Genetics
Episodes
Dr. Rhonda Patrick covers lithium microdosing, reducing homocysteine, aluminum's link to cancer, and beta-alanine and alpha-lipoic acid supplements.
Dr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
Dr. George Church discusses revolutionary technologies in the field of genetic engineering.
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Exercise Biomarkers Vitamin E Genetics Eyes Caffeine Folate Sulforaphane Sauna Antioxidant Dairy Polyphenol Supplements Wearable TechnologyDr. Rhonda Patrick covers lithium microdosing, reducing homocysteine, aluminum's link to cancer, and beta-alanine and alpha-lipoic acid supplements.
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Dr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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Dr. George Church discusses revolutionary technologies in the field of genetic engineering.
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In this clip, Dr. Ronald Krauss describes why it may be more beneficial to reduce LDL levels than to raise HDL levels.
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In this clip, Dr. Rhonda Patrick describes what Mendelian randomization studies are and how they are valuable instruments in the scientific toolbox.
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In this clip, Dr. Steve Horvath describes research suggesting that caloric restriction, especially when it is reversing obesity or metabolic syndrome, may slow epigenetic aging.
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In this clip, Dr. Steve Horvath discusses whether epigenetic clocks play causal roles in aging.
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Methylation and demethylation are critical processes in development and interfering with the enzymes that carry out these two opposing processes can play critical roles in epigenetic age.
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Some epigenetic clock evidence reinforces the idea that accelerated aging may be a consequence of chronic inflammation.
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As techniques are developed to differentiate and transdifferentiate cells from one cell type, such as a fibroblast, into another, such as a neuron, interesting patterns of effects on epigenetic age are revealed.
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A study using a mouse model of premature aging showed that short-term expression of four special factors which reverse epigenetic age ameliorated cellular and physiological hallmarks of aging and prolonged lifespan.
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Scientists have observed that the epigenetic clock of transplanted cells and their descendant lineages synchronize with the donor rather than the recipient, a fascinating phenomenon that offers promise for the idea of rejuvenation in humans.
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In this clip, Dr. Steve Horvath discusses how epigenetic aging differs from senescence-mediated aging.
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A person's epigenetic age correlates with their risk for developing major diseases of aging like cancer, Alzheimer's disease, and Parkinson's.
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The stability of methylation patterns on DNA samples means the data can be trusted more in the lab when investigating anti-aging interventions.
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In this clip, Dr. Steve Horvath explains the differences between chronological age and biological age.
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Evidence indicates that the heritability of epigenetic aging is about 40 percent. This is seen in supercentenarians and their offspring, who tend to age slower than their younger counterparts.
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Dr. Steve Horvath discusses epigenetic aging clocks and their use in predicting biological aging and healthspan.
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Dr. Steve Horvath found a way to measure biological aging – a type of "clock" – based on the methylation pattern of an organism's genome. This video primer explains the basics of epigenetic clocks, the topic of our interview with Dr. Steve Horvath.
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In this clip, Dr. Giselle Petzinger highlights some of the risk factors for Parkinson's disease, and discusses how this is likely a multifaceted problem.
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In this clip, Dr. Rhonda Patrick discusses the role that genetics plays in the immune system.
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COVID-19 Vitamin D Nutrition Exercise Microbiome Sleep Vitamin C Omega-3 Inflammation Immune System Virus Micronutrients Vitamin E Vaccine Genetics Testosterone Estrogen Zinc Fiber AutoimmunityCOVID-19 Q&A Part 2: Rhonda Patrick, Ph.D. answers subscriber questions in a multi-part series.
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In this clip, Tim Ferriss discusses his MTHFR status and his experience with vitamin supplementation.
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Rhonda explains NAD+: importance for aging, decline with age, boosters (nicotinamide riboside, nicotinamide mononucleotide), and data in animals and humans.
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In this clip, Dr. David Sinclair describes the major breakthroughs in aging research and the unique relationships that develop between researchers and the organisms they study.
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Dr. David Sinclair on Informational Theory of Aging, Nicotinamide Mononucleotide, Resveratrol & MoreDr. David Sinclair discusses the mechanisms that drive human aging and the importance of identifying ways to slow or reverse aging's effects.
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In this clip, Dr. Roland Griffiths and Dr. Rhonda Patrick discuss the effects of meditation on gene expression.
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Dr. Elissa Epel describes how pre-pregnancy parental health impacts offspring.
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Dr. Elissa Epel describes the effects of longer sperm telomere length on subsequent generations.
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Dr. Rhonda Patrick and Dr. Elissa Epel describe the factors that influence how we respond to diet.
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Dr. Elissa Epel gives a brief overview of telomeres and the enzyme telomerase and explains how they impact health and lifespan.
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Dr. Elissa Epel explains how aging syndromes can be passed to offspring via epigenetic mechanisms.
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Rhonda Nutrition Exercise Alzheimer's Aging Fasting Memory Genetics Mortality Sauna Time-Restricted Eating Cardiovascular Supplements Ketogenic DietDr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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Epigenetics Vitamin D Nutrition Exercise Aging Metabolism Sleep Diabetes Telomeres DNA Damage Stem Cells Stress Melatonin Vitamin E Genetics 23andMe Heat Stress Autophagy Autism Folate Sauna AntioxidantOur genes influence the way we absorb and metabolize micronutrients. Nutrigenomics looks at the influence genetic variation has over micronutrient absorption/metabolism and the biological consequences of this dynamic relationship.
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Dr. Rhonda Patrick talks about transgenerational effects of caloric restriction on longevity, B-vitamins silencing bad genes, cognitive stimulation reversing neurodegenerative disease, exercise increases neurogenesis, and ways in which vitamin D might influence aging.
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This video breaks down, point-by-point what gene polymorphisms you might look at, and how they relate to very specific micronutrients.
Topic Pages
News & Publications
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Even if you work out, spending most of your day sitting may still adversely affect your health in ways that don’t become apparent until later in life. A recent study found that 35-year-olds who engaged in 30 minutes of vigorous exercise each day had cholesterol levels comparable to those of sedentary 30-year-olds, suggesting that vigorous exercise can offset up to five years of age-related decline in heart health.
Researchers analyzed data from adults aged 28 to 49 who participated in the Colorado Adoption/Twin Study of Lifespan Behavioral Development and Cognitive Aging. They tracked the time participants spent sitting each day and how often they engaged in moderate or vigorous physical activity. To isolate the effects of behavior from shared genetics and environment, the researchers also compared identical twins with differing activity and sitting patterns. They examined two key health markers: body mass index and the ratio of total to high-density lipoprotein cholesterol—a strong predictor of heart disease risk.
They found that people who spent more time sitting tended to have higher body mass index and worse cholesterol ratios as they aged. However, among those who sat for the same amount of time—about four hours daily—participants who exercised vigorously for at least 30 minutes daily had cholesterol profiles that resembled those of people five years younger. In some cases, vigorous activity was associated with health markers typical of people up to 10 years younger, but the protective effect weakened with longer sitting durations. In other words, exercise helped—but only to a point.
These findings suggest that while vigorous exercise offers clear benefits, reducing sitting time is just as important for maintaining good health. “Exercise snacks” can offset the harmful effects of prolonged sitting. Learn more in this clip featuring Dr. Rhonda Patrick and Brady Holmer.
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While genes play a role in aging, lifestyle and environmental exposures—collectively called the exposome—may have a more robust effect on aging and longevity. A recent study found that the exposome contributes far more to premature death and age-related diseases than genetic risk alone.
Researchers analyzed data from nearly 500,000 people enrolled in the UK Biobank to measure the exposome’s role in aging. They identified environmental exposures linked to early death and biological aging, then used a proteomic age clock—a tool that tracks molecular signs of aging—to confirm which exposures accelerate the aging process. Finally, they compared the exposome’s influence on disease risk to that of genetic predisposition.
The exposome explained 17 percentage points more of the variation in mortality than genetic risk, which accounted for less than two percentage points. It was more strongly connected to lung, heart, and liver diseases, while genetic factors were more closely associated with certain cancers and dementias. The analysis identified three disease states and 22 biomarkers related to liver and kidney function, cardiovascular and metabolic health, inflammation, longevity, genetics, and vitamin and mineral status that independently drive biological aging and disease risk.
These findings suggest that the exposome is critical in shaping health and longevity. While genes contribute to some diseases, environmental exposures throughout life greatly influence aging and survival. Air pollution is an exposome element contributing to disease and early death. Learn how wearable devices measure the air pollution exposome in this episode featuring Dr. Michael Snyder.
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Donating blood is an act of generosity that saves lives, yet few donors think about how it affects their own health. Each donation triggers a surge in blood cell production, a process that could subtly shape the long-term health of blood-forming stem cells. A recent study found that frequent blood donation promotes the expansion of specific blood stem cell mutations that support healthy red blood cell production.
Researchers analyzed blood samples from 217 older men who had donated more than 100 times and compared them to 212 men who had donated fewer than 10 times. They looked for clonal hematopoiesis, a condition where blood stem cells acquire genetic changes that allow specific cell populations to expand. They also used gene-editing techniques to study how particular mutations behaved when exposed to erythropoietin, a hormone that increases after blood loss.
They found that the overall rate of clonal hematopoiesis was similar between frequent and infrequent donors. However, mutations in the DNMT3A gene showed distinct patterns in frequent donors. Some of these mutations responded to erythropoietin by expanding, while others, known to be associated with leukemia, were more likely to grow in response to interferon-gamma, a protein involved in the immune response. Further analysis revealed that the erythropoietin-responsive mutations tended to push blood stem cells toward making more red blood cells rather than leading to abnormal or harmful changes.
These findings suggest that repeated blood donation encourages the expansion of specific blood stem cell mutations, but the effects support normal blood cell production rather than increase disease risk. Blood donation also lowers levels of iron—a key nutrient that, in excess, harms the brain. Learn more in this episode featuring Dr. Gordon Lithgow.
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DHA-rich diet protects against memory deficits and loss of smell in Alzheimer's-prone APOE4 mice, reveals new study. link.springer.com
A diminished or lost sense of smell is a common feature of the early stages of Alzheimer’s disease and other forms of dementia. But a new study in mice that carry the APOE4 gene variant, the primary genetic risk factor for Alzheimer’s disease, shows that DHA – a type of omega-3 fatty acid found in fish – protects against these losses. APOE4-carrying mice that ate a DHA-rich diet retained their sense of smell and the ability to distinguish between objects based on their scent.
Researchers fed normal mice and APOE4 carriers a regular diet or one supplemented with DHA. Then, using MRI scans, they assessed the animals' brain structures and studied their behavior related to smell and the recognition of new objects. They also measured biomarkers related to cell death and inflammation.
They found that the APOE4-carrying mice given a regular diet exhibited memory deficits and difficulty adjusting to new smells and distinguishing between different objects. In addition, their brains showed increased signs of inflammation in the olfactory bulb – the area responsible for the sense of smell. However, APOE4-carrying mice that ate the DHA-rich diet did not exhibit these characteristics.
These findings suggest that a DHA-rich diet benefits APOE4 carriers. Learn more about the beneficial effects of DHA in our comprehensive omega-3 overview article.
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Time-restricted eating activates genes involved in metabolism and autophagy. www.sciencedaily.com
Time-restricted eating influences the activation of roughly 70 percent of all genes in mice, a new study shows. Mice that ate on a time-restricted schedule had fewer active genes involved in inflammation and oxidative stress and more active genes involved in metabolism and autophagy – a cellular defense mechanism.
Researchers fed two groups of mice a Western-style diet, which is high in fat and sugars, for seven weeks. One group was allowed to eat whenever they chose to, but the other group was allowed to eat only during a nine-hour window each day. At the end of the seven-week intervention, the researchers analyzed gene activity in the animals' tissues at different times of the day.
They found that time-restricted eating altered the activity of more than 80 percent of genes involved in protein synthesis, folding, and maintenance. They also found that time-restricted eating altered amino acid, fat, and glucose metabolism and re-aligned the circadian rhythms of the animals' organs.
These findings suggest that time-restricted eating influences gene activity in mice. If the findings translate to humans, they could have far-reaching implications for chronic metabolic disorders, neurodegenerative diseases, cancer, and other diseases. Learn more about the health benefits of time-restricted eating in this episode featuring Dr. Satchin Panda, the senior investigator for this study.
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In a mendelian randomization study, genetically predicted levels of interleukin 6 (IL-6) were associated with neuropsychiatric disorders. www.sciencedaily.com
IL-6 may drive inflammation in neuropsychiatric disorders.
Neuropsychiatric disorders are the leading cause of disability among people living in the United States, accounting for nearly 20 percent of all years of life lost to disability and premature death. Evidence suggests that brain inflammation is a key player in neuropsychiatric disorders, the effects of which may be bidirectional. A recent study identified potential links between inflammation and structural alterations in regions of the brain implicated in neuropsychiatric disorders.
The brains of people with neuropsychiatric disorders exhibit a range of abnormal structural alterations, but researchers don’t fully understand what drives these abnormalities. One possible player is interleukin-6 (IL-6), a cytokine that can cross the blood-brain barrier, increasing the barrier’s permeability and promoting brain inflammation. In turn, this inflammation can impair synaptic pruning, a natural process that occurs in the brain between early childhood and adulthood and eliminates extra synapses. Inappropriate synaptic pruning is associated with some neuropsychiatric disorders, including schizophrenia and autism.
The investigators searched for evidence of potential causality in the association between inflammatory cytokines and altered brain structure using Mendelian randomization, a research method that provides evidence of links between modifiable risk factors and disease based on genetic variants within a population. Using data from more than 20,000 adults enrolled in the UK Biobank study, the researchers looked for associations between genetic variants that influence levels of interleukin-6 (IL-6, a pro-inflammatory cytokine), as well as other inflammatory factors. and changes in gray matter volume in specific areas of the brain. They also examined postmortem brain tissue to assess gene expression in the brain areas of interest.
They found that genes that influence the production of pro-inflammatory molecules, especially IL-6, are strongly linked with brain structure in the temporal and frontal regions of the brain, areas of the brain commonly implicated in neuropsychiatric disorders. The postmortem analyses revealed that the overproduction of these pro-inflammatory genes is associated with disorders such as epilepsy, cognitive disorder, schizophrenia, psychotic disorder, and autism spectrum disorder.
These findings suggest that pro-inflammatory pathways, especially those associated with IL-6, are essential for normal brain structural development and IL-6 elevation may drive structural alterations implicated in neuropsychiatric disorders. Evidence suggests that heat stress reduces symptoms associated with depression, a type of neuropsychiatric disorder. Learn about a clinical trial that is investigating the benefits of heat stress in this episode featuring Dr. Ashley Mason.
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Data from nearly 80,000 twin pairs suggest that brain aneurysm ruptures are more commonly caused by environmental factors than by genes. (2010) www.sciencedaily.com
From the article:
During the past few decades, the genetic makeup has been regarded as playing a significant role in the development of SAH [subarachnoid haemorrhage]. Contrary to this belief, however, a twin study recently published in the journal Stroke showed that environmental factors account for most of the susceptibility to develop SAH Conducted in Finland, Sweden and Denmark, the study is the largest population level twin study in the world.
This means that instead of screening the close family members of SAH patients, the focus of preventive treatment may now be increasingly shifted to the efficient management of hypertension and smoking cessation intervention. This is what we do with other cardiovascular diseases as well."
The Nordic study combined data on almost 80,000 pairs of twins over several decades. All in all, the follow-up time of all of the twin pairs corresponds to a staggering 6 million person-years.
The researchers nevertheless emphasize that there are rare cases of families among whose members SAH is significantly more common than in the overall population. In these cases genetic factors are the principal cause underlying the development of the disease.
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Carriers of a gene variant that increases the chance of brain aneurysm by 37-48%, fivefold their risk if they smoke. (2010) www.sciencedaily.com
From the article:
Researchers have confirmed three gene changes that raise the risk that a blood vessel in the brain will weaken and balloon out (aneurysm), creating a life-threatening chance of rupture. Smoking, the biggest risk factor for brain aneurysm, is five times more dangerous in people with these gene variations. However, a second study on the same population notes that most people with aneurysm die of cancer or heart problems.
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In one study (Broderick, abstract 156), researchers found that the chance of an intracranial aneurysm increased between 37 percent and 48 percent for people who carried one copy of an identified risky gene variation. However, when the gene variant was combined with smoking the equivalent of one pack a day for 20 years, the risk increased more than five-fold. People with two copies of the gene variant were at even higher risk.
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Insomnia, hypertension and smoking, but not high triglyceride levels, are considered possible risk factors for brain aneurysm rupture. www.sciencedaily.com
From the article:
Data from several genome-wide association studies were used to gauge genetic associations to lifestyle and cardiometabolic risk factors. […] According to the analysis:
-A genetic predisposition for insomnia was associated with a 24% increased risk for intracranial aneurysm and aneurysmal subarachnoid hemorrhage.
-The risk for intracranial aneurysm was about three times higher for smokers vs. non-smokers.
-The risk for intracranial aneurysm was almost three times higher for each 10 mm Hg increase in diastolic blood pressure (the bottom number in a blood pressure reading).
-High triglyceride levels and high BMI did not demonstrate an increased risk for intracranial aneurysm and aneurysmal subarachnoid hemorrhage.
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Menopause disrupts sleep, accelerating biological aging www.sciencedaily.com
Menopause accelerates epigenetic aging.
Menopause, which typically occurs around the age of 52 years, is the cessation of a female’s menstrual cycle and signifies the loss of reproductive capacity. Evidence suggests that early menopause increases the risk for age-related disease and premature death. Findings from a 2016 study suggest that menopause accelerates epigenetic aging.
Epigenetics is a biological mechanism that regulates gene expression (how and when certain genes are turned on or off). Diet, lifestyle, and environmental exposures can drive epigenetic changes throughout a person’s lifespan to influence health and disease. Epigenetic age is based on a person’s DNA methylation profile and strongly correlates with their chronological age. However, some exceptions exist. For example, the epigenetic ages of semi-supercentenarians (people who live to be 105 to 109 years old) are markedly younger than their chronological ages.
The investigators analyzed the DNA methylation profiles of more than 3,100 women enrolled in four large observational studies (Women’s Health Initiative; InCHIANTI; Parkinson’s Disease, Environment, and Genes; and the National Survey of Health and Development) to identify links between epigenetic age and menopause. Their analysis was based on assessment of the biological age of cells taken from the women’s blood, saliva, and inner cheek. Because the age at which a female experiences menopause is heritable, they conducted a Mendelian randomization analysis to identify genetic links between age at menopause and epigenetic aging.
They found that menopause markedly accelerated epigenetic aging. Females who experienced earlier natural menopause were more likely to have “older” blood than those who experienced later menopause, but females who had surgical menopause (a surgical procedure in which the ovaries are removed) had older blood and saliva than those who experienced natural menopause. Cells taken from the inner cheek of females who took menopausal hormone therapies were younger than those who did not take hormones. They also found that a particular gene variant that influences the age at which a female experiences menopause also influences age acceleration.
These findings suggest that menopause accelerates epigenetic aging in females. The investigators conceded that their findings do not establish a cause-and-effect relationship, however. In a related study, researchers found that menopause-related sleep disorders, such as insomnia or poor sleep quality, contribute to the accelerated aging associated with menopause. Learn more about accelerated epigenetic aging in this episode featuring Dr. Steve Horvath.
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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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Carriers of a common BDNF genetic variant demonstrate more rapid decline from Alzheimer's disease. www.sciencedaily.com
BDNF plays critical roles in many aspects of cognitive function, including learning and memory formation. A single-nucleotide polymorphism (SNP) in the gene that encodes BDNF causes a substitution of the amino acid valine (Val) by methionine (Met) in a specific region of the DNA where the gene is located. Evidence suggests that carrying the Met allele (Met/Met or Val/Met genotype) is associated with lower BDNF expression.. A 2017 study found that amyloid-beta burden impaired BDNF-related learning and memory.
Amyloid-beta is a toxic 42-amino acid peptide that aggregates and forms plaques in the brain with age. Amyloid-beta is associated with Alzheimer’s disease, a progressive neurodegenerative disease that can occur in middle or old age and is the most common cause of dementia.
The study involved more than 1,000 adults (approximately 55 years at the beginning of the study) who were enrolled in a larger study of Alzheimer’s disease. Nearly 65 percent of the participants were at high risk for developing Alzheimer’s disease, having at least one parent diagnosed with the condition. Each of the participants underwent cognitive assessment and BDNF genotyping five times over a period of four to 11 years. In addition, a small cohort of participants underwent imaging studies to assess amyloid-beta burden.
The genotyping revealed that approximately one-third of the participants were carriers of the Met-66 allele. Compared to Val/Val carriers, Met-66 carriers showed steeper declines in cognitive function. In addition, Met-66 carriers with greater amyloid-beta burden showed an even greater cognitive decline, likely due to lower BDNF expression. These findings suggest that a SNP in the gene for BDNF influences cognitive health and could serve as a therapeutic target against Alzheimer’s disease.
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BDNF genetic variant predicts success in alcohol dependence treatment. www.sciencedaily.com
Alcohol dependence is a complex disorder that increases a person’s risk of death from all causes. Findings from a 2009 study suggest that variations in certain genes can impact the likelihood of relapsing following treatment.
BDNF is involved in neuronal growth and survival, as well as influencing neurotransmitters – chemical signals from the nervous system. Low BDNF levels have been linked to the development of depression, anxiety, and alcohol dependence.
Previous research has demonstrated that alcohol dependence has a genetic component. The current study investigated whether common variations in certain genes would have an effect on post-treatment relapse.
The prospective study involved 154 participants who met the criteria for alcohol dependence and were admitted to a treatment facility. The patients provided blood samples for genetic analysis and completed self-assessment questionnaires about depression, hopelessness, impulsivity, and the severity of their alcohol use. The authors followed up with participants for approximately one year to assess whether they had relapsed. Relapse was defined as any drinking during the observation period, with heavy drinking considered as more than four drinks per day for more than four consecutive days. During the follow-up period, 59 (48 percent) participants relapsed, with 48 returning to heavy drinking. The average time to relapse was 218 days.
The authors tested a genetic variant that resides in the BDNF gene, known as Val66Met. They observed that participants with the Val form of this gene were more likely to relapse compared to those with the Met version. Participants with two copies of the Val allele – one from each parent – had higher rates of relapse and shorter times to relapse when compared to carriers of at least one Met allele.
These findings suggest that BDNF influences a person’s ability to remain abstinent following treatment for alcohol dependence. With further evaluation, these findings may help clinicians to identify people at increased risk for post-treatment relapse and tailor their care plans.