Aging
Metformin featured article
Metformin is a drug commonly used to treat type 2 diabetes. It is the fourth most widely prescribed medication in the United States, with more than 80 million prescriptions for the drug written yearly. Metformin is in a class of drugs called biguanides, which impede liver gluconeogenesis (glucose production in the liver), thereby decreasing glucose uptake in the gut and increasing overall glucose utilization by improving insulin sensitivity in skeletal muscle and fat tissue. Multiple studies demonstrate that metformin reduces fasting blood glucose levels by as much as 3.9 mmol/L, corresponding to a nearly 2 percent decrease in HbA1c (a measure of long-term blood glucose control). Metformin is typically used in combination therapy incorporating dietary modification and other anti-diabetes drugs. Brand names of metformin sold in the United States include Glucophage, Glucophage XR, Fortamet, and Glumetza.
In recent decades, extensive research has focused on characterizing the...
Episodes
Dr. Rhonda Patrick discusses her supplement routine, Neu5Gc risks, Repatha and diabetes, heat stress, osteoporosis in men, and plyometrics.
In this clip, Dr. Rhonda Patrick discusses sauna benefits, VO2 max, HIIT, sulforaphane, and strategies to enhance cardiovascular health and longevity.
In this clip, Dr. Rhonda Patrick explores the causes of gray hair, its prevention, and potential remedies like exercise, supplements, and red light therapy.
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Dr. Rhonda Patrick discusses her supplement routine, Neu5Gc risks, Repatha and diabetes, heat stress, osteoporosis in men, and plyometrics.
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In this clip, Dr. Rhonda Patrick discusses sauna benefits, VO2 max, HIIT, sulforaphane, and strategies to enhance cardiovascular health and longevity.
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In this clip, Dr. Rhonda Patrick explores the causes of gray hair, its prevention, and potential remedies like exercise, supplements, and red light therapy.
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In this episode, we’re taking a deep dive into alcohol. We’ll explore the science, misconceptions, controversies, and health effects of this widely used drug.
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Dr. Levine details his research findings that show how a structured exercise regimen can reverse up to 20 years of heart aging.
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In this solo episode, I'm taking an in-depth look at magnesium – a critical yet frequently underestimated mineral in our health.
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In my keynote at LongevityFest 2023, I share powerful habits to delay aging and improve healthspan, presented at the American Academy of Anti-Aging Medicine.
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In this clip, Dr. Peter Attia reveals his personal pre-bed, sleep, diet, and exercise routines for optimal longevity.
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Dr. Peter Attia presents practical steps we can implement to improve our health, emphasizing the importance of each aspect while providing actionable advice.
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Dr. Rhonda Patrick describes strategies you can apply immediately to enhance your health and prevent chronic disease.
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In this clip, Dr. Martin Gibala weighs the risks vs. benefits of interval training across ages, highlighting its advantage over sedentary life.
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In this clip, Dr. Martin Gibala explains how vigorous activity activates both slow and fast-twitch muscles and the impact of aging on these fibers.
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In the clip, Dr. Gibala discusses high-intensity interval training's future, stressing translating research into public health applications.
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In this clip, Dr. Martin Gibala outlines the principle behind VILPA and discusses the ongoing research examining its potential impact on health and longevity.
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Dr. Martin Gibala discusses HIIT's health benefits and describes common HIIT protocols.
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Rhonda Aging Vitamin C Omega-3 Stem Cells Skin Sauna Protein Berberine Supplements Red Light TherapyDr. Rhonda Patrick explores growth hormone secretagogues, spermidine's longevity role, methylene blue, whey protein, and solutions for scar tissue in a Q&A.
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Rhonda Brain Diet Aging Hormones Omega-3 Fasting Memory Testosterone Dementia Development Skin CocoaDr. Rhonda Patrick explores taurine's longevity role, cocoa flavanols, training adaptations, and oral hyaluronic acid in a Q&A.
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In this clip, Dr. McGlory describes the mechanisms and implications of muscle disuse atrophy and the limitations of nutrition in combating this issue.
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In this clip, Dr. Axel Montagne discusses the potential of these emerging diagnostic tools in assessing an individual's risk of developing dementia.
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In this clip, Dr. Axel Montagne explains the damaging effects of chronic high blood pressure on the brain.
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In this clip, Dr. Axel Montagne discusses the feasibility of pursuing cyclophilin A, MMP9, or blood-brain barrier proteins to develop new Alzheimer's disease therapies.
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In this clip, Dr. Montagne discusses promising targets for protecting brain vessels to delay Alzheimer's.
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In this clip, Dr. Axel Montagne discusses how the brain transport of omega-3 DHA may be important for the prevention and possibly as a therapy for dementia.
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Many factors promote inflammation but reducing these factors in our lives will likely improve our aging.
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Dr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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Dr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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Dr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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Dr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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Dr. George Church discusses revolutionary technologies in the field of genetic engineering.
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Lifestyle factors and new technologies offer the promise of living longer, healthier lives, but is there a limit to the human lifespan? This episode explores the different theories supporting this hotly debated topic.
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In this clip, Dr. Stuart Phillips outlines steroid biochemistry and why he thinks testosterone boosters don't work.
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In this clip, Dr. Stuart Phillips describes how omega-3 fatty acids may contribute to slow age-related declines in muscle mass and strength.
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In this clip, Dr. Stuart Phillips discusses how growth hormone promotes collagen synthesis and how this might relate to muscle strength.
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In this clip, Dr. Stuart Phillips discusses whether it is important to distribute protein intake equally throughout the day.
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In this clip, Dr. Stuart Phillips describes how muscle mass and strength decline with age and outlines the importance to maintaining quality of life.
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In this clip, Dr. Stuart Phillips describes his current lifestyle to optimize health and longevity.
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In this clip, Dr. Stuart Phillips discusses whether plant-derived proteins can support hypertrophy.
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In this clip, Dr. Stuart Phillips discusses how building muscle reserves under adequate nutrition delays the disability threshold and contributes to more successful aging.
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In this clip, Dr. Stuart Phillips discusses creatine monohydrate and its effects on brain and muscle health.
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In this clip, Dr. Stuart Phillips discusses how heat stress promotes muscle health and reduces muscle loss.
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In this clip, Dr. Stuart Phillips discusses the implications of hormones in muscle mass growth and compares physiological to supraphysiological doses.
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In this clip, Dr. Stuart Phillips describes how muscle protein synthesis differs between young and older adults, and how the efficiency of protein use declines with age.
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In this clip, Dr. Stuart Phillips explains the importance of dietary protein quality and the role of the amino acid leucine in muscle protein synthesis.
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In this clip, Dr. Stuart Phillips discusses his concerns regarding the current protein recommended dietary allowances.
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In this clip, Dr. Stuart Phillips and Dr. Rhonda Patrick discuss the importance of building and maintaining muscle mass for longevity.
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Dr. Stuart Phillips discusses how exercise and nutrition influence skeletal muscle-protein turnover and muscle maintenance throughout the lifespan.
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In this clip, Dr. Levine shares the personal habits she's developed to slow the aging process including exercise, a plant-based diet, and time-restricted eating.
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In this clip, Drs. Patrick and Levine discuss the reliability of epigenetic age tests available to consumers.
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In this clip, Drs. Levine and Patrick discuss lifestyle factors that accelerate epigenetic aging including smoking cigarettes or having a low omega-3 index.
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In this clip, Drs. Levine and Patrick discuss the epigenetic changes that occur with age, including methylation of CpG sites.
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In this clip, Drs. Levine and Patrick discuss how genes that are important for embryonic development can tell us a lot about aging.
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Drs. Levine and Patrick discuss how and why individuals age at different rates and how menopause & obesity may increase an individual's rate of aging.
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In this clip, Drs. Levine and Patrick discuss the advantage of using epigenetic clocks in aging research to measure biological age.
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In this clip, Drs. Levine and Patrick discuss new advances in cellular aging research that show it's possible to reverse aging and generate new stem cells from already differentiated cells.
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In this clip, Drs. Levine and Patrick discuss definitions of aging used in science and why biological aging matters to scientists.
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In this clip, Drs. Levine and Patrick discuss genetic and environmental factors that can accelerate or slow epigenetic aging.
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Why "second generation" epigenetic clocks are better at detecting biological age | Dr. Morgan Levine ClipDr. Morgan Levine, describes the importance of this step in making her epigenetic clock PhenoAge and that of her postdoctoral mentor GrimAge more accurate in their ability to detect biological age and epigenetic age acceleration.
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In this clip, Dr. Dominic D'Agostino describes animal research that explores the mechanisms by which the ketogenic diet may benefit the brain.
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In this clip, Dr. Dominic D'Agostino discusses how ketones produced during fasting and ketosis protect against muscle loss.
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Dr. Morgan Levine discusses epigenetics and the application of epigenetic aging clocks in quantifying human aging.
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Fasting as Healthspan Maintenance, Relevance for Tissue Rejuvenation, Cancer & More | Rhonda Patrick ClipDr. Patrick explains some of the early evidence that suggests the value prolonged fasting (48+ hours) may have from the standpoint of tissue rejuvenation and healthspan maintenance, as well as relevance for other more specific conditions.
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In this clip, Dr. Valter Longo explains how certain macronutrients influence the insulin/IGF-1/growth hormone axis to modulate aging in many cell types.
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In this clip, Dr. Ronald Krauss discusses that in clinical practice, cholesterol particle size may be more relevant than the amount of cholesterol.
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In this clip, Bruce provides both an evolutionary and a molecular rationale for his theory.
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In this clip, Bruce Ames describes how folate is critical for the transferring of single-carbon groups between molecules.
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In this clip, Rhonda talks about the difference between vitamin K1 and K2.
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In this clip, Bruce Ames explains that recommended daily allowance (RDA) is set at two standard deviations above the estimated average requirement (EAR).
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In this clip, Bruce Ames explains that two carotenoids in the eye, lutein and zeaxanthin, are able to mitigate the harmful effects of singlet oxygen produced by sunlight.
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In this clip, Bruce Ames explains how vitamin D functions as both a vitamin and a hormone.
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In this clip, Bruce Ames says that although he eats a very healthy diet, he still takes a vitamin D supplement.
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In this clip, Bruce Ames emphasizes the importance of proper nutrition for prevention of diseases.
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In this clip, Dr. Krauss discusses the indications for the ion mobility test.
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In this clip, Rich Roll and Dr. Rhonda Patrick discuss how IGF-1 levels impact cancer risk.
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In this clip, Dr. Mark Mattson describes how ketone esters may improve brain health.
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In this clip, Dr. Mark Mattson discusses the importance of maintaining muscle mass during aging.
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Discussions on fasting, beta hydroxybutyrate & the fasting mimicking diet | Dr. Darya & Kevin Rose ClipIn this video, Dr. Darya & Kevin Rose talk about fasting, beta-hydroxybutyrate and the fasting-mimicking diet.
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Dr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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Dr. Peter Diamandis and Tony Robbins discuss the application of precision medicine and health technologies in slowing human aging.
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Rhonda Aging Breast Cancer Omega-3 Probiotics Coffee Vitamin B12 Vaccine Vitamin K Skin Sulforaphane Sauna Time-Restricted Eating Protein COVID-19 NAD+ Moringa SupplementsDr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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In this clip, Dr. Bill Harris highlights a novel area of research — the role omega-3s play in altering red blood cell biology.
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In this clip, Dr. Bill Harris discusses the impact omega-3 levels have on the risk of death from cardiovascular disease, cancer, and other diseases.
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Omega-3 Brain Aging Heart Disease Biomarkers Inflammation Immune System Pregnancy Mortality Polyunsaturated FatDr. Bill Harris discusses the roles that omega-3 fatty acids play in cardiovascular and neurocognitive health.
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Rhonda Vitamin D Aging Omega-3 Fasting Immune System Antioxidant Protein COVID-19 Moringa Supplements Ketogenic DietDr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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Compared to people with the lowest blood concentrations of EPA and DHA (combined), those with the highest blood concentrations were as much as 17 percent less likely to die from all causes of premature death.
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In this clip, Dr. Michael Snyder discusses how people age in distinct ways and at varying rates and how knowing our "ageotype" might offer targets for preventing age-related diseases.
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Genetics plays an important role in longevity, but there is also a strong lifestyle component. Dr. Snyder's research, using deep molecular measurements, indicates that when you exercise, a profound molecular change occurs — particularly when it comes to immune molecules.
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Rhonda Exercise Aging Vitamin C Omega-3 Stem Cells Fasting Magnesium Vitamin E Vaccine Vitamin K Allergies Resveratrol Sauna Time-Restricted Eating Blood Sugar Breast MilkDr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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In this clip, Dr. Steve Horvath describes research suggesting that caloric restriction, especially when it is reversing obesity or metabolic syndrome, may slow epigenetic aging.
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In this clip, Dr. Steve Horvath discusses whether epigenetic clocks play causal roles in aging.
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Methylation and demethylation are critical processes in development and interfering with the enzymes that carry out these two opposing processes can play critical roles in epigenetic age.
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Some epigenetic clock evidence reinforces the idea that accelerated aging may be a consequence of chronic inflammation.
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A study using a mouse model of premature aging showed that short-term expression of four special factors which reverse epigenetic age ameliorated cellular and physiological hallmarks of aging and prolonged lifespan.
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Scientists have observed that the epigenetic clock of transplanted cells and their descendant lineages synchronize with the donor rather than the recipient, a fascinating phenomenon that offers promise for the idea of rejuvenation in humans.
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Conventional health advice, such as healthy eating, physical activity, and education level are linked with slowed epigenetic aging, albeit weakly, and obesity, sleep deprivation, and smoking are linked with accelerated epigenetic aging.
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In this clip, Dr. Steve Horvath discusses how epigenetic aging differs from senescence-mediated aging.
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The DNAm GrimAge epigenetic clock may be a more reliable predictor of healthspan and lifespan than traditional hallmarks of aging like telomeres.
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How epigenetic predictions align with onset of cancer, Parkinson's and Alzheimer's | Steve Horvath ClipA person's epigenetic age correlates with their risk for developing major diseases of aging like cancer, Alzheimer's disease, and Parkinson's.
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The stability of methylation patterns on DNA samples means the data can be trusted more in the lab when investigating anti-aging interventions.
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The GrimAge clock (named for the Grim Reaper) predicts lifespan and healthspan in units of years and tests whether potential lifestyle interventions may slow or reverse biological aging.
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Horvath epigenetic aging clocks measure two types of age: biological aging vs. chronological aging ClipIn this clip, Dr. Steve Horvath explains the differences between chronological age and biological age.
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Sometimes a person's clinical biomarkers doesn't accurately reflect how well they are aging, but epigenetic clocks may give a more reliable insight into their aging.
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Evidence indicates that the heritability of epigenetic aging is about 40 percent. This is seen in supercentenarians and their offspring, who tend to age slower than their younger counterparts.
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Emerging evidence now suggests that supplemental omega-3 fatty acids or vitamin D slow epigenetic aging.
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Dr. Steve Horvath discusses epigenetic aging clocks and their use in predicting biological aging and healthspan.
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Dr. Steve Horvath found a way to measure biological aging – a type of "clock" – based on the methylation pattern of an organism's genome. This video primer explains the basics of epigenetic clocks, the topic of our interview with Dr. Steve Horvath.
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Rhonda Exercise Aging Sleep Telomeres Vitamin C Cholesterol Omega-3 DNA Damage Fasting Coffee Magnesium Eyes Calcium Time-Restricted Eating Breast Milk Moringa LactateDr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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In this clip, Dr. Giselle Petzinger describes her recommended components for an exercise program for people with Parkinson's disease.
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In this clip, Dr. Giselle Petzinger discusses how intense exercise can impact motor scores in people with Parkinson's disease.
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Dr. Giselle Petzinger discusses new findings in Parkinson's disease research, emphasizing exercise's role in delaying disease progression.
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In this clip, Dr. Rhonda Patrick discusses DHA bioavailability and describes her personal DHA regimen, which includes dietary and supplemental sources of omega-3 fatty acids.
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Sulforaphane increases brain glutathione: relevance in autism, TBI, brain aging | Rhonda Patrick ClipIn this clip, Dr. Rhonda Patrick describes advances in sulforaphane research that are particularly relevant to the brain.
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In this clip, Dr. Rhonda Patrick talks about the importance of obtaining adequate magnesium in the diet.
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Should healthy people take metformin? (benefits vs. negative exercise effects) | Rhonda Patrick ClipIn this clip, Dr. Rhonda Patrick gives her thoughts on whether healthy, active adults should take metformin.
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Dr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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In this clip, Tim Ferriss and Dr. Rhonda Patrick discuss the anti-cancer properties of the diabetes drug metformin.
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In this clip, Tim Ferriss outlines the biomarkers that he measures routinely to make sure his health is on-track while following a ketogenic diet
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Rhonda Vitamin D Brain Cancer Epigenetics Aging Hormones Diabetes Vitamin C Antibiotics Vitamin K Sulforaphane Sauna Glutathione Oxidative Stress NAD+ CardiovascularDr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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In this clip, Dr. Ray Cronise discusses his approach to choosing a diet to optimize healthspan.
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In this clip, Dr. Peter Attia discusses the role of the APOE4 gene variant and the associated risk for Alzheimer’s disease and cardiovascular disease.
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In this clip, Dr. Peter Attia and Dr. Rhonda Patrick discuss how a healthy digestive tract interacts with the immune system to curb inflammation.
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In this clip, Dr. Peter Attia describes his empirical strategy to obtain a personalized nutrition plan for longevity.
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In this clip, Dr. Peter Attia explains the complex relationship that exists between cancer cells, the immune system, and IGF-1.
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In this clip, Dr. Peter Attia explains the interrelated mTOR and IGF-1 growth pathways and the delicate balance required to limit accelerated aging.
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In this clip, Dr. Peter Attia explains the challenges involved in studying how diet and lifestyle affect longevity in humans.
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Rhonda explains NAD+: importance for aging, decline with age, boosters (nicotinamide riboside, nicotinamide mononucleotide), and data in animals and humans.
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Dr. Jed Fahey discusses the beneficial effects broccoli sprouts have in mediating the harmful effects of _H. pylori_.
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Dr. Jed Fahey describes the beneficial effects of sulforaphane in modulating the symptoms of autism and other brain disorders.
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Dr. Jed Fahey describes the current state of the science of understanding how sulforaphane influences longevity.
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Rhonda Nutrition Cancer Diet Aging Performance Omega-3 Fasting Magnesium Drug Sulforaphane Sauna NRF2Dr. Rhonda Patrick on Kevin Rose Show: metformin, magnesium L-threonate, fish oil, brain health, sulforaphane, goitrogenic activity, sauna, and more.
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In this clip, Dr. David Sinclair elaborates on his Informational Theory of Aging.
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In this clip, Dr. David Sinclair and Dr. Rhonda Patrick discuss the brain health benefits associated with NAD+ boosters.
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Resveratrol has positive impact on brain health & Alzheimer’s disease prevention | David Sinclair ClipIn this clip, Dr. David Sinclair and Dr. Rhonda Patrick discuss the brain health benefits associated with resveratrol.
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In this clip, Dr. David Sinclair identifies some of the practical considerations of resveratrol supplementation and discusses his personal use of the compound.
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In this clip, Dr. David Sinclair describes his personal sleep habits for optimal performance during his workday.
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In this clip, Dr. Rhonda Patrick describes her personal experience with sleep deprivation and her subsequent altered metabolism.
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In this clip, Dr. David Sinclair describes his personal resveratrol and nicotinamide mononucleotide supplementation habits.
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In this clip, Dr. David Sinclair discusses the economic issues associated with research using nicotinamide riboside and nicotinamide mononucleotide.
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In this clip, Dr. David Sinclair discusses the current state of research on nicotinamide mononucleotide.
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In this clip, Dr. David Sinclair discusses the stability issues encountered with nicotinamide riboside and nicotinamide mononucleotide.
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Nicotinamide Riboside vs. Nicotinamide Mononucleotide - dosing and effects on NAD+ | David Sinclair ClipIn this clip, Dr. David Sinclair discusses the current state of research on the NAD+ boosters nicotinamide riboside and nicotinamide mononucleotide.
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In this clip, Dr. David Sinclair identifies some of the practical considerations of resveratrol supplementation and discusses his personal use of the compound.
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In this clip, Dr. David Sinclair describes research demonstrating the beneficial effects of resveratrol on the cardiovascular system of monkeys.
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In this clip, Dr. David Sinclair describes how plant-based compounds activate cellular protective mechanisms in humans.
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In this clip, Dr. David Sinclair describes the NAD+ salvage pathway and how boosting cellular NAD+ levels may be beneficial in slowing aging.
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In this clip, Dr. Rhonda Patrick describes a study in which stem cell-derived retinal cells were used to treat macular degeneration in a human.
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In this clip, Dr. David Sinclair talks about the discovery of genes that can reset the Horvath epigenetic clock.
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In this clip, Dr. David Sinclair describes how epigenomic modifications can influence how an organism ages, potentially reversing years of age-related damage.
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In this clip, Dr. David Sinclair explains why NAD+ levels decrease with age.
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In this clip, Dr. David Sinclair describes the links between NAD+, sirtuins, and resveratrol in the aging process.
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In this clip, Dr. David Sinclair describes the role of NAD+ in the regulation of the body's circadian clock and sirtuin production.
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The link between sirtuins, calorie restriction, fasting, and the insulin pathway | David Sinclair ClipIn this clip, Dr. David Sinclair describes how sirtuins, caloric restriction, fasting, and the insulin-IGF-1 pathway converge to modulate aging and lifespan.
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In this clip, Dr. David Sinclair describes the major breakthroughs in aging research and the unique relationships that develop between researchers and the organisms they study.
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Dr. David Sinclair on Informational Theory of Aging, Nicotinamide Mononucleotide, Resveratrol & MoreDr. David Sinclair discusses the mechanisms that drive human aging and the importance of identifying ways to slow or reverse aging's effects.
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In this clip, Dr. Valter Longo describes the origins of the fasting-mimicking diet and explains how it enhances chemotherapeutic treatments.
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In this clip, Dr. Valter Longo describes the IGF-1 pathway and explains how defects in the pathway influence disease risk.
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Sauna use boosts lifespan and overall health supported by compelling data from observational, interventional, and mechanistic studies.
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Dr. Valter Longo defines the different fasting modalities, and compares and contrasts the variations of each in duration and degree of restrictiveness.
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Dr. Valter Longo explains how certain macronutrients influence the insulin/IGF-1/growth hormone axis to modulate aging in many cell types.
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Dr. Longo describes the promising research that suggests that one's risk for diseases over the next 10 years may be drastically reduced.
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Dr. Valter Longo highlights which biomarkers, both currently available and forthcoming, that he considers relevant when assessing longevity and biological age.
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Dr. Valter Longo discusses his new book "The Longevity Diet" and how his fasting-mimicking diet can treat or prevent several age-related diseases.
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Dr. Elissa Epel discusses potential concerns about supplementation and describes some of the studies that demonstrate the links between healthy lifestyle behaviors.
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Dr. Rhonda Patrick describes the dual nature of biochemical pathways involved in aging and explains how exercise tips the balance toward its beneficial properties.
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Drs. Rhonda Patrick and Jari Laukkanen discuss the benefits of sauna use in terms of cardiorespiratory fitness and mood.
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Drs. Rhonda Patrick and Jari Laukkanen discuss findings from a study linking sauna use and lower risk of death from cardiovascular disease.
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Dr. Eric Verdin describes the liver's functions and proposes that the ketogenic diet does not put any undue stress on the liver.
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Dr. Eric Verdin discusses several ways in which NAD+ supplementation can benefit mitochondrial health and play a protective role against aging.
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Dr. Eric Verdin explains how nicotinamide adenine dinucleotide levels diminish with age along with the ongoing research to understand the reasons why.
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Dr. Eric Verdin describes the emerging field of biomarkers of aging and the diverse strategies, including artificial intellegence, that are being employed.
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Dr. Eric Verdin discusses the idea that increasing protein levels too high while on a ketogenic diet may have adverse health effects.
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Dr. Eric Verdin describes how supplementing with exogenous ketone esters may confer some of the beneficial effects of the ketogenic diet.
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Dr. Eric Verdin discusses the role of beta-hydroxybutyrate in protecting against oxidative stress, both as a nutrient, but also as a transcription regulator.
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Dr. Eric Verdin explains how a cyclic or the portion-controlled ketogenic diet is linked to improvements in lifespan and memory in mice.
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Plausible mechanisms by which intermittent fasting may be effective against aging | Eric Verdin ClipDr. Eric Verdin describes how fasting or a fasting-mimicking diet can influence healthspan and lifespan including discussion of some of the potential mechanisms.
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Dr. Eric Verdin explains the importance of the insulin signaling pathway in aging and highlights both animal and human research in this area.
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Dr. Eric Verdin explains how exercise and nutrition form the cornerstone of strategies to slow aging, but exciting approaches are ahead.
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The longevity advantage of genetic deficiencies in growth hormone/IGF-1 signaling | Valter Longo ClipDr. Valter Longo discusses the longevity-conferring effects of diminishing the pro-aging IGF-1 pathway.
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IGF-1 plays a key role in the regenerative processes activated by prolonged fasting | Valter Longo ClipDr. Rhonda Patrick and Dr. Valter Longo discuss how IGF-1 is involved in the regenerative aspect of the two phases of fasting and refeeding.
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Dr. Valter Longo discusses the origin of the fasting-mimicking diet and a possible shift from a drug-centered mentality to one which allows the body to heal itself.
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Reversing immunosenescence — lymphocytes return to youthful levels after fasting (adaptive immunity) ClipDr. Valter Longo describes how fasting promotes the immune system to return to a more youthful profile.
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Dr. Valter Longo describes how a fasting-mimicking diet can reduce markers of inflammation, resetting our biological systems to a more youthful state.
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Dr. Valter Longo describes how prolonged fasting and subsequent refeeding, sends signals to the body to systematically shrink and rebuild organ systems.
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Dr. Valter Longo explains the benefits of a prolonged fast.
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Dr. Guido Kroemer describes how intermittent fasting recapitulates the life-extension benefits of caloric restriction without some of the drawbacks.
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Caloric Restriction Mimetics in Aging, Improved Cancer Chemotherapy, Autophagy Anti-Obesity Effect ClipDr. Guido Kroemer describes the autophagy-inducing effects of calorie restriction mimetics such as spermidine and resveratrol.
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Dr. Rhonda Patrick describes how bright light exposure drives cortisol release.
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Dr. Dale Bredesen identifies the defining characteristics of Alzheimer’s disease and enumerates its known subtypes.
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Dr. Dale Bredesen describes his novel dietary protocol, the Ketoflex 12/3, and how it improves cognitive function.
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Dr. Dale Bredesen discusses the potential brain-health benefits associated with a ketogenic diet.
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Circadian regulation of sleep leads to better health outcomes in infants and elderly | Matt Walker ClipDr. Matthew Walker explains how altering light-dark schedules can improve health outcomes in older adults and babies.
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Dr. Matthew Walker talks about the importance of identifying early-life windows of vulnerability to prevent or delay age-related cognitive decline.
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Dr. Matthew Walker describes how the different stages of sleep influence emotional and cardiovascular health.
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Dr. Elissa Epel describes how pre-pregnancy parental health impacts offspring.
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Dr. Elissa Epel describes the effects of longer sperm telomere length on subsequent generations.
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Dr. Elissa Epel describes how even small lifestyle changes can have an effect on telomere length and healthy aging to compress morbidity.
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Dr. Rhonda Patrick and Dr. Elissa Epel discuss how obesity affects genes in sperm DNA involved in metabolic health and cognitive function.
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Dr. Elissa Epel discusses the pros and cons associated with taking dietary supplements to lengthen telomeres.
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Dr. Elissa Epel discusses how cancer cells exploit the regenerative capacity of telomerase to perpetually divide, essentially becoming immortal.
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Dr. Elissa Epel discusses the harmful effects of what she calls a "toxic lifestyle," one that includes the consumption of sugar-sweetened beverages.
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Dr. Elissa Epel describes some of the studies that demonstrate the links between healthy lifestyle behaviors like exercise and discusses potential mechanisms.
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Dr. Elissa Epel describes the "low hanging fruit" – small, healthy lifestyle behaviors – that can have positive effects on telomere length and lifespan.
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Dr. Elissa Epel identifies some of the key differences in male and female biology and how they influence telomere length and aging.
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Telomeres explained: role in genomic stability, stem cells, replicative senescence | Elissa Epel ClipDr. Elissa Epel gives a brief overview of telomeres and the enzyme telomerase and explains how they impact health and lifespan.
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Dr. Elissa Epel discusses the importance of having an optimal ratio of telomerase to reduce the risk of chronic diseases and cancer.
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Dr. Elissa Epel explains how aging syndromes can be passed to offspring via epigenetic mechanisms.
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Dr. Elissa Epel describes how Mendelian randomization techniques provide insights into the dual nature of telomeres, as both a cause and a sign of aging.
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Dr. Elissa Epel describes how toxic stress modulates telomere length.
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Dr. Elissa Epel describes the beneficial effects of education on telomere length in the babies of low-income women.
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Dr. Elissa Epel describes the non-linear effects of exercise on telomere length.
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Dr. Elissa Epel discusses the mechanisms of healthy aging and the associations between stress, telomere length, addiction, eating, and metabolic health.
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Sleep Brain Alzheimer's Cancer Obesity Aging Performance Depression Immune System Stress Circadian Rhythm Behavior DementiaDr. Matthew Walker discusses the role of sleep in immunity, creativity, and aging.
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This episode features a Q&A session on fasting-related topics with Dr. Rhonda Patrick and Mike Maser of Zero Fasting Tracker.
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Dr. Dale Bredesen discusses treatments that may reverse symptoms of mild cognitive decline and Alzheimer’s disease.
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Dr. Valter Longo on Resetting Autoimmunity and Rejuvenating Systems with Prolonged Fasting & the FMDFasting Cancer Obesity Aging Heart Disease Diabetes Insulin Resistance Inflammation Stem Cells Immune System Tissue Repair Autophagy Apoptosis Insulin AutoimmunityDr. Valter Longo discusses fasting as a means to treat or prevent age-related diseases such as cancer, Alzheimer’s disease, and others.
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Rhonda Nutrition Exercise Alzheimer's Aging Fasting Memory Genetics Mortality Sauna Time-Restricted Eating Cardiovascular Supplements Ketogenic DietDr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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Dr. Rhonda Patrick makes her seventh appearance on the Joe Rogan Experience.
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Dr. Eric M. Verdin discusses the roles of the ketogenic diet, beta-hydroxybutyrate, HDAC inhibitors, NAD+, and more in the context of aging.
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Epigenetics Vitamin D Nutrition Exercise Aging Metabolism Sleep Diabetes Telomeres DNA Damage Stem Cells Stress Melatonin Vitamin E Genetics 23andMe Heat Stress Autophagy Autism Folate Sauna AntioxidantOur genes influence the way we absorb and metabolize micronutrients. Nutrigenomics looks at the influence genetic variation has over micronutrient absorption/metabolism and the biological consequences of this dynamic relationship.
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Dr. Rhonda Patrick talks about transgenerational effects of caloric restriction on longevity, B-vitamins silencing bad genes, cognitive stimulation reversing neurodegenerative disease, exercise increases neurogenesis, and ways in which vitamin D might influence aging.
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Aging Nutrition Cancer Podcast Fasting Multiple Sclerosis Autophagy Video Triglycerides Fatty Liver Time-Restricted Eating ProteinDr. Guido Kroemer discusses immunology, cancer biology, calorie-restriction mimetics, aging, and autophagy.
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Heat Stress Alzheimer's Aging Heart Disease Podcast Video Blood Pressure Protein Aerobic CardiovascularDr. Jari Laukkanen discusses the role of heat stress in the prevention of cardiovascular & Alzheimer’s disease.
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Dr. Judith Campisi discusses the role of cellular senescence in the aging process and the development of cancer.
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Dr. Gordon Lithgow discusses the roles of protein aggregation, iron overload, and others in the aging process.
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Science on refined sugar: mortality, aging, brain function, memory, neuroinflammation, cancer, sex hormones, addiction & more.
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Sulforaphane Brain Cancer Aging Heart Disease Insulin Resistance Inflammation Depression Behavior Mental Health Autism Mortality NRF2This podcast is about one of the most important biological pathways you could possibly take the time to learn about: the NRF2 pathway.
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Dr. Valter Longo discusses the role of fasting and the fasting-mimicking diet in longevity, cancer & multiple sclerosis.
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A modest change on the "micronutrient smoothie" that also talks about the beneficial compounds that don't qualify as micronutrients.
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Ray Cronise discusses the roles that cold stress, intermittent fasting, and weight loss play in human healthspan.
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Performance Brain Alzheimer's Cancer Gut Aging Ketosis Insulin Resistance Podcast Cholesterol Inflammation Immune System InsulinDr. Peter Attia discusses dietary strategies to promote longevity and optimal performance.
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Dr. Patrick's keynote lecture at MBOG Congres 2015 in the Netherlands covers micronutrient inadequacy and Dr. Bruce Ames' triage theory.
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Heat Stress Exercise Brain Aging Performance Heart Disease Depression Memory Anxiety Cold Stress MortalityThis episode is a presentation Dr. Rhonda Patrick delivered at the Biohacker Summit in Helsinki, Finland in 2016.
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Dr. Ronald Krauss discusses the role that LDL cholesterol plays in heart disease, dyslipidemia, and atherosclerosis.
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Rhonda explains chronic stress's impact on brain, gut, immune system, and aging. Meditation buffers and improves cognitive and biological aging.
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Dr. Aubrey de Grey discusses technologies that can repair the various types of damage that occur during the aging process.
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Obesity Nutrition Aging Heart Disease Insulin Resistance Cholesterol Inflammation Magnesium Vitamin K SeleniumDr. Bruce Ames discusses the CHORI Bar, a micronutrient- and fiber-dense nutrition bar developed in the Ames laboratory to manage obesity.
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In this video, Dr. Rhonda Patrick summarizes a recent study that found that frequency of sauna use was associated with increased decreased risk of death. Using the sauna 2-3 times per week was associated with 24% lower all-cause mortality and 4-7 times per week decreased all-cause mortality by 40%.
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Dr. Bruce Ames discusses his triage theory.
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Dr. Rhonda Patrick is on The Tim Ferriss Show in episode #12 entitled "Rhonda Patrick on Life Extension, Performance, and More".
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Dr. Rhonda Patrick makes her second appearance on the Joe Rogan Experience.
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Sauna Exercise Brain Aging Hormones Performance Insulin Resistance Depression Stress Heat Stress MuscleDr. Rhonda Patrick discusses how conditioning the body to heat stress through sauna use, called "hyperthermic conditioning" may cause adaptations that increase athletic endurance (by increasing plasma volume and blood flow to heart and muscles) and potentially even muscle mass.
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Dr. Rhonda Patrick makes her first appearance on the Joe Rogan Experience.
Topic Pages
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Aerobic exercise
Aerobic exercise mitigates aging by promoting mitochondrial biogenesis, enhancing telomerase activity, preserving proteostasis, and suppressing chronic inflammation.
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Age-related decline of muscle power (powerpenia)
Aging precipitates powerpenia by inducing type II fiber atrophy, motor-unit remodeling, mitochondrial dysfunction, and slowed excitation–contraction kinetics.
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Autophagy
With aging, mTOR-driven suppression of autophagy accumulates cellular damage, whereas autophagy activation extends lifespan by enhanced clearance.
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Berberine
Inhibiting mitochondrial respiratory complex I, berberine raises AMP/ATP ratio, activates AMPK, suppresses mTOR, enhancing autophagy and attenuating cellular aging.
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Beta-hydroxybutyrate
Beta-hydroxybutyrate inhibits class I HDACs and activates HCAR2, enhancing autophagy and oxidative-stress defenses, slowing cellular senescence.
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Caloric restriction
Caloric restriction retards organismal aging by attenuating IIS–mTOR signaling, augmenting autophagy, mitochondrial efficiency, and genomic maintenance.
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Creatine
Aging diminishes skeletal-muscle phosphocreatine availability; creatine supplementation restores ATP buffering, partially mitigating age-related bioenergetic decline.
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Epigenetic aging clocks
Epigenetic aging clocks are high-dimensional biomarkers reflecting systematic age-associated DNA methylation drift, without proven causal impact on aging.
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Fasting
Intermittent fasting lowers insulin/IGF-1 and mTOR signaling, enhances AMPK-driven autophagy, thus delaying systemic organismal aging.
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FOXO
Reduced insulin/IGF signaling during aging activates FOXO transcription factors that upregulate stress-resistance, autophagy and metabolic genes, prolonging lifespan.
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Hallmarks of aging
Aging results from cumulative, interdependent hallmarks—genomic instability, telomere erosion, epigenetic drift, proteostasis failure, mitochondrial dysfunction, cellular senescence—driving physiological decline.
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Hydrolyzed collagen
Orally absorbed hydrolyzed collagen peptides activate fibroblast receptors and downregulate matrix metalloproteinases, partially counteracting age-related dermal collagen loss.
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Metformin
Metformin activates AMPK and inhibits mitochondrial complex I–mTOR signaling, attenuating nutrient-sensing pathways mechanistically implicated in cellular aging.
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NAD+
Aging-associated NAD+ decline diminishes sirtuin-mediated deacetylation and PARP-dependent DNA repair, exacerbating mitochondrial dysfunction and cellular senescence.
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Nicotinamide mononucleotide
Nicotinamide mononucleotide replenishes age-related NAD⁺ decline, thereby modulating sirtuin-dependent mitochondrial function and DNA repair pathways.
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Nicotinamide riboside
Preclinically, nicotinamide riboside replenishes age-related NAD⁺ loss, activating sirtuin-mediated mitochondrial and genomic maintenance pathways.
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Omega-3 fatty acids
Omega-3 fatty acids modulate aging by attenuating inflammaging through specialized pro-resolving mediators, preserving telomeres, and improving mitochondrial membrane fluidity.
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Quercetin
Quercetin acts as a senolytic by suppressing PI3K/AKT and activating caspase-dependent apoptosis in senescent cells, attenuating age-related pathology.
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Rapamycin
Rapamycin alleviates aging phenotypes by inhibiting mTORC1 signaling, suppressing anabolic translation, and promoting autophagy-mediated cellular maintenance.
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Salmon roe
Salmon roe comprises lipid-rich oocytes containing omega-3 fatty acids, bioavailable proteins, phospholipids, vitamins A, D, E, and astaxanthin.
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Sauna
Repeated sauna heat stress induces heat-shock protein–dependent hormesis that may attenuate cellular senescence and systemic aging processes.
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Senescence
Aging entails progressive accumulation of senescent cells whose SASP-mediated paracrine effects promote tissue dysfunction and systemic decline.
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Sirtuins
Sirtuins are NAD⁺-dependent deacylases that sense cellular redox state, deacetylate targets, enhance genome stability, and delay aging.
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Toll-like receptors
Aging skews Toll-like receptor expression and NF-κB signaling, amplifying sterile proinflammatory cytokine production that drives inflammaging.
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Vitamin D
Aging decreases epidermal 7-dehydrocholesterol and renal 1α-hydroxylase, impairing vitamin D synthesis and accelerating immunosenescence.
News & Publications
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Consistency in daily activity rhythms can enhance cardiorespiratory fitness and walking efficiency up to 20% in older adults. pubmed.ncbi.nlm.nih.gov
A consistent daily schedule may do more than support sleep—it could also help maintain physical fitness as we age. Robust evidence suggests that disruptions in circadian rhythms, such as those caused by shift work or jet lag, are linked to poorer health outcomes. A recent study found that older adults with more regular daily activity patterns had better cardiorespiratory fitness and walked more efficiently than those with inconsistent routines.
Researchers analyzed data from nearly 800 older adults (average age 76) who wore wrist devices that continuously monitored their movement. They measured how active each person was during the day compared to nighttime rest, identified the time of day when each person was most active, and determined the consistency of these patterns from day to day. The researchers then examined how activity rhythms were related to peak oxygen uptake (a measure of cardiorespiratory fitness) and the energy required to walk at different speeds, while accounting for factors such as age, sex, race, height, and chronic health conditions.
Older adults who showed the greatest difference between daytime activity and nighttime rest had up to 20% better cardiorespiratory fitness and increased walking efficiency. Earlier times of peak activity were also associated with improved outcomes. Additionally, those who reached their peak activity at the same time each day tended to perform more effectively. These patterns encompassed all types of daily movement—including walking, cleaning, gardening, and shopping—not just formal exercise.
These findings suggest that consistent, rhythmic activity patterns play a crucial role in maintaining physical function and health as we age. Learn more about developing an early circadian pattern in this clip featuring Dr. Satchin Panda.
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Aging compromises muscle strength and bone density, altering the signaling pathways that coordinate their function. These pathways involve myokines—hormone-like proteins released by muscle during exercise that help regulate metabolism, enhance muscle performance, and support bone formation. A recent study found that levels of a myokine called cardiotrophin-like cytokine factor 1 decline sharply with age but rise by nearly 70% following resistance exercise in both humans and mice.
Researchers measured cardiotrophin-like cytokine factor 1 levels in muscle and blood samples from young and older adults before and after single and long-term resistance training sessions. In younger participants, a single session triggered a sharp rise in cardiotrophin-like cytokine factor 1 levels. In older adults, however, levels only increased after 12 weeks of consistent training. The researchers linked this diminished response to a decline in cytokine receptor-like factor 1, a companion protein required for the myokine’s release.
Then they restored cardiotrophin-like cytokine factor 1 levels in older mice and found that muscle strength, glucose tolerance, and mitochondrial activity improved. Bone density also increased as the myokine reduced bone-resorbing cells and boosted bone-forming cells. Blocking the myokine prevented these exercise benefits, confirming its essential role in maintaining musculoskeletal health.
These findings suggest that aging limits the body’s ability to produce key exercise-related proteins, potentially explaining why older adults respond more slowly to training. However, regular training counters these effects. Dietary protein intake influences the body’s response to training, too. Learn more in this clip featuring Dr. Stuart Phillips.
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The glymphatic system—the brain’s waste clearance network—uses cerebrospinal fluid to flush out toxic metabolic byproducts, including amyloid-beta, tau, and other protein aggregates. This clearance process plays a critical role in maintaining brain health and may help protect against neurodegenerative diseases, such as Alzheimer’s. A recent study in mice found that a network of lymphatic vessels in the neck aids glymphatic waste removal, and this system can be enhanced using a gentle, non-invasive technique.
Researchers viewed the lymphatic vessel function of mice using fluorescent tracers. They tracked how cerebrospinal fluid drained from spaces around the brain into lymphatic vessels near the base of the skull and then flowed through tissues near the eyes, nose, and mouth into superficial lymphatic vessels in the neck. Then, using a small mechanical device, they gently compressed the animals' skin in three areas: from around the eyes down to the jaw; from the side of the nose down to the jaw; and along specific lymphatic vessels leading to a lymph node under the jaw.
They found that about half of the cerebrospinal fluid outflow to the neck passed through the superficial lymphatic vessels. Older mice had fewer lymphatic vessels near the nose and roof of the mouth and exhibited reduced cerebrospinal fluid clearance. However, the lymphatics in the neck remained structurally intact and responsive to stimulation. When they applied the mechanical device to the skin, cerebrospinal outflow doubled, even in aged mice.
These findings suggest that poor glymphatic waste clearance in aging may be reversible by stimulating functional lymphatic vessels in the face. If this approach works in humans, it could offer a simple, noninvasive strategy to support brain health and reduce the risk of neurodegenerative disease. Deep sleep also promotes glymphatic clearance. Learn more in this clip featuring Dr. Matt Walker.
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Age-related macular degeneration, the leading cause of irreversible blindness in older adults, affects nearly 200 million people worldwide. This progressive disease erodes central vision, which is critical for reading, driving, and other daily activities. A recent study found that glucagon-like peptide-1 (GLP-1) receptor agonists, such as Ozempic, Wegovy, or others, may double the risk of developing neovascular age-related macular degeneration, the most serious form of the disease.
Researchers analyzed health records from more than 1.1 million people in Ontario, Canada, who had diabetes and were 66 or older. They created a matched study group of about 139,000 people, comparing those who used GLP-1 receptor agonists for at least six months to similar patients who didn’t use the drugs. The researchers tracked new cases of neovascular age-related macular degeneration over three years.
They found that people who used GLP-1 receptor agonists were more than twice as likely to develop neovascular age-related macular degeneration than those who didn’t use the drugs. About 0.2% (93) of the users developed the condition, compared to 0.1% (88) of non-users. Even after accounting for other risk factors, the difference remained consistent.
These findings suggest that while GLP-1 receptor agonists provide considerable health benefits, they may also pose an overlooked risk for serious vision problems. It’s noteworthy that diabetes is an independent risk factor for macular degeneration, and this study identified associations, not a cause-and-effect relationship. Learn more about GLP-1 drugs in Aliquot #128: The Expanding Role of Weight Loss Drugs
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Struggling to lift 5 kilograms (11 pounds)—the weight of a small dog or a full backpack—could indicate more than just aging. It might also be an early warning signal for declining health. A recent study found that this simple measure could help identify older adults at a greater risk of developing severe medical conditions.
Researchers tracked more than 51,000 people aged 50 and older across 15 European and Middle Eastern countries for up to five years. They used data from the Survey of Health, Ageing, and Retirement in Europe, which collected information on physical function, health status, and quality of life. They asked each participant a straightforward question: Do you have difficulty lifting 5 kilograms?
At the beginning of the study, nearly one in five participants reported difficulty lifting 5 kilograms. Over the next four years, these people were 9% more likely to report a lower quality of life, 8% more likely to develop depression, and 7% more likely to have poor handgrip strength. They also experienced mild to moderate increases in risk for conditions such as osteoarthritis, rheumatoid arthritis, diabetes, stroke, and Alzheimer’s disease. These effects were more pronounced in men than in women.
These findings suggest that a simple question about lifting something as ordinary as a grocery bag or a full laundry basket could present a practical, affordable method for identifying muscle weakness and flagging potential health issues, with no clinic or special equipment necessary. Power training can boost strength and improve functional movement, even for older adults. Learn more in this clip featuring Dr. Brad Schoenfeld.
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Compounds derived from cruciferous vegetables may influence not only disease prevention but also the fundamental processes of aging. A recent roundworm study found that sulforaphane, a bioactive compound derived from broccoli, extended lifespan by more than 50%, but only when taken early in life.
Scientists administered varying doses of sulforaphane to roundworms (a robust aging model) throughout different stages of their lives. They also monitored changes in gene activity over time to create an “aging clock” based on transcription patterns—essentially a readout of the worms' biological age determined by which genes were activated or deactivated.
The worms that received sulforaphane early in life lived considerably longer—more than 50% longer at the most effective dose—than untreated worms. The aging clock also showed that these worms appeared to be about 20% younger, biologically speaking, than untreated worms of the same chronological age. The most notable shifts in gene activity involved detoxification and stress-response pathways, suggesting that sulforaphane triggers system-wide protective responses early in life.
These findings suggest that sulforaphane could promote healthy aging by activating the body’s natural defense systems, but timing matters, with early-life intervention being crucial. Notably, most human clinical trials use sulforaphane doses ranging from 30 to 100 micromoles daily (approximately 5 to 18 milligrams). These doses are typically delivered as glucoraphanin—the precursor to sulforaphane—paired with myrosinase to enhance conversion in the body. Learn more about sulforaphane in this episode featuring Dr. Jed Fahey.
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Daily vitamin D3 supplements slow telomere shortening in older adults by 25% over four years, potentially reducing the risk of age-related diseases and premature death. ajcn.nutrition.org
Telomeres serve as protective caps at the ends of chromosomes, and when they shrink too much, cells stop dividing and age. Shorter telomeres have been linked to an increased risk for age-related diseases and premature death. A recent study found that daily vitamin D3 supplementation slowed telomere shortening by about 25% over four years in older adults.
Researchers recruited 1,031 participants from the large VITAL trial who took vitamin D3 (2,000 IU daily), omega-3 fatty acids (1 gram daily), both, or a placebo for four years. The researchers measured each person’s telomere length at the start of the study, then again two and four years later.
On average, telomeres shrank noticeably in the placebo group, but remained much more stable in the group taking vitamin D3. After four years, those taking vitamin D3 had telomeres preserved by an average of 140 base pairs—about 25% more than the loss observed in the placebo group. The benefits were most pronounced among participants under age 64 who didn’t smoke, maintained a healthy body weight, or weren’t taking medications for cholesterol, diabetes, or high blood pressure. Omega-3 fatty acid supplements had no apparent effect on telomere length.
These findings suggest that daily vitamin D3 supplements help slow cellular aging by reducing telomere erosion, particularly in people who are younger, healthier, or not already taking medications for chronic conditions. Learn more about vitamin D in our comprehensive overview article.
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One means of assessing cardiovascular health is the American Heart Association’s Life’s Essential 8, which takes into account one’s diet, physical activity, nicotine exposure, sleep, body mass index, blood pressure, cholesterol levels, and blood sugar. Maintaining high scores across these factors throughout young adulthood can reduce the risk of cardiovascular disease later in life. A recent study found that people with higher Life’s Essential 8 scores from ages 18 to 45 and those who showed improvement over this period were nearly 90% less likely to develop cardiovascular disease after age 45.
Researchers followed more than 4,800 participants from the Coronary Artery Risk Development in Young Adults study across four United States centers, collecting cardiovascular health data from 1985 to 2020. They analyzed the relationship between cumulative Life’s Essential 8 scores (measured over time from ages 18 to 45) and the risk of cardiovascular disease after age 45.
They found that participants with higher cumulative Life’s Essential 8 scores had considerably lower risks of both cardiovascular disease and early death. Those in the top quartile of scores had up to 88% lower risk of cardiovascular disease and 71% lower risk of mortality than those in the lowest quartile. And those whose Life’s Essential 8 score improved over the study period also experienced a reduced risk of developing cardiovascular disease in midlife.
These findings suggest that maintaining and improving cardiovascular health during young adulthood is crucial for lowering the risk of developing cardiovascular disease later in life. Sauna use is an excellent strategy for boosting cardiovascular health. Learn more in this episode featuring Dr. Rhonda Patrick.
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Regular infrared sauna use increases blood vessel density in aged muscles by 33%, though muscle size, strength, and protein synthesis remain unchanged. pubmed.ncbi.nlm.nih.gov
Scientists have speculated that regular heat exposure, such as that experienced in a sauna, might help aging muscles adapt in ways that preserve strength and mass. A recent study found that older adults who engaged in infrared sauna sessions regularly experienced a 33% increase in the number of small blood vessels surrounding their muscle fibers.
Researchers asked 14 healthy older adults (65 to 85 years old) to sit in an infrared sauna (60°C, 140°F) for 45 minutes, three times weekly, for eight weeks. They collected muscle biopsies before and after the heat exposure to measure capillarization—the number of capillaries around each muscle fiber—as well as muscle size. They also tracked muscle protein synthesis using amino acid infusions and ultrasound imaging to assess how well blood flowed through muscle tissue after eating. Finally, they measured leg strength using a one-repetition maximum test.
After eight weeks of heat therapy, participants had 31% to 33% more capillaries surrounding both type I and type II muscle fibers. However, muscle blood flow, protein synthesis rates, leg strength, and muscle size did not improve. Body weight, body composition, and walking speed also stayed the same. The only physical performance measure that improved was handgrip strength, which increased slightly. Interestingly, systolic blood pressure dropped by 2%, while diastolic pressure and resting heart rate were unchanged.
These findings suggest that passive heat treatment can increase blood vessel density in older muscle tissue, but this change alone doesn’t improve nutrient delivery, muscle building, or strength. Heat exposure might support muscle health in other ways, but it doesn’t appear to be a replacement for resistance or aerobic exercise. Learn more about the benefits of heat exposure in Aliquot #96: Thermal Stress, Part I: The Science Behind Heat Stress and its Positive Effects on Health.
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Once-weekly, low-volume resistance training boosts physical functioning, energy, and social engagement in older adults while reducing pain by up to 40% and improving strength by 30%. www.sciencedirect.com
Resistance training is a powerful tool for improving the health and well-being of older adults, but many guidelines focus on higher training volumes that may be difficult for some to achieve or maintain. A recent study found that once-weekly, low-volume resistance training boosted physical functioning, energy, and social engagement in older adults, reducing pain by up to 40% and improving strength by 30%.
Researchers assigned 31 older adults (average age, 66) to one of four groups. Participants trained once a week for six weeks, doing leg press exercises with either a slower, controlled pace or a more explosive effort and using lighter or heavier weekly exercise “doses” (either three or five sets of five repetitions). The researchers assessed the participants' quality of life, functional capacity, strength, and body mass at baseline and weeks 3 and 6.
They found that participants moved more easily, felt more energetic, and reported less pain after the intervention. Their balance and strength improved, and many participants reported more frequent physical activity—an average increase of 25%—and a 20% improvement in mental health. Most participants (85%) continued exercising after the study, and 95% said they would recommend the program. Many valued the structure and support, with 75% finding the shorter three-by-five routine practical and sustainable.
These findings suggest that lower-dose, once-weekly resistance training interventions can produce meaningful health improvements in older adults. One of the principal benefits of resistance training is building muscle, which is critical for maintaining health during aging. Learn how it’s never too late to start building muscle in this clip featuring Dr. Rhonda Patrick.
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As people age, sleeping problems become more common, often affecting mood, memory, and overall health. A recent study found that resistance training improves sleep in older adults better than other forms of exercise.
Researchers analyzed 25 clinical trials involving more than 2,100 people to see how different kinds of physical activity influenced sleep quality. They looked specifically at the Pittsburgh Sleep Quality Index, a subjective measure of a person’s sleep quality. The studies compared people who exercised to those who adhered to their usual routines, received health education, or did no physical activity at all.
Strength training was the most effective approach for improving sleep scores, followed by aerobic activity and then a combination of both. People who engaged in strength exercises were more likely to report better sleep, with the strongest improvement observed across all comparisons. Aerobic activity also helped but wasn’t as effective, and combined exercise had a more modest benefit.
These findings suggest that resistance training does more than build muscle—it also improves sleep. Resistance training builds bone, too, a critical component of aging well. Learn more in this clip featuring Dr. Brad Schoenfeld.
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Even if you work out, spending most of your day sitting may still adversely affect your health in ways that don’t become apparent until later in life. A recent study found that 35-year-olds who engaged in 30 minutes of vigorous exercise each day had cholesterol levels comparable to those of sedentary 30-year-olds, suggesting that vigorous exercise can offset up to five years of age-related decline in heart health.
Researchers analyzed data from adults aged 28 to 49 who participated in the Colorado Adoption/Twin Study of Lifespan Behavioral Development and Cognitive Aging. They tracked the time participants spent sitting each day and how often they engaged in moderate or vigorous physical activity. To isolate the effects of behavior from shared genetics and environment, the researchers also compared identical twins with differing activity and sitting patterns. They examined two key health markers: body mass index and the ratio of total to high-density lipoprotein cholesterol—a strong predictor of heart disease risk.
They found that people who spent more time sitting tended to have higher body mass index and worse cholesterol ratios as they aged. However, among those who sat for the same amount of time—about four hours daily—participants who exercised vigorously for at least 30 minutes daily had cholesterol profiles that resembled those of people five years younger. In some cases, vigorous activity was associated with health markers typical of people up to 10 years younger, but the protective effect weakened with longer sitting durations. In other words, exercise helped—but only to a point.
These findings suggest that while vigorous exercise offers clear benefits, reducing sitting time is just as important for maintaining good health. “Exercise snacks” can offset the harmful effects of prolonged sitting. Learn more in this clip featuring Dr. Rhonda Patrick and Brady Holmer.
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While genes play a role in aging, lifestyle and environmental exposures—collectively called the exposome—may have a more robust effect on aging and longevity. A recent study found that the exposome contributes far more to premature death and age-related diseases than genetic risk alone.
Researchers analyzed data from nearly 500,000 people enrolled in the UK Biobank to measure the exposome’s role in aging. They identified environmental exposures linked to early death and biological aging, then used a proteomic age clock—a tool that tracks molecular signs of aging—to confirm which exposures accelerate the aging process. Finally, they compared the exposome’s influence on disease risk to that of genetic predisposition.
The exposome explained 17 percentage points more of the variation in mortality than genetic risk, which accounted for less than two percentage points. It was more strongly connected to lung, heart, and liver diseases, while genetic factors were more closely associated with certain cancers and dementias. The analysis identified three disease states and 22 biomarkers related to liver and kidney function, cardiovascular and metabolic health, inflammation, longevity, genetics, and vitamin and mineral status that independently drive biological aging and disease risk.
These findings suggest that the exposome is critical in shaping health and longevity. While genes contribute to some diseases, environmental exposures throughout life greatly influence aging and survival. Air pollution is an exposome element contributing to disease and early death. Learn how wearable devices measure the air pollution exposome in this episode featuring Dr. Michael Snyder.
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With more than 80% of older adults in the U.S. having at least one chronic health condition, finding ways to support healthy aging has become a public health priority. A recent study found that people who followed healthy diets over the long term were more than twice as likely to age well—physically, mentally, and emotionally—even into their mid-70s.
Researchers followed adults for 30 years as part of two large, long-running health studies in the U.S. They looked at how closely people followed eight well-known dietary patterns, including the Alternative Healthy Eating Index (AHEI)—a scoring system that reflects how well someone’s diet aligns with current nutrition guidelines. Other patterns included the Mediterranean diet, the DASH diet, a plant-based diet, and the Planetary Health Diet.
The researchers also examined diets linked to higher levels of inflammation and insulin resistance and the amount of ultra-processed food people ate. They then compared these patterns to a comprehensive measure of healthy aging, including physical function, cognitive ability, mental health, and freedom from major chronic disease.
They found that people with the highest AHEI scores were 2.43 times more likely to maintain good overall health as they aged, up to 75. Similar benefits appeared for people who followed Mediterranean-style, MIND, and plant-based diets. In contrast, those who ate the most ultra-processed food or followed dietary patterns that drive inflammation and high blood glucose levels were less likely to age in good health.
These findings suggest that long-term dietary choices can meaningfully influence how well we age—not just how long we live. Learn more about lifestyle factors that prolong healthy aging in this episode featuring Dr. Rhonda Patrick.
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Your brain may be aging faster than the rest of your body. While some people maintain brain health well into old age, others experience structural decline much earlier. A recent study found that multiple health factors—including hypertension, diabetes, smoking, and low educational attainment—may speed up brain aging, increasing the risk of cognitive decline and neurodegenerative diseases.
Researchers analyzed brain scans and long-term health data from 964 adults in northern China, monitoring them for 16 years. They used machine learning to estimate brain age based on imaging techniques and compared brain aging among groups with various high-risk health factors. They also focused on people with high blood pressure to see how it affects brain structure.
They found that people with four or five high-risk factors had considerably older-looking brains than those with fewer risks, suggesting that multiple health problems may accelerate brain aging. Hypertension, high blood sugar, elevated creatinine (a feature of metabolic disease), smoking, and lower education were the strongest predictors of brain structure decline. However, hypertension had the strongest link, with hypertensive participants exhibiting more substantial structural deterioration.
These findings suggest maintaining good cardiovascular and metabolic health may help slow brain aging. Hypertension damages the brain’s microvasculature. Learn how exercise preserves these tiny blood vessels, helping to maintain cognitive health.
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Conventional wisdom suggests that cognitive skills begin to decline in early adulthood, but this assumption may be misleading. A recent study found that cognitive skills—specifically math and reading skills—actually improve into one’s forties before experiencing a decline, and using these skills regularly is crucial in determining how abilities change over time.
Researchers analyzed data from a previous German study that monitored more than 3,200 adult participants over time, allowing for the identification of genuine age-related changes in cognitive abilities. They also considered measurement errors that could skew results.
They found that math and reading skills continued to improve into the participants' forties. After that, literacy declined slightly, while numeracy dropped more sharply—but only for participants with below-average skill usage. Those who regularly engaged in complex tasks at work or home, particularly white-collar and highly educated participants, maintained or improved their skills well beyond midlife. However, women experienced steeper declines in numeracy as they aged.
These findings suggest that cognitive decline is not inevitable. Remaining mentally engaged through work and daily activities may help preserve or enhance cognitive abilities beyond middle age. Maintaining healthy blood flow to the brain through vigorous exercise can support cognitive function in aging. Learn more in this episode featuring Dr. Rhonda Patrick.
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Being socially active may delay dementia onset by five years. alz-journals.onlinelibrary.wiley.com
A lively social life might be one of the best defenses against dementia. With more than 50 million people affected worldwide and care costs soaring into the hundreds of billions, finding ways to delay dementia is a public health priority. A recent study found that older adults who were more socially active developed dementia about five years later than those who were the least socially engaged.
Researchers tracked nearly 2,000 older adults without dementia as part of the Rush Memory and Aging Project. Each year, participants underwent cognitive assessments to determine whether they had developed mild cognitive impairment or dementia.
Over nearly seven years of follow-up, 545 participants developed dementia, and 695 developed mild cognitive impairment. On average, the least socially active participants developed dementia at about age 87, while the most socially active participants developed it at about age 92—a five-year difference. The same pattern emerged for mild cognitive impairment.
These findings suggest that social activity could be a powerful, community-wide strategy for delaying dementia, ultimately improving older adults' quality of life and reducing healthcare costs. Dietary components, including omega-3 fatty acids, play a critical role in reducing the risk of dementia, too. Learn more in this episode featuring Dr. Rhonda Patrick.
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Pentadecanoic Acid (C15:0), an Essential Fatty Acid, Shares Clinically Relevant Cell-Based Activities with Leading Longevity-Enhancing Compounds pmc.ncbi.nlm.nih.gov
Pentadecanoic acid (C15:0) is an essential odd-chain saturated fatty acid with broad activities relevant to protecting cardiometabolic, immune, and liver health. C15:0 activates AMPK and inhibits mTOR, both of which are core components of the human longevity pathway. To assess the potential for C15:0 to enhance processes associated with longevity and healthspan, we used human cell-based molecular phenotyping assays to compare C15:0 with three longevity-enhancing candidates: acarbose, metformin, and rapamycin. C15:0 (n = 36 activities in 10 of 12 cell systems) and rapamycin (n = 32 activities in 12 of 12 systems) had the most clinically relevant, dose-dependent activities. At their optimal doses, C15:0 (17 µM) and rapamycin (9 µM) shared 24 activities across 10 cell systems, including anti-inflammatory (e.g., lowered MCP-1, TNFα, IL-10, IL-17A/F), antifibrotic, and anticancer activities, which are further supported by previously published in vitro and in vivo studies. Paired with prior demonstrated abilities for C15:0 to target longevity pathways, hallmarks of aging, aging rate biomarkers, and core components of type 2 diabetes, heart disease, cancer, and nonalcoholic fatty liver disease, our results support C15:0 as an essential nutrient with activities equivalent to, or surpassing, leading longevity-enhancing candidate compounds.
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Gray hair is often considered an inevitable part of aging, but evidence suggests lifestyle strategies—including diet—could slow it down. A recent study in mice found that luteolin, a plant-derived antioxidant, may help prevent hair graying by targeting key cellular processes.
Researchers tested the effects of three antioxidants—luteolin, hesperetin, and diosmetin—on hair graying in mice prone to premature graying. They applied the compounds topically and administered them orally, then analyzed changes in hair color, stem cell activity, and molecular markers associated with aging hair follicles.
Luteolin, but not the other antioxidants, substantially reduced hair graying in the mice. Both topical and oral luteolin helped maintain communication between hair follicle stem cells and melanocyte stem cells,which are essential for pigment production. Mice treated with luteolin also had fewer aging-related changes in these cells, suggesting it protects against age-related hair follicle dysfunction.
These findings suggest that luteolin is a promising candidate for an anti-graying treatment. Luteolin is abundant in celery, green pepper, broccoli, carrots, and olive oil, and is also available as a dietary supplement. Learn about other strategies to slow or prevent hair graying in this episode featuring Dr. Rhonda Patrick.
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Androgens shape more than just male traits—they may also influence the pace of aging. A recent study found that an epigenetic predictor called the androgen clock can precisely track cumulative androgen exposure, offering new insights into how these hormones affect biological aging.
To develop this model, researchers analyzed DNA methylation, a chemical modification that regulates gene activity and changes with age. They studied male-specific DNA methylation patterns in sheep and mice, identifying genetic sites that gradually lost methylation in males while remaining stable in females. Using this pattern, they created a clock that accurately estimates androgen exposure and tested whether altering hormone levels could change its ticking rate.
They found that supplementing female mice with androgens accelerated the clock while removing androgens in male sheep through castration halted it altogether. The model estimated the duration of androgen exposure in both species with an accuracy of a few months, indicating that androgens directly influence epigenetic aging and can precisely regulate this process.
These findings indicate that the androgen clock may be an effective tool for investigating how sex hormones influence aging. Learn more about epigenetic aging in this episode featuring Dr. Steve Horvath, one of the investigators involved in this study.
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Aging impairs mitochondrial function, disrupting the heart’s energy supply. Over time, this energy shortfall undermines cardiac cell function, driving the heart’s gradual decline. A recent study found that supplemental urolithin A—a bioactive compound derived from pomegranates and walnuts—boosts mitochondrial health and reduces pro-inflammatory lipids called ceramides, ultimately enhancing cardiac function.
Researchers investigated the effects of supplemental urolithin A in models of natural aging in mice and heart failure in rats and assessed its effects on plasma ceramide levels in healthy older adults. Mice received 50 milligrams per kilogram of urolithin A daily (in food) for eight weeks, rats received 50 milligrams per milliliter (in water) for 24 hours following a simulated heart attack, and the older adults took 1 gram of urolithin A (via supplement) or a placebo daily for two to four months.
Supplemental urolithin A improved systolic and diastolic cardiac function in models of natural aging and heart failure—an effect of the restoration of mitochondrial structure and enhanced mitophagy at the cellular level. Four months of urolithin A supplementation in healthy older adults significantly lowered plasma ceramides.
Ceramides are a class of bioactive lipids that contribute to cardiovascular disease by promoting inflammation, insulin resistance, and lipid accumulation in arteries. Elevated ceramide levels are linked to a higher risk of atherosclerosis and adverse cardiac events.
Urolithin A is a byproduct of gut microbial metabolism of ellagic acid, a bioactive compound found in pomegranates and walnuts. The capacity to form urolithin A from ellagic acid varies considerably from person to person (depending on gut microbial composition) and decreases with age. Pterostilbene, a compound found in blueberries and some supplements, boosts urolithin A conversion. Learn more in this clip featuring Dr. Rhonda Patrick.
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About half of your brain is white matter—a network of nerve fibers that allow for the exchange of information and communication within the brain. Aging and lifestyle factors can damage the white matter, increasing the risk of stroke, dementia, and disability. However, a recent study found that the brains of regular green tea drinkers have fewer white matter lesions than non-drinkers.
The study included nearly 8,800 older adults living in Japan. Participants provided information about their green tea and coffee consumption and underwent magnetic resonance imaging to assess their brain health and volume.
They found that higher green tea consumption correlated with fewer cerebral white matter lesions but had little effect on brain volumes, even after accounting for demographic, lifestyle, and health factors. People who drank about three cups (~20 ounces) of green tea daily had 3% less white matter damage in their brains than those who drank just one cup (~7 ounces). Those who drank around seven to eight glasses (~50 ounces) daily had 6% less damage. Coffee consumption did not affect white matter or brain volume, suggesting that green tea protects against white matter damage.
Green tea contains epigallocatechin gallate (EGCG), a polyphenolic compound that exerts robust antioxidant, anti-inflammatory, and neuroprotective effects. Evidence suggests that EGCG reduces the buildup of amyloid beta and tau—two proteins involved in the pathophysiology of Alzheimer’s disease. Learn more about EGCG and other polyphenols in our overview article.
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Cardiorespiratory fitness measures the body’s aerobic capacity—the ability to deliver oxygen to skeletal muscles—during sustained physical activity. A recent study found that better cardiorespiratory fitness boosts cognitive performance, even among people at greater risk for cognitive decline, such as older adults and APOE4 carriers.
Researchers collected information from more than 600 older adults regarding their age, sex, education, use of beta-blockers (drugs that lower heart rate), and APOE4 gene status (a genetic risk factor for Alzheimer’s). The participants underwent cardiorespiratory fitness testing on a treadmill. They also completed a comprehensive battery of neuropsychological tests to assess their cognitive function across multiple domains, including processing speed, executive function, working memory, episodic memory, and attention control.
Participants with higher cardiorespiratory fitness performed better on all cognitive assessment domains than those with poorer fitness—even among those at greater risk for cognitive decline, such as older adults and APOE4 carriers. Additionally, women, participants with fewer years of education, and those taking beta-blockers demonstrated greater cognitive performance in processing speed and executive function.
These findings suggest that better cardiorespiratory fitness in later life protects against cognitive decline.Although robust exercise is the best way to boost cardiorespiratory fitness, sauna use does, too. Learn more in our members-only report, Sauna Use: Implications for Aging and the Brain.
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Supplemental vitamin D is linked to a 40% lower risk of Alzheimer's in cognitively healthy older adults. alz-journals.onlinelibrary.wiley.com
As the global population ages and the risk of Alzheimer’s disease increases, identifying lifestyle factors that may prevent or forestall the disease is becoming increasingly important. A recent study found that people who take vitamin D supplements are 40% less likely to develop Alzheimer’s than those who don’t supplement.
The study involved more than 12,000 cognitively healthy older adults. Researchers gathered information about the participants' vitamin D supplementation practices and whether they developed Alzheimer’s over 10 years.
They found that participants who took any form of supplemental vitamin D (D2, D3, or D3 with calcium) had a 40% lower risk of developing Alzheimer’s than non-supplementers. This effect was more robust in women, those with normal cognition, and people without the APOE4 gene (a risk factor for Alzheimer’s).
These findings suggest that supplemental vitamin D protects against Alzheimer’s. However, this was an observational study, so other factors might have influenced the participants' Alzheimer’s risk. For example, those who took supplemental vitamin D had higher education than those who didn’t. Research suggests that higher educational attainment is associated with a lower risk of Alzheimer’s.
Nevertheless, vitamin D is essential for human health, and most people living in the U.S. have low vitamin D levels, potentially driving the growing number of Alzheimer’s cases. Learn more about vitamin D’s effects on the brain in this episode featuring Dr. Rhonda Patrick.
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Flaxseed oil is rich in alpha-linolenic acid (ALA), an omega-3 fatty acid. In the liver, ALA converts to docosahexaenoic acid (DHA), a crucial component of brain health. Evidence suggests that low DHA levels can impair cognitive function. However, a recent study in older adults found that supplemental flaxseed oil enhances cognitive function, particularly verbal fluency—the ability to retrieve and use words quickly.
The study involved 60 cognitively healthy older adults between the ages of 65 and 80. Half of the participants received 3.7 grams of flaxseed oil containing 2.2 grams of ALA daily for 12 weeks, and the other half received corn oil. Before and after the intervention, researchers assessed aspects of their cognitive function, including verbal fluency.
Verbal fluency relies on several cognitive skills, including recalling word meanings, finding the right words quickly, processing information efficiently, controlling impulses, holding and using information in the moment, switching between tasks or ideas, and adapting to new situations. It also involves multiple areas of the brain working together. Unfortunately, verbal fluency declines with age, impairing conversation and social interactions and serving as a predictor of Alzheimer’s disease.
The researchers found that participants who received the ALA-rich flaxseed oil supplement had higher verbal fluency than their peers who received the corn oil, suggesting that flaxseed oil is suitable for delivering crucial omega-3s to the brain. Learn more about the effects of omega-3s on brain health in this clip featuring Dr. Axel Montagne.
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Athletes exhibit 63% better working memory performance than sedentary people, underscoring the cognitive benefit of regular physical activity. www.tandfonline.com
Working memory, the brain’s system for temporarily storing and managing information, is crucial for recalling strategies and adapting to rapidly changing situations. A recent meta-analysis found that athletes outperform non-athletes by as much as 63% on working memory tasks.
Researchers analyzed 21 studies involving more than 1,400 participants across various sports, including basketball, football, and fencing. They assessed working memory through tasks like recalling sequences or matching stimuli after delays. The various studies compared athletes to non-athletes, including sedentary people, and examined factors like sports type and activity level.
The analysis revealed that athletes had a slight but consistent advantage in working memory compared to non-athletes, with a 30% improvement overall. When athletes were compared to sedentary people, their working memory performance was 63% better. However, the advantage dropped to just 15% when sedentary participants were excluded, suggesting a notable disadvantage for people with inactive lifestyles.
These findings suggest that sports expertise may enhance working memory, likely due to the cognitive demands of high-level performance. Moreover, sedentary lifestyles hinder working memory, underscoring the importance of regular physical activity for maintaining cognitive health. Physical activity also promotes longevity. Learn more about the longevity and brain-boosting effects of exercise in this episode featuring Dr. Rhonda Patrick.
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Eggs are a dietary paradox: high in cholesterol but rich in brain-boosting nutrients, including choline, lutein, and zeaxanthin. While some studies indicate that eggs maintain cognitive health, others report the converse. A recent study found that eating eggs may help women preserve semantic memory—crucial for language comprehension and factual recall—as they age.
Researchers analyzed data from 890 adults aged 55 and older. Participants reported their egg consumption using a food frequency questionnaire, and researchers measured their memory and thinking skills at two clinic visits about four years apart.
They found that women who ate five eggs weekly experienced less decline in verbal fluency, a measure of semantic memory, than those who ate fewer eggs. In men, researchers found no clear relationship between egg intake and changes in cognitive performance. Eating eggs did not appear to harm cognitive function in either sex.
These findings suggest that eggs play a small but beneficial role in preserving memory in women. They also align with other research demonstrating that people with moderate choline intake—roughly the amount in two eggs—are about half as likely to have low cognitive function than those with the lowest intake.
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Rapid increases in frailty levels, especially among women, amplify dementia risk by up to 73%. pubmed.ncbi.nlm.nih.gov
Frailty isn’t just about getting older—it’s a key indicator of biological age that can signal an increased risk for many health concerns, including dementia. A recent study found that rapid increases in frailty increase the risk of dementia by as much as 73%, especially among females.
Researchers analyzed data from four large studies involving nearly 88,000 adults aged 60 and older. They measured participants' frailty levels at the start and monitored their health, including the development of dementia, over several years.
They found that in the years before dementia began to manifest, frailty tended to increase. Participants with the most rapid increases in frailty were 18% to 73% more likely to develop dementia than those with slower frailty progression. Frailty was more common in females than males among those who developed dementia, with the greatest differences seen in the years leading up to dementia onset.
These findings suggest that measuring frailty could help identify people at greater risk for dementia, serving as an early target for strategies to reduce dementia risk through public health interventions and lifestyle changes. One powerful lifestyle approach for reducing dementia risk is exercise—especially the vigorous kind. Learn more in this episode featuring Dr. Rhonda Patrick.
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Rapamycin, a compound initially discovered as an antifungal agent, has garnered considerable interest in longevity research due to its ability to inhibit mTOR, a protein that plays a critical role in cellular growth and aging. Studies in animal models have demonstrated rapamycin’s potential to extend lifespan and improve healthspan. However, translating these findings into human applications has proven complex, as substantial risks often accompany the benefits.
Bryan Johnson is an internet personality who has made a name for himself by talking about his sometimes extravagant n=1 biohacking attempts to reverse aging. Recently, Johnson announced a reversal on his position on rapamycin: He thinks it might be making him age worse.
Johnson tested various rapamycin dosing protocols to explore its anti-aging potential while minimizing adverse effects. These protocols included weekly doses of 5, 6, and 10 milligrams, biweekly doses of 13 milligrams, and an alternating weekly schedule of 6 and 13 milligrams.
Although data from preclinical trials were promising, Johnson concluded that the long-term use of rapamycin in humans does not outweigh its drawbacks. Side effects, including intermittent skin and soft tissue infections, impaired lipid metabolism, elevated glucose levels, and increased resting heart rate, persisted regardless of dosage adjustments. After ruling out other potential causes, he attributed these issues to rapamycin and ultimately decided to discontinue its use.
Other research supports his observations, demonstrating that chronic rapamycin use can impair lipid profiles, induce insulin resistance, and contribute to glucose intolerance and pancreatic beta-cell toxicity. While anecdotal evidence suggests that rapamycin may slow tumor growth, its suppression of natural killer cells raises concerns about impaired immune surveillance and potentially increased cancer risk over time.
Further complicating the picture, a recent pre-print study presented new findings about rapamycin’s effects on aging. The study assessed the effects of rapamycin across 16 epigenetic aging clocks and found that it accelerated aging markers in humans. This analysis is noteworthy because most assessments have relied on only one or two aging clocks, raising concerns about the reliability of the findings.
As Johnson notes, longevity research is a rapidly evolving field that requires continuous scrutiny of emerging studies and biomarkers. For now, his experience underscores the importance of balancing potential benefits against risks when exploring experimental compounds like rapamycin. Learn more about rapamycin in our overview article.
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Mediterranean diet variations, rich in polyphenols and targeted at metabolic health, halve brain atrophy markers, slowing age-related brain shrinkage by up to 50% over 18 months. www.sciencedirect.com
Brain atrophy occurs naturally with aging, but certain factors such as type 2 diabetes, high blood pressure, and inflammation can accelerate this process, increasing the risk of cognitive decline. However, eating a healthy diet may help slow brain aging. A recent study found that two versions of the Mediterranean diet reduced markers of brain atrophy by 50% over 18 months compared to general healthy eating guidelines.
Researchers assigned participants aged 50 or older with abdominal obesity or abnormal blood lipids to one of three diets: one that followed standard healthy dietary guidelines, a calorie-restricted Mediterranean diet (which included walnuts and olive oil and substituted chicken and fish for lamb and beef), or a “green” calorie-restricted Mediterranean diet enriched with polyphenols from green tea and mankai, an aquatic plant. The participants underwent brain imaging to assess hippocampal atrophy, a key marker of brain aging, and the researchers tracked changes in body weight, blood sugar, and inflammation over the study period.
Participants following the green Mediterranean diet showed the greatest preservation of brain volume, particularly in the hippocampus. They also experienced improvements in HbA1c (a marker of long-term blood glucose control), insulin resistance, fasting glucose, and C-reactive protein. Improvements in blood sugar levels and inflammation were closely linked to better brain health outcomes, and greater intake of polyphenol-rich foods like mankai and green tea further enhanced these benefits.
Mankai, also called duckweed, is rich in polyphenols, omega-3 fatty acids, dietary fiber, and many micronutrients, including iron and vitamin B12. The polyphenols in mankai exert robust antioxidant activity and support healthy blood glucose levels—critical elements in maintaining brain health.
These findings suggest that diets rich in polyphenols and designed to improve metabolic health may help protect against age-related brain atrophy and keep the brain biologically younger. Learn more about the health benefits of polyphenols in our overview article.
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Physical activity at any intensity boosts mental speed almost immediately, equating cognitive function to that of people four years younger. pubmed.ncbi.nlm.nih.gov
Exercise boosts brain health, but some evidence suggests that even ordinary activities like dog walking or gardening can sharpen the mind. A recent study found that physical activity—no matter the intensity—can improve mental speed.
The study involved 90 healthy participants between the ages of 40 and 65. Using smartphones, participants reported their physical activity five times daily and completed brief cognitive tasks to measure mental speed and memory. The smartphones captured activity levels ranging from light chores to vigorous exercise and assessed how these influenced brain function in real-time.
The results indicated that being active within the previous 3.5 hours improved mental speed, equating to the cognitive function of someone four years younger. Both light and moderate-to-vigorous activities offered similar benefits. While memory accuracy did not improve, reaction times in memory tasks mirrored the gains in mental speed, especially in people who were more active overall.
These findings suggest that everyday physical activity can deliver immediate cognitive benefits, potentially offering a simple way to boost brain health at any intensity level. Learn more about the brain benefits of exercise in the Cognitive Enhancement Blueprint, a members-only perk.
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Frequent use of common household chemicals—including fluoride-based anti-caries agents, air fresheners, and disinfectants—increases the risk of cognitive decline in older adults. pubmed.ncbi.nlm.nih.gov
Cognitive decline—especially among older adults with dementia—can profoundly affect a person’s quality of life and increase their dependency on others. Evidence suggests that environmental exposures influence the risk of dementia. A recent study found that certain household chemicals, widely used for personal hygiene, cleaning, and disinfecting, may pose an unexpected risk for cognitive decline** in older adults.
Researchers analyzed data from a large cohort study of adults over 65. They evaluated how frequently the participants used eight common household chemicals, including insecticides, air fresheners, and disinfectants, and then examined whether these products were linked to declines in cognitive function.
They found that frequent use of anti-caries agents raised the likelihood of developing cognitive decline by 68%, while frequent use of air fresheners increased it by 148%, and disinfectants raised it by 40%. In general, more frequent chemical use was linked with worsening cognitive function.
Anti-caries agents prevent or reduce the development of dental caries, also known as cavities or tooth decay. Common anti-caries agents include fluoride mouth rinses, toothpaste formulations, and dental varnishes or sealants. Air fresheners contain various indoor pollutants, including phthalates and benzene. When these substances react with ozone, they create harmful byproducts that can harm the central nervous system. Sulforaphane, a bioactive compound derived from broccoli, boosts the excretion of pollutants like benzene. Learn more in this clip featuring Dr. Jed Fahey.
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'Endurance training' for the brain improves cognitive function in older adults, offsetting the effects of fatigue. www.sciencedirect.com
Mental fatigue can severely impair cognitive and physical performance, especially in older adults, increasing their risk of falls, accidents, and other health concerns. A recent study found that combining cognitive and physical exercise training may help improve mental and physical function in older adults, particularly when tired.
Researchers randomly assigned 24 women aged 65 to 78 to one of three groups: brain+exercise training, exercise-only training, or no training (control). The brain+exercise and exercise-only groups completed three weekly sessions for eight weeks consisting of 20 minutes of resistance training (squats and bicep curls) and 25 minutes of endurance exercise (walking outside). The brain training consisted of various assessments that measure reaction time and cognitive inhibition—the brain’s ability to block distractions or irrelevant information—completed four times throughout the study.
The researchers found that the brain+exercise and exercise-only groups performed better than the control group on cognitive and physical tasks regardless of how tired they were. However, the brain+exercise group showed greater improvements, particularly when tired. On average, cognitive performance increased by 7.8% in the brain+exercise group compared to 4.5% in the exercise-only group. Similarly, physical performance improved by nearly 30% in the brain+exercise group compared to 22.4% in the exercise-only group.
The findings from this small study suggest that combining cognitive and physical training boosts mental and physical abilities in older adults, particularly when tired. This approach may help mitigate age-related declines and reduce the risk of falls and other health complications. Learn about the brain-protective effects of physical exercise in this episode featuring Dr. Rhonda Patrick.
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Increased iron levels in the brain worsen cognitive test performance by as much as 10% in older adults, a phenomenon linked to brain atrophy and decline in memory and attention. pubmed.ncbi.nlm.nih.gov
Iron is an essential nutrient that participates in oxygen transport, energy production, and other critical processes. However, iron can accumulate in the brain, impairing memory and thinking abilities, especially in conditions like Alzheimer’s. A recent study found that older adults with higher brain iron levels perform poorly on cognitive tests.
Researchers used specialized MRI techniques to measure iron levels and atrophy in the brains of 770 older adults. Of these participants, 219 underwent cognitive testing roughly every year for about three years. The researchers focused on crucial brain regions associated with normal aging and Alzheimer’s disease to explore the relationship between iron buildup, brain atrophy, and cognitive performance.
They found that higher iron levels were linked to worse cognitive performance, particularly in memory and attention. Participants with the highest iron levels in aging-related brain regions were more likely to experience cognitive decline over time, performing up to 10% worse on cognitive tests than those with lower iron levels. Additionally, increased iron levels corresponded with more severe brain atrophy in these regions.
These findings suggest that brain iron accumulation impairs cognitive function and may be an early warning sign for the condition. Other lifestyle factors contribute to cognitive losses and brain atrophy, too, including alcohol consumption. Learn more in this episode featuring Dr. Rhonda Patrick.
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Increasing resistance training volume overcomes non-responsiveness in muscle growth in older adults, driving significant size and strength improvements. pubmed.ncbi.nlm.nih.gov
As we age, our muscles' response to resistance training diminishes to varying degrees, with some people responding and others not. This non-responsiveness can make maintaining muscle mass and strength challenging in later years. A recent study found that increasing resistance training volume—the number of sets performed—overcomes non-responsiveness in older adults.
The study involved 85 older adults (average age, 68) who completed a 10-week resistance training program. Participants followed a low-volume protocol (one set) for one leg and a high-volume protocol (four sets) on the other leg while performing knee extensions twice weekly. Researchers measured their muscle size and assessed their leg strength before and after the intervention.
They found that 51 participants didn’t respond to the low-volume training. However, they experienced considerable muscle size and strength improvements when they increased their volume. Responders—those who saw muscle gains from the one-set protocol—also benefited from the higher volume, but their strength gains were similar regardless of volume.
These findings suggest that older adults who don’t see improvements from resistance training can achieve meaningful gains by increasing the number of sets performed. Learn more about resistance training in this clip featuring Dr. Brad Schoenfeld.
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The gut-brain axis may hold more clues about cognitive decline than previously realized, with some evidence suggesting that gut microbial populations might influence brain health and cognitive function. A recent study found that older adults with cognitive impairment had distinct differences in their gut microbes compared to those without impairment.
Researchers assigned 229 adults aged 60 and older to one of two groups based on their cognitive function. They analyzed the diversity and composition of the participants' gut microbes and used machine learning to identify key bacterial species associated with cognitive impairment. They also investigated how lifestyle factors such as diet and exercise influenced these bacterial populations.
They found that participants with cognitive impairment had less diverse gut microbial populations than those without, indicating a potential link between less microbial diversity and cognitive decline. They noted that higher numbers of specific bacteria, including Megamonas, Blautia, and Veillonella, were associated with better cognitive function. They also found that higher fruit intake and regular exercise were linked to increased abundance of these beneficial species.
These findings suggest that maintaining a healthy gut microbiota through diet and exercise is essential in preserving cognitive function as we age. Time-restricted eating helps promote gut microbial diversity. Learn more in this clip featuring Dr. Satchin Panda.
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The brain’s hippocampus is vital for memory and learning but tends to shrink with age, contributing to cognitive decline. A recent study found that high-intensity interval training (HIIT) improves hippocampal-dependent cognitive abilities in older adults better than other forms of exercise.
Researchers randomly assigned 151 healthy adults aged 65 to 85 to one of three exercise regimens: low-intensity training, medium-intensity training, or HIIT. Over six months, participants attended 72 supervised sessions, underwent monthly cognitive testing, and provided blood samples. The researchers assessed the participants' brain volumes using magnetic resonance imaging (MRI) brain scans at various time points, with follow-ups continuing for five years.
They found that the HIIT group experienced marked improvements in hippocampal function. HIIT also reduced age-related brain volume loss, particularly in the hippocampus, and strengthened the connections between critical brain networks. The HIIT group’s cognitive improvements were associated with higher levels of brain-derived neurotrophic factor—a growth factor that supports brain function—and cortisol.
These findings suggest that HIIT protects against age-related cognitive decline and highlights its potential to preserve brain health in older adults. Learn more about the brain benefits of HIIT in this episode featuring Dr. Rhonda Patrick.
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Regular resistance training improves heart function in older women in just six months. link.springer.com
Keeping our hearts strong and healthy becomes increasingly challenging as we age, especially for older women. However, physical activity, especially resistance training, may benefit the heart. A recent study found that a 24-week resistance training program improved heart function in older women.
Researchers assigned 73 physically independent older women (average age, 68) to either an exercise training or sedentary group. The training group participated in a supervised resistance training program three times weekly for 24 weeks, using machines and free weights. Each session included exercises targeting the whole body, with three sets of eight to 12 repetitions each. The researchers measured the participants' cardiac function before and after the program.
They found that women in the training group experienced several improvements in heart function, including: - A 10.6% decrease in left ventricular volume versus a 1.1% increase in the sedentary group. - A 9.1% decrease in left atrial volume versus a 3.9% increase in the sedentary group. - Better heart relaxation, indicated by a 4.8% reduction in the diastolic function index.
These findings suggest that regular resistance training improves heart structure and function in older women, potentially reducing the risk of age-related cardiac decline. Finding the time for resistance training can be difficult, however. Listen as Drs. Brad Schoenfeld and Stuart Phillips describe time-efficient ways to incorporate resistance training into a busy schedule.
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Genes play critical roles in determining how long a person lives, but a new study suggests that the secret to longevity may be as simple as “food as medicine.” Centenarians—people who live 100 years or more—typically eat healthy, balanced diets and require fewer medications than their shorter-lived peers.
Researchers analyzed studies examining the lifestyles, medication use, and overall health of centenarians and near-centenarians aged 95 to 118. Their analysis included 34 studies and involved more than 59,000 participants.
They identified several healthy lifestyle habits of long-lived adults: Engaging in regular physical activity Avoiding alcohol and tobacco Adhering to a diverse, macronutrient-balanced diet Preferring less salty foods Using few medications—with just over four taken daily, primarily blood pressure medicines or other cardiovascular drugs
Multiple drug use—known as polypharmacy—is common in older adults. Defined as taking more than five medications daily, polypharmacy is linked with many adverse health effects, especially among older adults, who are at risk of a “prescription cascade”—where the side effects of drugs can be misdiagnosed as symptoms of another disease, creating a vicious cycle of more drug use.
This analysis suggests that using food as medicine—through healthy, balanced diets—combined with lower drug use contributes to healthy aging and longevity. Learn how other healthy lifestyle behaviors like exercise and dietary supplementation also promote longevity in this episode featuring Dr. Rhonda Patrick.
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Aging isn't linear—it may occur in two distinct bursts in our mid-40s and again around age 60. www.nature.com
We often think of aging as a steady, downhill slope, but a new study suggests aging happens in two distinct bursts—in our mid-40s and again around age 60—when massive shifts in crucial molecules involved in metabolism and other critical processes occur. These shifts may explain why our disease risk and other hallmarks of aging tend to spike at these pivotal times in our lives.
The study involved 108 adults aged 25 to 75 years living in the U.S. Researchers assessed changes in 135,000 molecular markers in the participants' blood, feces, and bodily fluids for up to seven years, yielding more than 246 billion data points.
They found that molecular changes occurred in two massive bursts rather than gradually, with changes in cardiovascular health, lipids, and alcohol metabolism appearing around 44 years of age, followed by shifts in crucial biological processes such as immune regulation and carbohydrate metabolism around 60 years.
These findings suggest that the progression of aging and related diseases is marked by distinct phases at specific ages. Some lifestyle behaviors can delay the changes that drive aging. Learn more about these powerful habits in this episode featuring Dr. Rhonda Patrick.
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Excess body fat in the arms and belly increases the risk of neurodegenerative disease. www.neurology.org
Although many factors influence whether a person develops neurodegenerative diseases like Alzheimer’s and other forms of dementia, excess body fat stands out as a notable risk factor. Some research suggests that where that body fat is located modulates that risk, with a new study finding that higher body fat in the arms and belly increases the likelihood of neurodegenerative disease.
The study involved more than 412,000 people enrolled in the UK Biobank study. Researchers measured the participants' body composition and tracked their health for about nine years.
They found that participants with greater muscle strength, bone density, and body fat in their legs were 6% to 25% less likely to develop neurodegenerative diseases. However, those with more body fat in their arms and bellies were 13% to 18% more likely to develop neurodegenerative diseases. Between 10% and 35% of the link between these body composition patterns and neurodegenerative diseases was attributable to the influence of cardiovascular diseases—particularly cerebrovascular diseases.
Cerebrovascular disease is an umbrella term for conditions that affect the blood vessels that supply the brain, such as strokes and aneurysms. Exercise helps maintain the health of these blood vessels, reducing the risk of neurodegenerative diseases. Learn more in this episode featuring Dr. Axel Montagne.
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Ketones may protect against cognitive decline by mitigating insulin resistance-induced neuronal damage. www.futurity.org
Insulin regulates many processes involved in memory and cognitive function. However, age-related insulin resistance in the brain disrupts neuronal synaptic activity and contributes to cognitive decline. A recent study found that ketones may protect the brain from age-related insulin resistance in the brain.
Researchers induced acute insulin resistance in mouse hippocampal tissue and determined its effects on neuronal function. Then, they administered beta-hydroxybutyrate, a type of ketone, to the tissues and evaluated the outcomes.
They found that insulin resistance adversely affected aspects of neuronal communication, including synaptic activity, axonal conduction, network synchronization, synaptic plasticity, and action potential properties. However, ketones restored these functions.
These findings suggest that ketones rescue the brain from the deleterious effects of acute insulin resistance. The high blood glucose levels associated with insulin resistance induce glucotoxicity, which causes structural damage and functional impairments of neuronal cells. Learn more about the effects of insulin resistance in the brain in this clip featuring Dr. Dale Bredesen.
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Initiating exercise later in life improves physical performance by up to 31%, demonstrating its beneficial effects against age-related decline. pubmed.ncbi.nlm.nih.gov
A sedentary lifestyle contributes to systemic inflammation, a critical player in the pathogenesis of many chronic diseases. However, evidence suggests it’s never too late to experience the benefits of regular exercise. A recent study found that physical performance measures in older adults who initiated an exercise regimen improved by as much as 31%.
Researchers collected data from two observational cohorts of older adults—an active group (318 participants) and a sedentary one (146 participants). All participants completed a battery of physical performance tests at baseline, six months, and one year later, including the six-minute walk test, the 30-second chair stand, and the timed up-and-go.
The researchers found that the two groups' physical performance differed considerably after one year. Exercising adults' performance improved in all measures, while sedentary adults' performance declined:
*A decrease indicates faster speed.
These findings suggest that regular, sustained exercise confers protection against age-related declines in physical performance in older adults. They also highlight the importance of interventions to reduce sedentary behavior and increase physical activity to support overall health and function. Learn more about how exercise, especially vigorous exercise, promotes longevity in this episode featuring Dr. Rhonda Patrick.
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Frequent nightmares linked to quadruple cognitive decline risk, especially among men. www.thelancet.com
Nightmares and bad dreams are common occurrences, with many adults experiencing them monthly. However, a growing body of evidence points to links between nightmares and cognitive function. A recent study found that people who have frequent nightmares have a fourfold greater risk for cognitive decline and dementia.
The study involved 605 adults enrolled in MIDUS, an ongoing survey of middle-aged and older adults living in the United States. Participants provided information about their sleep quality and distressing dream frequency over about seven years. They also completed cognitive tests and reported whether they had been diagnosed with dementia.
Middle-aged participants who had weekly distressing dreams were four times more likely to experience cognitive decline during the seven years than those without bad dreams. Older adults with weekly bad dreams were more than twice as likely to experience cognitive decline. The connection between bad dreams and cognitive decline was more robust among men.
These findings suggest that distressing dreams predict cognitive decline risk, potentially aiding early diagnosis and treatment. Dreams play essential roles in creativity and inspiration. Learn more in this clip featuring Dr. Matthew Walker.
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Chronic inflammation in early adulthood can impair cognitive performance by midlife, with 39% of young adults showing high inflammation levels. pubmed.ncbi.nlm.nih.gov
Research demonstrates that inflammation in later life harms the brain, increasing the risk of dementia and cognitive decline. However, scientists don’t fully understand the effects of inflammation that begins in early adulthood. A recent study found that inflammation during early adulthood markedly impairs cognitive performance in midlife.
The research involved more than 2,300 young adults (aged 24 to 58) enrolled in the Coronary Artery Risk Development in Young Adults study. Researchers tracked the participants' inflammation levels, measured by C-reactive protein (CRP), for about 18 years. Five years after their last CRP measurement, the participants completed tests that measured their verbal memory, processing speed, executive function, verbal fluency, category fluency, and overall cognition.
The researchers identified three inflammation patterns among the participants: lower stable (45%), moderate/increasing (16%), and consistently higher (39%). Participants with consistently higher CRP levels were 67 percent more likely to experience poor processing speed and 36 percent more likely to have poor executive function than those with stable, low CRP levels. Those with moderate/increasing CRP levels were twice as likely to have poor processing speed. There were no significant associations between CRP levels and memory, verbal fluency, category fluency, or overall cognition.
One of the many ways inflammation harms the brain is through its effects on pericytes, tiny cells that surround the brain’s blood vessels and help maintain the blood-brain barrier. Inflammation causes pericytes to release pro-inflammatory cytokines, compromising the barrier and facilitating neurodegeneration. Learn more about links between inflammation, pericytes, and cognitive decline in this clip featuring Dr. Axel Montagne.
These findings indicate that more than one-third of young adults have high inflammation levels, adversely affecting executive function and processing speed by midlife. They also underscore the importance of managing inflammation throughout life. Omega-3 fatty acids have potent anti-inflammatory effects. Learn more in this episode featuring Dr. Bill Harris.
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Older adults who used psychedelics exhibited better cognitive function and fewer depressive symptoms than non-users. journals.sagepub.com
Psychedelic drugs are hallucinogenic substances that alter cognition and perception, inducing visual and auditory changes and a “heightened state of consciousness.” They have a long history of traditional use in medicine and religion for their perceived ability to promote physical and mental health. A recent review found that older adults who have used psychedelic drugs tend to exhibit better cognitive functioning and fewer depressive symptoms than those who have not.
The study involved more than 2,500 adults between the ages of 42 and 92. Researchers assessed participants' executive function and episodic memory and enquired about their use of psychedelic drugs, including marijuana, LSD, or other hallucinogens (e.g., PCP, angel dust, peyote, ecstasy, mescaline, or Prozac), in the previous 12 months.
They found that participants who reported psychedelic use had better executive function but not episodic memory. They also tended to have fewer depressive symptoms.
Psychedelic drugs primarily act on serotonin receptors, particularly the 5-HT2A receptor, altering perception, mood, and cognition. These changes in brain activity and connectivity may promote neuroplasticity, potentially benefiting overall cognitive function and mental health. Learn more about psychedelic drugs in this episode featuring Dr. Roland Griffiths.
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As people age, they often experience muscle function and size declines, adversely affecting their health and overall quality of life. However, evidence suggests exercise can forestall these effects. A recent study found that one year of supervised resistance training with heavy loads exerts lasting benefits on muscle function in older adults.
Researchers conducted a randomized controlled trial involving 451 older adults at retirement age. They assigned participants to one of three groups: heavy resistance training, moderate-intensity training, or a non-exercising control group. They measured participants' leg extensor power, isometric leg strength, and body composition before and after the one-year intervention and again at two and four years after the study started.
They found that participants in the heavy resistance training group maintained their baseline isometric leg strength without notable decline over the four years. In contrast, participants in the moderate-intensity and control groups experienced decreased leg strength over time.
The heavy resistance training protocol involved a full-body workout performed three times a week, using machines in a commercial gym while under supervision. Participants spent the first six to eight weeks getting accustomed to the routine and then completed three sets of six to 12 repetitions for each exercise at about 70% to 85% of their maximum effort.
These findings suggest that one year of heavy resistance training can help preserve muscle function in older adults, potentially mitigating typical age-related declines in muscle strength. They also highlight the importance of incorporating resistance training into exercise programs for older adults to promote healthy aging. Learn more about resistance training for older adults in this clip featuring Dr. Brad Schoenfeld.
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Delirium is a sudden and severe state of confusion that can affect attention and cognitive function. It is particularly common in older adults after surgery or hospitalization, increasing their risk of death, institutionalization, and dementia. A 2022 study found that structural integrity of the anterior midcingulate cortex may predict and mitigate the risk of postoperative delirium.
The study involved 93 cognitively normal older adults undergoing elective surgery. Researchers divided the participants into two groups based on their performance on neuropsychological tests: “SuperAgers” (those whose cognitive function was comparable to that of young adults) and those whose cognitive function was typical for their ages. Participants underwent magnetic resonance imaging (MRI) to assess the structural integrity of various brain regions.
The researchers found that none of the SuperAgers experienced postoperative delirium, whereas 20 percent of the typical older adults did. Those who did not experience postoperative delirium exhibited enhanced structural integrity of the anterior midcingulate cortex.
The anterior midcingulate cortex is a brain region involved in a wide range of cognitive and motor functions. This critical area grows in response to activities that require considerable effort, such as exercise. Here’s what Dr. Andrew Huberman, our recent interview guest, had to say about it.
These findings suggest that greater structural integrity of the anterior midcingulate cortex protects against delirium and predicts cognitive resilience in older adults. They also align with other evidence demonstrating that SuperAgers exhibit greater cortical thickness in the anterior midcingulate cortex and lower incidence of Alzheimer’s disease. Learn more about the anterior midcingulate cortex in this episode featuring Dr. Andrew Huberman.
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The skin is the body’s first line of defense against environmental exposures. However, the skin changes considerably as we age, reducing its defense capacity. A 2021 study in mice found that sulforaphane, a bioactive compound derived from broccoli, mitigates age-related skin changes by activating Nrf2, a protein that participates in the body’s antioxidant defense system.
Researchers fed young and old mice regular mouse chow or chow supplemented with sulforaphane for three months. They assessed the antioxidant capacity and protein expression levels in the animals' skin. They also measured levels of reactive oxygen species and matrix metalloproteinase-9 (MMP9, a protein involved in tissue remodeling, inflammation, and wound healing), assessed epidermal and dermal thickness changes, and analyzed collagen content.
They found that sulforaphane reduced reactive oxygen species and MMP9 levels in older mice. It also increased the skin’s antioxidant capacity, as evidenced by enhanced Nrf2 production. They observed no difference in epidermal thickness between young and old SFN-treated mice, but dermal layers were thinner in older mice. Collagen content improved in young and old mice, with more substantial structural improvements observed in the older group.
These findings suggest that dietary supplementation with sulforaphane ameliorates age-related skin changes in mice by activating the Nrf2 pathway, enhancing antioxidant defenses and reducing oxidative stress.
Notably, the dose provided in this mouse study was very high, translating to about 2,500 milligrams of sulforaphane in humans – roughly the amount supplied in 63 cups of broccoli sprouts. Nevertheless, sulforaphane’s antioxidant-inducing capacity is well established, and consumption of sulforaphane-rich foods is associated with increased healthspan and lifespan. Broccoli sprouts are excellent sources of sulforaphane and are easy to grow at home. For tips on how to grow broccoli sprouts, check out our comprehensive Sprouting Guide, a members-only perk.
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Urolithin A, a compound derived from pomegranates and walnuts, boosts mitophagy and enhances cognitive function in aged mice. neurosciencenews.com
Mitochondrial function declines with aging, driving many age-related conditions, including Alzheimer’s disease. A recent study in mice found that urolithin A, a compound derived from pomegranates and walnuts, promotes mitophagy – the targeted destruction of damaged mitochondria – in the brain.
Researchers fed older mice urolithin A (200 milligrams per kilogram of body weight) daily for five months. They subjected the animals to various learning and memory tests, assessed their sense of smell, and examined their brains.
They found that urolithin A markedly improved the animals' learning, memory, and sense of smell, enhanced memory-related brain functions, and reduced the accumulation of amyloid-beta and tau protein (hallmarks of Alzheimer’s disease). Urolithin A also improved the function of lysosomes, cellular structures that play a crucial role in mitophagy, by breaking down and recycling damaged mitochondria.
These findings suggest that urolithin A boosts mitophagy in mice, improving brain health and cognitive function. Urolithin A is a byproduct of gut microbial metabolism of ellagic acid, a bioactive compound found in pomegranates and walnuts. The capacity to form urolithin A from ellagic acid varies considerably from person to person (depending on gut microbial composition) and decreases with age.
Due to the low quantities of ellagic acid in foods and the poor conversion rate, achieving a human dose comparable to that used in this study likely would require supplemental intake. Nevertheless, the findings align with other evidence suggesting that long-term dietary intake of foods containing ellagic acid benefits cognitive health.
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Diets rich in omega-3s and antioxidants slow brain aging and improve cognitive function in older adults. www.nature.com
While brain aging is an inevitable part of growing older, lifestyle factors, particularly diet, can influence the rate at which this aging occurs. A recent study found that older adults with diets rich in omega-3 fatty acids, antioxidants, and vitamins demonstrate slower brain aging and better performance on cognitive tests.
Researchers administered cognitive tests and brain imaging scans to 100 healthy older adults. They also measured 13 nutrition-related biomarkers in the participants' blood.
They identified two brain aging patterns among the participants, with one group exhibiting accelerated aging and the other slower aging. Further analysis revealed that distinct dietary patterns distinguished the two groups. In particular, the intake of specific nutrients positively influenced brain health and cognitive function, including: - Alpha-linolenic acid (an omega-3 fatty acid found in nuts and seeds, such as walnuts and chia) - Eicosapentaenoic acid (an omega-3 fatty acid found in fatty fish, such as salmon) - Lutein (a polyphenol found in green leafy vegetables, such as kale) - Zeaxanthin (a polyphenol found in brightly colored vegetables, such as orange bell peppers and butternut squash) - Vitamin E (found in seeds and nuts, such as sunflower seeds and hazelnuts) - Choline (found in a variety of foods, including eggs and soybeans) These patterns were consistent even when considering the participants' demographics, fitness levels, and body measurements.
These findings suggest that nutrient-rich diets are critical for maintaining cognitive health and decelerating the brain’s aging process. They also highlight the importance of dietary choices as potential tools to manage and mitigate age-related cognitive decline. Learn about other lifestyle choices that slow cognitive and physical aging in this episode featuring Dr. Rhonda Patrick.
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In older adults with type 2 diabetes, high-intensity resistance training decreases blood glucose levels by 12 percent and strengthens muscles by 33 percent. pubmed.ncbi.nlm.nih.gov
Type 2 diabetes is a metabolic disorder characterized by high blood glucose, increasing the risk for a wide range of complications, including kidney dysfunction, vision loss, and circulatory problems. However, evidence suggests that exercise improves blood glucose control. A 2002 study found that resistance training improved blood glucose control in people with type 2 diabetes.
The study involved 62 older adults with type 2 diabetes. Half of the participants engaged in a 16-week high-intensity resistance training program (gradually increasing in intensity), while the other half maintained their typical activities. Researchers measured participants' glycated hemoglobin levels (HbA1c, a measure of long-term blood glucose control), body composition, and muscle glycogen stores before and after the intervention.
They found that among resistance training participants, HbA1c decreased by approximately 12 percent, muscle glycogen increased by 31 percent, and muscle strength increased by 33 percent. Those who engaged in resistance training also experienced reductions in blood pressure and body fat, and their need for diabetes medications decreased.
These findings suggest that resistance training is a robust adjunct to type 2 diabetes treatments, effectively improving blood glucose control and metabolic health. Resistance training involves pushing or pulling against the resistance of an object, such as weights, bands, or even one’s body weight. Older adults starting a resistance training program may benefit from using lighter weights and performing more repetitions, especially if they have chronic joint problems. Learn more in this episode featuring Dr. Brad Schoenfeld.
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Creatine supplementation improves muscle strength and function, potentially averting functional disability in older adults. aspenjournals.onlinelibrary.wiley.com
Older adults often experience acquired functional disability – a newfound inability to carry out tasks necessary for independent living. This disability often arises due to the skeletal muscle wasting that can occur with acute periods of disuse, such as during hospitalization or illness. A recent systematic review found that creatine supplementation improved physical function in older adults at risk for acquired functional disability.
Researchers analyzed the findings of randomized controlled trials that investigated the effects of creatine supplementation on physical function in older adults. Their analysis included 33 trials and more than 1,000 participants, about half of whom had a chronic disease.
They found that creatine supplementation improved participants' handgrip strength, lean tissue mass, and upper-body muscle strength with few adverse effects. About two-thirds of the studies practiced creatine loading, with a daily maintenance dose ranging from 0.07 to 0.3 grams per kilogram of body weight. The most common dose was 5 grams daily. The investigators deemed the quality of evidence as “low” or “very low” due to study heterogeneity.
These findings suggest that creatine supplementation prevents acquired functional disability in older adults. A possible contributor to acquired functional disability is catabolic crisis, a phenomenon defined by periods of accelerated declines in muscle mass and functional capacity. Catabolic crisis can occur at any age but is more common among older adults, for whom injuries, surgeries, or prolonged illnesses dictate long and sometimes frequent periods of physical inactivity or immobilization. These cumulative insults drive older adults toward a disability threshold from which they might not recover. Omega-3 fatty acid supplementation may reduce the risk of catabolic crisis. Learn more in this episode featuring Dr. Chris McGlory.
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Regular moderate-intensity exercise is widely acknowledged for its longevity-promoting effects. However, scientific consensus on the effects of extreme endurance exercise on lifespan is divided. A recent study found that athletes who ran a sub-4-minute mile tend to live longer than the general population.
Researchers used data from a publicly available database of runners who have successfully run a sub-4-minute mile. They compared the lifespans of 200 of these runners with the life expectancies specific to each athlete’s country of origin.
They found that about one-third of the sub-4-minute mile runners had died, but those still alive had surpassed their predicted life expectancy by an average of 4.7 years. Interestingly, longevity benefits varied by decade, with those completing the mile in the 1950s, 1960s, and 1970s living longer by 9.2, 5.5, and 2.9 years, respectively, beyond their expected lifespan.
These findings suggest that high-level endurance training associated with running a sub-4-minute mile may increase longevity. They also challenge the notion that extreme endurance exercise is detrimental and support the benefits of vigorous physical activity for extending lifespan. Learn more about how vigorous exercise and other healthy lifestyle habits promote longevity in this episode featuring Dr. Rhonda Patrick.
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Older adults improve muscle strength, waist circumference, and cholesterol levels by boosting protein intake and engaging in regular exercise. onlinelibrary.wiley.com
Maintaining muscle mass as we age requires a comprehensive approach encompassing nutrition and regular physical activity. However, many older adults don’t consume adequate dietary protein and may lead sedentary lives, due to injuries, chronic illnesses, or joint problems. A recent study found that older adults who increased their dietary protein intake and engaged in regular exercise showed marked improvements in multiple health and fitness parameters.
The study involved 97 older adults (average age, 64) with low dietary protein intake (less than 1 gram per kilogram of body weight daily) who had experienced at least one fall in the past year. Half of the participants received a daily serving of a protein-enriched soup (providing 24 to 30 grams of protein) and engaged in one hour of group exercise (aerobic and resistance) each week for 12 weeks. The other half received nutrition education training at the beginning of the study and maintained their normal activity levels.
At the end of the study, sedentary participants showed improvements in handgrip strength only. However, the participants who consumed the protein-rich soup and exercised regularly showed improvements in waist circumference, walking distance, lower body strength, functional mobility, handgrip strength, nutritional status, serum triglycerides, HDL cholesterol, and DHEA-S.
DHEA-S (dehydroepiandrosterone sulfate) is a naturally occurring precursor to estrogen and testosterone. These steroid hormones exert anabolic effects by enhancing the bioavailability of insulin-like growth factor-1 in muscles, facilitating muscle growth and repair.
These findings suggest that increasing dietary protein and activity levels in older adults improves multiple health and fitness parameters. Interestingly, most of the participants in this study were female. Evidence suggests women typically consume less protein than men. In this clip, Dr. Stuart Phillips provides some insights to help older women get sufficient protein to support muscle health.
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Vision problems predict dementia risk nearly 10 years before diagnosis. www.ncbi.nlm.nih.gov
People with dementia often experience visual problems, which range in severity from difficulty seeing contrasts or colors to impaired understanding of spatial relationships. These visual problems typically manifest early in dementia, indicating that early vision testing may help identify those at risk. A recent study found that visual problems may predict dementia nearly 10 years before diagnosis.
The study involved more than 8,600 participants in a large, population-based prospective cohort. At the beginning of the study, participants took two visual sensitivity tests (simple and complex), which assess how quickly a person can process visual information and react to it. Researchers tracked the participants' cognitive and physical health for about 15 years.
They found that vision problems predicted participants' dementia risk an average of 9.6 years before a clinical diagnosis. A low score on the simple visual sensitivity test was associated with a 39 percent greater risk of developing dementia, and a low score on the complex test was associated with a 56 percent greater risk. These risks persisted even after accounting for the participants' ages. Interestingly, the vision testing was more sensitive to variables commonly associated with dementia risk (such as age, gender, and education) than traditional dementia assessments.
These findings suggest that visual problems predict future dementia risk. They also bolster previous research demonstrating that horizontal eye movements, such as those used when reading or viewing television, improve memory. Other lifestyle factors, including sleep, influence dementia risk, too. Learn more in this video featuring Dr. Rhonda Patrick.
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Evening exercise reduces the risk of early death in people with obesity by 61%, outperforming 33% risk reduction from morning exercise. diabetesjournals.org
Although obesity increases the risk of chronic disease and premature death, especially in those who have type 2 diabetes, exercise may counter some of those risks. However, the time of day a person exercises may influence the extent of risk reduction. A recent study found that moderate to vigorous physical activity in the evening reduced the risk of premature death by 61 percent in people with obesity.
Researchers asked nearly 30,000 adults with obesity, some of whom (3,000) had type 2 diabetes, how often they engaged in moderate to vigorous physical activity (lasting at least three continuous minutes) and whether they did so in the morning, afternoon, or evening. They tracked the participants' health for about eight years.
They found that engaging in moderate to vigorous physical activity in the evening reduced participants' risk of premature death from all causes by 61 percent. Afternoon exercise reduced the risk by 40 percent, and morning exercise reduced it by 33 percent. Similarly, evening exercise reduced the risk of cardiovascular disease by 36 percent and microvascular disease by 24 percent. They noted similar risk reductions in those who had type 2 diabetes.
These findings suggest that moderate to vigorous physical activity reduces the risk of chronic disease and premature death in people with obesity (including those with type 2 diabetes), but evening exercise confers the greatest benefit. Learn more about the health benefits of vigorous exercise in this episode featuring Dr. Rhonda Patrick.
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A ketogenic diet – a high-fat, low-carbohydrate dietary pattern – offers potential benefits in various health contexts, including weight management and seizure control. Some evidence suggests that the ketogenic diet is beneficial in preventing or treating neurodegenerative diseases, such as Alzheimer’s and dementia. A recent study in older mice found that a ketogenic diet improves memory functions and increases lifespan.
Researchers compared the effects of a seven-month ketogenic diet to a standard diet in mice prone to developing Alzheimer’s-like symptoms. They examined the hippocampal region of the animals' brains, a crucial area for memory and learning, to gauge the diet’s effects on synaptic plasticity – the brain’s ability to form and reorganize synaptic connections, especially in response to learning or new experiences.
They found that mice on the ketogenic diet experienced restoration of their long-term potentiation – a measure of synaptic strength and a fundamental mechanism for learning and memory – to levels comparable to healthy mice. They attributed this restoration to the marked elevation of beta-hydroxybutyrate (BHB), a ketone body produced during the ketogenic diet. They also found that the diet triggered enhancements in several key pathways and molecules associated with synaptic plasticity, including notable increases in specific enzymes and brain-derived neurotrophic factor (BDNF), particularly in female mice.
BDNF is crucial for cognitive functions, providing support for neuronal survival, growth, and differentiation and enhancing learning and memory by strengthening and creating synaptic pathways. Elevated BDNF levels correlate with better cognitive performance, whereas its deficiency is linked to various mental and neurodegenerative disorders, highlighting its significance in brain health. Learn more about BDNF in our overview article.
These findings suggest that a ketogenic diet ameliorates memory impairments and bolsters neuronal health in an Alzheimer’s mouse model, primarily through the action of BHB and its enhancement of synaptic plasticity. Learn more about beta-hydroxybutyrate in our overview article.
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Supplemental collagen improves skin appearance, reducing wrinkle depth by nearly half. www.dovepress.com
Collagen is crucial in maintaining the structural integrity of various tissues in the human body, and its decrease contributes markedly to the aging process. A recent study found that supplemental collagen combined with antioxidants substantially improved the appearance and health of skin and hair in adult women, reducing wrinkle depth by 48 percent.
The study involved 40 healthy adult women between the ages of 38 and 50. Participants consumed a commercially available collagen treatment containing collagen, hyaluronic acid, biotin, and vitamins C and E or a placebo for 56 days. Researchers evaluated various aspects of their skin, such as elasticity, hydration, brightness, and pigmentation, along with hair strength and hair fall (normal hair loss) before, during, and after the intervention.
They found that those who consumed the collagen treatment experienced a 48 percent reduction in wrinkle depth, a 39 percent reduction in fine lines, and a 16 percent increase in skin hydration compared to those who took a placebo. Their hair fall decreased by 28 percent versus 7 percent among those who took a placebo.
The findings from this small study suggest that supplemental collagen and antioxidants improve skin and hair health. Collagens are characterized by a triple helix arrangement, forming a sturdy, resilient structure. They serve general tissue assembly and maintenance functions, including tissue scaffolding, morphogenesis, and repair. Learn more about collagen in our overview article.
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A single session of high-intensity resistance training boosts memory and brain connectivity – particularly in the hippocampus – an indicator of enhanced cognitive health. onlinelibrary.wiley.com
High-intensity resistance training, also known as functional training, requires the body to exert considerable effort against weights or resistance. Evidence suggests this type of training confers myriad physical and mental health benefits, including improved metabolic function and mood, particularly in older adults. A recent study found that engaging in a single session of high-intensity resistance training enhanced memory capabilities.
The study involved 60 young, healthy adults who took memory tests and underwent resting-state functional magnetic resonance imaging of their brains. Then, half of the participants engaged in a single high-intensity resistance training session, while the other half did not. The training involved three resistant exercise sets at 75 to 80 percent of the participants' one-rep max, with one minute of rest between sets and a total duration of under seven minutes. Two days later, both groups repeated the memory tests and brain imaging scans.
Those who participated in the resistance exercise session exhibited marked improvements in memory recall compared to the non-exercising group. These memory improvements correlated with greater connectivity in the left posterior region of the hippocampus, an area involved in memory.
The findings from this small study suggest that just one session of high-intensity resistance training has considerable influence on memory, highlighting its potential to promote cognitive health and neural plasticity. Learn more about high-intensity resistance training in this clip featuring Dr. Martin Gibala.
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Even regular stretching exercises reduce the risk of premature death by 20 percent and boost cardiovascular health, study finds. www.ncbi.nlm.nih.gov
A recent study found that older adults who engaged in flexibility (stretching) exercises were 20 percent less likely to die prematurely than those who didn’t stretch.
The study involved more than 34,000 adults between the ages of 20 and 79 years. Participants provided information about the frequency and duration of their engagement in moderate- and vigorous-intensity aerobic physical activities, including aerobic, resistance, and flexibility exercises. Researchers tracked the participants' health for roughly 10 years and noted any deaths.
They found that engaging in just flexibility exercises like stretching or yoga five times per week reduced the risk of premature death from all causes by 20 percent and the risk of death from cardiovascular disease by 25 percent.
Stretching can take three forms – static, dynamic, and proprioceptive neuromuscular facilitation (PNF). Static stretching involves holding a stretch for 10 to 30 seconds, as seen in yoga poses, such as “downward-facing dog.” Dynamic stretching involves active movements, such as arm circles (used in warm-ups without holding the stretch) or elements of Tai Chi. PNF stretching is used primarily in physical therapy for flexibility and rehabilitation.
A 2014 review found that stretching’s effects vary by context. Dynamic stretching before exercise tends to improve strength, power, speed, and agility, enhancing sprint and agility test outcomes. Integrating dynamic stretching with exercises like front squats may further boost performance, but overdoing it can promote fatigue and hinder results. Although its effects on endurance sports are less certain, dynamic stretching is generally recommended in warm-ups for its benefits in speed and agility-focused activities.
Some evidence suggests that stretching may be particularly beneficial for older adults and those who are sedentary. For example, a comprehensive meta-analysis found that stretching exercises reduce arterial stiffness, heart rate, and diastolic blood pressure while improving vascular endothelial function in middle-aged and older adults. Stretching may reduce the risk of fall-related injuries in older adults by improving balance.
An abundance of research consistently singles out aerobic activities, especially at moderate to vigorous intensities, as the premier choice for improving health and extending life, as further supported by this study’s conclusions. However, the findings from this study point to the potential value of flexibility exercises. Although they may not offer the same cardiovascular benefits as aerobic activities, their beneficial effects on overall health are noteworthy. Embracing a diverse exercise regimen that includes aerobic and flexibility training may provide myriad health advantages. Learn more about the benefits of vigorous exercise in this episode featuring Dr. Martin Gibala.
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Yoga improves memory and boosts cognition in older women at risk for Alzheimer's, demonstrating increased hippocampal connectivity and expression of anti-aging markers. www.sciencedaily.com
Yoga is an ancient Indian practice that engages the mind and body through physical poses, breathing techniques, and meditation. Robust scientific evidence suggests that yoga benefits both mental and physical health. A new study found that Kundalini yoga – a type of yoga that involves specific postures, breathing techniques, and meditation – boosted cognition and memory in older women at risk of developing Alzheimer’s disease.
The study involved 63 older women who had self-reported memory problems and cerebrovascular conditions – risk factors for Alzheimer’s. About half the women participated in a weekly yoga session, while the other half participated in weekly memory training. Researchers assessed the women’s cognitive function and moods before and after the two interventions. They also measured markers of aging and inflammation in the women’s blood and assessed changes in their brains using magnetic resonance imaging (MRI).
They found that the women who participated in yoga experienced marked improvements in memory, increased connectivity in the hippocampus, and increased expression of anti-inflammatory and anti-aging markers** compared to those who did memory work only. The MRIs revealed that the brains of the women in the yoga group showed less age-related volume loss.
Women are at greater risk of developing Alzheimer’s disease than men, partly due to having higher rates of cardiovascular conditions, many of which share risk factors with Alzheimer’s. In addition, the decrease in protective estrogen during menopause may also amplify cognitive declines.
These findings suggest that Kundalini yoga benefits women at risk for Alzheimer’s disease. Evidence indicates that vigorous exercise can boost cognitive function, too. Learn more in this episode featuring Dr. Martin Gibala.
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Increased dietary fiber intake can help maintain muscle mass in older adults, potentially offering protection against age-related muscle loss. pubmed.ncbi.nlm.nih.gov
Sarcopenia is an age-related condition involving the gradual loss of muscle mass and strength. Older adults with sarcopenia are at greater risk for frailty, falls, loss of independence, and early death. A 2022 study found that higher dietary fiber intake maintains muscle mass in older adults.
Researchers assessed the physical capabilities (including balance, walking speed, and grip strength) of 981 older adults. They also measured their muscle mass using DEXA. Participants reported their dietary fiber intake and wore accelerometers to track their physical activity.
The DEXA scans revealed that women who consumed more fiber had considerably greater muscle mass than those who ate less. Men who consumed more fiber also had greater muscle mass, but only in those without metabolic syndrome. The associations were consistent even when considering physical activity and protein consumption.
These findings suggest that dietary fiber protects against muscle loss in older adults. Sources of dietary fiber include fruits, vegetables, whole grains, and legumes. People who follow a lower carbohydrate diet might find getting enough fiber challenging. Dr. Dominic D'Agostino provides some tips on how to get plenty of fiber even when following a ketogenic diet.
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Aging undermines the brain's capacity for maintaining working memory, with subtle declines in neuron activity and connectivity in the prefrontal cortex. www.sciencedaily.com
As the brain ages, cognitive functions decline, with working memory – a form of short-term memory necessary for reasoning, decision-making, and behavior – among the earliest affected. The brain’s prefrontal cortex is crucial in working memory, showing sustained activity during memory-guided behavior. A recent study in mice found that aging reduces the prefrontal cortex’s ability to maintain working memory, with older mice showing less effective communication between memory-coding neurons.
Using imaging techniques to see how neurons behave during memory tasks involving touch and sound, researchers tracked brain activity in mice of varying ages. They also used light-based interventions to temporarily disrupt brain activity, observing how this affected the animals' ability to perform the tasks.
They discovered that with aging, the prefrontal cortex had fewer neurons responsible for managing actions, and the signals from these neurons weakened. Furthermore, whereas young mice used both broad and specific memory strategies, older mice mainly relied on specific strategies, indicating a subtle decline in the brain’s memory circuits over time.
The researchers also observed a drop in the resting brain connections among neurons managing actions, beginning around middle age. This drop in connections became even more pronounced when the mice were doing tasks, suggesting that the brain’s ability to retain thoughts might weaken with age. Additionally, the brains of middle-aged mice were more easily disrupted by light-based interventions, hinting at a greater risk to their thought-retention processes as they age.
The findings in this mouse study suggest that aging leads to a marked decrease in brain connectivity and neuron activity in the prefrontal cortex, affecting memory retention and making it more susceptible to disruptions. The blood-brain barrier is a critical player in brain connectivity, and its impairment during aging contributes to cognitive dysfunction. Learn more in this episode featuring Dr. Axel Montagne.
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Multivitamin/mineral supplements enhance memory and cognitive function in older adults, a finding from the COSMOS trial. www.sciencedirect.com
As the global population ages, the number of people at risk for Alzheimer’s disease and other forms of dementia increases. A robust and growing body of evidence indicates that lifestyle influences the risk of developing dementia. A recent study found that multivitamin/mineral supplements improve memory and slow cognitive aging in older adults – roughly equivalent to reducing cognitive aging by two years.
Researchers investigated the effects of multivitamin/mineral supplementation on cognitive function in a subset of participants enrolled in the COSMOS study, a randomized, double-blind, placebo-controlled trial involving more than 21,000 older adults (60 years or older) in the U.S. Participants in COSMOS were randomly assigned to receive one of three interventions: cocoa extract (providing 500 milligrams of flavanols daily, including 80 milligrams of epicatechin), a multivitamin/mineral supplement, or both, daily for two years. A fourth group received a placebo. In the subset, called COSMOS-Clinic, 573 participants underwent extensive brain function tests before and after the study and again two years later.
They found that multivitamin/mineral supplementation conferred modest improvements in overall cognitive function over two years in participants enrolled in the subset, particularly in episodic memory – the ability to recall specific events, experiences, and contextual details from one’s past. They did not observe improvements in the participants' executive function or attention. However, a meta-analysis involving more than 5,000 participants from the COSMOS-Clinic, COSMOS-Mind, and COSMOS-Web studies demonstrated that multivitamin/mineral supplementation markedly improved overall cognition and episodic memory.
These findings from the COSMOS trials suggest that multivitamin/mineral supplementation – a low-cost, low-effort intervention – improves cognitive function in older adults. They also highlight the role of adequate nutrition throughout the lifespan and support the “micronutrient triage theory” – the idea that the body prioritizes the utilization of micronutrients for metabolic pathways needed for survival and reproduction over those used for long-term health. Learn more about micronutrient triage theory in this clip featuring Dr. Bruce Ames.
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With age, cognitive and metabolic dysfunction increases, often coinciding. However, evidence suggests that consuming berries improves cognitive and metabolic health. A recent study found that strawberry consumption improved memory and mood in overweight people with mild cognitive decline.
Researchers recruited 34 overweight middle-aged adults with insulin resistance who reported mild cognitive decline. Half of the participants consumed a strawberry powder supplement daily for 12 weeks, while the other half consumed a placebo. Both groups abstained from all berry consumption throughout the study. The researchers assessed the participants' cognitive and metabolic functions and moods before and after the intervention.
They found that those who consumed the strawberry powder exhibited better memory function and fewer symptoms of depression than those who consumed the placebo. However, they did not show any improvements in metabolic function.
These findings suggest that strawberry supplementation improves cognitive function in middle-aged adults, potentially reducing the risk of dementia, but has little effect on metabolic function. The study’s authors attributed the lack of metabolic response to the relatively low dose and the study’s short duration.
Strawberries are rich in anthocyanins, a class of polyphenolic compounds that exert potent antidiabetic, anticancer, anti-inflammatory, and anti-obesity effects in humans. Anthocyanins lend their characteristic blue, red, or purple hues to strawberries, blueberries, and other fruits and vegetables. Learn about other polyphenols in our overview article.
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Smoking cigarettes damages multiple organs, including the brain, possibly explaining why as many as 14 percent of Alzheimer’s cases worldwide are linked to smoking. A new study shows that cigarette smoking reduces brain volume, accelerating normal brain aging.
Researchers investigated the relationship between smoking and brain volume in more than 32,000 adults enrolled in the UK Biobank study. They used a set of guidelines (called Bradford Hill’s criteria) to determine whether a potential cause-and-effect relationship exists between a specific factor (such as smoking) and a health outcome (such as a disease). They also investigated whether genetic factors predispose some people to initiate smoking.
They found that regular smoking, especially heavier smoking, was linked to notable brain shrinkage, especially in terms of total gray matter volume. The more years a person smoked, the greater the shrinkage. They also found that daily smoking played a role in the relationship between the genetic risk score for smoking initiation and the total gray matter volume.
These findings suggest that smoking cigarettes reduces drives brain volume losses, effectively aging the brain prematurely. They also align with other research demonstrating that regular (daily or nearly daily) cigarette smoking increases relative brain aging, driving poor cognitive function and declines in fluid intelligence. Many habits like smoking (and overeating) can be broken using mindfulness techniques. Learn more in this clip featuring Dr. Ashley Mason.
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Hearing aids reduce the risk of early death in older adults with hearing loss by 24 percent. www.thelancet.com
Hearing loss is a common feature of aging and a known risk factor for poor quality of life, depression, dementia, and early death. Roughly two-thirds of adults over 70 have some degree of hearing loss, but few seek out treatment. A recent study found that hearing aids reduce the risk of premature death in older adults with hearing loss by 24 percent.
The study involved more than 9,800 adults (average age, 48 years) enrolled in the NHANES studies. Participants underwent hearing tests and completed questionnaires about their hearing aid use over a ten-year period.
The tests and questionnaires revealed that nearly 15 percent of the participants had some hearing loss. However, fewer than 13 percent of those with hearing loss regularly used hearing aids. Those with hearing loss who did wear hearing aids were 24 percent less likely to die prematurely than those who didn’t, even after taking demographics, hearing levels, and medical history into account.
These findings suggest hearing aids reduce the risk of premature death in older adults with hearing loss. Other evidence demonstrates that hearing aids benefit older adults at high risk for cognitive decline. Interestingly, another study found that the risk of developing mild hearing loss was nearly 30 percent lower among people who adhered to healthy dietary patterns such as the DASH diet or the Mediterranean diet, suggesting that diet may play a role in preventing mild hearing loss.
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Roughly half of all adults living in the U.S. have hypertension, with men affected more than women (48 percent versus 43 percent, respectively). However, the sex differences in hypertension prevalence aren’t consistent throughout the lifespan: Women who are 65 and older are more likely to have hypertension than men, raising concerns that current blood pressure recommendations should consider sex. Now, findings from a new study suggest that having an average systolic blood pressure of 160 mm Hg or higher increases the risk of dying from cardiovascular disease (CVD) among women by 113 percent.
Researchers drew on data from more than 53,000 middle-aged adults enrolled in the NHANES studies. Over about ten years, they measured the participants' blood pressures three times and averaged the measures. They also tracked the participants' CVD-related death rates.
They found that links between blood pressure measures and CVD-related deaths differed by sex. Women experience a 61 percent increased risk of cardiovascular death when systolic blood pressure reaches between 130-139 mm Hg, and it soars to 113 percent when at 160 mm Hg or higher. In comparison, men see a 76 percent increased risk only when systolic measures are 160 mm Hg or higher.
When considering diastolic blood pressure, men had a higher risk of dying from CVD if measures were too low (below 70 mm Hg) or too high (80 mm Hg or more), compared to the risk associated with measures between 70 and 80 mm Hg. Again, for women, the risk was higher with diastolic measures that were too low (below 50 mm Hg) or too high (80 mm Hg or higher).
These findings suggest that having high blood pressure markedly increases the risk of death from CVD, and this risk begins at much lower measures among women than men.
Nearly two-thirds of adults in the United States have high blood pressure, defined as having a systolic pressure of 130 mmHg or higher or a diastolic pressure of 80 mmHg or higher. High blood pressure increases a person’s risk for heart disease and stroke and contributes to small vessel disease, a major risk factor for cardiovascular disease, dementia, and stroke. However, lifestyle factors, such as sauna use, help maintain healthy blood pressure. Learn more in this clip featuring Dr. Jari Laukkanen.
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Even minimal exercise linked to 47 percent lower anxiety risk in older adults. www.sciencedirect.com
Many older adults have generalized anxiety disorder, a persistent feeling of anxiety or dread that interferes with everyday life. Evidence suggests that physical activity alleviates symptoms of anxiety, but scientists don’t know how much activity is optimal. A recent study found that older adults who engaged in regular physical activity were 47 percent less likely to experience symptoms of anxiety than those who engaged in no activity.
Researchers drew on data from more than 7,600 older adults enrolled in The Irish Longitudinal Study on Ageing (TILDA). They gathered information about the participants' physical activity levels, worry symptoms, and anxiety levels over ten years. They assessed the participants' activity levels and categorized them as having no, low, medium, or high activity levels.
They found that participants with high activity levels were 31 percent less likely to develop anxiety than those with no activity. However, participants who engaged in even minimal moderate-intensity physical activity – equivalent to just 10 minutes a day, five times a week – were 47 percent less likely to develop anxiety than those with no activity.
These findings suggest that even a small amount of physical activity has robust effects on mood in older adults, markedly reducing the risk of developing anxiety. They also align with previous research, which found that older adults enrolled in TILDA who met WHO physical activity guidelines were 63 percent less likely to develop generalized anxiety disorder than those who did not.
Exercise supports the health of pericytes, tiny contractile cells surrounding the brain’s capillaries that regulate vascular blood flow and maintain blood-brain barrier integrity. Pericytes detach from the blood vessels in aging, driving the pathophysiology of neurological dysfunction, vascular dementia, and mood disorders like anxiety. Learn more in this episode featuring Dr. Axel Montagne.
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Medications induce gray hair re-pigmentation, pointing to potential future therapies. www.ncbi.nlm.nih.gov
Graying hair is a cardinal sign of aging, typically beginning in a person’s fourth or fifth decade. Nutritional deficiencies, including low intake of protein, vitamin B12, iron, and copper, can contribute to premature graying. However, a recent review found that some medications may promote gray hair re-pigmentation.
Researchers reviewed 27 studies and case reports of medication-induced gray hair re-pigmentation, totaling 133 patients. They categorized the various drugs as anti-inflammatories, stimulators of melanogenesis (the production of melanin, the pigment responsible for hair, skin, and eye color), vitamins, medications that accumulate in tissues, and those with an undetermined mechanism. Then, they ranked the quality of the evidence for each study or report.
They found that medications that reduce inflammation or stimulate melanogenesis can promote diffuse re-pigmentation of gray hair. They also found that vitamin B complex supplementation may contribute to the darkening of gray hair, but they cautioned that evidence supporting this finding was weak.
These findings suggest that certain medications induce gray hair re-pigmentation. Although these drugs aren’t presently recommended for treating gray hair, their mechanisms provide insights into potential targets for future medications aimed at hair re-pigmentation.
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Naringenin, a citrus fruit flavonoid, preserves muscle mass in aging while enhancing exercise capacity and aerobic metabolism efficiency (animal study). medicalxpress.com
Muscle mass declines markedly with age, with up to 8 percent muscle mass loss occurring per decade after age 30. Evidence suggests that naringenin, a flavonoid compound found in citrus fruits, maintains muscle mass in aging. Mice that ate a diet supplemented with naringenin showed improved muscle endurance and grip strength.
Researchers supplemented the diets of young adult mice, middle-aged mice, and mice prone to muscular dystrophy (accelerated muscle loss) with naringenin. Then, they assessed naringenin’s effects on exercise capacity and aerobic metabolic levels in skeletal muscle.
They found that young adult and middle-aged mice receiving naringenin could run farther than those that did not. Middle-aged mice also showed improved grip strength and increased calf muscle size. Mice prone to developing muscular dystrophy ran farther and showed improved grip strength.
The researchers attributed these improvements in muscle endurance to naringenin’s capacity to increase the number of oxidative myofibers (muscle fibers that use oxygen) and improve the overall efficiency of aerobic metabolism in the body. They found that Sp1, a transcription factor that influences gene expression in muscle, likely mediated naringenin’s effects.
These findings indicate that naringenin may preserve muscle mass in aging and disease. Other dietary components, such as omega-3 fatty acids, influence muscle maintenance, too. Learn more in this episode featuring Dr. Chris McGlory.
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Vitamin D, best known for maintaining calcium balance and bone health, is critical in many physiological processes, including blood pressure regulation, immune function, and cell growth. Evidence now suggests vitamin D also influences body composition and muscle strength. A recent study in mice showed that high vitamin D intake increased muscle strength and mass without altering body weight.
Researchers fed mice one of three diets, providing low, normal, and high doses of vitamin D for four weeks to achieve deficient, insufficient, and sufficient vitamin D concentrations, respectively. At the end of the fourth week, they assessed the animals' grip strength (a measure of muscle function) and body composition.
They found that compared to low or normal vitamin D intake, high intake increased grip strength and lean mass and decreased fat mass without altering the animals' weights. High intake also impaired myostatin production and increased the animals' leptin sensitivity and energy expenditure without altering their activity levels.
Leptin is a satiety hormone that signals the brain to balance energy. When body fat increases or decreases, blood concentrations of leptin change accordingly. Higher leptin levels signal the brain to reduce hunger and boost energy use. However, in obesity, the body becomes less responsive to leptin, dulling its effects on appetite and energy expenditure.
These findings suggest that vitamin D influences body composition and metabolism by preferentially allocating calories toward muscle development and overall growth rather than fat storage. They also highlight the intricate relationship between obesity and vitamin D status. Learn more about vitamin D in our comprehensive overview article.
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Dementia cases could surpass previous estimates by 40 percent, highlighting the need for prevention. medicalxpress.com
Nearly 50 million people worldwide live with Alzheimer’s disease or another form of dementia — a number projected to triple in the coming decades. However, a recent study suggests the number could be even higher, as much as 40 percent more than previous estimates.
Researchers analyzed data from the English Longitudinal Study of Ageing, a long-term study of older adults living in England and Wales. They identified dementia cases from among more than 90,000 people. Then, they analyzed how dementia incidence changed over time based on age, sex, and education.
They found that dementia incidence decreased by 28.8 percent between 2002 and 2008 and then increased by 25.2 percent between 2008 and 2016 (nearly 3 percent per year). People with lower educational attainment experienced a slower decline in dementia during 2002-2008 and a more rapid increase after 2008, demonstrating growing disparities. The researchers predicted that if dementia incidence continues to rise at the same pace observed from 2008 to 2016, the number of people living with dementia will roughly double by 2040.
These findings suggest that the number of people with dementia will be markedly higher in the coming decades. Evidence suggests lifestyle factors influence a person’s dementia risk. Learn how sauna use, exercise, sleep, and dietary components, such as omega-3 fatty acids and sulforaphane exert robust anti-aging effects on the brain, potentially preventing or forestalling dementia.
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Accelerated biological aging is linked to a 40 percent higher risk of vascular dementia and stroke. medicalxpress.com
Aging is the collective physiological, functional, and mental changes that accrue in a biological organism over time. However, people age at different rates, a consequence of both genetic and environmental factors. A recent study found that people whose biological age is five years older than their chronological age are roughly 40 percent more likely to develop vascular dementia or experience a stroke than those whose biological and chronological ages align.
Using 18 routinely measured clinical biomarkers, researchers calculated the biological ages of more than 325,000 people enrolled in the UK Biobank study. Then, they evaluated how older biological age influenced the occurrence of neurological conditions, including dementia of all types, stroke, Parkinson’s disease, and motor neuron disease, over a nine-year follow-up period.
They found that nearly 1,400 participants developed dementia, and more than 2,500 experienced a stroke. Having an older biological age that was five years older than chronological age increased the participants' risk of dementia by 26 percent, vascular dementia by 41 percent, and stroke by 39 percent. The findings were consistent even after considering various disease-specific risk factors.
These findings suggest that accelerated biological aging markedly increases the risk of dementia and stroke. Age acceleration can result from intrinsic factors, such as normal metabolism and genetics, or extrinsic factors, such as diet, smoking, and exercise. Learn how epigenetic changes influence biological aging in our overview article.
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Lifelong choline supplementation provides a potential shield against Alzheimer's disease in mice. www.ncbi.nlm.nih.gov
Choline, an essential nutrient found in eggs, meat, fish, beans, and nuts, supports the production of acetylcholine, a neurotransmitter involved in neurogenesis, synapse formation, learning, and memory. Most people living in the US don’t consume enough choline – 550 milligrams per day for men and 425 milligrams per day for women – potentially increasing their risk for various diseases. A 2019 study in mice found that lifelong choline supplementation prevented Alzheimer’s disease and preserved cognitive function.
Researchers fed mice susceptible to developing Alzheimer’s disease a regular diet or a diet supplemented with choline from early life to old age. When the mice reached the age of 10 months, the researchers assessed the animals' memory function and examined their brain tissue.
They found that mice that received lifelong choline supplementation had better spatial memory and fewer amyloid-beta plaques in their brains than those on a regular diet. They also found that the mechanisms driving these effects were related to reduced amyloid-beta peptide synthesis, a dampened microglia inflammatory response, and downregulation of the alpha-7 nicotinic acetylcholine and sigma-1 receptors, both of which are critical for various neurological processes.
These findings suggest that lifelong choline supplementation mitigates Alzheimer’s disease pathology and maintains cognitive function in mice susceptible to the disease. Other research showed that mice that ate a choline-poor diet had higher brain levels of amyloid-beta and tau – two proteins implicated in the pathogenesis of Alzheimer’s disease – than those that ate a choline-rich diet. The mice that ate a choline-poor diet also gained weight, showed signs of altered metabolism, liver damage, and enlarged hearts, and performed poorly on motor skills tests.
More than 55 million people worldwide live with Alzheimer’s disease. Learn more about the disease and how to prevent it in this episode featuring Dr. Dale Bredesen.
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Hyperbaric oxygen therapy reverses aspects of the cellular aging process in older adults, boosting immune cell function. www.sciencedaily.com
Hyperbaric oxygen therapy involves exposure to oxygen at up to three times the normal pressure, increasing the amount of oxygen the blood can carry. A 2020 study found that hyperbaric oxygen therapy prevented telomere shortening and cellular senescence – hallmarks of cellular aging – in older adults, effectively reversing the aging process.
The study involved 35 older adults who underwent 60 hyperbaric oxygen therapy treatments over three months. Using blood samples the participants provided before, during, and after the intervention, researchers assessed the participants' immune cell telomere length and senescence.
They noted a 20 percent or greater increase in T helper, T cytotoxic, natural killer, and B cell telomere length following the hyperbaric treatments. B cell telomeres showed the greatest change, increasing as much as 52 percent post-treatment. B cells facilitate adaptive immunity – producing antibodies against bacterial, viral, and toxic exposures. The number of senescent T helper cells decreased by roughly 37 percent; senescent T cytotoxic cells decreased by 11 percent.
Telomeres are short, repetitive sequences of DNA located on the ends of chromosomes. They form a protective “cap” – a sort of disposable buffer that gradually shortens with age – that prevents chromosomes from losing genes or sticking to other chromosomes during cell division. When the telomeres on a cell’s chromosomes get too short, the cell stops dividing or dies. Learn more about telomeres in this episode featuring Dr. Elisa Epel.
Cellular senescence is the condition or process of deterioration that occurs with age. Cells that acquire enough damage can become senescent, rendering them metabolically inactive and unable to replicate. Senescent cells often release proinflammatory cytokines, driving the deterioration of neighboring healthy cells. Learn more about cellular senescence in this episode featuring Dr. Judith Campisi.
These findings suggest that hyperbaric oxygen therapy reverses some of the effects of aging in immune cells. However, this study was small and had no control group. Future research with larger groups may shed more light on the effectiveness of hyperbaric oxygen in slowing or reversing cellular aging.
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Dietary AGEs linked to overeating and 30 percent shorter lifespan in worms. www.sciencedaily.com
Advanced glycation end-products (AGEs) form when the sugars, amino acids, and fats in food encounter heat. The molecules in the foods rearrange, forming brown polymers (a process known as the Maillard reaction) and creating the deep flavors of browned barley in beer, roasted coffee, seared meats, and French fries. A recent study in worms shows that dietary AGEs promote overeating and reduce lifespan by as much as 30 percent in those genetically susceptible.
Researchers investigated the health effects of AGEs in Caenorhabditis elegans, a type of roundworm often used to model human aging. Specifically, they looked at the effects of dietary AGEs derived from methylglyoxal, a byproduct of glycolysis and lipid peroxidation.
They found that worms lacking the gene for glyoxalase, an enzyme that protects the body from methylglyoxal-derived AGEs, showed increased appetite when exposed to AGEs. They also found that the methylglyoxal-derived AGE known as MG-H1 influences the production of the neurotransmitter tyramine, ultimately contributing to the harmful effects of AGEs, including increased feeding, decreased lifespan, and neuronal damage.
These findings suggest that dietary AGEs promote overeating and reduce lifespan by as much as 30 percent in genetically susceptible organisms. Although AGEs are present in the diet, they also form in the body during normal glucose metabolism. However, if high AGE levels accumulate in the tissues and blood, they can become pathogenic, driving many chronic diseases, including diabetes, atherosclerosis, Alzheimer’s disease, macular degeneration, and kidney failure. The body clears excess AGEs via the liver (and possibly the kidney)00462-3/fulltext), but the clearance rate declines with age.
Evidence suggests that a low carbohydrate diet inhibits AGE formation. The ketogenic diet typically restricts carbohydrate intake to roughly 10 percent or less of one’s calories. Learn more about the ketogenic diet and its health effects in this episode featuring Dr. Dominic D'Agostino.
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Greater blood pressure variability is linked with cognitive decline in older adults. www.sciencedaily.com
Scientists have long understood that high blood pressure increases a person’s risk for cognitive decline and dementia. Now, evidence suggests that blood pressure variability carries similar risks. A recent study found that older adults with higher blood pressure variability performed worse on cognitive tests than those with lower variability.
Blood pressure variability occurs in response to various physiological and environmental factors that influence arterial blood pressure. Scientists classify blood pressure variability according to five types: short-term (beat to beat), short-term (24 hours), mid-term (day to day), long-term (less than five years), or very long-term (more than five years). People with high blood pressure tend to have higher variability than those with normal pressure.
Researchers measured the blood pressure of 70 older adults (aged 60 to 80) without dementia over several days. The participants took cognitive tests and underwent tests to determine their arterial stiffness – a well-established cardiovascular risk factor for cognitive impairment and closely linked with high blood pressure.
The researchers found that regardless of the participants' average blood pressure, those with high systolic short-term exhibited poor attention and psychomotor speed, and those with mid-term blood pressure variability showed poor executive function. Those with higher systolic short-term blood pressure variability tended to have higher arterial stiffness.
These findings suggest that higher blood pressure variability influences cognitive function, potentially reflecting early-stage decline better than average blood pressure. They also underscore the importance of maintaining healthy blood pressure throughout the lifespan. Learn how lifetime high blood pressure increases dementia risk in this clip featuring Dr. Axel Montagne.
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Longevity study reveals key blood markers increase chances of living to 100 and beyond. www.sciencealert.com
By the year 2050, the number of centenarians – people who are 100 years or older – is expected to increase fivefold. Many factors promote centenarians' extraordinary longevity and likely involve the interaction of both lifestyle and genetic variables. A recent study has found that the blood of centenarians differs from their younger counterparts.
The study followed more than 44,000 people from their mid-60s to late 90s until they died. Of these, 1224 of them lived to 100 years old. Using blood samples collected earlier in the participants' lives, researchers assessed 12 blood-related biomarkers previously associated with aging or early death, including those associated with inflammation and indicators of malnutrition, anemia, and liver, kidney, and metabolic function.
They found that higher levels of total cholesterol and iron and lower levels of glucose, creatinine, uric acid, and several enzymes involved in metabolism increased the likelihood of reaching 100 years. Notably, centenarians exhibited strikingly consistent biomarker profiles, even from age 65 and beyond, displaying more favorable values than their shorter-lived counterparts.
Centenarians often carry genetic variants called single-nucleotide polymorphisms associated with longevity. They tend to develop disease much later in life than people of average age span, a phenomenon called “compression of morbidity,” and have longer telomere lengths than adults two to three decades younger. The highest concentrations of centenarians worldwide live in Okinawa, Japan; Sardinia, Italy; Nicoya, Costa Rica; Ikaria, Greece; and Loma Linda, California.
The findings from this study demonstrate that biomarkers related to various genetic or lifestyle influences may contribute to greater longevity. Inflammation also plays a role in longevity. Learn more in this clip featuring Dr. Valter Longo.
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Agricultural PM2.5 pollution significantly worse for dementia risk: 13 percent increase compared to 5 percent from wildfires. www.sciencedaily.com
Particulate matter in air pollution is a mixture of solid particles and liquid droplets. It forms fine inhalable particles with diameters typically 2.5 micrograms (PM2.5) or less. Exposure to particulate matter promotes oxidative stress and increases the risk of developing many chronic diseases, including cardiovascular disease, cancer, hypertension, and diabetes. A recent study found that particulate matter in air pollution from agriculture increases the risk of dementia in older adults.
The study involved more than 27,000 adults enrolled in the Environmental Predictors of Cognitive Health and Aging study. Participants were over the age of 50 and dementia-free at the time of enrollment. Using spatiotemporal and chemical transport models, researchers assessed the participants' exposure to PM2.5 from nine emission sources over a 10-year period.
They found that exposure to higher levels of PM2.5 increased the risk of dementia by 8 percent. When they examined specific PM2.5 sources, they discovered that agriculture PM2.5 increased dementia risk by 13 percent, while wildfire PM2.5 increased risk by 5 percent.
These findings suggest that reducing PM2.5 pollution, particularly from agricultural and wildfire sources, could benefit cognitive health in older adults. However, further research is necessary to validate these findings and explore potential intervention strategies.
Evidence suggests that sulforaphane, a bioactive compound derived from broccoli, counters some of the harmful effects of particulate matter. Learn more about sulforaphane in our comprehensive overview article.
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Strength training raises resting metabolic rate by 9 percent in men, countering age-associated energy expenditure decreases. pubmed.ncbi.nlm.nih.gov
As people age, their total energy expenditure (total calories burned in a day) decreases primarily due to declines in resting metabolic rate and the energy expenditure of physical activity, driving increases in body fat. Strength training increases fat-free mass (muscle mass), offering a promising intervention to offset these declines. A 2001 study found that strength training increased resting metabolic rate in men, regardless of age, by 9 percent.
The study involved young and older men and women participating in a supervised strength training program three days a week for 24 weeks. Participants maintained their usual diet and body weight throughout the study period. Researchers assessed the participants' resting metabolic rate and energy expenditure of physical activity before and after the intervention.
They found that strength training increased the participants' resting metabolic rate by 7 percent, regardless of age. However, they observed a gender-related difference, with men experiencing a 9 percent increase in resting metabolic rate, while women did not experience a notable increase. This effect persisted even after adjusting for fat-free mass.
These findings suggest that strength training increases resting metabolic rate, an effect influenced by gender but not age. Learn more about the benefits of strength training in this episode featuring Dr. Brad Schoenfeld.
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Playing American football linked to a 61 percent higher risk of parkinsonism and Parkinson's disease. neurosciencenews.com
The relationship between repetitive blows to the head (as in boxing) and parkinsonism and Parkinson’s disease is well established. However, scientists don’t fully understand the relationship between American football and these conditions. A recent study found that playing American football increases a person’s risk of parkinsonism and Parkinson’s disease by 61 percent.
Researchers conducted a cross-sectional study using data from 1,875 men enrolled in the Fox Insight study, in which participants completed online questionnaires regarding their health status. They collected data on aspects of football participation, including duration of play, highest level played, and age at first exposure. The analysis accounted for various factors, including age, education, medical history, body mass index, concussions, and family history of Parkinson’s disease.
They found that those who had played football were 61 percent more likely to report having parkinsonism or Parkinson’s disease than those who did not. Those who experienced higher levels of play (such as college or professional level) were nearly three times more likely to report being diagnosed with these conditions.
Parkinsonism is an umbrella term that describes a group of neurological disorders that share similar symptoms with Parkinson’s disease, including tremors, muscle stiffness, slow movement, and difficulties with balance and coordination. Parkinson’s disease is the primary cause of parkinsonism, driving approximately 80 percent of all cases.
These findings suggest that playing American football markedly increases the risk of parkinsonism and Parkinson’s disease. However, this study does not prove causation but highlights a potential link between sports-related head injuries and long-term neurological consequences. Learn more about Parkinson’s disease in this episode featuring Dr. Giselle Petzinger.
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"Exercise snacks" – short bursts of activity interspersed throughout the day – boost fitness levels in sedentary adults. pubmed.ncbi.nlm.nih.gov
Sedentary behavior is associated with an increased risk of many chronic diseases. Evidence suggests that “exercise snacks” – brief, isolated intervals of vigorous exercise, each lasting less than one minute and typically performed multiple times throughout the day – may counter the harmful effects of sedentary behavior. A 2022 study found that vigorous stair-climbing increased participants' peak oxygen uptake by approximately 5 percent.
The study involved 24 healthy, sedentary young adults. For six weeks, half of the participants engaged in three bouts of vigorous stair climbing (60 steps in a three-flight stairwell) daily, with one to four hours of rest in between, three days a week. The other half did not participate in any training. Researchers measured the participants' peak oxygen uptake and power output before and after the intervention.
At the end of the intervention, the stair-climbing participants' peak oxygen uptake had increased by approximately 5 percent, and peak power output increased by 12 percent. Participants maintained a consistent rate of perceived exertion of 5, indicating a “hard” level, and their heart rate remained relatively stable at approximately 85 percent of the age-predicted maximum.
These findings suggest that integrating brief periods of intense exercise into one’s daily routine can improve cardiorespiratory fitness in sedentary adults. They also align with previous research showing that exercise snacks improve insulin sensitivity in people with insulin resistance.
A key benefit of exercise snacks is that they eliminate the need for specialized equipment and the scheduling of leisure time for structured exercise. They are easily integrated into everyday activities, whether inserting short bursts of activity between tasks or incorporating them into daily routines at home, work, or school. Exercise snacks can also reduce blood glucose levels in people with type 2 diabetes. Learn more in this clip featuring Dr. Martin Gibala.
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Delta-9-tetrahydrocannabinol – better known as THC – is the primary psychoactive compound found in cannabis. THC binds to endocannabinoid system receptors, eliciting a wide range of physical effects and producing the “high” associated with its use. A new study suggests that THC reverses brain aging in old mice.
Researchers injected old mice with a microdose of THC that was roughly three to four orders of magnitude lower than a typical dose. Then, they assessed gene expression in the animals' hippocampal tissue at five days and five weeks post-treatment.
After just five days, they found that the microdose THC treatment altered the expression of 18 genes related to neurogenesis (the production of new nerve cells). THC altered the expression of 88 genes related to nerve cell survival and development five weeks post-treatment. Interestingly, THC did not affect brain-derived neurotrophic factor, a protein noted for its effects on neurogenesis.
These findings suggest that a single microdose of THC exerts potent, enduring effects on the rodent brain and may have potential applications in humans. It also aligns with results from a compelling case study in which THC microdosing ameliorated symptoms of Alzheimer’s disease. Lactate, a molecule produced during vigorous exercise, also has robust effects on the brain, influencing neurogenesis and promoting cognitive function. Learn more in this episode featuring Dr. George Brooks.
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Higher fish and omega-3 intake linked to 12 percent lower hip fracture risk. www.nutraingredients-asia.com
Hip fractures can lead to a decline in self-reliance, diminished quality of life, and feelings of depression. However, some research suggests that consuming fish and omega-3 fatty acids influences a person’s risk of experiencing a hip fracture. A 2019 meta-analysis and systematic review found that higher fish and omega-3 intake reduces the risk of hip fracture by as much as 12 percent.
Researchers reviewed the findings of 10 studies involving nearly 300,000 people. Seven of the studies followed people over time (prospective), and three compared groups with and without fractures (case-control).
They found that people who consumed more fish had a lower risk of hip fractures, even when combining the results from prospective and case-control studies. They found the same protective effect for those who consumed higher omega-3s in their diets. Notably, the protective effect of fish and omega-3 intake remained only when considering larger prospective studies (involving 10,000 participants or more) or studies that included body mass index as a factor.
These findings suggest that dietary intake of fish and omega-3s might promote bone health and reduce the risk of hip fractures. Other studies have proposed mechanisms by which omega-3s exert their beneficial effects. For example, one study found that DHA inhibits osteoclast formation and subsequent bone resorption by inhibiting the production of TNF-alpha, a pro-inflammatory molecule. A separate study demonstrated that resolvin, a byproduct of omega-3 metabolism, promotes bone preservation under inflammatory conditions and influences the PI3K-AKT pathway, a major signaling pathway implicated in many human diseases, including osteoporosis.
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Cardiovascular aging is characterized by marked functional decline and increased cardiovascular disease risk. Evidence suggests that flavonols, a broad class of bioactive compounds found in cocoa and other fruits, exert cardioprotective effects, bolstering cardiorespiratory fitness. A recent study shows that older adults who took cocoa flavonols experienced a nearly 10 percent gain in peak oxygen consumption, a marker of cardiorespiratory fitness, during exercise.
Researchers conducted a study involving 68 healthy older adults aged 55 to 79. Half of the participants took 1,000 milligrams of cocoa flavonols daily for a month, while the other half took a placebo. The researchers measured the participants' peak oxygen consumption during exercise and assessed other aspects of their cardiovascular health, including blood pressure and blood vessel health.
They found that participants who took the cocoa flavonols showed marked improvements in their cardiorespiratory fitness. Their oxygen use during exercise increased by nearly 10 percent, and their exercise capacity increased by more than 6 percent. Their resting systolic and diastolic blood pressures decreased by 5.4 mmHg and 2.9 mmHg, respectively, and their blood vessel function improved by 1.3 percent. Those who took the placebo didn’t demonstrate these improvements.
These findings suggest that cocoa flavonols benefit older adults' cardiovascular health by improving fitness levels and other health markers, potentially promoting better heart health in aging. Interestingly, the benefits of cardiorespiratory fitness extend to cognitive function, too. Learn more in this clip featuring Dr. Axel Montagne.
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Hearing aids show promise in reducing dementia risk by half in high-risk older adults, new study reveals. www.cnn.com
Older adults with hearing loss are more likely to experience cognitive decline and an increased risk of developing dementia. However, a new study suggests that hearing aids can moderate this risk. Older adults with hearing loss who wore hearing aids were nearly half as likely to develop dementia as those who didn’t.
Researchers recruited nearly 1,000 older adults aged 70 to 84 with untreated hearing loss. About half of the participants received hearing aids, and the other half received health education counseling. The researchers assessed the participants' cognitive function every six months for three years.
They found no difference in cognitive decline between the two groups when considering the entire cohort. However, when they looked at specific subgroups, they found that the effect of hearing aids on cognitive change varied according to the participants' risk profiles. Specifically, hearing aids appeared to reduce cognitive change in older adults with a higher risk of decline but not in those with a lower risk.
These findings suggest that hearing aids benefit older adults with a higher risk of cognitive decline. Approximately two-thirds of all adults over 70 have some degree of hearing loss. Evidence suggests that adhering to healthy dietary patterns such as the DASH diet or the Mediterranean diet reduces the risk of mild hearing loss by nearly 30 percent, highlighting potential links between diet, dementia, and hearing loss. Learn more about dietary strategies to reduce the risk of dementia in this episode featuring Dr. Dale Bredesen.
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Vitamin D is a steroid hormone that plays critical roles in many physiological processes, including blood pressure regulation, immune function, and cell growth. Findings from a new study suggest that vitamin D prevents dementia. People who took vitamin D were 40 percent less likely to develop dementia than those who didn’t.
The study involved more than 12,000 older adults who did not have dementia at enrollment. Researchers categorized the participants based on their vitamin D exposure: those exposed to vitamin D before dementia onset and those not exposed before dementia onset. They also examined different forms of vitamin D (calcium + vitamin D, cholecalciferol [D3], and ergocalciferol [D2]) to see if their effects on dementia rates varied and explored potential interactions with other risk factors for dementia, such as age, sex, education, race, cognitive function, depression, and apolipoprotein E4 (APOE4) status.
They found that participants exposed to vitamin D had a 40 percent lower risk of developing dementia. They were also dementia-free longer than those without vitamin D exposure. These effects were evident across various forms of vitamin D. Further analysis revealed that sex, cognitive status, and APOE4 status influenced the extent of vitamin D’s effects on dementia risk. For example, females, people with normal cognitive function, and those who did not carry the APOE4 gene variant seemed to gain greater protection against dementia.
These findings suggest that vitamin D supplementation holds promise as a preventive measure for dementia, especially for people at higher risk of developing the condition. However, more research is required to fully understand the mechanisms behind this association and establish specific vitamin D supplementation guidelines to reduce dementia risk. Learn more about vitamin D in our comprehensive overview article.
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Every 1 percent drop in body weight slows brain aging by nearly nine months, highlighting the substantial, and often overlooked, neuroprotective benef elifesciences.org
Excess body fat harms multiple organ systems, including the central nervous system, potentially accelerating brain aging. A new study shows that a 1 percent weight loss delays brain aging by nearly nine months.
Researchers conducted a study involving 102 participants enrolled in the DIRECT-PLUS study who underwent an 18-month lifestyle intervention to promote weight loss. Using magnetic resonance imaging, the researchers assessed the resting-state functional connectivity in the participants' brains and predicted their brain ages. They also evaluated how various health factors, such as body measurements, blood markers, and fat deposits, affect brain aging.
They found that the brain age prediction model accurately predicted the participants' chronological ages. They also found that brain aging slowed by 8.9 months for every 1 percent of body weight loss, an effect linked with improved liver health and reduced liver, visceral, and subcutaneous fat. Their analysis revealed that lower consumption of processed foods, sweets, and beverages delayed brain aging.
These findings suggest that weight loss may benefit the brain’s aging process, potentially slowing its aging trajectory. They also underscore the importance of maintaining a healthy weight throughout the lifespan to support overall brain health. Sulforaphane, a bioactive compound derived from broccoli, benefits brain health and may influence its aging, too. Learn more in this episode featuring Dr. Rhonda Patrick.
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Daily multivitamin supplementation boosts memory in older adults, particularly those with cardiovascular disease. neurosciencenews.com
Short-term memory – such as remembering a list of items or numbers shortly after hearing them – is particularly vulnerable as we age. But a new study shows that multivitamin/multimineral supplementation bolsters short-term memory in older adults, especially those with cardiovascular disease.
The study involved more than 3,500 older adults (average age, 71 years) enrolled in the COSMOS trial. About half of the participants took a daily multivitamin/multimineral supplement for three years, and the other half took a placebo. All participants completed a battery of cognitive tests at the one-, two-, and three-year points.
The tests revealed that those who took the supplement performed better on short-term memory tests than those who took the placebo, an effect that endured over the entire three-year study. Participants with cardiovascular disease scored lower on memory tests initially, but after taking the multivitamin/multimineral supplements for a year, their memory scores improved, reaching a level comparable to those without cardiovascular disease.
These findings suggest that multivitamin/multimineral supplementation benefits short-term memory in older adults. The study’s authors proposed that the cognitive effects of multivitamin/multimineral intervention may occur by activating vitamin and mineral receptors in the hippocampus, given its prominent role in recall memory. Learn how vitamins and minerals influence other aspects of aging in this episode featuring Dr. Bruce Ames.
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Older women and those with obesity clear alcohol from their systems 52 percent faster, according to new research. www.technologynetworks.com
The effects of alcohol vary between people, largely due to differences in alcohol absorption rates and metabolism in the gut. A new study has found that older women and those with obesity clear alcohol from their systems 52 percent faster than younger women and those with healthy weights.
Researchers analyzed the findings of three studies that investigated alcohol clearance rates in 143 women. They used a computer-assisted alcohol infusion system to model the self-administration of alcohol. They also measured the women’s body fat via DEXA or bioelectrical impedance.
They found that women with obesity, particularly those who were older, cleared alcohol 52 percent faster than women with a healthy weight. They also found that age and lean body mass explained 72 percent of the differences in the alcohol elimination rate among women.
These findings suggest that women with obesity eliminate alcohol faster than leaner women, likely due to the increase in fat-free mass that often accompanies obesity, especially in older women. Drinking alcohol increases a person’s risk for many chronic diseases, but exercise can help reduce alcohol cravings. Learn more in this short video featuring Dr. Rhonda Patrick.
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Novel collagen supplement containing glycine-proline dipeptide improves qualities of skin aging and health, such as wrinkle formation, roughness, and academic.oup.com
Ultraviolet (UV) light exposure – from the sun or tanning beds – causes premature skin aging, a process called photoaging. But a new study in mice found that supplemental collagen, which is rich in the glycine-proline dipeptide, protects against the damaging effects of UV light exposure. Mice that received collagen during regular exposure to UV light had fewer wrinkles and other signs of photoaging than those that didn’t.
Researchers exposed young mice to one of four treatments for 12 weeks: UV light only; UV light plus low-dose collagen (300 milligrams per kilogram); UV light plus high-dose collagen (500 milligrams per kilogram); or neither exposure. They measured the animals' plasma collagen concentrations, and then, at the end of the study, they assessed the animals' skin for signs of photoaging.
They found that collagen concentrations increased considerably within 30 minutes of consumption. They also found that both low- and high-dose collagen reduced wrinkle development and skin thinning and improved the skin’s hydration.
These findings suggest supplemental collagen protects against photoaging in mice, aligning with a recent review and meta-analysis. Interestingly, some evidence suggests collagen supplementation in the setting of exercise recovery reduces joint pain and improves joint functionality but appears to have no significant effect on post-exercise muscle protein synthesis necessary for hypertrophy and muscle collagen protein synthesis.
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Omega-3 supplementation in mice reverses aging effects on brain's lipid rafts, enhancing cognitive function. onlinelibrary.wiley.com
Lipid rafts – cholesterol-filled “bubbles” found in neuronal cell membranes – play a crucial role in synaptic plasticity and memory formation. However, lipid rafts undergo extensive changes during aging, ultimately contributing to cognitive decline. A new study in mice shows that omega-3 fatty acids preserve lipid raft integrity and bolster cognitive function.
Researchers fed young and old female mice a regular diet or a diet supplemented with omega-3 fatty acids. Then they examined the animals' brains to determine the omega-3s' effects on the structure and properties of the lipid rafts.
They found that older mice fed a regular diet exhibited changes consistent with lipid raft aging, including reduced omega-3 fatty acid concentrations, increased membrane lipid saturation, and altered lipid composition. However, omega-3 supplementation reversed these changes to the point where they resembled the lipid rafts typically seen in younger mice. In addition, omega-3 supplementation influenced the distribution and accumulation of glutamate receptors and ion channels involved in synaptic plasticity, potentially influencing memory formation.
These findings suggest that omega-3 fatty acids counteract age-related changes in the brain, specifically in lipid rafts, and preserve cognitive function and memory in aging. Learn more about omega-3s' roles in preserving cognitive function in this clip featuring Dr. Axel Montagne.
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DHA-rich diet protects against memory deficits and loss of smell in Alzheimer's-prone APOE4 mice, reveals new study. link.springer.com
A diminished or lost sense of smell is a common feature of the early stages of Alzheimer’s disease and other forms of dementia. But a new study in mice that carry the APOE4 gene variant, the primary genetic risk factor for Alzheimer’s disease, shows that DHA – a type of omega-3 fatty acid found in fish – protects against these losses. APOE4-carrying mice that ate a DHA-rich diet retained their sense of smell and the ability to distinguish between objects based on their scent.
Researchers fed normal mice and APOE4 carriers a regular diet or one supplemented with DHA. Then, using MRI scans, they assessed the animals' brain structures and studied their behavior related to smell and the recognition of new objects. They also measured biomarkers related to cell death and inflammation.
They found that the APOE4-carrying mice given a regular diet exhibited memory deficits and difficulty adjusting to new smells and distinguishing between different objects. In addition, their brains showed increased signs of inflammation in the olfactory bulb – the area responsible for the sense of smell. However, APOE4-carrying mice that ate the DHA-rich diet did not exhibit these characteristics.
These findings suggest that a DHA-rich diet benefits APOE4 carriers. Learn more about the beneficial effects of DHA in our comprehensive omega-3 overview article.
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The unique balance of gut viruses, termed the virome, may hold the secret to centenarians' longevity, new research proposes. healthsciences.ku.dk
The gut virome – the collection of viruses inhabiting the gut – plays a crucial role in shaping the immune system and defending against infections throughout the lifespan. A new study shows that centenarians' viromes differ from those of younger people, potentially contributing to their longevity.
Researchers examined the gut viromes of centenarians and compared them with those of younger people. Then they analyzed the viruses' auxiliary metabolic gene activity. Auxiliary metabolic genes are found in bacteriophages – viruses that infect bacteria. They help viruses manipulate their host cells' metabolism to facilitate viral replication.
They found that the centenarians exhibited more diverse viromes than younger people. In addition, the centenarians' viromes demonstrated increased lytic activity, indicating that their viromes were more active in infecting and destroying bacterial cells. Finally, they found that the centenarians' gut viruses possessed an abundance of auxiliary metabolic genes involved in sulfate metabolism, the byproducts of which promote gut integrity and pathogen resistance.
These findings suggest that centenarians' viromes differ markedly from those of younger people in terms of makeup and activity, potentially contributing to centenarians' healthspan and longevity. Learn more about the role gut microbial populations play in human health in this episode featuring Dr. Eran Elinav.
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Resistance training – not just aerobic exercise – found to enhance skin health and potentially counteract skin aging. www.nature.com
Aerobic exercise has profound effects on the human body – including the skin. Now findings from a new study suggest that resistance training slows skin aging. Women who engaged in resistance training had thicker, more resilient skin than women who engaged in aerobic exercise alone.
Researchers compared the effects of aerobic versus resistance training on skin aging in 56 sedentary, middle-aged women. The participants engaged in a twice-weekly supervised exercise program involving either aerobic or resistance training for 16 weeks. The researchers evaluated the participants' skin properties, body composition, and physical capacity before and after the intervention.
They found that both types of training improved skin elasticity and structure, but only resistance training increased the thickness of the dermis, the inner layer of the skin. Resistance training also increased levels of biglycan, a protein that promotes wound healing and skin resilience via its interactions with collagen. The researchers also noted an increase in the expression of genes related to the skin cells' extracellular matrix.
These findings suggest that resistance training enhances several aspects of skin health, slowing the effects of skin aging. They also highlight yet another way in which resistance training bolsters health. Learn about other strategies to promote healthy, resilient skin in this Aliquot featuring Dr. Rhonda Patrick.
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Taurine supplementation extends life by 12 percent in animal studies, pointing to a potentially promising anti-aging strategy that may highlight the r www.cuimc.columbia.edu
Taurine is an amino acid that participates in immune health and neurological function. Findings from a recent study suggest that taurine influences longevity. Mice that received supplemental taurine lived as much as 12 percent longer than those that didn’t.
Researchers conducted a multi-part experiment in several species. First, they measured blood taurine concentrations in mice, monkeys, and humans at different ages and found that taurine decreased in all three species over time. Notably, taurine concentrations were 80 percent lower in older adult humans than in young children.
Then they gave middle-aged mice either taurine (1,000 milligrams per kilogram of body weight) or an inactive substance once daily until their natural deaths. Among mice that received taurine, median lifespan increased by 10 to 12 percent, roughly equivalent to about eight years in humans. They repeated their experiment in monkeys, worms, and yeast and observed similar effects. They also found that taurine reduced several hallmarks of aging in all the species studied, including cellular senescence, mitochondrial dysfunction, DNA damage, and inflammation.
Finally, they measured blood taurine concentrations in humans following an acute bout of exercise. They found that exercise increased the levels of taurine metabolites in the blood, providing a potential mechanism for the anti-aging effects of exercise.
These findings suggest that supplemental taurine reverses age-related taurine declines and extends both healthspan and lifespan in several species. Learn about other nutrients that influence aging in this episode featuring longevity expert Dr. Bruce Ames.
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Openness – a sense of curiosity, open-mindedness, and interest in new experiences – is critical to preserving cognitive function as we age. A new study has found that a tiny region in the brain called the locus coeruleus may provide the link between openness and better cognitive health. People with greater locus coeruleus integrity demonstrated more openness and – interestingly – had higher intelligence.
Researchers gave 135 young adults a battery of tests to gauge their openness and intelligence. Then, using an imaging technique called voxel-based morphometry, they measured the participants' locus coeruleus volumes.
They found that the participants with greater locus coeruleus volumes tended to have more openness and higher intelligence, regardless of age, gender, or total brain volume. Because locus coeruleus volume is associated with cognitive function, these findings suggest that activities that maintain locus coeruleus volume may be beneficial for preserving cognitive function.
The locus coeruleus is the primary region of the brain responsible for norepinephrine production. It is located in the pons and participates in the body’s response to stress, attention, emotion, motivation, decision-making, learning, and memory. Poor sleep has profound effects on locus coeruleus integrity and cognitive function. Learn more about the brain effects of poor sleep in this episode featuring Dr. Matt Walker.
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A new study finds that exercise maintains critical connections in the brains of older adults while boosting fitness. Older adults who walked regularly performed better on tests of cognitive function and memory and had better cardiorespiratory fitness.
The study involved 33 older adults (average age, 78 years). Participants walked on a treadmill for 30 minutes a day, four times a week, for 12 weeks and underwent tests before and after the intervention to assess their physical and cognitive performance. In addition, researchers performed functional MRIs to examine the neural connections in their brains.
They found that participants' cardiorespiratory fitness improved by more than 10 percent. They also demonstrated improvements in cognitive performance, particularly in verbal fluency, verbal learning, and memory. The MRIs revealed that participants experienced increased connectivity between the default mode network and regions of the brain involved in memory.
The default mode network is a collection of interconnected neural structures involved in attention and focus. Disturbances in default mode network connectivity are associated with poor working memory, reduced performance, and work-related productivity losses.
Although this was a small study, it supports a growing body of evidence suggesting exercise is a potent strategy for staving off cognitive decline in aging. One contributor to cognitive decline is the loss of blood-brain barrier integrity. Learn how vigorous exercise helps maintain blood-brain barrier integrity as we age in this episode featuring Dr. Axel Montagne.
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Creatine supplementation improves bone quality but not bone density in postmenopausal women. pubmed.ncbi.nlm.nih.gov
Previous research has shown that creatine supplementation increases bone mass. But a recent trial in postmenopausal women found that creatine had little effect on bone mineral density. It did, however, improve aspects of bone quality.
Researchers studied the effects of creatine monohydrate supplementation on the bone health of 237 postmenopausal women. Half of the participants took creatine (0.14 grams per kilogram of body weight of creatine, ~10 grams for a 160-pound female) daily for two years, while the other half took a placebo. All the participants engaged in a walking and resistance training exercise program. The researchers measured the women’s bone mineral density and other aspects of bone before and after the two-year intervention.
They found that the creatine supplements had no significant effects on the women’s bone mineral density of the femoral neck, total hip, or lumbar spine compared to the placebo. However, creatine did improve aspects of their bone quality. Women who took creatine showed improvements in the section modulus (how resistant the bone is to bending and breaking) and the buckling ratio (how well the bone can withstand compression and maintain its shape without collapsing) at the narrow part of the femoral neck.
Creatine is a nitrogen-containing compound that is produced in the liver and kidneys and is stored in the brain and muscles. It plays essential roles in the recycling of ATP and is widely used as a dietary supplement to build and maintain muscle mass.
These findings suggest that supplemental creatine in conjunction with exercise did not affect bone mineral density in postmenopausal women, but it did improve certain aspects of bone quality. However, robust data support resistance training as a means to build bone mass. Learn more in this episode featuring Dr. Brad Schoenfeld.
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Exercise, vitamin D, and cognitive training boost cognitive function. link.springer.com
Changes in brain function and connectivity often occur many years before the clinical manifestation of cognitive impairment and dementia. A new study shows that lifestyle modifications, including exercise, vitamin D intake, and cognitive training, improve functional brain connectivity in older adults with mild cognitive impairment.
The study involved 120 older adults (ages 60 to 80 years) with mild cognitive impairment. The participants engaged in 30 minutes of cognitive training and 60 minutes of exercise three times a week for 20 weeks. Thirty-eight of the participants received vitamin D supplements, while the remainder received a placebo. Researchers measured the participants' functional brain connectivity using MRI before and after the interventions.
They found that physical exercise alone, exercise combined with cognitive training, or exercise combined with both cognitive training and vitamin D supplementation increased functional brain connectivity in regions of the brain’s default mode network, including the hippocampus and angular gyrus.
The default mode network is a collection of interconnected neural structures involved in attention and focus. Disturbances in default mode network connectivity are associated with poor working memory, reduced performance, and work-related productivity losses.
This study’s findings suggest that lifestyle behaviors, particularly exercise, enhance functional brain connectivity, potentially staving off age-associated cognitive decline. Learn more about the effects of exercise on the brain in this episode featuring Dr. Axel Montagne.
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Blocking the body's antiviral immune response holds promise for Alzheimer's disease prevention. medicalxpress.com
The immune system plays important, and sometimes surprising, roles in brain health. A new study in mice found that blocking components of the antiviral immune response may make the brain more resilient to the effects of abnormal tau – potentially preventing Alzheimer’s disease and other forms of dementia.
Tau is a protein found in the brain. Abnormal tau can form aggregates called tau tangles – one of the defining characteristics of Alzheimer’s disease – activating antiviral response pathways and interfering with normal brain function and cognition.
Researchers studied the effects of exposure to abnormal tau on microglia, the brain’s resident immune cells. They found that when microglia were exposed to abnormal tau, the mitochondria became “leaky,” releasing their DNA into the cellular fluid. The immune system inappropriately interpreted the leaked DNA as a viral attack, triggering an immune response that promoted the release of type-I interferon, a cytokine that drives the antiviral immune response. Interrupting the pathways involved in this response restored normal brain function.
These findings suggest that suppressing the inappropriate immune response to abnormal tau exposure could provide a means to prevent or treat the tau-associated pathologies common in Alzheimer’s disease and dementia. Learn about other strategies to reduce the risk of Alzheimer’s disease in this episode featuring Dr. Dale Bredesen.
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Low bone density may increase dementia risk. www.medscape.com
A new study shows that having low bone density may increase a person’s risk for cerebral small vessel disease – a driver of dementia. People with the lowest bone density in their upper femur were twice as likely to develop dementia over a ten-year period than those with the highest bone density.
Researchers categorized nearly 1,200 people over the age of 50 years according to their small vessel health status and bone density. They also measured serum bone turnover markers and microRNAs related to cerebral small vessel disease and bone metabolism.
They found that cerebral small vessel disease scores increased as bone mineral density decreased. They also found that levels of microRNA-378f, a non-coding RNA molecule that inhibits bone formation, were higher among participants with low bone density.
In older adults, dementia and low bone mineral density often coincide. In addition, physical inactivity and poor nutrition, common among people with dementia, can accelerate bone loss. Scientists don’t fully understand the extent to which bone loss is present before the onset of dementia, however. (Read more about bone health in the two reviews presented below.)
The findings from this study suggest that bone and brain health are closely linked, possibly via a bone-brain axis that regulates brain health. However, whether bone loss causes cerebral small vessel disease and subsequent dementia remains unclear. The findings also highlight the importance of maintaining bone health throughout the lifespan. Learn how resistance exercise helps increase bone density in this clip featuring Dr. Brad Schoenfeld.
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Untreated sleep apnea may impair men's social cognition – the ability to understand and recognize social cues and emotions. www.sciencealert.com
Untreated sleep apnea may harm the brain, a new study shows. Middle-aged men with sleep apnea performed worse on tests of cognitive and social function than healthy men.
Researchers compared 27 middle-aged men who had either mild or severe untreated sleep apnea with seven healthy men. Each of the men underwent a sleep study and apnea assessment and took a battery of neuropsychological tests.
The researchers found that the men with sleep apnea had worse cognitive function, including poorer attention, memory, and decision-making capabilities, compared to the healthy men. They also found that sleep apnea impaired the men’s social cognition – the ability to understand and recognize social cues and emotions. Social cognition can be impaired in certain mental health conditions, such as depression, and may be connected to sleep patterns.
Sleep apnea is a common, but serious, sleep disorder characterized by brief moments of paused or shallow breathing. People with sleep apnea are at greater risk of high blood pressure, stroke, abnormal heart rhythms, heart failure, diabetes, weight gain, and heart attacks.
The findings from this small study suggest that sleep apnea impairs cognitive function as early as middle age in men. Larger studies that also include women are needed to confirm the role that sleep apnea plays in cognitive decline. Learn about the role that sleep plays in preventing dementia in this short video featuring Dr. Rhonda Patrick.
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High blood pressure in early adulthood is linked to late-life neurodegeneration and loss of white matter integrity. www.news-medical.net
A new study shows that having high blood pressure in early adulthood harms brain health later in life, especially in men. Men who had high blood pressure as young adults had poorer brain health than those with normal blood pressure.
Researchers performed brain scans on 427 older adults to assess their brain volume and white matter integrity. Then they compared the scans of those who had high blood pressure in early adulthood (between the ages of 30 and 40 years) with those who had normal blood pressure.
They found that those who had high blood pressure had lower brain volumes and poorer white matter integrity – an indication of impaired cognitive plasticity. The link between high blood pressure and lower brain volume was stronger in men, especially in the frontal cortex and cerebral gray matter.
These findings suggest that prolonged exposure to high blood pressure has marked effects on brain health later in life, increasing one’s risk of dementia. Exercise can have profound blood pressure-reducing effects, however. Learn more about the brain-protective effects of exercise in this clip featuring Dr. Axel Montagne.
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Greater, more intense physical activity may preserve brain volume – especially in the hippocampus, an area of the brain involved in memory. Physichttps://neurosciencenews.com/physical-activity-neuroprotection-21177/al activity boosts brain health.
Being more physically active is associated with having larger brain volume, a 2022 study found. The greatest brain-enhancing effects were seen in those who engaged in moderate- to vigorous-intensity exercises.
The study involved more than 2,500 adults between the ages of 30 and 94 years. The participants wore wrist accelerometers to track their activity levels and underwent brain scans to assess their brain volume, cortical thickness, and gray matter density.
The scans revealed that physical activity had a marked, dose-dependent effect on the participants' brain health. Those with greater, more intense physical activity levels exhibited larger brain volumes – especially in the hippocampus, an area of the brain involved in memory – than those with lower, less intense levels. However, the beneficial effects of physical activity on brain health were particularly evident when comparing the brain volumes of those who engaged in moderate physical activity to those who were sedentary, suggesting that even small increases in physical activity can boost brain health and reduce brain volume losses associated with aging.
The beneficial effects of physical activity may be related to exercise-induced production of brain-derived neurotrophic factor (BDNF), a protein that controls and promotes the growth of new neurons. BDNF is active in the hippocampus, cortex, cerebellum, and basal forebrain – areas involved in learning, long term memory, and executive function. Learn more about the brain-boosting effects of BDNF in our comprehensive overview article.
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Higher cardiovascular fitness delays brain aging and the onset of dementia in women, a 2018 study showed. Women with high cardiovascular fitness levels experienced nearly a decade’s delay in dementia onset than those with moderate fitness levels.
The study involved 191 middle-aged women. Participants completed a cycling test to gauge their cardiovascular fitness and underwent regular neuropsychiatric testing to determine if they developed dementia during their lifetime.
Compared to women with moderate cardiovascular fitness levels, women with high cardiovascular fitness levels were 88 percent less likely to develop dementia. However, those with low fitness levels were 41 percent more likely to develop dementia. Higher fitness delayed the onset of dementia by 9.5 years compared to those with moderate fitness.
Cardiovascular fitness is a measure of how well the heart, lungs, and blood vessels transport oxygen to the muscles during exercise. Exercise contributes to cardiovascular fitness because it exerts robust effects on the cardiovascular system, boosting heart rate, blood pressure, and cardiac output. Interestingly, sauna use exerts similar effects on the cardiovascular system. Learn more in our overview article.
These findings suggest that cardiovascular fitness protects against dementia in women. Learn more about the effects of cardiovascular fitness on brain health in this short video featuring Dr. Rhonda Patrick.
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Magnesium may delay age-related brain shrinkage. www.medscape.com
Magnesium may protect the brain from age-related volume losses, a new study showed. People with the highest magnesium intake had larger brain volumes than those with lower intake – a protective effect that corresponded to roughly one year less aging.
The study involved more than 6,000 adults between the ages of 40 and 73 years enrolled in the UK Biobank study. The participants completed questionnaires about their typical daily magnesium intake. They also underwent brain scans that measured their brain volumes and identified the presence of white matter lesions – areas in the brain that often indicate cerebral small blood vessel disease, a risk factor for dementia.
The scans revealed that participants with the highest magnesium intake – 550 milligrams or more daily – had larger gray matter and hippocampal volumes than those with normal intake (about 350 milligrams daily). In middle-aged adults, this effect on brain health corresponded to about one year of aging. The protective effects of magnesium were more pronounced in women than in men.
Magnesium is an essential mineral. It is found in green leafy vegetables, legumes, nuts, seeds, and whole grains, and is widely available as a dietary supplement. Evidence suggests that low magnesium levels are involved in the pathogenesis of various age-related brain disorders. In addition, people with Alzheimer’s disease often have lower magnesium levels than healthy people. More than half of people living in the United States likely have magnesium deficiency
These findings suggest that magnesium protects the brain against age-related volume losses, which are associated with dementia. It also aligns with other research showing that people who follow the MIND diet, which emphasizes the consumption of magnesium-rich green leafy vegetables, were 40 percent less likely to develop Alzheimer’s disease.
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A new study found that regular cycling may slow sarcopenia – the age-related loss of muscle mass and strength. Men who cycled regularly had larger, leaner gluteus muscles than inactive men.
The study involved two groups of men: 28 who were physically inactive and had not practiced sports for an average of 27 years and 28 who were trained recreational male cyclists, had cycled more than 4,300 miles in the past year, and had been cycling for an average of 15 years. Researchers used magnetic resonance imaging to determine the volume of the participants' gluteus maximus and gluteus medius muscles, which are situated in and around the buttocks, as well as the percentage of fat infiltration within those muscles.
They found that the inactive group tended to be heavier than the cyclists. They also found that the cyclists had larger gluteus maximus and gluteus medius muscles than the males in the inactive group. On average, the cyclists had 7 percent less fat infiltration in the gluteus maximus and 5 percent less in the gluteus medius than the males in the inactive group.
Research suggests that physical inactivity promotes muscle fat infiltration and progressive muscle weakness, driving sarcopenia – the age-related loss of muscle tissue. However, exercise and appropriate nutritional support may forestall these muscle losses. Learn how exercise and dietary protein play roles in slowing age-related muscle loss in this episode featuring Dr. Stuart Phillips.
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Vitamin D may reduce the risk of developing Alzheimer's disease. www.sciencedaily.com
Taking vitamin D may prevent Alzheimer’s disease, a new study shows. People who took vitamin D were 40 percent less likely to develop Alzheimer’s disease than those who did not.
The study involved more than 12,000 adults who were dementia-free at the time of enrollment. Participants provided information about their vitamin D intake and underwent regular cognitive evaluations over a period of 10 years.
Even after taking other risk factors into account, such as age, sex, education, race, cognitive diagnosis, depression, and whether they carried the APOE4 gene, people who took vitamin D were 40 percent less likely to develop Alzheimer’s disease during the study period than those who did not. APOE4 carriers who took vitamin D were 33 percent less likely to develop the disease than carriers who did not. Interestingly, women were more likely than men to develop Alzheimer’s disease, but taking vitamin D countered this effect.
Vitamin D is a fat-soluble vitamin that is stored in the liver and fatty tissues of the body. Perhaps best known for its role in maintaining calcium balance and bone health, vitamin D plays critical roles in many physiological processes, such as blood pressure regulation, immune function, and cell growth. Poor vitamin D status is implicated in the pathogenesis of many acute and chronic diseases, including rickets, osteoporosis, multiple sclerosis, and cancer. Evidence suggests that low vitamin D concentrations are linked with severe outcomes in COVID-19.
The findings from this large study suggest that vitamin D protects the brain against Alzheimer’s disease. The researchers did not measure the participants' blood vitamin D concentrations, so they could not identify cutoffs that define risk. However, the Endocrine Society has determined that vitamin D concentrations less than 20 ng/mL (50 nmol/L) define “deficiency,” and concentrations ranging from 52.5 to 72.5 nmol/L (21 to 29 ng/mL) define “insufficiency.” They also recommend widespread testing for at-risk populations. Learn more about vitamin D in our overview article.
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As little as nine minutes of moderate or vigorous activity daily may improve cognitive function. www.news-medical.net
A new study shows that engaging in even a few minutes of daily exercise improves memory and cognitive function. Middle-aged adults who engaged in just nine minutes of moderate to vigorous activity daily performed better on tests of memory, planning, and organization than those who engaged in sedentary or light activities.
Researchers tracked the activity patterns of nearly 4,500 adults over a period of a week. The participants took cognitive tests that assessed their verbal memory and executive function – the ability to plan, monitor, and execute one’s goals.
People who engaged in moderate to vigorous activity scored higher on the cognitive tests than those who were sedentary or engaged in only light activity. Surprisingly, just nine minutes of moderate to vigorous activity markedly improved cognitive performance versus sedentary activity.
Physical activity is a broad term that includes exercise, work-related exertion, and even some hobbies. Moderate-intensity physical activities, which include activities like brisk walking, doubles tennis, or raking leaves, increase a person’s heart rate to about 50 to 60 percent of their maximum. Vigorous-intensity physical activities, which include activities like running, swimming, or cycling, increase the heart rate to 70 to 80 percent of one’s maximum.
Robust evidence demonstrates that vigorous activity maintains the blood-brain barrier, a critical component of brain health and cognitive function. Learn more in this episode featuring Dr. Axel Montagne.
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Three or more concussions may worsen brain function later in life. www.sciencedaily.com
Experiencing multiple concussions increases a person’s risk of poor brain function later in life, a new study shows. People who experienced three or more concussions exhibited cognitive deficits that worsened with each subsequent concussion.
Researchers collected self-reported concussion histories from more than 5,700 adults between 50 and 70 years old. They administered cognitive tests to gauge changes in the participants' brain function every year for up to four years.
They found that participants who experienced three mild concussions in their lifetime had difficulty with attention and performing complex tasks later in life. Participants who experienced four mild concussions had difficulty with processing speed and working memory – an aspect of cognitive function that allows a person to remember information for relevant tasks. However, experiencing even one moderate-to-severe concussion impaired the participants' attention and the ability to perform complex tasks and process information.
These findings underscore the risks associated with even mild brain injury. Some evidence suggests that lactate and ketones may be beneficial in treating brain injury. Learn more in this clip featuring Dr. Dominic D'Agostino.
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The effects of obesity on the brain mirror those of Alzheimer's disease. www.sciencedaily.com
Excess body weight drives gray matter losses similar to those seen in Alzheimer’s disease, a new study shows. The brains of people who were obese showed marked signs of gray matter atrophy in areas of the brain responsible for attention, problem-solving, and reasoning.
Using neuroimaging data, researchers compared the grey matter patterns of more than 1,300 older adults. Participants included those with Alzheimer’s disease and those who were cognitively healthy, obese but otherwise healthy, or lean.
The scientists found that obesity and Alzheimer’s disease had similar effects on the brain. Both conditions were associated with gray matter atrophy in the right temporoparietal cortex (an area involved in attention) and the left prefrontal cortex (an area involved in reason, problem-solving, and comprehension). They also found that obesity-related gray matter atrophy patterns didn’t overlap with amyloid-beta or tau protein distribution in the brains of people with Alzheimer’s disease. Amyloid-beta and tau accumulation are widely considered hallmarks of Alzheimer’s disease.
Excess body weight drives many metabolic disorders, including type 2 diabetes, hypertension, and dyslipidemia. Recent evidence demonstrates that excess body weight impairs cognitive function. The findings from this study suggest that excess body weight drives gray matter losses similar to those seen in Alzheimer’s disease.
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Growth hormone cuts fracture risk in half for women with osteoporosis. endocrinenews.endocrine.org
Growth hormone improves bone density and reduces the risk of fractures in women with osteoporosis, according to a 2015 study. Women who received growth hormone were half as likely to experience a fracture over a 10-year period than women who did not.
The study involved 80 women (50 to 70 years old) who had osteoporosis and were taking estrogen-based hormone replacement therapy. Researchers randomly assigned the women to receive daily injections of either a low or high dose of growth hormone for three years or a placebo for 18 months. All the women took daily vitamin D and calcium supplements for the study’s duration. The researchers measured the women’s body composition and bone mass at regular intervals.
They found that women who received growth hormone injections showed marked improvements in their bone mineral density and bone mineral content compared to those who received the placebo. Over the 10-year period, the number of fractures among the women who received growth hormone dropped from 56 percent to 28 percent, whereas fractures among those who received the placebo increased from 8 percent to 32 percent.
Growth hormone, a peptide hormone produced in the pineal gland, promotes growth in childhood and adolescence. During middle age, growth hormone production decreases. Some evidence suggests that because growth hormone is secreted at night (during sleep), not getting enough sleep may hinder growth hormone release, exacerbating age-related bone loss. Learn how body temperature can influence how well you sleep at night in this clip featuring Dr. Matthew Walker.
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Vitamin D deficiency may cause the brain to age faster. www.valleycentral.com
According to findings from a recent study, the brains of people with vitamin D deficiency age faster than those with adequate vitamin D levels. This is particularly true for males.
Researchers measured blood vitamin D concentrations in the blood of more than 1,800 healthy adults. Then they scanned the participant’s brains to assess their brain aging. They calculated the participants' brain age based on chronological age and brain volume.
They found that participants with vitamin D deficiency (which the researchers defined as less than 16.08 nanograms (ng) per milliliter (ml) for the purposes of this study) were more likely to have accelerated brain aging, as evidenced by lower total brain and gray matter volumes. Interestingly, the association between low vitamin D concentrations and older brain age was only statistically significant for male participants.
Vitamin D is a fat-soluble vitamin that is stored in the liver and fatty tissues of the body. Perhaps best known for its role in maintaining calcium balance and bone health, vitamin D plays critical roles in many physiological processes. Poor vitamin D status is implicated in the pathogenesis of many acute and chronic diseases, including osteoporosis, multiple sclerosis, and cancer.
Although the researchers that conducted this study used 16.08 ng/ml as the cutoff for vitamin D deficiency, public health experts and physicians disagree regarding the appropriate cutoffs and terminology that define vitamin D status. Learn more about vitamin D in our overview article.
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Rising blood pressure in young adulthood damages brain blood vessels, reducing blood flow to the brain. journals.lww.com
Gradual increases in blood pressure from young adulthood to middle age increased the risk of poor brain health in older age, a 2022 study found. Having higher blood pressure over time damaged the brain’s delicate blood vessels, reducing blood flow to the brain.
The study involved 885 adults whose blood pressures were monitored regularly over a 30-year period. Using magnetic resonance imaging studies, researchers assessed the participants' brain health at the beginning and end of the study period.
The researchers found that participants who had either high blood pressure in young adulthood or moderate blood pressure that gradually increased over time showed marked signs of microvascular disease in the white matter of their brains. The two groups also showed reduced blood flow in the gray matter of their brains.
Microvascular disease, also called small vessel disease, is a condition characterized by blood vessel dysfunction. It commonly occurs with aging and contributes to the development of cardiovascular disease, dementia, and stroke. Small vessel disease in the brain contributes to approximately 50 percent of dementia cases worldwide.
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Lowering blood pressure reduces the risk of dementia. www.sciencedaily.com
Lowering high blood pressure later in life reduced a person’s risk of dementia by 13 percent, a recent study has found. This was true even after considering other factors that increase dementia risk.
Researchers analyzed the findings of five large studies investigating the effects of reducing blood pressure in older adults (average age, 69 years) on the risk of dementia. The studies involved more than 28,000 people from 20 countries and spanned roughly four years.
They found that reducing high blood pressure cut the risk of a person developing dementia by approximately 13 percent, even after considering a person’s age, sex, history of stroke, body mass index, and whether they had diabetes. When they looked at specific ranges of systolic blood pressure, they noted that the greatest risk reduction – 23 percent – was seen among those whose systolic pressure was less than 147 mmHg.
Nearly two-thirds of adults living in the United States have high blood pressure, defined as having a systolic pressure of 130 mmHg or higher or a diastolic pressure of 80 mmHg or higher. High blood pressure increases a person’s risk for heart disease and stroke and contributes to small vessel disease, a major risk factor for cardiovascular disease, dementia, and stroke.
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Hot water baths before bedtime reduce the risk of hypertension. www.eurekalert.org
Older adults who regularly bathed in hot springs in the evening were less likely to have hypertension, a new study has found. Having hypertension markedly increased the likelihood of having other chronic diseases, however.
Researchers gathered information about the hot spring bathing habits and overall health of more than 10,000 older adults. The participants lived near Beppu, Japan, an area known for its many hot springs.
They found that older adults who regularly bathed in hot springs in the evening were approximately 15 percent less likely to have hypertension. Older adults who didn’t frequent the hot springs were roughly 50 percent more likely to have type 2 diabetes, heart arrhythmia, stroke, gout, or abnormal blood lipids.
Evidence suggests that chronic mental stress promotes hypertension. Research has shown that bathing in hot springs improves mental health and reduces stress. Other research has shown that hot water bathing before bedtime promotes faster sleep onset and better sleep quality, which could reduce the risk of developing hypertension.
Exercise, hot baths, and sauna use may have similar effects on promoting sleep and reducing blood pressure. Learn more about the effects of sauna use on hypertension in this clip featuring Dr. Jari Laukkanen.
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Staying hydrated is essential for health and longevity. www.sciencedaily.com
Poor hydration associated with a more advanced biological age.
Press release: https://www.sciencedaily.com/releases/2023/01/230102100941.htm
Drinking plenty of fluids promotes a long, healthy life, a recent study has found. Older adults who were well-hydrated were less likely to develop chronic diseases and die young compared to their less-hydrated peers.
Normal blood sodium levels typically fall between 135 and 146 millimoles per liter (mmol/l). As hydration decreases, blood sodium levels decrease, so researchers measured blood sodium levels in nearly 12,000 older adults. They calculated the participants' biological ages (based on several markers of cardiometabolic health and lifestyle factors) and assessed their risk of disease and early death.
The researchers found that participants with blood sodium levels above 142 mmol/l, suggesting poorer hydration, were 50 percent more likely to have a biological age that was older than their chronological age. Having an older biological age, in turn, increased the participants' risk for chronic diseases by 70 percent and their risk of dying prematurely by 59 percent.
A person’s fluid needs vary according to weight, activity level, and individual sweat losses. In general, drinking one-half to one ounce of water for each pound of body weight per day is adequate. However, exercise, sauna use, and other activities can increase fluid needs markedly. For example, a person can lose roughly one pound (~0.5 kilograms) in a single traditional sauna session.
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Estrogen may protect against cocaine-induced brain dysfunction by improving brain blood flow - progesterone and testosterone may be detrimental.(2001) www.sciencedaily.com
From the article:
Lead researcher Marc Kaufman and his colleagues first established the rate of blood flow to the brain in male and female occasional cocaine users. An intravenous dose of cocaine (0.4 mg/kg) was administered to nine men and 13 women. Men were studied once while women were examined during different phases of their menstrual cycle phases (days 3-8, follicular phase and 18-24, leutial phase) after the beginning of menstruation.
[…]
In the follicular phase, when estrogen levels are high and progesterone levels are low, cocaine did not alter the amount of blood in the brain. By contrast, a 10 percent reduction in blood was found in women during their luteal menstrual cycle phase, when progesterone levels rise; male subjects incurred a 20 percent loss. These findings suggest that cocaine’s effects on blood vessels in the brain differ as a function of sex and menstrual cycle phase, and imply that progesterone in women and testosterone in men may enhance cocaine-induced vasoconstriction, while estrogen in women may blunt cocaine’s vascular effects.
[…]
Such benefits could extend beyond drug using populations. For example, treatments that improve brain blood flow might also benefit the elderly, many of whom experience reductions of blood flow to the brain as a result of aging.
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Women with the highest vitamin K1 intake were nearly half as likely to require long-term hospitalization due to hip fracture compared to women with the lowest intake, a recent study shows. Those with higher vitamin K1 intake were nearly one-third less likely to experience any kind of fracture that required hospitalization.
Researchers tracked hip fractures among more than 1,300 older women (70 years and older) living in Australia for about 15 years. They also assessed the women’s vitamin K1 intake using food frequency questionnaires and measured their blood vitamin D concentrations.
They found that nearly 11 percent of the women experienced a hip fracture and 28 percent experienced any type of fracture that required hospitalization during the study period. When compared to women with the lowest vitamin K1 intake, those with the highest intake were 49 percent less likely to require hospitalization due to hip fracture and were 31 percent less like to require hospitalization due to any type of fracture. This was true regardless of the women’s vitamin D status.
Vitamin K is a fat-soluble vitamin that participates in blood clotting, bone metabolism, prevention of blood vessel mineralization, and regulation of various cellular functions. The body has limited vitamin K storage capacity, so the body recycles it in a vitamin K redox cycle and reuses it multiple times. Naturally occurring forms of vitamin K include phylloquinone (vitamin K1) and a family of molecules called menaquinones (vitamin K2). Vitamin K1 is synthesized by plants and is the major form of vitamin K in the diet.
The findings from this study suggest that vitamin K1 is essential for bone health in older women and underscore the importance of adequate dietary intake of this essential nutrient. The study investigators noted that just one or two servings of vitamin K1-rich foods daily were sufficient to achieve levels high enough to protect against fracture. Sources of vitamin K1 include kale, Swiss chard, spinach, and other green leafy vegetables.
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Resistance training reverses age-related muscle loss in older women. www.sciencedirect.com
Resistance exercise reduces symptoms of sarcopenia – age-related muscle loss – in older women, a new study has found. Women who engaged in resistance training saw improvements in muscle size, strength, and function.
Researchers studied the effects of resistance training in 38 women who were 70 years of age or older. About half of the women engaged in a supervised resistance training program for six months, while the other half did not. The researchers assessed the women’s body composition, strength, and capacity to perform basic fitness tests.
They found that half of the women who engaged in the resistance training experienced remission of their sarcopenia, demonstrated by increases in muscular mass, decreases in fat mass, and enhanced muscular strength and performance in their arms and legs. The women who trained also performed better on tests of leg function and strength as well as balance.
Sarcopenia is an age-related condition characterized by a progressive loss of muscle mass and associated strength. Because the condition begins as early as one’s 30s, a person in their 70s may have lost as much as half of their muscle mass.
This study demonstrates that resistance training rebuilds muscle mass in older women. Having sufficient muscle mass markedly reduces a person’s risk of dying prematurely, and actively challenging those muscles, through regular physical activity and exercise, may extend a person’s life by several years. Learn more in this clip featuring Dr. Stuart Phillips.
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Higher protein intake reduces the risk of hip fracture in women. www.clinicalnutritionjournal.com
For every 25 grams of protein consumed per day – about the amount in a four-ounce serving of fish – the risk of hip fracture in underweight women drops by nearly half, a recent study has found. Drinking tea or coffee reduces the risk of hip fracture, too.
Researchers tracked the health of more than 26,000 middle-aged women for about 22 years. The women provided information about the types and quantities of foods they ate on a regular basis.
The researchers found that for every 25 grams of protein consumed per day, the women’s risk of experiencing a hip fracture decreased by 14 percent. However, when the researchers separated the women according to whether they were underweight, healthy weight, or overweight, they found that for every 25 grams of protein consumed per day, the risk of hip fracture for a woman who was underweight decreased by 45 percent.
Other dietary components influenced hip fracture risk, too. For example, for every additional cup of tea or coffee the women consumed, their risk decreased by 4 percent. And although calcium and vitamin D play important roles in bone health, their consumption reduced hip fracture risk only in women who were underweight.
These findings suggest that dietary protein protects against hip fractures, especially in women who are underweight. Learn more about the importance of dietary protein in this episode featuring Dr. Stuart Phillips.
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For every 25 grams of protein consumed per day – about the amount in a four-ounce serving of fish – the risk of hip fracture in underweight women drops by nearly half, a recent study has found. Drinking tea or coffee reduces the risk of hip fracture, too.
Researchers tracked the health of more than 26,000 middle-aged women for about 22 years. The women provided information about the types and quantities of foods they ate on a regular basis.
The researchers found that for every 25 grams of protein consumed per day, the women’s risk of experiencing a hip fracture decreased by 14 percent. However, when the researchers separated the women according to whether they were underweight, healthy weight, or overweight, they found that for every 25 grams of protein consumed per day, the risk of hip fracture for a woman who was underweight decreased by 45 percent.
Other dietary components influenced hip fracture risk, too. For example, for every additional cup of tea or coffee the women consumed, their risk decreased by 4 percent. And although calcium and vitamin D play important roles in bone health, their consumption reduced hip fracture risk only in women who were underweight.
These findings suggest that dietary protein protects against hip fractures, especially in women who are underweight. Learn more about the importance of dietary protein in this episode featuring Dr. Stuart Phillips.
- Read full publication.00393-4/fulltext#secsectitle0010)
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Why our bones need resistance training for old age. link.springer.com
High-load resistance training restores bone mineral density in people who have osteoporosis and osteopenia, a 2021 analysis of several studies found. Those who engaged in the training experienced improvements in their motor function and reported few adverse events.
Researchers analyzed the findings of nine randomized controlled trials involving nearly 500 women and men with either osteoporosis or osteopenia. The various studies examined changes in the bone mineral density of the participants' lower extremities and spine after engaging in resistance training interventions versus not.
The researchers found that resistance training increased the bone mineral density of the lumbar spine, femoral neck, and total hip. The greatest benefits were obtained in the lumbar spine, an area that is particularly vulnerable to the damaging effects of bone loss.
High-load resistance training involves using heavier weights and performing fewer repetitions (typically 8 to 12 per set per exercise) than ordinary resistance training. Evidence suggests that high-load resistance training strengthens the lower extremities more effectively than training with lighter loads.
The findings from this analysis suggest that performing high-load resistance training reverses the bone loss that accompanies osteoporosis and osteopenia. However, the researchers cautioned that the variability in the studies' designs and outcomes and the possibility of publication bias (the tendency to publish only favorable findings) make generalizing their findings difficult.
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Levels of a hormone produced in the testes predict age-related diseases in men. www.independent.co.uk
Men who have low levels of a hormone called INSL3 are more likely to develop chronic, age-related diseases later in life, a 2021 study showed. The men also had low sex hormone production.
Researchers measured INSL3 levels in the blood of more than 3,300 men between the ages of 40 and 79 years. They collected data about the men’s overall health, sexual function, and lifestyle behaviors, such as whether they smoked or drank alcohol.
They found that having low INSL3 levels was associated with hypogonadism, a condition in which the sex organs produce little or no sex hormones. Having low INSL3 was also associated with reduced sexual function, bone mineral density, and physical activity, as well as increased occurrence of hypertension, cardiovascular disease, cancer, and diabetes.
INSL3, or insulin-like peptide 3, is produced in the Leydig cells of the testes and, to a lesser degree, the theca cells of the ovaries. Although it plays important roles in male reproductive maturation and health, evidence suggests it affects other aspects of human health, including bone and muscle physiology, brain function, and others.
These findings suggest that INSL3 is a robust biomarker of sexual function and future disease risk in men. Factors that may influence INSL3 production include childhood body mass index, prepubertal nutrition, and genetics.
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Testosterone levels are subject to a circadian rhythm, peaking in the early morning hours and then falling by at least 43%. (2003) onlinelibrary.wiley.com
From the publication:
Total testosterone
Each subject in both the old and young groups showed a marked diurnal variation in serum total testosterone, with a minimum decrease (peak to nadir) of 43% of the peak value. In each group, 50% of the subjects reached a nadir of < 10 nmol/l, while all subjects in both groups had a peak level of > 10 nmol/l. […] A significant difference between the young and older mean total testosterone was shown at three sampling times: 06·00, 07·00 and 07·30 h, when the young group showed a higher mean concentration at each of the three times. In both groups, the acrophase occurred at 07·30 h.
Bioavailable testosterone
Both groups display a significant circadian rhythm. No significant difference was demonstrated in mesor or acrophase but a significant difference was shown in amplitude. The acrophase in both groups coincide at 07·24 h, similar to that for the total testosterone. Significant differences between the young and middle-aged groups in the mean bioavailable testosterone were seen at 04·30, 05·30, 06·00, 07·30 and 09·30 h.
Free testosterone
A highly significant circadian rhythm was observed in the young group and in the older group. As with the bioavailable testosterone, there was no significant difference between the two groups in mesor and acrophase but a significant difference was seen in amplitude. The acrophase was calculated as occurring at 07·18 h in the young group and 07·05 h in the older men. Significant differences in the mean free testosterone concentration were seen at 05·00, 05·30, 06·00, 06·30, 07·00, 07·30, 09·00, 09·30, 10·00 and 18·00 h.
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Low vitamin D levels promote brain aging. www.sciencedirect.com
Low vitamin D levels promote brain aging and loss of brain volume and gray matter.
A recent study found that the brains of people with low vitamin D levels age faster. Having high vitamin D levels may protect the brain, however.
Researchers measured vitamin D levels and reviewed MRI brain studies of more than 1,800 adults to identify associations between vitamin D levels and total brain, gray matter, and hippocampal volumes. They found that having low vitamin D levels was closely tied to brain aging. As vitamin D levels decreased, total brain and gray matter volumes decreased as well, particularly in males.
Between the ages of 30 and 40 years, the connections between cells in a person’s brain begin to diminish, causing the brain to shrink in volume. The rate of shrinkage increases as a person reaches the age of 60, impairing thinking, memory, and executive function. The loss of brain volume is a hallmark of Alzheimer’s disease.
These findings suggest that vitamin D plays a role in protecting the brain from the effects of aging. Vitamin D plays many other roles in human health. Learn more about vitamin D in our overview article.
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Having a large waistline can almost double your risk of dying prematurely even if your body mass index is within the 'normal' range www.sciencedaily.com
Having a large waist circumference may double a person’s risk of premature death.
People with a large waist circumference were roughly twice as likely to die prematurely compared to those with a smaller waist, according to a 2008 study. Notably, every two-inch increase in waist circumference increased the risk of premature death by 17 percent in males and 13 percent in females.
Researchers took various body measurements (body mass index [BMI], waist circumference, and waist-to-hip ratio) from nearly 360,000 adults enrolled in EPIC, an ongoing study in Europe. Then they investigated possible links between these measures and the risk of premature death over a period of about ten years.
They found that males who had a BMI of 25.3 and females who had a BMI of 24.3 were the least likely to die during the study period. However, a person’s waist circumference and waist-to-hip ratio were strongly linked with the risk of dying, even after considering factors that influence risk, including BMI, educational level, smoking status, alcohol consumption, physical activity, and height. For any given BMI, they noted that every five-centimeter (two-inch) increase in waist circumference markedly increased the risk of premature death.
A large waist circumference may be an indicator of visceral fat – body fat that is stored in the abdominal cavity and plays a central role in the links between obesity and systemic inflammation. Health experts recommend having a waist circumference of 40 inches or less for males and 35 inches or less for females.
Similarly, a large waist-to-hip ratio may increase a person’s risk of cardiovascular disease. The World Health Organization recommends having a waist-to-hip ratio of 0.9 or less for males and 0.85 or less for females.
See the Digest story below to learn how heavy drinking may influence waist circumference.
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The beneficial effects of 6 months of testosterone treatment on frailty in older men were not maintained 6 months after treatment. (2010) www.sciencedaily.com
From the article:
Frailty is an age-related state of physical limitation caused by the loss of muscle mass and function and can lead to adverse clinical outcomes such as dependency, institutionalization and death. Testosterone levels naturally decline with aging and testosterone replacement is a common therapy. Short-term testosterone treatment in frail elderly men has been shown to improve muscle mass and strength, but until now it has been unclear whether these effects could be maintained post-treatment.
[…]
In this study, researchers evaluated 274 intermediate-frail and frail elderly men aged 65-90 years with low testosterone levels. Study participants received either a testosterone gel or placebo for six months. Assessments were carried out at baseline, the end of treatment and six months after treatment cessation. Researchers found that the increased lean body mass, muscle strength and quality of life after six months of testosterone treatment were not maintained six months after treatment.
“At present, the optimal duration of anabolic hormonal intervention to produce sustained benefits in treating frailty in older men is unknown,” said Wu. “To best interrupt the downward spiral into frailty a greater emphasis should be placed on a multi-disciplinary interventional approach including resistance exercise, diet and other lifestyle options, in conjunction with pharmacological agents.”
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Older men with higher testosterone levels may lose less muscle mass as they age. (2011) www.sciencedaily.com
From the article:
“Our study finds that men, aged 65 years and older, with higher testosterone levels lost less muscle mass, especially in their arms and legs, than men this age who had lower testosterone levels,” said Erin LeBlanc, MD, of Kaiser Permanente Northwest in Portland, OR and lead author of the study. “Men who had higher testosterone levels before they lost weight also lost less leg function and could stand up more easily from a chair than men who had lower testosterone levels before they lost weight.”
In this study, researchers used data from 1,183 men aged 65 years or older and tested the hypothesis that higher baseline measures of sex steroids are associated with lesser declines in lean mass and maintenance of physical performance over an average follow-up of 4.5 years. Body composition was measured using dual energy x-ray absorptiometry (DXA) scans and physical performance was measured through a series of exercises that assessed grip strength, lower extremity power, walking speed and the ability to rise from a chair without the use of arms.
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Testosterone replacement may help mobility limited older men improve and maintain aerobic capacity. (2014) www.sciencedaily.com
From the article:
To investigate whether testosterone supplementation improves measures of aerobic function ― the peak oxygen uptake and the gas exchange lactate threshold ― Dr. Storer and his colleagues analayzed data from subjects in a larger randomized controlled study of men over age 65 who had low testosterone levels and difficulty performing the usual physical activities of daily living. For 6 months, 28 men in one group received 10 milligrams of testosterone gel and 36 men in a second group received a placebo gel. All subjects completed a cycle exercise test to measure their peak aerobic fitness before and after the 6 month study.
The men taking testosterone displayed a slight improvement in aerobic fitness while those taking placebo showed a slight decline. This small increase in aerobic capacity in the testosterone group eliminated the expected decrease that men generally experience with natural aging.
Among the men taking testosterone, the age-related decline in the peak oxygen uptake was 3.4 times less than expected, while the rate of decline among the men taking placebo accelerated to nearly twice the expected rate. The decrease in gas exchange lactate threshold was significantly smaller in the testosterone group than in the placebo group. Longer term studies are needed to evaluate safety and durability of effect.
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A drop in testosterone levels over time is more likely to result from a man’s behavioral and health changes than by aging, study suggests. (2012) www.sciencedaily.com
From the article:
On average, testosterone levels did not decline significantly over five years; rather, they decreased less than 1 percent each year, the authors reported. However, when the investigators analyzed the data by subgroups, they found that certain factors were linked to lower testosterone levels at five years than at the beginning of the study.
“Men who had declines in testosterone were more likely to be those who became obese, had stopped smoking or were depressed at either clinic visit,” Wittert said. “While stopping smoking may be a cause of a slight decrease in testosterone, the benefit of quitting smoking is huge.”
[…]
Unmarried men in the study had greater testosterone reductions than did married men. Wittert attributed this finding to past research showing that married men tend to be healthier and happier than unmarried men. “Also, regular sexual activity tends to increase testosterone,” he explained.
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Higher levels of omega-3s in mid-life protect the brain from shrinkage and preserve cognitive function. www.nutritionaloutlook.com
Having higher blood levels of omega-3 fatty acids in midlife is linked with greater brain volume and better cognitive function, potentially reducing the risk of cognitive decline later in life, new research finds. The fatty acids may also protect the brain against white matter hyperintensities – areas in the brain that often indicate cerebral small blood vessel disease, a risk factor for dementia.
Researchers measured the red blood cell concentrations of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) of more than 2,100 middle-aged adults and calculated each participant’s Omega-3 Index, which gauges long-term exposure to EPA + DHA in red blood cells. They measured the participants' brain volumes, reviewed their scores on cognitive tests, and determined whether they were carriers of APOE-4, a gene that influences dementia risk.
They found that the effects of omega-3s differed according to APOE-4 status. Whereas non-carriers of APOE-4 who had a higher Omega-3 Index or DHA concentrations had larger hippocampal volumes, APOE-4 carriers who had higher EPA concentrations tended to have better abstract reasoning. APOE-4 carriers also had fewer white matter hyperintensities if all their omega-3 measures were higher.
Omega-3 fatty acids play critical roles in human health and may reduce the risk of many aging-related diseases. The findings from this study suggest that having higher blood concentrations of omega-3s in mid-life preserves brain health and promotes aspects of cognitive function. Learn more about the Omega-3 Index in this clip featuring Dr. Bill Harris.
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In men with Alzheimer's disease, free testosterone levels were about half those of healthy men. (2004) www.sciencedaily.com
From the article:
Dr. Resnick, Scott Moffat, Ph.D., and their colleagues evaluated the testosterone levels of 574 men, ages 32 to 87, who participated in the Baltimore Longitudinal Study of Aging (BLSA). The investigators examined free and total testosterone levels-measured over an average of 19 years-in relationship to subsequent diagnosis of AD. Based on physical, neurological and neuropsychological exams, 54 of the 574 men were diagnosed with AD.
The research team found that for every 50 percent increase in the free testosterone index in the bloodstream, there was about a 26 percent decrease in the risk of developing AD. Although overall free testosterone levels fell over time, these levels dropped more precipitously in those men who later developed AD. In fact, at the end of the study, men who were diagnosed with AD, on average, had about half the levels of circulating free testosterone as men who didn’t develop the disease. In some cases, the drop-offs in free testosterone levels associated with AD were detected up to a decade before diagnosis.
Previously, Dr. Resnick and her colleagues found that older men with high levels of circulating free testosterone have better visual and verbal memory and perform spatial tasks more adeptly than their peers.
“It is quite possible that circulating free testosterone has a broad range of influences on the aging brain,” Dr. Resnick said.
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The marketing and prescribing of testosterone and growth hormone for aging-associated problems is disease mongering, experts say. (2015) www.sciencedaily.com
From the article:
The epidemic of testosterone prescribing over the last decade has been primarily pushing testosterone as a tonic for sexual dysfunction and/or reduced energy in middle-aged men, neither of which are genuine testosterone deficiency states.“
[…]
“Clearly, previous attempts to warn doctors and the public of this disease mongering that is potentially medically harmful and costly have not been effective. Now however,” said Perls, “with the FDA’s recent dual commission findings that testosterone treatment is not indicated for age-associated decline in serum testosterone, alternatively called ‘andropause,’ ‘late-onset hypogonadism’ and marketed as ‘low T,’ we have the opportunity to highlight why hormone replacement (also euphemistically called "bioidentical hormone replacement”) for aging with not only testosterone but also growth hormone is disease mongering, that the conjured benefits are unfounded and are far outweighed by the risks, and to provide suggestions about how this deceptive practice can be stopped."
The authors point out that for many men, testosterone does not decline with age among men retaining excellent general health, and if it does, the decline is due to common underlying problems such as obesity and poor fitness. Those who hawk testosterone and growth hormone have developed advertising and in some cases professional-appearing questionnaires that focus on common complaints among older men such as decreased energy, feeling sad, sleep problems, decreased physical performance or increased fat.
Additionally, the authors highlight that many times, a testosterone level won’t even be obtained and the patient is told that, simply based on these common symptoms alone or with minor reductions in serum testosterone, they have “late onset hypogonadism,” or that their erectile dysfunction may be improved with testosterone treatment.
In the case of growth hormone, the FDA requires that doctors perform a test to demonstrate that the body does not produce enough growth hormone. “Those who market and sell HGH for these common symptoms nearly never perform the test because if they did a properly performed test, it would almost never be positive because the diseases that cause growth hormone deficiency in adults, such as pituitary gland tumors, are very rare,” said Perls.
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Higher testosterone levels may be associated with better cognitive function in older men. (2002) www.sciencedaily.com
From the article:
“Our study only looked at natural testosterone levels and so it doesn’t prove that testosterone supplements can prevent cognitive decline. We will need results of large randomized clinical trials in older men before we can confidently say that testosterone supplements are beneficial and safe,” she said.
Taking testosterone, or over-the-counter supplements that boost levels of the hormone, can have side effects including increased risk of prostate cancer, increased cholesterol levels, acne and male pattern baldness, Yaffe said.
[…]
The cognitive tests measured concentration, memory, attention, language, and other cognitive skills. When scores on these tests decline significantly, or are well below average, this serves as a warning of a high risk of Alzheimer’s disease, Yaffe said.
In addition to testosterone, the researchers measured estrogen and sex hormone binding globulin, a protein that binds these two hormones. Although testosterone was linked to better scores on the tests, estrogen had essentially no effect on performance, Yaffe said. Previous studies of women have shown that higher estrogen levels can reduce their risk of cognitive decline.
Other research has shown that men have higher levels of both estrogen and testosterone than women, and that women have a 30 percent greater risk of developing Alzheimer’s Disease, Yaffe said. Some researchers hypothesize that women’s increased Alzheimer’s risk is related to lower hormone levels.
This study doesn’t explain how testosterone acts on the brain, Yaffe said, but other studies of mice have shown that the parts of the brain that handle learning and memory tasks are replete with receptors for testosterone.
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Testosterone therapy may boost sexual function and mood in older men with low testosterone levels. (2016) www.sciencedaily.com
From the article:
Yale enrolled the largest number of participants at any one site (84 of 790) for these double-blind, placebo-controlled trials that investigated the efficacy of testosterone gel for multiple outcomes, including sexual function, physical function, and vitality.
The researchers found that men who received testosterone therapy for one year, versus those on placebo, saw significant improvements in sexual function, including sexual activity, sexual desire, and erectile function.
[…]
While participants enrolled in the trial that assessed physical function did not see significant improvements in their walking ability – as measured by an increase of 50 meters or more in their distance walked in 6 minutes – an increase was found when all study participants were evaluated. In addition, men enrolled in the vitality trial saw modest benefits in terms of improved mood and fewer depressive symptoms.
While the results were somewhat mixed, Gill noted an overall benefit that had not been seen in previous studies. “One way of interpreting the results across trials is a global impression of change,” he said. “We found that testosterone improved men’s impression that their sexual desire, walking ability, energy level, and overall health were better.”
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Testosterone administration to deficient older men did not affect atherosclerosis rates, sexual function, or health-related quality of life. (2015) www.sciencedaily.com
From the article:
Shalender Bhasin, M.B.B.S., of Brigham and Women’s Hospital, Harvard Medical School, Boston, and colleagues randomly assigned 308 men 60 years or older with low or low-normal testosterone levels to receive 7.5 g of 1 percent testosterone (n = 156) or placebo (n = 152) gel packets daily for 3 years. The dose was adjusted to achieve testosterone levels between 500 and 900 ng/dL. Characteristics were similar between groups at study entry: patients were an average age of 68 years; 42 percent had hypertension; 15 percent, diabetes; 15 percent, cardiovascular disease; and 27 percent, obesity.
The researchers found that the rates of subclinical atherosclerosis progression, as measured by changes in common carotid artery intima-media thickness or coronary artery calcium, did not differ significantly between men assigned to the testosterone or placebo groups. Changes in intima-media thickness or calcium scores were not associated with change in testosterone levels among individuals assigned to receive testosterone.
Sexual desire, erectile function, overall sexual function scores, partner intimacy, and health-related quality of life did not differ significantly between groups. Hematocrit (a measure of red blood cells) and prostate-specific antigen levels increased more in testosterone group.
The authors write that this trial was not designed to determine the effects of testosterone on CVD events, and that a substantially larger trial would be needed to determine this.
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Low testosterone levels may be associated with up to 40% higher risk of falling in older men. (2006) www.sciencedaily.com
From the article:
Eric Orwoll, M.D., Oregon Health & Science University, Portland, and colleagues studied 2,587 men age 65 to 99 (average age 73) who enrolled in the Osteoporotic Fractures in Men (MrOS) Study between 2000 and 2002.
[…]
During the course of the study, which continued until March 2005, 56 percent of the men fell at least once. Those with lower bioavailable testosterone levels were significantly more likely to fall and to fall multiple times than those with higher levels–among the one-fourth of participants with the lowest testosterone levels, the risk for falling was 40 percent higher than among the one-fourth with the highest testosterone levels. The association was stronger in younger men (ages 65 to 69) and not apparent in men older than 80.
The association remained the same when the researchers factored in the scores on physical performance tests.
“Bioavailable testosterone concentration is associated with measures of physical performance, but the association of testosterone level to the risk of falling is apparent regardless of physical performance,” the authors write. “Thus, the mechanisms by which testosterone level affects the propensity to fall may involve other pathways.” For example, low testosterone levels could impair vision, thinking processes or coordination, increasing the risk for falls.
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Plant-based dietary components may prevent cognitive decline. www.sciencedaily.com
Although epidemiological and observational data support the role of nutrition in maintaining cognitive health in aging, establishing which components of a diet support brain health is difficult and error-prone when relying on food intake surveys and biomarker studies. A recent metabolomics study identified specific dietary components associated with either preventing or promoting cognitive decline.
Metabolomics is an emerging field of study that involves the measurement of all metabolites – the intermediate or end products of metabolism – in a biological specimen. Many metabolites are produced when food is digested and further metabolized by gut microbes.
The investigators analyzed food-related and microbiota-derived metabolites in the blood of more than 800 adults living in two distinct regions of France. The participants completed a battery of neuropsychological tests and provided information about their overall health.
The investigators found that plant-based food metabolites (from cocoa, coffee, mushrooms, and red wine) and microbiota-derived metabolites (from microbial metabolism of polyphenol-rich apples, cocoa, green tea, blueberries, oranges, and pomegranates) appeared to exert a protective effect against cognitive decline. Conversely, metabolites derived from caffeine, alcohol, and artificial sweeteners appeared to promote cognitive decline.
These findings suggest that specific plant-based dietary components protect against cognitive decline and support the rationale for a plant-rich diet. Some evidence suggests that a ketogenic diet promotes cognitive function and protects the brain against cognitive decline. Learn how to incorporate fiber-rich plant-based foods into a ketogenic diet in this clip featuring Dr. Dominic D'Agostino.
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Older adults who engage in leisure time physical activities have lower risk of premature death.
Leisure time physical activity is a broad term that refers to physical activities performed outside work or typical household responsibilities. Examples include exercise, sports, dancing, gardening, and walking. Findings from a recent study suggest that certain leisure time physical activities are associated with a lower risk of death from all causes of premature death, including cardiovascular disease and cancer, in older adults.
Most public health organizations recommend that adults of all ages should engage in at least 150 minutes of moderate-intensity aerobic physical exercise or at least 75 minutes of vigorous-intensity aerobic physical exercise each week, or an equivalent combination of both. The bulk of the research focused on the benefits of physical activity has been in younger people, the findings of which might not be translatable to older adults.
The investigators drew on data from 272,500 older adults (average age, 70 years) enrolled in the National Institutes of Health-AARP Diet and Health Study, an ongoing study of associations between diet and cancer. Participants provided information about their demographics, height, weight, smoking status, mood, educational level, and alcohol consumption. They also answered questions about the average amount of time they spent per week during the previous year engaging in cycling, swimming laps, playing racquet sports, playing golf, walking for exercise, jogging or running, and other aerobic exercises. The investigators calculated the participants' average leisure time activity levels in terms of metabolic equivalents, or METs, a measure of the rate of energy expended per unit of time.
They found that playing racquet sports was associated with a 16 percent reduction in the risk of death from any cause and running was associated with a 15 percent reduction. The other activities conferred protection as well, but to a lesser extent. Achieving the recommended amount of physical activity through any combination of the seven leisure time activities reduced the risk of death by 13 percent. The protective effects of leisure time physical activity were dose-dependent to a degree, with greater duration conferring greater reduction in risk, but levels beyond those recommended showed diminishing returns.
These findings suggest that older adults who meet physical activity guidelines through leisure time physical activities, especially aerobic activities such as racquet sports or running, have a reduced risk of premature death from all causes. Learn about the benefits of aerobic exercise in our overview article.
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Higher diet quality relates to decelerated epigenetic aging academic.oup.com
The DASH Diet slows epigenetic aging.
The DASH Diet (Dietary Approaches to Stop Hypertension) is a dietary pattern that emphasizes heart-healthy eating. Widely recognized for its evidence-based guidelines, DASH is rich in fruits, vegetables, fish, poultry, legumes, and healthy fats and is low in saturated fats and sweets. Findings from a 2021 study suggest that the DASH diet slows epigenetic aging.
Epigenetic age acceleration is a phenomenon that occurs when an individual’s epigenetic (biological) age exceeds their chronological age. Early research relied on measures of either intrinsic or extrinsic factors to measure age acceleration. Newer methods rely on clinical and functional biomarkers, which have stronger predictive abilities for the time to chronic diseases and death.
The study utilized data from nearly 2,000 adults (average age, 67 years) who were enrolled in the Framingham Heart Study Offspring Cohort. Investigators collected information about the participants' usual dietary intake and assigned a score based on the overall quality and adherence to DASH guidelines. They also collected blood samples from the participants for analysis and determination of their DNA methylation status using three epigenetic age acceleration measures: Dunedin Pace of Aging Methylation, GrimAge acceleration, and PhenoAge acceleration.
They found that all three age acceleration measures indicated that having a higher DASH score was associated with slowed epigenetic aging, even after taking age, sex, smoking status, body mass index, physical activity, alcohol consumption, and caloric intake into consideration. This slow aging translated to roughly one additional year of life. Higher intakes of vegetables, fruits, nuts, legumes, and whole grains were associated with slower aging, while higher intakes of red and processed meat and sodium were associated with faster aging.
These findings suggest that the DASH dietary pattern slow epigenetic aging and underscores the importance of implementing lifestyle modifications to promote health and longevity. Learn more about epigenetic age acceleration in these clips featuring epigenetics experts Dr. Steve Horvath and Dr. Morgan Levine.
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Exceeding current exercise recommendations protects against premature death.
Most public health organizations recommend that adults of all ages engage in 150 to 300 minutes of moderate-intensity aerobic physical exercise or 75 to 150 minutes of vigorous-intensity aerobic physical exercise each week, or an equivalent combination of both. Most adults fall far short of these recommendations, however. Evidence from a recent study suggests that people who exceed current exercise recommendations are less likely to die prematurely than those who exercise less.
Exercise stresses the human body, eliciting a wide array of protective mechanisms that work together to condition the body for future stressors, a biological phenomenon known as hormesis. Hormesis is a compensatory defense response to a stressor that is disproportionate to the stressor’s magnitude.
The study involved more than 116,000 adults enrolled in the Nurses' Health Study and the Health Professionals Follow-up Study, two ongoing studies focused on identifying risk factors that drive chronic disease. Twice a year for a period of 30 years, participants provided information about their lifestyles and physical activity, including the intensity and duration. The investigators tracked death rates and causes of death among the participants.
They found that approximately 47,000 of the participants died during the 30 years of follow-up. Compared to participants who didn’t exercise at all, those who met the moderate-intensity exercise guideline during their lives were 19 to 25 percent less likely to die prematurely. Those who met the vigorous-intensity guideline were 19 to 31 percent less likely to die prematurely.
However, exercising even more conferred greater protection against premature death. Participants who engaged in 300 to 599 minutes of moderate-intensity exercise each week (double the guideline) were 3 to 13 percent less likely to die prematurely, and those who engaged in 150 to 299 minutes of vigorous-intensity exercise each week (double the guideline) were 2 to 4 percent less likely to die prematurely.
These findings suggest that meeting or exceeding current exercise guidelines markedly reduces the risk of dying prematurely and underscores the importance of regularly engaging in physical activity. Learn about the many health benefits of aerobic exercise in our overview article.
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Age, gender and body size are better predictors of aortic aneurysm than atherosclerosis and hypertension. (2003) www.eurekalert.org
From the article:
“Atherosclerotic plaques and the risk factors that cause them, including hypertension, classically have been considered important potential causes of the expansion of the aorta,” says Bijoy Khandheria, M.D., a Mayo Clinic cardiologist and study author. “Intuitively, it makes sense that high blood pressure would stretch the vessel walls and make them more likely to become enlarged. This study shows that while these risk factors are highly important in a host of diseases and conditions, they are bit players when it comes to causing the dilatation of the aorta that can lead to aneurysm.”
[…]
The study found that age, gender and body size together account for one-third or more of the cases of aortic dilatation, while atherosclerosis and related risk factors only explained 3 percent.
“There has been a tendency recently to refer to aneurysms as ‘athersclerotic aneurysms,’” explains Dr. Khandheria. “But the fact that plaques – even complex or severe ones – are very common, while aneurysms are rare, supports the conclusion that atherosclerosis and its risk factors are not likely to blame for aneurysms in the major blood vessels of the chest. Other factors and processes, including genetic diseases similar to Marfan syndrome, seem to be more important.
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Smokers may be nearly twice as likely to develop an abdominal aortic aneurysm. (2016) www.eurekalert.org
From the article:
The study found the lifetime risk of an abdominal aortic aneurysm were: 1 in 17 among all study participants; 1 in 9 among current smokers; 1 in 9 among those in the top third of smoking pack-years (number of cigarettes smoked over a lifetime), whether a current or former smoker; 1 in 12 among current female smokers.
Researchers also found those who had quit smoking for 3-8 years (recent quitters) still had an approximately 2.6 to 3.5 fold increased risk for both clinical and asymptomatic abdominal aortic aneurysm in the next 15 years compared to never smokers. Their lifetime risk was 6.6 percent higher than long-term quitters.
For women, authors note the steep increase in risk is particularly concerning given the United States Preventive Services Task Force recommends that current or former male smokers undergo an ultrasound screening for an abdominal aortic aneurysm once between the ages of 65 and 75 but makes no such recommendation for women.
[…]
The study also found that being older, white, or having high levels of bad cholesterol also increased the risk of abdominal aortic aneurysm.
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Stress accelerates immune aging. www.sciencedaily.com
Stress ages the immune system.
Psychosocial stress, such as that experienced with discrimination or trauma, has profound effects on the human body. For example, evidence suggests that stress alters the immune system, driving inflammatory processes and impairing antiviral responses. Findings from a recent study demonstrate that stress accelerates immune aging.
Immune function wanes as the body ages, a phenomenon referred to as immunosenescence. This gradual deterioration of the immune system is widely considered the primary driver of the increased rate of infections and cancers in older adults. Multiple factors promote immunosenescence, including genetics, nutrition, exercise, and pathogen exposures, among others.
The investigators analyzed blood samples taken from more than 5,700 participants over the age of 50 years who were enrolled in the Health and Retirement Study, an ongoing study of older adults living in the United States. They measured the types and characteristics of the participants' immune cells, including CD4+ naïve (immature) cells, CD4+ differentiated (mature) cells, CD8+ naïve cells, and CD8+ differentiated cells, as well as the ratio of CD4+ to CD8+. Having more immature cells is indicative of a younger immune cell profile. The participants provided information about their socioeconomic status, lifestyle practices, and lifetime exposures to various stressors, including stressful life events, chronic stress, everyday discrimination, lifetime discrimination, and life trauma.
The investigators found that participants who had experienced more stress had fewer immature CD4+ cells and more mature CD4+ cells. Similarly, those who had experienced more stress had fewer immature CD8+ cells and more CD8+ cells. Those who had experienced high lifetime discrimination and chronic stress tended to have a lower CD4+ to CD8+ ratio, an indicator of impaired immune function. However, some of the harmful effects of stress were partly ameliorated by lifestyle factors, such as not smoking or drinking alcohol, and maintaining a healthy weight.
These findings suggest that psychosocial stress accelerates immune aging, potentially driving disease and premature death in vulnerable groups. However, lifestyle practices may moderate this risk. Interestingly, evidence suggests that a fasting-mimicking diet promotes the return of a more youthful immune cell profile. Learn more in this clip featuring Dr. Valter Longo.
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Association Between Dietary Fiber Intake and All-Cause and Cardiovascular Mortality in Middle Aged and Elderly Adults With Chronic Kidney Disease www.ncbi.nlm.nih.gov
High dietary fiber intake reduces the risk of premature death among people with chronic kidney disease.
Chronic kidney disease, an umbrella term for a variety of conditions that impair kidney function, affects as many as 700 million people worldwide. The primary causes of chronic kidney disease are diabetes and hypertension32977-0/fulltext). Findings from a recent study suggest that high dietary fiber intake reduces the risk of premature death among people with chronic kidney disease.
Dietary fiber refers to the indigestible components of plant-based foods. A growing body of evidence indicates that eating a fiber-rich diet decreases the risks of many chronic diseases, such as coronary heart disease, stroke, hypertension, diabetes, and some types of cancer, including breast cancer and colon cancer. Public health recommendations for fiber intake vary based on a person’s age and sex. For example, adult females need between 22 and 28 grams of fiber per day, and adult males need between 28 and 34 grams per day. Most people living in the United States only get about half of the recommended amounts of fiber daily.
The study involved nearly 3,900 adults (average age, 63 years) who had chronic kidney disease and were enrolled in the Korean Genome and Epidemiology Study. The investigators collected information regarding the participants' diets (including fiber intake), lifestyle habits (such as smoking or exercising), alcohol intake, and overall health. They tracked the participants for about ten years and noted whether the participants died and, if so, their cause of death.
During the ten-year period, 602 of the participants died; of these, 149 died from cardiovascular diseases. The participants' average daily fiber intake was approximately 5 grams per day. The participants who consumed the most fiber were 37 percent less likely to die from all causes of premature death than those who consumed the least, even when considering age, sex, body mass index, smoking, exercise, hypertension, diabetes, and abnormal blood lipids. When the investigators looked at specific causes of death, they found that participants who consumed the most fiber were 44 percent less likely to die from cardiovascular diseases than those who consumed the least.
These findings suggest that dietary fiber markedly reduces the risk of premature death in people with chronic kidney disease. Interestingly, people with chronic kidney disease are often advised to reduce their intake of fiber-rich vegetables, fruits, nuts, legumes, and whole grains because these foods also contain phosphates and potassium, which carry risks in the setting of poor kidney function. However, dietary counseling regarding which foods to avoid can offset some of these risks and encourage healthy consumption of dietary fiber.
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Creatine supplementation and aging musculoskeletal health link.springer.com
Creatine prevents age-related muscle losses.
Creatine is a nitrogen-containing compound that is produced in the liver and kidneys and stored in the brain and muscles. It plays essential roles in the recycling of adenosine triphosphate, or ATP. Creatine is also present in the diet in meat and seafood and is widely used as a dietary supplement to build and maintain muscle mass. Although creatine is available in many forms, the bulk of the research on the compound has centered on creatine monohydrate. Evidence from a 2013 meta-analysis suggests that creatine prevents age-related muscle losses.
Sarcopenia, the progressive loss of skeletal muscle mass and strength that occurs with aging, begins as early as one’s 30s or 40s. By the time a person reaches their 80s, they may have lost as much as half of their total muscle mass. As a result, sarcopenia is one of the leading causes of functional decline and loss of independence in older adults. Contributing factors for sarcopenia include poor nutrition, low physical activity, and inflammation, among others. However, evidence suggests that resistance exercise can prevent or reverse sarcopenia.
The investigators conducted a meta-analysis, a type of study that analyzes the data derived from multiple studies using objective, statistical formulas to identify a common effect. Their analysis included 13 studies that examined the effects of creatine supplementation and resistance exercise on muscle mass and other health indicators in adults over the age of 50 years.
They found that creatine supplementation, in combination with resistance exercise, promotes muscle accretion and builds strength in older adults more effectively than resistance exercise alone. Their analysis also revealed that creatine supplementation benefits bone health by increasing bone mineral density and improving markers of bone biology.
These findings suggest that creatine and resistance exercise work in a synergistic fashion to promote muscle mass and strength in older adults. However, the investigators cautioned that although creatine is widely considered safe for most people, its effects on people with kidney dysfunction aren’t known and further research in older adults is warranted. [Watch this clip in which Dr. Stuart Phillips discusses the benefits of creatine on muscle protein synthesis.](LINK)
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Vitamin D deficiency is associated with the development of dementia.
Vitamin D is a fat-soluble vitamin that plays critical roles in many physiological processes, such as blood pressure regulation, immune function, and cell growth. Poor vitamin D status is implicated in the pathogenesis of many acute and chronic diseases, including rickets, osteoporosis, multiple sclerosis, cancer, and COVID-19. Evidence from a recent study suggests that vitamin D deficiency is associated with the development of dementia.
Health experts disagree on the terminology and cutoffs used to determine vitamin D status. The Institute of Medicine (IOM) has determined that serum vitamin D concentrations less than 30 nmol/L (less than 12 ng/mL) place people “at risk for vitamin D deficiency”; those ranging from 30 to 50 nmol/L (12 to 20 ng/mL) place some populations “at risk for inadequacy”; and those of 50 nmol/L (20 ng/mL) or greater are considered “sufficient.” However, the Endocrine Society has suggested that vitamin D concentrations ranging from 52.5 to 72.5 nmol/L (21 to 29 ng/mL) define “insufficiency,” and those less than 20 ng/mL (50 nmol/L) define “deficiency.”
The study involved more than 425,000 healthy adults (ages 60 to 73 years) enrolled in the UK Biobank study who had undergone magnetic resonance imaging (MRI) studies to assess brain volumes and whose vitamin D status was known. The investigators categorized the participants according to their vitamin D status based on literature and Institute of Medicine and Endocrine Society Clinical Practice guidelines. They collected information about the participants' demographics, lifestyles, and various health factors and tracked the participants for approximately 10 years. Then they used Mendelian randomization, a research method that provides evidence of links between modifiable risk factors and disease based on genetic variants within a population, to identify causal links between vitamin D status and brain health, dementia, and stroke.
They found that lower total brain volume tended to reflect a higher rate of dementia and stroke. The participants with low vitamin D concentrations were more likely to have lower brain volumes, an increased risk for dementia and stroke, and more white matter hyperintensities (brain lesions that indicate small vessel disease) than those with high concentrations. Vitamin D conferred the greatest protection against dementia at concentrations of 50 to 74.9 nmol/L. The Mendelian randomization revealed that participants whose concentrations were less than 25 nmol/L were 54 percent more likely to develop dementia.
These findings suggest that low vitamin D increases a person’s risk for dementia. The authors suggested that as many as 17 percent of dementia cases might be prevented by achieving vitamin D sufficiency (50 nmol/L). Learn more about the beneficial health effects of vitamin D in our overview article.
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BMI is positively associated with accelerated epigenetic aging in twin pairs discordant for BMI (~one month per 1-unit BMI increase) onlinelibrary.wiley.com
Higher BMI is associated with epigenetic age acceleration.
Obesity exerts profound effects on the human body, ranging from alterations in the gut microbiota to an increased risk for many chronic diseases. Body mass index (BMI) is a proxy for body fatness and is strongly correlated with disease risk with aging. Findings from a recent study suggest that BMI is associated with epigenetic age acceleration.
Epigenetic age acceleration is a phenomenon that occurs when an individual’s epigenetic (biological) age exceeds their chronological age and can be the result of either intrinsic or extrinsic factors. Intrinsic factors are largely driven by internal physiological factors such as normal metabolism and genetics. Extrinsic factors are those associated with lifestyle and environmental exposures, such as diet, smoking, or exercise.
To rule out the effects of genetics and shared environments, the investigators used data from the Finnish Twin Cohort, an ongoing study of twins and twin families. They gathered BMI data and metabolic health parameters for more than 1,400 participants, including both monozygotic (identical) and dizygotic (fraternal) twins. They measured the participants' epigenetic ages using GrimAge, a type of epigenetic clock that predicts lifespan and healthspan in units of months or years, and tests the effects of lifestyle on biological aging.
They found that for every one-unit increase in BMI, the twins exhibited approximately one month of accelerated epigenetic aging. In twin pairs where one twin was heavier than the other, the heavier twin’s epigenetic age was approximately 5 months older than the lighter twin. They also found that age acceleration was associated with insulin resistance, a risk factor for type 2 diabetes.
These findings suggest that having a higher BMI accelerates epigenetic aging and underscores the importance of maintaining a healthy body weight throughout the lifespan. To learn more about epigenetics and accelerated epigenetic aging, check out these resources, including an overview article and these episodes featuring epigenetic experts Dr. Steve Horvath and Dr. Morgan Levine.
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Air pollution may attenuate the beneficial association vigorous physical activity with low white-matter hyperintensity volume n.neurology.org
Air pollution negates some of the beneficial effects of vigorous-intensity exercise.
Components present in air pollution – a mixture of toxic chemicals, gases, and particulate matter – can cross biological barriers, including the blood-brain barrier. Exposure to air pollutants is associated with poor health outcomes and an increased risk for both acute and chronic diseases. A recent study suggests that air pollution negates some, but not all, of the beneficial effects of vigorous-intensity aerobic exercise.
Robust evidence demonstrates that vigorous-intensity aerobic exercise (defined as activity that achieves a heart rate that is 70 to 80 percent of one’s maximum) benefits brain health. For example, vigorous-intensity aerobic exercise appears to activate the endocannabinoid system to promote motor sequence memory and learning. Other evidence suggests it improves mood.
The study involved 8,600 adult participants enrolled in the UK Biobank study. Participants wore wrist accelerometers to track their physical activity. They also underwent magnetic resonance imaging (MRI) to assess their structural brain volumes and identify the presence of white matter hyperintensities – areas of the brain that show up as distinct white areas on MRIs and indicate cerebral small blood vessel disease. The investigators estimated the participants' exposure to air pollution based on where the participants lived.
The investigators found that the more physically active participants were, the less their brains showed evidence of shrinkage, and the fewer white matter hyperintensities they exhibited – an effect roughly equivalent to being three years younger. Participants who were exposed to more air pollution exhibited greater brain shrinkage than those with less exposure – about the amount observed in one year of normal aging. However, participants who exercised the most and had the most exposure to air pollution demonstrated no evidence of more brain shrinkage, but they exhibited more white matter hyperintensities, especially if they engaged in vigorous-intensity aerobic exercise.
These findings support earlier studies that demonstrate the beneficial health effects of vigorous-intensity exercise on the brain but suggest that exercising in areas where air pollution is high negates some of these benefits. The authors recommended that because most air pollution comes from vehicle exhaust, people should exercise in areas far from heavily trafficked roads.
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Periodontal Condition Is Correlated with Deep and Subcortical White Matter Hyperintensity Lesions in Japanese Adults www.mdpi.com
Gum disease may increase the risk of white matter hyperintensities, a type of brain lesion.
White matter hyperintensities are brain lesions that appear as intense white spots on magnetic resonance imaging (MRI) scans. They are often indicators of cerebral small blood vessel disease and are considered a risk factor for dementia. High blood pressure is the primary contributor to white matter hyperintensity formation, but other factors likely play roles, as well. Findings from a 2020 study suggest that periodontitis is associated with white matter hyperintensities.
Periodontitis is a chronic inflammatory condition of the gums, characterized by red, tender, swollen, or bleeding gums. It is typically caused by poor oral hygiene and is more common with age, manifesting in more than two-thirds of adults over the age of 65 years. Periodontitis is diagnosed using a periodontal probe, which is used to assess the depth of pockets in the gum. In a healthy mouth, a pocket can be anywhere from 1 to 3 millimeters deep. Deeper pockets are indicators of gum inflammation and disease.
The study involved more than 400 adults (average age, 54 years) who underwent a routine dental exam that included pocket depth probing. The investigators performed MRI scans on the participants to identify the presence of white matter hyperintensities, which were classified according to their size, number, and severity. They gathered information about the participants' general health and lifestyles and measured their C-reactive protein (CRP, a biomarker of inflammation). They found that nearly half of the participants had white matter hyperintensities. Those who did were nearly three times more likely to be at least 65 years old, more than twice as likely to have elevated systolic blood pressure, and nearly twice as likely to have deeper pocket depth (6 millimeters or more). Having white matter hyperintensities was not associated with the participants' CRP levels.
These findings suggest that older age, elevated blood pressure, and periodontitis are associated with an increased risk of developing white matter hyperintensities, but inflammation is not a driver of this association. Evidence indicates that white matter hyperintensities are predictive of the amount and degree of leakage of the blood-brain barrier leakage. Learn more in our overview article.
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From the article:
Systemic immune-inflammation index (SII) is a novel inflammatory marker based on the composition ratio of blood cell counts. In this study, we evaluated the association between the SII and cerebral small vessel disease (cSVD) in health check-up participants. We evaluated participants from our health check-up registry between 2006 and 2013. The SII was calculated using the following formula: SII = (platelet count × neutrophil count)/lymphocyte count. cSVD was assessed by considering white matter hyperintensity (WMH) volume, lacunes, and cerebral microbleeds (CMBs). A total of 3187 participants were assessed. In multivariable linear regression analysis, the SII was significantly related to WMH volume [β = 0.120, 95% confidence interval (CI) 0.050–0.189]. However, lacunes and CMBs showed no statistical significance with the SII. In the subgroup analysis by age, the SII was significantly associated with WMH volume only in participants aged ≥ 60 years (β = 0.225, 95% CI 0.068–0.381). In conclusion, a high SII was associated with cSVD. Since this association was more pronounced in WMH than in lacunes or CMBs, WMH might be closer to the inflammation-related pathological mechanisms.
Age-related changes in systemic inflammation:
Interestingly, the close association between the SII and WMH volume in our study was significant only in older participants aged ≥ 60 years. This might be related to the aging-related changes in the homeostatic maintenance of our body’s inflammation and immunity (e.g., inflammaging, immunosenescence, and homeostenosis)
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Obese when compared to those with normal body fat had much higher inflammation: 53% higher CRP, 30% higher TNF-a, 17% higher WBC count, 42% higher IL6 linkinghub.elsevier.com
Strong link between accumulated visceral fat and chronic inflammation.
A person’s waist-to-hip ratio compares their waist measurement to that of their hips. A high ratio can be an indicator of excess fat accumulation around the waist, often referred to as visceral fat. Findings from a 2005 study suggest that visceral fat is associated with markers of inflammation.
Visceral fat is stored in the abdominal cavity near the liver, pancreas, and intestines. The accumulation of visceral fat is linked to increased risk of cardiovascular disease and other chronic diseases. Many factors drive visceral fat accumulation, including poor sleep, an obesogenic diet, and sugar-sweetened beverage intake, among others.
The study involved more than 3,000 healthy males and females (18 to 89 years old) living in Greece. The investigators calculated the participants' body mass index (BMI) and measured their waist and hip circumferences. Participants provided blood samples for the assessment of inflammatory biomarkers, including C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-alpha), amyloid A (an apolipoprotein secreted in the acute stage of inflammation), white blood cells, and interleukin-6 (IL-6).
The investigators found that approximately 36 percent of the males and 43 percent of the females had excess visceral fat. Approximately 20 percent of the males and 15 percent of the females had obesity. Participants with greater visceral fat had 53 percent higher CRP, 30 percent higher TNF-alpha), 26 percent amyloid A, 17 percent higher white blood cell counts, and 42 percent higher IL-6, compared to participants with normal fat distribution. The relationship between visceral fat and inflammatory markers was stronger than that between obesity and inflammation, even when considering the participants' age, income, education, and other potential confounding factors.
These findings suggest that visceral fat and inflammatory processes are linked. The investigators posited that excess accumulation of visceral fat may increase the risk for cardiovascular disease by driving inflammation.
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Fecal microbial transplants from young to old mice reverse the hallmarks of aging. www.sciencedaily.com
Scientists have identified several hallmarks of aging – observable biological patterns of dysfunction that occur as an organism ages. These hallmarks both drive and are the result of inflammaging, the chronic, low-grade inflammation that occurs with aging. Findings from a recent study suggest that fecal microbial transplants reverse the hallmarks of aging.
As a person ages, the overall makeup of the population of microbes that inhabit their gut undergoes extensive changes. These changes are associated with increased inflammation, altered metabolic health and immune function, and an increased risk of chronic disease. Fecal microbial transplant is a therapeutic strategy that involves transfer of microbial-rich feces from a donor to a recipient. The goal of fecal microbial transplant is to restore the microbial balance in the gut of the recipient as a means to improve health.
The investigators performed fecal microbial transplants first between young mice and aged mice and then vice versa. They sequenced the bacterial populations in the fecal samples before and after transplantation. Then they assessed the effects of the transplants on inflammatory hallmarks of aging (specifically, protein levels, immune function, and behavior).
They found that fecal microbial transplantation from aged to young mice elevated systemic and tissue markers of inflammaging, accelerated age-related inflammation in the central nervous system and retina, drove the loss of key functional proteins in the retina, and promoted intestinal barrier permeability (sometimes referred to as “leaky gut”). However, transplantation from young to old mice reversed these effects.
These findings suggest that age-related changes in the gut microbiota promote inflammation, driving increased gut permeability, retina dysfunction, and impaired brain health, and contributing to the hallmarks of aging. Learn more about the hallmarks of aging in our comprehensive overview article.
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Repeated head injury damage the blood-brain barrier and produce an autoimmune response that promotes neurological disease www.sciencedaily.com
From the article:
A new study suggests that brain injury from repeat blows to the head – observed among football players and soldiers – might not be a traumatic phenomenon, but an autoimmune phenomenon. It indicates that brain injury may be the result of an out-of-control immune response, much like multiple sclerosis. This is an entirely new way of thinking about how trauma could cause long term degeneration and opens the door to investigating a vaccine/drug to prevent head trauma.
[…]
Researchers found that S100B, a well-accepted protein biomarker for traumatic brain injury, was present in varying degrees in the blood samples of the 67 football players after every game – even though none of them suffered a concussion. This demonstrates that even the most routine hits have some impact on the blood-brain barrier and possibly the brain itself, Bazarian said.
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Inherited Parkinson's LRRK2 mutations promote excessive inflammatory cytokines that cross blood-brain barrier, trigger neuron damage via microglia www.sciencedaily.com
From the article:
Suspecting that the LRRK2 mutations might be acting outside of the brain, the researchers used an agent – the outer shell of bacteria, called lippopolysaccharide (LPS) – that causes an immune reaction. LPS itself does not pass into the brain, nor do the immune cells it activates, which made it ideal for testing whether this second hit was acting directly in the brain.
When the researchers gave the bacterial fragments to the mice carrying the two most common LRRK2 gene mutations, the immune reaction became a “cytokine storm,” with inflammatory mediators rising to levels that 3-5 times higher than a normal reaction to LPS. These inflammatory mediators were produced by T and B immune cells expressing the LRRK2 mutation.
Despite the fact that LPS did not cross the blood-brain barrier, the researchers showed that the elevated cytokines were able to enter the brain, creating an environment that caused the microglia to activate pathologically and destroy the brain region involved in movement.
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Repurposed chemo drug acting on the blood-brain barrier shows dose-dependent increase of dopamine in Parkinson's disease patients www.sciencedaily.com
Repurposed chemo drug inactivates protein that destroy’s the blood-brain barrier in Parkinson’s disease:
The current part of the study just published, examined the cerebrospinal fluid of patients via epigenomics, which is a systematic analysis of the global state of gene expression, in correlation with continuing clinical outcomes. The new analysis helps explain the clinical findings.
Nilotinib inactivated a protein (DDR1) that was destroying the ability of the blood brain barrier to function properly. When DDR1 was inhibited, normal transport of molecules in and out of the brain filter resumed, and inflammation declined to the point that dopamine, the neurotransmitter depleted by the disease process, was being produced again.
After 27 months, nilotinib was found to be safe, and patients who received nilotinib showed a dose-dependent increase of dopamine, the chemical lost as a result of neuronal destruction.
First study to show blood-brain barrier as therapeutic target for Parkinson’s disease:
“Not only does nilotinib flip on the brain’s garbage disposal system to eliminate bad toxic proteins, but it appears to also repair the blood brain barrier to allow this toxic waste to leave the brain and to allow nutrients in,” Moussa explains. “Parkinson’s disease is generally believed to involve mitochondrial or energy deficits that can be caused by environmental toxins or by toxic protein accumulation; it has never been identified as a vascular disease.”
“To our knowledge, this is the first study to show that the body’s blood brain barrier potentially offers a target for the treatment for Parkinson’s disease,” Moussa says.
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Environmental toxins inhaled through nose may induce inflammation which culminates in the deposit of Lewy bodies in the brain, promoting Parkinson's www.sciencedaily.com
Lewy bodies found in olfactory areas suggest not only is lost smell a sign of neural damage, but rather a direct link to the mechanism creating the disorder:
The loss of a sense of smell is known to be one of the earliest signs of Parkinson’s disease (PD) and can even appear years before the characteristic tremors and loss of motor function are seen. Some scientists believe that olfactory dysfunction may not just be a sign of broader neural damage, but rather may have a more direct linkage to the generation of the disorder itself. In support of this idea, deposits of a protein called alpha-synuclein that form Lewy bodies can be found in olfactory areas, as well as in dying dopamine neurons whose loss triggers PD, and mutations in the gene encoding alpha-synuclein produce PD.
Inflammation triggered in the areas where the olfactory neurons project (recapitulated by lipopolysaccharide) culminate in alpha-synuclein that can cross the blood-brain barrier:
Results of the study, published in the journal Brain Pathology, showed that application of an irritating component of a bacterium’s cell wall induces inflammation in the areas exactly where the olfactory neurons project, called the olfactory bulb. Moreover, these areas show the hallmark signs of PD, depositions of alpha-synuclein, the core components of Lewy bodies. PD is characterized by progressive motor and non-motor symptoms linked to alpha-synuclein pathology and the loss of dopaminergic neurons in the nigrostriatal system. Toxic aggregates of alpha-synuclein can arise from either overexpression of the protein, changes in protein modifications, and from hereditary mutations.
[…]
“Data from our study show that the bacterial trigger does not move across the blood-brain barrier,” said Quan. “Rather, a sequential inflammatory activation of the olfactory mucosa triggers a subsequent expression of inflammatory molecules within the brain, propagating the inflammation.”
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Processes contributing to cancer may reduce risk of Alzheimer's disease, according to post-mortem analysis www.the-scientist.com
From the article:
Thanks to those data, which showed participants with cancer had fewer hallmarks of Alzheimer’s disease in their brains as well as a reduced likelihood of neurodegenerative symptoms during their lifetimes, lead study author Erin Abner, a University of Kentucky epidemiologist and aging researcher and her team were able to offer the clearest picture yet of a molecular mechanism that seems to link the two diseases.
“The connection is becoming more and more apparent,” New York University cancer researcher Eva Hernando-Monge, who didn’t work on the study, tells The Scientist.
They investigated cancer deaths for traces of Alzheimer’s:
As cohort members passed away, the team autopsied their brains to look for biomarkers associated with Alzheimer’s disease, including structures such as neurofibrillary tangles and neuritic plaques. They also noted when someone carried the APOE ε4 allele, a known genetic risk factor for the neurodegenerative condition.
[…]
The analysis revealed “less Alzheimer’s pathology in the people who had cancer, both amyloid and tau,” Abner says. “We also saw evidence [that] another amyloid pathology—cerebral amyloid angiopathy, which is amyloid aggregation in blood vessel walls—was lower.
Mechanisms of the cancer-Alzheimer’s anti-relationship:
Processes related to cell growth and survival, as well as the production of specific molecules including the antistress response protein vimentin and the enzyme carbonic anhydrase, are all upregulated in cancer, he finds. Alzheimer’s occurs when these processes and proteins are downregulated.
Another review, published in Molecular Psychiatry in 2021, identifies the proteins p53 and PIN1 as implicated in both cancer and Alzheimer’s. PIN1 overexpression is associated with myriad cancers, but its absence is linked to the formation of the Alzheimer’s biomarkers tracked in the Brain study. Meanwhile, p53 has a well-established anticancer role, but can also contribute to neurodegenerative disease.
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Amyloid-beta can travel, cancer-like, to brain from other parts of body: insights from parabiosis experiments www.sciencedaily.com
From the article:
The scientists demonstrated this cancer-like mobility through a technique called parabiosis: surgically attaching two specimens together so they share the same blood supply for several months. […] Normal mice that had been joined to genetically modified partners for a year “contracted” Alzheimer’s disease. Song says the amyloid-beta traveled from the genetically-modified mice to the brains of their normal partners, where it accumulated and began to inflict damage.
The problem is partly due to an increased permissiveness of the blood-brain barrier as we age that allows entry from other parts of the body:
“The blood-brain barrier weakens as we age,” says Song, a Canada Research Chair in Alzheimer’s Disease and the Jack Brown and Family Professor. “That might allow more amyloid beta to infiltrate the brain, supplementing what is produced by the brain itself and accelerating the deterioration.”
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50% of all dementias and Alzheimers may start with leaky blood-brain barrier www.sciencedaily.com
From the article:
“Many scientists have focused their Alzheimer’s disease research on the buildup of toxic amyloid and tau proteins in the brain, but this study and others from my lab show that the problem starts earlier – with leaky blood vessels in the brain,” said Berislav Zlokovic, senior author of the study
Reducing fibrinogen that enters the brain through leaky gatekeeping may be important for preventing decline:
Fibrinogen develops blood clots so wounds can heal. When gatekeeper cells are compromised, an unhealthy amount of fibrinogen slinks into the brain and causes white matter and brain structures, including axons (nerve fibers) and oligodendrocytes (cells that produces myelin), to die.
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Leaky blood-brain barrier caused by cerebral small vessel disease increases the prevalence of white-matter hyperintensities and brain damage www.sciencedaily.com
Poor blood-brain barrier integrity drives white matter losses.
White matter hyperintensities are areas in the brain that appear as intense white spots on magnetic resonance imaging (MRI) scans. They are often indicators of cerebral small blood vessel disease and are considered a risk factor for dementia. A 2021 study found that breaches in blood-brain barrier integrity are associated with brain tissue losses and precede the appearance of white matter hyperintensities.
The blood-brain barrier, a specialized system of endothelial cells that shields the brain from toxins present in the blood, supplies the brain’s tissues with vital nutrients and substances necessary for neuronal and metabolic function. The structural integrity of the blood-brain barrier is therefore critical for homeostatic maintenance of the brain microenvironment.
The study involved 43 patients (average age 58 years) who had been diagnosed with cerebral small vessel disease, as evidenced by having experienced a stroke or demonstrating mild cognitive impairment. At the beginning of the study and two years later, participants underwent a variety of MRI techniques that quantified their overall blood-brain barrier permeability as well as the areas surrounding white matter hyperintensities.
The MRIs revealed that participants who had the greatest amount of leaky brain tissue at the beginning of the study exhibited greater white matter tissue losses two years later. These tissue losses translated to greater permeability, a phenomenon particularly evident in the areas surrounding the brain lesions associated with white matter hyperintensities.
These findings suggest that losses in blood-brain barrier integrity damage brain tissue, driving increased permeability and white matter losses. In turn, these changes potentiate the disease processes associated with cerebral small vessel disease. Learn more about the blood-brain barrier in our overview article.
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Alzheimer’s risk allele APOE4 triggers early breakdowns in blood-brain barrier, predicting cognitive decline www.sciencedaily.com
From the article:
Severe damage to vascular cells called pericytes was linked to more severe cognitive problems in APOE4 carriers. APOE4 seems to speed up breakdown of the blood-brain barrier by activating an inflammatory pathway in blood vessels, which is associated with pericyte injury."
[…]
Zlokovic’s previous research shows that people who develop early memory problems also experience the most leakage in their brain’s blood vessels – independent of amyloid plaque or tau, two common contributors to Alzheimer’s. The leakage starts when cells called pericytes, which line the walls of blood vessels in the brain and maintain blood-brain barrier integrity, are damaged.
[…]
In participants who had the APOE4 gene, researchers found damaged capillaries in the brain’s memory center, the hippocampus and medial temporal lobe. The damage correlated with increased levels of a protein that causes inflammation, cyclophilin A – an early sign of the disease in people already at higher risk of developing Alzheimer’s.
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Inhibiting the Mfsd2a transporter that brings omega-3 DHA into the brain promotes leakage of brain barrier www.sciencedaily.com
Impaired transport of DHA disrupts the blood-brain barrier.
Lipid rafts – cholesterol-filled “bubbles” found in the cell membrane – serve as staging areas for many cellular activities. One type of lipid raft, called caveolae, facilitates the transport of substances across the membrane of endothelial cells. Findings from a 2017 study demonstrate that suppression of caveolae-mediated transport in brain endothelial cells protects the integrity of the blood-brain barrier.
The blood-brain barrier is a highly selective semi-permeable barrier made up of endothelial cells connected via tight junctions. This barrier separates the circulating blood from the brain’s extracellular fluid and prevents the entry of substances that may be neurotoxic. Disruption of the blood-brain barrier has been implicated in the pathogenesis of neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and multiple sclerosis, among others.
The investigators' previous research showed that a critical player in blood-brain barrier function is Mfsd2a, a transmembrane protein found exclusively on the endothelial cells that line blood vessels on the barrier. Mfsd2a participates in lipid transport and is the sole means by which lysophospholipid DHA, the brain’s preferred form of DHA (a type of omega-3 fatty acid) is delivered to the brain.
Using mice that carried a mutation that blocked Mfsd2a’s capacity to transport DHA, the investigators assessed blood-brain barrier function as well as caveolae formation and activity in the animals' brains. Then they compared the lipid composition of brain endothelial cells to lung epithelial cells, which lack Mfsd2a.
They found that mice that lacked Mfsd2a function had leakier blood-brain barriers and greater caveolae formation and activity than normal mice. They also found that brain endothelial cells had higher lipid concentrations than lung epithelial cells. The most abundant lipid in the brain endothelial cells was DHA, which was found in concentrations that were two to five times higher.
These findings suggest that Mfsd2a-mediated transport of lipids, particularly DHA, impairs caveolae activity, thereby preserving blood-brain integrity. Learn more about links between Mfsd2a, DHA, and brain health in this open-access peer-reviewed article by Dr. Rhonda Patrick..
[Learn more about the blood-brain barrier in our overview article.](LINK)
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Leaking of the blood-brain barrier disrupts healthy aging and memory www.sciencedaily.com
Abstract:
“The blood–brain barrier (BBB) protects the central nervous system (CNS) from unregulated exposure to the blood and its contents. The BBB also controls the blood-to-brain and brain-to-blood permeation of many substances, resulting in nourishment of the CNS, its homeostatic regulation and communication between the CNS and peripheral tissues. The cells forming the BBB communicate with cells of the brain and in the periphery. This highly regulated interface changes with healthy aging. Here, we review those changes, starting with morphology and disruption. Transporter changes include those for amyloid beta peptide, glucose and drugs. Brain fluid dynamics, pericyte health and basement membrane and glycocalyx compositions are all altered with healthy aging. Carrying the ApoE4 allele leads to an acceleration of most of the BBB’s age-related changes. We discuss how alterations in the BBB that occur with healthy aging reflect adaptation to the postreproductive phase of life and may affect vulnerability to age-associated diseases.”
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Menopause disrupts sleep, accelerating biological aging www.sciencedaily.com
Menopause accelerates epigenetic aging.
Menopause, which typically occurs around the age of 52 years, is the cessation of a female’s menstrual cycle and signifies the loss of reproductive capacity. Evidence suggests that early menopause increases the risk for age-related disease and premature death. Findings from a 2016 study suggest that menopause accelerates epigenetic aging.
Epigenetics is a biological mechanism that regulates gene expression (how and when certain genes are turned on or off). Diet, lifestyle, and environmental exposures can drive epigenetic changes throughout a person’s lifespan to influence health and disease. Epigenetic age is based on a person’s DNA methylation profile and strongly correlates with their chronological age. However, some exceptions exist. For example, the epigenetic ages of semi-supercentenarians (people who live to be 105 to 109 years old) are markedly younger than their chronological ages.
The investigators analyzed the DNA methylation profiles of more than 3,100 women enrolled in four large observational studies (Women’s Health Initiative; InCHIANTI; Parkinson’s Disease, Environment, and Genes; and the National Survey of Health and Development) to identify links between epigenetic age and menopause. Their analysis was based on assessment of the biological age of cells taken from the women’s blood, saliva, and inner cheek. Because the age at which a female experiences menopause is heritable, they conducted a Mendelian randomization analysis to identify genetic links between age at menopause and epigenetic aging.
They found that menopause markedly accelerated epigenetic aging. Females who experienced earlier natural menopause were more likely to have “older” blood than those who experienced later menopause, but females who had surgical menopause (a surgical procedure in which the ovaries are removed) had older blood and saliva than those who experienced natural menopause. Cells taken from the inner cheek of females who took menopausal hormone therapies were younger than those who did not take hormones. They also found that a particular gene variant that influences the age at which a female experiences menopause also influences age acceleration.
These findings suggest that menopause accelerates epigenetic aging in females. The investigators conceded that their findings do not establish a cause-and-effect relationship, however. In a related study, researchers found that menopause-related sleep disorders, such as insomnia or poor sleep quality, contribute to the accelerated aging associated with menopause. Learn more about accelerated epigenetic aging in this episode featuring Dr. Steve Horvath.
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Childhood cancer survivors have epigenetic alterations that increase biological age www.sciencedaily.com
Genetic links between childhood cancer and accelerated epigenetic aging identified.
Childhood cancer is relatively rare, affecting just one in 6,500 children each year. In recent decades, the overall survival rate for children with cancer has increased from 10 percent to 85 percent, due to early diagnosis and marked advancements in treatment. However, findings from a new study suggest that some survivors of childhood cancer are genetically susceptible to experiencing accelerated epigenetic aging.
Epigenetic age acceleration is a phenomenon that occurs when a person’s epigenetic age exceeds their chronological age. Acceleration may be either intrinsic or extrinsic. Intrinsic aging is largely driven by internal physiological factors such as normal metabolism and genetics, whereas extrinsic aging is associated with lifestyle and environmental exposures, such as diet, tobacco use, ultraviolet radiation, and mental illness.
The investigators performed a genome-wide association study, a type of observational study that associates specific genetic variations with particular diseases, using multiple epigenetic aging clocks. Their assessment was based on blood-derived DNA from approximately 2,400 childhood cancer survivors and 500 people who had never had cancer.
They identified single nucleotide polymorphisms, or variants, in two areas of the survivors' DNA – the ¬¬SELP gene and the HLA region – that drive accelerated aging and are associated with age-related disease. The SELP gene encodes for a protein called P-selectin, a cell adhesion molecule that plays roles in atherosclerosis and peripheral artery disease. Its activity is increased in the setting of Alzheimer’s disease. The HLA, or human leukocyte antigen, region is an area on chromosome six that plays important roles in immunity. Mutations in the HLA region, which can occur following exposure to genotoxic drugs (such as chemotherapy) are associated with increased risk for autoimmune disorders, such as type 1 diabetes and celiac disease.
These findings suggest that genetic variants increase the risk of accelerated epigenetic aging among childhood cancer survivors and underscore the importance of identifying children at risk. Learn about epigenetic aging acceleration in this clip featuring Dr. Steve Horvath.
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Mid-life long duration antibiotic use of >= two months linked to poorer scores in cognition, learning, working memory, and attention in later life www.sciencealert.com
Antibiotic use in midlife increases a person’s risk for neuropsychiatric diseases.
Antibiotics are prescribed for a wide range of infectious diseases. In 2015, healthcare providers in the United States wrote nearly 270 million antibiotic prescriptions – more than 800 antibiotic prescriptions for every 1,000 people. Health experts estimate that 30 percent of these prescriptions were likely unnecessary. Findings from a new study suggest that antibiotic use in midlife increases a person’s risk for neuropsychiatric diseases.
The study included approximately 15,000 midlife participants (average age, 55 years) enrolled in the Nurses’ Health Study II, an ongoing prospective cohort study of female nurses. The participants completed questionnaires regarding their general health, diet, lifestyle, and medication use during the previous four years, including antibiotic use and the reason for which the antibiotic was prescribed. The investigators categorized the participants' cumulative antibiotic use as none, one to 14 days, 15 days to two months, and two months or more. Participants also completed a battery of neuropsychological tests.
The investigators found that participants who took antibiotics for at least two months over the previous four years were more likely to perform worse on neuropsychological tests than participants who did not take antibiotics. The influence of antibiotic use on neuropsychological test scores was roughly equivalent to three to four years of aging. These findings held true even after considering other factors that could influence cognitive function, including age and coexisting illnesses.
These findings suggest that longer exposure to antibiotics in midlife negatively influences cognitive health, underscoring the importance of moderating antibiotic use in older adults. They also support findings from animal studies that suggest antibiotic use early in life alters neuropeptide signaling pathways that influence behavioral development. Learn more about the effects of antibiotic use in early life in this clip featuring Dr. Eran Elinav.
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The secret to staying young: New research highlights power of life long exercise to keep muscles healthy www.sciencedaily.com
Lifelong exercise protects older adults from losing muscle mass and function with age.
With age, muscles shrink in size and lose strength, a process called sarcopenia that can increase frailty and reduce the quality of life for older adults. In people with sarcopenia, muscle fibers contain fewer satellite cells (i.e., muscle stem cells) and progressively lose their connections to nerves, a process called denervation. Findings of a new report show that lifelong exercisers have more youthful muscles that resist denervation.
Satellite cells are stem cells that proliferate, fuse together, and form the long tubular structures than comprise muscle fibers. Satellite cells are necessary for muscle repair and growth after exercise, a process called hypertrophy, due to their connection with cells that produce growth factors and deliver nutrients. Previous research demonstrates that exercise interventions that last several weeks can reverse muscle denervation in older adults with frailty; however, the preventive effects of lifelong exercise have yet to be investigated.
The authors recruited 15 moderately active young men (average age, 26 years), 16 older men who were lifelong exercisers (average age, 73 years), and 15 older men who lived a sedentary lifestyle (average age, 73 years). On their first visit to the lab, participants completed a bout of heavy resistance training on only one side of their body so that the researchers could compare the effects of exercise and sedentary behavior in each person. The researchers also measured maximum muscle strength and body composition and collected a blood sample. Participants provided another blood sample two days and six days after the exercise challenge and provided a muscle biopsy sample six days after.
Lifelong exercisers had muscles that were more resistant to fatigue during exercise compared to sedentary young and older adults. Compared with sedentary older adults, lifelong exercisers had more satellite cells in their muscles connected to type 2 myofibrils, which are important for fast-twitch muscle movement, but no difference in connection to type 1 slow-twitch myofibrils. Muscles from lifelong exercisers also expressed high levels of mRNA for acetylcholine receptors, which are necessary for preventing denervation.
These results show that lifelong exercisers maintained a more youthful muscle profile due to increased connections with muscle- and nerve-supporting satellite cells. People who started life with a sedentary lifestyle can still reap the longevity-promoting benefits of exercise. Starting a new aerobic exercise habit, even at age 70, cuts heart disease death in half.
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Hyperbaric oxygen trial discovered a lengthening of up to 38% of the telomeres, decrease of up to 37% in senescent cells in certain cell populations www.sciencedaily.com
Routine hyperbaric treatment increased telomere length and reduced senescence in humans.
With age, tissues lose their ability to function properly, leading to an increased risk of cancer, cardiovascular disease, and Alzheimer’s disease, among others. Cells become exhausted from replication over time and enter a state of senescence, meaning they will no longer reproduce because they are damaged. Findings of a new report demonstrate the ability of hyperbaric treatments to reduce the number of senescent immune cells.
Hyperbaric (i.e., high air pressure) treatments use increased atmospheric pressure and oxygen content to enhance the total amount of oxygen dissolved in the body, accelerating wound healing. Some forms of routine hyperbaric therapy cause the body to react as if it were experiencing hypoxia (i.e., low blood oxygen), a phenomenon called the hyperoxic-hypoxic paradox. Although some of the hypoxia-associated effects of hyperbaric treatments, such as sirtuin activation, stem cell proliferation, mitochondrial biogenesis, and neurogenesis, are associated with longevity, the effects of hyperbaric therapy on cellular senescence are unknown.
The authors recruited 35 participants aged 60 and older who did not have cognitive decline and lived independently. Participants completed 60 hyperbaric treatments distributed as five sessions per week for three months. Each session consisted of 90 minutes of breathing 100 percent oxygen at a pressure twice that of normal barometric pressure. The researchers collected blood samples at multiple time points to measure markers of senescence in peripheral blood mononuclear cells, which include T cell, B cells, monocytes, and natural killer cells.
By the 30th hyperbaric treatment, participants experienced statistically significant increases in telomere length, a marker of reduced senescence rate, in T-helper cells, B cells, and natural killer cells. Following all 60 treatments, telomere length increased by 30 percent in T-helper cells, 38 percent in B cells, and 22 percent in natural killer cells. Demonstrating further benefit, hyperbaric treatment reduced the number of senescent T-helper cells by 12 percent and cytotoxic T cells by 11 percent after 60 sessions.
These results show, for the first time in humans, that routine hyperbaric treatment reduced the rate of aging in immune cells. However, because this study utilized a small sample, reported large variations in the data, and did not contain a control group, these results must be replicated with future research before they can be fully interpreted.
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Discovery highlights why women are more susceptible to Alzheimer's disease: follicle-stimulating hormone (FSH) may be a major pathogenic factor www.eurekalert.org
From the article:
“During menopause, the serum concentration of FSH strongly increases, binding to the cognate FSH receptor on neurons and activating the C/EBPβ/AEP pathway. This results in Aβ and Tau pathologies, leading to the development of AD,” said Dr. Zaidi Mone, co-corresponding author of the study and a tenured professor at the Mount Sinai School of Medicine in New York.
The researchers employed different methods to demonstrate this finding. Using ovariectomized mice, they used anti-FSH antibody treatment to block FSH and inactivate the C/EBPβ/AEP pathway. They also deleted FSH receptor (FSHR) expression in neurons to abolish the binding of FSH to FSHR in the hippocampus. Both of these methods alleviated pathology and cognitive dysfunction. In addition, knockdown of C/EBPβ in the AD mice model decreased AD pathologies.
Besides working with female mice, the researchers also injected FSH into male mice and discovered that FSH promoted AD pathologies.
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β-Hydroxybutyrate, the body's major source of energy during exercise or fasting, blocks histone deacetylases that otherwise promote oxidative stress www.sciencedaily.com
From the article:
“Over the years, studies have found that restricting calories slows aging and increases longevity – however the mechanism of this effect has remained elusive” Dr. Verdin said. Dr. Verdin, the paper’s senior author, directs the Center for HIV & Aging at Gladstone and is also a professor at the University of California, San Francisco, with which Gladstone is affiliated. “Here, we find that βOHB – the body’s major source of energy during exercise or fasting – blocks a class of enzymes that would otherwise promote oxidative stress, thus protecting cells from aging.”
[…]
Normally HDACs keep a pair of genes, called Foxo3a and Mt2, switched off. But increased levels of βOHB block the HDACs from doing so, which by default activates the two genes. Once activated, these genes kick-start a process that helps cells resist oxidative stress. This discovery not only identifies a novel signaling role for βOHB, but it could also represent a way to slow the detrimental effects of aging in all cells of the body.
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D-beta-hydroxybutyrate supplementation restored impaired brain function and protected against neurodegeneration in mouse model of Parkinson's disease www.sciencedaily.com
From the article:
Infusion of D-beta-hydroxybutyrate (D-beta-HB) to mice suffering from Parkinson disease restored impaired brain function and protected against neurodegeneration and motor skill abnormalities.
[…]
Przedborski and colleagues administered the neurotoxin MPTP to mice, which caused dopaminergic neurodegeneration and deficits in the mitochondrial electron transport chain reminiscent of Parkinson disease. Using this model of disease, the authors showed that the infusion of the ketone body D-beta-HB restored mitochondrial respiration and protected against MPTP-induced neurodegeneration and motor deficits. The study supports a critical role for mitochondrial defect in Parkinson disease.
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Maintaining a lower systolic blood pressure (less than 120 mm Hg) may reduce the amount of white matter lesions, reducing risk of dementia www.sciencedaily.com
Maintaining a systolic blood pressure of 120 or less may protect against dementia and cognitive decline. Nearly two-thirds of adults living in the United States have hypertension (high blood pressure), defined as having a systolic pressure of 130 or higher or a diastolic pressure of 80 or higher. Hypertension damages small blood vessels in the eyes, kidneys, and other tissues, increasing the risk for disease and dysfunction. A 2019 study found that intensive blood pressure control in patients with hypertension reduces the risk of developing small blood vessel damage-related white matter lesions in the brain.
Intensive blood pressure control is an aggressive treatment protocol for hypertension that seeks to achieve a target systolic blood pressure goal of 120 or less. This differs from standard treatment protocols, which stipulate that within three months of starting medication therapy to reduce high blood pressure, a patient’s target pressures (systolic and diastolic) should be less than 140/90. After three months, the target pressures should be less than 130/80.
White matter lesions are areas in the brain that appear as intense white spots on magnetic resonance imaging (MRI) scans. They are often indicators of small blood vessel disease and are considered a risk factor for dementia.
The study involved 670 adults (average age, 67 years) who had hypertension. Roughly half of the participants underwent intensive blood pressure control treatment, while the other half underwent standard treatment. The investigators performed MRI scans of all participants at the beginning of the intervention and again about four years later.
They found that participants who underwent intensive blood pressure control had fewer white matter lesions in their brains compared to those who underwent the standard treatment. Interestingly, those who underwent intensive treatment exhibited greater brain volume losses than those who underwent standard treatment, but this difference was not statistically significant.
These findings suggest that intensive blood pressure control reduces white matter lesions in the brains of people with hypertension and support findings from a related study that demonstrated that intensive blood pressure control may reduce the risk of adverse cognitive outcomes.
Hypertension is highly preventable with lifestyle modifications that involve diet and exercise. For example, dietary components, such as potassium and magnesiumquercetin and vitamin D lower blood pressure. Aerobic exercise also lowers blood pressure. Learn about other beneficial effects of aerobic exercise in our overview article.
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Exercise increases activity of anti-aging sirtuin enzymes in older adults with obesity. www.mdpi.com
Older adults were asked to complete twice-weekly aerobic and strength training for 12 weeks. Some participants were advised to consume a healthier diet during the exercise training. Other participants were given two grams of omega-3-rich oil from Calanus finmarchicus. The investigators also evaluated a control group of participants who did not exercise, change their diet, or take the supplement. The investigators measured the activity of sirtuin enzymes 1, 3, and 5 in the blood.
All three groups who completed the exercise training had significant increases in the activity of sirtuin enzymes 1 and 3. Participants who completed the exercise training and also followed a healthy diet plan had the greatest increase in sirtuin activity compared to the control group. The activity of sirtuin enzyme 5 did not change significantly for any group.
The authors stated that their report is the first to demonstrate the effects of chronic exercise and healthy eating on sirtuin activity.
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Mechanical forces of pressure and movement from exercise increases the formation of bone and lymphocytes, enhancing the ability to clear infection www.sciencedaily.com
From the article:
Researchers from the Morrison laboratory discovered that forces created from walking or running are transmitted from bone surfaces along arteriolar blood vessels into the marrow inside bones. Bone-forming cells that line the outside of the arterioles sense these forces and are induced to proliferate. This not only allows the formation of new bone cells, which helps to thicken bones, but the bone-forming cells also secrete a growth factor that increases the frequency of cells that form lymphocytes around the arterioles. Lymphocytes are the B and T cells that allow the immune system to fight infections.
When the ability of the bone-forming cells to sense pressure caused by movement, also known as mechanical forces, was inactivated, it reduced the formation of new bone cells and lymphocytes, causing bones to become thinner and reducing the ability of mice to clear a bacterial infection.
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Exercise may improve thinking skills and thicken areas of the brain in people as young as 20 www.sciencedaily.com
From the article:
Researchers found that aerobic exercise increased thinking skills. From the beginning of the study to the end, those who did aerobic exercise improved their overall scores on executive function tests by 0.50 points, which was a statistically significant difference from those who did stretching and toning, who improved by 0.25 points. […] “Since a difference of 0.5 standard deviations is equivalent to 20 years of age-related difference in performance on these tests, the people who exercised were testing as if they were about 10 years younger at age 40 and about 20 years younger at age 60,” Stern said.
Increased thickness of the outer layer of the brain in the left frontal area:
“Since a difference of 0.5 standard deviations is equivalent to 20 years of age-related difference in performance on these tests, the people who exercised were testing as if they were about 10 years younger at age 40 and about 20 years younger at age 60,” Stern said.
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Rebalancing gut microbiome with butyrate lengthens survival in mouse model of ALS by repairing intestinal permeability www.sciencedaily.com
From the article:
In a mouse model of ALS, the compound butyrate helped correct a gut microbiome imbalance and reduced gut leakiness – both symptoms of ALS. The treated mice lived also longer compared to mice that weren’t given butyrate.
[…]
When the researchers fed the ALS-prone mice butyrate in their water, starting when the mice were 35 to 42 days old, the mice showed a restored gut microbiome profile and improved gut integrity. Butyrate-treated mice also showed improved neuromuscular function and delayed onset of ALS symptoms. Treated mice showed symptoms at 150 days old compared to control mice at about 110 days. Treated mice also lived an average 38 days longer than mice not given butyrate.
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Long-term distance cycling reduces hallmarks of aging: thymic involution - "cyclists' thymuses were making as many T cells as those of a young person" www.sciencedaily.com
From the article:
The study recruited 125 amateur cyclists aged 55 to 79, 84 of which were male and 41 were female. The men had to be able to cycle 100 km in under 6.5 hours, while the women had to be able to cycle 60 km in 5.5 hours.
[…]
The cyclists also did not increase their body fat or cholesterol levels with age and the men’s testosterone levels also remained high, suggesting that they may have avoided most of the male menopause.
More surprisingly, the study also revealed that the benefits of exercise extend beyond muscle as the cyclists also had an immune system that did not seem to have aged either.
An organ called the thymus, which makes immune cells called T cells, starts to shrink from the age of 20 and makes less T cells. In this study, however, the cyclists' thymuses were making as many T cells as those of a young person.
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Gene enhancers activated by exercise are hotspots of inter-individual variation and linked to cognitive abilities www.sciencedaily.com
From the article:
The scientists discovered that after completing the endurance training program, the structure of many enhancers in the skeletal muscle of the young men had been altered. By connecting the enhancers to genetic databases, they discovered that many of the regulated enhancers have already been identified as hotspots of genetic variation between individuals – hotspots that have been associated with human disease.
The scientists speculate that the beneficial effects of exercise on organs distant from muscle, like the brain, may largely be mediated by regulating the secretion of muscle factors. In particular, they found that exercise remodels enhancer activity in skeletal muscle that are linked to cognitive abilities, which opens for the identification of exercise training-induced secreted muscle factors targeting the brain.
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A high-polyphenol diet is protective against age-related brain shrinkage. www.eurekalert.org
“The effect of diet on age-related brain atrophy is largely unproven.
This 18-month clinical trial longitudinally measured brain structure volumes by magnetic-resonance-imaging…Abdominally obese/dyslipidemic participants were randomly assigned to (1)-healthy dietary guidelines (HDG), (2)-Mediterranean (MED) diet, or (3)-Green-MED diet (MED diet higher in polyphenols and lower in red/processed meat). All subjects received free gym memberships and physical activity guidance. Both MED groups consumed 28g/day walnuts (+440 mg/d polyphenols). The Green-MED group consumed green-tea (3-4 cups/day) and Mankai (Wolffia-globosa strain, 100g frozen-cubes/day) green shake (+800mg/day polyphenols).
Compared to younger participants, atrophy was accelerated among those ≥ 50 years. In subjects ≥50years, HOC decline and LVV expansion were attenuated in both MED groups, with the best outcomes among Green-MED diet participants, as compared to HDG. Similar patterns were observed among younger subjects. Improved insulin sensitivity over the trial was the strongest parameter associated with brain atrophy attenuation (p<0.05). Greater Mankai, green-tea and walnuts intake and less red and processed meat were significantly and independently associated with reduced HOC decline (p<0.05). Elevated urinary levels of the Mankai-derived polyphenols: urolithin-A (r = 0.24;p = 0.013) and tyrosol (r = 0.26;p = 0.007) were significantly associated with lower HOC decline.
A Green-MED, high-polyphenol diet, rich in Mankai, green tea and walnuts and low in red/processed meat is potentially neuroprotective for age-related brain atrophy."
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Exercise reverses aspects of brain aging: improvements in executive function, mental flexibility, verbal fluency, and blood flow to the brain neurosciencenews.com
Aging drives an array of physiological, functional, and mental changes in the human body. It is the primary risk factor for many chronic diseases in humans, including cancer, Alzheimer’s disease, and cardiovascular disease. Findings from a 2020 study suggest that exercise reverses some of the harmful effects of aging on the brain.
Scientists have identified strong links between regular physical exercise and brain health. Some of the mechanisms that drive the beneficial effects of exercise on the brain include increases in brain volume and connectivity, improved blood flow, enhanced synaptic plasticity, and increased neurogenesis – the formation of new neurons.
The intervention study involved 206 healthy, cognitively intact middle-aged and older adults (average age, 66 years) with low physical activity levels. The participants engaged in a supervised aerobic exercise program three days per week, gradually increasing from 20 to 40 minutes over a period of six months. They also completed an unsupervised exercise session one day per week during the six-month period. The authors of the study assessed the participants' cognitive performance, cerebrovascular function, and overall fitness on three separate occasions over a period of 12 months.
After completing the six months of exercise, the authors of the study noted that the study participants improved by nearly 6 percent on measures of working memory, flexible thinking, and self-control. They improved by nearly 2.5 percent on tests of verbal fluency, comparable to abilities seen in person five years younger. Blood flow to the brain increased by nearly 3 percent, suggesting that cerebrovascular function is a critical aspect of maintaining or improving memory and verbal skills.
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Six months of daily aerobic exercise directly impacts tests of executive function, mental flexibility, self-correction, and verbal fluency www.sciencedaily.com
From the article:
Participants were enrolled in a supervised aerobic exercise program held three days a week. As they progressed through the program, they increased their workout from an average of 20 minutes a day to an average of at least 40 minutes. In addition, people were asked to work out on their own once a week.
Researchers found that after six months of exercise, participants improved by 5.7% on tests of executive function, which includes mental flexibility and self-correction. Verbal fluency, which tests how quickly you can retrieve information, increased by 2.4%.
[…]
Before and after six months of aerobic activity, the participants' average peak blood flow to the brain was measured using ultrasound. Blood flow rose from an average of 51.3 centimeters per second (cm/sec) to an average of 52.7 cm/sec, a 2.8% increase. The increase in blood flow with exercise was associated with a number of modest but significant improvements in aspects of thinking that usually decline as we age, Poulin said.
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Some people appear to age slower (or faster) than others, exhibiting vastly different age-related physical changes and disease risks. Recognition of this biological phenomenon has given rise to the concept of biological age – a measure of a person’s physiological and functional state. Scientists use a variety of means to gauge biological age, including methylation markers, gray matter volume, and facial aging. Findings from a recent study suggest that retinas provide useful biomarkers in determining a person’s biological age.
The retina is a thin, multicellular layer lining the rear, interior portion of the eye. It plays critical roles in the cascade of events involved in visual processing, converting the energy of photons of the visible light spectrum into biochemical signals and transmitting those signals to the brain. Poor retinal health is often an indicator of systemic illness, such as cardiovascular disease or nutritional deficiency.
The authors of the study viewed more than 80,000 retinal images collected from adults (average age, 55 years) participating in the UK Biobank Study. They also collected information about the participants' demographics, lifestyles, and overall health. The researchers used deep learning, a type of machine learning that mimics the way humans learn, to analyze images of the retinas and assign a biological age, which they referred to as “retinal age.” Then they calculated the retinal age gap – the difference between retinal age and chronological age. Having a positive retinal age gap was reflective of an older-appearing retina; having a negative retinal age gap was reflective of a younger-appearing retina. Finally, the researchers looked at links between retinal age gap and all causes of premature death.
They found that their machine learning model accurately predicted retinal age and chronological age to within 3.5 years. For every year of positive retinal age gap difference, the risk of premature death from any cause increased 2 percent. Having positive retinal age gaps greater than three years increased the risk of premature death from specific diseases (other than cardiovascular disease or cancer) by as much as 67 percent. These findings held true even after taking other factors into account, such as body weight, high blood pressure, or smoking.
These findings suggest that retinal age, as predicted via deep learning, is a powerful predictor of biological age and premature death risk. Collecting retinal images is a low-cost, non-invasive procedure that may be beneficial in identifying people at risk for premature disease and death. Learn about other strategies for predicting biological age in our overview article on epigenetic aging clocks.
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A growing body of evidence indicates that exercise supports cognitive health throughout the lifespan, even into one’s later years. Scientists don’t fully understand the mechanisms that drive the beneficial effects of exercise, but some studies suggest that it increases brain volume, while others suggest that it reduces the brain’s toxic burden. Findings from a recent study suggest that exercise maintains synapses in the brains of older adults.
Synapses are junctions between neighboring neurons, where the exchange of electrical signals and neuronal communication occurs. Synaptic formation and integrity are necessary for the establishment and maintenance of the brain’s neural networks and the precision of its circuitry. The loss of synapses promotes the collapse of neural networks important for memory and cognition and drive the dementia associated with Alzheimer’s disease. Key players in synaptic integrity are synaptic proteins, which play critical roles in neurotransmission and neuronal development.
The investigators drew on data from the Rush Memory and Aging Project, an ongoing study of aging and Alzheimer’s disease among older adults. More than 400 older adults participated in the study. They wore activity monitors to track their movement and exercise throughout the day for up to 10 days. They also agreed to donate their brains upon their death for postmortem evaluation, during which the investigators measured the presence of synaptic proteins in the participants' brain tissue.
They found that older adults who exercised regularly had higher levels of synaptic proteins in their brains. The proteins were present in multiple brain regions, including areas involved in memory and cognitive function, and were highest when activity levels were measured within two years of death, suggesting that without sufficient exercise, the proteins diminished over time.
These findings suggest that exercise preserves synaptic integrity via enhanced production of synaptic proteins, potentially providing protection against Alzheimer’s disease. Learn how exercise affects other aspects of brain health in this episode featuring Dr. Giselle Petzinger.
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Zinc deficiency promotes inflammation and weakens immunity, especially in older adults. pubmed.ncbi.nlm.nih.gov
Vitamins and minerals are utilized by a wide array of enzymes that protect cells and DNA from damage. Zinc, in particular, is essential for maintaining DNA integrity and adequate antioxidant defenses. A new paper reviewing the work of Dr. Bruce Ames and others highlights the importance of zinc in promoting longevity and preventing chronic diseases.
Zinc is a metallic mineral that is consumed in the diet from foods such as meat, shellfish, legumes, and fortified foods. Severe zinc deficiency results in growth retardation, hair loss, skin sores, and depressed immunity and is uncommon in developed nations. However, marginal deficiency, which is asymptomatic and dangerous over long periods of time, is likely very common. Children, older adults, and people with altered gastrointestinal function are particularly susceptible to zinc deficiency.
Zinc is concentrated in the nuclei of cells where it functions to stabilize chromatin (large structures of spooled DNA) and catalyze chemical reactions for DNA repair, replication, and transcription. Along with other metals such as copper, iron, and magnesium, zinc is essential for balancing oxidative and reductive reactions in the cellular environment. One enzyme, copper-zinc superoxide dismutase, neutralizes hydrogen peroxide radicals by accepting an electron at its copper site. By absorbing reactive oxygen species, antioxidant compounds prevent damage to structures such as lipid membranes, enzymes, and DNA.
The immune system is a major producer of hydrogen peroxide and other oxygen radicals, which attack pathogens and recycle damaged host cells. Adequate zinc intake is essential for moderating the inflammatory response. In particular, zinc inhibits activation of the NF-kappaB pathway, driving the production of inflammatory cytokines such as tumor necrosis factor-alpha. Zinc deficiency increases the risk of developing neurodegenerative and autoimmune diseases through mechanisms that involve over-activation of inflammatory pathways.
Zinc deficiency further increases one’s risk of disease by reducing the number of pathogen-fighting cells such as antibody-producing B cells, natural killer cells, and monocytes. Reduced pathogenic immunity and increased chronic inflammation are common in old age, but they begin in middle-adulthood and progress over time in parallel, with decreasing zinc absorption and retention. Zinc supplementation in older adults reduces inflammation while increasing production of new immune cells and strengthening the body’s response to vaccines.
Overall, zinc deficiency accelerates the aging process by impairing antioxidant production and cellular repair mechanisms, over-activating inflammatory pathways, and reducing pathogen defenses. The authors conclude there is good evidence to suggest that supplementing with at least 20 milligrams of zinc per day may be an effective strategy for reducing the adverse effects of aging on the immune system.
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Diet is superior to drugs and bioactive compounds for metabolic health and longevity. www.sciencedaily.com
Nutrient sensing – a cell’s capacity to recognize and respond to fuel sources – plays a critical role in human health, ultimately influencing the aging process and susceptibility to age-related disease. Findings from a recent study suggest that dietary interventions exert powerful effects on proteins produced in the liver, fundamentally “reprogramming” nutrient-sensing pathways.
Multiple studies have investigated the possibility that dietary strategies or drugs can alter nutrient-sensing pathways to improve metabolic health and extend lifespan. For example, robust evidence indicates that intermittent fasting and calorie restriction prolong lifespan in rodents and monkeys. Other findings suggest that altering dietary composition, such as increasing or decreasing protein, fat, or carbohydrate content, also influences longevity. Similarly, many drugs and bioactive compounds have demonstrated longevity-promoting qualities.
The study investigators assessed the effects of various diets and drugs on liver protein production in mice, using the Geometric Framework for Nutrition, a research tool that identifies links between diet, health, and disease. Diets included in the analysis varied in terms of overall nutrient content and calories. Drugs under study included metformin (an anti-diabetes drug), rapamycin (an anti-parasitic drug), and resveratrol (a bioactive compound derived from certain fruits and vegetables).
Diets with lower caloric content accelerated production of proteins required for overall protein synthesis (particularly genes for a cellular machine called the spliceosome). As dietary protein content increased, oxidative stress in mitochondria increased. Higher protein content also increased SLC25A51, a cellular protein involved in the transport of nicotinamide adenine dinucleotide (NAD+). NAD+ participates in many aspects of metabolism, and its depletion has been implicated in the onset and progression of metabolic dysregulation. Interestingly, anti-aging drugs diminished the effects of diet. For example, metformin and rapamycin impaired mitochondrial responses to protein, and resveratrol decreased the response to fats and carbohydrates.
These findings suggest that diet dramatically influences cellular processes involved in metabolism and longevity and is superior to current anti-aging drugs and compounds. Learn more about dietary strategies, drugs, and bioactive compounds that may promote longevity in our overview articles about caloric restriction, time-restricted eating, metformin, and resveratrol.
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Higher diet quality is associated with lower epigenetic age. academic.oup.com
A diet rich in plant foods, lean protein, and healthy fat is associated with a reduced risk of death from cardiovascular disease, cancer, and all causes; however, many of the cellular and molecular mechanisms of these relationships are unknown. One of the mechanisms that controls a person’s response to diet and risk of disease is epigenetic modification. Findings of a new investigation detail the relationship between healthy eating and epigenetic and biological age.
While a person’s genetic code does not change over time, the pattern of epigenetic markers attached to DNA does change with age. Epigenetic modifications include the addition and subtraction of methyl groups, naturally occurring processes that regulate gene expression. These changes are quantifiable and serve as a means to gauge biological age, which is often different from chronological age. Epigenetic aging clocks use an organism’s DNA methylation profile biomarker of aging based on alterations in an organism’s DNA methylation profile and can be used to predict likelihood of death (i.e., mortality).
The investigators utilized data from the Sister Study, an observational study of over 50,000 females in the United States who had a biological sister diagnosed with breast cancer, but were free from cancer themselves. These participants provided data about their dietary habits and provided a blood sample for the measurement of epigenetic age and other factors. Next, the authors analyzed the diet data and calculated four scores of diet quality that aligned with dietary recommendations from the USDA and other sources. The authors analyzed a subsample of almost 3,000 participants in order to calculate epigenetic age using the Hannum, Horvath, PhenoAge, and GrimAge clocks.
The data revealed only a weak association between higher diet quality and epigenetic age as measured by the two aging clocks designed as predictors of chronological age (Horvath and Hannum clocks). However, there was a strong relationship between diet quality and epigenetic age calculated by the two clocks designed to estimate mortality (PhenoAge and GrimAge clocks). This highlights the differences between aging clock designs, but it also supports a relationship between diet quality and disease risk that is mediated by epigenetic changes. The relationship between increased diet quality and reduced mortality-related epigenetic age was strongest among participants who did not meet exercise recommendations. Smoking status and age did not significantly alter these statistical relationships.
These findings demonstrate that higher diet quality is associated with a lower biological age as estimated by epigenetic clocks designed to predict mortality. Learn more about epigenetics from expert Dr. Steve Horvath, creator of the Horvath epigenetic aging clock, in this episode of the FoundMyFitness podcast.
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Scientists use animal models to answer a variety of scientific questions about humans, from basic science to the pathophysiology of complex diseases. The reliability of these models is based on remarkable similarities in the biology of most mammals and the fact that many human diseases often affect other animal species. Findings from a recent study suggest that glucose homeostasis in aging differs between some commonly studied animals and humans.
As humans age, they experience significant changes in glucose metabolism and body composition. For example, insulin resistance is common among older adults, increasing their risk for type 2 diabetes. In addition, a person’s fat mass typically increases and muscle mass and bone mineral density decrease.
The authors of the study compared the trajectories, change rates, and death rates associated with fasting blood glucose, body weight, and fat mass in mice, nonhuman primates, and humans across their lifespans. They drew on data from the Study of Longitudinal Aging in Mice, the Nonhuman Primate Study, and the Baltimore Longitudinal Study of Aging.
They found that body weight and body fat across the three species followed similar trajectories, typically peaking in mid to late life and decreasing thereafter. However, fasting blood glucose levels decreased as the mice aged but increased as the nonhuman primates and humans aged. Having low glucose in mice and high glucose in nonhuman primates and humans translated to higher death rates.
These findings suggest that aging-related changes in glucose homeostasis differ among species and underscore the need for choosing appropriate animal models in aging research.
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Neural tube defects (e.g., spina bifida, hydranencephaly) are a group of birth defects caused by incomplete development of the outer layers of the brain or spinal cord. Prenatal folate supplementation prevents an estimated 70 percent of neural tube defects, but additional therapies are needed. A recent report describes the relationship between maternal diabetes and abnormal cell aging in the fetal nervous system in mice.
Previous research has demonstrated a relationship between maternal diabetes and the incidence of neural tube defects in mice; however, the mechanisms that drive this relationship are unknown. High blood glucose levels cause oxidative damage and promote cellular senescence, a state in which cells are not metabolically active and do not reproduce. Aging cells accumulate damage over time and become senescent. In adults, an excess of senescent cells can promote inflammation and disease. In the developing fetus, senescence is vital for tissue remodeling and the building of limbs and organs. However, inappropriate senescence may lead to abnormal development.
The investigators used multiple mouse models in their study. In a first experiment, they used a strain of mice that develop diabetes and compared them to wild-type mice that are not predisposed to any disease. They injected pregnant females from both groups with either rapamycin, a compound that slows cellular aging by inhibiting the enzyme mTOR, or a placebo. In a second experiment, they used diabetic and non-diabetic strains of knockout mice, whose genomes do not contain the gene FoxO3a, a regulator of aging that may slow cellular senescence.
Maternal diabetes increased the abundance of biomarkers of cellular senescence and DNA damage in the lining of the brain in offspring. Pregnant diabetic mice that were exposed to rapamycin had offspring with lower levels of senescence biomarkers and fewer neural tube defects compared to placebo. Offspring from FoxO3a knockout mice experienced the same decrease in senescence biomarkers and neural tube defect rates as rapamycin-treated mice.
These results elucidate the mechanisms by which maternal diabetes can cause birth defects through metabolic changes that accelerate aging. Learn more about the role of cellular senescence in aging in this episode featuring Dr. Judith Campisi.
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Irisin, a muscle hormone, mediates the neuroprotective effects of exercise. www.massgeneral.org
Aging causes brain changes that impair cognitive function, even in people who do not have Alzheimer’s disease or dementia. However, lifestyle factors like diet and exercise have significant influence over the rate of cognitive decline. Previous research has shown that exercise improves brain health and cognitive function during aging. A new report details the role of the muscle hormone irisin in the neuroprotective effects of exercise
Irisin, a type of myokine, is a hormone secreted from muscle in response to exercise. Previous research has shown that irisin may mediate some of the beneficial effects of exercise on the brain by stimulating the production of brain-derived neurotrophic factor (BDNF), a growth factor that increases neuroplasticity. Irisin is a fragment of the prohormone FNDC5, which is attached to the membranes of muscle cells. During exercise, irisin is cleaved from FNDC5 and circulates throughout the body to induce adaptations to exercise.
The authors used mice of varying ages who lack the genes necessary to produce FNDC5, called knock-outs, and genetically-normal mice, called wild-type. Both groups of mice completed exercise testing to measure balance, grip strength, endurance, and motor coordination; a water maze test to measure spatial learning ability and memory; and an open field test to measure locomotor activity levels, anxiety, and willingness to explore. In order to study the effects of irisin supplementation, the investigators conducted a second experiment in which they administered exogenous (i.e., made outside the body) irisin to a strain of mice who develop an Alzherimer’s-like dementia at an early age due to loss of FNDC5 function. The investigators measured structural and psychological changes in the brain throughout both experiments.
Both knock-out and wild-type mice exercised the same amount during testing. However, unlike the wild-type mice, knock-out mice did not show exercise-induced improvements in spatial learning and memory. Aged knock-out mice had more cognitive decline than wild-type mice and were less likely to prefer novel objects, a behavior associated with loss of function in the hippocampus, the brain region most associated with memory loss in dementia. Indeed, aged knock-out mice showed abnormal neuronal activation patterns in the dentate gyrus, a structure within the hippocampus that contributes to memory formation.
In contrast to knock-out mice and sedentary wild-type mice, wild-type mice who exercised had increased dendritic complexity and length in the dentate gyrus. This demonstrates the ability of exercise to improve neuronal structure and function in brain areas associated with memory through mechanisms involving irisin. Regular injections with exogenous irisin significantly improved performance on spatial learning and memory tasks in mice with Alzheimer’s-like dementia compared to untreated mice. These improvements may have been caused by dampening of overactive glial activity, leading to reduced inflammation.
Taken together, these data suggest that irisin is essential for mediating the beneficial effects of exercise on cognitive function. The authors concluded that these data also demonstrate the efficacy of exogenous irisin administration in regulating cognitive function in mice with Alzheimer’s-like dementia, providing support for future use of irisin therapies in humans with dementia.
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Fecal microbiota transplantation from young mice reverses aging effects. www.sciencedaily.com
Declines in brain function are common with age owing to metabolic and immune alterations that include changes to the gut microbiota, the community of microorganisms that inhabit the intestines. While a diverse microbial community with many species of beneficial bacteria is associated with improved nutrition and reduced inflammation, older adults (especially residents of long-term care facilities) have perturbations in microbiota composition that increase the risk for cognitive decline and frailty. Findings of a report released this month show that fecal microbiota transplantation from young to aged mice reverses age-associated cognitive impairment.
Fecal microbiota transplantation is a therapy in which microbes are isolated from the stool of a donor, processed, filtered, and administered to a recipient by nasogastric tube or enema. Previous research demonstrates the efficacy of fecal microbiota transplantation in treating infection with Clostridium difficile, a hospital-acquired infection that is difficult to treat with antibiotics, and a growing list of other diseases such as inflammatory bowel disease, metabolic syndrome, neurodevelopmental disorders (e.g., autism), and autoimmune diseases. Fecal microbiota transplantation improves health partially by increasing microbiota alpha diversity, meaning the number of species in an individual’s microbiota, also called “richess.” A microbiota with high richness is more likely to contain key beneficial species, such as those that produce neuroprotective short chain fatty acids.
Given the wide range of diseases associated with gastrointestinal microbiota composition, its effects on aging are an area of intense interest. Prior investigations have demonstrated that transfer of the fecal microbiota from aged mice to young mice alters immunity, neurogenesis, and cognition; however, the consequence of fecal transplantation from young mice to aged mice is unknown.
The investigators performed their experiment using young and aged male mice. They assigned aged mice to receive a fecal microbiota transplant from either a young mouse (the experimental group) or aged mouse (the control group). For further comparison, the researchers also assigned a group of young mice to receive a fecal microbiota transplant from another young mouse. Mice received the fecal microbiota transplant treatments once per day for three days, then twice weekly for four weeks. The mice completed a battery of tests to assess cognitive function. The researchers collected fecal samples in order to sequence the DNA of the microbiota and blood samples in order to measure hormones, cytokines, and other immune markers before and after the four weeks of treatment. Finally, they analyzed changes to gene expression and metabolism in the hippocampus, the brain region most-associated with age-related cognitive decline.
At baseline, young and aged mice had distinctly different microbiota composition. Following four weeks of microbiota transplantation, young mice, aged mice receiving a young transplant, and aged mice receiving an aged transplant all had similar microbiota composition. Aged mice tended to have more over-reactive T cells, dendritic cells, and macrophages, especially in the lymph nodes that line the intestines. Aged mice also showed enlargement of microglia (the predominant immune cells in the brain), a common feature of neurodegenerative diseases. Microbiota transplantation from young mice reversed these age-related effects on brain and peripheral immunity. Amino acid metabolism in the hippocampus, which is necessary for neurotransmission and cognition, was impaired in aged mice, but restored following microbiota transplantation from young mice. Finally, the improved hippocampal metabolism in aged mice that received a young microbiota transplant translated to increased learning and long-term memory and reduced anxiety-related behaviors compared to aged mice receiving an aged microbiota transplant.
These results reveal the potential benefits of fecal microbiota transplantation from young donors as a therapy to promote healthy aging.
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Human lifespan may not have a limit. www.sciencedaily.com
Since the 1990s, longevity researchers have attempted to estimate the maximum human lifespan; however, supercentenarians (i.e., people who live beyond 110 years) routinely break these estimates. Additional research is needed to provide more accurate models of aging for use in planning government programs and economic policy. Authors of a paper released this year report their updated estimates for the maximum age at death in the year 2100.
The existence of a fixed age limit for humans is an area of debate, with some scientists theorizing that biological processes like the shortening of telomeres are irreversible, determined by genetics, and a strong predictor of death. However, others argue that there is no limit to human lifespan and that age-related risk of death plateaus around 110 years of age. This uncertainty is partly due to a lack of consistent record keeping with verified age information. Research institutions have recently created systems such as the International Database on Longevity, a database containing validated supercentenarian life lengths from 15 countries, to aid in future research.
The investigators used a statistical model created by the authors of a 2017 report on maximum lifespan. This model estimates the survival probability of supercentenarians, meaning the likelihood of surviving each year beyond age 110 years. For the current report, the researchers used updated data from the International Database on Longevity, which currently includes records from more than 1,100 supercentenarians and almost 14,000 semi-supercentenarians (people who live between 105 and 109 years). They also added additional projections to the model regarding future levels of fertility and life expectancy across multiple countries and extended the projection window to the year 2100.
The authors found that the probability of breaking the current maximum reported age at death (122 years and 164 days, set by Jeanne Calment of France) this century is nearly 100 percent; the probability of a person reaching age 126 is approximately 89 percent; and the probability of a person reaching age 130 is nearly 13 percent. While the model did not exclude the possibility of a person living to 135 or 140 years this century, it is extremely unlikely. These estimates are in line with most other projections.
The authors concluded that these data do not support the existence of a maximum human age and forecast substantial increases in the number of supercentenarians in the coming decades.
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Depression is associated with muscle loss in older adults. journals.plos.org
Sarcopenia, the loss of muscle mass with age, is related to falling, poor oral health, and chronic disease. Sarcopenia is a progressive disorder, but early interventions with diet and exercise may improve health outcomes. Authors of a new report investigated the relationship between sarcopenia progression, depression, dementia, and hypertension.
Body composition shifts across the lifespan, with a progression toward lower muscle mass and increased fat mass after age of 60. Because fat and muscle participate in whole-body metabolism and hormone signaling, this shift in body composition contributes to the development of age-related diseases. Previous research has reported a link between sarcopenia, cognitive impairment, and depressive symptoms in older Korean men, but research is needed in additional demographic groups.
The authors collected data from more than 750 adults aged 60 years and older living in Japan. Participants completed surveys to measure depression and dementia status and underwent a physical examination that included the measurement of blood pressure, height, muscle mass, grip strength, and walking speed. The investigators classified participants as having sarcopenia if they had low skeletal muscle index (i.e., the ratio of the muscle in a person’s arms and legs to their height), poor grip strength, and slower walking speed. They defined pre-sarcopenia as having a low skeletal muscle index with normal grip strength and walking speed. Finally, they classified participants with a normal skeletal muscle index as robust.
Sarcopenia was associated with increased age and depression severity, but reduced hypertension. Compared to robust participants, those with pre-sarcopenia were more likely to have depression and hypertension. However, sarcopenia was not associated with dementia, which the authors noted may have been due to the small number of participants (only 49) with dementia.
The authors suggested that future research should explore strategies for management of depression, dementia, and hypertension in the prevention of sarcopenia.
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Graying of hair is related to psychological stress but may be reversible. www.scientificamerican.com
The loss of hair pigmentation (graying) is a hallmark of aging. Although it typically begins during a person’s twenties, the timing and extent of graying vary according to genetics and interactions between biological and psychological factors. Graying is generally considered irreversible, but findings from a recent study demonstrate that graying is not necessarily a linear process and may be reversible.
One of the primary drivers of graying is oxidative stress, which damages the pigment-producing region of the hair shaft. Oxidative stress occurs during the process of oxidative phosphorylation (the generation of energy) in mitochondria and can be reflective of exposures to both physical and psychological stressors. Evidence suggests that depigmented hairs may exhibit altered mitochondrial energy metabolism. Interestingly, case and anecdotal reports suggest that hair re-pigmentation can occur, causing bicolor hairs.
The authors of the study collected dark, depigmented, and bicolor hairs from 14 healthy young adults (average age, 35 years) who did not color, bleach, or chemically treat their hair. The authors digitally mapped pigmentation patterns in the hairs over time and assessed protein content in the hair shafts. Some of the participants completed a retrospective stress assessment questionnaire using a life event calendar, in which they recorded major events over a given time. Then the authors overlaid the hair pigmentation patterns on the participants' life events.
The authors found that depigmentation and re-pigmentation events corresponded with specific moments in the participants' lives, with depigmentation linked to stressful events (such as marital discord) and re-pigmentation linked with non-stressful events (such as a vacation). The authors also found that depigmented hairs contained more proteins linked to mitochondrial function and energy use, suggesting that mitochondria and metabolism are involved in the graying process.
These findings suggest that graying of hair is a more malleable process than once thought and indicate that studying changes in hair color may provide insights into how psychological stressors influence health.
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Creatine intake improves cognitive performance in older adults. link.springer.com
Cognitive decline is a personally challenging issue that degrades the quality of life for those affected. It is also a growing public health burden, with one in nine adults aged 65 years and older living with some level of cognitive impairment. Previous research has identified dietary components that reduce age-related cognitive impairment, including vitamin E, folate, and vitamin D. Authors of a new report investigated the effects of creatine on cognitive function in older adults.
Creatine is a compound found primarily in the brain and muscle that is involved with the production of energy in the form of adenosine triphosphate (ATP). Creatine is obtained in the diet from red meat, poultry, fish, and seafood and is also available as a dietary supplement. In older adults, metabolic dysfunction decreases cellular energy, potentially contributing to cognitive decline. One meta-analysis found that dietary creatine improves aspects of cognitive function in young and older healthy adults.
The authors of the current study analyzed data from more than 1,300 participants (average age, 71 years) in the National Health and Nutrition Examination Survey (NHANES), a long-term study collecting lifestyle and health data from people living in the United States. Participants completed cognitive testing and a 24-hour dietary recall during an interview with NHANES staff. The researchers analyzed the dietary data for foods containing creatine and calculated each participant’s estimated daily creatine intake. This assessment did not include supplemental creatine.
Participants with higher dietary creatine intake tended to have higher cognitive scores, even after taking into account other nutrition factors and socioeconomic status. Participants in the top 50 percent of creatine intake consumed more than 0.95 grams of creatine per day, the amount in about 14 ounces of cooked beef or fish. These participants performed better on cognitive testing than those in the bottom 50 percent.
These findings suggest creatine from food may be protective against age-related cognitive decline. Future research is needed to determine a dose of creatine that improves cognition without damaging kidney health, which is a concern for older adult populations.
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Altering energy metabolism lengthens healthspan and lifespan in mice. www.eurekalert.org
Metabolic dysfunction escalates with age and increases the risk of frailty and chronic disease. Many investigational antiaging drugs target enzymes involved in energy metabolism, such as mammalian target of rapamycin (mTOR) and insulin-like growth factor (IGF)-1. Findings of a new study in mice detail the role of sirtuins in energy metabolism and healthy aging.
Sirtuins are enzymes that play key roles in healthspan and longevity in multiple organisms. They are linked to the regulation of a variety of metabolic processes, including the release of insulin, mobilization of lipids, response to stress, and modulation of lifespan. Sirtuins respond to physiological changes in energy levels, thereby regulating energy homeostasis and health.
When fasting or exercising, the liver helps maintain blood sugar levels using the alternating processes of glycogenolysis (the breakdown of glycogen) and gluconeogenesis (the creation of new glucose). In glycogenolysis, single glucose molecules are released from larger glucose chains, called glycogen, for use as energy. Because the body stores a limited amount of glycogen, the liver uses gluconeogenesis to create glucose from non-carbohydrate precursors, such as lactate and glycerol. The role of gluconeogenesis in aging is unclear, with one study reporting an increase in gluconeogenesis with age in rats and other studies in rats reporting decreased gluconeogenic ability.
Using breeding techniques, the investigators produced a line of mice with livers that over-express the sirtuin enzyme SIRT6, which increases during fasting and regulates glucose metabolism. The researchers bred these mice with normal mice to produce litters with a mix of genotypes. Using this technique, the researchers were able to compare aging processes among littermates, which reduced confounding factors in their analyses.
Compared to their normal siblings, male SIRT6 mice exhibited a 27 percent increase in average lifespan and an 11 percent increase in maximal lifespan. Female SIRT6 mice showed a 15 percent increase in both average and maximal lifespan. Normal mice experienced greater metabolic dysfunction, performed less physical activity, and developed more inflammatory and degenerative diseases with age compared to SIRT6 mice. A series of metabolic tests revealed that SIRT6 mice had increased gluconeogenic gene expression in the liver and enhanced glycerol release from adipose tissue, which provided extra fuel for gluconeogenesis.
The authors concluded that SIRT6 controls healthspan and lifespan through regulating energy metabolism. This mechanistically complicated study will provide the groundwork for future aging research in humans.
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Diet and lifestyle intervention reduced epigenetic age by two years in just eight weeks. www.ncbi.nlm.nih.gov
Age-related diseases like heart disease, diabetes, dementia, and cancers are on the rise, placing a significant burden on the healthcare system and economy. Interventions that can slow the aging process by just two years could save almost $7 trillion over 50 years and increase health and quality of life. Authors of a recent report tested the effects of a diet and lifestyle intervention on the reversal of epigenetic aging.
Epigenetic aging is a way to predict an individual’s risk of age-related disease by biological means instead of just chronology. Epigenetics is a biological mechanism that regulates gene expression (how and when certain genes are turned on or off). Diet, lifestyle, and environmental exposures can drive epigenetic changes throughout an individual’s lifespan to influence aging. The record of these changes can be used to predict biological age. Lifestyle interventions may be able to slow biological aging by reversing some epigenetic modifications.
The authors of the study enrolled 43 healthy males between the ages of 50 and 72 years. They randomly assigned half of the participants to complete an eight-week diet and lifestyle intervention, while the other half did not. The intervention included a diet rich in vegetables (e.g., leafy greens, beets, and cruciferous and other colored vegetables), low-glycemic fruit (e.g., blueberries), seeds, animal proteins, liver, and eggs. The researchers advised participants to choose organic over conventional produce and meat; avoid eating between 7 p.m. and 7 a.m.; stay hydrated; cook with healthy oils (e.g., coconut, olive, or flaxseed oils); avoid sugar, dairy, grains, and beans; and avoid plastic containers. They gave participants a supplement rich in bioactive plant compounds (like quercetin or green tea extract) and a probiotic with the bacteria, Lactobacillus plantarum. They also asked participants to exercise for 30 minutes five days per week, sleep for at least seven hours per night, and manage stress with prescribed breathing exercises. They measured DNA methylation patterns before and after the intervention period to assess changes in the epigenome.
The diet and lifestyle intervention significantly decreased epigenetic age by more than three years by the end of the eight-week trial compared to participants in the control group. Compared to their own baseline epigenetic age, participants who completed the intervention reversed their epigenetic clocks by almost two years, although this relationship was not statistically significant. The intervention also increased serum folate by 15 percent and reduced blood triglyceride levels by 25 percent.
This study is the first randomized controlled trial to find that diet and lifestyle interventions may reverse epigenetic aging in healthy adult males. The authors note that large-scale trials with longer durations are needed to confirm their results.
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Age-related brain shrinkage is slower among non-industrialized populations. www.sciencedaily.com
The brain shrinks with age, a process called brain atrophy, and a faster rate of shrinkage is associated with dementia and cognitive and functional impairments. Heart disease risk factors such as high cholesterol, diabetes, and hypertension are common in industrialized populations and increase the risk of brain atrophy. Findings of a recent report compare rates of brain atrophy in industrialized and non-industrialized populations.
The indigenous Tsimane people of lowland Bolivia live by foraging, hunting, fishing, and horticulture in the Amazon basin. The Tsimane have the lowest prevalence of coronary heart disease of any known population, likely due to their highly active lifestyle and diet rich in fiber, unsaturated fats, and omega-3 fats. Their lifestyle also puts the Tsimane at a high risk of infection, causing chronically increased immune activity and inflammation, risk factors for both heart disease and brain atrophy.
This study included over 700 participants aged 60 years or older from a long-term study measuring lifestyle and health status in Tsimane adults. Clinic staff regularly visited participants in their villages to record infections and inflammation, heart disease risk factors, diet, and physical activity. The participants visited a nearby city to complete a computerized tomography (CT) scan of their heads to measure brain volume. The researchers compared these results to brain volume measurements from participants in the United States and Europe.
When compared to industrialized populations, the Tsimane had a significantly slower rate of brain volume loss with age. Compared to one sample of 500 participants aged 40 to 70 years in the Netherlands, Tismane adults in the same age range had half the rate of brain atrophy.
The authors concluded that slower rates of brain atrophy, along with diet and lifestyle factors and low heart disease risk among the Tsimane protect brain health despite high levels of chronic inflammation caused by infection. Future research should explore the relationship between infection, heart disease risk, and dementia.
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Maximum human lifespan may be 150 years. www.scientificamerican.com
Aging involves a progressive decline in the body’s ability to heal from damage (a property known as resilience) and a gradual increase in the risk of age-related diseases like cancers, diabetes, and cardiovascular diseases. Aging research aims to increase lifespan and healthspan through pharmacological and lifestyle interventions that enhance cellular repair and reduce exposure to harmful substances. Findings of a recent report propose a possible maximum age for humans.
As the field of aging research grows, several aging “clocks” have been proposed as ways to measure biological age. These clocks use blood markers, DNA patterns, and physical activity measures to estimate the risk of age-related disease more accurately than chronological age. In younger populations, chronological age and biological age are more closely related, but as populations age, the variation of biological age increases. By modeling the rate of these aging dynamics, calculating a theoretical maximum human lifespan is possible.
The authors collected data from over 500,000 participants of the National Health and Nutrition Examination Survey (NHANES), a long-term study of people living in the United States (US), and the United Kingdom (UK) Biobank, a long-term study of people living in the UK. They based their assessments on participants' complete blood count, which measures the number and type of white blood cells, red blood cells, and platelets and the concentration of hemoglobin. They also retrieved physical activity data measured using a wrist-worn activity tracker from more than 5,000 NHANES participants.
The authors created a statistical model and trained it to predict the risk of disease and death using blood marker data and disease and death rates from the US and UK databases. The model produced a single risk value called the Dynamic Organism State Indicator, which could be used to accurately predict the onset of numerous age-related diseases. The model predicted a loss of resilience and a maximum life span between ages 120 and 150 years. The authors used activity tracker data to create a second model of maximum lifespan, which predicted a maximum age between 110 and 170 years.
The authors concluded that human life does have a maximum length due to loss of resilience that cannot be extended by any known interventions. However, they suggested their research may be a step toward the development of life-extending therapies.
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Long-lived adults have highly efficient DNA repair mechanisms. www.eurekalert.org
Semi-supercentenarians and supercentenarians – people who live to the age of 105 years and beyond – personify healthy aging, having avoided the diseases and concomitant disabilities that many adults experience, such as cardiovascular disease, diabetes, cancer, and cognitive decline. Genetics play key roles in longevity and healthy aging. Findings from a recent study indicate that semi-supercentenarians and supercentenarians have unique genetic profiles characterized by highly efficient DNA repair mechanisms.
DNA repair is a cellular defense mechanism that helps maintain genomic integrity. Research had identified five DNA repair pathways, which are active throughout the varied stages of the cell cycle. Failure of these pathways contributes to genomic instability, a hallmark of many chronic diseases.
The study involved 81 semi-supercentenarians (105 years or older) and supercentenarians (110 years or older) who were matched with 36 healthy adults (average age, 68 years) living in the same regions of Italy. Using blood samples collected from the participants, the investigators conducted whole-genome sequencing to identify genetic differences between the two groups and to create a risk score for cardiovascular disease, the leading cause of death worldwide. They compared their findings with those of a similar recent study.
The authors of the study identified five genetic variants among the participants, some of which are involved in DNA repair, mitochondrial function, and elimination of reactive oxygen species – a driver of inflammation. The participants also had fewer naturally occurring mutations, potentially conferring a protective effect against many chronic diseases. They replicated their findings in the other study.
These data suggest that people who live longer, healthier lives share similar genetic profiles that provide protection against many chronic diseases and promote healthy aging. Learn more about healthy aging in this episode featuring aging expert Dr. Judith Campisi.
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Omega-3 supplementation reduces inflammation and cellular aging in response to social stress. www.nature.com
Omega-3 fatty acid consumption reduces the risk of death from cardiovascular disease and all causes. By reducing inflammation, lengthening telomeres, and blunting the body’s response to stress, omega-3 fatty acids lessen the effects of aging on a cellular level. Authors of a recent study tested the effects of omega-3 supplementation on inflammation and telomere length in response to stress.
Telomeres are often compared to the plastic tips on the end of shoelaces (aiglets) because telomeres protect chromosomes from fraying on the ends. Both acute and chronic stress increase inflammation, which can cause chromosomes to become frayed when telomeres are short. Once chromosomes lose their telomeres, their DNA cannot be replicated, and this accelerates aging.
The randomized, controlled intervention trial included 138 sedentary, adults with overweight between the ages of 40 and 85 years. The participants received daily supplements providing 2.5 grams of omega-3s, 1.25 grams of omega-3s, or a placebo for four months. Before and after the intervention, the participants took the Trier Social Stress Test, a testing platform in which a person must deliver a speech and perform mental arithmetic in front of an audience. Participants also provided blood and saliva samples as a means to measure cortisol (a stress hormone), telomerase (an enzyme that helps maintain telomere length); anti-inflammatory cytokines, including interleukin (IL)-10 (IL-10); and pro-inflammatory cytokines, including IL-6, IL-12, and tumor necrosis factor-alpha (TNF-alpha).
Following the stress test, participants in the placebo group experienced a 24 percent reduction in telomerase activity and a 26 reduction in IL-10; however, both omega-3 groups were protected from this response. This relationship was statistically significant and accounted for baseline stress reactivity, age, waist circumference, and sex. Participants who received 2.5 grams of omega-3s had a 19 percent reduction in cortisol levels and a 33 percent reduction in IL-6 compared to the placebo group.
The authors concluded that by reducing inflammation and stress hormone levels, omega-3 supplementation may boost cellular repair and slow aging. This decrease in stress response may also translate to reduced risk of depression, making these findings relevant to mental health as well.
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Supplemental glycine and cysteine restore glutathione levels and correct several markers of aging. www.sciencedaily.com
Glutathione is an antioxidant compound produced by the body’s cells. It helps prevent damage from oxidative stress caused by the production of reactive oxygen species, a key contributor to the aging process. Glutathione levels decrease with aging. Findings from a new study suggest that supplemental glycine and cysteine restore glutathione levels and correct several markers of aging.
Glycine and cysteine (commonly provided as N-acetylcysteine, or NAC) are amino acids. They play critical roles in the body’s synthesis of glutathione. Glycine and cysteine levels are typically lower in older adults and people with metabolic disease.
The authors of the study conducted a 36-week trial of glycine and cysteine (GlyNAC) supplementation in 16 healthy old (average age, 74 years) and young adults (average age, 24 years). The authors drew blood from the participants and assessed their metabolic, physical, and cognitive health at baseline and at 12, 24, and 36 weeks after the start of the intervention. Assessments included measures of mitochondrial fuel oxidation, oxidative stress, inflammation, glucose metabolism, body composition, and strength tests, among others. The old adults took a GlyNAC supplement (dose varied according to the participants' bodyweight) every day for 24 weeks; the young adults did not take a GlyNAC supplement.
Twenty-four weeks of supplemental GlyNAC restored red blood cell levels of glutathione, reduced oxidative stress, and improved mitochondrial function. Markers of inflammation, endothelial dysfunction, glucose metabolism, and genomic damage decreased. Measures of cognition, strength, and body composition improved. Discontinuation of supplemental GlyNAC negated these improvements.
These findings suggest that supplemental GlyNAC provides a viable means to improve several measures of metabolic, physical, and cognitive health in older adults. This was a very small study, however, and lacked a blinded placebo group. Further study is warranted.
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Body mass index (BMI) is a measure of body size that is calculated by dividing a person’s weight by their height. A wealth of research has demonstrated that having a body mass index outside of the normal range (18.5 to 25) increases the risk of death. However, body mass index does not differentiate fat and muscle mass. Authors of a new report investigated the effects of body composition on risk of death.
Extra body fat has been shown to increase the risk of developing a number of chronic lifestyle diseases, while increased muscle (fat-free) mass has been shown to decrease disease risk. Previous research has demonstrated mixed results for the effect of body composition and risk of death, likely due to differences in study design.
The authors combined data from seven studies with over 16,000 participants between the ages of 20 and 93 years collected between 1994 and 2008. Researchers measured body composition using bioelectrical impedance and adjusted for age and sex. They also interviewed participants about their health, lifestyle, and socioeconomic factors and tracked them for an average of 14 years.
After adjusting for a number of demographic and lifestyle factors, the researchers found that having body fat below or above the normal range increased risk of death among the participants. Those with high body fat (37 kilograms) had a 56 percent greater risk of death, while those with highest fat-free mass had a 30 percent lower risk of death.
The authors concluded that fat mass and fat-free mass have opposite effects on the risk of death. They noted that their study included a large number of participants and a long follow-up period, which strengthened the quality of their results.
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Decreased brain derived neurotrophic factor, physical activity, and brain volume are associated with greater memory impairment. www.nature.com
Brain derived neurotrophic factor (BDNF) is a growth factor associated with decreased risk of dementia and improved cognitive function in humans. While BDNF promotes brain cell growth plasticity, its precursor form, called proBDNF, has the opposite effect, promoting cell death. The authors of a recent report investigated the relationship between blood levels of pro-BDNF and memory loss.
The effects of Alzheimer’s disease on the brain can be observed 10 to15 years before the onset of dementia, which presents the opportunity for early detection. Even though BDNF is known to cross the blood-brain barrier, whether blood levels of BDNF are reflective of BDNF activity in the brain is unclear. Establishing blood biomarkers of dementia risk provides the ability for early intervention.
The authors recruited 256 older adults (average age, 68 years) without dementia. They analyzed magnetic resonance imaging (MRI) scans of the participants’ brains and measured blood levels of BDNF and proBDNF. Participants completed questionnaires to measure memory and physical activity habits.
The investigators reported that increased age and decreased physical activity were associated with poorer memory performance. MRI findings showed decreased volume in the hippocampus, the region of the brain associated with memory, in those with worse memory scores. Finally, the authors reported that decreased blood levels of BDNF, but not pro-BDNF, were associated with worse memory performance.
These results echo earlier findings that exercise is associated with greater BDNF activity and better memory performance. The authors conclude the measuring blood levels of BDNF may be an effective strategy for early detection of dementia.
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Omega-3 fatty acids may reduce muscle loss in older adults. www.ncbi.nlm.nih.gov
Sarcopenia is an age-related progressive condition characterized by the loss of skeletal muscle mass and strength. It is one of the leading causes of functional decline and loss of independence in older adults. Contributing factors for sarcopenia include poor nutrition, low physical activity, and inflammation, among others. Findings from a recent meta-analysis suggest that omega-3 fatty acids are beneficial in preventing or treating sarcopenia.
Omega-3 fatty acids participate in a wide range of physiological processes and are essential for human health. Some evidence demonstrates that omega-3 fatty acids play roles in muscle mass synthesis and function. Omega-3 fatty acids include alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). ALA is found mainly in plant oils such as flaxseed, soybean, and canola oils. DHA and EPA are found in fish and other seafood. The human body can convert some ALA into EPA and then to DHA, but the process is very inefficient.
The authors analyzed data from 10 randomized controlled intervention trials investigating the effects of increased omega-3 fatty acid intake on skeletal muscle mass, muscle strength, or muscle performance. More than 550 adults aged 60 years and older were included in the studies, the duration of which spanned 10 to 24 weeks. Outcomes included changes in muscle mass, muscle strength, or physical performance, assessed by walking time or the Timed Up & Go Test (TUG).
The trials provided omega-3 fatty acids from a variety of sources, including fish oil, flax oil, and healthy dietary patterns that adhered to a low omega-6 to omega-3 ratio. Doses ranged from 0.16 to 2.6 gram per day of EPA and from 0 to 1.8 grams per day of DHA. One study provided 14.0 gram per day of ALA. The participants saw increases in muscle mass of about 0.33 kilograms (~11 ounces), and their TUG test times decreased by 30 seconds. Participants who consumed more than 2 grams of omega-3s per day saw greater improvements, with increases in muscle mass of 0.67 kilograms (~1.8 pounds). Among those enrolled in interventions lasting six months or longer, walking times improved by nearly 2 meters per second.
These findings suggest that nutritional interventions that include dietary and/or supplemental omega-3 fatty acids improve muscle mass and physical performance in older adults. The relatively small number of trials and the varying doses, duration, and study designs limit the application of the findings, however.
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Gene therapy slows aging in mice. www.reuters.com
Cellular senescence is the condition or process of cellular deterioration that occurs with age. Senescent cells often release inflammatory proteins that can damage neighboring healthy cells. Understanding the genetic and epigenetic bases of cellular senescence is instrumental in developing interventions to slow aging. A recent report identifies a gene therapy strategy to slow aging in mice.
Gene therapy is a technique in which altered (mutated) genes are corrected as a means to prevent or treat disease. One type of gene therapy involves inactivating a mutated gene that is functioning improperly.
The study investigators conducted a genome-wide screen of mesenchymal precursor cells (a descendant of embryonic stem cells) that carried genes for Werner syndrome and Hutchinson-Gilford progeria syndrome – conditions characterized by rapid, accelerated aging. They found that the primary driver of the accelerated aging in both syndromes was KAT7, an enzyme involved in histone modification.
Then the investigators inactivated the KAT7 gene in normally aging mice and prematurely aging mice and found that inactivation of the gene extended the animals' lifespan. They did not observe any toxicities or adverse events in the animals.
These findings suggest that inactivation of critical genes involved in aging syndromes extends lifespan in mice and shows promise as a strategy to slow aging in humans.
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Dietary patterns that include cheese and wine may promote cognitive health. www.research.iastate.edu
Fluid intelligence – the ability to creatively solve problems without prior knowledge or learning – declines with age. Greater losses of fluid intelligence are associated with increased risk of Alzheimer’s disease. Findings from a recent study suggest that dietary factors protect against fluid intelligence losses.
Nutrition plays critical roles in maintaining cognitive health. Evidence indicates that adherence to dietary patterns that include fruits, vegetables, nuts, and olive oil reduces the risk of developing Alzheimer’s disease. People who carry gene variants that increase their risk of Alzheimer’s disease may benefit from consuming foods that are rich in DHA, a type of omega-3 fatty acid.
The study involved nearly 1,800 people between the ages of 46 and 77 years who were enrolled in the UK Biobank Prospective Study. The participants completed three fluid intelligence tests over a period of several years to assess their ability to creatively solve problems without prior knowledge or learning. They also completed food frequency questionnaires regarding their dietary intake.
The authors of the study found that daily cheese consumption provided the most protection against age-related fluid intelligence losses. They also found that alcohol consumption, especially red wine, provided protection. Eating lamb was associated with better cognitive performance but eating other types of red meat was not. In general, eating too much salt promoted cognitive decline, especially among high-risk groups.
These findings suggest that dietary modifications can promote cognitive health in aging. One mechanism that may drive these benefits is autophagy, a cellular recycling program that is crucial in maintaining neuronal health. Caloric restriction mimetics, such as spermidine (present in aged cheese) and resveratrol (present in red wine), “trick” cells into inducing autophagy even in the setting of sufficient nutrient levels. Watch Dr. Guido Kroemer describe the autophagy-inducing effects of calorie restriction mimetics such as spermidine and resveratrol.
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Experimental drug protocol demonstrates reversal of epigenetic aging. www.ncbi.nlm.nih.gov
The human immune system loses function with age in a process known as immunosenescence. Previous research has reported on the ability of a number of drugs to impact the aging process; however, these studies have not measured the ability to reverse epigenetic aging. Research from epigenetics expert Steve Horvath is the first to demonstrate the reversal of epigenetic aging and immunosenescence of the thymus with drug therapy.
The thymus is an immune organ necessary for the development of T cell populations. After the age of approximately 63, a process called thymic involution severely impairs T cell function and is linked to increases in cancer, infection, autoimmune conditions, chronic inflammation, and heart disease.
Nine participants between the ages of 51 and 65 years were given a drug protocol that included recombinant human growth hormone to reverse signs of immunosenescence. Because growth hormone can increase insulin production to a harmful degree, the authors used metformin, a common diabetes drug, and dehydroepiandrosterone, a steroid precursor, to control symptoms of diabetes. The investigators collected white blood cells to measure immune characteristics and epigenetic age.
Following one year of treatment, the authors reported an average decrease in epigenetic age of 1.5 years over baseline, meaning they reversed epigenetic age by 2.5 years over the course of the study. Participants demonstrated an increase in t cell production and an increase in the leukocyte/monocyte ratio, a measure of immune cell populations that is associated with less inflammation and lower rates of several cancers. Monocytes use a lot of nicotinamide adenine dinucleotide (NAD+), which is an important energy source for cells. The authors suggested this decrease in monocytes and subsequent increase in NAD+ may be responsible for the reversal of epigenetic aging.
The main purpose of this pilot trial was to determine the safety and efficacy of the study treatment. Larger studies with a control group are needed to expand on these results.
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Losing weight between early adulthood and midlife can reduce the chance of premature death. www.sciencedaily.com
Obesity is a global health problem that impacts a person’s quality of life and lifespan. Findings from a recent study suggest that losing weight between early adulthood and midlife influences the risk of death from all causes.
To estimate the weight status of people in the US, researchers often turn to the National Health and Nutrition Examination Survey, or NHANES — a large, continuously updated dataset that represents the health of the US population.
Previous research has demonstrated that weight gain between early adulthood and midlife has negative consequences for longevity. The current study investigated whether weight loss during this time of life would affect the risk of death from all causes.
The authors of the study examined NHANES data encompassing more than 24,000 people aged 40 to 74 years. They weighed participants at baseline, and each person recalled how much they weighed at age 25 years (early adulthood) and 10 years before the start of the study. The authors studied the relationship between the participants' body mass index (BMI, a proxy for body fatness) at various time points and their probability of dying during the study period.
They determined that carrying extra weight during early adulthood and midlife, as measured by a BMI above the normal range, accounted for more than 12 percent of premature deaths in the US. Furthermore, they estimated that if obese participants lost weight during the period between early adulthood and midlife — such that their BMI fell into the overweight category — more than 3 percent of early deaths could have been avoided.
These findings suggest that maintaining a normal weight during the period from early adulthood to midlife reduces the risk of mortality from all causes. Moreover, these findings indicate that even modest weight loss during this time of life reduces the risk of mortality from all causes.
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Preclinical evidence suggests BDNF may be a potent interventional tool in Alzheimer's and brain aging by directly improving learning and memory www.sciencedaily.com
From the article:
For these experiments, the researchers injected the BDNF gene or protein in a series of cell culture and animal models, including transgenic mouse models of Alzheimer’s disease; aged rats; rats with induced damage to the entorhinal cortex; aged rhesus monkeys, and monkeys with entorhinal cortex damage.
In each case, when compared with control groups not treated with BDNF, the treated animals demonstrated significant improvement in the performance of a variety of learning and memory tests. Notably, the brains of the treated animals also exhibited restored BDNF gene expression, enhanced cell size, improved cell signaling, and activation of function in neurons that would otherwise have degenerated, compared to untreated animals. These benefits extended to the degenerating hippocampus where short-term memory is processed, one of the first regions of the brain to suffer damage in Alzheimer’s disease.
[…]
“In this series of studies, we have shown that BDNF targets the cortical cells themselves, preventing their death, stimulating their function, and improving learning and memory. Thus, BDNF treatment can potentially provide long-lasting protection by slowing, or even stopping disease progression in the cortical regions that receive treatment.”
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BDNF from aerobic exercise may reduce loss of photoreceptor cells in macular degeneration: exercise reduced cell death by 50% in animal model www.sciencedaily.com
From the article:
In the current study, the scientists trained mice to run on a treadmill for one hour per day, five days per week, for two weeks. After the animals were exposed to toxic bright light – a commonly used model of retinal degeneration – they exercised for two more weeks. The exercised animals lost only half the number of photoreceptor cells as animals that spent the equivalent amount of time on a stationary treadmill.
Additionally, the retinal cells of exercised mice were more responsive to light and had higher levels of a growth- and health-promoting protein called brain-derived neurotrophic factor (BDNF), which previous studies have linked to the beneficial effects of exercise. When the scientists blocked the receptors for BDNF in the exercised mice, they discovered that retinal function in the exercised mice was as poor as in the inactive mice, effectively eliminating the protective effects of the aerobic exercise.
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Faster rates of mutation speed aging and impair fertility. www.eurekalert.org
Researchers in the field of aging have posited several theories to explain how and why the body ages. One of these theories, the somatic mutation theory of aging, is based on the idea that DNA damage accumulates over time – the result of day-to-day living and oxidative stress. A variety of mechanisms within cells can repair DNA damage and prevent potentially harmful mutations. These repair mechanisms become less efficient as the body ages, however, promoting age-related disease and decline. A new study suggests that loss of the body’s capacity to repair itself starts during adolescence and could influence fertility among women.
The authors of the study assessed germline mutation rates based on blood samples from 41 three-generation families enrolled in a large, multigenerational study in the United States. Germline mutation rates are typically higher among men can vary considerably among people of the same sex.
The analysis revealed that a faster age-adjusted mutation rate increased all-cause mortality rates in both sexes. The rate of DNA mutations increased considerably during adolescence, but later onset of menstruation appeared to slow the rate. In addition, the mutation rate varied, with some participants acquiring mutations at a rate three-fold faster than others. People with slower mutation rates were more likely to have been born to younger parents.
The authors predicted that a faster mutation rate shortened a person’s life as much as five years – roughly equivalent to the effects of smoking or a sedentary lifestyle. The mutation rate also appeared to influence fertility among women, with a faster rate associated with fewer live births and older age at the time of their last child.
These findings suggest that germline mutation rates serve as markers of reproductive and systemic aging and interventions geared toward reducing mutation rates to those found before puberty could have beneficial effects in terms of reducing the incidence of disease and death.
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Aging is the progressive accumulation of damage that occurs to an organism over time, eventually leading to disease and death. Findings from a new study suggest that diluting the blood of old mice can reverse some of the deleterious effects of aging.
Previous studies have shown that therapeutic plasma exchange via heterochronic parabiosis, a procedure in which two organisms of different ages are joined so that they share a common blood supply, elicits improvements in the older organism and declines in the younger, suggesting that young blood rejuvenates whereas old blood deteriorates. Similar effects have been observed in studies in which blood between old and young organisms was transfused, without the need for joining the two.
The authors of the new study capitalized on these findings. Over a period of 30 minutes, they gradually replaced half of the platelet-rich plasma in old and young mice with a saline and albumin solution, effectively diluting the plasma and compensating for any albumin losses. Six days later, they assessed the effects of the dilution on aspects of muscle, brain, and liver health.
Diluting the blood of old mice enhanced muscle repair, increased neurogenesis in the hippocampus, and decreased fat stores and fibrosis in the liver – recapitulating the effects of heterochronic blood exchange. The overall composition of the blood proteins shifted toward a more favorable one that coordinated tissue maintenance and improved immune responses. The procedure had no effects on the young mice.
The authors of the study suggested that there are proteins in old blood that are responsible for accelerating aging. Diluting plasma altered cell signaling pathways, subsequently influencing the expression of genes involved in aspects of physiological functioning. They further suggested that this type of procedure could be used to promote health and longevity in humans.
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Exercise improves blood flow to the brain and cognitive function in older adults. www.sciencedaily.com
Poor blood flow to the brain, a common feature of aging, is associated with an increased risk of stroke and cognitive dysfunction. A recent study demonstrated that exercise improves brain blood flow and improves cognitive function in older adults.
The intervention study involved 206 healthy, cognitively intact middle-aged and older adults (average age, 66 years) with low physical activity levels. The participants engaged in a supervised aerobic exercise program three days per week, gradually increasing from 20 to 40 minutes over a period of six months. They also completed an unsupervised exercise session one day per week during the six-month period. The authors of the study assessed the participants' cognitive performance, cerebrovascular function, and overall fitness on three separate occasions over a period of 12 months.
After completing the six months of exercise, the authors of the study noted that the study participants improved by nearly 6 percent on measures of working memory, flexible thinking, and self-control. They improved by nearly 2.5 percent on tests of verbal fluency, comparable to abilities seen in person five years younger. Blood flow to the brain increased by nearly 3 percent, suggesting that cerebrovascular function is a critical aspect of maintaining or improving memory and verbal skills.
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Omega-3 fatty acids decrease oxidative stress and affect biomarkers of aging. www.sciencedaily.com
As the human body ages several changes occur, including the gradual erosion of the protective caps on the ends of chromosomes, known as telomeres. A 2012 study suggests that supplementing with omega-3 fatty acids can counteract telomere shortening and slow aging.
Telomeres function as a protective buffer against DNA loss during replication and DNA damage caused by inflammation, reactive oxygen species, and other chemical compounds. Telomeres get shorter with age and telomere length is a biological marker for age.
Previous research has demonstrated that many factors can affect the rate of telomere shortening. The dietary balance of the essential polyunsaturated fatty acids (PUFAs) omega-3 and omega-6 — which influence inflammation — might be a factor. The current study investigated whether blood levels of these polyunsaturated fatty acids affect telomere stability.
The double-blind randomized controlled trial involved 106 adults between the ages of 40 and 85 years who were sedentary and overweight. The authors of the study provided participants with a supplement containing 1.25 grams or 2.5 grams of omega-3 fatty acids or a placebo. To evaluate the influence of the omega-3 fatty acids versus placebo, the authors measured telomere length, telomerase activity, and markers of oxidative stress (known as F2-isoprostanes). They found that supplementation at both doses lowered the omega-6 to omega-3 fatty acid ratio in the blood, which was associated with longer telomere length. They also observed that omega-3 fatty acid supplementation decreased markers of oxidative stress by 15 percent.
These findings suggest that consumption of omega-3 fatty acids in quantities high enough to lower the omega-6 to omega-3 ratio in the blood can slow aging.
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Vitamin C supplementation restores lifespan in mice with Werner's syndrome (an advanced aging phenotype) www.sciencedaily.com
From the article:
Scientists treated both normal mice and mice with a mutation in the gene responsible for Werner’s syndrome (WRN gene) with vitamin C in drinking water. Before treatment, the mice with a mutated WRN gene were fat, diabetic, and developing heart disease and cancer. After treatment, the mutant mice were as healthy as the normal mice and lived a normal lifespan. Vitamin C also improved how the mice stored and burned fat, decreased tissue inflammation and decreased oxidative stress in the WRN mice.
From actual publication, rather than press release:
Daily ascorbate supplementation allowed [Werner mice] to recover a normal mean life span and healthy aging. Although the number of animals used in each cohort was not big enough for a statistical testing on maximum life span, ascorbate treatment did prevent the appearance of Werner syndrome characteristic redox imbalance and related genomic damage. It also prevented the liver proinflammatory status observed in [Werner mice].
What’s someone unexpected about the fact that additional vitamin C restoring mean lifespan is the fact that Werner syndrome is associated with higher-than-usual ascorbate status rather than reduced, so supplementing with vitamin C being beneficial may be somewhat counter to expectation:
Interestingly, blood ascorbate levels increased with phenotypic progression in [Werner mice]. Ascorbate being protective, it is possible that the retention of vitamin C is a defense mechanism to counterbalance the age‐dependent rise in oxidative stress. We cannot rule out, however, the possibility that the increased ascorbate levels observed in [Werner mice] are due to a modification in ascorbate metabolism only specific to these mice.
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Healthy lifestyle reduces risk of disease and death. www.eurekalert.org
Cardiovascular disease is a broad class of diseases that involve the heart or blood vessels, including stroke, hypertension, thrombosis, heart failure, and atherosclerosis. As much as 90 percent of cardiovascular disease may be attributable to lifestyle factors and, therefore, preventable. A recent study found that having better cardiovascular health during one’s midlife years may reduce risk of premature death later in life.
The American Heart Association has developed a scoring system that describes a person’s cardiovascular health based on measures of various lifestyle behaviors, such as smoking, diet, and physical activity, and known cardiovascular disease risk factors, such as blood pressure, body mass index, and blood glucose and cholesterol levels. Having a higher cardiovascular health score is associated with reduced markers of disease, longer telomeres, and better vascular function and, consequently, lower risk of cardiovascular disease, diabetes, and premature death.
The prospective cohort study, which spanned a 16-year period, drew on data from the Framingham Heart Study Offspring investigation and involved 1,445 men and women whose average age was 60 years. The authors of the study found that for every five-year period that a person had intermediate or ideal cardiovascular health, they had a 33 percent lower risk for high blood pressure, 27 percent lower risk for diabetes or cardiovascular disease, 25 percent lower risk for diabetes, and 14 percent lower risk for premature death, compared to people who were in poor cardiovascular health. These findings held true regardless of age or sex.
Sauna use is a lifestyle behavior that has been shown to improve cardiovascular health. A large study of health outcomes in more than 2,300 middle-aged men from eastern Finland identified strong, dose-dependent links between sauna use and reduced cardiovascular-related death and disease. Compared to men who used the sauna once weekly, men who used the sauna four to seven times per week were 50 percent less likely to die from cardiovascular-related causes. Watch this clip in which Drs. Rhonda Patrick and Jari Laukkanen discuss these findings.
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Mental stress and lifestyle can predict lifespan. www.eurekalert.org
The average life expectancy of people living in the United States is roughly 79 years. Several factors influence how long a person lives, however, such as diet, physical activity, and smoking. A new study suggests that mental stress shortens life expectancy by nearly three years.
Mental stress can affect the immune, digestive, cardiovascular, sleep, and reproductive systems, eliciting a wide range of symptoms, including headaches, sleeplessness, sadness, anger, or irritability. Prolonged stress can promote continued strain on the body, contributing to serious health problems, such as heart disease, high blood pressure, diabetes, and other illnesses, including mental disorders such as depression or anxiety.
The study was based on data drawn from cross-sectional health surveys conducted every five years in Finland, spanning a 20-year period between 1987 and 2007 and including approximately 35,000 adults. The study participants were generally healthy and were between the ages of 25 and 74 years. The authors of the study conducted a statistical analysis of death rates using a model that included risk factors commonly associated with longevity, such as socioeconomic background, medical history, lifestyle, lifestyle satisfaction, and biological risk factors.
They found that some factors decreased the risk of premature death such as eating fruits and berries daily or almost daily (15 percent lower), having a higher level of education (10 percent lower), or frequent engagement in leisure-time physical activity (25 percent lower). Factors that increased risk included smoking (67 percent higher) or having diabetes (100 percent higher), both of which correlated to nearly seven years' shorter lifespan. Having high levels of stress decreased lifespan among men by nearly three years.
To learn more about the harmful effects of stress, watch this clip featuring Dr. Elissa Epel in which she describes how stress can modulate telomere length, a marker of aging.
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Brain aging emerges in the late 40's but dietary ketosis increases overall brain activity and stabilizes functional networks. news.stonybrook.edu
Insulin resistance and poor blood glucose control – defining characteristics of type 2 diabetes – drive changes associated with brain aging and cognitive decline. A growing body of evidence suggests that dementia is the manifestation of insulin resistance and altered metabolism in the brain. A recent study suggests that dietary patterns that promote ketosis improve brain metabolism and function.
Ketosis is a metabolic state that results in the body’s production and use of ketones (byproducts of fatty acid metabolism). It occurs under conditions of fasting, starvation, and low carbohydrate intake. Ketones induce physiological and metabolic responses to promote brain health.
The study had multiple components. First, the authors of the study investigated the time course of human brain aging. Using functional MRI (fMRI) data from more than 900 people between the ages of 18 and 88 years, they determined that neural network stability is a biomarker of brain aging, and the loss of network stability manifests as early as the fifth decade of life (average age, 47 years). They found that the greatest changes in the brain occur around the age of 60 years.
Then they performed fMRI scans on 12 young adults (average age, 28 years) to assess how different energy sources – glucose versus ketones – alter brain function. Each participant underwent three scans under different dietary conditions: a normal diet without fasting, a normal diet with overnight fasting, or a ketogenic diet for one week. They performed fMRI scans on 30 young adults (average age 29 years) 30 minutes after they took an oral bolus of either glucose or ketones or after following their normal diet with overnight fasting. The authors of the study measured the participants' blood glucose and ketone levels before and after each of the scans.
The fMRI scans revealed that ketones increased overall brain activity and stabilized functional networks, but glucose had the opposite effect, regardless of whether the ketones were produced endogenously or supplied from exogenous sources. These findings suggest that dietary interventions that increase ketone production may be useful in mitigating the harmful effects of glucose on the brain.
Certain dietary patterns promote ketosis. For example, the Ketoflex 12/3 diet, a form of time-restrictive eating that limits the period during which a person eats to a 12-hour window at least three hours before bedtime, promotes the production of ketones. Watch this clip in which Dr. Dale Bredesen describes this novel dietary protocol and how it improves cognitive function.
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Adherence to the Mediterranean diet for one year promotes gut bacteria linked to healthy aging in older adults. www.sciencedaily.com
Frailty is a syndrome that commonly manifests in older adults. It carries an increased risk for poor health outcomes including falls, disability, hospitalization, and death. A key driver in the development of frailty is inflammation, which often accompanies diet-induced changes in the gut microbiota. Findings from a recent study suggest that eating a Mediterranean diet, which is rich in fruits, vegetables, legumes, fish, and fiber, and low in saturated fat and red meat, alters the gut microbiome in older adults to reduce the risk of frailty.
The intervention study involved more than 600 older, non-, pre-frail, or frail older adults living throughout Europe. Roughly half of the participants followed a Mediterranean diet for one year, while the other half, which served as the control group, ate their regular diets. Before and after the one-year intervention, the authors of the study profiled the microbial makeup of the participants' gut microbiome. Whereas the microbiome of the participants from the northern European countries shared many similarities, the participants from Italy had a distinct microbiome.
At the end of the study, the participants who adhered to the Mediterranean diet showed reductions in biomarkers associated with inflammation (such as C-reactive protein and interleukin 17) and improvements in frailty-associated measures (such as handgrip strength, gait speed time, and cognitive function). The authors of the study observed notable changes in the participants' gut microbiomes, which were associated with higher numbers of bacteria that produce short-chain fatty acids – byproducts of dietary fiber metabolism that reduce gut inflammation.
These findings suggest that dietary interventions that promote adherence to a Mediterranean diet may be beneficial in reducing the risk of developing frailty among older adults due to changes in gut microbiota and reduced inflammation.
Interestingly, some of the benefits observed among the participants in this study may be related to their increased intake of essential vitamins and minerals. Without these nutrients, the body has to compensate for the shortages – a concept known as “triaging.” Long-term compensation contributes to aging. Watch this clip in which Dr. Bruce Ames explains this phenomenon in what he calls his triage theory.
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The negative effects of obesity mimic the aging process. www.sciencedaily.com
World health experts estimate that nearly 1.9 billion adults and 380 million children are overweight or obese. Having excess body fatness carries many risks, including increased risk for cardiovascular disease, type 2 diabetes, Alzheimer’s disease, and many types of cancer. A recent review suggests that the effects of obesity are similar to those associated with aging.
Obesity, a condition characterized by access body fatness, is commonly defined as being 20 percent above a person’s ideal body weight, which corresponds to having a body mass index greater than 30. Research indicates that obesity roughly doubles a person’s risk of premature death.
Aging, the progressive accumulation of damage that occurs to an organism over time, eventually leads to disease and death. These damages drive genomic dysfunction, compromised immunity, poor metabolic function, and increased risk of chronic diseases such as type 2 diabetes, Alzheimer’s disease, cardiovascular disease, and cancer.
The authors of the review point out that obesity’s association with aging is exemplified by the fact that obesity decreases telomere length in humans by 240 base pairs, which roughly corresponds to 9 years of aging. Telomeres are distinctive structures comprised of short, repetitive sequences of DNA located on the ends of chromosomes. They form a protective “cap” – a sort of disposable buffer that gradually shortens with age. Shortened telomeres promote genomic instability and are associated with shorter lifespan. According to the authors, research indicates that obesity reduces life expectancy by 5.8 years in men and 7.1 years in women after the age of 40.
The authors went on to posit that the similarities between obesity and aging are driven by shared molecular- and cellular-level mechanisms, including increased levels of reactive oxygen species, mitochondrial dysfunction, cellular senescence, increased apoptosis, impaired autophagy, and increased inflammation. These mechanisms work together in a synergistic fashion to promote the early onset of many age-related conditions. Finally, the authors suggested that viewing obesity as a disease of aging is critical to understanding the condition and identifying better ways to prevent or treat it.
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Dietary olive oil may improve healthspan and delay aging by switching on the activity of sirtuins. www.sciencedaily.com
Olive oil, the principal fat consumed in the Mediterranean diet, is widely consumed for its flavor, versatility, and health-promoting attributes. A recent study demonstrates that the monounsaturated fats (MUFAs) in olive oil may extend lifespan by switching on the activity of key cellular proteins called sirtuins.
Monounsaturated fats are dietary fats found in plant foods, such as nuts, avocados, and vegetable oils, especially olive oil, which contains approximately 75 percent of the MUFA known as oleic acid. The body stores MUFAs in lipid droplets – intracellular fat storage depots that facilitate the movement and signaling activities of fatty acids. During times of increased energy demand (such as during exercise) or decreased energy supply (such as during fasting), the fatty acids stored in lipid droplets can be released for the body’s use.
Sirtuins are highly conserved enzymes that play key roles in healthspan and longevity in multiple organisms. Sirtuin 1 (SIRT1) is linked to the regulation of a variety of metabolic processes, including the release of insulin, mobilization of lipids, response to stress, and modulation of lifespan.
The authors of the study first investigated the role of perilipin 5 (PLIN5), a protein found in lipid droplets that regulates fatty acid oxidation in oxidative tissues. They found that PLIN5 binds to lipid droplet MUFAs and delivers them to the cell nucleus, where they modulate the activity of SIRT1.
Then they studied the effects of MUFA consumption in mice. They fed the mice a control diet rich in lard and soybean oil or a diet rich in olive oil for 12 weeks. The mice that ate the olive oil-rich diet lost weight and had higher energy expenditure than mice fed the control diet. These effects were attributed to activation of SIRT1.
These findings suggest that the health-promoting benefits associated with the Mediterranean diet may be attributable to the diet’s high olive oil content. In addition, olive oil as part of a healthy eating pattern such as the Mediterranean diet may increase healthspan and longevity.
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Alcohol and cigarettes may accelerate brain aging. www.inverse.com
How well (and how quickly) we age depends on a confluence of genetic, environmental, and lifestyle factors. Some lifestyle behaviors, such as alcohol consumption and cigarette smoking, elicit harmful effects on multiple body systems that can accumulate over time to modulate aging. A new study demonstrates that alcohol consumption and cigarette smoking accelerate brain aging, in particular.
Research indicates that smoking cigarettes alters multiple structural aspects of the brain. For example, smokers tend to have less gray matter density and volume in the frontal, occipital, and temporal lobes – areas related to a wide range of brain function. Similarly, heavy alcohol use is associated with reduced gray and white matter volumes in the medial-prefrontal and orbitofrontal cortices.
The authors of the study assessed relative brain age, a comparative measure of brain aging between people of the same chronological age, to determine if a person’s brain is aging at a different rate relative to their peers. The study was based on analysis of brain-imaging data collected from more than 17,000 UK Biobank participants who were of European ancestry and were cognitively normal. After determining the participants' relative brain age, they studied the association of relative brain age with cigarette smoking, alcohol consumption, and genetic variants.
They found that regular (daily or nearly daily) cigarette smoking or alcohol consumption increased relative brain aging. Every gram of alcohol (~20 grams in 1 fluid ounce) consumed per day was linked to one week of accelerated brain aging and each year spent smoking one pack of cigarettes per day was linked to 11 days of accelerated brain aging.
These increases in brain aging were associated with poor cognitive function and declines in fluid intelligence, the ability to creatively solve problems without prior knowledge or learning. They also identified two single nucleotide polymorphisms associated with accelerated brain aging.
While it is important to note that the effect of alcohol on brain aging was only seen in daily or almost daily drinkers, these findings provide useful insights into how cigarette smoking and alcohol consumption influence brain aging and highlight the need for future research to fully elucidate the factors associated with how the brain ages.
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Stress has far-reaching effects on the human body, including increased risk of chronic disease and other conditions associated with aging. Anecdotal reports suggest that stress can contribute to the premature graying of hair. Findings from a recent study in mice suggest that acute stress depletes melanocyte stem cell populations to promote the graying of hair.
Melanocyte stem cells are undifferentiated cells found in the region of hair associated with growth. They give rise to melanocytes, the mature, melanin-forming cells that provide color to growing hair.
Both mental and physical stress activate the body’s sympathetic nervous system, one of the two main divisions of the autonomic nervous system (the other being the parasympathetic nervous system). The sympathetic nervous system’s primary purpose is to stimulate the body’s fight-or-flight response to stress. A critical element in this response is noradrenaline, a type of hormone and neurotransmitter that plays a role in vigilance and conditioned fear.
The authors of the study induced acute stress in mice and noted that the mice exhibited increased numbers of gray hairs. This increased graying was attributed to the activation of sympathetic nerves in the region in which the stem cells reside and subsequent release of noradrenaline, which promoted stem cell proliferation, differentiation, migration, and eventual depletion.
These findings suggest that neuronal activity induced by an acute stressor can drive stem cell loss and illustrate how overall mental and physical health influence stem cell health.
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Decreasing the insulin signaling pathway and the TOR pathway increased lifespan of worms by 500 percent. www.eurekalert.org
The insulin and insulin-like signaling (IIS) pathways and the target of rapamycin (TOR) pathway are critical elements of the aging process. Findings from a new study suggest that decreasing the activity of these highly conserved pathways markedly increases the lifespan of worms.
The IIS pathways are involved in maintaining glucose homeostasis. They facilitate the uptake of glucose into fat and muscle cells while inhibiting gluconeogenesis – the production of glucose in the liver. These pathways are dysregulated in obesity and type 2 diabetes.
The TOR pathway senses amino acid concentrations and regulates cell growth, cell proliferation, cell motility, cell survival, protein synthesis, autophagy, and transcription. It integrates other pathways including insulin, growth factors (such as IGF-1), and amino acids and plays a key role in mammalian metabolism and physiology. The pathway is dysregulated in many human diseases, such as diabetes, obesity, depression, and certain cancers.
The study focused on altering the activity of orthologs of these pathways (called DAF-2 and RSKS-1) in C. elegans, a type of nematode worm, which is often used in aging studies. The authors of the study introduced double mutations in the worms to block the activities of DAF-2 and RSKS-1 and conducted genome-wide translational state analysis to identify genes associated with the worms' lifespan.
Knocking DAF-2 and RSK-1 elicited a synergistic effect that increased the lifespan of the worms by 500 percent, suggesting that regulation of these two pathways is integral to the aging process in worms. Watch this clip for learn more about the evidence that altered growth hormone and insulin signaling may improve healthspan in humans, too.
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Drinking tea at least three times a week is linked with a longer and healthier life. www.eurekalert.org
Tea is one of the most commonly consumed beverages in the world, especially in Asian countries. It is rich in tannins, catechins, and other polyphenolic compounds that elicit beneficial health effects associated with reduced risk of cardiovascular disease, cancer, and type 2 diabetes. A recent study suggests that habitual tea drinkers may live longer than non-habitual drinkers.
The prospective cohort study involved more than 100,000 adults living in China who completed questionnaires about their tea consumption. Those who drank tea three or more times per week were classified as habitual tea drinkers, while those who drank tea fewer than three times per week were classified as non-habitual tea drinkers. Hospital records and death certificates provided data about mortality rates and causes among the participants during a follow-up period of approximately eight years, on average.
The findings revealed that habitual tea drinkers were 22 percent less likely to die heart disease and stroke and were 15 percent less likely to die from all causes of premature death compared to non-habitual drinkers. The habitual tea drinkers were also more likely to live longer (about one year and three months) and cardiovascular disease-free (nearly one and one-half years) than non-habitual drinkers.
These findings underscore the role of diet in improving healthspan and longevity and suggest that minor modifications can markedly influence disease risk.
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Higher cardiorespiratory fitness associated with increases in gray matter volume. newsnetwork.mayoclinic.org
Cardiorespiratory fitness is a measure of the body’s ability to deliver oxygen to skeletal muscles during sustained physical activity. Findings from a new study suggest that higher cardiorespiratory fitness may increase the brain’s gray matter.
Gray matter contains the cell bodies, dendrites, and axon terminals of neurons in the brain. Loss of gray matter is associated with cognitive decline and memory loss – hallmarks of dementia. Physical inactivity promotes gray matter losses and is a major risk factor for dementia.
The new study involved more than 2,100 adults between the ages of 21 and 84 years living in Germany. The authors of the study assessed the participants' cardiorespiratory fitness based on peak oxygen uptake during exercise on a stationary bike. They also measured the participants' gray matter and total brain volume using magnetic resonance imaging (MRI).
The MRI analysis revealed that for a single standard deviation increase in peak oxygen uptake, gray matter volume increased by more than 5 cubic centimeters in regions associated with emotion, memory encoding, learning, and decision making. These findings suggest that physical activity that promotes cardiorespiratory fitness might be a means to prevent dementia associated with gray matter losses.
Sauna bathing is an exercise mimetic and promotes many of the cardiovascular benefits associated with exercise. Dr. Rhonda Patrick describes some of these effects in this podcast.
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Cognitive-behavioral therapy reduces symptoms of social anxiety disorder and improves biomarkers of aging. www.nature.com
Telomeres are distinctive structures comprised of short, repetitive sequences of DNA located on the ends of chromosomes that prevent chromosomes from losing genes or sticking to other chromosomes during cell division. Telomere attrition, a biomarker of aging, is commonly associated with mental health conditions such as social anxiety disorder. Protection against telomere shortening is provided by activation of the enzymes telomerase and glutathione peroxidase. Findings from a new study suggest that cognitive behavior therapy reduces telomere attrition by activating these protective mechanisms.
Social anxiety disorder, also known as social phobia, is a mental health condition characterized by an intense, persistent fear of being judged, negatively evaluated, or rejected by others. Approximately 15 million people living in the United States have been diagnosed with social anxiety.
The study involved 46 people with social anxiety disorder. The participants' plasma levels of telomerase and glutathione peroxidase were measured before and nine weeks after receiving cognitive behavior therapy. The participants' anxiety was assessed via self-report.
Following cognitive behavioral therapy, the participants' social anxiety symptoms decreased significantly. Increases in telomerase and glutathione peroxidase activity were associated with reduced social anxiety, suggesting that cellular protective mechanisms may be involved in mediating anxiety symptoms and adding to a growing body of evidence that stress and anxiety accelerate biological aging.
Lifestyle factors such as exercise and meditation have also been shown to improve symptoms of anxiety and biomarkers of aging. Meditation, in particular, slows biological aging by slowing the shortening of telomeres. Studies by telomere experts Elizabeth Blackburn at UCSF and Elisa Epel show that meditation buffers the stress that shortens telomeres and activates the gene that encodes for telomerase.
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A compound that blocks a key inflammatory pathway in the brain reverses cognitive decline in mice. news.berkeley.edu
Cognitive decline is a common feature of aging, affecting more than 16 million people living in the United States. Findings from a new study in mice suggest that reducing inflammation in the brain may slow or reverse cognitive decline.
Chronic inflammation is a key element of the aging process and drives many age-related diseases and conditions. The blood-brain barrier (BBB) is critical to healthy brain function, but chronic, systemic inflammation may cause changes in the BBB, allowing toxic blood-borne molecules to enter the brain. For example, rodent models of traumatic brain injury (TBI) demonstrate that loss of BBB function following TBI allows albumin, a type of protein, to enter the brain. This, in turn, activates the transforming growth factor-beta (TGF-ß) signaling pathway, which drives a pro-inflammatory environment and compromises cognitive function. Roughly two-thirds of all adults over the age of 70 years have some degree of BBB dysfunction.
The authors of this study measured serum albumin in mice and found that it was detectable in the brains of mice as early as 12 months of age (which corresponds roughly to “middle age”), suggesting that BBB dysfunction occurred much earlier than commonly believed. Then they gave the mice a drug that inhibited the action of the TGF-ß receptor, impairing TGF-ß signaling and reversing the accompanying cognitive dysfunction.
These findings suggest that reducing inflammation in the brain could serve as a means to restore cognitive function in older adults.
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A group of proteins identified in human plasma predicts both chronological and biological age. www.sciencedaily.com
Aging is the primary risk factor for many chronic diseases in humans, including cancer, Alzheimer’s disease, and cardiovascular disease. Individuals age at different rates, however, a phenomenon observed across sexes, ethnic groups, and races. A recent study has identified a group of proteins in human plasma that predicts both chronological and biological age.
Proteins regulate key cellular pathways. The overall composition of proteins in the body changes with time, reflecting the effects of aging. Blood is the primary vehicle for most of the body’s proteins, and some studies have shown that transfusing the blood of young mice into old mice restores cognitive function to a more youthful phenotype.
The authors of this study analyzed blood samples from more than 4,300 healthy adults between the ages of 18 and 95 years to quantify proteins involved in signaling, metabolism, and other physiological functions. They found that hundreds of proteins – many of which are associated with age-related diseases – changed at specific times in a person’s life, typically at the ages of 34, 60, and 78 years.
The proteins that changed varied by sex, emphasizing the importance of including more women in clinical trials. In addition, the findings highlight the dynamic nature of aging and suggest that blood may be a useful tissue for identifying proteins that alter the aging process as a means to develop disease prevention strategies and more targeted treatments.
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Gut bacteria may alter the aging process of the human brain through the production of butyrate www.sciencedaily.com
The gut microbiota is a complex and dynamic population of microorganisms that is subject to change throughout an individual’s lifespan in response to the aging process. Findings from a new study demonstrate that altering the gut microbial population may alter the aging process of the human brain.
The authors of the study transplanted gut microbiota samples from healthy young or old mice into young germ-free mice. Eight weeks after the transplant, the mice that received microbial samples from the old mice demonstrated increased neurogenesis – the process of forming new neurons – in the hippocampus region of their brains.
Further analysis revealed that these mice also had larger numbers of butyrate-producing microbes in their colons. Butyrate, a short-chain fatty acid, is produced during bacterial fermentation in the human colon and has wide-ranging effects on human physiology. In this study, butyrate was associated with an increase in growth factors and subsequent activation of key longevity signaling pathways in the livers of the recipient mice. When butyrate alone was given to the recipient mice it promoted neurogenesis, as well.
The findings from this study may have relevance for dietary interventions to maintain or improve brain health.
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Mild hearing loss – when hearing is still considered normal – is linked to cognitive decline. www.sciencedaily.com
Approximately two-thirds of all adults over the age of 70 have some degree of hearing loss. Few people seek out treatment, however. A recent study found that even mild hearing loss – when hearing is still considered normal by most people – is linked to cognitive decline.
The participants in the cross-sectional study, which included more than 6,000 men and women who were 50 years or older (average age, 59 years) and living in the United States, were part of the Hispanic Community Health Study and the National Health and Nutrition Examination Study (NHANES). Each of the participants completed a series of tests to gauge neurocognitive function. They also underwent audiometry tests to assess their hearing.
The association between cognitive decline and hearing loss first appears with mild hearing loss and progresses in a dose-dependent manner as hearing worsens. The authors of the study used statistical models to identify associations between hearing loss and cognitive decline. They found that for every 10 dB decrease in hearing, cognitive function decreased as well, especially among those who were in the earliest stage of hearing loss.
Interestingly, a related study found that the risk of developing mild hearing loss was nearly 30 percent lower among people who adhered to healthy dietary patterns such as the DASH diet or the Mediterranean diet, suggesting that diet may play a role in preventing mild hearing loss.
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Supercentenarians have high level of cytotoxic T cells, which can kill cancer cells. www.sciencedaily.com
Supercentenarians – people who live to be 110 years of age or older – have long healthspans, free of disease and the physical and cognitive decline that commonly accompany aging. A critical factor in their long, healthy lives is a robust immune system. Findings from a new study reveal that supercentenarians have high levels of cytotoxic CD4 T-cells, a specialized type of white blood cell.
CD4 T-cells are key elements in the body’s antigen-specific immune response. They destroy virus-infected and malignant cells by triggering apoptosis – a type of cellular self-destruct mechanism that rids the body of damaged or aged cells. CD4 T-cells are considered “helper” cells in that they assist other cells in the immune response.
The authors of the study collected circulating immune cells in the blood of seven supercentenarians and five controls, who were between the ages of 50 and 80 years. They found that the supercentenarians had considerably higher levels of CD4 T-cells than the controls, and these CD4 T-cells had unique cytotoxic capabilities. Furthermore, they found that the cytotoxic cells had arisen via clonal expansion, the process by which daughter cells arise from a single parent cell.
Cytotoxic CD4 T-cells are rare, even among young people, but they play key roles in immunosurveillance and can kill cancer cells. These findings shed light on how supercentenarians maintain good health throughout their lives.
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12 weeks of high-intensity interval training improves memory by 30% in older adults between the ages of 60 and 88. www.sciencedaily.com
Cognitive decline and associated memory loss are common features of aging, affecting approximately 16 million people living in the United States. A recent study found that high-intensity interval training improves memory in older adults.
The study involved 64 sedentary older adults between the ages of 60 and 88 years who were randomized to participate in 12 weeks of high-intensity interval training, moderate continuous training, or stretching (which served as the control group). Each of the participants' memory and executive functions were assessed before the training began.
The participants in the high-intensity group performed four intervals of high-intensity exercise on a treadmill for four minutes, followed by a period of recovery. The participants in the moderate continuous group performed a single set of moderate-intensity aerobic exercise for approximately 50 minutes.
At the end of the study period, participants who engaged in high-intensity exercise performed better on memory tests than those who engaged in moderate continuous training or stretching only. The participants who saw the greatest fitness gains also saw the greatest memory improvements. Both high-intensity interval and moderate continuous exercise improved executive function in the participants.
These findings suggest that aerobic exercise, especially if it includes high-intensity interval training, has the potential to enhance memory in older adults.
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Human longevity was associated with decreased levels of genes involved in neural overactivity. www.nature.com
Healthy brain activity is achieved by maintaining a balance between neural excitation and inhibition. Impairment in this balance is related to many neurological and neurodegenerative disorders, including epilepsy, autism, Parkinson’s, Alzheimer’s, and schizophrenia. In Caenorhabditis elegans, a model organism for studying both the nervous system and aging, neural excitation increases with age and age-related cognitive decline, but lifespan increases with inhibition. A recent study demonstrates that extended longevity in humans is associated with lower levels of genes related to neural excitation.
The multi-arm study focused on three organisms: C. elegans, humans, and mice. The authors of the study found that global inhibition of neural excitation increased the lifespan of C. elegans. RNA sequencing and microarray analysis of human genes revealed that long-lived people (older than 85 years) have higher levels of REST, a gene-silencing transcription factor that downregulates neural excitation-related genes. In addition, they found that mice that are deficient in REST exhibit higher levels of neural excitation. REST and lower levels of neural excitation activate FOXO1, a longevity-associated transcription factor in mammals, suggesting that REST regulates a conserved mechanism of aging.
The authors of the study suggested that REST activation and subsequent reduction of excitatory neural activity may be a means to slow aging in humans.
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Metformin supplementation prevented gains in lean muscle mass in healthy people 65 years and older who engaged in resistance training. onlinelibrary.wiley.com
Age-related skeletal muscle mass and strength is a leading cause of the functional decline and loss of independence in older adults. Resistance training exercise is a highly effective strategy for maintaining or building muscle mass. A new study suggests that metformin, a drug commonly used to treat type 2 diabetes, blunts the effects of resistance training.
Metformin is in a class of drugs called biguanides, which act by decreasing liver gluconeogenesis (the production of glucose in the liver), decreasing glucose uptake in the gut, and increasing overall glucose utilization by improving insulin sensitivity in skeletal muscle and fat tissue. Scientific evidence suggests that metformin modulates aging processes to improve healthspan and extend lifespan in multiple organisms.
The present study involved 94 healthy men and women aged 65 years and older who were randomized to take either a 1,700-milligram dose of metformin daily (a typical dose prescribed for diabetes and prediabetes) or a placebo for 14 weeks. The participants also performed supervised resistance training for the duration of the study. At the end of the study, participants who took the placebo exhibited greater gains in lean body mass and thigh muscle mass than those who took metformin.
Although metformin is a safe and effective treatment for type 2 diabetes, these findings underscore concerns about the possible negative effects of metformin use in healthy older adults.
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The senolytic drug combination of dasatinib and quercetin cleared senescent cells from obese mice in a study by researchers at the Mayo Clinic in Rochester, Minnesota funded by NIA. When the senescent cells were removed, cell growth resumed in the brain regions involved in that process, also known as neurogenesis, and obesity-related anxiety behavior decreased.
Abstract cellsOver time, accumulation of senescent cells may slow or stop cell regeneration and tissue maintenance, thus contributing to tissue aging.
Clearing senescent cells from the brain and other tissues can delay, prevent, or alleviate multiple age-related disorders.
The combination of dasatinib and quercetin was recently shown to prevent cell damage, delay physical dysfunction, and, when used in naturally aging mice, extend their life span.
The researchers sought to determine whether anxiety-like behavior in obesity can be caused by increased senescent cell burden.
When the senescent cells had been eliminated from the mice brains, anxious behavior decreased and new nerve cell growth in the brain was detected.
The scientists note that the data show that senescent cells play a role in causing impaired cell growth due to obesity.
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Animal study demonstrates fungus C. albicans can cross the blood-brain barrier and may promote neurodegenerative disease, such as Alzheimer's www.sciencedaily.com
A common type of fungus, Candida albicans, was shown to cross the blood-brain barrier and trigger an inflammatory response in the brain that results in memory impairment (mouse study).
These findings raise the possibility that fungal infections may play a role in the development of chronic neurodegenerative disorders, such as Alzheimer’s disease. Dr. Dale Bredesen talks about this is the recent podcast episode I did with him.
Check that out here: https://www.foundmyfitness.com/episodes/dale-bredesen
From the article:
“We thought that yeast would not enter the brain, but it does,” Corry said. “In the brain, the yeast triggered the activity of microglia, a resident type of immune cell. The cells became very active ‘eating and digesting’ the yeast. They also produced a number of molecules that mediated an inflammatory response leading to the capture of the yeasts inside a granule-type structure inside the brain. We called it fungus-induced glial granuloma, or FIGG.”
The mice cleared the yeast infection in about 10 days; however, the microglia remained active and the FIGGs persisted well past this point, out to at least day 21. Intriguingly, as the FIGGs formed, amyloid precursor proteins accumulated within the periphery and amyloid beta molecules built up around yeast cells captured at the center of FIGGs. These amyloid molecules are typically found in plaques that are the trademark of Alzheimer’s disease. […] Intriguingly, as the FIGGs formed, amyloid precursor proteins accumulated within the periphery and amyloid beta molecules built up around yeast cells captured at the center of FIGGs. These amyloid molecules are typically found in plaques that are the trademark of Alzheimer’s disease.
[…]
“The results prompted us to consider the possibility that in some cases, fungi also could be involved in the development of chronic neurodegenerative disorders, such as Alzheimer’s, Parkinson’s and multiple sclerosis. We are currently exploring this possibility.”
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A new study by my mentor Dr. Bruce Ames proposes that 10 known compounds be classified as potential longevity vitamins due to their interaction with proteins that protect against diseases of aging. The concept is based on the Triage Theory, which classifies proteins and enzymes as either survival proteins, needed for survival and reproduction, or longevity proteins, which protect against future damage and are sacrificed in case of vitamin shortage, leading to an acceleration of insidious diseases of aging.
These putative “longevity vitamins” include: ergothioneine (a fungal antioxidant found in mushrooms), queuine (a bacterial metabolite found in the gut), PQQ (a bacterial metabolite in soil that is taken up by plants ), lutein and zeaxanthin (concentrated in leafy greens), lycopene (found in tomatoes), alpha- and beta-carotene, and cryptoxanthin (all plant antioxidant carotenoids), astaxanthin (a marine carotenoid found in salmon and krill), and taurine (found in meat).
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Beta-hydroxybutyrate production from fasting or a ketogenic diet may reduce the production of senescent cells associated with vascular aging www.sciencedaily.com
Fasting or beta-hydroxybutyrate administration reduces cellular senescence.
Beta-hydroxybutyrate (BHB) is a ketone produced by the body during times of carbohydrate scarcity such as those encountered while practicing a ketogenic diet, fasting, or exercise, which have all demonstrated the ability to extend healthspan and lifespan. However, the precise effects of beta-hydroxybutyrate on the cellular mechanisms of aging are not well understood. Findings of one report show that BHB administration and fasting both reduce senescence in mice.
Senescence occurs when a damaged cell terminates its normal cycles of growth and reproduction for the purpose of preventing the accumulation of damaged DNA or mitochondria. While senescence plays a vital role in human development and wound healing, the accumulation of senescent cells is associated with diseases of aging such as Alzheimer’s disease, Parkinson’s disease, cardiovascular disease, type 2 diabetes, and glaucoma. Lifestyle habits or drugs that increase beta-hydroxybutyrate may extend healthspan and reduce disease risk by slowing the rate of senescence.
The researchers conducted an experiment that involved culturing human vascular endothelial (i.e., blood vessel cells) from the umbilical cord and aorta, followed by an experiment with mice. To compare the effects of BHB supplementation and fasting, the researchers fed one group of mice a normal diet, then randomly assigned them to receive an injection of BHB or a placebo after they had fasted for just five hours. Using a second group of mice, the researchers randomly assigned half of the group to fast for 72 hours and the other half to eat normally. In both the cell culture and mice experiments, the researchers measured changes in gene expression and metabolic activity.
The researchers found that BHB reduced senescence in vascular cells due to increased expression of the transcription factor Oct4, which is a protein that binds to DNA and regulates cell regeneration and stem cell differentiation. Compared to mice who received a placebo injection, mice who received BHB had reduced senescence in vascular cells through the same Oct4 pathway as in cell culture. Mice who fasted also robustly activated Oct4, leading to activation of senescence-associated markers such as mTOR inhibition and AMPK activation, two pathways that modulate lifespan.
Prior to this study, it was not known whether Oct4 was active in adult cells; however, these results show fasting or BHB administration activates youth-associated DNA factors that reduce senescence in mice and cell culture. Future studies are needed to translate these results into relevant use for humans because humans have very different nutritional needs than mice to cells in culture.
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Expression of specific inflammasome gene modules stratifies older individuals into two extreme clinical and immunological states (2017) www.nature.com
Abstract: Low-grade, chronic inflammation has been associated with many diseases of aging, but the mechanisms responsible for producing this inflammation remain unclear. Inflammasomes can drive chronic inflammation in the context of an infectious disease or cellular stress, and they trigger the maturation of interleukin-1β (IL-1β). Here we find that the expression of specific inflammasome gene modules stratifies older individuals into two extremes: those with constitutive expression of IL-1β, nucleotide metabolism dysfunction, elevated oxidative stress, high rates of hypertension and arterial stiffness; and those without constitutive expression of IL-1β, who lack these characteristics. Adenine and N4-acetylcytidine, nucleotide-derived metabolites that are detectable in the blood of the former group, prime and activate the NLRC4 inflammasome, induce the production of IL-1β, activate platelets and neutrophils and elevate blood pressure in mice. In individuals over 85 years of age, the elevated expression of inflammasome gene modules was associated with all-cause mortality. Thus, targeting inflammasome components may ameliorate chronic inflammation and various other age-associated conditions.
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Cell-Autonomous Regulation of Astrocyte Activation by the Circadian Clock Protein BMAL1 papers.ssrn.com
Abstract
Circadian clock dysfunction is a common symptom of aging and neurodegenerative diseases, though its impact on brain health is poorly understood. Astrocyte activation occurs in response to diverse insults, and plays a critical role in brain health and disease. We report that the core clock protein BMAL1 regulates astrogliosis in a synergistic manner via a cell-autonomous mechanism, and via a lesser non-cell-autonomous signal from neurons. Astrocyte-specific Bmal1 deletion induces astrocyte activation in vitro and in vivo, mediated in part by suppression of glutathione-s-transferase signaling. Functionally, loss of Bmal1 in astrocytes promotes neuronal death in vitro. Our results demonstrate that the core clock protein BMAL1 regulates astrocyte activation and function in vivo, elucidating a novel mechanism by which the circadian clock could influence many aspects of brain function and neurologic disease.
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Abstract:
Purpose of review - We systematically appraised randomized controlled trials proposing exercise to influence cognition in older adults to (1) assess the methodologic quality using Cochrane criteria; (2) describe various exercise dose measures and assess their relationship with improved cognitive performance; and (3) identify consistent patterns of reported effects on cognition.
Recent findings: There was overall good methodologic quality in all 98 included studies. The assessment of the relationship between improved cognition and various measures of exercise dose (session duration, weekly minutes, frequency, total weeks, and total hours) revealed a significant correlation with total hours. Improvements in global cognition, processing speed/attention, and executive function were most stable and consistent.
Summary: We found that exercising for at least 52 hours [over the course of 6 months is the minimum amount needed] is associated with improved cognitive performance in older adults with and without cognitive impairment. Exercise modes supported by evidence are aerobic, resistance (strength) training, mind–body exercises, or combinations of these interventions.
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Dietary Restriction Improves Intestinal Cellular Fitness to Enhance Gut Barrier Function and Lifespan in D. Melanogaster papers.ssrn.com
Loss of gut integrity is linked to various human diseases including inflammatory bowel disease. However, the mechanisms which lead to loss of barrier function remain poorly understood. Using D. melanogaster, we demonstrate that dietary restriction (DR) slows the age-related decline in intestinal integrity by enhancing enterocyte cellular fitness through upregulation of dMyc in the intestinal epithelium. Reduction of dMyc in enterocytes induces cell death through JNK signaling leading to increased gut permeability and reduced lifespan upon DR. Genetic mosaic and epistasis analyses suggest that cell competition, whereby neighboring cells eliminate unfit cells by apoptosis, mediates cell death in enterocytes with reduced levels of dMyc. Reducing enterocyte apoptosis partially rescued the increased gut permeability and shortened lifespan upon loss of dMyc. We propose that dMyc acts as a barometer of enterocyte cell fitness impacting intestinal homeostasis in response to changes in diet and age.
Akagi, Kazutaka and Wilson, Kenneth A. and Katewa, Subhash D. and Ortega, Mauricio and Simmons, Jesse and Kapuria, Subir and Sharma, Amit and Jasper, Heinrich and Kapahi, Pankaj, Dietary Restriction Improves Intestinal Cellular Fitness to Enhance Gut Barrier Function and Lifespan in D. Melanogaster (2018). Available at SSRN:
https://ssrn.com/abstract=3155743 or http://dx.doi.org/10.2139/ssrn.3155743
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Hair Regeneration by Small Molecules That Activate Autophagy papers.ssrn.com
Hair plays important roles, ranging from the conservation of body heat to the preservation of psychological well-being. Hair loss or alopecia affects millions worldwide and can occur because of aging, hormonal dysfunction, autoimmunity, or as a side effect of cancer treatment. Methods that can be used to regrow hair are highly sought after, but lacking. Here we report that hair regeneration can be stimulated by small molecules that activate autophagy, including the longevity metabolites α-ketoglutarate and α-ketobutyrate, and the prescription drugs rapamycin and metformin which impinge on TOR and AMPK signaling.
Chai, Min and Jiang, Meisheng and Vergnes, Laurent and Fu, Xudong and de Barros, Stéphanie C. and Jiao, Jing and Herschman, Harvey R. and Crooks, Gay M. and Reue, Karen and Huang, Jing, Hair Regeneration by Small Molecules That Activate Autophagy (2018). Available at SSRN: https://ssrn.com/abstract=3188356 or http://dx.doi.org/10.2139/ssrn.3188356
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Epigenetic drift of H3K27me3 in aging links glycolysis to healthy longevity in Drosophila | eLife elifesciences.org
Abstract: Epigenetic alteration has been implicated in aging. However, the mechanism by which epigenetic change impacts aging remains to be understood. H3K27me3, a highly conserved histone modification signifying transcriptional repression, is marked and maintained by Polycomb Repressive Complexes (PRCs). Here, we explore the mechanism by which age-modulated increase of H3K27me3 impacts adult lifespan. Using Drosophila, we reveal that aging leads to loss of fidelity in epigenetic marking and drift of H3K27me3 and consequential reduction in the expression of glycolytic genes with negative effects on energy production and redox state. We show that a reduction of H3K27me3 by PRCs-deficiency promotes glycolysis and healthy lifespan. While perturbing glycolysis diminishes the pro-lifespan benefits mediated by PRCs-deficiency, transgenic increase of glycolytic genes in wild-type animals extends longevity. Together, we propose that epigenetic drift of H3K27me3 is one of the molecular mechanisms that contribute to aging and that stimulation of glycolysis promotes metabolic health and longevity.
Discussion: Aging is a complex process that can be regulated by a network of multiple mechanisms. It has been well-established that enhancing NAD+ biogenesis promotes healthy lifespan (Anderson et al., 2002; Balan et al., 2008; Mills et al., 2016). As noted, supplementation of NAD+ precursors profoundly elevates energy metabolism by increasing the expression of genes in the TCA cycle as well as glycolysis in C. elegans (Mouchiroud et al., 2013), and promotes glucose metabolism with increased flux through pentose phosphate and glycolytic pathways in mice on a high-fat diet (Mitchell et al., 2018). Therefore, it would be interesting to test whether the life-benefit effects of NAD+ might be through at least in part by the activation of glycolysis. Intriguingly, while declining intracellular NAD+ and thus increased NADH/NAD+ ratio correlate with aging (Zhu et al., 2015), our experiments in Drosophila demonstrate that increased ratios of GSH/(GSH +GSSG) and NADH/NAD+ due to enhanced glycolytic activities may provide a simple but effective way to retard aging. The oxidative phosphorylation, although produces more ATP than glycolysis, can yield intracellular ROS. The accumulation of ROS is the leading proposed cause of decline in cellular function and integrity in aging (Balaban et al., 2005). Thus, modulating H3K27me3 may reprogram bioenergetic decline during aging, which in effect reduces cellular damage and deterioration. Importantly, mammalian glycolytic genes have also been shown as PRCs targets (Brookes et al., 2012). Future investigations, including in-depth comparative analysis of PRCs and glycolytic pathway in the aging process in both flies and humans, may harness common operative mechanisms that modulate metabolic homeostasis and healthy longevity. Given the reversible nature of epigenetic pathways, this study proffers a tempting strategy against age-associated physiological decline and disease.
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Disruption of the beclin 1–BCL2 autophagy regulatory complex promotes longevity in mice www.nature.com
[Abstract]
Autophagy increases the lifespan of model organisms; however, its role in promoting mammalian longevity is less well-established. Here we report lifespan and healthspan extension in a mouse model with increased basal autophagy. To determine the effects of constitutively increased autophagy on mammalian health, we generated targeted mutant mice with a Phe121Ala mutation in beclin 1 (Becn1F121A/F121A) that decreases its interaction with the negative regulator BCL2. We demonstrate that the interaction between beclin 1 and BCL2 is disrupted in several tissues in Becn1F121A/F121A knock-in mice in association with higher levels of basal autophagic flux.
Compared to wild-type littermates, the lifespan of both male and female knock-in mice is significantly increased. The healthspan of the knock-in mice also improves, as phenotypes such as age-related renal and cardiac pathological changes and spontaneous tumorigenesis are diminished. Moreover, mice deficient in the anti-ageing protein klotho3 have increased beclin 1 and BCL2 interaction and decreased autophagy. These phenotypes, along with premature lethality and infertility, are escued by the beclin 1(F121A) mutation. Together, our data demonstrate that disruption of the beclin 1–BCL2 complex is an effective mechanism to increase autophagy, prevent premature ageing, improve healthspan and promote longevity in mammals.
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Following five healthy lifestyle habits may increase life expectancy by decade or more. www.eurekalert.org
Eating a healthy diet, regular exercise (at least 30 minutes or more per day of moderate to vigorous exercise), maintaining a healthy body weight, not drinking too much alcohol (up to about one 5-ounce glass of wine per day for women, or up to two glasses for men), and not smoking during adulthood may add more than a decade to life expectancy.
There was also a dose-response relationship between each individual healthy lifestyle behavior and a reduced risk of early death and the combination of all five healthy behaviors was linked with the most additional years of life.
Women who maintained all five of these healthy habits gained, on average, 14 years of life, and men gained 12 years, compared with those who didn’t maintain healthy habits over the 30-year study period.
Those individuals that maintained the healthiest lifestyles were 82% less likely to die from cardiovascular disease and 65% less likely to die from cancer compared with those with the least healthy lifestyles.
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A new study shows the "obesity paradox,” the idea that obese people live longer than those of normal weight, may be explained by muscle mass. journals.plos.org
A new study shows the “obesity paradox,” the idea that obese people live longer than those of normal weight, may be explained by muscle mass.
After accounting for muscle mass, high BMI no longer associates with greater survival. Some have hypothesized that excess fat stores are beneficial for counteracting episodes of catabolic stress. However, the risk of death increased with low muscle mass and greater body fat.
This study also found that skeletal muscle mass was an independent risk factor for mortality in the general population, and this was more pronounced among younger adults…which is interesting because most studies on muscle mass and mortality focus on a geriatric population.
Skeletal muscle mass could directly influence survival and could protect against loss of functional status due to aging or the onset of chronic disease. However, since this is an observational nature study, a causal relationship cannot be determined. There is always the possibility that there may be other confounding health-related factors that were not accounted for.
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New research suggests that mammals may become less responsive to light as a signal that resets the circadian clock as they age. www.sciencedaily.com
The research was done in mice and found that the glutamate receptor (NMDA), which used to transmit light information, became less effective in resetting the circadian clock during the aging process.
It is unclear how much of this translates to humans and whether this means that older people may need more bright light exposure to reset the circadian clock, which in turn affects sleep onset and quality.
Light entrains the circadian clock to our 24-hour day through melanopsin, a photopigment in the eye that is specialized for communicating circadian information instead of image formation.
Additionally, the eye is known to undergo structural changes with age, which can also impact circadian training. Light information is decoded by a subset of retinal ganglion cells expressing the melanopsin photopigment. Melanopsin is specialized for communicating circadian information.
To learn more how the important role early bright light exposure plays in circadian training, check out my first podcast episode with Dr. Satchin Panda, who discovered melanopsin. You can click on the timeline for the specific time points when we discuss the role bright light plays in resetting the clock.
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Pilot study finds supplementation with nicotinamide riboside improves blood pressure/arterial health particularly in individuals with hypertension. www.genengnews.com
A pilot study finds supplementation with nicotinamide riboside (500 mg, twice a day) improves blood pressure and arterial health particularly in individuals with mild hypertension (compared to placebo). The decrease in blood pressure could translate to a 25% reduction in heart attack risk.
The study also found that 1,000 mg daily of nicotinamide riboside boosted levels increased NAD+ by 60%.
Nicotinamide riboside is a form of vitamin B3 that is converted into NAD+. NAD+ is a cofactor for many metabolic enzymes and becomes depleted across various tissues as we age. This causes the mitochondria to suffer and mitochondrial decay is also thought to also be a key driver of aging.
To learn more about the role of nicotinamide riboside and NAD+ in aging…check out my conversation with Dr. Eric Verdin. Click on the timeline for the exact time point when we discuss nicotinamide riboside.
Dr. Eric Verdin Episode: https://www.foundmyfitness.com/episodes/eric-verdin
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Why is Stem Cells Therapy Good for Anti Aging? - Stemfinitycord Malaysia stemfinitycord.co
Stem cell therapy is a type of cell therapy where stem cells are introduced into the damaged tissue to treat the disorder or the injury. Mesenchymal stem cells (MSCs) are used in most stem cell therapy. They’re non-hematopoietic cell precursors initially found in the bone marrow, but actually present in many other tissues. Mesenchymal stem cells (MSCs) in culture are adherent, proliferating, and capable of multilineage differentiation into several tissues of mesenchymal origin, such as bone marrow stroma, adipose tissue (body fat), bone, cartilage, tendon, skeletal muscle and etc.
So Why is Stem Cells Therapy Good for Anti Aging?
In short, stem cells therapy was heavily emphasised to have the capacity to repair, renew and replace damaged tissue is a good anti aging treatment.
As shown below are the functions of Mesenchymal stem cells (MSCs) therapy: - Help facilitate growth of new blood vessels, a process known as angiogenesis which leads to improved blood flow in tissue - An anti-inflammatory effect which fastens wound healing - After aiding wound healing, it helps in reducing size of scarred tissue such as infected cardiomyocytes (heart cells) or wound to joint injury - Repair of damaged tissue which then leads to renewal of healthy tissue - Relief if symptoms related to any chronic diseases - Vast improvement in the immune system against disease - Better digestion and elimination of constipation - More flexible joints and discs - Improvement in skin elasticity and thickness - Reducing facial pigmentation, and adding a glow to your skin - Diminishing fine lines and wrinkles - Improving skin complexion - Tightening and shrinking open pores - Removing dark circles
No more joints problems, no more constipation, better appearance, overall human health improves!
The list is non-exhaustive when it comes to stem cells therapy. All these benefits brought by stem cells therapy are exactly the definition of anti aging if not reviving old age.
Visit more information on: http://stemfinitycord.co/
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Small molecule modulation of splicing factor expression is associated with rescue from cellular senescence bmccellbiol.biomedcentral.com
During the ageing process, both senescent and non-senescent cells lose a degree of response to cellular stressors. The upstream causes of this are as yet unclear, but may include changes in genes controlling alternative splicing; a major regulator of gene expression which ensures genomic plasticity. Here, we provide evidence that treatment with novel analogues of the stilbene compound resveratrol is associated not only with restoration of splicing factor expression but also with amelioration of multiple cellular senescence phenotypes in senescent human primary fibroblasts. At present, the precise mechanisms behind these observations are unclear, but may involve both the restoration of a more ‘youthful’ pattern of alternative splicing, and also effects of specific splicing factors on telomere maintenance. We propose therefore that splicing factors, and the upstream drivers of splicing factor expression may prove promising as druggable targets to ameliorate ageing phenotypes and hold promise as anti-degenerative compounds effective in human cells in the future.
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Clearing out senescent cells can extend healthspan by 25% in mice. Great summary of current state of research on senescence! www.scientificamerican.com
Cellular senescence is so important when we discuss aging and cancer because as our cells accumulate damage, which naturally happens as we age there are only so many outcomes that we can expect. The first possibility is that the cells can die. The next is that they can become senescent where they stop dividing but stay alive all-the-while secreting molecules that influence surrounding tissue… or the worst of all possible outcomes, the cells can really go off the rails and become malignant. Accumulating senescent cells is inevitable but there are varying strategies of how to tackle senescence and this is of great interest to the field of aging. There are ways to clear out senescent cells with drugs or even dietary and lifestyle interventions. Not only are there ways to kill senescent cells, there are also ways to influence what sort of molecules they produce, possibly limiting the inflammatory ones… even without killing them. To learn more about this…watch the episode of my podcast with Dr. Judy Campisi. She talks about the role of cellular senescence in the aging process and cancer, what causes senescence, and how viable lifestyle interventions (ie. fasting) and certain compounds (ie. senolytics) that can clear senescent cells may be plausible life extension strategies. Campisi episode: https://www.youtube.com/watch?v=adg3vUez3EU
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People who consumed 3-4 servings of fruits, vegetables, legumes, and a higher fat consumption (35% of energy) was associated with lower mortality. www.sciencedaily.com
A diet consisting more than 60% of energy from carbohydrates (including refined) was related to higher mortality, although not with the risk of cardiovascular disease. The research on dietary fats found that they are not associated with major cardiovascular disease, but higher fat consumption was associated with lower mortality; this was seen for all major types of fats (saturated fats, polyunsaturated fats, and monounsaturated fats), with saturated fats being associated with lower stroke risk. The data are from the Prospective Urban Rural Epidemiology (PURE) study which followed more than 135,000 people from 18 low-income, middle-income, and high-income countries. The study asked people about their diet and followed them for an average of seven and half years. The data was adjusted for age, sex, energy intake, current smoking status, urban or rural location, physical activity, baseline diabetes, education, and other dietary variables (white meat, red meat, bread, and cereal intake). However, this is a prospective study which means causation cannot be established.
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Genetically lowering plasma insulin levels by 25% extended median lifespan by 11% in female mice fed a low-calorie/high-carb/low-fat diet and by 3% in female mice fed a high-calorie/high-fat/low-carb diet.
This study looked at the effects of genetically lowering insulin levels in older mice. Unfortunately, the male mice did not have lower plasma levels of insulin despite genetically lowering insulin-genes and so the effect on lifespan could not be determined in male mice.
The female mice were fed two diets: (diet A: moderate-energy diet of 4.68 kcal/g, with 20% of calories from protein, 25% from fat, and 55% from carbohydrate; diet B: high-energy diet of 5.56 kcal/g, with 16% of calories from protein, 58% from fat, and 26% from carbohydrate).
Interestingly, the lowering of circulating insulin through gene manipulation had a more profound effect on median lifespan in female mice fed the low-calorie/high-carb/low-fat diet (11% extension) versus the high-calorie/low-carb/high-fat diet (3% extension). It is important to note that diets A and B were not matched for the type of fat content, protein levels, or micronutrient composition, so there are numerous potential factors that could have impacted diet-dependent outcomes.
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Telomeres are tiny caps on the ends of chromosomes that protect our DNA from damage. They get shorter every year and are a biological marker for aging. Exercise is one of the most robust ways to slow telomere attrition and someone that is very physically active may have a biological age that is even 10 years younger than their chronological age. In this study, a high level of exercise was defined as 30 minutes of jogging per day for 5 days a week for women and 40 minutes per day for men. Get out there and sweat!
FTA:
Exercise science professor Larry Tucker found adults with high physical activity levels have telomeres with a biological aging advantage of nine years over those who are sedentary, and a seven-year advantage compared to those who are moderately active. To be highly active, women had to engage in 30 minutes of jogging per day (40 minutes for men), five days a week.
“If you want to see a real difference in slowing your biological aging, it appears that a little exercise won’t cut it,” Tucker said. “You have to work out regularly at high levels.”
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A conserved NAD+ binding pocket that regulates protein-protein interactions during aging | Science science.sciencemag.org
This is from a press release on www.eurekalert.org “UNSW researchers have made a discovery that could lead to a revolutionary drug that actually reverses ageing, improves DNA repair and could even help NASA get its astronauts to Mars.”
From the link above “NAD+ binding modulates protein interactions An unexpected function of the oxidized form of nicotinamide adenine dinucleotide (NAD+) could underlie some effects of aging and propensity to age-related diseases. Li et al. found that the protein DBC1 (deleted in breast cancer 1) contains a domain that specifically binds NAD+. Binding of NAD+ inhibited the interaction of DBC1 with PARP1 [poly(adenosine diphosphate–ribose) polymerase 1], an enzyme important in DNA repair. Activity of PARP1 is inhibited by interaction with DBC1. Thus, the reduced abundance of NAD+ associated with aging may decrease PARP1 activity by promoting the interaction of PARP1 with DBC1. This mechanism could help explain the reported rejuvenating actions of NAD+ supplementation in older animals.”
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Daily tea consumption (green, black or oolong) was associated with a 50% reduced risk of cognitive decline. www.sciencedaily.com
Daily tea consumption (green, black or oolong) was associated with a 50% reduced risk of cognitive decline and a 86% lower risk in people genetically predisposed (ApoE4 gene) for Alzheimer’s disease.
The mechanism for the cognitive benefit is unclear and may include catechins, theaflavins, thearubigins and L-theanine which are all anti-inflammatory and have antioxidant activity. However, caffeine itself cannot be ruled out as a contributing factor as well.
While this data is an association and does not prove causation, the data was adjusted for many different factors that affect health and it still found the 50% and 86% reductions. The health factors that were adjusted for in the analysis included age, gender, education, smoking, alcohol consumption, body mass index, hypertension, diabetes, heart diseases, stroke, depression, ApoE4, physical activity, social and productive activities, vegetable and fruit consumption, fish consumption, and daily coffee consumption.
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Using sauna 4-7x per week lowered dementia risk by 66% & Alzheimer's risk by 65% after adjusting for diet/lifestyle. ageing.oxfordjournals.org
This study included over 2,000 middle-aged men that were followed for 20 years. The results were adjusted for many possible confounding factors including baseline age, alcohol consumption, BMI, physical exercise, socioeconomic status, systolic blood pressure, smoking status, type 2 diabetes, previous heart attack, resting heart rate and serum low-density lipoprotein cholesterol.
One of the reasons I find this study so compelling even though it is associative data and does not establish causality is because the sauna activates heat shock proteins, which have been shown in countless animal studies to play a causal role in preventing Alzheimer’s disease and other neurodegenerative diseases.
Anyone that follows me knows that I talk about saunas ALOT. I have a couple of videos where I discuss the effects of the sauna on longevity and in muscle mass and endurance. I discuss the role of heat shock proteins in both videos. I also have free reports with references covering all these topics that you can download on my website (foundmyfitness.com). Sauna longevity video: https://www.youtube.com/watch?v=eWKBsh7YTXQ Sauna muscle/endurance video: https://www.youtube.com/watch?v=aHOlM-wlNjM&t=1s
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Is there any research or even supported notion behind the idea that exogenous use of various hormones that are stimulated via heat stress (such as growth hormone) would disrupt the body’s affinity to respond to the hormetic stress?
I understand that there probably is not much to go off of, but this is more of a question of theorizing exogenous introduction of various compounds on natural pathways that stimulate these.
If Dr. Rhonda P had to guess, what would she think? I could see it being both synergistic and disruptive.
Have we looked at the effects of fasted sauna use vs non fasted as well? This is something i do, post workout, typically fasted for 20 hours.
THANKS
https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-2007-971895 http://europepmc.org/abstract/med/3218898
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Epitalon is a peptide that can actually lengthen your telomeres by an incredible amount.
Discovered in the late 1980’s by Prof. Vladimir Khavinson from St. Petersburg, Russia, Epitalon has been shown in studies to increase resistance to emotional stress, act as an antioxidant and decrease age-related changes in immune and neuroendocrine systems. It is also one of the few substances able to activate telomerase which renews (or elongates) telomeres. Telomeres help protect human DNA from damage and other cancer-causing errors.
Has anyone here tried it? Do you think it is safe?
One person stated that he is 49, but had the telomeres of a 55-year-old man. After taking Epitalon his telomere length is up by 1,000 base pairs. He now essentially has the telomere length of a ten-year-old.
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People with the highest fiber intake had ~80% greater chance of living long & healthy life out of all other dietary factors looked at. www.sciencedaily.com
other factors including total carbohydrate intake, glycemic index, glycemic load, and sugar intake. Successful aging was defined as including an absence of disability, depressive symptoms, cognitive impairment, respiratory symptoms, and chronic diseases including cancer, coronary artery disease, and stroke.
The gut is a major source of inflammation and also the major regulator of the immune system. Fermentable fiber feeds the beneficial bacteria in the gut which then prevents them from being forced to cannibalize the gut barrier (which causes inflammation) and it allows them to produce signaling molecules (short chain fatty acids) which make the immune system better. Also, many foods that contain fiber such as vegetables and fruits also have many important micronutrients and other plant compounds that play a role in successful aging. For more on the importance of fiber in successful aging watch my interview with the authors of The Good Gut, Drs. Justin and Erica Sonnenburg: https://youtu.be/gOZcbNw7sng
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Gastrodin promotes the secretion of brain-derived neurotrophic factor in the injured spinal cord www.ncbi.nlm.nih.gov
Abstract: Gastrodin, an active component of tall gastrodia tuber, is widely used in the treatment of dizziness, paralysis, epilepsy, stroke and dementia, and exhibits a neuroprotective effect. A rat model of spinal cord injury was established using Allen’s method, and gastrodin was administered via the subarachnoid cavity and by intraperitoneal injection for 7 days. Results show that gastrodin promoted the secretion of brain-derived neurotrophic factor in rats with spinal cord injury. After gastrodin treatment, the maximum angle of the inclined plane test, and the Basso, Beattie and Bresnahan scores increased. Moreover, gastrodin improved neural tissue recovery in the injured spinal cord. These results demonstrate that gastrodin promotes the secretion of brain-derived neurotrophic factor, contributes to the recovery of neurological function, and protects neural cells against injury.
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Why Broth is Beautiful: Essential Roles for Proline, Glycine and Gelatin - Weston A Price www.westonaprice.org
Gelatin’s traditional reputation as a health restorer has hinged primarily on its ability to soothe the GI tract. “Gelatin lines the mucous membrane of the intestinal tract and guards against further injurious action on the part of the ingesta,” wrote Erich Cohn of the Medical Polyclinic of the University of Bonn back in 1905. Cohn recommended gelatin to people with “intestinal catarrh”–an inflammation of the mucus membrane now called irritable bowel syndrome. Interestingly, the type of gelatin used in follow-up experiments done on people with even more serious intestinal diseases was specified as a “concentrated calves foot broth.”37 This form of gelatin would have been rich in cartilage and bone and presumably provide a better amino acid profile than straight collagen. A 1999 German study also proved the truth of the saying “Man ist was man isst.” Their study was inspired by reports of the positive influence of gelatin on degenerative diseases of the musculo-skeletal system and curiosity about the “therapeutic mechanism and the absorption dynamics.” Mice fed radioactive gelatin hydrolysate were compared to control mice administered radioactive proline. They found that 95 percent of the gelatin was absorbed within the first 12 hours, and the labeled gelatin found in the tissues was similar to that of labeled proline with one exception–the absorption and accumulation of gelatin in the cartilage was twice as high. This suggested a salutary effect of gelatin on cartilage metabolism that would not occur with the ingestion of proline alone. They concluded, “These results demonstrate intestinal absorption and cartilage tissue accumulation of gelatin hydrolysate and suggest a potential mechanism for previously observed clinical benefits of orally administed gelatin.”51 - See more at: http://www.westonaprice.org/health-topics/why-broth-is-beautiful-essential-roles-for-proline-glycine-and-gelatin/#sthash.G5l30GLj.dpuf
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New 20-page report on cryotherapy just released! Cold shock boosts norepinephrine up to 5-fold & increase type of immune cell that kills tumor cells. www.foundmyfitness.comExercise Brain Alzheimer's Aging Metabolism Inflammation Memory Immune System Norepinephrine Protein
This 20-page report explains how cold shock is a type of hormesis, which is a description of a type of stress that, in the right doses, is enough to shock the body and kick off adaptive processes and response mechanisms that are hardwired into our genes, and, once on, are able to create a resilience that actually exceeds what was needed to counter the initial stimuli. Rhonda discusses how cold exposure increases norepinephrine up to 5-fold in the brain and what the temperature and duration needed to do this are, how norepinephrine has an effect on mood, vigilance, focus, and attention, how cold exposure increases cold shock proteins including one in the brain that repairs damaged synapses and in muscle prevents atrophy, how cold-induced norepinephrine lowers inflammation and pain by decreasing the levels of 3 inflammatory mediators, how chronic cold shock may increase immune cell numbers and particularly a type of immune cell that kills cancer cells, how cold exposure increases metabolic rate, the number of mitochondria, and the burning of fat, what the effects of different cold exposure temperatures and timing are on athletic performance, recovery time, and muscle mass, and the differences between various types of cold shock modalities, including cold water immersion and whole body cryotherapy.
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Pomegranate is metabolized by gut bacteria to produce anti-inflammatory compound Urolithin A that prevents brain plaques. www.sciencedaily.com
Computational studies suggest urolithin A crosses the blood-brain barrier.
From the article:
Alzheimer’s disease is associated with ß-amyloid (Aß) fibrillation, a process in which amyloid proteins in the brain form clumps. To fight the formation of these fibrils, however, a molecule would have to cross the blood-brain barrier – a series of cell junctions that prevent certain substances from entering the brain. In previous work, the researchers showed that a pomegranate extract has anti-Alzheimer’s effects in animals, but they did not identify the compounds responsible.
[…]
Computational studies found that polyphenols could not cross the blood-brain barrier, but that urolithins could. Urolithins are anti-inflammatory and neuroprotective compounds that are formed when ellagitannins, a type of polyphenol, are metabolized by gut bacteria. The researchers then showed that urolithins reduced Aß fibrillation levels in vitro.
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The reason old folk sleep less found: neurons responsible for regulating sleep patterns in "ventrolateral preoptic nucleus" die off www.huffingtonpost.com
The method by which this area was found to be critical is particularly interesting.
FTA:
Saper analyzed a dataset of almost 1,000 subjects who had entered into a memory and aging study back in 1997, when they were all healthy 65-year-olds. As part of the study, they had all agreed to wear a small watch-sized device on their wrists for about 7 to 10 days, every two years, that would record all their movements. Upon their deaths, their brains were donated to science, so research could continue.
Saper chose 45 brains to examine, based on whether or not the ventrolateral preoptic nucleus was still intact. First he stained the brain in order to find the cluster of neurons, which were located in a similar part of the human brain as the rats' brains.
Then he linked the neurons found in the brain to the rest-activity behavior data collected in that person’s final year of life. He found that the fewer neurons one had, the more sleep fragmentation that person experienced in the last year of life. Brains with the largest amount of neurons (over 6,000) belonged to people with longer, uninterrupted sleep.
Another key finding from the study: The link between fewer neurons and less sleep was even more pronounced in people who had died with Alzheimer’s disease.