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DNA Damage

Episodes

magnesium

The Science of Magnesium and Its Role in Aging and Disease | Dr. Rhonda Patrick

Posted on March 15th 2024 (over 1 year)

In this solo episode, I'm taking an in-depth look at magnesium – a critical yet frequently underestimated mineral in our health.

genetic engineering

Dr. George Church: Rewriting Genomes to Eradicate Disease and Aging

Posted on August 23rd 2022 (almost 3 years)

Dr. George Church discusses revolutionary technologies in the field of genetic engineering.

epigenetics

How epigenetic aging works and how it might be reversed | Dr. Morgan Levine

Posted on May 22nd 2022 (about 3 years)

In this clip, Drs. Levine and Patrick discuss the epigenetic changes that occur with age, including methylation of CpG sites.

Topic Pages

  • Epigenetic aging clocks

    DNA damage drives repair-linked chromatin remodeling and methyltransferase recruitment, accelerating CpG methylation trajectories captured by epigenetic aging clocks.

  • NAD+

    DNA strand breaks activate PARP1, rapidly consuming NAD+ for poly(ADP-ribosyl)ation and depleting intracellular NAD+ stores.

  • Nicotinamide mononucleotide

    DNA damage hyperactivates PARP, depleting cellular NAD+, whereas nicotinamide mononucleotide restores NAD+ pools, supporting PARP-dependent repair.

News & Publications

  • Melatonin supplementation may heighten DNA repair in night shift workers during daytime sleep, potentially reducing cancer risk. oem.bmj.com
    Cancer Sleep DNA Damage Circadian Rhythm Melatonin Supplements

    Working night shifts may increase the risk of cancer by disrupting the production of melatonin, a hormone essential for DNA repair. This disruption can impair the body’s ability to repair oxidative DNA damage, potentially contributing to cancer development. A recent study found that melatonin supplementation could improve the repair of oxidative DNA damage in night shift workers.

    The researchers conducted a four-week randomized, placebo-controlled trial with 40 night shift workers, providing them a 3-milligram dose of melatonin before their daytime sleep periods. They collected urine samples during daytime sleep and nighttime work periods, measuring 8-hydroxy-2′-deoxyguanosine (8-OH-dG), a marker of DNA repair capacity.

    They found that melatonin supplementation nearly doubled 8-OH-dG excretion during daytime sleep, indicating improved DNA repair. However, they observed no difference in 8-OH-dG excretion during the night shift. Although the melatonin group experienced a slight decrease in wakefulness after falling asleep, the researchers found no differences in total sleep duration or sleepiness levels between the two groups.

    The findings from this small study suggest that melatonin supplementation enhances oxidative DNA repair in night shift workers, offering the potential for reducing cancer risk. More extensive studies may identify optimal dosages and the long-term effects of melatonin supplementation in this population. Learn about the pros and cons of melatonin supplementation in this clip featuring Dr. Satchin Panda.

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  • A newly developed "androgen clock" precisely tracks long-term androgen exposure. www.pnas.org
    Epigenetics Aging Hormones DNA Damage

    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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  • Exposure to benzyl butyl phthalate, a common plastic additive in everyday items, was found to cause extensive reproductive cell disruption and DNA damage. journals.plos.org
    Metabolism Inflammation DNA Damage Pollution Environment Genome

    The risks of everyday plastics may go beyond environmental concerns, affecting our reproductive health on a cellular level. Benzyl butyl phthalate (BBP), a common plastic additive found in toys, cleaning products, food packaging, and cosmetics, has been linked to reproductive and developmental impairments. A recent study in worms found that BPP induced abnormalities in chromosome segregation and increased cell death in reproductive cells.

    Researchers exposed C. elegans, a type of roundworm, to four different concentrations of BBP: 1, 10, 100, and 500 micromolar. Then, they measured the chemical’s effects on the worms' chromosomes and cell structure while tracking its metabolism into two primary byproducts: monobutyl phthalate and monobenzyl phthalate.

    They found that exposure to 10 micromolar BBP induced considerable cellular disruption, increasing germ cell apoptosis, abnormalities in chromosome structure, and elevated levels of DNA damage throughout the reproductive tissues. The compound also triggered increased oxidative stress and affected critical genes involved in cell cycle progression and oxidative metabolism.

    These findings suggest that BBP exposure profoundly affects reproductive health by impairing the cellular processes necessary for healthy chromosome segregation and genomic stability. A person’s phthalate burden may contribute to poor metabolic function, inflammation, and cognitive dysfunction. Learn how sauna use induces substantial sweat losses, promoting the excretion of toxic compounds like BBP.

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  • Low magnesium levels drive DNA damage, especially among people with high homocysteine. link.springer.com
    DNA Damage Magnesium Homocysteine

    Magnesium is critical for various biochemical processes, including DNA repair and replication. It also helps regulate homocysteine, an amino acid that, when elevated, can increase the risk of heart disease and other serious health problems. A recent study found that low magnesium levels might contribute to increased DNA damage, particularly when accompanied by high homocysteine levels.

    Researchers measured the blood levels of magnesium, homocysteine, folate, and vitamin B12 in 172 healthy middle-aged people. They also assessed DNA damage by examining specific biomarkers in the blood cells, such as micronuclei, nucleoplasmic bridges, and nuclear buds.

    They found that participants with low magnesium and high homocysteine levels had more DNA damage markers than those with high magnesium and low homocysteine levels. While males had slightly higher magnesium and homocysteine levels, females tended to have greater numbers of specific DNA damage markers, particularly micronuclei. Despite these differences, the general pattern remained, with lower magnesium and higher homocysteine linked to increased DNA damage.

    These findings indicate that maintaining higher magnesium levels might protect against DNA damage, particularly for people with high homocysteine. They also underscore the importance of adequate magnesium intake in overall health and its potential role in reducing the risk of diseases linked to DNA damage. Learn more about the health effects of magnesium in this episode featuring Dr. Rhonda Patrick and our comprehensive overview article.

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  • Hyperbaric oxygen therapy reverses aspects of the cellular aging process in older adults, boosting immune cell function. www.sciencedaily.com
    Aging Telomeres DNA Damage Immune System Senescence

    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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  • 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
    Aging Inflammation DNA Damage Mitochondria Taurine

    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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  • Omega-3 fatty acids protect against DNA damage. pubs.rsc.org
    Omega-3 DNA Damage

    Cellular DNA is subject to tens of thousands of injuries each day that arise from both endogenous sources, such as free radicals produced during normal metabolism, and exogenous sources, such as cytotoxic drugs, ionizing radiation, and cigarette smoke, among others. DNA damage induces genomic instability, a hallmark of aging. Evidence from a 2020 study suggests that omega-3 fatty acids protect against DNA damage.

    The study involved 140 healthy children and adolescents (aged 9 to 13 years). Researchers assessed the children’s body measurements and collected blood samples to measure nutritional status (particularly the omega-3 fatty acids EPA and DHA, retinol, beta-carotene, and riboflavin) and DNA damage.

    They found that a higher intake of the omega-3 fatty acids EPA and DHA was associated with less DNA damage. These findings held true even after considering other factors that influence DNA integrity, such as the children’s age, sex, body mass index, and others. The authors posited that the DNA-protective effects of EPA and DHA may be related to their capacity to resolve inflammation, a consequence of DNA damage.

    These findings suggest that omega-3s reduce DNA damage in children. [Learn more about omega-3s in our overview article.](LINK)

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  • Zinc deficiency promotes inflammation and weakens immunity, especially in older adults. pubmed.ncbi.nlm.nih.gov
    Aging Inflammation DNA Damage Immune System Zinc

    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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  • Daily consumption of dark roast coffee reduces DNA damage in healthy adults. link.springer.com
    DNA Damage Coffee Antioxidant

    DNA damage occurs with normal metabolism and upon exposure to toxic environmental factors. It is associated with the development of some cancers, cardiovascular diseases, diabetes, and inflammatory bowel diseases. Coffee contains a number of compounds with antioxidant properties, and previous research has shown that coffee and coffee extracts may reduce DNA damage in colon cells and white blood cells. Findings of this randomized controlled trial detail the effects of daily coffee consumption on DNA damage in healthy adults.

    Coffee constituents such as caffeic acid, catechol, hydroxyhydroquinone, trigonelline, and alkylpyridinium compounds enhance cellular protection by activating Nrf2, a transcription factor that regulates the expression of antioxidant proteins like glutathione. Of these constituents, the alkylpyridinium compounds, which are produced during roasting, were the most robust activators of Nrf2. One study comparing dark and medium roast coffee blends found that both blends reduced DNA damage; however, this study did not include a control group.

    The researchers recruited 100 healthy adults to participate in their study and randomly assigned them to one of two groups that were matched for weight and age. During a preconditioning period, they asked participants to consume at least 16 ounces of water per day and to avoid coffee, tea, and other caffeine-containing beverages and foods for four weeks. During the intervention period, participants in one group consumed 16 ounces of freshly brewed dark roast coffee blend per day for four weeks while the other group continued to drink water and avoid coffee. Participants gave blood samples at baseline and at the end of each four-week period for the measurement of DNA damage, using a test called the comet assay, which measures DNA strand breaks.

    DNA damage did not change between the preconditioning and intervention period for participants in the water group, while participants in the coffee group had a reduction in DNA damage. Compared to their baseline intake of coffee and other antioxidant-rich foods and beverages, participants who consumed the study coffee treatment had a significant 23 percent reduction in DNA damage levels. These effects were similar between males and females.

    The authors concluded that regular consumption of dark roast coffee reduces DNA damage in healthy adults compared to water consumption. They advise that future studies should compare the effects of different kinds of coffee (e.g., light, medium, and dark roast) on DNA damage and health.

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  • Long-lived adults have highly efficient DNA repair mechanisms. www.eurekalert.org
    Aging DNA Damage

    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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  • Faster rates of mutation speed aging and impair fertility. www.eurekalert.org
    Aging DNA Damage

    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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  • Omega-3 fatty acids may reduce DNA damage in children. pubmed.ncbi.nlm.nih.gov
    Omega-3 DNA Damage

    DNA damage, a major contributor to aging, occurs from exposure to byproducts of cellular metabolism, environmental chemicals, and radiation from sunlight. If not repaired, DNA damage can be detrimental and is associated with diseases such as cardiovascular disease and cancer. A new study suggests that higher levels of omega-3 fatty acids are associated with lower DNA damage in children and adolescents.

    Omega-3 fatty acids are essential because the body cannot make them, and they must be obtained from the diet. They include eicosapentaenoic acid, or EPA, and docosahexaenoic acid, or DHA. EPA and DHA, found in fish and other seafood, play key roles in controlling inflammation. Dietary nutrients provide important cofactors that are needed for DNA repair enzymes to function properly.

    Previous research has examined the relationship between nutrients and DNA damage in adults. The current study investigated whether the blood levels of omega-3 fatty acids and some vitamins are associated with the level of DNA damage in healthy children and adolescents.

    This cross-sectional study involved 140 children between the ages of nine and 14 years. The authors measured blood biomarkers including retinol, beta-carotene, riboflavin, and red blood cell levels of EPA and DHA. They assessed DNA damage using a sensitive test known as the comet assay. The authors analyzed the data using two different statistical techniques and found that DNA damage was inversely correlated with EPA and DHA levels in the blood. Plasma retinol and beta-carotene were also inversely correlated with DNA damage, but only with one of the statistical methods.

    These findings suggest that having adequate levels of the omega-3 fatty acids DHA and EPA in the blood is beneficial in reducing the risk of DNA damage. This reduction in DNA damage may decrease the risk of certain diseases while increasing healthspan and longevity.

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  • Vitamin C part of crucial pathway that eliminates toxic byproducts of fat metabolism www.sciencedaily.com
    Metabolism Vitamin C DNA Damage Fat

    From the article:

    “It’s true that vitamin C does react with oxidized lipids to form potential genotoxins,” said Balz Frei, professor and director of the Linus Pauling Institute, and co-author on this study. “But the process does not stop there. We found in human studies that the remaining vitamin C in the body continues to react with these toxins to form conjugates - different types of molecules with a covalent bond - that appear to be harmless.”

    In human tests, the OSU scientists found in blood plasma extraordinarily high levels of these conjugates, which show this protective effect of vitamin C against toxic lipids.

    “Prior to this, we never knew what indicators to look for that would demonstrate the protective role of vitamin C against oxidized lipids,” Stevens said. “Now that we see them, it becomes very clear how vitamin C can provide a protective role against these oxidized lipids and the toxins derived from them. And this isn’t just test tube chemistry, this is the way our bodies work.

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  • Folate deficiency leads to harmful chromosome abnormalities causing cells to inherit the incorrect amount of DNA and chromosome abnormalities. www.eurekalert.org
    DNA Damage Folate

    Folate deficiency leads to harmful chromosome abnormalities causing cells to inherit the incorrect amount of DNA and can even lead to the loss of an entire chromosome.

    Folate is high in dark leafy greens. Folate has long been known to be important for the production of new DNA because it is important for making a DNA nucleotide called thymine. It has also been shown to play an important roll in cell division (called mitosis) but this new study sheds light on a potential mechanism for why it is important for proper chromosomal segregation during cell division.

    This study analyzed the part or area of the genome called FRAXA, which contains an extensive so-called CGG sequence, a genetic code. Folate deficiency caused abnormalities in cells with an abnormally long CGG sequence and how the entire X chromosome became unstable in cases of long exposure to folate deficiency.

    Folate is high in dark leafy greens like chard, kale, spinach, etc.

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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
    Aging Ketosis Heart Disease DNA Damage Fasting Ketogenic Diet

    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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  • Why is Stem Cells Therapy Good for Anti Aging? - Stemfinitycord Malaysia stemfinitycord.co
    Exercise Diet Obesity Aging DNA Damage Stem Cells Tissue Repair Estrogen Skin Calcium Antioxidant

    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
    Aging Telomeres DNA Damage

    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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  • A conserved NAD+ binding pocket that regulates protein-protein interactions during aging | Science science.sciencemag.org
    Aging DNA Damage Protein

    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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