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Obesity

Episodes

exercise

Dr. Layne Norton on Building Muscle – Insights on Diet, Training, and Supplements

Posted on August 26th 2024 (10 months)

Dr. Layne Norton and I discuss fat loss, resistance training, seed oils, the carnivore diet, artificial sweeteners, and much more.

rhonda
Premium

Q&A #35 with Dr. Rhonda Patrick (4/30/2022)

Posted on April 30th 2022 (about 3 years)

Dr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.

fasting

Do healthy people benefit from intermittent fasting? | Dr. Mark Mattson

Posted on April 2nd 2022 (about 3 years)

In this clip, Dr. Mark Mattson predicts that intermittent fasting benefits both overweight and healthy weight people.

Topic Pages

  • Blood-brain barrier

    Obesity-induced systemic inflammation, oxidative stress and dyslipidemia compromise blood-brain barrier endothelial tight junctions, increasing permeability.

  • Fasting

    Fasting decreases insulin and increases glucagon, activating adipose lipolysis and AMPK signaling, thereby promoting negative energy balance and reducing obesity.

  • Nicotinamide mononucleotide

    In obese models, NMN elevates NAD+, activating SIRT1 and AMPK pathways that enhance mitochondrial fatty acid oxidation and reduce adiposity.

  • Nicotinamide riboside

    Nicotinamide riboside elevates NAD+, activating sirtuin- and AMPK-mediated mitochondrial biogenesis, thereby enhancing energy expenditure and countering obesity.

  • Sodium (Salt)

    High dietary sodium promotes obesity through thirst-stimulated energy-dense beverage intake and hyperosmolarity-induced adipogenic inflammation.

  • Sugar-sweetened beverages (SSBs)

    Chronic SSB intake promotes obesity by delivering rapidly absorbable sugars, spiking insulin, enhancing hepatic de novo lipogenesis and caloric surplus.

  • Ultra-processed Foods (UPFs)

    Chronic ultra-processed food intake induces obesity by fostering energy surplus via hyper-palatable formulation, high glycemic load, and satiety attenuation.

News & Publications

  • Artificial sweetener sucralose may disrupt the brain's appetite regulation by mimicking sweetness without increasing blood sugar, leading to increased hunger and altered brain activity. www.nature.com
    Brain Diet Obesity Sugar Weight Loss

    Artificial sweeteners like sucralose are marketed as healthier alternatives to sugar, but they may send mixed signals to the brain. A recent study found that sucralose increased hunger and altered activity in the part of the brain that regulates appetite, with effects differing by body weight.

    Researchers asked 75 young adults—some with a healthy weight and some with overweight or obesity—to drink a beverage sweetened with either sucralose (often marketed as Splenda), sucrose (table sugar), or plain water on three separate occasions. Afterward, the researchers measured the participants' blood glucose levels, collected their self-reported hunger ratings, and conducted brain scans to examine activity and connectivity in key regions involved in appetite control.

    Compared to sugar, sucralose increased blood flow to the hypothalamus and promoted stronger feelings of hunger. Sucralose also heightened hypothalamic activity more than water but didn’t influence hunger. Only sugar elevated blood glucose levels, an increase linked to reduced activity in the hunger-regulating regions of the brain.

    Interestingly, the brain’s response to sucralose differed based on body weight: In people with a healthy weight, sucralose enhanced connections between the hypothalamus and areas involved in attention and decision-making. In those with overweight, sucralose diminished connections to brain regions that process bodily sensations. And those with obesity exhibited little to no change in these neural connections. Compared to water, both sweeteners elicited distinct patterns of brain activity depending on weight status.

    These findings suggest that sucralose interferes with the brain’s normal appetite-regulating signals by mimicking sweetness without delivering the expected rise in blood sugar. This mismatch appears to increase hunger and alter brain connectivity in ways that vary depending on body weight. Artificial sweeteners also affect the gut microbiome. Learn more in this clip featuring Dr. Eran Elinav.

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  • Intermittent fasting three nonconsecutive days per week coupled with regular exercise promotes more weight loss than daily calorie restriction. www.acpjournals.org
    Diet Obesity Fasting Weight Loss

    Diets that require daily calorie cutting are hard to adhere to, and most people gain the weight back within a year. Intermittent fasting, which involves eating very little on some days and freely on others, might offer a more sustainable alternative. A recent study found that fasting three nonconsecutive days per week promoted more weight loss than daily calorie restriction as part of a comprehensive weight loss program.

    Researchers assigned 165 adults aged 18 to 60 with a body mass index between 27 and 46 to one of two diet plans. One group followed a 4:3 intermittent fasting schedule, eating freely on four days of the week and cutting calories by 80% on three nonconsecutive days each week. The second group followed a daily calorie restriction (about 34% less than baseline needs) to match the same total weekly calorie reduction. Both groups also participated in a year-long behavioral weight loss program that included group support and a goal of 300 minutes of moderate exercise weekly.

    After 12 months, participants in the intermittent fasting group lost roughly 6.4 pounds more, on average, than those in the daily calorie restriction group. Just over three-fourths of participants completed the study. The difference in weight loss between the two groups was small but statistically meaningful.

    These findings suggest that intermittent fasting offers a modest advantage over daily calorie restriction for people trying to lose weight, especially when paired with regular exercise and behavioral support. Learn more about the health benefits of intermittent fasting in this clip featuring Dr. Mark Mattson.

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  • Sleep disruption reduces the newly discovered hormone 'raptin,' potentially increasing appetite and promoting weight gain. www.nature.com
    Diet Obesity Sleep Hormones

    Sleepless nights don’t just leave you tired—they may also interfere with your body’s ability to regulate hunger. Researchers have long known that poor sleep increases the risk of obesity, but the biological link has remained elusive. A recent study found that a sleep-triggered hormone called raptin helps control appetite and may explain why people who don’t get enough sleep are more likely to gain weight.

    Researchers examined brain activity, hormone levels, and eating behavior under different sleep conditions in mice and humans. They identified a previously unknown hormone, which they named raptin, and tracked where and when it was released. They also studied the effects of a genetic variant that blocks raptin production and examined hormone levels in people with sleep deficiency, obesity, and nighttime eating syndrome.

    They discovered that raptin is produced in a part of the brain that regulates hunger and hormone secretion and is released during sleep. When sleep is disrupted, raptin levels drop. In lab experiments, raptin acted on specific receptors in the brain and stomach to reduce appetite and slow stomach emptying. People with obesity and sleep deficiency had lower levels of raptin, while those who underwent therapy to improve sleep showed increases in the hormone. A genetic variant that blocks raptin production was linked to night-time overeating and obesity.

    These findings indicate that raptin explains how sleep influences weight gain and appetite. Learn more about the effects of sleep deprivation in Aliquot #27: Health consequences of sleep deprivation, part I: Metabolic & immune health and Aliquot #28: Health consequences of sleep deprivation, Part 2: Mental & cognitive health

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  • Watching screens while eating boosts food intake, especially among women, potentially driving overeating. www.sciencedirect.com
    Diet Obesity

    Many people eat without thinking while watching TV, scrolling on their phones, or working on a computer. This habit is more than just a distraction—it can influence how much people eat and what types of foods they choose. A recent study found that screen use increases food intake, especially among women, regardless of what’s on the screen.

    Researchers conducted a systematic review and meta-analysis, analyzing data from 23 experimental studies involving nearly 1,900 participants. They compared food intake between those who watched screens while eating and those who did not, as well as among groups exposed to different types of screen content, such as food-related images or weight-control messages.

    They found that watching a screen while eating increased food consumption, particularly among women. Screen content modestly influenced intake, and duration mattered. For example, food cues slightly increased intake when screen time was under 30 minutes. However, when exposure lasted longer, food intake remained elevated regardless of the content, suggesting prolonged screen use drives overeating.

    These findings suggest that simply having a screen on during meals may encourage overeating, no matter what’s being watched. Reducing screen exposure during meals could be a simple way to help regulate food intake and support healthier eating habits. Learn about the effects of screen time on kids in this episode featuring Dr. Rhonda Patrick.

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  • Poor cardiorespiratory fitness may double the risk of early death, regardless of body weight. bjsm.bmj.com
    Exercise Obesity Cardiovascular

    How fit you are may matter more than how much you weigh when it comes to your risk of dying early. A recent review and meta-analysis found that poor cardiorespiratory fitness increases the risk of early death from cardiovascular disease and other causes, regardless of body weight.

    Researchers analyzed the findings of 20 studies investigating the effects of cardiorespiratory fitness and body weight on the rates of early death from cardiovascular disease and all other causes. The various studies included nearly 400,000 participants and compared the risks among people who were overweight or obese to those who were normal weight.

    They found that overweight, fit people were about 50% more likely to die from cardiovascular disease and had roughly the same overall risk of early death as those with normal weight. Obese, fit people were 62% more likely to die from cardiovascular disease and had an 11% higher overall risk of early death, but these differences were not statistically significant.

    However, being unfit was linked to a much higher risk of death. Normal-weight people who were unfit were about twice as likely to die from cardiovascular disease and all causes. Overweight, unfit people had roughly 2.5 times the risk of cardiovascular death and 82% higher overall risk of early death. Obese, unfit people had more than triple the risk of cardiovascular death and twice the risk of dying from any cause compared to those with normal weight.

    These findings suggest that cardiorespiratory fitness robustly predicts the risk of early death from cardiovascular disease and other causes. Vigorous exercise, such as high-intensity interval training, is a great way to boost cardiorespiratory fitness and prevent early death. Learn more in this episode featuring Dr. Rhonda Patrick.

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  • The brain's vagus nerve controls fat absorption in the intestine—a possible pathway for managing obesity. pubmed.ncbi.nlm.nih.gov
    Brain Diet Obesity Fat Isothiocyanates

    Fat is a vital energy source, but when consumed in excess, it can promote obesity. However, the amount of fat the body absorbs may be more related to the brain than the gut. A recent study in mice found that signals from the brain’s vagus nerve regulate fat uptake in the intestine, offering a potential means to moderate obesity.

    Researchers manipulated the dorsal motor nucleus of the vagus (DMV), which plays a crucial role in digestion. They inactivated DMV neurons that connect to the jejunum (the middle portion of the intestine), shortening the length of the microvilli in the gut and reducing fat absorption. However, stimulating DMV neurons increased fat absorption and promoted weight gain. Finally, they injected mice with puerarin, a bioactive compound derived from the kudzu plant, and found that the compound mimicked the effect of DMV suppression, further reducing fat absorption.

    These findings suggest that controlling the DMV-vagus-jejunum pathway could provide a novel approach to managing fat absorption and weight. They also highlight yet another way the brain-gut axis influences human health.

    Puerarin is an isothiocyanate, a class of sulfur-containing compounds known for their potent anti-inflammatory, anti-cancer, and anti-obesity effects. Sulforaphane, another well-known isothiocyanate, shares many of these beneficial properties. To learn more about the health effects of sulforaphane, check out our overview article.

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  • Cardiovascular risk and obesity accelerate brain atrophy in men a decade before similar effects occur in women, potentially increasing dementia risk. jnnp.bmj.com
    Brain Obesity Cardiovascular

    Cardiovascular health affects more than the heart—it shapes the brain. A recent study found that cardiovascular risk and obesity contribute to brain atrophy in men and women, with effects manifesting earlier in men.

    Researchers analyzed data from more than 34,000 adults aged 45 to 82 enrolled in the UK Biobank study. They measured the participants' grey matter volume, assessed their cardiovascular risk, and calculated the fat volume under their skin and around their internal organs.

    They found that men experienced considerable grey matter volume losses linked to cardiovascular risk and obesity between ages 55 and 64. However, volume losses in women manifested a decade later, between ages 65 and 74. These patterns were evident regardless of whether participants carried the APOE4 gene, a key genetic risk factor for Alzheimer’s disease.

    These findings suggest that cardiovascular disease-related dementia risks manifest earlier in men, underscoring the importance of tailoring interventions based on sex. One of the mechanisms linking cardiovascular disease, obesity, and dementia is vascular dysfunction, which contributes to blood-brain barrier failure. Learn more about vascular dysfunction in this clip featuring Dr. Axel Montagne.

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  • Diagnosis of type 2 diabetes before the age of 50 nearly doubles the risk of dementia, while concurrent obesity triples the risk. journals.plos.org
    Obesity Diabetes Dementia

    Type 2 diabetes is becoming increasingly common among younger adults, shifting from its traditional association with older populations. A recent study found that the age at which a person develops type 2 diabetes influences their risk of developing dementia, with obesity more than tripling risk, especially at younger ages.

    Researchers tracked more than 1,200 adults aged 50 and older who had diabetes but no dementia at the start of the study. They grouped participants based on the age they were diagnosed with diabetes—before age 50, in their 50s, 60s, or 70s—and by whether they had obesity. They tracked new dementia cases for about 10 years, using cognitive assessments and considering factors like lifestyle and medication use.

    They found that people diagnosed with diabetes at younger ages had higher dementia risks than those diagnosed after 70. Those diagnosed before age 50 were nearly twice as likely to develop dementia, and obesity more than tripled this risk. Among obese participants diagnosed with diabetes before age 50, dementia risk was highest.

    These findings suggest that diabetes, especially in the setting of obesity, markedly increases dementia risk. Self-monitoring of blood glucose levels can help identify pre-diabetes—a precursor to diabetes—providing a window of opportunity to prevent the disease with lifestyle and dietary changes. Learn more in this clip featuring Dr. Michael Snyder.

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  • Long-term intervention with calorie restriction and high-intensity interval training doubles insulin sensitivity and greatly improves liver function in people with a form of fatty liver disease. pubmed.ncbi.nlm.nih.gov
    Exercise Obesity Metabolism Insulin Resistance Fatty Liver

    Metabolic dysfunction-associated steatohepatitis (MASH) is a form of fatty liver disease that promotes inflammation and damage over time. Closely connected to conditions like obesity and insulin resistance, MASH affects nearly one-third of people worldwide. A recent study found that a long-term intervention combining calorie restriction and high-intensity interval training (HIIT) in people with MASH improved liver function, doubling insulin sensitivity.

    Researchers assigned people with MASH to either a treatment group (16 participants) that received lifestyle counseling and exercise training or a control group (eight participants) that continued with standard medical care. The treatment group engaged in supervised HIIT three times a week while reducing caloric intake. The researchers assessed the participants' liver fat, measured blood biochemistries, and evaluated insulin sensitivity before and after the intervention.

    They found that the treatment group experienced notable reductions in body weight, fat mass, and liver injury. Their cardiorespiratory fitness improved considerably, and they exhibited a twofold increase in peripheral insulin sensitivity compared to the control group. Both groups saw reductions in total energy intake and liver fat.

    These findings suggest that combining caloric restriction with regular high-intensity exercise can yield marked improvements in liver health and insulin sensitivity, likely by redistributing excess nutrients to skeletal muscle. Learn more about calorie restriction in this clip featuring Dr. David Sinclair, and HIIT in this clip featuring Dr. Martin Gibala.

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  • High-protein, low-calorie diets—whether animal or plant-based—lead to an average weight loss of ~18 pounds and improved glucose metabolism in people at risk for type 2 diabetes. dom-pubs.pericles-prod.literatumonline.com
    Diet Obesity Diabetes Muscle Protein Weight Loss

    The global obesity epidemic is driving a marked increase in the incidence of type 2 diabetes, and some experts estimate that by 2024, more than 780 million adults worldwide will develop the disease. A recent study found that high-protein, low-calorie diets promote weight loss and improve cardiometabolic markers in people at risk for type 2 diabetes.

    The study involved 117 adults with either prediabetes or type 2 diabetes and a body mass index (BMI) over 27.5—considered overweight or obese. Participants consumed an animal- or plant-based high-protein diet that provided 35% of their total calories for six months. The remainder of their calories came from fat (30%) and carbohydrates (35%).

    Participants in both groups saw similar improvements in body composition, including an average weight loss of approximately 8 kilograms (~18 pounds) and reduced visceral (abdominal) fat. Glucose metabolism indicators, such as fasting glucose and glycated hemoglobin levels, improved equally in both groups, as did lipid levels, liver enzymes, and inflammatory markers.

    These findings suggest that high-protein, low-calorie diets—whether animal- or plant-based—can improve body composition, glucose metabolism, and other cardiometabolic markers in people with prediabetes or type 2 diabetes.

    Dietary protein supports muscle hypertrophy and maintenance—critical aspects of glucose metabolism. Learn how to optimize protein intake to support muscle health when following a plant-based diet in this clip featuring Dr. Luc van Loon.

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  • Fasting-based dietary strategies, including intermittent fasting and time-restricted eating, show slight superiority over calorie restriction for promoting weight loss and improving insulin sensitivity. www.mdpi.com
    Diet Obesity Metabolism Fasting Time-Restricted Eating Weight Loss

    With millions worldwide affected by obesity-linked conditions like diabetes and cardiovascular disease, understanding which dietary methods are most effective has become crucial. A recent review and meta-analysis found that fasting-based strategies are slightly more effective for promoting weight loss and improving insulin sensitivity than calorie restriction.

    Researchers reviewed 10 randomized controlled trials involving more than 600 participants to compare the effects of fasting-based and calorie-restricted diets on weight loss and metabolic health. Fasting-based strategies included intermittent fasting, time-restricted eating, and alternate-day fasting, while continuous calorie restriction involved reducing daily caloric intake by 20% to 40% without meal timing changes.

    They found that both methods effectively reduced body weight, with participants losing around 5.5 to 6.5 kilograms (roughly 12 to 14 pounds) after six months. Fasting-based approaches had a slight edge in short-term weight and fat loss—about 1 kilogram (2.2 pounds) more than calorie restriction—but both approaches had similar effects on lean body mass, waist and hip circumference, blood pressure, lipid levels, and glucose metabolism. Notably, fasting-based methods also lowered fasting insulin levels and improved insulin sensitivity.

    These findings suggest that while both methods support weight loss, fasting-based diets may offer additional short-term metabolic benefits. Learn more about fasting-based diets and calorie restriction from these great resources:

    What type of fasting is best? Caloric restriction vs. periodic fasting and the importance of re-feeding after a fast The link between sirtuins, calorie restriction, fasting, and the insulin pathway Topic article: Fasting

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  • Middle-aged adults with higher leptin availability, a hormone that regulates appetite and weight, show stronger brain structures and cognitive functions, potentially shielding against Alzheimer's. alz-journals.onlinelibrary.wiley.com
    Brain Alzheimer's Obesity Hormones

    Obesity has long been associated with a higher risk of developing Alzheimer’s disease, but scientists don’t fully understand what drives this link. However, some research indicates that leptin, a hormone that regulates appetite and body weight, may be vital in protecting brain health. A recent study found that middle-aged adults with higher leptin bioavailability had better brain structure and cognitive function than those with lower levels.

    Researchers analyzed data from more than 2,200 cognitively healthy participants enrolled in the Framingham Heart Study. They measured leptin and related markers in the participants' blood and tested their cognitive function. Then, they assessed their brain structure using magnetic resonance imaging scans to measure white matter integrity and signs of brain atrophy.

    They found that participants with greater leptin bioavailability had better white matter integrity, indicated by reduced brain degeneration markers and better brain connectivity. However, participants with higher levels of a leptin-related marker called soluble leptin receptor were more likely to have poorer brain structure.

    These findings suggest that leptin protects brain health, potentially reducing the risk of dementia later in life. They also highlight how metabolic health in midlife can influence cognitive aging, especially for those with obesity. Poor sleep can suppress the effects of leptin, ultimately impairing metabolic function. Learn more in this clip featuring Dr. Matt Walker.

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  • Excess body fat reduces semen quality, potentially contributing to infertility. www.nature.com
    Obesity Pregnancy

    Infertility is a growing public health concern, and poor semen quality plays a role in as many as 70% of all infertility cases. A recent review and meta-analysis found that men with obesity had lower semen volume, sperm number, and motility and fewer normal-shaped sperm than men with healthy body weight.

    The reviewers analyzed the findings of studies investigating links between body mass index (BMI) and semen quality. Their analysis included 50 studies involving more than 71,000 men.

    They found that compared to men with a healthy BMI, men with obesity had lower semen volume, sperm number, and motility and fewer normal-shaped sperm. These reductions in semen quality were more pronounced among the men with the highest BMIs. Men with overweight had lower semen volume and motility than healthy-weight men.

    These findings suggest that excess body fat reduces semen quality, potentially contributing to infertility. Many other factors influence semen quality, including age, lifestyle factors (such as smoking, excess alcohol consumption, and poor sleep quality), and environmental exposure (such as air pollution, extreme temperatures, and microplastic exposure).

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  • Genetics plays a key role in the body's response to exercise. scitechdaily.com
    Exercise Obesity Metabolism Diabetes Genetics

    Many factors influence the extent to which exercise promotes weight loss, including exercise intensity, dietary habits, and overall lifestyle. Evidence suggests genetic differences play a role, too. A recent study found that mice with certain variants of PGC1-alpha—a key regulator of metabolism—consume less oxygen and burn less fat during workouts and are more likely to gain weight despite increased activity.

    Researchers analyzed gene expression in mice to determine the distribution of the three variants of PGC1-alpha: A, B, and C. Then, they assessed the animals' muscle growth, fat burning, and oxygen consumption during rest, short-term exercise, and long-term exercise. They performed the same assessments on 20 men, half of whom had type 2 diabetes.

    They found that although the three variants have similar functions, the A variant is widely distributed throughout the body, but the B and C variants are primarily found in brown adipose tissue, skeletal muscle, and the heart. They found that mice lacking the B and C variants had a diminished response to exercise, consuming less oxygen and burning less fat. These mice gained weight, developed high insulin levels, and were intolerant of cold temperatures. Men who had higher expression of the B and C variants consumed more oxygen and had less body fat, even among those with type 2 diabetes.

    These findings suggest that variants of PGC1-alpha influence the body’s response to exercise and highlight potential strategies for treating obesity.

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  • Taurine supplementation can help regulate blood glucose and lower blood pressure, reducing risk factors associated with metabolic syndrome. pubmed.ncbi.nlm.nih.gov
    Obesity Diabetes Cholesterol Triglycerides Blood Pressure Metabolic Syndrome Taurine Stroke Cardiovascular Supplements

    Metabolic syndrome is a cluster of conditions that includes hypertension, high blood glucose, excess abdominal fat, and abnormal blood lipids. Having metabolic syndrome markedly increases a person’s risk of cardiovascular disease, type 2 diabetes, and stroke. A recent meta-analysis found that taurine supplementation improves conditions associated with metabolic syndrome.

    Researchers analyzed the findings of 25 studies (with more than 1,000 participants) investigating links between taurine supplementation and metabolic syndrome. They also explored the effects of taurine dose and examined secondary outcomes of taurine supplementation, including body composition, lipid profile, and blood glucose control.

    They found that taurine doses ranged from 0.5 to 6 grams, with study durations ranging from five days to one year. On average, taurine supplementation reduced systolic blood pressure by 4 mmHg, diastolic blood pressure by 1.5 mmHg, fasting blood glucose by 6 milligrams per deciliter, and triglycerides by 18 milligrams per deciliter. The researchers did not observe an effect on high-density lipoprotein cholesterol. The reduction in diastolic blood pressure and fasting blood glucose was dose-dependent, with higher doses eliciting more robust effects.

    These findings suggest that taurine supplementation improves factors associated with metabolic syndrome. Interestingly, other research shows that an acute bout of exercise increases blood taurine levels, providing a mechanistic link between exercise and better metabolic health.

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  • Appetite control varies widely with different weight-loss interventions. onlinelibrary.wiley.com
    Diet Obesity Weight Loss

    The body’s appetite feedback circuit is a sophisticated system that regulates hunger and satiety to maintain energy balance. Suppressing this circuit is essential to successful weight loss before reaching a plateau. A recent study found that weight-loss interventions vary in their capacity to overcome the body’s appetite feedback circuits by as much as threefold.

    A researcher used a validated mathematical model to simulate the body’s weight-loss response to calorie restriction, glucagon-like peptide receptor agonists (GLP-1 RAs, a class of drugs primarily used to treat type 2 diabetes and obesity), and bariatric (gastric bypass) surgery. The model predicted how these interventions influenced body weight by simulating changes in caloric intake, energy use, and appetite over time.

    He found that weight loss plateaued at around 12 months with calorie restriction and at around 24 months with GLP-1 RAs or gastric bypass surgery. The drugs and surgery were between 40 and 70 percent more effective at suppressing appetite than calorie restriction, aligning with data indicating that most people find calorie restriction challenging to adhere to, especially for an extended period.

    These findings suggest that weight-loss interventions vary in their capacity to overcome the body’s appetite feedback circuits, influencing their effectiveness. Unfortunately, many people regain weight after successful weight loss, possibly due to changes in their gut microbiome. Learn more in this episode featuring Dr. Eran Elinav.

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  • Higher-dose omega-3 supplementation elevates blood levels, even in Alzheimer’s high-risk APOE4 carriers, but obesity may hinder its brain availability. content.iospress.com
    Brain Alzheimer's Obesity Omega-3 Genetics Dementia

    Omega-3 fatty acids play critical roles in maintaining brain health and function, potentially reducing the risk of developing Alzheimer’s disease. People who carry the APOE4 gene variant and those with obesity have a higher risk of developing the disease, suggesting that differences in metabolism could be a factor. A 2022 study found that obesity influenced the amount of omega-3 in plasma phospholipid form that is important for brain transport.

    Fifty people (half of whom carried the APOE4 gene) took 2.5 grams of combined docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) daily for six months. Because omega-3 fatty acids must be in the free fatty acid form or phospholipid form to cross the blood-brain barrier, researchers measured these forms of the fatty acids in the participants' plasma before and after the intervention. They also investigated whether APOE genotype or body mass index (BMI, a proxy for overweight and obesity) influenced these measures.

    They found that supplemental omega-3s increased by up to fourfold in all participants, regardless of APOE status. However, participants with a high BMI experienced lower plasma phospholipid omega-3 increases than those with a low BMI. Having a high BMI is a well-established risk factor for Alzheimer’s disease. Interestingly, APOE4 did not influence the amount of plasma phospholipid omega-3.

    They also lend support to evidence suggesting that APOE4 carriers do not respond to lower dose omega-3 supplementation as well as non carriers possibly because they do not transport DHA in free fatty acid form across the blood-brain barrier as well. However, the transport of the phospholipid form of DHA across the blood-brain barrier bypasses the default in tight junctions, potentially providing a better means of DHA transport for people with the APOE4 gene and lowering their risk of developing the disease. Learn more about APOE4 and DHA transport in this peer-reviewed article by 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
    Exercise Obesity Aging Diabetes Mortality

    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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  • Apple cider vinegar promotes weight loss and improves metabolism in young people with overweight or obesity. nutrition.bmj.com
    Diet Obesity Metabolism Weight Loss Polyphenol

    Obesity and overweight are growing global public health concerns, especially among young people. Evidence suggests that apple cider vinegar supports weight loss and improves metabolic health. A recent study found that young people who took apple cider vinegar for 12 weeks lost more weight and exhibited better metabolic parameters than those who took a placebo.

    The study involved 120 teens and young adults with overweight or obesity. Participants received 5, 10, or 15 milliliters (5 milliliters = 1 teaspoon) of apple cider vinegar or a placebo diluted in water daily for 12 weeks. They didn’t make any changes to their diets or activity levels. Researchers measured the participants' anthropometrics (weight, body mass index, waist/hip circumferences, and body fat ratio) and blood glucose, triglyceride, and cholesterol levels at the beginning of the study and again at four-week intervals.

    They found that participants who took apple cider vinegar lost weight in a dose- and time-dependent manner, with those taking higher doses manifesting the greatest weight loss, which increased as the study progressed. All anthropometric measures improved, too, as did blood glucose, triglyceride, and cholesterol levels. None of the participants taking the vinegar experienced any adverse or ill effects.

    These findings suggest that apple cider vinegar promotes weight loss and improves metabolic parameters in young people with overweight or obesity. The investigators noted that these effects occurred without changes to the participants' diets or activity levels, suggesting the effects arose from the vinegar itself. Apple cider vinegar is made by fermenting apple juice. It is rich in vitamins, minerals, amino acids, and polyphenols such as flavonoids, which may confer some of apple cider vinegar’s benefits. Learn about the health benefits of other polyphenols in our overview article.

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  • What are the optimal time-restricted eating patterns for cardiovascular wellness? pubmed.ncbi.nlm.nih.gov
    Diet Obesity Diabetes Cholesterol Time-Restricted Eating Blood Pressure Cardiovascular

    Time-restricted eating is a dietary pattern that restricts the time during which a person eats to a specific window, such as a “16:8" pattern, where they fast for 16 hours a day and consume food only during the remaining eight hours. Evidence suggests that time-restricted eating improves cognitive function, supports weight loss, and reduces systemic inflammation. Findings from a recent review and meta-analysis suggest that time-restricted eating also reduces the risk of cardiovascular disease.

    Researchers analyzed the findings of 33 studies involving 1,725 participants investigating the effects of time-restricted eating on markers of cardiovascular health. They conducted a sub-group analysis to determine how age, health characteristics, and eating patterns influenced the effects of time-restricted eating.

    They found that the effects of time-restricted eating on cardiovascular disease varied according to a person’s risk factors, age, and when they ate. The table below presents their findings for the optimal time-restricted eating for different groups.

    This meta-analysis and review identifies the optimal time-restricted eating interventions for blood pressure, obesity, lipids, and glucose. It effectively provides a best-practices guide for people interested in implementing time-restricted eating as a lifestyle modification to improve cardiovascular health. Learn more about time-restricted eating in this episode featuring Dr. Satchin Panda.

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  • Obesity triggers mitochondrial fragmentation, hindering fat-burning efforts. www.sciencedaily.com
    Diet Obesity Mitochondria Fat

    Obesity, which affects more than 40 percent of U.S. adults, arises when the body stores excess fat, primarily in adipose tissue. While adipose tissue is an important source of energy, its capacity to produce energy in the setting of obesity diminishes, complicating weight loss efforts. A recent study demonstrates that obesity promotes fragmentation of the mitochondria in adipose cells, resulting in smaller and less effective mitochondria with reduced fat-burning capacity.

    Researchers fed mice an obesogenic diet and assessed its effects on their fat cells' mitochondrial function. Then, they analyzed gene activity in fat samples collected from people with obesity.

    They found that after eating a high-fat diet, mitochondria in the animals' adipose cells underwent fragmentation, forming smaller, less efficient mitochondria with diminished fat-burning capabilities. This metabolic alteration was orchestrated by the activity of RaIA, a molecule that serves various roles, one of which involves assisting in the breakdown of dysfunctional mitochondria. Deleting this gene in the mice prevented excessive weight gain despite consuming an obesogenic diet, highlighting RaIA’s crucial role in transitioning from a healthy weight to obesity. They also found evidence of increased gene activity in people with obesity that corresponded with persistent elevation in RalA.

    These findings suggest that obesity induces fragmentation of mitochondria, compromising their function and driving a vicious cycle of diminished fat-burning capability and increased body fat gain. Evidence suggests cold exposure and fasting promote weight loss. Learn more in this episode featuring Dr. Ray Cronise.

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  • A single 8-ounce serving of 100 percent fruit juice daily promotes weight gain in children. pubmed.ncbi.nlm.nih.gov
    Nutrition Diet Obesity Polyphenol

    Whole fruits are rich in vitamins, minerals, and bioactive compounds that promote health. They also contain essential fiber, which supports digestion and regulates blood sugar levels. Fruit juices, on the other hand, contain little fiber, are high in natural sugars, and can cause rapid blood sugar spikes, impairing metabolism. A recent systematic review and meta-analysis found that consuming 100 percent fruit juice promotes weight gain in children.

    Researchers analyzed the findings of 42 randomized clinical trials investigating the effects of consuming 100 percent fruit juice on body weight. The various trials included more than 45,000 children and 268,000 adults.

    They found that for every additional serving of juice (defined as 8 ounces) per day, the children showed a modest increase in body mass index, a proxy for body fatness. However, the findings in adults were mixed, with studies that didn’t adjust for caloric intake observing greater body weight gain than those that didn’t.

    These findings suggest that a single serving of 100 percent fruit juice daily promotes weight gain in children – a noteworthy finding considering that roughly half of children and teens in the U.S. consume at least one serving of fruit juice a day. An 8-ounce serving of 100 percent orange juice contains about 110 calories and 20 grams of sugar, while a medium-sized whole orange contains approximately 62 calories and 12 grams of sugar. Encouraging the consumption of whole fruits versus fruit juices may influence body weight in children.

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  • Vitamin D increases muscle strength and mass without altering body weight in mice. www.biorxiv.org
    Vitamin D Obesity Aging Metabolism Hormones Muscle

    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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  • The gut microbiome alters the brain's response to tempting foods, affecting dietary choices. www.sciencedaily.com
    Brain Obesity Microbiome Prebiotics

    The brain’s reward centers react more strongly to the sight of tempting food than to less tempting options, driving food choices. Evidence suggests the gut microbiome influences these neural activity patterns, ultimately modulating body weight and metabolic health. A recent study found that inulin, a prebiotic derived from chicory root, alters the gut microbiome, reducing the intensity of the brain’s reward system activation.

    Researchers gave 59 overweight young to middle-aged adults 30 grams of inulin or a placebo every day for two weeks. Then, the participants underwent functional MRI scans while viewing images of various foods and rating the foods' desirability. Finally, they ate the most desired food and underwent more MRIs. After a two-week break, they switched to the alternate treatment. The researchers collected blood and fecal samples from the participants before and after the two interventions.

    They found that the participants' reward-related brain activation in response to high-calorie food stimuli decreased after consuming the prebiotic inulin. A shift in the gut microbial composition accompanied these changes.

    These findings suggest that prebiotics influence dietary choices via alterations in the gut microbiome. They also highlight the complex interplay between the gut, brain, and the body’s microbial partners. Learn more about the gut microbiome in this episode featuring Dr. Eran Elinav.

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  • Jet lag causes rats to overeat, linking circadian rhythm disruption to altered appetite regulation and weight gain. www.sciencedaily.com
    Obesity Sleep Hormones Circadian Rhythm

    Circadian rhythms regulate the body’s many physiological processes, including those influencing appetite. Disrupted rhythms, such as those occurring with shift work or jet lag, can alter appetite, contributing to weight gain. A recent study showed that rats with jet lag ate 460 percent more food during their resting phase than non-jet-lagged rats.

    Researchers studied two groups of rats: one that experienced typical light/dark cues (a control group) and one that experienced reversed cues (a “jet-lagged” group) for five days. They monitored the animals' food intake and measured levels of glucocorticoids, a class of hormones that regulate behavior, sleep-wake cycles, and metabolism.

    They found that jet-lagged animals demonstrated dysregulated orexigenic hypothalamic neuropeptide, a glucocorticoid hormone that regulates appetite. This dysregulation increased their desire to eat during their inactive phase (when they typically rest), consuming 460 percent more food than the control group. The overeating rats didn’t gain weight during the study period, likely due to the short duration.

    These findings suggest that circadian rhythm disruption alters glucocorticoid levels in rats, driving increased food consumption. Although the animals didn’t gain weight during the study, longer disruption (as in shift work) may drive considerable weight gain. The study’s authors posited that maintaining a consistent daily schedule and regular meals may help mitigate the effects of circadian rhythm disruption. Learn more about how shift work and jet lag influence circadian rhythms in this clip featuring Dr. Satchin Panda.

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  • Impairment of associative learning caused by obesity and insulin insensitivity offset by anti-obesity drug liraglutide in recent study www.sciencedaily.com
    Obesity Diabetes Memory

    Associative learning is a psychological process that occurs when two initially unrelated elements, such as objects, sights, sounds, ideas, or behaviors, become linked in the brain. Classic examples include associating pain with touching a hot stove or connecting foodborne illness with eating a particular food. People with obesity and poor insulin sensitivity have impaired associative learning. However, a recent study shows that liraglutide, a drug used to treat type 2 diabetes and obesity, restores associative learning capability in people with obesity.

    The study involved 54 adults, half with normal body weight (high insulin sensitivity) and half with obesity (reduced insulin sensitivity). Researchers gave participants either liraglutide or a placebo in the evening and tested their learning abilities the next morning.

    They found that people with obesity and reduced insulin sensitivity encountered difficulties when attempting to establish connections between sensory signals, and their brain activity related to learning was weaker than in normal-weight individuals. However, just one dose of liraglutide reversed these issues in people with obesity and reduced insulin sensitivity, exhibiting brain activity comparable to that of normal-weight participants, indicating that the drug improved their learning abilities.

    Liraglutide is a glucagon-like peptide 1 receptor agonist (GLP-1RA), a type of drug used to treat type 2 diabetes, overweight, and obesity. GLP-1RA medications work in the pancreas to lower blood glucose levels by promoting the production and release of insulin. They also support beta cells synthesis, growth, and survival while reducing their apoptosis rate.

    These findings suggest that liraglutide, an anti-obesity drug, affects brain activity in people with obesity and reduced insulin sensitivity. This study was small, however, so validating the results requires more research.

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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
    Brain Obesity Aging Dementia Sulforaphane Weight Loss Neurodegeneration

    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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  • Study reveals a sixfold decrease in C-reactive protein levels among obese women who took omega-3s during pregnancy. www.ncbi.nlm.nih.gov
    Obesity Omega-3 Inflammation Pregnancy Supplements CRP

    Pregnant women with obesity often experience high levels of inflammation. But a new study shows that omega-3s may reduce inflammation during pregnancy. Women with obesity who took omega-3 fatty acids during their pregnancies experienced a sixfold reduction in C-reactive protein, a marker of inflammation.

    The study involved 49 pregnant women with obesity. Half of the women took an omega-3 supplement providing 800 milligrams of docosahexaenoic acid (DHA) and 1,200 milligrams of eicosapentaenoic acid (EPA) daily, starting before week 16 of their pregnancies and continuing until delivery. The other half took a placebo containing wheat germ oil. Researchers measured the women’s inflammatory biomarkers before and after the intervention.

    They found that the women’s omega-3 levels increased markedly following the intervention, and their C-reactive protein levels decreased sixfold. Inflammatory gene expression in adipose and placental tissues also decreased.

    These findings suggest that omega-3 fatty acids reduce inflammation in pregnant women with obesity, aligning with evidence demonstrating that omega-3 fatty acids modulate inflammation by inhibiting the production of pro-inflammatory cytokines and eicosanoids. Furthermore, byproducts of omega-3 metabolism called specialized pro-resolving mediators, or SPMs, help resolve inflammation. Learn more about SPMs in this clip featuring omega-3 expert Dr. Bill Harris.

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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
    Obesity Aging Metabolism Alcohol

    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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  • Obesity disrupts the brain's sensing of glucose and lipid signals; MRIs reveal dysregulation and altered dopamine release, which persists even after w www.genengnews.com
    Nutrition Brain Obesity

    Signals from the foods we consume help regulate eating behaviors, such as whether we should stop or continue eating. A new study has found that obesity diminishes the brain’s responses to these signals, and weight loss doesn’t correct the problem.

    The study involved 60 participants: 30 with a healthy body weight and 30 with obesity. To avoid the influence of taste or preference cues on brain activity, they infused glucose, lipids (fats), and water (as a control) directly into the participants' stomachs. Then they measured the participants' brain activities and dopamine release in the striatum, an area involved in reward and motivation. To determine whether weight loss influenced this brain activity, they repeated the experiment 12 weeks later, after the participants achieved a 10 percent weight loss through dieting.

    They found that the brain responded to glucose and lipids in participants with healthy body weight. However, obesity impaired the brain’s response to these nutrients. Interestingly, the impaired brain responses did not improve, even after successful weight loss.

    These findings suggest that impaired brain responses to the signals sent after eating may contribute to overeating and obesity. They also provide insights into why many people struggle to maintain weight loss, as their brains continue to resist these signals even after significant weight reduction.

    Notably, this was a relatively small study, and the amount of weight loss – just 10 percent – might have been insufficient to induce global changes in the brain regarding nutrient sensing. Future studies that include more participants and induce greater weight loss may provide different results.

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  • Vitamin D may be critical in building strong muscles and combating obesity. www.biorxiv.org
    Vitamin D Obesity Muscle

    Poor strength and muscle mass are linked with many disease states, including obesity, diabetes, and chronic inflammation. A new study in mice shows that vitamin D is critical in building and maintaining muscle. Mice with higher vitamin D levels had greater strength and muscle mass and less fat mass than those with lower levels.

    Researchers fed mice three different diets over a period of 12 weeks to induce deficient, normal, and high blood concentrations of vitamin D. They measured the animals' strength and body composition before and after each dietary intervention. They also measured levels of myostatin (a hormone that inhibits muscle growth) and leptin (a hormone that maintains bodyfat stores) in the animals' blood.

    They found that vitamin D-deficient mice had poor strength and low muscle mass. Boosting vitamin D levels to normal (20-30 ng/mL) increased the animals' muscle strength but did not increase muscle mass. However, raising vitamin D to high concentrations increased both strength and muscle mass. This increase occurred without a corresponding weight increase but with a decrease in fat mass, implying that vitamin D redistributed dietary calories from fat to muscle. Higher vitamin D concentrations were associated with reductions in myostatin levels and increases in leptin levels.

    These findings suggest that high vitamin D concentrations decrease myostatin production and increase leptin production, redirecting excess calories to muscle growth instead of fat storage. Learn more about the health benefits of vitamin D in our comprehensive overview article.

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  • Overeating during pregnancy and breastfeeding may prime offspring for overeating and weight gain later in life. www.sciencedaily.com
    Obesity Pregnancy

    Exposure to a high-fat, obesogenic diet during pregnancy and breastfeeding may contribute to poor eating habits and obesity later in life, a new study in mice shows. Mice whose mothers ate an unhealthy diet tended to overeat and gain more weight than mice whose mothers ate a healthy diet.

    Researchers fed female mice one of two diets – a high-fat, obesogenic chow, or a balanced, healthy chow – before, during, and after their pregnancies and lactation. After weaning, the animals' pups were given unlimited access to healthy chow initially and then allowed unlimited access to the high-fat obesogenic chow. The researchers monitored the pups' food intake and body weights and studied their brain connections.

    The pups whose mothers ate the high-fat diet were heavier at birth than those whose mothers ate the healthy chow, but their weights normalized after eating the healthy chow. When given access to the high-fat chow, both groups of pups overate and gained weight. However, the pups whose mothers had eaten the high-fat chow overate more (and subsequently gained more weight) than those whose mothers ate the healthy chow, due to differences in brain connections – a consequence of overnutrition during pregnancy and lactation.

    These findings suggest that overnutrition during pregnancy primes offspring for adult overeating and weight gain. Learn about other ways in which parental health influences offspring health in this clip featuring Dr. Elissa Eppel.

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  • The effects of obesity on the brain mirror those of Alzheimer's disease. www.sciencedaily.com
    Brain Alzheimer's Obesity Aging

    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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  • Early-life obesity increases the risk of macular degeneration later in life. www.sciencedaily.com
    Obesity Metabolism Inflammation Immune System Eyes

    Obesity in early life induces changes in immune cells that may increase the risk of macular degeneration later in life, a study in mice has found. These changes linger even after weight loss and the restoration of normal metabolism.

    Researchers fed mice a diet that promoted weight gain early in life. Then they studied the effects of having excess body fat on the animals' adipose tissue macrophages – a type of immune cell found in fat. Later, they put the mice on a diet that promoted weight loss.

    They found that having excess body fat induced epigenetic changes in the macrophages that, in turn, induced an inflammatory response. This pro-inflammatory response persisted even after the mice lost weight. They also found that the macrophages could migrate from the fatty tissue to other parts of the body, including the eyes, where they could contribute to the onset of macular degeneration.

    Macular degeneration is the leading cause of blindness worldwide. Having excess body fat is the second leading risk factor for macular degeneration. In fact, a person’s risk of developing macular degeneration increases by 75 percent with each 0.1 increase in their waist-to-hip ratio – a measure of abdominal obesity.

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  • Estrogen's effects on fat-mobilization promotes a pear shape in pre-menopausal women, but may promote abdominal accumulation after menopause. www.sciencedaily.com
    Exercise Obesity Hormones Fat Estrogen

    From the article:

    Gavin and her colleagues recruited 17 overweight-to-obese premenopausal women, all between the ages of 18 and 44 years old. […] Participants performed this [submaximal] exercise both by itself and while the [fat-mobilizing] drugs were being infused. To test the effects of estrogen, the researchers also performed each of these conditions while estrogen was also being slowly infused into participants' fat deposits.

    Results

    The researchers found that estrogen’s effects differed tremendously depending on the fat-mobilizing interventions themselves and where the fat deposit was located. For example, estrogen blunted fat breakdown in the abdomen if it was infused while a particular fat-mobilization drug called isoproterenol was also being infused, but it didn’t have this effect in the buttocks. When a second fat mobilizing drug was given along with the first while participants were at rest, fat breakdown didn’t change any further. However, when both drugs were injected together during exercise or when the volunteers exercised without the drugs, fat breakdown increased in the abdomen, but less so in the buttocks.

    Importance of the Findings

    These results suggest that estrogen has different effects within fat tissue depending on its location. Together, these effects could help maintain premenopausal women’s “pear” shape even in the face of exercise or other signals the body receives to break down fat. They could also help generate some new ideas on how estrogen in fat may influence why postmenopausal women tend to accumulate more fat in the abdomen.

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  • Estrogen-sensitive brain circuit may help women control obesity by stimulating physical activity and thermogenesis, animal study suggests. (2022) www.sciencedaily.com
    Brain Obesity Metabolism Hormones Estrogen Thermogenesis

    From the article:

    The team reveals in the journal Science Advances an estrogen-activated neurocircuit that stimulates thermogenesis, or body heat production, and physical activity in animal models. The circuit begins in neurons located in a region of the hypothalamus called the ventrolateral subdivision of the ventromedial hypothalamic nucleus (vlVMH). These neurons interact with estrogen via estrogen receptor-alpha (ER-alpha) and respond to the hormone by connecting to and communicating with serotonin-producing neurons located in another brain region called dorsal raphe nucleus (DRN).

    The circuit not only responds to estrogen, but also to changes in ambient temperature and in the nutritional status of the animal. Interestingly, the circuit seems to be functional in males but, at this point, its physiological relevance is not clear.

    […]

    “For example, the circuit can be activated when it’s cold, stimulating thermogenesis and physical activity, which would help the animal stay warm,” Xu said. “The circuit can be inhibited when the animal is hungry, which would shut down thermogenesis and physical activity, saving energy to adapt to the lack of nutrients.”

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  • Estrogens may act on distinct hypothalamic neurons to regulate energy homeostasis and reproduction, mouse study suggests. (2011) www.sciencedaily.com
    Brain Obesity Metabolism Hormones Estrogen Neuron Metabolic Syndrome

    From the article:

    “When women approach menopause, they gain weight in fat and their energy expenditure goes down,” says Deborah Clegg of the University of Texas Southwestern Medical Center. Estrogen levels decline and women grow increasingly susceptible to obesity and metabolic syndrome.

    Estrogen acts on receptors found throughout the body, in fat, on ovaries and in muscle. But when it comes to the hormone’s influence on metabolism, Clegg suspected receptors in the brain.

    […]

    The researchers showed female mice lacking ERα [estrogen receptor-α (ERα)] in one part of the brain (the hypothalamic steroidogenic factor-1 or SF1 neurons) gained weight without eating any more. Loss of ERα from another brain area (the hypothalamic pro-opiomelanocortin or POMC neurons) had the opposite effect: animals ate more without gaining weight. Loss of ERα receptors in those same neurons also led to various problems in ovulation and fertility.

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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
    Obesity Aging Mortality Metabolic Syndrome

    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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  • Heavy drinking into older age adds 4 cm to waistline www.sciencedaily.com
    Obesity Alcohol Metabolic Syndrome

    Heavy drinking in later life increases stroke risk and contributes to a larger waist circumference.

    Heavy drinking into one’s later life could add more than two inches to their waistline, a new study finds. Drinking heavily also contributes to a greater risk of cardiovascular disease and liver dysfunction.

    Researchers asked more than 4,800 people (average age, 69 years) living in the United Kingdom about their alcohol consumption habits. They also took their body measurements and collected information about their overall health.

    They found that people who drank heavily in later life were more likely to have higher blood pressure, higher stroke risk, and worse liver function than non-heavy drinkers. Heavy lifetime drinkers were also more likely to have a larger waist circumference – as much as 5.47 centimeters (~2.15 inches) larger – even if they cut back on their alcohol consumption before the age of 50.

    Other research has shown that heavy drinking contributes to a large waist circumference, which is associated with a greater risk for cardiovascular disease and type 2 diabetes. Cutting back on alcohol consumption may help reduce waist circumference. Learn how exercise can help reduce cravings for alcohol.

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  • Several environmental and lifestyle factors can lower testosterone levels. (2020) www.tandfonline.com
    Vitamin D Diet Obesity Sleep Hormones Stress Magnesium Testosterone Zinc Polyphenol Oxidative Stress

    From the publication:

    Many factors, including external, environmental and internal factors, influence testosterone levels. The impact of energy intake derived from a testosterone-boosting diet depends on a human body mass. In the case of people of healthy body mass, insufficient energy intake may result in a reduction in testosterone levels in men. The same energy deficit in obese people, may, in turn, result in a neutral or positive impact on the levels of the hormone. Undoubtedly, nutritional deficiency, and particularly of such nutrients as zinc, magnesium, vitamin D, together with low polyphenols intake, affects the HPG [hypothalamic–pituitary–gonadal] axis. The levels of mental and oxidative stress can also adversely impact the axis. The higher the cortisol levels in a human body, or the higher its daily fluctuation, the lower the testosterone levels. What is more, the effect seems to be strengthened by excessive body weight, which is related to the increased oxidative stress affecting the functions of the Leydig cells. Other factors which might disrupt testosterone synthesis may be the length and quality of sleep. Even though the issue is relatively unknown, it appears that both sleep deprivation (shorter than five hours) and low quality of sleep (sleeping with the light on, sleeping during the day, under the influence of alcohol) impact the testosterone levels negatively.

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  • Testosterone therapy may play a small role in temporarily exacerbating or inducing changes in obstructive sleep apnea. (2021) www.sciencedirect.com
    Obesity Sleep Hormones Testosterone Weight Loss

    From the publication:

    The best current evidence suggests that short-term, high-dose testosterone administration mildly worsens OSA [obstructive sleep apnea]. Longer-term TTh [testosterone therapy] in subjects undergoing concomitant weight loss was shown to mildly worsen OSA but only initially. By 18 weeks, patients demonstrated return to baseline levels of OSA risk. These results suggest that TTh’s role in exacerbating OSA is small and may be time limited. However, it is also possible that weight loss acted as a confounding factor. Additional studies are needed to determine if men who are more obese at baseline have a higher risk of developing OSA with TTh than nonobese men. Why testosterone would have a timedependent effect, however, remains unanswered. Regarding the mechanisms by which TTh may worsen OSA, anatomic TTh-induced airway changes and altered sleep stage architecture have been largely refuted. The mechanism of action is more likely related to altered hypoxic and hypercapnic ventilatory response with testosterone administration, though work is still needed to resolve inconsistencies in currently available studies. Until these questions are more fully understood, clinicians may choose to exercise caution in prescribing TTh to individuals with severe, untreated OSA.

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  • Obstructive sleep apnea may have a suppressive effect on serum testosterone levels in men, independent of BMI and age. (2021) onlinelibrary.wiley.com
    Obesity Sleep Hormones Testosterone

    Sleep apnea increases the risk of low testosterone.

    Men with sleep apnea are more likely to have low testosterone levels, according to a 2021 study. Men with severe apnea are at the greatest risk of low testosterone.

    Researchers reviewed the findings of 18 studies involving more than 1,800 men that examined links between sleep apnea and male testosterone levels. Then they analyzed a subset of the studies after matching the men’s age, body mass index, and severity of their sleep apnea.

    They found that the men with sleep apnea were more likely to have low testosterone levels, even after considering their age and body mass index. However, the subset analysis revealed that this relationship was only notable for those with severe apnea.

    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.

    This review identifies links between sleep apnea and testosterone levels. It also underscores the importance of diagnosing and treating sleep apnea, particularly among men whose apnea is more severe.

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  • Testosterone levels improved in obese men following a common weight-loss operation. (2015) www.eurekalert.org
    Obesity Hormones Testosterone Weight Loss

    From the article:

    The aim of the study was to investigate the effect of surgical weight loss following sleeve gastrectomy [removement of about 75 percent of the stomach] on serum testosterone, DHEA (a precursor to testosterone), and prostate-specific antigen (PSA). This clinical study involved 24 obese male patients undergoing gastric sleeve surgery, also called sleeve gastrectomy, at Stanford Hospital. Serum testosterone, DHEA, and PSA were measured before and at three, six, and 12 months after the procedure.

    The researchers found that the study group experienced a significant increase in average serum testosterone after undergoing sleeve gastrectomy. At 12 months, testosterone had increased on average from 295 to 423 ng/dL. The normal range for circulating testosterone is 300 to 1000 ng/dL. A person is diagnosed with low serum testosterone when the level drops below 300 ng/dL.

    Before the procedure, 63 percent of participants had low testosterone and afterwards, only 41 percent did. The average BMI was 46 before surgery and 31 after the operation. In addition, DHEA also rose, from 12.8 to 39.6 ng/mL, and serum PSA concentration rose over 12 months from 0.62 to 0.75 ng/mL with no change in PSA mass, which is a marker for prostate cancer progression.

    […]

    “When you are obese, your fat becomes converted to estrogen, which will compete with testosterone and drive it down,” Dr. Morton said. “The nice thing about what this process does is it creates an autotransfusion of testosterone from yourself. This process occurs because you are losing weight, and therefore losing that estrogen, causing your natural testosterone stores to rise. It’s actually really helpful across the board for these patients.”

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  • Obese teen boys showed up to 50 percent less testosterone than lean boys. (2012) www.sciencedaily.com
    Obesity Hormones Sex Testosterone Weight Loss

    From the article:

    We were surprised to observe a 50 percent reduction in testosterone in this pediatric study because these obese males were young and were not diabetic,“ says Paresh Dandona, MD, PhD, SUNY Distinguished Professor in the Department of Medicine, chief of the Division of Endocrinology, Diabetes and Metabolism in the UB medical school and first author on the study. "The implications of our findings are, frankly, horrendous because these boys are potentially impotent and infertile,” says Dandona. “The message is a grim one with massive epidemiological implications.”

    The small study included 25 obese and 25 lean males and was controlled for age and level of sexual maturity. Concentrations of total and free testosterone and estradiol, an estrogen hormone, were measured in morning fasting blood samples. The results need to be confirmed with a larger number of subjects, Dandona says.

    […]

    “The good news is that we know that testosterone levels do return to normal in obese adult males who undergo gastric bypass surgery,” says Dandona. “It’s possible that levels also will return to normal through weight loss as a result of lifestyle change, although this needs to be confirmed by larger studies.”

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  • In overweight and obese men, higher testosterone levels may be associated with poorer sleep quality. (2014) www.sciencedaily.com
    Obesity Sleep Hormones Testosterone

    From the publication:

    The research team performed a polysomnogram, or overnight sleep study, in 44 men ages 20 to 50 years who were overweight or obese. All subjects were otherwise healthy and were nonsmokers. Their selection for the study did not consider whether they had symptoms or a history of sleep apnea, according to Van Cauter. However, the sleep study showed that 29 (66 percent) of the men did have OSA [obstructive sleep apnea], which she said was moderately severe in most cases.

    […]

    Later analyses demonstrated that higher total testosterone level strongly correlated with more shallow sleep. This association, Van Cauter said, was independent from the presence of other factors known to decrease sleep quality, such as age, race/ethnicity and OSA [obstructive sleep apnea] severity.

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  • Weight loss reduced the prevalence of low testosterone levels in overweight, middle-aged men with prediabetes by 46%. (2012) www.sciencedaily.com
    Obesity Hormones Diabetes Testosterone Weight Loss

    From the article:

    The study population had 891 middle-aged men, with an average age of 54 years. The men were randomly assigned to receive one of three treatments: 293 men to lifestyle modification, 305 to the diabetes drug metformin and 293 to inactive placebo pills. Lifestyle modifications consisted of exercising for 150 minutes a week and eating less fat and fewer calories.

    The results showed that low testosterone levels are common in overweight men with prediabetes, Hayes said. At the beginning of the study, nearly one in four men had low testosterone levels, considered to be below 300 nanograms per deciliter.

    With lifestyle modification, the prevalence of low testosterone levels decreased from about 20 percent to 11 percent after one year, a 46 percent decrease, the authors reported. The prevalence of low testosterone was unchanged in the metformin group (24.8 versus 23.8 percent) and the placebo group (25.6 versus 24.6 percent).

    Men in the lifestyle modification group lost an average of about 17 pounds (7.8 kilograms) over the one-year study, according to the abstract. The increase in testosterone levels in that group correlated with decreasing body weight and waist size.

    “Losing weight not only reduces the risk of prediabetic men progressing to diabetes but also appears to increase their body’s production of testosterone,” Hayes said.

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  • Low testosterone levels may herald rheumatoid arthritis in men. (2013) www.sciencedaily.com
    Obesity Hormones Inflammation Testosterone Tobacco Arthritis

    From the article:

    Sex hormones are thought to play a part in the development of rheumatoid arthritis, and both men and women with the condition tend to have lower levels of testosterone in their blood than healthy people. But it is not clear whether this is a contributory factor or a consequence of the disease.

    The researchers based their findings on participants of the Swedish Malmo Preventive Medicine Program (MPMP), which began in 1974 and tracked the health of more than 33,000 people born between 1921 and 1949.

    […]

    After taking account of smoking and body mass index, both of which can affect the risk of rheumatoid arthritis, **men with lower levels of testosterone in their blood samples were more likely to develop the disease.

    This was **statistically significant for those who tested negative for rheumatoid factor when they were diagnosed.

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  • In overweight men with vitamin D deficiency, testosterone levels increased significantly after taking 3320 IU of vitamin D daily for one year. (2011) pubmed.ncbi.nlm.nih.gov
    Vitamin D Obesity Hormones Testosterone

    From the publication:

    Healthy overweight men undergoing a weight reduction program who participated in a randomized controlled trial were analyzed for testosterone levels. The entire study included 200 nondiabetic subjects, of whom 165 participants (54 men) completed the trial. Participants received either 83 μg (3,332 IU) vitamin D daily for 1 year (n = 31) or placebo (n =2 3). Initial 25(OH)D concentrations were in the deficiency range (< 50 nmol/l) and testosterone values were at the lower end of the reference range (9.09-55.28 nmol/l for males aged 20-49 years) in both groups. Mean circulating 25(OH)D concentrations increased significantly by 53.5 nmol/l in the vitamin D group, but remained almost constant in the placebo group. Compared to baseline values, a significant increase in total testosterone levels (from 10.7 ± 3.9 nmol/l to 13.4 ± 4.7 nmol/l; p < 0.001), bioactive testosterone (from 5.21 ± 1.87 nmol/l to 6.25 ± 2.01 nmol/l; p = 0.001), and free testosterone levels (from 0.222 ± 0.080 nmol/l to 0.267 ± 0.087 nmol/l; p = 0.001) were observed in the vitamin D supplemented group. By contrast, there was no significant change in any testosterone measure in the placebo group. Our results suggest that vitamin D supplementation might increase testosterone levels. Further randomized controlled trials are warranted to confirm this hypothesis.

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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
    Obesity Aging Hormones Depression Mental Health Sex Testosterone

    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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  • Testosterone-deficient men on testosterone therapy lost 6.6 pounds more body fat while dieting but maintained muscle mass. (2016) www.sciencedaily.com
    Diet Obesity Hormones Fat Testosterone Muscle

    From the article:

    For the first 10 weeks, all participants were placed on a strict 600 kcal per day very-low calorie diet. They were also encouraged to abstain from alcohol and perform at least 30 minutes a day of moderate exercise. From the 11th through the 56th week, participants in both groups used a weight-maintenance diet based on the Australian Commonwealth Scientific and Industrial Research Organisation (CSIRO) Total Wellbeing Diet comprising of normal foods.

    Every 10 weeks over the 56-week-long study, 49 men also received injections of 1,000mg of intramuscular testosterone undecanoate, and 51 took placebo.

    At the end of 56 weeks, both groups lost roughly 11 kg (24.2 lb). But those in the testosterone group lost almost exclusively fat, while those on placebo lost both lean and fat. The men taking testosterone lost 3 kg (6.6 lb) more body fat than those on placebo and maintained their muscle mass, while those on placebo lost 3.5 kg (7.7 lb) of muscle mass.

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  • In a study, 40% of obese and 50% of obese diabetic participants had low testosterone levels. (2010) www.sciencedaily.com
    Obesity Hormones Diabetes Testosterone

    From the article:

    Results of a study published online ahead of print in the journal Diabetes Care, conducted by University at Buffalo endocrinologists, showed that 40 percent of obese participants involved in the Hypogonadism in Males (HIM) study had lower-than-normal testosterone readings.

    The percentage rose to 50 percent among obese men with diabetes. Results also revealed that as body mass index (BMI) – a relationship of weight-to-height – increased, testosterone levels fell.

    “The effect of diabetes on lowering testosterone levels was similar to that of a weight gain of approximately 20 pounds,” says Sandeep Dhindsa, MD, an endocrinology specialist in the UB Department of Medicine and first author on the study.

    […]

    This is the largest analysis of the association between obesity and low testosterone, and the first to compare prevalence of low testosterone with obesity and diabetes separately and together. The study shows that obesity and diabetes may exert independent influences on testosterone concentrations.

    […]

    UB endocrinologists published a study in Diabetes Care in 2008 showing that more than 50 percent of men between 18 and 35 years old with type 2 diabetes had lower than normal testosterone levels.

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  • In a study of men with low testosterone, 56% of study participants suffered from depression or showed depressive symptoms. (2015) www.sciencedaily.com
    Obesity Sleep Hormones Depression Mental Health Sex Testosterone

    From the article:

    The research, slated to publish online on July 1 in the Journal of Sexual Medicine, involved 200 adult men, aged 20-77, with a mean age of 48 years old, who were referred for borderline total testosterone levels between 200 and 350 ng/dL. Information gathered included demographics, medical histories, medication use, signs and symptoms of hypogonadism, and assessments of depressive symptoms and/or a known diagnosis of depression or use of an antidepressant.

    Depression and/or depressive symptoms were present in 56 percent of the subjects. Furthermore, one quarter of the men in the study were taking antidepressants and that the men had high rates of obesity and low rates of physical activity. The most common symptoms were erectile dysfunction, decreased libido, fewer morning erections, low energy, and sleep disturbances.

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  • Omega-3 supplementation altered interleukin-6 levels by -12% (vs +36% in placebo group) and TNF-α by -2.3% (vs +12% in placebo group). (2012) www.sciencedaily.com
    Obesity Omega-3 Inflammation IL-6 TNF-Alpha

    From the article:

    The scientists recruited 138 adults – 45 men and 93 women – who were in good health, but who were either overweight or obese and lived sedentary lives. Their average age was 51 years. Based on body mass index, a measure of weight relative to height, 91 percent of the participants were overweight and 47 percent were obese.

    […]

    Participants received either a placebo or one of two different doses of omega-3 fatty acids – either 2.5 grams or 1.25 grams per day. The supplements were calibrated to contain a ratio of the two fish oil fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), of seven to one. Previous research has suggested that EPA has more anti-inflammatory properties than does DHA.

    After four months, participants who had taken the omega-3 supplements had significantly lower levels in their blood of two proteins that are markers of inflammation, also called pro-inflammatory cytokines. The low-dose group showed an average 10 percent decrease in the cytokine interleukin-6 (IL-6), and the high-dose group’s overall IL-6 dropped by 12 percent. In comparison, those taking a placebo saw an overall 36 percent increase in IL-6 by the end of the study.

    Levels of the cytokine tumor necrosis factor-alpha (TNF-a) also dropped, but in a more modest way, by 0.2 percent and 2.3 percent in the low- and high-dose groups, respectively. The placebo group’s TNF-a increased by an average of 12 percent.

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  • New insights on how some individuals with obesity can lose weight medicalxpress.com
    Exercise Obesity Mitochondria

    Exercise boosts mitochondrial function and promotes weight loss among people who struggle to lose weight with dieting alone.

    Most weight loss programs focus on reducing caloric intake. Although this strategy works for many people, a subset of people with obesity are diet-resistant – failing to lose weight even when adhering to a low-calorie diet. Findings from a new study suggest that exercise promotes weight loss in diet-resistant women by boosting mitochondrial function.

    Mitochondria are tiny cellular organelles that produce energy in the presence of oxygen. They are often referred to as the “powerhouses of the cell” because of their role in the production of ATP. Mitochondrial dysfunction, the disruption of normal mitochondrial function that occurs over time, is a driver of many chronic diseases, such as cancer, type 2 diabetes, and cardiovascular disease, and is a hallmark of aging.

    The investigators enrolled 20 women with obesity for the study. Half of the women had exhibited diet resistance when following a 900-calorie-per-day diet, while the other half had exhibited diet sensitivity. Both groups participated in a supervised, six-week exercise program that included both aerobic and resistance exercises, performed three times per week. The investigators assessed the women’s body composition and metabolic markers and collected muscle tissue samples for biopsy.

    They found that at the end of the six-week exercise program, the women who were diet resistant exhibited improved body composition and muscle metabolism and increased numbers of muscle mitochondria. The exercise program elicited only minimal effects in women who were diet sensitive. Interestingly, the diet-sensitive women exhibited risk factors associated with metabolic syndrome, suggesting that diet-sensitive obesity confers a greater risk for cardiometabolic disease.

    These findings demonstrate that exercise promotes weight loss and metabolic health in women with obesity and diet resistance and may confer greater health benefits than rapid diet-induced weight loss. Learn more about the benefits of exercise in our overview article.

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  • Babies Breastfed for a Year or More Better Protected Against Adult Obesity www.newsweek.com
    Obesity Development Breast Milk

    Breastfeeding for a year or longer protects infants against obesity in later life.

    Obesity is a condition in which a person has too much body fat. Having obesity increases a person’s risk for many chronic diseases, including diabetes, heart disease, cancer, and others. New research suggests that breastfeeding for a year or longer protects infants against obesity in later life.

    Breastfeeding is the biologically superior way to feed an infant. The American Academy of Pediatrics recommends exclusive breastfeeding for the first six months of an infant’s life and then continued breastfeeding while introducing age-appropriate foods until an infant is 12 months old or older. This provides the infant optimal nutrition and immunity while supporting growth and development.

    To model short-term versus long-term breastfeeding in humans, the investigators weaned one group of rat pups at three weeks of age (typical weaning time) and another group at four weeks of age (delayed weaning time, comparable to a year or more in humans). Once the animals were weaned, half of each group were fed a normal diet, and half were fed a high-fat diet until they reached adulthood. The investigators measured the animals' bodyweight, analyzed their body composition, and measured their energy expenditure.

    They found that rats that ate a normal diet and were weaned at the typical and delayed times did not differ in terms of bodyweight in adulthood. But rats that had a delayed wean time and were fed a high-fat diet were leaner than those that were weaned at the typical time and fed a high-fat diet. The delayed rats also had higher energy expenditures and more active brown fat, a type of fatty tissue involved in thermogenesis, or heat production. The delayed rats' brown fat contained higher quantities of various proteins involved in thermogenesis, including fibroblast growth factor 21 (FGF21). FGF21 activates neurons in the brain involved in metabolic regulation.

    These findings suggest that prolonged breastfeeding protects against obesity in later life, likely mediated by the influence of FGF21 on metabolic regulation. Learn more about the beneficial effects of breastfeeding for both infants and mothers 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
    Obesity Epigenetics Aging Metabolic Syndrome

    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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  • 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
    Obesity Aging Metabolism Inflammation Immune System Metabolic Syndrome IL-6

    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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  • Lost memory in menopause explained: Estrogen provides a protective role in mitigating effects of visceral fat on brain structural networks and memory jamanetwork.com
    Brain Alzheimer's Obesity Memory Estrogen Visceral Fat

    Estrogen mitigates the association between visceral fat on cognitive decline.

    Estradiol, a form of estrogen, is the primary female sex hormone. It participates in menstrual cycle regulation and drives the development of female secondary sex characteristics, such as breasts, a wider pelvis, and gynoid fat – fat that forms around the hips, thighs, and breasts. Evidence suggests that estradiol exerts both cardioprotective and neuroprotective effects. Findings from a 2020 study demonstrate that estradiol mitigates the association between visceral fat on cognitive decline.

    Cognitive decline is characterized by altered brain structural networks and accelerated degeneration with aging. Scientists don’t fully understand the biological mechanisms that drive cognitive decline, but evidence indicates that visceral fat – a type of fat that accumulates in the abdominal cavity – may play a role. Visceral fat is metabolically active and is associated with increased markers of inflammation and oxidative stress, and decreased levels of anti-inflammatory proteins, such as adiponectin

    The cross-sectional study involved 974 cognitively healthy females and males (average age, ~50 years). Using magnetic resonance imaging, the investigators measured the participants' gray matter volume, cerebral cortex area, intracranial blood vessels, and visceral fat. They also measured estradiol concentrations in a subset (390) of the females. All the participants completed neuropsychological testing to assess memory performance.

    The investigators found that visceral fat exacerbated the harmful effects of aging on the brain’s structural networks in both females and males. However, estradiol mitigated some of these effects in the females, but not the males. Females between the ages of 35 and 55 years (the period surrounding menopause) who had lower estradiol concentrations were more likely to exhibit greater structural network impairments and worse memory performance.

    These findings suggest that estradiol mitigates some of the harmful effects of visceral fat on the brain’s structural networks and cognitive health. Interestingly, the fasting-mimicking diet preferentially depletes visceral fat. Learn more in this clip featuring Dr. Valter Longo.

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  • Gut microbiota predicts body fat change following a low-energy diet. genomemedicine.biomedcentral.com
    Diet Obesity Microbiome

    Very low-calorie diets elicit extensive changes to the gut microbiota, influencing weight loss.

    Many popular diet programs emphasize calorie reduction as a means to lose weight. However, this approach to weight loss minimizes evidence suggesting that the gut microbiota plays important roles in body weight and likely influences the host’s metabolic response to diet. Findings from a recent study suggest that very low-calorie diets elicit extensive changes to the gut microbiota, influencing how much weight a person loses when dieting.

    Low-calorie diets (1,200 to 1,500 calories per day) and very low-calorie diets (less than 800 calories per day) have gained popularity in recent decades. These diets often rely on the use of meal replacements, typically in the form of ready-made meals, shakes, or bars. When combined with behavior modification, evidence suggests that low-calorie and very low-calorie diets are useful strategies for losing weight.

    The investigators drew on data from the PREVIEW study, a three-year lifestyle intervention study aimed at type-2 diabetes prevention. The current study involved more than 2,200 adults (aged 20 to 70 years) with overweight or obesity and pre-diabetes. Participants consumed a meal replacement that provided approximately 810 calories and 13 grams of fiber daily for eight weeks. They were also allowed to consume up to 400 grams (about 200 calories) of non-starchy vegetables daily. Before and after the intervention, participants provided fecal samples for microbial sequencing.

    The investigators observed that the overall makeup of the participants' gut microbial populations underwent considerable changes over the eight-week intervention. Not only did microbial numbers (termed “richness”) increase, but the diversity of microbes increased, as well. In addition, the numbers of bacteria that may be beneficial for metabolic health, such as Akkermansia and _ Christensenellaceae_, increased, but butyrate production decreased, an indication of fewer butyrate-producing microbes. Butyrate plays important roles in maintaining gut health. These changes were correlated with changes in body fat and weight.

    These findings suggest that very low-calorie diets induce marked changes in the overall composition of microbes in the gut, influencing changes in body fat and weight. Other issues complicate weight loss, however. For example, excess body weight has profound, deleterious effects on the gut microbiome, driving dysbiosis and impairing critical aspects of nutrient metabolism. Of particular concern is the inability to metabolize flavonoids, some of which participate in fat metabolism. This dysbiosis persists, even after weight loss, likely promoting recurrent (or “yo-yo”) obesity. Learn more about this phenomenon in this clip featuring Dr. Eran Elinav.

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  • Strict 12-week keto without calorie counting: participants lost >5% percent body fat, 44% of their visceral fat, and 48% better insulin sensitivity www.sciencedaily.com
    Diet Obesity Ketosis Insulin Resistance Metabolic Syndrome Visceral Fat Ketogenic Diet

    This is a Jeff Volek study and used hard biomarkers, checking ketones daily.

    From the article:

    In the study, which appears in the journal Military Medicine, participants on the keto diet lost an average of almost 17 pounds and were able, with support of counselors, to maintain ketosis for 12 weeks. As a group, they lost more than 5 percent of their body fat, almost 44 percent of their belly, or visceral, fat and had a 48 percent improvement in insulin sensitivity – a marker that predicts risk of diabetes.

    […]

    The ketogenic diets in the study included no caloric restrictions, just guidance about what to eat and what to avoid. Carbs were restricted to about 30 to 50 grams daily, with an emphasis on nuts and non-starchy vegetables.

    […]

    Keto diet participants had near-daily check-ins during which they reported blood ketone measurements from a self-administered finger-prick test and received feedback, usually through text messages, from the research team. Ketosis was defined as a blood concentration of ketones, chemicals made in the liver, between 0.5 and 5.0 mM (millimolar).

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  • Visceral fat and total brain volume inversely linked independent of BMI and insulin resistance: a relationship between dementia and obesity www.sciencedaily.com
    Brain Obesity Insulin Resistance Metabolic Syndrome Visceral Fat

    From the article:

    Preliminary findings suggest a relationship between obesity and dementia that could lead to promising prevention strategies in the future.

    […]

    “Our results confirm the inverse association of increasing BMI with lower brain volumes in older adults and with younger, middle-aged adults and extends the findings to a much larger study sample,” […] “More importantly our data suggests a stronger connection between central obesity, particularly the visceral fat component of abdominal obesity, and risk of dementia and Alzheimer’s disease,” Dr. Seshadri added. The research showed the association between visceral adipose tissue and total brain volume was most robust and was also independent of BMI and insulin resistance."

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  • PCB exposure linked to increased visceral fat: "persistent compound PCB189 was related to a high proportion of fat in the abdomen" www.sciencedaily.com
    Obesity Pollution Metabolic Syndrome Visceral Fat

    Exposure to PCBs may increase visceral fat.

    Persistent organic pollutants are ubiquitous environmental toxicants that pose considerable threats to human health. These compounds typically degrade slowly and are often referred to as “forever compounds.” A 2012 study found that exposure to the organic pollutants polychlorinated biphenyls (PCBs) was associated with having increased visceral fat.

    PCBs were historically used in industrial and chemical applications, such as coolants, transformer insulators, capacitors, motors, paints, and electrical wire coatings. Although PCBs have been banned in the United States, the compounds are widespread in the environment. Exposure to PCBs is associated with an increased risk of adverse health effects, including many chronic disorders, such as cardiovascular disease, diabetes, hypertension, melanoma, and non-Hodgkin’s lymphoma. PCB exposure may also be linked to neurodegenerative disease PCBs bioaccumulate in human muscle and adipose tissue, brain, liver, and lungs and have long elimination half-lives, ranging from 10 to 15 years.

    The cross-sectional study involved more than 1,000 adults (70 years and older) living in Sweden. Participants provided information about their medical histories, education level, exercise habits, smoking habits, and medication use. A subset of 287 participants underwent magnetic resonance imaging to assess body fat location and quantity. Investigators collected blood samples from the participants to detect the presence of persistent organic pollutants.

    They found that higher blood concentrations of the organic pollutant PCB189, a highly chlorinated PCB, were associated with having greater quantities of visceral fat, suggesting that environmental exposures influence fat deposition in humans. Interestingly, PCB189 exposure and increased visceral fat are associated with type 2 diabetes, potentially providing a mechanistic link between body fat and diabetes risk.

    Although exposure to persistent organic pollutants is likely unavoidable, some PCBs are excreted in sweat. Sauna use, which induces copious sweating, may promote PCB excretion. Learn more about the beneficial health effects of sauna use in our overview article.

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  • Visceral fat may be less circadian than (healthier) subcutaneous fat: only subcutaneous showed circadian rhythmicity in insulin sensitivity www.sciencedaily.com
    Obesity Insulin Resistance Circadian Rhythm Insulin Metabolic Syndrome Visceral Fat

    From the article:

    Using samples of adipose tissue from both visceral fat and subcutaneous fat from 18 people who underwent gastric bypass surgery, researchers found that subcutaneous fat has an intrinsic circadian rhythm in insulin sensitivity. Insulin sensitivity reached its maximum around noon, and was more than 50 percent higher than at midnight. Interestingly, the rhythm was not observed in visceral fat.

    […]

    “Our study demonstrates that subcutaneous human fat tissue has an internal clock that is able to regulate insulin sensitivity even when outside of the body. This tissue rhythm matches well with what has been observed in humans overall when examining how people cope with a meal or sugar load,”

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  • Weighted vests may produce changes in body mass through perturbation of a homeostatic "gravitostat," a system regulating appetite by sensing weight www.sciencedaily.com
    Exercise Obesity Metabolic Syndrome

    Exploiting the “gravitostat,” a novel homeostatic mechanism that regulates body weight, promotes weight loss.

    Having overweight or obesity increases a person’s risk of developing many chronic diseases. But losing weight loss is challenging, partly due to homeostatic mechanisms that regulate body weight. Findings from a 2020 study suggest that exploiting a novel homeostatic weight-regulating mechanism called the gravitostat promotes weight loss in humans.

    The concept of the gravitostat first emerged in 2017, when scientists implanted small weights into the abdomens of mice and found that the animals’ food intake decreased, promoting weight loss and improving glucose tolerance. They suggested that the gravitostat regulates weight via a negative feedback system involving bone cells called osteocytes. Because osteocytes can sense changes in bone strain, the investigators proposed that increasing the animals’ body weight activated a biological sensor that communicated with the osteocytes of weight-bearing bones to drive changes in eating behaviors and subsequent weight loss.

    In the 2020 study, the investigators conducted a randomized controlled trial involving 69 adults with mild obesity (body mass index of 30-35). About half of the participants wore a heavy weighted vest (11 percent of their body weight) for eight hours every day for three weeks, while the other half wore a light vest (1 percent of their body weight). Before and after the intervention, the investigators weighed the participants and analyzed their body composition using bioelectrical impedance.

    They found that participants who wore the heavy vest lost an average of 1.37 percent more bodyweight than those who wore the light vest, translating to about 3.5 pounds. Those who wore the heavy vests also lost fat mass and gained fat-free mass. These findings suggest that the gravitostat regulates body weight in humans and exploiting it provides a possible strategy for losing weight.

    Overcoming other aspects of bodyweight homeostasis might still prove challenging, however. Research from Dr. Eran Elinav’s lab suggests that metabolic parameters normalize with weight loss, but characteristics of the microbiome remain unchanged. In other words, the microbiome holds a memory of past obesity that promotes weight regain. Preclinical studies indicate that repeated weight cycling shifts gut microbes to a configuration with an altered ability to metabolize flavonoids — compounds that usually help promote the burning of excess energy by adipose tissue. Learn more in this clip featuring Dr. Eran Elinav.

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  • Visceral fat intimately linked with the hypertensive effect of obesity: "only abdominal fat remained independently associated with hypertension" www.sciencedaily.com
    Obesity Blood Pressure Metabolic Syndrome Visceral Fat

    From the article:

    For this study, 903 patients enrolled in the Dallas Heart Study were followed for an average of seven years to track development of hypertension. […] Patients also received imaging of visceral fat, or fat located deep in the abdominal cavity between the organs; subcutaneous fat, or visible fat located all over the body; and lower-body fat.

    […]

    At the end of the study period, 25 percent of patients developed hypertension. While higher BMI was associated with increased incidence of hypertension, when abdominal fat content, overall fat content and lower-body fat content were factored in, only abdominal fat remained independently associated with hypertension.

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  • Retinol-binding protein 4 (RBP4) may be a biomarker for visceral fat accumulation: levels of RBP4 double or triple in concentration compared to normal www.sciencedaily.com
    Obesity Biomarkers Metabolic Syndrome Carotenoids Visceral Fat

    From the article:

    The researchers, including Barbara Kahn and Timothy Graham of Harvard Medical School and Matthias Blüher of the University of Leipzig in Germany, showed that “retinol-binding protein 4” (RBP4) is produced in much greater amounts by visceral fat compared to the subcutaneous fat that lies just beneath the skin. Moreover, they report that blood serum levels of RBP4 jump in people who are obese, who have double or even triple the concentrations found in individuals of normal weight.

    […]

    The only known function of RBP4 was to carry vitamin A (also known as retinol) in the blood, Kahn said.

    Large gene expression changes in visceral fat:

    n a study of 196 people, the researchers now reveal that RBP4 is indeed preferentially produced in the deep fat that covers organs of the belly. RBP4 gene expression activity levels spiked about 60-fold in the visceral fat of viscerally obese relative to lean study participants, they found. By comparison, visceral fat RBP4 concentrations were increased just 12-fold in obese individuals with a preponderance of subcutaneous fat.

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  • Removing the visceral fat in female mice reduces intestinal tumors and extends survival (a sex-specific effect) www.sciencedaily.com
    Cancer Obesity Metabolic Syndrome Visceral Fat

    From the article:

    “There has been some skepticism as to whether obesity per se is a bona fide cancer risk factor, rather than the habits that fuel it, including a poor diet and a sedentary lifestyle,” […] “Although those other lifestyle choices play a role, this study unequivocally demonstrates that visceral adiposity is causally linked to intestinal cancer.”

    There was a sex-specific effect:

    The researchers then subdivided the groups by gender. In female mice, the removal of visceral fat was significantly related to a reduction in intestinal tumors, but calorie restriction was not. In male mice, calorie restriction had a significant effect on intestinal tumors, but removal of visceral fat did not.

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  • Greater visceral and total body fat associated with vascular brain injury and impaired cognitive scores www.sciencedaily.com
    Brain Obesity Dementia Metabolic Syndrome Blood-Brain Barrier Small Vessel Disease Visceral Fat

    From the article:

    In the study, 9,166 participants were measured by bioelectrical impedance analysis to assess their total body fat.

    As well, 6,733 of the participants underwent magnetic resonance imaging (MRI) to measure abdominal fat packed around the organs known as visceral fat, and the MRI also assessed vascular brain injury – areas in the brain affected by reduced blood flow to the brain.

    […]

    Co-author Eric Smith, a neurologist, scientist and an associate professor of clinical neurosciences at the University of Calgary, said that “preserving cognitive function is one of the best ways to prevent dementia in old age. This study suggests that one of the ways that good nutrition and physical activity prevent dementia may be by maintaining healthy weight and body fat percentage.”

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  • Plasmacytoid dendritic cells (pDCs) are a special immune cell that accumulate in visceral fat, producing lymphoid structures driving secondary disease www.sciencedaily.com
    Obesity Inflammation Immune System Metabolic Syndrome Visceral Fat

    An obesogenic diet drives immune cell activation.

    Although the role of dietary fat intake in obesity is a matter of considerable controversy, research has identified complex interrelationships between dietary components, inflammation, and immune function. For example, some evidence suggests that consumption of a diet high in fat drives inflammatory processes in the central nervous system and peripheral tissues, including the liver, adipose tissue, skeletal muscle, and gut, promoting metabolic dysfunction and weight gain. Findings from a recent study suggest that a high-fat diet promotes the activity of plasmacytoid dendritic cells, a type of immune cell.

    Plasmacytoid dendritic cells, also known as natural interferon-producing cells, are critical components of both the innate and adaptive immune response. These specialized cells secrete copious amounts of type 1 interferons in response to a viral infection and then differentiate into professional antigen-presenting cells, which can stimulate T cell activity. Chronic stimulation of the plasmacytoid dendritic cells is linked with the development of autoimmune disorders and certain types of cancer. Although plasmacytoid dendritic cells are somewhat rare, they have been identified in visceral adipose tissue.

    The investigators fed multiple groups of mice either a high-fat diet or standard chow for three weeks. They gave one group of mice on the high-fat diet a drug that blocks the migration of plasmacytoid dendritic cells into the visceral adipose tissue. Then they analyzed the animals’ blood, peripheral tissue, lymphatic organs, and visceral adipose tissue for the presence of plasmacytoid dendritic cells.

    They found that after three weeks of a high-fat diet, plasmacytoid dendritic cells increased in the blood, liver, spleen, and visceral adipose tissue. The cells were especially abundant in fat-associated lymphoid clusters within the visceral adipose tissue. The animals on the high-fat diet gained weight and exhibited poor glucose tolerance, indicating metabolic dysfunction. Their visceral adipose tissue weight doubled during the three-week diet. Animals that received the drug that blocked plasmacytoid dendritic cell migration did not gain weight and demonstrated better glucose tolerance.

    These findings suggest that an obesogenic diet drives visceral and peripheral weight gain, promotes glucose intolerance, and increases immune cell activation in the visceral adipose tissue of mice.

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  • An unexpected way to shed visceral fat through the sebaceous gland: "We believe that we are the first group to show a non-hormonal way to induce this" www.sciencedaily.com
    Obesity Metabolic Syndrome Visceral Fat

    From the article:

    Treating obese mice with the cytokine known as TSLP led to significant abdominal fat and weight loss compared to controls […] Unexpectedly, the fat loss was notassociated with decreased food intake or faster metabolism. Instead, the researchers discovered that TSLP stimulated the immune system to release lipids through the skin’s oil-producing sebaceous glands.

    Thymic stromal lymphopoietin:

    Thymic stromal lymphopoietin (TSLP) is a cytokine – a type of immune system protein – involved in asthma and other allergic diseases. The Kambayashi research group has been investigating the expanded role of this cytokine to activate Type 2 immune cells and expand T regulatory cells. Since past studies have indicated that these cells can regulate energy metabolism, the researchers predicted that treating overweight mice with TSLP could stimulate an immune response, which could subsequently counteract some of the harmful effects of obesity.

    “When I looked at the coats of the TSLP-treated mice, I noticed that they glistened in the light. I always knew exactly which mice had been treated, because they were so much shinier than the others,” he said. Kambayashi considered a far-fetched idea – was their greasy hair a sign that the mice were “sweating” out fat from their skin?

    Does this mechanism exist in humans?

    To examine whether TSLP could potentially play a role in the control of oil secretion in humans, the researchers then examined TSLPand a panel of 18 sebaceous gland-associated genes in a publicly-available dataset. This revealed that TSLPexpression is significantly and positively correlated with sebaceous gland gene expression in healthy human skin.

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  • Visceral fat may cause pathogenic obesity reinforced through a cycle of chronic inflammation www.sciencedaily.com
    Obesity Inflammation Metabolic Syndrome Intestinal Permeability Visceral Fat

    Scientist proposes that the bodies decision to promote visceral fat rather than subcutaneous fat may be due to underlying biological switches triggered partly by malnutrition.

    The evolutionary advantage of visceral fat:

    Sometimes called “the abdominal policeman,” a VAT-rich structure called the omentum, a loosely hanging fold of the membrane lining the abdominal cavity, sticks to wounds, foreign objects such as shrapnel and infection sites like a bandage full of antibiotics. In fact, surgeons sometimes use pieces of omentum to control severe postoperative infections. VAT surrounds the small intestine, defending the body from ingested pathogens and toxins.

    […]

    In the past, the role of visceral fat as part of the immune system may have been more widely important than it is today because starvation and infections were more common. West-Eberhard proposes that in fetuses subject to nutritional stress, more energy may be stored as fat around the abdominal organs rather than as fat under the skin (subcutaneous fat or SAT).

    Chronic inflammatory feedback loop promotes development of visceral fat:

    In overweight individuals, a dangerous feedback loop may develop: increased VAT leads to increased chronic inflammation, which, in turn, leads to increased insulin resistance leading to further VAT storage and increased susceptibility to disease.

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  • Brain insulin sensitivity determines fat distribution: insulin sensitivity in the hypothalamus form little visceral, but no influence on subcutaneous www.sciencedaily.com
    Exercise Brain Obesity Metabolic Syndrome Visceral Fat

    From the article:

    If the person’s brain responds sensitively to the hormone, a significant amount of weight can be lost, unhealthy visceral fat reduced, and the weight loss can be maintained over the long term. However, If the person’s brain responds only slightly or not at all to insulin, the person only loses some weight at the beginning of the intervention and then experiences weight regain. Over the long term, the visceral fat also increases.

    […]

    Since the insulin action in the hypothalamus is crucial for the regulation of peripheral energy metabolism, the researchers also investigated how insulin sensitivity in this area of the brain is related to the distribution of body fat. For this purpose, they examined a cross-sectional cohort of 112 participants. The analysis of the data showed that people with high insulin sensitivity in the hypothalamus form little visceral fat. However, insulin sensitivity has no influence on the mass of subcutaneous fat.

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  • Sugar-sweetened drinks linked to increased visceral fat www.sciencedaily.com
    Obesity Sugar Metabolic Syndrome Sugar-Sweetened Beverages Visceral Fat

    Sugar-sweetened beverage intake increases visceral fat.

    Subcutaneous fat is stored just beneath the skin. Commonly associated with a “pear” shape, subcutaneous fat may protect against some diseases. Visceral fat, on the other hand, is stored in the abdominal cavity close to internal organs such as the liver, pancreas, and intestines. An excess of visceral fat, often referred to as central obesity or abdominal obesity, is commonly associated with an “apple” shape and an increased risk of developing many chronic diseases. Findings from a 2016 study suggest that sugar-sweetened beverage intake increases visceral fat deposition.

    Sugar-sweetened beverages include commonly consumed products such as soda, sports drinks, energy drinks, and other beverages that contain added sugars. Many sugar-sweetened beverages exceed the recommended maximum daily added sugar intake of 25 grams in a single serving. They are the leading contributor to sugar intake among people living in the United States.

    The investigation involved 1,160 participants enrolled in the Third Generation of the Framingham Heart Study who underwent repeated computed tomography scans (approximately six years apart) to assess the amount of fat in their abdominal region, including subcutaneous fat and visceral fat. Participants provided information about their dietary intake, physical activity, overall health, and whether they smoked. Investigators categorized the participants according to their sugar-sweetened beverage or diet soda intake, ranging from non-consumers (drinking none to less than one serving per month) to daily consumers (drinking one or more servings per day.

    They found that sugar-sweetened beverage intake was associated with visceral fat gain in a dose-dependent manner, with daily consumers gaining 29 percent more visceral fat over a six-year period than non-consumers. These findings held true even after accounting for the participants' age, gender, physical activity, body mass index, and other factors. Drinking diet soda was not associated with visceral fat gain.

    These findings suggest that drinking sugar-sweetened beverages increases visceral fat, potentially contributing to an increased risk of chronic disease. Learn more about sugar-sweetened beverages in our overview article.

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  • Even low exercise groups prevents accumulation of visceral fat (vigorous sees declines): highest level saw a 6.9 percent decrease in visceral fat www.sciencedaily.com
    Exercise Obesity Aerobic Visceral Fat

    From 2005.

    From the article:

    To better understand the effects of differing amounts of exercise, the researchers studied 175 overweight sedentary men and women who were beginning to show signs of lipid problems. They were randomized into one of four groups: no exercise, low dose/moderate intensity (equivalent of 12 miles of walking per week), low dose/vigorous intensity (12 miles of jogging per week) or high dose/vigorous intensity (20 miles of jogging per week).

    […]

    “On the other hand, participants who exercised at a level equivalent to 17 miles of jogging each week saw significant declines in visceral fat, subcutaneous abdominal fat and total abdominal fat,” Slentz continued. “While this may seem like a lot of exercise, our previously sedentary and overweight subjects were quite capable of doing this amount.”

    Specifically, those participants exercising at the highest level saw a 6.9 percent decrease in visceral fat and a 7 percent decrease in subcutaneous fat.

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  • Fibroblast growth factor-2 released by visceral fat tumorigenic: "when the fat secretions had more of FGF2, more of the cells formed cancerous tumors" www.sciencedaily.com
    Cancer Obesity Metabolic Syndrome Visceral Fat

    From the article:

    A new Michigan State University study now offers new details showing that a certain protein released from fat in the body can cause a non-cancerous cell to turn into a cancerous one. The federally funded research also found that a lower layer of abdominal fat, when compared to fat just under the skin, is the more likely culprit, releasing even more of this protein and encouraging tumor growth.

    […]

    “Our study suggests that body mass index, or BMI, may not be the best indicator,” Bernard said. “It’s abdominal obesity, and even more specifically, levels of a protein called fibroblast growth factor-2 that may be a better indicator of the risk of cells becoming cancerous.”

    […]

    She also collected visceral fat tissue from women undergoing hysterectomies and found that when the fat secretions had more of the FGF2 protein, more of the cells formed cancerous tumors when transferred into mice.

    Read more
  • For every 10-gram increase in soluble fiber eaten per day, visceral fat [but not subcutaneous] was reduced by 3.7 percent over five years www.sciencedaily.com
    Exercise Diet Obesity Fiber Visceral Fat

    From the article:

    According to a new study by researchers at Wake Forest Baptist Medical Center, the way to zero in and reduce visceral fat is simple: eat more soluble fiber from vegetables, fruit and beans, and engage in moderate activity.

    The study found that for every 10-gram increase in soluble fiber eaten per day, visceral fat was reduced by 3.7 percent over five years. In addition, increased moderate activity resulted in a 7.4 percent decrease in the rate of visceral fat accumulation over the same time period.

    […]

    Researchers found that increased soluble fiber intake was associated with a decreased rate of accumulated visceral fat, but not subcutaneous fat.

    “There is mounting evidence that eating more soluble fiber and increasing exercise reduces visceral or belly fat, although we still don’t know how it works,” Hairston said. “Although the fiber-obesity relationship has been extensively studied, the relationship between fiber and specific fat deposits has not. Our study is valuable because it provides specific information on how dietary fiber, especially soluble fiber, may affect weight accumulation through abdominal fat deposits.”

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  • Inadequate sleep may preferentially act as a trigger for visceral fat accumulation (randomized controlled crossover study) www.sciencedaily.com
    Diet Obesity Sleep Metabolic Syndrome Visceral Fat

    Inadequate sleep drives abdominal fat gains.

    Visceral fat is body fat that is stored in the abdominal cavity near the liver, pancreas, and intestines. The accumulation of visceral fat is linked to type 2 diabetes, insulin resistance, inflammatory diseases, certain types of cancer, cardiovascular disease, and other obesity-related conditions. Findings from a recent study suggest that not getting enough sleep increases the risk of developing excess visceral fat.

    Sleep is essential for human health. Not getting enough sleep or having poor, fragmented sleep promotes the development of many chronic illnesses, including cardiovascular disease, hypertension, diabetes, stroke, obesity, and depression. Scientists don’t fully understand the mechanisms that drive these effects, but some evidence suggests that disturbances in circadian rhythms play vital roles.

    The trial involved 12 healthy young adults (aged 19 to 39 years) who engaged in an in-patient sleep study. Participants were allowed to have either a full night of sleep (nine hours of sleep opportunity) or restricted sleep (four hours of sleep opportunity) for two weeks. After a three-month washout period, participants repeated the study with the opposite sleep experience. The investigators measured the participants’ caloric intake, energy expenditure, body weight, body composition, and fat distribution throughout the study period.

    They found that when participants were sleep-restricted, they consumed approximately 13 percent more protein and 17 percent more fat (translating to about 300 calories) daily, but their overall energy expenditure did not change. Sleep-restricted participants also gained weight. Much of this weight was in the abdominal area, with a 9 percent increase in total abdominal fat area and an 11 percent increase in visceral fat, compared to when they got a full night’s sleep.

    These findings suggest that insufficient sleep increases caloric intake and promotes weight gain and visceral fat increases. Learn more about the harmful health effects of insufficient sleep in this episode featuring sleep expert Dr. Matt Walker.

    Read more
  • Chronic systemic inflammation induced by lipopolysaccharide can cause microglia to attack the blood-brain barrier www.sciencedaily.com
    Obesity Inflammation Immune System Toll-Like Receptors Blood-Brain Barrier Lipopolysaccharide

    Obesity promotes circulation of lipopolysaccharide. In animals, chronic systemic inflammation, experimentally induced by injection with LPS, also known as “LPS challenge,” can cause microglia into the brain to switch from protecting the blood-brain barrier to damaging it.

    From the article:

    Nearly 50 percent of all dementias, including Alzheimer’s, begins with the breakdown of the smallest blood vessels in the brain and their protective “gatekeeper cells,” according to a Keck School of Medicine of USC study.

    […]

    A key point of interest was the systemic inflammation induced by injecting the mice with an inflammation-inducing substance. Such injections resulted in the movement of microglia to the blood vessels and increased the permeability of the blood-brain barrier within a few days. Then, the microglia initially acted to protect the blood-brain barrier and limit increases in permeability, but as inflammation progressed, the microglia reversed their behavior by attacking the components of the blood-brain barrier, thus increasing the barrier’s permeability. The subsequent leakage of molecules into the brain had the potential to cause widespread inflammation in the brain and consequent damage to neurons (cells of the nerves).

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  • Hunger inhibition hormone leptin directly contributes to cardiovascular disease in those desensitized by obesity by increasing cardiovascular activity www.sciencedaily.com
    Brain Obesity Heart Disease Satiety Blood Pressure Metabolic Syndrome

    From the article:

    In both cell culture and animal models, the researchers have shown that fat-derived leptin directly activates aldosterone synthase expression in the adrenal glands, resulting in production of more of the steroid hormone aldosterone.

    High aldosterone levels are known to contribute to widespread inflammation, blood vessel stiffness and scarring, enlargement and stiffness of the heart, impaired insulin sensitivity and more.

    Aldosterone, which is produced by the adrenal gland, has a direct effect on blood pressure by regulating salt-water balance in the body. High levels of aldosterone are an obesity hallmark and a leading cause of metabolic and cardiovascular problems. But exactly how it gets high in obesity was a mystery.

    Read more
  • Excess artificial light exposure increases risk of obesity in preschool aged children www.sciencedaily.com
    Obesity Sleep Circadian Rhythm Development Blue Light

    Artificial light exposure increases the risk for obesity among children. Light is the primary signal that entrains the body’s master clock to set its 24-hour circadian cycle. Consequently, the body is synchronized to external light-dark cycles. In recent decades, exposure to light from artificial sources (rather than natural ones) has increased, paralleling the global increases in obesity among adults. Findings from a 2016 study suggest that exposure to artificial light increases the risk for obesity among children.

    Global health experts estimate that more than 42 million children under the age of five years have obesity, roughly one-fourth of whom live in developing nations. Obesity increases a person’s risk for developing chronic diseases such as type 2 diabetes, heart disease, and some cancers. It also imposes considerable financial costs at the individual, healthcare system, and national level.

    The study involved 48 preschool-aged children receiving daycare services in Australia. The investigators measured the children’s baseline body mass index (BMI), sleep duration and timing, light exposure, and physical activity levels via clinical assessment, parent questionnaires, and light and activity trackers. They repeated these measures 12 months later.

    They found that at baseline, children who had longer early exposure to moderate intensity light (such as that from artificial sources) were more likely to have higher BMI, while children who had longer afternoon exposure to bright light (such as that from natural sources) tended to have lower BMI. At the second assessment, the investigators found that even after taking into account sleep duration and timing, BMI, and activity levels, children who had more total light exposure at baseline (due to having earlier exposure) gained more weight than their peers. Specifically, for every hour earlier that the children were exposed to light, they experienced a 0.6 unit increase in BMI. The investigators posited that although this was a small increase, it could be an indicator of a life-long trajectory toward weight gain.

    These findings suggest that greater light exposure, especially when it occurs early in the day from artificial light sources, contributes to weight gain in children. Interestingly, adults that receive early exposure to bright light typically sleep better – a key to maintaining a healthy weight. Learn more in this clip featuring Dr. Matthew Walker.

    Read more
  • Inflammatory injury from obesity is mediated by activation of TLR4 (but may be ameliorated by omega-3) www.sciencedaily.com
    Brain Obesity Omega-3 Inflammation Toll-Like Receptors Lipopolysaccharide

    Knocking out TLR4 in mice ameliorates obesity-associated inflammation, which may come as no surprise since increased circulation of LPS (a potent activator of TLR4) has been implicated in obesity due to associations with increased presence of LPS binding protein.

    While genetically knocking out TLR4 is probably not a practical solution to the inflammatory cascade associated with human obesity, which may also be a smoking gun in obesity-associated brain shrinkage and diminished cognition, dietary intake of omega-3 fatty acids EPA and DHA may at least be partly ameliorative (see review). Additionally, a study in breast cancer patients showed that 5 grams per day of EPA and DHA ultimately lead to hypermethylation (usually interpreted as suppressive) of TLR4.

    From the article:

    When a person consumes more calories than needed, the excess calories are stored in the form of triglycerides inside fat tissue, also known as white adipose tissue (WAT). Researchers know that in obese people, WAT becomes overworked, fat cells begin to die, and immune cells become activated. But the exact mechanism by which this inflammation occurs isn’t fully understood.

    […]

    After five months on a high-fat diet, the mice lacking Tlr4 had gained just as much weight, and just as much fat, as other mice on a high-fat diet. But the genetically engineered mice – with [fibro-inflammatory progenitors] that could no longer generate the same signals – no longer had high levels of inflammation. Instead, the levels of inflammatory molecules in their WAT were closer to the levels seen in mice on low-fat diets.

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  • Cardio exercise increases the production of FGF21 3x more than strength training: a hormone with relevance to metabolic disorders www.sciencedaily.com
    Exercise Obesity Diabetes Aerobic Strength FGF21

    From the article:

    In a new study published in the scientific Journal of Clinical Investigation – Insight, the researchers show that cardio training on an exercise bike causes three times as large an increase in the production of the hormone FGF21 than strength training with weights. FGF21 has a lot of positive effects on metabolism.

    […]

    Endurance training on a bicycle has such a marked effect on the metabolic hormone that we know ought to take a closer look at whether this regulation of FGF21 is directly related to the health-improving effects of cardio exercise. FGF21’s potential as a drug against diabetes, obesity and similar metabolic disorders is currently being tested, so the fact that we are able to increase the production ourselves through training is interesting', Christoffer Clemmensen elaborates.

    Read more
  • A high-polyphenol diet is protective against age-related brain shrinkage. www.eurekalert.org
    Brain Alzheimer's Obesity Aging Green Tea Nuts Dementia Urolithin A

    “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."

    Read more
  • Long-term weight-loss reduces cancer risk in adults with obesity and type 2 diabetes. www.sciencedaily.com
    Cancer Obesity Diabetes

    Obesity and type 2 diabetes cause perturbations in metabolism and immunity that increase the risk of cancer. Bariatric surgery is the most effective intervention for substantial and enduring weight loss in those with obesity and has been shown to [reverse type 2 diabetes](​​https://pubmed.ncbi.nlm.nih.gov/33485454/) and reduce cancer risk. Findings of a recent report demonstrate a lower risk of cancer in patients with obesity and diabetes up to 31 years following bariatric surgery.

    Weight gain occurs when the body stores excess calories in the form of fat in adipose tissue depots around the body. As the amount of energy stored increases, the body’s tolerance for glucose and other fuels decreases, leading to insulin resistance and type 2 diabetes. The high circulating levels of glucose, insulin, insulin-like growth factors, and inflammatory proteins observed in type 2 diabetes increase cancer cell proliferation and suppress apoptosis (programmed cell death). Reducing energy stores through bariatric surgery or other weight-loss therapies restores insulin sensitivity and reduces cancer risk.

    The authors collected data from an ongoing trial with over 4,000 participants investigating the long-term effects of bariatric surgery in adults with obesity and type 2 diabetes. At their baseline visit, participants underwent a physical exam, gave a blood sample, and completed questionnaires regarding health and lifestyle factors. Participants chose to undergo bariatric surgery or receive conventional obesity treatment during the years of 1987 and 2001. They continue to provide additional questionnaire data and blood samples as the study remains ongoing. The investigators followed participants in the current sample for an average of 21 years.

    Participants who chose to undergo bariatric surgery lost an average of 60 pounds two years after the baseline visit, compared to just 7 pounds in participants who received standard obesity treatment. These levels of weight loss remained stable 10 years after the baseline visit. At two years follow-up, 70 percent of participants who underwent surgery had diabetes remission, compared to 34 percent at 10 years follow-up. Bariatric surgery reduced cancer risk by 48 percent in women and 37 percent in the whole group. Participants who underwent surgery and maintained diabetes remission after 10 years had 55 percent reduction in cancer risk compared to participants with diabetes at 10 years follow-up. Participants who did not undergo surgery but achieved diabetes remission had an even greater risk reduction of 60 percent at 10 years follow-up.

    These findings support long-term weight-loss, including bariatric surgery, as a strategy to reduce type 2 diabetes and cancer risk among adults with obesity.

    Read more
  • Fat cells relay pro-cancer signals to tumors, especially in people with obesity and type 2 diabetes. www.inverse.com
    Cancer Obesity Breast Cancer Fat

    Obesity and metabolic diseases are strong risk factors for the development and progression of metastatic breast cancers in women who have completed menopause. Breast tumors contain a large number of white blood cells and adipocytes (i.e., fat cells); however, the role of adipocytes in metastatic breast cancer is unknown. Findings of a new report show that adipocytes shed molecular droplets called exosomes that relay cancer-promoting signals.

    Adipocytes play a critical role in the tumor microenvironment, releasing proinflammatory cytokines such as interleukin-6 and tumor necrosis factor-alpha and fats that act as fuel for tumor growth. Tumor metastasis is induced by changes in gene expression that increase cell movement and angiogenesis (i.e., the growth of new blood vessels) and decrease cell death and adhesion (i.e., how tightly cells cling to each other). The mechanisms by which adipocytes deliver these pro-cancer and pro-metastatic signals is understudied.

    The investigators obtained estrogen receptor-positive breast cancer cells and co-cultured them with adipocytes that were collected from female patients with or without type 2 diabetes who underwent bariatric (weight-loss) surgery. The researchers measured changes in gene and protein expression and performed fluorescence imaging to observe physical changes to adipocytes and cancer cells.

    When cultured with adipocytes from patients with obesity, cancer cells increased expression of genes important for a process called epithelial-to-mesenchymal transition, a key stage of tumor metastasis. Compared to exosomes produced by adipocytes from participants without type 2 diabetes, exosomes from participants with diabetes increased the expression of metastasis genes in cancer cells to a greater extent. Microscope imaging revealed that cancer cells from participants with diabetes underwent physical changes associated with metastasis as well as gene expression.

    These results revealed that exosomes shed from adipocytes act as the mechanism for delivery of pro-cancer compounds from adipocytes to breast cancer cells. Also, the strength of this pro-cancer signaling increased as insulin resistance increased. This study provides important insight into the relationship between obesity and cancer.

    Read more
  • Insulin improves dopamine signaling in regions of the brain associated with eating behavior. www.sciencedaily.com
    Obesity Insulin Dopamine

    Insulin signaling in the brain influences behavior, weight regulation, motivation, and cognition. Previous research demonstrates that insulin resistance reduces brain volume and cognitive function in middle-aged adults. Results of a new study demonstrate that insulin interacts with dopamine to modulate reward-based behavior and whole-body metabolism.

    Dopamine is a neurotransmitter that regulates activity of the mesocorticolimbic system, a region of the brain involved in reward-based learning. Mesocorticolimbic circuits transmit information from the midbrain to the ventral and dorsal striatum, prefrontal cortex, amygdala, and hippocampus to coordinate emotions, memories, and impulses involved in eating and other rewarding behaviors. Previous research has demonstrated that insulin interacts with dopamine, altering activity of the mesocorticolimbic systems, inducing feelings of satiety and decreasing high-calorie food seeking. However, much of the existing research has been conducted in mice, using very high levels of insulin, making translation to humans difficult.

    The investigators assigned ten male participants (average age, 27 years) with a normal BMI (average BMI, 24) to receive either intranasal insulin or a placebo and undergo a combined PET and MRI scan after having fasted overnight. The researchers gave participants an injection of a radioactive marker called [11C]-raclopride that binds to dopamine receptors so they could measure dopamine-related brain activity during the scan. Participants also completed surveys to assess eating behavior and provided a blood sample for measurement of insulin and other hormones.

    Following administration of intranasal insulin, [11C]-raclopride synaptic binding potential increased in the ventral and dorsal striatum, suggesting an increase in the number of dopamine receptors in these regions. Accordingly, synaptic dopamine concentrations (dopamine that has not bound to a receptor and internalized by the neuron) decreased. Ultimately, this increase in dopamine signaling reduced resting-state activity in the ventral and dorsal striatum and improved functioning of mesocorticolimbic circuits 15 to 45 minutes after insulin exposure. As the participants' response to insulin exposure increased, so did their scores on tests of subjective wellbeing and cognitive control.

    This study, which demonstrated the effects of intranasal insulin on dopamine activity in the mesocorticolimbic system, has important implications for reward-based learning, eating behavior, and obesity. Future research should include participants with insulin resistance to gain a better understanding of the effects of obesity and metabolic disease on the brain.

    Read more
  • The SARS-CoV-2 virus infects adipose tissue, increasing inflammation during COVID-19 illness. www.biorxiv.org
    Obesity COVID-19

    The SARS-CoV-2 virus, which causes COVID-19, has infected over 255 million individuals worldwide. Obesity and related diseases such as type 2 diabetes and hypertension are strong independent risk factors for infection, severe disease, and death. Findings of a new report indicate that SARS-CoV-2 infiltrates adipose tissue, causing inflammation and worsening disease severity.

    Severe COVID-19 is characterized by immune hyperreactivity that creates systemic inflammation mediated by excessive production of pro-inflammatory proteins. Obesity is also characterized by excessive immune reactivity and inflammation, potentially putting people with obesity at greater risk of COVID-19 complications. However, further investigation is needed to understand the mechanisms by which obesity increases COVID-19 severity and whether these mechanisms are independent of type 2 diabetes, hypertension, and other obesity-related conditions.

    The investigators recruited adults with obesity who were patients of a bariatric surgery center and had not had a SARS-CoV-2 infection. They collected adipose tissue samples from multiple fat depots around the body such as subcutaneous fat (under the skin), visceral fat (wrapped around internal organs), and pericardial and epicardial fat (around the heart) on the day participants underwent bariatric surgery. The researchers also collected adipose tissue samples from adults who had died from COVID-19 illness. They isolated cells from the connective tissue, sorted them based on type (such as mature adipocyte, pre-adipocyte, and adipose tissue macrophage), and characterized their gene expression and surface receptor population. Then, they exposed the cells to the SARS-CoV-2 virus and observed changes.

    The authors found that the SARS-CoV-2 virus infects adipose tissue from multiple depots around the body, but that macrophages were the main cell type infected. They found low expression of the angiotensin converting enzyme (ACE)-2 receptor in these macrophages, indicating that the virus enters through a different route than the primary entry point in cells of the lungs and gut. Upon exposure to the SARS-CoV-2 virus, these cells increased production of pro-inflammatory cytokines. In adipose tissue samples from participants who had died of COVID-19, the investigators found SARS-CoV-2 infection in mature adipocytes in addition to macrophages.

    These results are the first to show that the SARS-CoV-2 virus can infect adipose tissue in vivo and that this tissue type may contribute to excess inflammation during COVID-19 illness, especially in older adults with a higher BMI.

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  • Patients with obesity and COVID-19 produce mostly autoimmune SARS-CoV-2 antibodies, not neutralizing. pubmed.ncbi.nlm.nih.gov
    Obesity Immune System COVID-19 Autoimmunity

    Obesity is a strong independent risk factor for COVID-19, the disease caused by the SARS-CoV-2 virus. Previous research has shown that people with obesity generate fewer antibodies in response to viral infection or vaccination; however, whether antibody quality is also affected by obesity is unknown. Findings published in a new report show that the majority of the antibodies found in people with obesity are autoimmune and not able to neutralize the SAR-CoV-2 virus, putting individuals with obesity at greater risk of severe COVID-19.

    Obesity increases the rate of inflammaging, the process of chronic low-grade inflammation that wears down the body’s tissues over time, putting people with obesity at greater risk of many diseases. Inflammaging increases the risk of autoimmunity by increasing the concentration of damaged cellular components in the blood, potentially triggering the immune system to generate antibodies against its own cells. Previous research has shown that many patients with severe COVID-19 generate autoimmune antibodies that increase the risk of long-term complications. Because people with obesity experience increased baseline inflammaging, they may be at greater risk of developing long-term autoimmune complications for COVID-19; however, no published studies have yet addressed this concern.

    The investigators collected blood from 15 participants with a lean BMI (less than 25) and 15 participants with an obese BMI (greater than 30) who tested positive for SARS-CoV-2. The investigators also collected blood from 30 participants who had not had a SARS-CoV-2 infection and were matched for age, sex, and BMI. The researchers measured the concentration of neutralizing antibodies (meaning antibodies that bind to the SARS-CoV-2 spike protein and prevent viral entry into cells), non-neutralizing antibodies, and autoimmune antibodies.

    Participants with obesity had fewer SARS-CoV-2 antibodies than participants with a lean BMI, confirming previous reports. While all 15 SARS-CoV-2-positive participants with a lean BMI had circulating neutralizing antibodies, only a few participants with obesity did. The researchers found that SARS-CoV-2 infection increased the concentration of autoimmune antibodies in all patients, but the concentration of autoimmune antibodies was always higher in participants with obesity. Finally, they found that participants with the highest concentration of autoimmune antibodies also had the highest levels of serum C-reactive protein, a marker of chronic inflammation, suggesting that inflammation is integral to developing autoimmunity.

    These data confirm previous reports that obesity reduces the effectiveness of the immune response in COVID-19 patients and increases the risk of autoimmunity.

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  • Older adults with a higher BMI spread more infectious SARS-CoV-2 aerosol particles. www.pnas.org
    Obesity Pollution COVID-19

    The SARS-CoV-2 virus is transmitted through aerosols that are generated when an infected person breathes, talks, sneezes, or coughs. The amount and size of aerosol droplets a person exhales can vary drastically between individuals and may be affected by diet and age. Findings of a recent study suggest that humans and non-human primates with greater age and body mass index (BMI) produce more aerosol droplets during COVID-19 infection.

    Aerosol droplets are produced when air passes over mucus-coated airways during breathing. This mucus determines the size of aerosol droplets produced. A healthy mucus layer forms large droplets, while a dysfunctional mucus layer produces droplets that aerosolize into many smaller infectious droplets. Mucus structure and composition are influenced by age, environment, disease, and the microbiota. A Western, obesity-promoting diet is often deficient in fiber, starving the beneficial bacteria in the gut that produce metabolites such as short chain fatty acids that regulate the lung mucus barrier. Older adults also experience degradation of the lung mucus layer, potentially influencing aerosol droplet size.

    The researchers recruited 194 participants from the United States. They asked participants to breathe into a particle detector to measure the quantity of exhaled particles in the size range of three to five micrometers. They characterized participants who exhaled 156 particles per liter of air or less during the breath test as low spreaders and participants above this level of superspreaders. The particle detector was connected to an air filter that collected the particles so the concentration of SARS-CoV-2 virus could be measured. The investigators also used a sample of eight non-human primates to better understand the effects of SARS-CoV-2 infection. The investigators exposed rhesus macaques and green monkeys to either the SARS-CoV-2 or tuberculosis virus and monitored them for up to 60 days. The non-human primates performed a similar breath test as the one used in the human participants.

    The authors found no relationship between sex and aerosol particle number; however, there were significant statistical relationships among age, BMI, and particle size. The strongest correlation was found between particle size and BMI-years, which is calculated as BMI multiplied by age. Participants in the bottom 50 percent for BMI-years exhaled significantly less aerosol than participants in the top 50 percent. In non-human primates, SARS-CoV-2 or tuberculosis infection increased the number of aerosol particles exhaled in proportion to the amount of viral RNA measured from mucus swabs.

    The authors concluded that age, BMI, and active infection decrease aerosol particle size and may contribute to viral spread. Future models of pandemic progression should take these factors into account.

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  • Metabolic adaptation “cancels out” some of the calorie-burning effects of exercise. www.sciencedirect.com
    Exercise Obesity Metabolism

    Traditionally, governments and public health authorities have placed a high emphasis on recommending physical activity as a means of combating weight gain and obesity. Yet, randomized controlled trials have found exercise alone to have a relatively modest effect on body weight, yielding weight loss averages in the order of 4 to 11 pounds (2 to 5 kilograms) in people with overweight and obesity. Some researchers have posited that metabolic adaptation causes the body to compensate for energy burned during exercise by reducing the baseline metabolic rate and ultimately “canceling out” some of the exercise-induced calorie deficit. Findings from a recent study indicate that much of the effort of exercise is lost to energy compensation, especially among people with excess bodyweight.

    The researchers’ analysis revolved around energy expenditure data collected in a cohort of more than 1,700 healthy adults, excluding those involved in competitive sports training or were pregnant or breastfeeding. They focused on three measures: baseline energy expenditure (i.e., the energy required to fuel basic functions such as respiration, tissue repair, and immune defense, minus any physical activity), total energy expenditure (i.e., total calories burned over the same period of time), and physical activity expenditure (inferred by subtracting baseline from total energy expenditure).

    Looking at the relationships between the three types of energy expenditure, the researchers corroborated what many smaller studies have suggested. That is, the more energy a person used during physical activity, the more their baseline metabolism slowed down to avoid a calorie deficit. The result of this adaptation is that total energy expenditure is approximately 28 percent lower on active days than might be expected given the number of calories burned during physical activity.

    This metabolic compensation was independent of the participants' sex or age. However, it was significantly affected by fat mass and body mass index (BMI), as individuals in the 90th percentile of BMI recouped approximately 49 percent of calories burned through physical activity by lowering their baseline metabolism.

    These findings suggest that exercise may be a considerably less effective weight loss tool for people with overweight or obesity. They also raise interesting questions about causality, such as whether people who have overweight are better metabolic “compensators” because of their high level of adiposity (which may have hormonal and signaling properties conducive to this form of adaptation) or whether they become overweight because they start out life by being better “compensators” and are more likely exceed their baseline metabolic needs with food. The possibility of innate differences in compensation receives some support from evidence for significant ethnic disparities in baseline metabolism. It is worth mentioning that exercise benefits human health independently of potential weight loss, through effects such as improved endothelial cell function, neurogenesis, glucose regulation, and inflammation.

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  • High fructose diets promote survival of intestinal cells and improve nutrient absorption – possibly promoting cancer. www.cancer.gov
    Cancer Obesity Sugar

    Since the introduction of high fructose corn syrup in the 1960s, fructose consumption has tripled worldwide. Excess sugar consumption degrades health by contributing to obesity and promoting cancer initiation and progression. Findings of a recent report elucidate the mechanisms by which fructose improves survival of and nutrient absorption by intestinal cells.

    Fructose absorption begins in the epithelium (i.e., skin-like cells) of the small intestine, which measures approximately 320 square feet in surface area (about the size of a small studio apartment). This massive surface area is arranged like shag carpet, with structures called “villi” that protrude from the intestine wall. The longer the villi, the greater the surface area and number of intestinal epithelial cells available to absorb nutrients, such as fat or iron. Previous research has shown that fructose can lead to excessive intestinal epithelial growth (called hyperplasia) and cancer; however, the effects of fructose on non-cancerous intestinal epithelial cells is unknown.

    The investigators gave mice access to normal drinking water or drinking water with 25 percent high-fructose corn syrup (soda contains about 10 percent) for four weeks. Then they fed mice either a normal diet with no fructose, a high-fat diet with no fructose, or a high-fat diet with sucrose, which contains 50 percent fructose and 50 percent glucose. The researchers measured nutrient composition of the feces and examined the intestinal epithelium for changes.

    Mice consuming high-fructose corn syrup in their drinking water showed a 25 to 40 percent increase in intestinal villus length compared to mice consuming normal drinking water. As villus length increased, weight gain and dietary fat absorption also increased. Mice consuming a high-fat diet and fructose gained more weight and had longer intestinal villi than mice consuming a high-fat diet with no fructose, despite consuming and expending the same amount of calories. These mice had less fat in their feces, suggesting an increase in nutrient absorption. The researchers found that intestinal epithelial cells isolated from mice consuming fructose were better able to withstand low-oxygen conditions (called hypoxia), which is a common cause of intestinal cell death.

    The authors concluded that high fructose diets increase intestinal villi length and nutrient absorption capacity. These findings provide greater insight into the pathogenesis of intestinal cancer.

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  • Daily avocado consumption improves body fat distribution and reduces visceral fat apple.news
    Nutrition Diet Obesity Metabolic Syndrome Weight Loss Visceral Fat

    Seventy percent of adults living in the United States have overweight (BMI greater than 25) or obesity (BMI greater than 30), putting them at increased risk of metabolic disease. Extra fat stored around the body promotes inflammation and insulin resistance, but extra abdominal fat is particularly dangerous. Findings of a recent report suggest consuming foods rich in unsaturated fat and dietary fiber may improve fat distribution in females.

    Fat stored in the lower body, called subcutaneous fat, is located just under the skin. Fat stored in the abdominal region, called visceral fat, is wrapped around the internal organs (e.g., the liver, pancreas, and intestines). Visceral fat interferes with lipid metabolism in the liver, promoting insulin resistance, type 2 diabetes, and non-alcoholic fatty liver disease. A diet that includes avocados, which are rich in mono-unsaturated fats and dietary fiber, is associated with lower abdominal obesity.

    The investigators recruited 105 adults between the ages of 25 and 45 years who had overweight or obesity. They assigned participants to receive meals with avocado (about one Hass avocado) or meals without avocado that were matched for calories and total fat. The two meals contained different amounts of saturated fat, unsaturated fat, and fiber. Participants consumed their assigned meals once per day for 12 weeks and were told not to change their diet in other ways. Participants completed an oral glucose tolerance test to measure insulin resistance and had their body composition measured using X-ray.

    In females, avocado consumption decreased visceral adiposity and the ratio of visceral to subcutaneous fat, indicating an improvement in body fat distribution. Both males and females in the control group experienced a loss of subcutaneous fat and an increase in the ratio of visceral to subcutaneous fat, indicating a worsening of body composition over the 12 weeks. Avocado consumption had no effect on insulin resistance.

    The authors concluded that avocado consumption improved body fat distribution in females, but had no effects on body fat distribution in males or on insulin resistance in either males or females.

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  • Redefining the causes of obesity. www.sciencedaily.com
    Diet Obesity Ketogenic Diet

    Obesity is a complex, multifactorial disease influenced by genetic, molecular, environmental, and behavioral factors. Characterized as having excessive body fat, obesity affects more than 650 million people worldwide and markedly increases a person’s risk for many chronic diseases, including cardiovascular disease, type 2 diabetes, cancer, and depression, among others. The authors of a recent report challenge the prevailing theory regarding the root causes of obesity.

    A widely espoused concept in bodyweight management is the “eat less, exercise more” model, based on the principle that the number of calories consumed must be equivalent to (or less than) the number of calories expended. This model is supported by evidence suggesting that consuming high-fat foods drives overconsumption of calories due the foods' high caloric levels, poor ability to provide satisfaction and fullness, and high “pleasure factor.” However, this concept, which forms the basis for national dietary guidelines, public health messaging, and dietary counseling, is inherently flawed, because it fails to take into consideration the biological mechanisms that promote weight gain. Ultimately it places blame on people with obesity and promotes stigmatization.

    In recent decades, scientists have proposed a new model for explaining the root causes of obesity. In this model, body fat accumulation arises from hormonal responses to the consumption of high-glycemic load carbohydrates, ultimately driving a vicious cycle of body fat accumulation, hunger, and food intake. Commonly referred to as the “carbohydrate-insulin” model of obesity, this new paradigm reverses causation and provides a starting point for developing testable hypotheses.

    The concepts presented in this report suggest that what a person eats, rather than how much, plays key roles in body weight management. The authors of the report posited that if the carbohydrate-insulin model is accurate, dietary modifications that limit carbohydrate intake, such as a ketogenic diet, may alter hormonal responses and promote fat oxidation and weight loss. Learn more about the health benefits of the ketogenic diet in this clip featuring Dr. Dominic D'Agostino.

    Link to full publication.

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  • Maternal body weight influences risk of ADHD and obesity in offspring. apple.news
    Brain Obesity Pregnancy ADHD Genetics

    A woman’s body weight before and during pregnancy can have profound health effects on both mother and child. Women with obesity are at greater risk for developing pregnancy complications that can impair infant neurodevelopment, such as gestational diabetes, preeclampsia, preterm birth, and birth trauma. Findings from a new study suggest that maternal obesity contributes to attention deficit hyperactivity disorder (ADHD) and obesity in offspring.

    ADHD is a neuro-behavioral condition characterized by inattention and/or hyperactive or impulsive behavior that interferes with functioning, learning, or development. Obesity is characterized as having excessive body fat – typically defined as having greater than 25 percent body fat for males and greater than 33 percent body fat for females.

    The study included nearly 3,000 Finnish women and their offspring (~9,400 children). The authors of the study collected information about the children’s behavior and attention span from mothers and teachers. They gathered anthropometric data to determine the mothers' and children’s body mass index (BMI), a proxy for body fatness. They used Mendelian randomization and polygenic risk scores to assess risk for ADHD and/or obesity. Mendelian randomization is a research method that provides evidence of links between modifiable risk factors and disease based on genetic variants within a population. A polygenic risk score estimates a person’s genetic propensity for developing a trait or disease.

    They found that children whose mothers had a high BMI were more likely to develop ADHD, independent of genetic makeup. The Mendelian randomization analysis identified a bidirectional link between developing ADHD and obesity-related traits, suggesting that certain genetic variations may predispose children to both ADHD and obesity concurrently. The polygenic risk score revealed evidence for genetic overlap between having ADHD and greater BMI.

    These finding suggest that both genetic and prenatal environmental factors influence the likelihood that a woman’s child will develop ADHD and obesity. They also underscore the importance of maintaining a healthy maternal body weight before and during pregnancy.

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  • Co-supplementation with magnesium and vitamin D aids weight loss, improves mood, and reduces systemic inflammation. pubmed.ncbi.nlm.nih.gov
    Vitamin D Obesity Inflammation Depression Magnesium IL-6

    For decades, deficiencies in micronutrients such as magnesium and vitamin D have been linked to conditions such as depression and obesity, as well as their associated hallmarks of systemic inflammation. These observations raise questions about whether certain nutritional inadequacies might play a causal role in these conditions and whether supplementation may help regulate symptom severity. Now, a recent randomized double-blind placebo-controlled clinical trial reveals that co-supplementation with magnesium and vitamin D significantly decreases depression scores and body weight in healthy women with obesity.

    The study recruited 102 women with obesity (body mass index, 30–40; ages, 20-45 years) with mild-to-moderate depression and no indication of other health issues such as hormonal dysfunction, autoimmune disease, or diabetes. The study investigators randomly allocated the women to one of four groups to receive varying combinations of a weekly soft gel containing 50,000 international units (IU) of vitamin D, a daily tablet of 250 milligrams magnesium, and/or a placebo. The groups comprised:

    1) Co-supplementation: weekly vitamin D + daily magnesium

    2) Vitamin D only: weekly vitamin D + daily magnesium placebo

    3) Magnesium only: daily magnesium + weekly vitamin D placebo

    4) Control: weekly vitamin D placebo + daily magnesium placebo

    The investigators collected participants’ blood samples at baseline and following eight weeks of supplementation. The samples revealed that while the women on average had adequate baseline serum levels of magnesium and borderline-adequate levels of vitamin D, their health outcomes and biomarkers nonetheless showed the greatest improvements as a result of co-supplementation with both micronutrients. For instance, women who received both magnesium and vitamin D lost more weight over the duration of the intervention compared to all the other groups, in the absence of any observed changes in their dietary patterns. They also showed the greatest average reduction in depression scores over time, although all participants (including controls) exhibited some degree of symptom relief after the eight-week intervention - an observation the researchers attributed in part to the placebo effect.

    The women’s blood samples revealed a similar picture, with co-supplementation outperforming all other conditions (although individual supplementation with either vitamin D or magnesium still yielded significant improvements over controls). For instance, combining magnesium and vitamin D achieved the greatest reduction in plasma levels of pro-inflammatory tumor necrosis factor alpha (TNF-α), C-reactive protein (CRP), and interleukin 6 (IL-6). It also generated the highest boost in brain-derived neurotrophic factor (BDNF) and sirtuin-1 (SIRT1) – a protein widely known for its involvement in regulating autophagy and longevity-promoting genes.

    These findings reveal that co-supplementation with a weekly 50,000 IU dose of vitamin D and a daily 250 mg of magnesium can aid weight loss, enhance mood, and improve a host of blood biomarkers pertaining to systemic inflammation, brain functioning, and longevity. Moreover, the fact that positive health outcomes can be observed despite an absence of marked micronutrient deficiencies raises the possibility that current medical guidelines on adequate ranges of plasma levels and RDAs for vitamin D and magnesium, respectively, may be insufficiently high for optimal health outcomes.

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  • Lean people may still have metabolic dysfunction: a healthy BMI can still have negative metabolic consequences of visceral fat www.cell.com
    Obesity Metabolic Syndrome Visceral Fat

    The body mass index (BMI) is a ratio of weight to height and is one tool for measuring body size in health care and research. Epidemiological research indicates that individuals with a healthy BMI (between 20 and 25) have the lowest risk of cardiovascular disease and death compared to individuals with underweight (BMI less than 18.5), overweight (BMI between 25 and 30), and obesity (BMI greater than 30); however, some people with a healthy BMI experience metabolic dysfunction and an increased risk of death. Authors of the following report explore the condition lipodystrophy, its physiological causes, and its prevalence in the general population.

    Lipodystrophy is a condition in which the amount and/or distribution of fat tissue in the body is abnormal. Visceral fat is fat stored in the abdomen and is associated with insulin resistance, elevated triglycerides, and fatty liver. This is in contrast to fat stored in the lower body, called subcutaneous fat, which is not associated with metabolic dysfunction. In short-term studies, people with a healthy BMI and an increased waist-to-hip ratio (i.e., ratio of visceral to subcutaneous fat) are at a three times greater risk of death than people with obesity and no metabolic dysfunction, a condition referred to as metabolically healthy obesity. However, long-term studies (those with greater than 10 years' follow-up) show that people with metabolically healthy obesity have a 24 percent increased risk of death, suggesting metabolically healthy obesity is a transient stage between metabolic health and metabolic disease.

    The authors recruited almost 1,000 Caucasian/white participants of varying weight status who were at an increased risk of cardiometabolic disease based on weight, family and personal history of diabetes, and elevated glucose levels. The researchers used magnetic resonance imaging (MRI) to precisely measure body fat amount and distribution. They also measured blood pressure, fasting triglyceride levels, fasting glucose, the inflammatory marker C-reactive protein, insulin resistance, and carotid intima thickness (a measure of atherosclerosis). They defined good metabolic health as having two or fewer of the following criteria: blood pressure greater than 130/85 millimeters of mercury or the use of blood pressure medication; fasting triglycerides greater than 150 milligrams per deciliter; fasting HDL cholesterol (i.e., good cholesterol) less than 40 milligrams per deciliter in males or less than 50 milligrams per deciliter for females; fasting glucose greater than 100 milligrams per deciliter or the use of diabetic medication; C-reactive protein level in the 90th percentile or above; or insulin resistance in the 90th percentile or above.

    Compared to people with a healthy BMI and good metabolic health, those with a healthy BMI and more than two metabolic risk factors had more insulin resistance, nonalcoholic fatty liver disease, visceral obesity, less lower body subcutaneous fat, and increased atherosclerosis. However, they did not have an increased prevalence of high blood pressure, high triglycerides, low good cholesterol, or increased inflammation. Compared to people with a healthy BMI and metabolic dysfunction, people with overweight or obesity and metabolic dysfunction had a gradual increase in the prevalence of visceral adiposity, fatty liver, insulin resistance, atherosclerosis, and low subcutaneous fat volume in the lower body as BMI increased. This means that metabolic dysfunction in people with a healthy BMI is most characterized by insulin resistance and atherosclerosis and is most strongly associated with lower subcutaneous fat in the lower body than visceral adiposity in the abdomen. The authors used this to support the existence of a lipodystrophy phenotype in people with a healthy BMI.

    The authors conclude that some people with a healthy BMI may still have lipodystrophy that puts them at an increased disease risk compared to individuals with a healthy BMI and normal fat distribution. They recommend early testing of insulin sensitivity and use of medications that increase insulin sensitivity in people with lipodystrophy to lower disease risk.

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  • A very-low-calorie diet increases harmful gut bacteria. www.sciencedaily.com
    Obesity Microbiome Fasting Antibiotics

    The gut microbiota is composed of the community of bacteria, archaea, fungi, and viruses that live in the human intestine and is unique to each individual. Diet can modulate the structure and function of the gut microbiota in ways that either increase or decrease disease risk. Findings of a new report detail the effects of a very-low-calorie diet on the gut microbiota, weight loss, and infection risk.

    Following the absorption of most macronutrients (carbohydrates, fats, and proteins) and micronutrients (vitamins and minerals) present in food in the small intestine, undigested food travels to the large intestine where microbes metabolize any remaining nutrients. The amount and type of food consumed in the diet directly affect the amount and type of microbes that can flourish in the large intestine. Consuming a wide variety of foods in the diet supports a wide variety of microbes, while restricting certain foods or restricting caloric intake may reduce the abundance and diversity of the microbiota, a risk factor for disease.

    The authors of the report recruited 80 females who had completed menopause and who had overweight or obesity. They randomized participants to complete a medically supervised weight-loss program or to maintain a stable weight for 16 weeks. Participants in the weight-loss program consumed a very-low-calorie diet (800 calories per day) for eight weeks, followed by four weeks of a conventional low-calorie diet and four weeks of a weight maintenance diet. The researchers sequenced DNA from the participants' gut microbiota to determine the number and type of microbes present. Finally, they collected gut microbiota samples from the baseline and 12-week timepoints from the participants who lost the most weight during the weight loss program. They transplanted these samples into germ-free mice, which lack a microbiota.

    Participants in the weight-loss program lost an average of 14 percent of their body weight (about 27 pounds) after 12 weeks. A very-low-calorie diet reduced the abundance and diversity of microbes in the gut, but these changes were reversed when participants returned to a normal diet. Microbiota samples from the participants in the very-low-calorie diet intervention were enriched in Clostridioides difficile, a gastrointestinal pathogen (commonly referred to as “C. diff.”). This increase was associated with a reduction in the production of bile acids, which aid in dietary fat digestion and are protective against gastrointestinal pathogens. Mice that received a microbiota transplant from the very-low-calorie diet timepoint lost significantly more body weight due to changes in microbiota structure and reduced nutrient absorption, compared to mice that received a microbiota transplant from baseline.

    This research highlights the importance of diet in the interplay between pathogenic and beneficial microbes in the gut microbiota.

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  • Daily apple consumption decreases multiple markers of obesity-associated inflammation. academic.oup.com
    Diet Obesity Inflammation Polyphenol Intestinal Permeability Endotoxemia Lipopolysaccharide IL-6

    Obesity is characterized by chronic low-grade inflammation, which contributes to the development of cardiovascular disease. While processed foods and beverages high in saturated fats and simple sugars are associated with a higher risk of cardiovascular disease, diets rich in plant-based foods, including fruits, are associated with a lower risk. Findings of a recent report detail the effects of daily apple consumption on inflammation, endotoxemia, and metabolism.

    Causes of obesity-associated inflammation include leaky gut, a condition where the intestinal barrier is compromised, leading to increased levels of bacterial endotoxin (toxins that are released when bacteria die) in the bloodstream (called endotoxemia). This increase in endotoxin levels activates white blood cells to secrete pro-inflammatory cytokines such as interleukin (IL)-6 and IL-17. Plant foods such as apples are beneficial for people with obesity because they are rich in bioactive compounds that decrease inflammation and dietary fibers that strengthen the gut barrier.

    The researchers recruited 46 participants with overweight and obesity and directed them to avoid foods and beverages rich in polyphenols and/or dietary fibers (e.g., coffee, vegetables, grains, beans, and red/purple/blue fruits) for two weeks. Next, they assigned half of the participants to consume three Gala apples per day for six weeks or to avoid apples. Both groups continued to eat a diet with limited polyphenols and dietary fibers. Participants provided blood samples for the collection of white blood cells and measurement of pro-inflammatory cytokines. After isolating the white blood cells, the researchers stimulated them with endotoxin and measured their response.

    Apple consumption decreased plasma C-reactive protein (a pro-inflammatory cytokine) by 17 percent, IL-6 by 12 percent, and endotoxin-binding protein by 20 percent compared with no apple consumption. White blood cells from participants who consumed apples secreted 28 percent less IL-6 and 11 percent less IL-17. While apple consumption increased total antioxidant capacity in blood by 10 percent, it had no effect on cardiovascular disease markers.

    These findings suggest that six weeks of daily Gala apple consumption helped mitigate inflammation in those consuming a diet low in polyphenols and fiber, a common feature of the Western diet pattern. Apple consumption may decrease cardiovascular disease risk in those with obesity, even without weight loss.

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  • Drinking oolong tea promotes fat burning. www.eurekalert.org
    Obesity Green Tea Polyphenol

    Tea from the leaves of the Camelia sinensis plant is one of the most widely consumed beverages worldwide. Its consumption is associated with a variety of beneficial health effects. Findings from a recent study suggest that oolong tea consumption promotes weight loss.

    Many types of tea from Camelia sinensis exist, but they are generally classified as green, oolong, or black. The differences in the three types arise during processing, where they undergo various degrees of oxidation. Green tea is unoxidized; oolong tea is partially oxidized; and black tea is fully oxidized. Tea contains several bioactive compounds, including catechins and caffeine. Catechins are polyphenolic compounds that exert antioxidant properties. Caffeine is a potent stimulant.

    The intervention study involved 12 healthy non-obese men between the ages of 20 and 56 years. The participants consumed one of three beverages at breakfast and lunch for three 14-day sessions: oolong tea containing 51.8 milligrams of caffeine and 48.5 milligrams of catechins; a beverage containing 51.8 milligrams of caffeine; or a placebo beverage. A washout period of about two weeks separated each session. The men drank no other beverages containing caffeine or alcohol during the study period. They underwent 24-hour indirect calorimetry to monitor their metabolism and polysomnographic sleep recording to gauge their sleep quality.

    The authors of the study found that fat oxidation increased by roughly 20 percent when the participants drank the oolong tea or pure caffeine beverage, but not when they drank the placebo beverage. The effects of consuming oolong tea continued to a greater degree while the participants were asleep. Neither of the caffeine-containing beverages promoted an increase in the men’s energy expenditure, and none of the men exhibited alterations in sleep quality, suggesting that they developed a tolerance to the stimulatory effects of caffeine.

    These findings suggest that oolong tea stimulates fat oxidation, especially during the overnight fast.

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  • Brown fat is linked with lower risk of some chronic diseases. www.sciencedaily.com
    Obesity Cold Stress Brown Fat

    Obesity, or having excess body fat, is a known risk factor for a wide range of diseases, including diabetes, cancer, and dementia. Findings from a new study indicate that having brown fat is linked with lower risk of some chronic diseases.

    Brown fat, also known as brown adipose tissue, is found in all mammals and is particularly abundant in newborns. Unlike white fat, brown fat is a metabolically active tissue that is rich in mitochondria. It helps maintain body temperature during cold exposure, during which its uptake of glucose is eightfold higher than that of muscle tissues.

    The authors of the retrospective case-control investigation reviewed imaging reports from more than 52,000 adults who had undergone diagnostic positron emission tomography (PET) scans (nearly 135,000 total scans). They also reviewed the participants' health records.

    The PET scans revealed that nearly 10 percent of the study participants had detectable brown fat. Those who had brown fat were less likely to have type 2 diabetes, abnormal lipid levels, coronary artery disease, cerebrovascular disease, congestive heart failure, and hypertension. They were also more likely to have favorable blood glucose, triglyceride, and high-density lipoprotein levels. These effects were greatest in people who had obesity or overweight. The authors suggested that having brown fat might counteract some of the harmful effects of obesity.

    These findings indicate that brown fat may protect against some diseases and suggest that adopting lifestyle behaviors that promote production of brown fat, such as exercise or cold exposure, may be beneficial. Some nutrients and bioactive compounds, such as curcumin, capsaicin, resveratrol, and omega-3 fatty acids, may increase brown fat production, too.

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  • A Western diet impairs odor-related learning and memory in mice. www.sciencedaily.com
    Obesity

    Loss of olfactory system function – the sense of smell – is an early indicator of cognitive decline in people with type 2 diabetes and obesity. A new study in mice demonstrates the negative effects of a high-fat, high-sugar Western dietary pattern on odor-related learning and memory.

    Smell is an important regulator of behavior and memory, especially in non-human animals like mice. Olfactory system dysfunction may be due to decreased neurogenesis in the olfactory regions of the brains. In this way, changes in smell may signal decreased neurogenesis in other areas of the brain, which may indicate cognitive decline and Alzheimer’s disease progression.

    The investigators fed mice either standard chow, a high-fat diet (54 percent of calories from fat), or a Western diet (42 percent of calories from fat, 34 percent of calories from sugar) for eight months. They measured body weight, blood glucose, olfactory learning and memory, and cellular mechanisms of smell.

    After just three months of consuming a Western diet, mice showed declines in odor-related learning and memory. Weight gain and loss of glucose control were similar between the mice eating the Western and high-fat diets, but higher than among the mice eating the standard chow. After eight months, the mice consuming the Western and high-fat diets exhibited a diminished sense of smell and impaired olfactory learning and memory. However, the authors were unable to detect cellular changes related to this outcome.

    These findings add to a growing number of studies investigating the role of diet and obesity in cognitive decline. The authors encourage future researchers to investigate the interactions between olfactory and endocrine systems in people with obesity and type 2 diabetes.

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  • Obesity impairs brain neuroplasticity, increasing the risk for dementia and cognitive decline. www.unisa.edu.au
    Brain Obesity

    Having obesity increases a person’s risk for developing many chronic diseases, including dementia. The global prevalence of obesity is approximately 13 percent. A recent study suggests that obesity impairs brain neuroplasticity.

    Neuroplasticity, the brain’s capacity to reorganize itself in response to changes in its environment, is critical during periods of learning, psychological stress, and trauma. Some evidence suggests that obesity impairs neuroplasticity. People with dementia and Alzheimer’s disease often have impaired neuroplasticity.

    The study involved 30 young adults, 14 of whom had obesity and 16 of whom had healthy body weights. The authors of the study measured the participants' brain plasticity using a technique called theta burst transcranial magnetic stimulation (cTBS) – a procedure involving repeated pulses of electrical stimulation. They applied cTBS to the motor cortex of the participants' brains (an area responsible for the planning, control, and execution of voluntary movements) to briefly suppress excitability, a nerve’s capacity to produce an action potential.

    They found that cTBS suppressed cortical excitability in the participants in the healthy weight group but not among those in the obese group, suggesting impaired neuroplasticity among those with obesity.

    The authors of the study suggested that the reduced neuroplasticity observed among the obese participants might be due to inflammation, a common feature in obesity and a key driver in many chronic diseases. However, they also posited that the impairments were due to reduced levels of brain-derived neurotrophic factor (BDNF) – a cell signaling protein that plays key roles in a number of signaling pathways. BDNF levels and signaling are often decreased in the setting of obesity, but exercise increases BDNF levels.

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  • Probiotics may help manage obesity in children and adolescents. www.sciencedaily.com
    Obesity Supplements

    Nearly one in five children and adolescents living in the United States has overweight or obesity, placing them at risk for many chronic diseases, including heart disease and diabetes. A study presented at the European Endocrine Society’s recent conference suggests that probiotics can help manage obesity in young people.

    Probiotic bacteria are widely defined as live microorganisms that, when consumed in sufficient amounts, confer a health benefit on the consumer. They contain a variety of microorganisms, but Lactobacillus and Bifidobacterium bacteria are among the most common. Probiotics can be found in yogurt and other fermented foods and are widely available as dietary supplements.

    The authors of study were particularly interested in the effects of supplemental Bifidobacteria. They placed 100 obese children and teens between the ages of six and 18 years on a reduced calorie diet and then randomly assigned them to receive either a Bifidobacteria probiotic or a placebo. The authors measured the effects of the probiotic supplement in terms of body weight, metabolism, and gut microbial composition.

    They found that the children who took the probiotics while following the reduced calorie diet had reduced waist circumference, body mass, insulin function, and had fewer harmful bacteria in their gut. These findings demonstrate that probiotic supplementation may augment the beneficial effects of calorie reduction in children and adolescents with obesity.

    For the most part, however, usage of probiotic supplements has preceded the scientific evidence of their efficacy. Many probiotic supplements contain insufficient numbers of bacteria to elicit a beneficial response and many are not stored properly to maintain the viability of the bacteria they supposedly contain. Watch this clip in which Drs. Jed Fahey and Rhonda Patrick discuss concerns about the safety and efficacy of probiotic supplements.

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  • Consuming a diet with a high omega-6 to omega-3 fatty acid ratio during pregnancy may contribute to overeating in offspring. www.sciencedaily.com
    Obesity Lactate

    Maternal consumption of omega-6 and omega-3 fatty acids is essential for fetal brain development. Maintaining the proper balance of these two fatty acids is critical, but the typical Western diet is high in omega-6s and low in omega-3s. Findings from a new study in mice suggest that a high omega-6 to omega-3 fatty acid ratio of intake during pregnancy alters dopamine signaling, contributing to overeating in offspring.

    Dopamine is a neurotransmitter best known for its role in motor activity, motivation, and pleasure control. When exposed to a rewarding stimulus, the brain responds by increasing dopamine release to motivate behavior. Neurons that release dopamine are activated when a reward is expected.

    The authors of the study fed female mice either regular mouse chow or chow that was high in omega-6 fatty acids and low in omega-3s. The mice began eating their respective diets before mating and then throughout pregnancy and lactation. After the offspring were weaned, they ate the same diets as their mothers.

    The authors measured how much of a sucrose-containing solution (three solutions containing 3, 10, or 30 percent sucrose) the mice consumed after being water-deprived or when allowed to consume freely. Then they examined whether the mice preferred only sucrose-containing solutions or a high-fat diet after being food deprived. Finally, they administered a dopamine-inhibiting drug to the mice to determine if dopamine signaling influenced the mice’s eating behaviors.

    The mice that had been fed the high omega-6/low omega-3 diet consumed far more sucrose solution whether they were water-deprived or allowed to consume freely, compared to the mice fed the regular diet. The high omega-6/low omega-3 mice also consumed higher quantities of sucrose solution or high-fat foods after being food-deprived. Administration of the dopamine inhibitor reduced the animals' intake, however.

    These findings suggest that mice that are fed a diet with a high omega-6 to omega-3 ratio from conception through early life develop a stronger preference for highly palatable foods, many of which can contribute to obesity and other chronic health conditions. Foods high in omega-3 fatty acids include salmon and their roe, shellfish, walnuts, and flaxseed. For a fun, tasty way to eat salmon roe, check out this episode in which Dr. Rhonda Patrick shares her recipe for salmon roe stacks.

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  • Soluble fiber supplementation improves body weight and metabolism in adults with overweight and obesity. academic.oup.com
    Obesity Microbiome

    More than two-thirds of adults living in the United States have overweight or obesity. Having overweight or obesity increases a person’s risk of developing metabolic disorders such as diabetes. Findings from a 2017 review indicate that dietary fiber supplementation reduces body weight and improves metabolism in adults with overweight or obesity.

    Dietary fiber is classified as either soluble or insoluble. Soluble fiber, which is found in grains, nuts, seeds, legumes, and some vegetables and fruits, dissolves in water and may reduce blood glucose and cholesterol levels. Insoluble fiber, which is found in wheat bran, vegetables, and whole grains, does not dissolve in water. It promotes digestive health. Processed foods are typically low in fiber.

    According to the Dietary Guidelines for Americans, the recommendations for combined fiber intake vary according to age and sex. Women need between 22 and 28 grams of fiber per day, and men 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 on a daily basis.

    The authors of the review analyzed the findings of 12 randomized controlled trials involving more than 600 participants enrolled in interventions lasting between two and 17 weeks. Their analysis revealed that supplementation elicited beneficial effects on the study participants, with modest but notable improvements observed in BMI, body weight, body fat, fasting glucose, and fasting insulin, compared with the effects of placebo treatments. The authors of the review noted that the types of soluble fiber and dosages varied considerably across the 12 studies, however.

    These findings suggest that soluble fiber supplementation is a promising strategy for improving weight and metabolic health in people with overweight or obesity and supports efforts to increase fiber content of processed foods.

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  • Losing weight between early adulthood and midlife can reduce the chance of premature death. www.sciencedaily.com
    Obesity Aging

    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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  • Alpha-lipoic acid supplements promote weight loss in obese people who are otherwise healthy. www.sciencedaily.com
    Obesity

    Obesity is a major contributor to many of the leading causes of death, including cardiovascular disease, stroke, diabetes, and cancer. More than 650 million adults are obese worldwide. Findings from a new study suggest that alpha-lipoic acid promotes weight loss in obese adults.

    Alpha-lipoic acid is a naturally occurring substance present in the human body and in some foods. It is a powerful antioxidant that amplifies the beneficial effects of other antioxidants in the body such as glutathione and coenzyme Q10. Alpha-lipoic acid participates in metabolism by inhibiting fatty acid and triglyceride synthesis and, in turn, promoting fatty acid oxidation, triglyceride clearance from the liver, and fat loss. Dietary sources of alpha-lipoic acid include spinach, broccoli, and organ meats, among others. It is widely available as a dietary supplement.

    The randomized, double-blind, controlled trial involved 81 overweight or obese adults between the ages of 21 and 60 years who had elevated triglycerides but were otherwise healthy. Half of the participants took 600 milligrams of alpha-lipoic acid per day, while the other half took a placebo. The participants were asked to not change their diet or physical activity for the duration of the 24-week study. The authors of the study took anthropometric measures, checked vital signs, and collected blood and urine samples from the participants at the beginning of the trial, at week 12, and at week 24.

    The authors found that the participants who took alpha-lipoic acid did not experience changes in their triglyceride levels, but they did lose body weight. The greatest losses were observed among women and obese participants, who lost as much as 5 percent of body weight. Those who took alpha-lipoic acid also had higher levels of antioxidant enzyme expression, which is associated with reduced inflammation – a key driver in many diseases.

    These findings demonstrate that alpha-lipoic acid reduces body fat in overweight or obese people, independent of dietary or physical activity changes.

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  • Consuming carotenoid-rich vegetables reduces visceral body fat in obese men. pubmed.ncbi.nlm.nih.gov
    Diet Obesity Carotenoids Visceral Fat

    Carotenoids are red, yellow, and orange pigments found in fruits and vegetables that exert antioxidant, anti-inflammatory, and anticancer properties. Lycopene (which is found in tomatoes and watermelon) and lutein (which is found in green leafy vegetables) are among the most abundant carotenoids in the human diet. Findings from a recent study suggest that consuming vegetables that are high in lycopene and lutein can help reduce visceral fat in obese men.

    Visceral fat is body fat that is stored in the abdominal cavity close to internal organs such as the liver, pancreas, and intestines. In contrast to subcutaneous fat, which is located under the skin, visceral fat plays a central role in the interrelationship between obesity and systemic inflammation through its secretion of proinflammatory cytokines. The accumulation of visceral fat is linked to type 2 diabetes, insulin resistance, inflammatory diseases, certain types of cancer, cardiovascular disease, and other obesity-related diseases.

    The randomized, double-blinded, controlled clinical trial involved 28 men between the ages of 40 and 65 years who were overweight or obese. The authors of the eight-week study randomly assigned the participants to consume a beverage containing one of four edible pastes that contained high lycopene/high lutein; high lycopene/low lutein; low lycopene/high lutein; or low lycopene/low lutein. The authors measured the levels of carotenoids in the participants' plasma.

    The participants' carotenoid levels increased in every group and they experienced no adverse effects. Their visceral fat levels decreased for all groups, too, but waist circumference decreased only for the men in the high lycopene/low lutein group.

    These findings suggest that high carotenoid intake can help with weight loss. They also support epidemiological data indicating that vegetable intake can play a positive role in modulating body weight. For a tasty way to include more carotenoids in your diet, check out this video in which Dr. Rhonda Patrick shows how to make her carotenoid-rich smoothie.

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  • Omega-3 DHA intake increases hypothalamic neurogenesis in mice. diabetes.diabetesjournals.org
    Brain Obesity Omega-3 BDNF

    Saturated fatty acid intake induces inflammation in the hypothalamus that can eventually lead to apoptosis of hypothalamic neurons and subsequent loss of the control of caloric intake and energy expenditure. The overall health of hypothalamic neurons requires their regular renewal, a process known as neurogenesis, which is impaired in obesity. Findings from a 2016 study showed that docosahexaenoic acid (DHA), a type of polyunsaturated fatty acid (PUFA), increased hypothalamic neurogenesis in mice.

    DHA is an omega-3 fatty acid found in the human brain and the meat of fatty fish. DHA plays a key role in the development of eye and nerve tissues and is essential for normal brain function in humans.

    The authors of the study conducted a six-protocol study in mice. They fed the mice a high-fat diet for eight weeks and then fed them diets containing varying concentrations and types of fats, including flaxseed oil and DHA. They also injected DHA or BDNF, a growth factor involved in neurogenesis, into the brains of the mice.

    Mice that ate the DHA-containing diet showed improvements in body mass, glucose metabolism, activity levels, and response to leptin, a hormone involved in appetite control. Both the DHA-containing diet and the injected DHA increased levels of hypothalamic neurogenesis at rates similar to or superior to those observed with BDNF.

    These findings suggest that dietary intake of PUFAs such as DHA show promise as a strategy to ameliorate hypothalamic neuronal losses associated with obesity.

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  • From the blood to the brain: BDNF-producing blood cells travels to the hypothalamus in adults, regulating and suppressing appetite [animal research] www.sciencedaily.com
    Brain Obesity BDNF

    From the article:

    We knew that blood cells produced BDNF,“[…] "We didn’t know why it was produced in blood cells.”

    Dr. Hiroshi Urabe and Dr. Hideto Kojima, current and former postdoctoral fellows in Chan’s laboratory respectively, looked for BDNF in the brains of mice who had not been fed for about 24 hours. The bone marrow-derived cells had been marked with a fluorescent protein that showed up on microscopy. To their surprise, they found cells producing BDNF in a part of the brain’s hypothalamus called the paraventricular nucleus.

    “We knew that in embryonic development, some blood cells do go to the brain and become microglial cells,” said Chan. […]“This is the first time we have shown that this happens in adulthood. Blood cells can go to one part of the brain and become physically changed to become microglial-like cells.”

    A new way to affect appetite and obesity?

    When normal bone marrow cells that produce BDNF are injected into the third ventricle (a fluid-filled cavity in the brain) of mice that lack BDNF, they no longer have the urge to overeat, said Chan.

    All in all, the studies represent a new mechanism by which these bone-marrow derived cells control feeding through BDNF and could provide a new avenue to attack obesity, said Chan.

    He and his colleagues hypothesize that the bone marrow cells that produce BDNF fine tune the appetite response, although a host of different appetite-controlling hormones produced by the regular nerve cells in the hypothalamus do the lion’s share of the work.

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  • BDNF response in obese subjects is better under in high-intensity conditions rather than moderate-intensity: addressing cognitive dysfunction in obese www.sciencedaily.com
    Exercise Brain Obesity Aerobic BDNF Lactate

    From the article:

    Results of study, published in the journal Experimental Biology and Medicine, show that the BDNF response to acute high-intensity interval exercise was greater than continuous moderate-intensity exercise in obese subjects when compared to normal-weight subjects. Similarly, although acute high-intensity interval exercise induced greater blood lactate and plasma cortisol levels than continuous moderate-intensity exercise, obese subjects produced less blood lactate, but showed no difference in cortisol than normal-weight subjects.

    These findings suggest that acute high-intensity interval exercise may be a more effective protocol to upregulate BDNF expression in an obese population, independent of increased lactate and cortisol levels.

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  • Environmental enrichment alone produces browning of fat and enhanced weight control not accountable by exercise alone [animal study]
    Brain Obesity Memory Fat BDNF Thermogenesis

    From the article:

    “Up to now the only known approach to inducing brown fat has been through exposure to chronic cold. Our research reveals a novel way of doing this without cold exposure. We show that animals living in an enriched environment become lean and resistant to diet-induced obesity, even in the presence of unlimited food.”

    […]

    The current study used a similarly designed environment, with 15-20 mice housed in large containers equipped with running wheels, tunnels, huts, wood toys, a maze, and nesting material, in addition to unlimited food and water.

    Key findings include the following:

    • Enriched animals showed a significant reduction in abdominal white fat mass (49 percent less than controls).

    • Exercise (running in a wheel) alone did not account for the changes in body composition and metabolism of enriched animals.

    • Fed a high fat diet (45 percent fat), enriched animals gained 29 percent less weight than control mice and remained lean, with no change in food intake. Enriched animals also had a higher body temperature, suggesting that greater energy output, not suppressed appetite, led to the resistance to obesity.

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  • Increases in brain-derived neurotrophic factor from aerobic exercise associated with appetite suppression, weight loss, and improved blood pressure www.sciencedaily.com
    Exercise Brain Obesity Blood Pressure Aerobic Weight Loss BDNF

    From the article:

    The team evaluated blood levels of BDNF before and after a three-month program of aerobic exercise in 15 overweight or obese men and women. The seven men and eight women, ages 26 to 51, worked out on a treadmill and bicycle. They were asked about their calorie intake and told to continue eating their usual number of calories. The participants were unaware that one of the study’s objectives was to evaluate changes in food intake.

    At the end of the study, the subjects had decreased BMI, waist circumference, and blood pressure, the data showed. They also reported consuming fewer calories than at the beginning of the study. Over the three months, BDNF levels greatly increased. This higher the concentration of BDNF, the less the subject’s intake of calories and the greater the weight loss, Araya said.

    Thus, it is possible that increases in BDNF suppress appetite, she said. They did not test appetite suppression directly, but some past studies have shown that aerobic exercise suppresses appetite.

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  • Cardiorespiratory fitness and body composition influence brain health. www.eurekalert.org
    Exercise Brain Obesity

    A growing body of research demonstrates that exercise has beneficial effects on brain health. N-acetyl aspartic acid (NAA) is a compound found in the central nervous system that serves as a biomarker of neuronal health and energy production. Findings from a new study indicate that lower body fat and higher cardiorespiratory fitness are positively correlated with NAA levels.

    Cardiorespiratory fitness is a measure of the body’s ability to deliver oxygen to skeletal muscles during sustained physical activity. It is commonly measured by VO2 max, a person’s maximum rate of oxygen consumption while under maximal physical stress. Cardiorespiratory fitness is linked with lower body fat composition.

    The study involved 290 healthy young adults (average age, 24 years). Each of the participants' body composition and cardiorespiratory fitness were assessed. Then the participants underwent magnetic resonance spectroscopy (MRS) to assess their NAA levels.

    The MRS scans revealed that participants with less body fat and higher levels of cardiorespiratory fitness had higher levels of NAA in the white matter of their brains. This association was driven primarily by a participant’s whole-body total percent fat, suggesting that body fat might have negative effects on brain health. Exercise exerts a wide range of beneficial effects on brain health. Watch this podcast featuring Dr. Rhonda Patrick in which she describes how exercise might be useful in treating or reducing the risk of depression.

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  • Omega-3 fatty acids decrease oxidative stress and affect biomarkers of aging. www.sciencedaily.com
    Obesity Aging Omega-3 Inflammation

    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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  • As a cofactor in the biosynthesis of carnitine, vitamin C may have a role in enhancing PPAR-alpha-dependent fatty acid oxidation www.nature.com
    Obesity Vitamin C Fatty Liver Weight Loss Visceral Fat

    From the publication:

    Ascorbic acid is a known cofactor in the biosynthesis of carnitine, a molecule that has an obligatory role in fatty acid oxidation […] Ascorbic acid supplementation increased the mRNA levels of PPARα and its target enzymes involved in fatty acid β-oxidation in visceral adipose tissues. Consistent with the effects of ascorbic acid on visceral obesity, ascorbic acid not only inhibited hepatic steatosis but also increased the mRNA levels of PPARα-dependent fatty acid β-oxidation genes in livers. Similarly, hepatic inflammation, fibrosis, and apoptosis were also decreased during ascorbic acid-induced inhibition of visceral obesity. In addition, serum levels of alanine aminotransferase, aspartate aminotransferase, total cholesterol, and LDL cholesterol were lower in HFD-AA-fed mice than in those of HFD-fed mice.

    A few bullet points:

    • Reduced visceral obesity
    • Reduced hepatic inflammation
    • Increased expression of PPAR-a
    • Improved markers of liver health and cholesterol

    Related: studies in humans have shown reduced vitamin C status directly impacts fat oxidation in response to exercise.

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  • Vitamin C reduces C-reactive protein among some groups of people. www.sciencedaily.com
    Obesity Vitamin C Inflammation

    Inflammation is a biological response triggered by the immune system in response to a physical injury or infection. Vitamin C’s immune-boosting and antioxidant properties can mediate the body’s inflammatory response, reducing the symptoms or risk of various diseases. Evidence suggests that vitamin C can lower C-reactive protein, a marker of inflammation.

    C-reactive protein (CRP) is a protein that increases in the blood with inflammation and infection as well as following a heart attack, surgery, or trauma. It is one of several proteins that are often referred to as acute phase reactants. Blood levels of CRP greater than 1 milligram per liter are indicative of elevated cardiovascular disease risk.

    The randomized study involved nearly 400 healthy adults (average age, 44 years) who took 1 gram of vitamin C, 800 international units of vitamin E, or a placebo every day for two months. The findings revealed that vitamin E had no effect on lowering CRP; however, vitamin C supplementation decreased CRP 16.7 percent compared to pre-treatment measurements, but only in participants who had baseline CRP levels above 1 milligram per liter. This reduction in CRP was comparable to those achieved with statins (cholesterol-lowering drugs).

    Interestingly, the study identified a strong link between obesity and elevated CRP levels. Whereas 25 percent of normal-weight people had elevated CRP levels of CRP, 50 percent of overweight participants and 75 percent of obese participants had elevated levels.

    These findings suggest that vitamin C might be able to decrease inflammation to a similar magnitude as some statins in people at a higher risk of cardiovascular disease based on CRP levels.

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  • Diet-induced thermogenesis is higher after breakfast than after dinner. academic.oup.com
    Obesity Fasting Protein Dairy

    Eating increases the body’s metabolic rate, a phenomenon referred to as diet-induced thermogenesis (also known as the “thermic effect” of food). Diet-induced thermogenesis begins about an hour after eating, peaks about two hours later, and then maintains a steady level for several more hours. Approximately 5 to 15 percent of a person’s daily energy expenditure– an estimate of how many calories a person burns per day – is due to diet-induced thermogenesis.

    A few factors influence the degree of diet-induced thermogenesis, including meal size, macronutrient content (protein versus fat, for example) and environmental temperature. Age and physical activity may also play roles in diet-induced thermogenesis. Findings from a new study suggest that circadian variations in energy expenditure influence diet-induced thermogenesis.

    The randomized, cross-over, laboratory study involved 16 healthy, normal-weight men. Each of the men ate three meals per day in the laboratory for three days and maintained a regular sleep pattern. The authors of the study conducted indirect calorimetry tests to determine the participants' energy expenditure and collected participants' blood samples before and after meals to gauge glucose tolerance. The participants rated their feelings of hunger on a Likert scale.

    Meals consisted of a high-calorie breakfast and low-calorie dinner or the converse – a low-calorie breakfast and a high-calorie dinner. The high-calorie meals provided 69 percent of the participants' calorie needs and the low-calorie meals provided 11 percent. All lunches were identical and provided 20 percent of the participants' calorie needs.

    The indirect calorimetry tests revealed that the participants' diet-induced thermogenesis after breakfast was generally 2.5 times higher than after dinner. The participants' glucose levels were, on average, lower after breakfast than after dinner. Glucose levels were 17 percent higher after eating the low-calorie dinner compared with levels after eating the low-calorie breakfast. The participants reported having greater feelings of hunger, especially for sweet foods, on days when they ate the low-calorie breakfast.

    These findings highlight the role of circadian variation in metabolism and underscore the need for modifying food intake to exploit this variation.

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  • Obesity promotes diversity and virulence of influenza virus. www.eurekalert.org
    Obesity Immune System Protein

    Global estimates indicate that more than half of all adults are either overweight or obese. Obesity carries many health risks because it impairs the body’s immune response and creates a pro-inflammatory environment. In particular, being obese increases the disease severity of influenza infection. A recent study suggests that the impaired immune response commonly exhibited in people who are obese promotes the emergence of more virulent influenza strains.

    Influenza is a highly contagious respiratory infection caused by the influenza virus. More than 20,000 people die every year in the United States from influenza-related complications. Many different influenza viruses exist, and they undergo constant change, necessitating regular changes to influenza vaccines. Some of the changes to the influenza virus are due to the health and nutritional status of infected hosts. For example, diet-induced oxidative stress, micronutrient status, and aging can influence influenza virus virulence.

    The authors of the study serially infected lean and obese mice with the influenza virus to replicate the spread of influenza within the real-world setting. They found that serial infection of obese mice promoted changes in the virus that produced more virulent strains of the virus. The key driver associated with these changes was an impaired interferon response. Interferons are proteins produced by the body’s cells as a defensive response to viruses. This delayed interferon response also occurred in obesity-derived human bronchial epithelial cells.

    These findings suggest that obesity promotes influenza virus diversity and virulence and underscores concerns about the growing obesity problem.

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  • Excess visceral fat promotes inflammation and drives cognitive decline. www.eurekalert.org
    Brain Obesity Depression Neurons Protein Metabolic Syndrome NLRP3 Visceral Fat

    Visceral fat – body fat that is stored in the abdominal cavity in close proximity to important internal organs such as the liver, pancreas, and intestines – plays a central role in the interrelationship between obesity and systemic inflammation. Excess visceral fat, often referred to as central or abdominal obesity, is a strong predictor of age-related cognitive decline. A new study in mice demonstrates that having excess visceral fat may impair cognition by activating the NLRP3 inflammasome and promoting the release of interleukin-1 beta (IL-1β).

    Inflammasomes are large, intracellular complexes that detect and respond to internal and external threats. Activation of inflammasomes has been implicated in a host of inflammatory disorders. Cryopyrin, also known as NLRP3, is a protein that drives the formation and activation of the NLRP3 inflammasome.

    Interleukin-1 beta is a proinflammatory protein present in many cells. NLRP3 inflammasome-driven release of IL-1β activates microglia, the brain’s resident immune cells. Microglia serve an essential role in maintaining brain microenvironment homeostasis. Acute activation of microglia modulates inflammation and neurotoxicity, but chronic activation promotes brain inflammation and harm.

    The authors of the study first determined that mice lacking the gene for NLRP3 did not experience visceral fat-induced brain inflammation and cognitive decline. They also determined that when visceral fat from normal, obese mice was transplanted into these mice, they exhibited higher levels of IL-1β in their hippocampus, an area of the brain associated with memory (in particular, the consolidation of short-term memories to long-term memories), learning, and spatial navigation.

    To understand the effects of IL-1β on brain function, the authors of the study fed the mice a high- or low-fat diet for 12 weeks and then assessed the animals' capacity to navigate a water maze. The mice that ate the higher-fat diet experienced greater difficulties negotiating the water maze, compared to those that ate the lower-fat diet. Examination of the animals' brains revealed that the mice that ate the high-fat diet (as well as those that received the fat transplants) had weaker synapses between the neurons involved in learning and memory.

    These findings suggest that chronic inflammation driven by excess visceral fat may contribute to cognitive decline by promoting the release of IL-1β and increasing inflammation. Inflammation drives other aspects of brain dysfunction, including those associated with depression. Watch this clip in which Dr. Charles Raison discusses how a pro-inflammatory environment can contribute to the risk of depression.

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  • The negative effects of obesity mimic the aging process. www.sciencedaily.com
    Obesity Aging

    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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  • Children of women exposed to parabens during pregnancy are at greater risk of being obese. www.sciencedaily.com
    Obesity Epigenetics Satiety Neurons

    Obesity is a growing problem worldwide, especially among children and young adults. Many factors contribute to obesity, including environmental exposures, which can drive epigenetic changes. Findings from a new study suggest that maternal exposure to parabens may increase the risk of obesity among children.

    Parabens are widely used synthetic compounds that exert antibacterial and antifungal properties. They are commonly used in cosmetics, drugs, and some foods. Parabens can be ingested or absorbed through the skin. Some evidence suggests that parabens are endocrine disruptors.

    The study had multiple arms that included an analysis of epidemiological data from the German LINA study and an experimental study in mice that simulated paraben exposure during pregnancy. The epidemiological data revealed that the children of women who had high exposure to parabens during pregnancy (assessed by urinary excretion) were more likely to be obese, an effect that was more pronounced in girls. Findings from the mouse study suggested that this increased risk of obesity was driven by epigenetic mechanisms associated with the altered expression of the proopiomelanocortin gene (known as POMC), which plays critical roles in the neuronal regulation of appetite, satiety, and food intake.

    These findings suggest that prenatal environmental exposures to everyday compounds such as parabens may have far-reaching effects on the health of offspring.

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  • Abdominal obesity is associated with fatal heart attacks and strokes independent of other risk factors. www.escardio.org
    Obesity Heart Disease Weight Loss

    Myocardial infarction (MI), commonly referred to as heart attack, occurs when one of the heart’s coronary arteries is blocked suddenly or has poor blood flow. One of the principal risk factors for MI in men and women is abdominal obesity. The relative risk of recurrent cardiovascular disease-related death after having MI is approximately 30 percent higher than the risk among people without MI. Findings from a recent study suggest that abdominal obesity increases the risk of a fatal recurrent MI or stroke.

    According to the World Health Organization, the waist circumference range for increased cardiovascular risk is 94 to 102 centimeters for men and 80 to 88 centimeters for women. Values above this range place people at greatly increased risk. Waist circumference measurement is particularly relevant in people whose body mass index is normal or overweight.

    The study was based on data gathered from more than 22,000 people living in Sweden who were between the ages of 35 and 77 years old and had experienced their first MI. The participants were followed for approximately four years for recurrent cardiovascular events, including nonfatal MI, coronary heart disease death, or stroke.

    The findings indicated that during the follow-up period, 7.3 percent of the men and 7.9 percent of the women had a recurrent cardiovascular event. The majority of the study participants had a waist circumference that was higher than the WHO’s recommended thresholds. Having a larger waist circumference was associated with roughly 20 percent greater risk of recurrent cardiovascular-related event, regardless of age, body mass index, or other risk factors, especially in men. Interestingly, participants who were overweight were less likely to experience a recurrent cardiovascular disease-related event compared to those who were normal weight or obese.

    These findings demonstrate that waist circumference may be a useful tool in the clinical setting for identifying patients at increased risk for recurrent MI and suggest that strategies to reduce abdominal fat (such as lifestyle modification) may reduce the risk of fatal heart attacks and strokes.

    Read more
  • Boys whose mothers were overweight or obese during pregnancy scored 5 or more points lower on IQ tests at age 7. www.sciencedaily.com
    Brain Obesity Pregnancy Intelligence

    Many factors influence a child’s growth and development, including parenting styles, environmental exposures, socioeconomic status, and maternal health. Maternal obesity, in particular, drives inflammatory, hormonal, and metabolic dysfunction that may adversely affect a developing fetus. Findings from a new study indicate that boys born to obese women perform poorly in measures of motor skills and intelligence compared to children born to healthy weight women.

    The study involved 368 children born to low-income African American or Dominican women living in the United States. The children underwent motor skill and intelligence testing at the ages of 3 and 7 years, respectively. The women were weighed before and during their pregnancies.

    Boys born to women who were overweight or obese during pregnancy scored poorly on motor skills tests at age 3. Similarly, boys whose mothers were overweight or obese during pregnancy scored 5 or more points lower on intelligence tests, compared to boys whose mothers were a healthy weight. Girls did not exhibit differences in motor skills or intelligence. Interestingly, a nurturing home environment modulated some, but not all, of the negative effects of maternal obesity on development.

    Although this was a prospective study and causation cannot be established, these findings point to the importance of maternal nutritional status before and during pregnancy. Unfortunately, this study did not control for important confounders such as diet during pregnancy or whether mothers breastfed their sons. Breastfeeding has been linked to intelligence in children.

    It is noteworthy that the negative effects of maternal obesity were only found in boys and not girls. Other studies have shown that exposure to lead or fluoride in-utero has a negative effect on intelligence in boys. It seems as though boys are particularly vulnerable during fetal development.

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  • Obese adolescents have decreased white matter in a brain region that connects the right and left hemispheres of the brain (compared to healthy teens). www.sciencedaily.com
    Brain Obesity Inflammation Insulin

    Obese adolescents have decreased white matter in a brain region that connects the right and left hemispheres of the brain (compared to healthy teens). These changes correlated with markers of inflammation and insulin resistance.

    Approximately 20 percent of teens living in the United States are obese. Obesity negatively affects multiple organ systems, including the nervous system. Findings from a new study indicate that the white matter in the brains of obese teens is lower than that of healthy teens.

    Obesity is associated with chronic low-grade inflammation, which can drive many disease processes. A specialized magnetic resonance imaging technique, called diffusion tensor imaging (DTI), can measure this inflammation in the brain.

    A study involving 59 obese adolescents and 61 normal weight adolescents between the ages of 12 and 16 years used DTI to measure damage to the white matter in the teens' brains. The imaging results revealed that areas of the corpus callosum, a bundle of nerve fibers that connects the left and right hemispheres of the brain, as well as areas of the middle orbitofrontal gyrus, an area responsible for emotional control and reward circuits, were diminished in the obese teens' brains. Damage in these areas was correlated with altered levels of insulin, inflammatory markers, and leptin, a key regulator of appetite, and insulin.

    Future research with DTI imaging techniques may reveal whether these changes in the structure of obese teens' brains are reversible.

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  • Obesity can break down our protective blood brain barrier resulting in problems with learning and memory: overactivity of adenosine in obesity www.sciencedaily.com
    Brain Alzheimer's Obesity Diabetes Coffee Insulin Blood Sugar Blood-Brain Barrier Lipopolysaccharide

    Diet-induced insulin resistance caused blood vessels to become leaky which impaired blood and oxygen flow to a brain region involved in learning and memory (animal evidence).

    Obesity and insulin resistance are associated with a leaky blood-brain barrier. This new animal study found that a high-sugar combined with a high-fat diet caused shrinkage of the tight junctions between endothelial cells that make up the blood-brain barrier and actual holes in those cells.

    Obesity is known to increase toll-like receptor activation through a variety of mechanisms. One of the mechanisms is through through associated increases of circulating of lipopolysaccharide. Another mechanism is the leaking of fatty acids from fatty acids, triggering toll-like receptors through the recognition of damage-associated molecular patterns (DAMPs). (See “obesity” section of toll-like receptor article.)

    Furthermore, LPS challenge in animal studies induces microglia in the brain to attack and damage the blood-brain barrier.

    Blocking adenosine may play a role in preventing impairment of the blood-brain barrier by diet-induced obesity

    However, adenosine, which helps us sleep and helps regulate our blood pressure and is blocked by caffeine may play a role in preventing some of the damaging effects obesity has on the blood-brain barrier, which promotes dementia.

    From the article:

    They knew that chronic activation of the receptor Adora2a [an adenosine receptor] on the endothelial cells that line this important barrier in our brain can let factors from the blood enter the brain and affect the function of our neurons.

    Now Medical College of Georgia scientists have shown that when they block Adora2a in a model of diet-induced obesity, this important barrier function is maintained.

    […]

    In the brain, adenosine is a neurotransmitter that helps us sleep and helps regulate our blood pressure; in the body it’s also a component of the cell fuel adenosine triphosphate, or ATP. Adenosine also activates receptors Adora1a and Adora2a on endothelial cells, which normally supports healthy relationships between brain activity and blood flow.

    Problems arise with chronic activation, particularly in the brain, which is what happens with obesity, says Stranahan.

    People who have obesity and diabetes have higher rates of cognitive impairment as they age and most of the related structural changes are in the hippocampus, a center of learning and memory and Stranahan’s focus of study. Fat is a source of inflammation and there is evidence that reducing chronic inflammation in the brain helps prevent obesity-related memory loss.

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  • A high-fat diet promotes depression-like behavior in mice by suppressing hypothalamic PKA signaling papers.ssrn.com
    Brain Obesity Depression Saturated Fat Protein

    Obesity is associated with an increased risk of depression. The aim of the present study was to investigate whether obesity is a causative factor for the development of depression and what is the molecular pathway(s) that link these two disorders. Using lipidomic and transcriptomic methods we identified a mechanism that links exposure to a high-fat diet (HFD) in mice with alterations in hypothalamic function that lead to depression. Consumption of an HFD selectively induced accumulation of palmitic acid in the hypothalamus, suppressed the 3´, 5´-cyclic AMP (cAMP)/protein kinase A (PKA) signaling pathway, and increased the concentration of free-fatty acid receptor 1 (FFAR1). Deficiency of phosphodiesterase 4A (PDE4A), an enzyme that degrades cAMP and modulates stimulatory regulative G-protein (Gs)-coupled G protein-coupled receptor signaling, protected animals either from genetic- or dietary induced depression phenotype.

    These findings suggest that dietary intake of saturated fats disrupts hypothalamic functions by suppressing cAMP/PKA signaling through activation of PDE4A. FFAR1 inhibition and/or an increase of cAMP signaling in the hypothalamus could offer potential therapeutic targets to counteract the effects of dietary or genetically induced obesity on depression.

    https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3188483

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  • Probiotic Bifidobacterium strains and galactooligosaccharides improve intestinal barrier function in obese adults microbiomejournal.biomedcentral.com
    Gut Obesity Probiotics Prebiotics Endotoxemia Lipopolysaccharide

    Full Title: Probiotic Bifidobacterium strains and galactooligosaccharides improve intestinal barrier function in obese adults but show no synergism when used together as synbiotics

    Background: One way to improve both the ecological performance and functionality of probiotic bacteria is by combining them with a prebiotic in the form of a synbiotic. However, the degree to which such synbiotic formulations improve probiotic strain functionality in humans has not been tested systematically. Our goal was to use a randomized, double-blind, placebo-controlled, parallel-arm clinical trial in obese humans to compare the ecological and physiological impact of the prebiotic galactooligosaccharides (GOS) and the probiotic strains Bifidobacterium adolescentis IVS-1 (autochthonous and selected via in vivo selection) and Bifidobacterium lactis BB-12 (commercial probiotic allochthonous to the human gut) when used on their own or as synbiotic combinations. After 3 weeks of consumption, strain-specific quantitative real-time PCR and 16S rRNA gene sequencing were performed on fecal samples to assess changes in the microbiota. Intestinal permeability was determined by measuring sugar recovery in urine by GC after consumption of a sugar mixture. Serum-based endotoxin exposure was also assessed.

    Results: IVS-1 reached significantly higher cell numbers in fecal samples than BB-12 (P < 0.01) and, remarkably, its administration induced an increase in total bifidobacteria that was comparable to that of GOS. Although GOS showed a clear bifidogenic effect on the resident gut microbiota, both probiotic strains showed only a non-significant trend of higher fecal cell numbers when administered with GOS. Post-aspirin sucralose:lactulose ratios were reduced in groups IVS-1 (P = 0.050), IVS-1 + GOS (P = 0.022), and GOS (P = 0.010), while sucralose excretion was reduced with BB-12 (P = 0.002) and GOS (P = 0.020), indicating improvements in colonic permeability but no synergistic effects. No changes in markers of endotoxemia were observed.

    Conclusion: This study demonstrated that “autochthony” of the probiotic strain has a larger effect on ecological performance than the provision of a prebiotic substrate, likely due to competitive interactions with members of the resident microbiota. Although the synbiotic combinations tested in this study did not demonstrate functional synergism, our findings clearly showed that the pro- and prebiotic components by themselves improved markers of colonic permeability, providing a rational for their use in pathologies with an underlying leakiness of the gut.

    Keywords: Synbiotic, Probiotic, Prebiotic, Obesity, Gut barrier function, Autochthonous, Allochthonous, Galactooligosaccharide, Bifidobacteria, Bifidobacterium

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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
    Obesity Aging Muscle Weight Loss

    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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  • Interlinking the kynurenine pathway, obesity, depression, and inflammation. www.ncbi.nlm.nih.gov
    Abstract Obesity Inflammation Depression

    [Abstract]

    Obesity and depression are among the most pressing health problems in the contemporary world. Obesity and depression share a bidirectional relationship, whereby each condition increases the risk of the other. By inference, shared pathways may underpin the comorbidity between obesity and depression. Activation of cell-mediated immunity (CMI) is a key factor in the pathophysiology of depression. CMI cytokines, including IFN-γ, TNFα and IL-1β, induce the catabolism of tryptophan (TRY) by stimulating indoleamine 2,3-dioxygenase (IDO) resulting in the synthesis of kynurenine (KYN) and other tryptophan catabolites (TRYCATs). In the CNS, TRYCATs have been related to oxidative damage, inflammation, mitochondrial dysfunction, cytotoxicity, excitotoxicity, neurotoxicity and lowered neuroplasticity. The pathophysiology of obesity is also associated with a state of aberrant inflammation that activates aryl hydrocarbon receptor (AHR), a pathway involved in the detection of intracellular or environmental changes as well as with increases in the production of TRYCATs, being KYN an agonists of AHR. Both AHR and TRYCATS are involved in obesity and related metabolic disorders. These changes in the TRYCAT pathway may contribute to the onset of neuropsychiatric symptoms in obesity.

    This paper reviews the role of immune activation, IDO stimulation and increased TRYCAT production in the pathophysiology of depression and obesity. Here we suggest that increased synthesis of detrimental TRYCATs is implicated in comorbid obesity and depression and is a new drug target to treat both diseases.

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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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  • Young men had increased body fat in response to later meal timing independent of food content and activity level. ajcn.nutrition.org
    Diet Obesity Circadian Rhythm Time-Restricted Eating

    The study found that the timing of food intake relative to melatonin onset, a marker of a person’s biological night, is associated with higher percent body fat. Individuals with high body fat percentages consumed most of their calories shortly before going to sleep when melatonin levels were high, compared to individuals with lower percentages of body fat.

    To learn more about the benefits of time-restricted eating and how to practice it check out my podcasts with Dr. Satchin Panda. To learn more about how late night eating affects cancer risk check out my podcast with Dr. Ruth Patterson. Both podcasts are available on iTunes and YouTube (called foundmyfitness).

    Satchin Panda podcast: https://www.youtube.com/watch?v=-R-eqJDQ2nU Ruth Patterson podcast: https://www.youtube.com/watch?v=8qlrB84xp5g

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  • VSL#3 improved HDL, insulin sensitivity, LDL, atherogenic factors, and inflammation www.ncbi.nlm.nih.gov
    Gut Obesity Microbiome Insulin Resistance Cholesterol Omega-3 Inflammation Microbes VSL#3 Insulin Triglycerides

    FTA

    … a clinical trial in 60 overweight (BMI > 25), healthy adults, aged 40-60 years. After initial screening, the subjects were randomized into four groups with 15 per group. The four groups received, respectively, placebo, omega-3 fatty acid, probiotic VSL#3, or both omega-3 and probiotic, for 6 weeks. […] The probiotic (VSL#3) supplemented group had a significant reduction in total cholesterol, triglyceride, LDL, and VLDL and had increased HDL (P < 0.05) value. VSL#3 improved insulin sensitivity (P < 0.01), decreased hsCRP and favorably affected the composition of gut microbiota. Omega-3 had a significant effect on insulin sensitivity and hsCRP but had no effect on gut microbiota. The addition of omega-3 fatty acid with VSL#3 had a more pronounced effect on HDL, insulin sensitivity and hsCRP. Table showing statistics of the study.

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  • Sulforaphane (found in broccoli sprouts) causes 20% fat loss by changing gut bacteria & increasing mitochondria in fat in mice. www.sciencedaily.com
    Gut Obesity Microbiome Metabolism Inflammation Sulforaphane Fatty Liver NRF2 Endotoxemia Lipopolysaccharide Visceral Fat

    Sulforaphane from broccoli sprouts causes 20% visceral fat loss by changing gut bacteria and increasing mitochondria in fat in mice. The mice fed sulforaphane also lowered fatty liver and reduced blood glucose levels. Sulforaphane reduced inflammation by decreasing a species of bacteria in the gut that is responsible for producing endotoxin, which is a major source of inflammation. Also, sulforaphane increased the levels of UCP1, which is responsible for increasing mitochondrial biogenesis (the generation of new mitochondria) in fat (called browning of fat). The browning of fat increases fat metabolism and can lead to fat loss. There have been human studies showing that sulforaphane decreases inflammatory biomarkers and improves blood glucose levels. It will be interesting to see future studies looking at these two new functions of sulforaphane in humans. For more information check out my video on sulforaphane or my podcast with Dr. Jed Fahey, who discovered broccoli sprouts are the best source of sulforaphane. Sulforaphane video: https://youtu.be/zz4YVJ4aRfg Sulforaphane podcast: https://youtu.be/Q0lBVCpq8jc

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