Stress
Episodes
In this clip, Dr. Mark Mattson delivers an overview of the research investigating the effects of intermittent fasting on female and stress hormones.
In this clip, Dr. Mark Mattson describes the importance of incorporating rest, recovery, and refeeding into one's routine.
In this clip, Dr. Ashley Mason describes how mindfulness, a cognitive behavioral strategy, can help mitigate harmful behaviors like overeating and smoking.
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In this clip, Dr. Mark Mattson delivers an overview of the research investigating the effects of intermittent fasting on female and stress hormones.
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In this clip, Dr. Mark Mattson describes the importance of incorporating rest, recovery, and refeeding into one's routine.
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In this clip, Dr. Ashley Mason describes how mindfulness, a cognitive behavioral strategy, can help mitigate harmful behaviors like overeating and smoking.
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In this clip, Dr. Ashley Mason describes how cognitive behavioral therapy for insomnia helps people take control of their thoughts to improve their sleep.
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Dr. Mark Mattson discusses how stress is essential to human survival and how exercise and intermittent fasting induce stress to promote health.
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Dr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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In this clip, Tim Ferriss and Dr. Rhonda Patrick discuss acute versus chronic inflammation and how supplemental antioxidants can negate some of the benefits of exercise.
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In this clip, Wim Hof gives us some insight into how his fascination with the cold originally began.
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Dr. Elissa Epel identifies several biohacks that show promise as strategies to reduce stress and lengthen telomeres.
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Drs. Rhonda Patrick and Jari Laukkanen discuss the benefits of sauna use in terms of cardiorespiratory fitness and mood.
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Fasting associated with sickness behavior critical to surviving bacterial infection | Guido Kroemer ClipDr. Guido Kroemer describes how fasting associated with sickness behavior is critical to surviving infection.
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Dr. Matthew Walker discusses how anxiety affects sleep and identifies ways to manage that stress to improve sleep.
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Dr. Elissa Epel describes how toxic stress modulates telomere length.
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Dr. Elissa Epel discusses the mechanisms of healthy aging and the associations between stress, telomere length, addiction, eating, and metabolic health.
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Sleep Brain Alzheimer's Cancer Obesity Aging Performance Depression Immune System Stress Circadian Rhythm Behavior DementiaDr. Matthew Walker discusses the role of sleep in immunity, creativity, and aging.
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Epigenetics Vitamin D Nutrition Exercise Aging Metabolism Sleep Diabetes Telomeres DNA Damage Stem Cells Stress Melatonin Vitamin E Genetics 23andMe Heat Stress Autophagy Autism Folate Sauna AntioxidantOur genes influence the way we absorb and metabolize micronutrients. Nutrigenomics looks at the influence genetic variation has over micronutrient absorption/metabolism and the biological consequences of this dynamic relationship.
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Systemic inflammation is an important mechanism that research shows may have a very interesting relationship with depression.
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Rhonda explains chronic stress's impact on brain, gut, immune system, and aging. Meditation buffers and improves cognitive and biological aging.
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Sauna Exercise Brain Aging Hormones Performance Insulin Resistance Depression Stress Heat Stress MuscleDr. Rhonda Patrick discusses how conditioning the body to heat stress through sauna use, called "hyperthermic conditioning" may cause adaptations that increase athletic endurance (by increasing plasma volume and blood flow to heart and muscles) and potentially even muscle mass.
Topic Pages
News & Publications
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Chronic stress inhibits autophagy—the brain's recycling system—but restoring its functionality yields rapid antidepressant effects. pubmed.ncbi.nlm.nih.gov
In small doses, stress can sharpen focus and improve resilience, but chronic stress gradually erodes emotional stability, increasing the risk of major depressive disorder. A recent study found that autophagy—the brain’s recycling and housekeeping system—helps maintain emotional stability by removing old or damaged proteins.
Researchers explored how short-term and long-term stress influenced autophagy in mice and investigated whether antidepressant drugs could restore this process. Employing genetic techniques, the researchers selectively inhibited or enhanced autophagy in a region of the brain called the lateral habenula and then monitored how the animals reacted to stress.
They found that acute stress activated autophagy, while chronic stress inhibited it. When autophagy ceased functioning properly, stress-related behaviors increased. However, restoring autophagy—even briefly—produced rapid antidepressant-like effects. Drugs commonly used to treat depression also reactivated autophagy in this brain region. Additional experiments indicated that autophagy helps regulate brain cell activity by breaking down excess glutamate receptors, which are often overactive in depression.
These findings suggest that disrupted autophagy in the lateral habenula plays a central role in how chronic stress contributes to depression. Learn more about autophagy in this episode featuring Dr. Guido Kroemer.
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Stress damages the heart and blood vessels, increasing the risk of cardiovascular events like heart attack or stroke. Stress can also drive people to make poor dietary choices, often leading to overeating or consuming high-fat, low-nutrient foods instead of healthier options like fruits and vegetables. A recent study found that cocoa flavanols help counteract the harmful effects of stress and unhealthy meals on the heart and blood vessels.
The study involved 23 healthy young adults. Each participant ate a high-fat meal (buttered croissants, cheese, and whole milk) paired with either a high-flavanol cocoa drink or a low-flavanol cocoa drink before completing an eight-minute stress task. Researchers measured their blood vessel function, brain oxygen levels, blood flow, blood pressure, and mood multiple times before and after the stress challenge.
Participants who drank the high-flavanol cocoa maintained better blood vessel function after stress than those who consumed the low-flavanol drink. Blood vessel function declined considerably within 30 minutes of the stress task in the low-flavanol group but was preserved with high flavanol intake. At 90 minutes, blood vessel function improved beyond pre-stress levels in the high-flavanol group. The two groups had similar stress-related changes in blood pressure, brain oxygenation, and mood.
The findings from this small study suggest that flavanol-rich foods help protect the cardiovascular system during stressful periods, even when accompanied by unhealthy meals. Flavanols are polyphenolic compounds in dark chocolate, berries, apples, and tea. Evidence suggests flavanols exert potent antioxidant and anti-inflammatory properties. Learn more about flavanols and other polyphenols in our overview article.
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Mild cognitive impairment is often a precursor to Alzheimer’s disease, marking the initial stages of cognitive decline that precede more severe dementia. Evidence suggests lifestyle factors mediate the progression of mild cognitive impairment. A recent study found that intensive lifestyle modification improves cognitive and functional performance and slows disease progression in older adults with mild cognitive impairment.
Researchers conducted a randomized controlled trial involving 49 participants aged 45-90 with mild cognitive impairment or early dementia due to Alzheimer’s disease. Half of the participants received the usual care, while the other half received a 20-week intensive lifestyle intervention. The researchers assessed the participants' cognitive and functional performance and measured plasma biomarkers associated with Alzheimer’s before and after the intervention.
They found that participants in the intervention group showed considerable improvements in cognition and function compared to the control group. In addition, Aβ42/40 ratios increased in the intervention group but decreased in the control group.
The Aβ42/40 ratio is a measure of the relative levels of two forms of amyloid-beta protein (Aβ42 and Aβ40) in the blood or cerebrospinal fluid. It is a biomarker used to assess the presence and progression of Alzheimer’s disease. Lower ratios typically indicate higher levels of brain amyloid-beta plaques, a hallmark of the disease. An increase in the Aβ42/40 ratio, as observed in the intervention group, suggests a potential reversal or slowing of amyloid-beta plaque accumulation, indicating an improvement in disease pathology.
These findings suggest that intensive lifestyle modification has profound effects on Alzheimer’s disease progression in older adults with mild cognitive impairment. FoundMyFitness has a wealth of information about the various components used in this intensive protocol, which included:
- Diet: A whole-food, minimally processed, plant-based diet, high in complex carbohydrates and low in harmful fats and refined sugars.
- Exercise: Daily aerobic activities and resistance training exercises three times weekly.
- Stress management: Daily meditation, yoga, stretching, relaxation exercises, and breathing technique sessions.
- Group support: Group sessions, including supervised exercise, stress management practices, support groups, and lifestyle lectures, three times weekly.
- Supplements: Daily supplements, including omega-3 fatty acids, curcumin, a multivitamin/mineral, coenzyme Q10, vitamin C, vitamin B12, magnesium L-threonate, lion’s mane mushroom, and a probiotic.
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Oral contraceptives influence how women process stress, disrupting the typical hormonal adjustment seen during social interactions. www.sciencedaily.com
Oral contraceptives are widely known for their role in preventing pregnancy, but evidence suggests they also influence the body’s stress response. A recent study shows that women who took oral contraceptives had lower levels of adrenocorticotropic hormone (ACTH), a component of the hypothalamic-pituitary-adrenal axis typically produced in response to stress.
Researchers measured blood ACTH levels in 131 young women before and after the women participated in group activities designed to promote social bonding and reduce stress. The participants completed questionnaires about their moods before and after the activities.
They found that ACTH levels decreased among women not using contraceptives during the stress-buffering group activities, but this effect varied depending on their menstrual cycle phase. However, women using oral contraceptives did not experience the same decrease in ACTH levels during the group activities, regardless of their menstrual cycle phase.
These findings suggest that oral contraceptives not only affect the reproductive system but also influence the body’s response to stress. Learn about other effects of oral contraceptives in this clip from a live Q&A with Dr. Rhonda Patrick.
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Breathing exercises reduce stress and improve mental health. www.news-medical.net
Breathwork improves mental health, a new study shows. People who practiced breathwork reported less anxiety, depression, and mental stress, regardless of how frequently they engaged in the practice.
Researchers reviewed the findings of 12 randomized controlled trials that investigated the effects of breathwork on stress. The breathwork techniques were presented in person, remotely, or via both.
They found that slow-breathing exercises improved participants' mental health, regardless of how the techniques were presented. Participants who practiced breathwork reported having less anxiety, depression, and mental stress, compared to those who did not practice breathwork. Surprisingly, the researchers didn’t identify a dose-response effect with breathwork, aligning with other findings in which just a single breathwork session reduced anxiety.
Breathwork is an umbrella term that refers to various breathing exercises and techniques. Evidence suggests that breathwork improves heart rate variability and promotes resilience to stress. People often engage in breathwork as part of general relaxation practices, yoga, or meditation. Learn more about the benefits of meditation in this audio episode featuring Dr. Rhonda Patrick.
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Perimenopausal estradiol fluctuations may increase women's sensitivity to social rejection and vulnerability to developing depressive symptoms. (2015) www.sciencedaily.com
From the article:
In addition, the menopausal transition and early postmenopausal period are times of particularly increased vulnerability to depression for women, with rates of MDD [major depressive disorder] and clinical elevations in depressive symptoms doubling or even tripling compared to premenopausal and late postmenopausal rates. A substantial proportion of women–between 26% and 33%–will develop clinically significant depressive symptoms within the context of perimenopausal hormonal flux.
The common physiological change occurring during the menopausal transition is extreme variability in estradiol concentrations, thus prompting the 12-month placebo-controlled randomized trial evaluating the mood and cardiovascular benefits of transdermal estradiol in perimenopausal women. The findings from the placebo group found that, in general, estradiol variability led to the development of depressive symptoms, as well as greater anger/irritability and feelings of rejection. More specifically, the findings suggest that perimenopausal estradiol fluctuation may increase women’s sensitivity to social rejection, and when this sensitivity is combined with psycho-social stressors such as divorce or bereavement, women are particularly vulnerable to developing clinically significant depressive symptoms. Of note, however, is that the effect of estradiol variability on mood is not the same in all women and, if a severe life stress did not occur, estradiol variability did not lead to depression. Very severe life stresses were defined and included divorce or separation, serious illness of a close relative or friend, significant current financial issues, physical or sexual abuse or assault, significant arrest of self or loved one.
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Several environmental and lifestyle factors can lower testosterone levels. (2020) www.tandfonline.comVitamin 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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Improving sleep, diet, fitness, and weight may be alternatives to testosterone therapy. (2018) www.sciencedirect.com
From the publication:
Patient interest in fertility and testicular size preservation and a desire to avoid lifelong medical therapy with testosterone drives the need to identify non-TTh [non-testosterone therapy] for hypogonadism. Medical therapies that can stimulate endogenous testosterone production include hCG [human chorionic gonadotropin], AIs [aromatase inhibitors], and SERMs [selective estrogen receptor modulators], all of which demonstrate efficacy in increasing serum testosterone levels and good safety profiles. Natural therapies to increase testosterone production include diet and exercise, weight loss, improved sleep, decreasing stress, and varicocele repair. Diet, exercise, and weight loss provide a means to potentially reverse comorbidities that are closely linked to hypogonadism. Improvements in sleep quality and duration and decreasing stress are additional lifestyle modifications that can improve testosterone levels without the need for lifelong medication. Varicocele repair also can increase testosterone levels, although rigorous data supporting its use remain lacking. Patients considering TTh should be counseled on disease modification and the possibility of discontinuing TTh in the future, before initiation of therapy, and the alternatives discussed in this review also should be considered first in appropriate candidates.
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Diet, exercise, and weight loss
– 12-wk lifestyle modification program involving aerobic exercise and diet modification significantly increased mean testosterone levels
– 52-wk program of diet and exercise significantly increased mean serum testosterone levels
– Individuals who lost 10% of weight between visits showed a significant increase in testosterone levels
– Weight loss through low-calorie diets or bariatric surgery was associated with significant increases in total testosterone levels
Improvements in sleep
– Men with OSA treated with UPPP had significant 3-mo postoperative increases in testosterone levels
– Restriction of sleep to 5 h/night decreased testosterone levels by 10-15%
Stress reduction
– Men with high stress levels had significantly lower serum testosterone levels compared with controls
– Men with higher work stress had higher than expected incidence of hypogonadism
Varicocele repair
– Varicocelectomy significantly increased mean testosterone levels
– Varicocele repair significantly increased testosterone levels
– Significantly increased total testosterone levels were found at 12-mo follow-up after varicocelectomy
– Mean serum total testosterone significantly increased after varicocelectomy
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Stress-induced chronic inflammation is associated with depression and other diseases. (2015) www.sciencedaily.com
From the article:
The authors found that in addition to being linked to numerous physical health issues, including cancer and diabetes, systemic inflammation is linked to mental health issues such as depression. Among patients suffering from clinical depression, concentrations of two inflammatory markers, CRP and IL-6, were elevated by up to 50 percent.
Fagundes said chronic inflammation is most common in individuals who have experienced stress in their lives, including lower socio-economic status or those who experienced abuse or neglect as children. Other contributing factors are a high-fat diet and high body mass index.
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The study also found that depression caused by chronic inflammation is resistant to traditional therapy methods, but can be treated with activities such as yoga, meditation NSAIDS and exercise.
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Social stress-triggered increase of interleukin-6 in the brain exacerbates an animal model of multiple sclerosis. (2007) www.sciencedaily.com
From the article:
To create a stressful environment, researchers housed three young male mice together for several weeks. After the mice established a stable social hierarchy, researchers introduced an older aggressive male into the residence for a couple of hours. The intruder exhibits aggressive behavior – posturing, fighting, wounding, pursuit – that results in submissive behaviors and social defeat in the younger resident mice. This procedure was repeated for three consecutive nightly two-hour sessions with one night off, followed by an additional three nightly sessions. To keep the mice from getting used to the intruder, a new intruder was introduced for each session.
What they found was this stress appears to elevate levels of IL-6, which subsequently increases the severity of the MS-like illness. Furthermore, using specific IL-6 neutralizing antibody treatments during the stress exposure can prevent the stress-related worsening of the disease, said the authors.
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Furthermore, interventions that prevented or reversed the stress-induced increases in IL-6 in the mouse model may have implications for humans, said Meagher. It is possible that the adverse effects of social conflict on people who are vulnerable to certain inflammatory diseases may be prevented or reversed by treatments aimed at blocking increases in this cytokine. Recent evidence suggests that some potential interventions include certain anti-inflammatory drugs, exercise, antidepressant medication, omega-3 fatty acids, and mindfulness relaxation training. However, human clinical trials are needed to fully evaluate this issue.
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Exercising, drinking coffee and having sex are triggers that raise rupture risks for brain aneurysm, retrospective study finds. (2011) www.sciencedaily.com
From the article:
Calculating population attributable risk – the fraction of subarachnoid hemorrhages that can be attributed to a particular trigger factor – the researchers identified the eight factors and their contribution to the risk as:
-Coffee consumption (10.6 percent)
-Vigorous physical exercise (7.9 percent)
-Nose blowing (5.4 percent)
-Sexual intercourse (4.3 percent)
-Straining to defecate (3.6 percent)
-Cola consumption (3.5 percent)
-Being startled (2.7 percent)
-Being angry (1.3 percent)
“All of the triggers induce a sudden and short increase in blood pressure, which seems a possible common cause for aneurysmal rupture,” said Monique H.M. Vlak, M.D., lead author of the study and a neurologist at the University Medical Center in Utrecht, the Netherlands.
Risk was higher shortly after drinking alcohol, but decreased quickly, researchers said.
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Although physical activity had triggering potential, researchers don’t advise refraining from it because it’s also an important factor in lowering risk of other cardiovascular diseases.
“Reducing caffeine consumption or treating constipated patients with unruptured IAs with laxatives may lower the risk of subarachnoid hemorrhage,” Vlak said. “Whether prescribing antihypertensive drugs to patients with unruptured IAs is beneficial in terms of preventing aneurysmal rupture still needs to be further investigated.”
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Retirement may not provide relief from work-related hypertension, increasing the risk for diseases such as aneurysms. (2009) www.sciencedaily.com
Hypertension is diagnosed when blood pressure on the artery walls is consistently too high. This condition can eventually damage cells of the arteries' inner lining, leading to angina, heart attack, stroke, aneurysm, kidney failure and other serious health problems.
“People’s occupations during their working years can clearly be a risk for hypertension after they retire,” said senior study author Paul Leigh, a professor with the Center for Healthcare Policy and Research and the Department of Public Health Sciences at UC Davis. “The body seems to have built up a stress reaction that takes years to ramp down and may last well beyond age 75.”
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What they found with retirees was consistent with studies of those who are currently employed: higher-status occupations are associated with less hypertension than lower-status occupations.
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Unlike executives and professionals like architects and engineers, Leigh explained, workers in positions such as sales, administrative support, construction and food preparation have little control over decision-making, are under pressure to get a specified amount of work done in a certain amount of time and may feel inadequate about their positions in the workplace hierarchy. Consequently, their stress levels tend to be higher, which can lead to high blood pressure and, eventually, hypertension.
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Stress accelerates immune aging. www.sciencedaily.com
Stress ages the immune system.
Psychosocial stress, such as that experienced with discrimination or trauma, has profound effects on the human body. For example, evidence suggests that stress alters the immune system, driving inflammatory processes and impairing antiviral responses. Findings from a recent study demonstrate that stress accelerates immune aging.
Immune function wanes as the body ages, a phenomenon referred to as immunosenescence. This gradual deterioration of the immune system is widely considered the primary driver of the increased rate of infections and cancers in older adults. Multiple factors promote immunosenescence, including genetics, nutrition, exercise, and pathogen exposures, among others.
The investigators analyzed blood samples taken from more than 5,700 participants over the age of 50 years who were enrolled in the Health and Retirement Study, an ongoing study of older adults living in the United States. They measured the types and characteristics of the participants' immune cells, including CD4+ naïve (immature) cells, CD4+ differentiated (mature) cells, CD8+ naïve cells, and CD8+ differentiated cells, as well as the ratio of CD4+ to CD8+. Having more immature cells is indicative of a younger immune cell profile. The participants provided information about their socioeconomic status, lifestyle practices, and lifetime exposures to various stressors, including stressful life events, chronic stress, everyday discrimination, lifetime discrimination, and life trauma.
The investigators found that participants who had experienced more stress had fewer immature CD4+ cells and more mature CD4+ cells. Similarly, those who had experienced more stress had fewer immature CD8+ cells and more CD8+ cells. Those who had experienced high lifetime discrimination and chronic stress tended to have a lower CD4+ to CD8+ ratio, an indicator of impaired immune function. However, some of the harmful effects of stress were partly ameliorated by lifestyle factors, such as not smoking or drinking alcohol, and maintaining a healthy weight.
These findings suggest that psychosocial stress accelerates immune aging, potentially driving disease and premature death in vulnerable groups. However, lifestyle practices may moderate this risk. Interestingly, evidence suggests that a fasting-mimicking diet promotes the return of a more youthful immune cell profile. Learn more in this clip featuring Dr. Valter Longo.
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Ketones produced during fasting or a ketogenic diet promote muscle stem cell survival.
Fasting – the voluntary abstention from food and drink – is widely appreciated for its beneficial effects on human metabolism and healthspan. Evidence suggests that fasting flips a metabolic “switch,” liberating fat stores via fatty acid oxidation and ketone production. Findings from a recent study suggest that ketones induce a deep resting state in muscle stem cells, protecting them from future stressors.
Ketones are molecules produced by the liver during the breakdown of fatty acids. Ketone production occurs during periods of low food intake (fasting), ketogenic diets, starvation, or prolonged intense exercise. There are three types of ketones produced in the body: acetoacetate, beta-hydroxybutyrate, and acetone. Ketones are readily used as energy by a diverse array of cell types, including neurons.
Next, they examined muscle stem cells from both groups and found that the fasted animals' cells were smaller; had less mitochondrial content, RNA content, and basal oxygen consumption; and exhibited delayed cell division, compared to cells of non-fasting animals. Interestingly, the fasted animals' cells exhibited greater resilience to environmental stressors, such as oxidative stress and low nutrient availability.
Then the investigators treated muscle stem cells from the non-fasting mice with beta-hydroxybutyrate, a type of ketone. The cells exhibited similar resistance, likely due to beta-hydroxybutyrate’s actions as a histone deacetylase (HDAC) inhibitor. HDAC inhibition is associated with improved cellular resilience and longevity.
These findings suggest that ketones, particularly beta-hydroxybutyrate, induce a deep resting state in muscle stem cells, protecting them from future stressors. Learn more about beta-hydroxybutyrate in our overview article.
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Omega-3 supplementation reduces inflammation and cellular aging in response to social stress. www.nature.com
Omega-3 fatty acid consumption reduces the risk of death from cardiovascular disease and all causes. By reducing inflammation, lengthening telomeres, and blunting the body’s response to stress, omega-3 fatty acids lessen the effects of aging on a cellular level. Authors of a recent study tested the effects of omega-3 supplementation on inflammation and telomere length in response to stress.
Telomeres are often compared to the plastic tips on the end of shoelaces (aiglets) because telomeres protect chromosomes from fraying on the ends. Both acute and chronic stress increase inflammation, which can cause chromosomes to become frayed when telomeres are short. Once chromosomes lose their telomeres, their DNA cannot be replicated, and this accelerates aging.
The randomized, controlled intervention trial included 138 sedentary, adults with overweight between the ages of 40 and 85 years. The participants received daily supplements providing 2.5 grams of omega-3s, 1.25 grams of omega-3s, or a placebo for four months. Before and after the intervention, the participants took the Trier Social Stress Test, a testing platform in which a person must deliver a speech and perform mental arithmetic in front of an audience. Participants also provided blood and saliva samples as a means to measure cortisol (a stress hormone), telomerase (an enzyme that helps maintain telomere length); anti-inflammatory cytokines, including interleukin (IL)-10 (IL-10); and pro-inflammatory cytokines, including IL-6, IL-12, and tumor necrosis factor-alpha (TNF-alpha).
Following the stress test, participants in the placebo group experienced a 24 percent reduction in telomerase activity and a 26 reduction in IL-10; however, both omega-3 groups were protected from this response. This relationship was statistically significant and accounted for baseline stress reactivity, age, waist circumference, and sex. Participants who received 2.5 grams of omega-3s had a 19 percent reduction in cortisol levels and a 33 percent reduction in IL-6 compared to the placebo group.
The authors concluded that by reducing inflammation and stress hormone levels, omega-3 supplementation may boost cellular repair and slow aging. This decrease in stress response may also translate to reduced risk of depression, making these findings relevant to mental health as well.
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Stress is essential to human survival. Long-term exposure to stress, however, increases a person’s risk of developing many chronic diseases. A recent review suggests that sauna bathing protects the body from the harmful effects of high stress occupations and describes the mechanisms that drive the protection.
People who work in high-stress occupations, such as firefighters, first responders, and military members, are exposed to both physiological and psychological stressors – often referred to as dual stressors. These dual stressors activate physiological responses to stress that ultimately drive inflammation, the underlying cause of many chronic diseases, including atherosclerosis, diabetes, rheumatoid arthritis, and dementia. Many people in high-stress occupations also work long or irregular hours and may have poor or inconsistent dietary patterns.
Sauna bathing exposes the body to extreme heat. This exposure – a form of stress – increases the body’s core temperature and activates a wide array of protective mechanisms that work together to condition the body for future stressors, a biological phenomenon known as hormesis. Hormesis is a compensatory defense response to a stressor that is disproportionate to the stressor’s magnitude.
The mechanisms that drive the effects of sauna bathing include activation of heat shock proteins and pro- and anti-inflammatory cytokines; decreased blood pressure and arterial stiffness; and multiple improvements in cardiovascular function. Sauna bathing also improves several aspects of metabolic function, primarily via activation of adenosine monophosphate-activated protein kinase (AMPK), a master regulator of cellular energy homeostasis. AMPK activation influences gene expression and inhibits cellular processes that drive oxidative stress.
The findings summarized in this review suggest that sauna bathing shows promise as a strategy to ameliorate the harmful effects of the dual stressors experienced by people working in high-stress occupations. Learn more about sauna bathing in our overview article.
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Bipolar disorder patients experience generalized impaired cellular resilience and broad reductions in BDNF that may contribute to the disease www.sciencedaily.com
From the article:
Effective neuronal plasticity also depends on neurotrophins, which are regulatory factors that promote development and survival of brain cells. Brain-derived neurotrophic factor (BDNF) is the neurotrophin mostly found in the brain. It has been extensively investigated in bipolar disorder patients and has been suggested as a hallmark of bipolar disorder. Indeed, some studies have shown that the levels of BDNF in the serum of bipolar disorder patients are reduced whenever patients undergo a period of depression, hypomania, or mania. Other studies have shown that regardless of mood state, bipolar disorder patients present reduced levels of BDNF. Overall, changes in BDNF levels seem to be a characteristic found in bipolar disorder patients that may contribute to the pathophysiology of the disease.
Immediate early genes:
Immediate early genes (IEGs) are a class of genes that respond very rapidly to environmental stimuli, and that includes stress. IEGs respond to a stressor by activating other genes that lead to neuronal plasticity, the ability of brain cells to change in form and function in response to changes in the environment. Ultimately, it is the process of neuronal plasticity that gives the brain the ability to learn from and adapt to new experiences.
One type of protein produced by IEGs is the so-called Early Growth Response (EGR) proteins, which translate environmental influence into long-term changes in the brain. These proteins are found throughout the brain and are highly produced in response to environmental changes such as stressful stimuli and sleep deprivation. Without the action played out by these proteins, brain cells and the brain itself cannot appropriately respond to the many stimuli that are constantly received from the environment.
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in a previous study done by the group in 2016, one type of IEG gene known as EGR3, that normally responds to environmental events and stressful stimuli, was found repressed in the brain of bipolar disorder patients, suggesting that when facing a stressor, the EGR3 in bipolar disorder patients does not respond to the stimulus appropriately. Indeed, bipolar disorder patients are highly prone to stress and have more difficulties dealing with stress or adapting to it if compared to healthy individuals. What the research group is now suggesting is that both EGR3 and BDNF may each play a critical role in the impaired cellular resilience seen in bipolar disorder, and that each of these two genes may affect each other’s expression in the cell. “We believe that the reduced level of BDNF that has been extensively observed in bipolar disorder patients is caused by the fact that EGR3 is repressed in the brain of bipolar disorder patients. The two molecules are interconnected in a regulatory pathway that is disrupted in bipolar disorder patients,”
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Large doses of vitamin C might mitigate the body's stress response, thereby improving immunity. www.sciencedaily.com
The human body responds to mental stress by releasing hormones called corticosteroids, triggering the body’s fight or flight response. Chronic activation of these hormones can impair immune function, increasing susceptibility to infection and disease. Findings from an early study in mice demonstrate that vitamin C mitigates the body’s stress response, thereby improving immunity.
The authors of the study immobilized mice for an hour every day for three weeks to induce stress. They also fed the mice 200 milligrams of vitamin C daily – roughly equivalent to several grams per day in humans. A control group of mice also received vitamin C but they were not subjected to stress.
The stressed mice that received large doses of vitamin C in their diets exhibited fewer signs of stress as evidenced by lower levels of corticosteroid hormones as well as other physical manifestations, such as weight loss. The mice also exhibited higher levels of IgG, the most abundant antibody in circulation, responsible for binding a broad selection of pathogens, including viruses, bacteria, and fungi, to prevent infection. Interestingly, the non-stressed mice that received large doses of vitamin C exhibited even greater increases in IgG, suggesting that stress cancels out some of the beneficial effects of the vitamin.
These findings suggest that high dose vitamin C might improve immune function, especially during times of mental and physical stress.
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Stress has far-reaching effects on the human body, including increased risk of chronic disease and other conditions associated with aging. Anecdotal reports suggest that stress can contribute to the premature graying of hair. Findings from a recent study in mice suggest that acute stress depletes melanocyte stem cell populations to promote the graying of hair.
Melanocyte stem cells are undifferentiated cells found in the region of hair associated with growth. They give rise to melanocytes, the mature, melanin-forming cells that provide color to growing hair.
Both mental and physical stress activate the body’s sympathetic nervous system, one of the two main divisions of the autonomic nervous system (the other being the parasympathetic nervous system). The sympathetic nervous system’s primary purpose is to stimulate the body’s fight-or-flight response to stress. A critical element in this response is noradrenaline, a type of hormone and neurotransmitter that plays a role in vigilance and conditioned fear.
The authors of the study induced acute stress in mice and noted that the mice exhibited increased numbers of gray hairs. This increased graying was attributed to the activation of sympathetic nerves in the region in which the stem cells reside and subsequent release of noradrenaline, which promoted stem cell proliferation, differentiation, migration, and eventual depletion.
These findings suggest that neuronal activity induced by an acute stressor can drive stem cell loss and illustrate how overall mental and physical health influence stem cell health.
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Human longevity was associated with decreased levels of genes involved in neural overactivity. www.nature.com
Healthy brain activity is achieved by maintaining a balance between neural excitation and inhibition. Impairment in this balance is related to many neurological and neurodegenerative disorders, including epilepsy, autism, Parkinson’s, Alzheimer’s, and schizophrenia. In Caenorhabditis elegans, a model organism for studying both the nervous system and aging, neural excitation increases with age and age-related cognitive decline, but lifespan increases with inhibition. A recent study demonstrates that extended longevity in humans is associated with lower levels of genes related to neural excitation.
The multi-arm study focused on three organisms: C. elegans, humans, and mice. The authors of the study found that global inhibition of neural excitation increased the lifespan of C. elegans. RNA sequencing and microarray analysis of human genes revealed that long-lived people (older than 85 years) have higher levels of REST, a gene-silencing transcription factor that downregulates neural excitation-related genes. In addition, they found that mice that are deficient in REST exhibit higher levels of neural excitation. REST and lower levels of neural excitation activate FOXO1, a longevity-associated transcription factor in mammals, suggesting that REST regulates a conserved mechanism of aging.
The authors of the study suggested that REST activation and subsequent reduction of excitatory neural activity may be a means to slow aging in humans.
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Abstract
Although sleep appears to be broadly conserved in animals, the physiological functions of sleep remain unclear. In this study, we sought to identify a physiological defect common to a diverse group of short-sleeping Drosophila mutants, which might provide insight into the function and regulation of sleep. We found that these short-sleeping mutants share a common phenotype of sensitivity to acute oxidative stress, exhibiting shorter survival times than controls. We further showed that increasing sleep in wild-type flies using genetic or pharmacological approaches increases survival after oxidative challenge. Moreover, reducing oxidative stress in the neurons of wild-type flies by overexpression of antioxidant genes reduces the amount of sleep. Together, these results support the hypothesis that a key function of sleep is to defend against oxidative stress and also point to a reciprocal role for reactive oxygen species (ROS) in neurons in the regulation of sleep.
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Acid Suspends the Circadian Clock in Hypoxia through Inhibition of mTOR. - PubMed - NCBI www.ncbi.nlm.nih.gov
Citation: Cell. 2018 Jun 28;174(1):72-87.e32. doi: 10.1016/j.cell.2018.05.009. Epub 2018 May 31.
Abstract Recent reports indicate that hypoxia influences the circadian clock through the transcriptional activities of hypoxia-inducible factors (HIFs) at clock genes. Unexpectedly, we uncover a profound disruption of the circadian clock and diurnal transcriptome when hypoxic cells are permitted to acidify to recapitulate the tumor microenvironment. Buffering against acidification or inhibiting lactic acid production fully rescues circadian oscillation. Acidification of several human and murine cell lines, as well as primary murine T cells, suppresses mechanistic target of rapamycin complex 1 (mTORC1) signaling, a key regulator of translation in response to metabolic status. We find that acid drives peripheral redistribution of normally perinuclear lysosomes away from perinuclear RHEB, thereby inhibiting the activity of lysosome-bound mTOR. Restoring mTORC1 signaling and the translation it governs rescues clock oscillation. Our findings thus reveal a model in which acid produced during the cellular metabolic response to hypoxia suppresses the circadian clock through diminished translation of clock constituents.
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Just watched the interview, and it’s easy to see why people do it. He seems very authentic, and his enthusiasm is infectious!
What I was wondering though.. why is an immune response to endotoxin injection a bad thing? Or put another way, why is it better for adrenaline to kick in instead of the immune system… seems counterintutive, no? Or at least, I always thought stress horomones (Cortisol, Adrenaline) are PRO-inflammatory, much like the cytokines that norephinephrine wants to supress.
Minus the epinephrine inducing breathing technique of letting in, more than you let out, is the Wim Hof Method the same as doing Whole Body Cryotherapy (as touted by Tony Robbins)?
I think I’d like to buy his ($200?) course, but doesn’t seem like any theory is covered in it… i.e. why cold exposure increases norephinephrine, and why that may be useful for treating psychological disorders. Can purely physiological / generic disorders (ex. TMAU) be improved?
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FTA:
Vinclozolin is a fungicide commonly used by farmers to treat fruits and vegetables.
To test the effects of stress on rats, the researchers confined some of them to soft, warm cylinders for six hours a day for three weeks. This was done during adolescence, a developmentally sensitive time of life for rats, just as for humans. Months later, the researchers tested the brain chemistry, brain function, gene expression and behavior of the rats as adults.
They discovered that for female rats, ancestral exposure to vinclozolin alone or stress during the animal’s adolescence alone had negligible effects on the rats' hormonal balance and behavior. However, the combination of ancestral exposure and stress caused the female rats to have dramatically higher levels of corticosterone (a stress hormone similar to cortisol in humans), higher expression of genes associated with anxiety and more anxious behaviors.
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The anxiolytic effect of cannabidiol on chronically stressed mice depends on hippocampal neurogenesis: involvement of the endocannabinoid system journals.cambridge.org
Cannabidiol (CBD), the main non-psychotomimetic component of the plant Cannabis sativa, exerts therapeutically promising effects on human mental health such as inhibition of psychosis, anxiety and depression. However, the mechanistic bases of CBD action are unclear. Here we investigate the potential involvement of hippocampal neurogenesis in the anxiolytic effect of CBD in mice subjected to 14 d chronic unpredictable stress (CUS). Repeated administration of CBD (30 mg/kg i.p., 2 h after each daily stressor) increased hippocampal progenitor proliferation and neurogenesis in wild-type mice. Ganciclovir administration to GFAP-thymidine kinase (GFAP-TK) transgenic mice, which express thymidine kinase in adult neural progenitor cells, abrogated CBD-induced hippocampal neurogenesis. CBD administration prevented the anxiogenic effect of CUS in wild type but not in GFAP-TK mice as evidenced in the novelty suppressed feeding test and the elevated plus maze. This anxiolytic effect of CBD involved the participation of the CB1 cannabinoid receptor, as CBD administration increased hippocampal anandamide levels and administration of the CB1–selective antagonist AM251 prevented CBD actions. Studies conducted with hippocampal progenitor cells in culture showed that CBD promotes progenitor proliferation and cell cycle progression and mimics the proliferative effect of CB1 and CB2 cannabinoid receptor activation. Moreover, antagonists of these two receptors or endocannabinoid depletion by fatty acid amide hydrolase overexpression prevented CBD-induced cell proliferation. These findings support that the anxiolytic effect of chronic CBD administration in stressed mice depends on its proneurogenic action in the adult hippocampus by facilitating endocannabinoid-mediated signalling.