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Epigenetics and Obesity

The AHA! Team — Tue, 03 Dec 2024 06:06:42 +0000

Michael Greger M.D. FACLM via Nutrition Facts – Identical twins don’t just share DNA; they also share a uterus. Identical twins don’t just share DNA; they also share a uterus. Might that help account for some of their metabolic similarities? “Fetal overnutrition, evidenced by large infant birth weight for gestational age, is a strong predictor of obesity in childhood and later life.” Could it be that you are what your mom ate? A dramatic illustration from the animal world is the crossbreeding of Shetland ponies with massive draft horses. Either way, the offspring are half pony/half horse, but when carried in the pony uterus, they come out much smaller, as you can see below and at 0:47 in my video The Role of Epigenetics in the Obesity Epidemic. (Thank heavens for the pony mother!) This is presumably the same reason why the mule (horse mom and donkey dad) is larger than the hinny (donkey mom and horse dad). The way you test this in people is to study the size of babies from surrogates after in vitro fertilization. Who do you think most determines the birth weight of a test-tube baby? Is it the donor mom who provided all the DNA or the surrogate who provided the intrauterine environment? When it was put to the test, the womb won. Incredibly, a baby who had a thin biological mother but was born to a surrogate with obesity may harbor a greater risk of becoming obese than a baby with a heavier biological mother but born to a slim surrogate. The researchers “concluded that the environment provided by the human mother is more important than her genetic contribution to birth weight.” The most compelling data come from comparing obesity rates in siblings born to the same mother, before and after her bariatric surgery. Compared to their brothers and sisters born before the surgery, those born when mom weighed about 100 pounds less had lower rates of inflammation, metabolic derangements, and, most critically, three times less risk of developing severe obesity—35 percent of those born before the weight loss were affected, compared to 11 percent born after. The researchers concluded that “these data emphasize how critical it is to prevent obesity and treat it effectively to prevent further transmission to future generations.” Hold on. Mom had the same DNA before and after surgery. She passed down the same genes. How could her weight during pregnancy affect the weight destiny of her children any differently? Darwin himself admitted, “In my opinion, the greatest error which I have committed, has been not allowing sufﬁcient weight to the direct action of the environment, i.e. food…independently of natural selection.” We finally figured out the mechanism by which this can happen—epigenetics. Epigenetics, which means “above genetics,” layers an extra level of information on top of the DNA sequence that can be affected by our surroundings, as well as potentially passed on to our children. This is thought to explain the “developmental programming” that can occur in the womb, depending on the weight of the mother—or even the grandmother. Since all the eggs in your infant daughter’s ovaries are already preformed before birth, a mother’s weight status during pregnancy could potentially affect the obesity risk of her grandchildren, too. Either way, you can imagine how this could result in an intergenerational vicious cycle where obesity begets obesity. Is there anything we can do about it? Well, breastfed infants may be at lower risk for later obesity, though the benefits may be confined to those who are exclusively breastfed, as the effect may be due to growth factors triggered by exposure to the excess protein in baby formula, as you can see below and at 3:51 in my video. The breastfeeding data are controversial, though, with charges leveled of a “white hat bias.” That’s the concern that public health researchers might disproportionally shelve research results that don’t fit some goal for the greater good. (In this case, preferably publishing breastfeeding studies showing more positive results.) But, of course, that criticism came from someone who works for an infant formula company. Breast is best, regardless. However, its role in the childhood obesity epidemic remains arguably uncertain. Prevention may be the key. Given the epigenetic influence of maternal weight during pregnancy, a symposium of experts on pediatric nutrition concluded that “planning of pregnancy, including prior optimization of maternal weight and metabolic condition, offers a safe means to initiate the prevention rather than treatment of pediatric obesity.” Easier said than done, but overweight moms-to-be may take comfort in the fact that after the weight loss in the surgery study, even the moms who gave birth to kids with three times lower risk were still, on average, obese themselves, suggesting weight loss before pregnancy is not an all-or-nothing proposition. What triggered the whole obesity epidemic to begin with? There are a multitude of factors, and I covered many of them in my 11-video series on the epidemic in the related posts below. We are what our moms ate in other ways, too. Check out: Heart Disease May Start in the Womb Maternal Diet May Affect Stress Responses in Children Flashback Friday: The Effect of Animal Protein on Stress Hormones, Testosterone, and Pregnancy Key Takeaways Babies who are born larger are at higher risk of obesity later in life, suggesting early metabolic programming by maternal diet. The intrauterine environment significantly influences birth weight and later obesity risk, potentially outweighing genetic contributions from the biological mother. A baby with a thin biological mother but born to a surrogate with obesity may harbor a greater risk of future obesity than a baby with a heavier biological mother but born to a slim surrogate. Siblings born to the same mother before and after her bariatric surgery show reduced obesity risk in later-born children, highlighting the critical role of maternal weight during pregnancy. Epigenetics explain how environmental factors, like maternal weight, can influence gene expression and obesity risk across generations. Breastfeeding, especially exclusive breastfeeding, may lower obesity risk in children, contrasting with potential risks associated with formula feeding and excess protein exposure. To read the original article click here.

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Giant Viruses Found on Greenland Ice Sheet

The AHA! Team — Fri, 11 Oct 2024 08:39:57 +0000

Aarhus University via EurekAlert! – The viruses probably regulate the growth of snow algae on the ice by infecting them. Knowing how to control these viruses could help us reduce some of the ice from melting Every spring when the sun rises in the Arctic after months of darkness, life returns. The polar bears pop up from their winter lairs, the arctic tern soar back from their long journey south and the musk oxen wade north. But the animals are not the only life being reawakened by the spring sun. Algae lying dormant on the ice starts blooming in spring blackening large areas of the ice. When the ice blackens it’s ability to reflect the sun diminishes and this accelerates the melting of the ice. Increased melting exacerbates global warming. But researchers might have found a way to control the snow algae growth – and maybe in the long run reduce some of the ice from melting. Living on the ice alongside the algae, postdoc Laura Perini from the Department of Environmental Science at Aarhus University and her colleagues, have found giant viruses. She suspects that the viruses feed on the snow algae and could work as a natural control mechanism on the algae blooms. – We don’t know a lot about the viruses, but I think they could be useful as a way of alleviating ice melting caused by algal blooms. How specific they are and how efficient it would be, we do not know yet. But by exploring them further, we hope to answer some of those questions, she says. Bigger than bacteria Viruses are normally much smaller than bacteria. Regular viruses measure 20-200 nanometers in size, whereas a typical bacteria is 2-3 micrometers. In other words, a normal virus is around 1000 times smaller than a bacteria. That is not the case with giant viruses though. Giant viruses grow to the size of 2,5 micrometers. That is bigger than most bacteria. But the giant viruses are not only bigger in size. Their genome is much bigger than regular viruses. Bacteriophages – virus infecting bacteria – have between 100.000 and 200.000 letters in their genome. Giant viruses have around 2.500.000. Never found on the ice before Giant viruses were first discovered in 1981, when researchers found them in the ocean. These viruses had specialized in infecting green algae in the sea. Later, giant viruses were found in soil on land and even in humans. But it’s the first time that giant viruses have been found living on the surface ice and snow dominated by microalgae, Laura Perini explains. – We analyzed samples from dark ice, red snow and melting holes (cryoconite). In both the dark ice and red snow we found signatures of active giant viruses. And that is the first time they’ve been found on surface ice and snow containing a high abundance of pigmented microalgae. A few years ago everyone thought this part of the world to be barren and devoid of life. But today we know that several microorganisms live there – including the giant viruses. – There’s a whole ecosystem surrounding the algae. Besides bacteria, filamentous fungi and yeasts, there are protists eating the algae, different species of fungi parasitizing them and the giant viruses that we found, infecting them. – In order to understand the biological controls acting on the algal blooms, we need to study these last three groups. Haven’t seen them with the naked eye Even though the viruses are giant, they can’t be seen with the naked eye. Laura Perini hasn’t even seen them with a light microscope yet. But she hopes to do so in the future. – The way we discovered the viruses was by analyzing all the DNA in the samples we took. By sifting through this huge dataset looking for specific marker genes, we found sequences that have high similarity to known giant viruses, she explains. To make sure that the viral DNA didn’t come from long dead microorganisms, but from living and active viruses, they also extracted all the mRNA from the sample. When the sequences of the DNA that form genes are activated, they are transcribed into single stranded pieces called mRNA. These pieces work as recipes for building the proteins the virus needs. If they are present the virus is alive. – In the total mRNA sequenced from the samples, we found the same markers as in the total DNA, so we know they have been transcribed. It means that the viruses are living and active on the ice, she says. DNA and RNA in viruses At the center of the giant viruses is a cluster of DNA. That DNA contains all the genetic information or recipes needed to create proteins – the chemical compounds that are doing most of the work in the virus. But in order to use those recipes, the virus needs to transcribe them from double-stranded DNA to single stranded mRNA. Normal viruses can’t do that. Instead they have strands of RNA floating around in the cell waiting to be activated, when the virus infects an organism and hijacks its cellular production facilities. Giant viruses can do that themselves which makes them very different from normal viruses. Whereas DNA from dead viruses can be found in samples, mRNA is broken down much faster. mRNA is therefore an important marker of viral activity. In other words mRNA-recipes of certain proteins show that the viruses are alive and kicking. Not sure exactly how they work Because giant viruses are a relatively new discovery not a lot is known about them. In contrast to most other viruses they have a lot of active genes that enable them to repair, replicate, transcribe and translate DNA. But why that is and exactly what they use it for is not known. – Which hosts the giant viruses infect, we can’t link exactly. Some of them may be infecting protists while others attack the snow algae. We simply can’t be sure yet, Laura Perini says. She’s working hard on discovering more about the giant viruses and has more research coming out soon. – We keep studying the giant viruses to learn more about their interactions and what is exactly is their role in the ecosystem. Later this year we’ll release another scientific with some more info on giant viruses infecting a cultivated microalgae thriving on the surface ice of the Greenland Ice Sheet, she concludes. Journal Microbiome DOI 10.1186/s40168-024-01796-y To read the original article click here.

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Researchers Discover Genetic Connections to Alcohol Consumption

The AHA! Team — Fri, 14 Jun 2024 08:22:49 +0000

University of California San Diego via News-Medical – A research group centered at the University of California San Diego School of Medicine has drilled deep into a dataset of over 3 million individuals compiled by the direct-to-consumer genetics company 23andMe, Inc., and found intriguing connections between genetic factors influencing alcohol consumption and their relationship with other disorders. A research group centered at the University of California San Diego School of Medicine has drilled deep into a dataset of over 3 million individuals compiled by the direct-to-consumer genetics company 23andMe, Inc., and found intriguing connections between genetic factors influencing alcohol consumption and their relationship with other disorders. The study was recently published in the Lancet eBioMedicine. Sandra Sanchez-Roige, Ph.D., corresponding author and associate professor at UC San Diego School of Medicine Department of Psychiatry, explained that the study used genetic data to broadly classify individuals as being European, Latin American and African American. Such classifications “are needed to avoid a statistical genetics pitfall called population stratification,” noted co-author Abraham A. Palmer, Ph.D., professor and vice chair for basic research in the psychiatry department. Researchers analyzed genetic data from the 3 million 23andMe research participants The researchers analyzed genetic data from the 3 million 23andMe research participants, focusing on three specific little snippets of DNA known as single-nucleotide polymorphisms, or SNPs. Sanchez-Roige explained that variants, or alleles, of these particular SNPs are “protective” against a variety of alcohol behaviors, from excessive alcohol drinking to alcohol use disorder. One of the alcohol-protective variants they considered is very rare: the most prevalent among the three alleles found in the study showed up in 232 individuals of the 2,619,939 European cohort, 29 of the 446,646 Latin American cohort and in 7 of the 146,776 African American cohort; others are much more common. These variants affect how the body metabolizes ethanol – the intoxicating chemical in alcoholic beverages. “The people who have the minor allele variant of the SNP convert ethanol to acetaldehyde very rapidly. And that causes a lot of negative effects.” – Sandra Sanchez-Roige, Ph.D., corresponding author and associate professor at UC San Diego School of Medicine Department of Psychiatry She went on to say that the resulting nausea eclipses any pleasurable effects of alcohol – think of a bad hangover that sets in almost immediately. “These variants are primarily associated with how much someone may consume alcohol,” she said. “And they also tend to prevent alcohol use disorder, because these variants are primarily associated with the quantity of alcohol someone may drink.” Sanchez-Roige explained that the SNP variants’ influence on alcohol consumption are well researched, but her group took a “hypothesis-free” approach to the 23andMe dataset, which contains survey data on thousands of traits and behaviors. The researchers wanted to find out if the three SNP variants might have any other effects beyond alcohol consumption. Sanchez-Roige and Palmer noted that their group has developed a 10-year partnership with 23andMe that has focused on numerous traits, especially those with relevance for addiction. This work is the basis of an academic collaboration through the 23andMe Research Program. They data-mined the analyses of DNA from saliva samples submitted by consenting 23andMe research participants, as well as the responses to the surveys of health and behavior available from the 23andMe database, and found a constellation of associations, not necessarily connected with alcohol. Individuals with the alcohol-protecting alleles had generally better health, including less chronic fatigue and needing less daily assistance with daily tasks. But the paper notes individuals with the alcohol-protective alleles also had worse health outcomes in certain areas: more lifetime tobacco use, more emotional eating, more Graves’ disease and hyperthyroidism. Individuals with the alcohol-protective alleles also reported totally unexpected differences, such as more malaria, more myopia and several cancers, particularly more skin cancer and lung cancer, and more migraine with aura. Sanchez-Roige acknowledged that there is a chicken-and-egg aspect to their findings. For example: Cardiovascular disease is just one of a number of maladies known to be associated with alcohol consumption. “So is alcohol consumption leading to these conditions?” she asks. Palmer finishes the thought: “Or do these genetic differences influence traits like malaria and skin cancer in a manner that is independent of alcohol consumption?” Sanchez-Roige said that such broad, hypothesis-free studies are only possible if researchers have access to very large sets of data. Many datasets, including the one used in the study, rely heavily on individuals with European ancestry. “It is important to include individuals from different ancestral backgrounds in genetic studies because it provides a more complete understanding of the genetic basis of alcohol behaviors and other conditions, all of which contributes to a more inclusive and accurate understanding of human health,” she said. “The study of only one group of genetically similar individuals (for example, individuals of shared European ancestry) could worsen health disparities by aiding discoveries that will disproportionately benefit only that population.” She said their study opens numerous doors for future research, chasing down possible connections between the alcohol-protective alleles and conditions that have no apparent connection with alcohol consumption. “Understanding the underlying mechanisms of these effects could have implications for treatments and preventative medicine,” Sanchez-Roige noted. Co-authors on the paper from the University of California San Diego School of Medicine Department of Psychiatry are Mariela V. Jennings, Natasia S. Courchesne-Krak, Renata B. Cupertino and Sevim B. Bianchi. Sandra Sanchez-Roige is also associated with the Department of Medicine, Division of Genetic Medicine, Vanderbilt University. Other co-authors are: José Jaime Martínez-Magaña, Department of Psychiatry, Division of Human Genetics, Yale University School of Medicine; Laura Vilar-Ribó, Psychiatric Genetics Unit, Group of Psychiatry, Mental Health and Addiction, Vall d’Hebron Research Institute, Universitat Autònoma de Barcelona, Barcelona, Spain; Alexander S. Hatoum, Department of Psychology & Brain Sciences, Washington University in St. Louis; Elizabeth G. Atkinson, Department of Molecular and Human Genetics, Baylor College of Medicine; Paola Giusti-Rodriguez, Department of Psychiatry, University of Florida College of Medicine; Janitza L. Montalvo-Ortiz, Department of Psychiatry, Division of Human Genetics, Yale University School of Medicine, National Center of Posttraumatic Stress Disorder, VA CT Healthcare Center; Joel Gelernter, VA CT Healthcare Center, Department of Psychiatry, West Haven CT; and Departments of Psychiatry, Genetics & Neuroscience, Yale Univ. School of Medicine; María Soler Artigas, Psychiatric Genetics Unit, Group of Psychiatry, Mental Health and Addiction, Vall d’Hebron Research Institute, Universitat Autònoma de Barcelona, Barcelona, Spain; Department of Mental Health, Hospital Universitari Vall d’Hebron, Barcelona; Biomedical Network Research Centre on Mental Health (CIBERSAM), Madrid; and Department of Genetics, Microbiology, and Statistics, Faculty of Biology, Universitat de Barcelona; Howard J. Edenberg, Department of Biochemistry and Molecular Biology, Indiana University School of Medicine; and the 23andMe Inc. Research Team, including Sarah L. Elson and Pierre Fontanillas. The study was funded, in part, by Tobacco-Related Disease Research Program grants T32IR5226 and 28IR-0070, National Institute of Health (NIH) National Institute of Drug Abuse (NIDA) DP1DA054394, and NIH National Institute of Mental Health (NIMH) R25MH081482. Source: University of California San Diego Journal reference: Jennings, M. V., et al. (2024) A phenome-wide association and Mendelian randomisation study of alcohol use variants in a diverse cohort comprising over 3 million individuals. Lancet eBioMedicine. doi.org/10.1016/j.ebiom.2024.105086. To read the original article click here.

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How Oxygen Radicals Protect Against Cancer

AHA Publisher — Thu, 29 Apr 2021 07:00:06 +0000

Goethe University Frankfurt via EurekAlert – Originally, oxygen radicals – reactive oxygen species, or ROS for short – were considered to be exclusively harmful in the body. They are produced, for example, by smoking or UV radiation. Because of their high reactivity, they can damage many important molecules in cells, including the hereditary molecule DNA. As a result, there is a risk of inflammatory reactions and the degeneration of affected cells into cancer cells. Because of their damaging effect, however, ROS are also deliberately produced by the body, for example by immune or lung epithelial cells, which destroy invading bacteria and viruses with ROS. This requires relatively high ROS concentrations. In low concentrations, on the other hand, ROS play an important role as signalling molecules. For these tasks, ROS are specifically produced by a whole group of enzymes. One representative of this group of enzymes is Nox4, which continuously produces small amounts of H2O2. Nox4 is found in almost all body cells, where its product H2O2 maintains a large number of specialised signaling functions, contributing, for example, to the inhibition of inflammatory reactions. Researchers at Goethe University Frankfurt, led by Professor Katrin Schröder, have now discovered that by producing H2O2, Nox4 can even prevent the development of cancer. They examined mice that were unable to produce Nox4 due to a genetic modification. When these mice were exposed to a carcinogenic environmental toxin (cancerogen), the probability that they would develop a tumour doubled. Since the mice suffered from very different types of tumours such as skin sarcomas and colon carcinomas, the researchers suspected that Nox4 has a fundamental influence on cellular health. Molecular investigations showed that the H2O2 formed by Nox4 keeps a cascade going that prevents certain important signalling proteins (phosphatases) from entering the cell nucleus. If Nox4 and consequently H2O2 are absent, those signalling proteins migrate into the cell nucleus and as a consequence, severe DNA damage is hardly recognised. Severe DNA damage – e.g. double strand breaks – occurs somewhere in the body every day. Cells react very sensitively to such DNA damage, setting a whole repertoire of repair enzymes in motion. If this does not help, the cell activates its cell death programme – a precautionary measure of the body against cancer. When such damage goes unrecognised, as occurs in the absence of Nox4, it spurs cancer formation. Prof. Katrin Schröder explains the research results: “If Nox4 is missing and there is therefore no H2O2, the cells no longer recognise DNA damage. Mutations accumulate and damaged cells continue to multiply. If an environmental toxin is added that massively damages the DNA, the damage is no longer recognised and repaired. The affected cells are not eliminated either, but multiply, sometimes very quickly and uncontrollably, which eventually leads to the development of tumours. A small amount of H2O2 thus maintains an internal balance in the cell that protects the cells from degeneration.” To read the original article click here.

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Accelerated Cellular Aging Associated With Mortality Seen in Depressed Individuals

AHA Publisher — Tue, 13 Apr 2021 07:00:25 +0000

Walter Reed Army Institute of Research via EurekAlert – Cells from healthy individuals with major depressive disorder were found to have higher than expected rates of methylation at specific sites on their DNA, when compared to cells from healthy individuals without MDD, according to a study by a multidisciplinary team of Walter Reed Army Institute of Research and University of California San Francisco scientists, in collaboration with others. Methylation is a process by which DNA is chemically modified at specific sites, resulting in changes in the expression of certain genes. Methylation of particular sets of genes, called “DNA methylation clocks,” typically change in predictable ways as people age, but the rate of these changes varies between people. Methylation patterns in individuals with MDD suggested that their DNA methylation cellular age was, on average, accelerated relative to matched healthy controls. In the study, published in Translational Psychiatry, blood samples from 49 individuals with MDD were compared to 60 healthy control subjects of the same chronological age using the ‘GrimAge’ clock–a mathematical algorithm designed to predict an individual’s remaining lifespan based on cellular methylation patterns. Individuals with MDD showed a significantly higher GrimAge score, suggesting increased mortality risk compared to healthy individuals of the same chronological age–an average of approximately two years on the GrimAge clock. The individuals with MDD were unmedicated prior to the study and showed no outward signs of age-related pathology, as they and the healthy controls were screened for physical health before entry into the study. The methylation patterns associated with mortality risk persisted even after accounting for lifestyle factors like smoking and BMI. These findings provide new insight into the increased mortality and morbidity associated with the condition, suggesting that there is an underlying biological mechanism accelerating cellular aging in some MDD sufferers. “This is shifting the way we understand depression, from a purely mental or psychiatric disease, limited to processes in the brain, to a whole-body disease,” said Katerina Protsenko, a medical student at UCSF and lead author of the study. “This should fundamentally alter the way we approach depression and how we think about it–as a part of overall health.” MDD is one of the most prevalent health concerns globally. According to the World health Organization, some 300 million people (4.4% of the population) suffer from some form of depression. MDD is associated with higher incidence and mortality related to increased rates of cardiovascular disease, diabetes, and Alzheimer’s disease among sufferers. “One of the things that’s remarkable about depression is that sufferers have unexpectedly higher rates of age-related physical illnesses and early mortality, even after accounting for things like suicide and lifestyle habits,” said Dr. Owen Wolkowitz, professor of psychiatry and a member of UCSF’s Weill Institute for Neurosciences, co-senior author of the study. “That’s always been a mystery, and that’s what led us to look for signs of aging at the cellular level.” The researchers say that they don’t yet know if depression causes altered methylation in certain individuals, or if depression and methylation are both related to another underlying factor. It is possible that some individuals may have a genetic predisposition to produce specific methylation patterns in response to stressors, but this has not been well-studied. Alterations in methylation patterns have previously been observed in individuals with post-traumatic stress disorder. “These findings will allow us to better understand the relationships between behavioral health disorders–for example, 60% of PTSD cases are co-morbid with MDD. Elucidating these mechanistic and biochemical underpinnings will improve efforts to develop targeted diagnostic and treatment strategies, ultimately improving patient care,” said Dr. Marti Jett, WRAIR chief scientist. Previous research from the group used GrimAge to study men with combat PTSD. Moving forward, the researchers hope to determine whether pharmacological treatments or therapy may mitigate some methylation changes related to MDD in hopes of normalizing the cellular aging process in affected individuals before it advances. Also, although the “GrimAge” methylation clock has been associated with mortality in other populations, no studies have yet prospectively determined whether this methylation pattern also predicts mortality in MDD. “As we continue our studies, we hope to find out whether addressing the MDD with anti-depressants or other treatments alters the methylation patterns, which would give us some indication that these patterns are dynamic and can be changed,” said Dr. Synthia Mellon, professor in the Department of Obstetrics, Gynecology and the Reproductive Sciences at UCSF and co-senior author of the study. To read the original article click here.

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How to Use Blood Tests & Biomarkers to Improve Your Mental Health

AHA Publisher — Fri, 26 Feb 2021 08:00:37 +0000

Dr. Caroline Leaf – Words like “health”, “wellbeing” and “longevity” are often thrown around, but what do they actually mean, and what do they mean for you? In this podcast (episode #258) and blog, I speak with Dr. Gil Blander, director, founder and chief scientist at InsideTracker, about how InsideTracker can improve your mental and physical health, my own experience with InsideTracker, how to not become too stressed or obsessed with biohacking, data and numbers and still enjoy good health, how thinking affects your health and metabolism, and how to proactively have a long and quality-filled life! At a young age, Dr. Blander was stunned by the early death of a family member. His commitment to advance the field of human longevity was made there and then. Working alongside some of the world leaders in aging research, such as MIT biologist Dr. Leonard Guarente and Harvard geneticist Dr. David Sinclair, he came up with the idea for an automated, algorithm-based personalized nutrition and lifestyle platform, founding InsideTracker to help people from all walks of life live better, longer and happier lives. At InsideTracker, they believe the most impactful science and technology products result from constant learning and data. They create evidence-based solutions that are simple, clear, and actionable, based on your unique biology and experiences. They cut through the “noise” by analyzing your blood, your DNA, your lifestyle and nutrition habits, and tell you how to live, look, age, and perform better for you. InsideTracker products have already helped thousands of people optimize their health by improving their bodies from the inside out, using personalized recommendations for nutrition, supplements, and lifestyle. They are optimizing everyone, from athletes to busy professionals and stressed-out parents! As Dr. Blander notes, personalized health choices based on data, which is at the heart of what InsideTracker does, is one of the most powerful weapons for fighting chronic disease, improving mental health, and increasing longevity. Your blood, DNA and habits are a goldmine of data. They’re a snapshot of your body in time; they tell you what’s going right, what’s not. They give you a window into how your brain and body are functioning. And the team at InsideTracker can tell you how to use this data to improve, including what to eat, how to exercise, what your body needs and more! This is important for both our mental and physical health. We can use biological markers like blood glucose levels, white blood cell counts (which is one marker of our inflammatory response to stress or a lack of quality sleep) and cortisol levels to examine how these impact our overall cognition and mental health, and what we can do to improve our stress resilience, sleep, clarity of thought and self-regulation. We can even use this data to start acting to prevent or heal inflammatory, age-related diseases like Alzheimer’s! Of course, there can be downsides to “biohacking” our health in this way. Although there are many health benefits to tracking our biomarkers, we need to be careful that we don’t become obsessed with our health data and stress about “biohacking” our life, especially if we are not trained to read or understand the results. Take the data and make sense of it with the help of a professional (like the highly-qualified team at InsideTracker), but don’t overload yourself with data and become obsessed with it, which can negatively impact your overall mental and physical health! We need to recognize that platforms like InsideTracker are guides, not the whole picture of everything that is going on all the time. Using these health guides to track your biomarkers in real time can be incredibly empowering—you don’t have to just follow a trend and hope it works for you, as Dr. Blander notes. You can see, over time, how your eating habits, exercise habits and your other lifestyle choices affect your health. Tracking your health using platforms like InsideTracker helps you understand what is going on in your brain and body, which permits you to make sustainable changes and improve your overall health and longevity. It puts the quality of your life in your hands! To read the original article click here. For more articles from Dr. Leaf click here.

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Study Reveals Birth Defects Caused by Flame Retardant

AHA Publisher — Fri, 19 Jun 2020 07:00:01 +0000

University of Georgia via Newswise – *Research focuses on man’s exposure prior to conception. A new study from the University of Georgia has shown that exposure to a now-banned flame retardant can alter the genetic code in sperm, leading to major health defects in children of exposed parents. Published recently in Scientific Reports, the study is the first to investigate how polybrominated biphenyl-153 (PBB153), the primary chemical component of the flame retardant FireMaster, impacts paternal reproduction. In 1973, an estimated 6.5 million Michigan residents were exposed to PBB153 when FireMaster was accidentally sent to state grain mills where it made its way into the food supply. In the decades since, a range of health problems including skin discoloration, headache, dizziness, joint pain and even some cancers have been linked to the exposure. More striking, the children of those who were exposed seemed to experience a host of health issues as well, including reports of hernia or buildup in the scrotum for newborn sons and a higher chance of stillbirth or miscarriage among adult daughters. Yet, little work has been done to understand how the chemical exposure could have impacted genes passed from an exposed father, said study author Katherine Greeson. Relatively new idea “It is still a relatively new idea that a man’s exposures prior to conception can impact the health of his children,” said Greeson, an environmental health science doctoral student in Charles Easley’s lab at UGA’s College of Public Health and Regenerative Bioscience Center. “Most studies where a toxic effect is observed in children look only to the mothers and the same has been true of studies conducted on PBB153,” she said. Greeson and a team of researchers from UGA and Emory University used a unique combination of observational and laboratory approaches to demonstrate how PBB153 acted on sperm cells. “Typically, scientific studies are either epidemiological in nature and inherently observational or focus on bench science, but in this study, we did both,” said Greeson. This approach allowed the researchers to mimic the known blood exposure levels of PBB153 in a lab environment. “We were uniquely able to recreate this effect using our previously characterized human stem cell model for spermatogenesis,” she said, “which allowed us to study the mechanism that causes this effect in humans.” The team looked at the expression of different genes in their human spermatogenesis model after dosing with PBB153 and found marked alterations in gene expression between dosed and undosed cells, specifically at genes important to development, such as embryonic organ, limb, muscle, and nervous system development. Changes to the DNA “PBB153 causes changes to the DNA in sperm in a way that changes how the genes are turned on and off,” said Greeson. “PBB153 seems to turn on these genes in sperm which should be turned off,” said Greeson, which may explain some of the endocrine-related health issues observed in the children of exposed parents. Though the study used this model to directly replicate exposure to PBB153, Greeson says this approach could be used to better understand the impact of other environmental exposures on reproduction, including large-scale accidental exposures to toxic chemicals or everyday exposures. More studies combining epidemiology “Hopefully this work will lead to more studies combining epidemiology and bench science in the future, which will tell us more about why we’re seeing an effect from an environmental exposure in human populations and encourage experimental studies to more closely mimic human exposures,” she said. To read the original article click here.

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Extinguishing Fearful Memories Depends on the Flexibility of Your DNA

AHA Publisher — Thu, 07 May 2020 07:00:19 +0000

University of Queensland via EurekAlert – Fear is an important survival mechanism and so too is the ability to inhibit fear when it’s no longer needed. In order to counter-balance fear, the brain engages in fear extinction. In this process, memories are formed during non-fearful experiences with similar environmental elements. These non-fearful memories then compete with the original fear memory. Now, in a new paper published in the journal Nature Neuroscience, the University of Queensland’s Professor Tim Bredy and his colleagues show that the ability to extinguish fearful memories in this way relies on the flexibility of your DNA. Flexible DNA “DNA can adopt a variety of different structures,” says Dr Paul Marshall, a researcher at UQ’s Queensland Brain Institute and lead author of the study. “The most common and most widely recognized form is the ‘B-DNA’ double helix, which twists in a clockwise direction. But, with a slight rearrangement of how DNA base-pairs connect with one another, DNA can form other helical structures, such as Z-DNA.” Z-DNA is a counter-clockwise twisted version of B-DNA, he explains. Imagine for a moment, that each of your hands is a DNA strand, the thumbs the bases. If you hold both hands out in front of you, palms out, so that your thumbs touch, this is how two bases connect in B-DNA. If you now flip your wrists so that your palms face inward and your pinkies touch, this is how bases flip-out during Z-DNA formation. If you keep rotating your hand and now re-join the thumbs this is what happens when Z-DNA is stabilized into a new twist. Turning Inside Out Z-DNA occurs over short regions and only certain sequences can turn inside-out like this. For a long time, no one knew why it existed at all. “We now know that Z-DNA appears wherever genes are being turned on,” says Dr Marshall. “It’s a marker of gene activity.” “Scientists have also noticed a connection between Z-DNA and certain diseases, including cancer, and high levels of Z-DNA have been found in the brains of people who had Alzheimer’s Disease.” This potential link with memory intrigued Dr Marshall and Professor Bredy, especially since the formation of fear extinction memories involves rapid changes in gene activity. To find out more, they turned their attention to an enzyme called ADAR1, which recognizes and latches onto Z-DNA. ADAR1 is known to play a role in RNA editing, which is important for modifying protein functions in the cell. Evidence also suggests that ADAR1 can convert Z-DNA back into B-DNA. “ADAR1 is doing a lot of things at once, but that’s what makes it interesting,” says Dr Marshall. Unable to Form Non-Fearful Memories He and his colleagues turned off the ADAR1 gene in mice, specifically in a part of the brain known to play a role in fear extinction. As a result, although the mice could still form fear memories, they were unable to form non-fearful memories. In short, they lost the capacity for fear extinction. The researchers observed a similar effect when they mutated ADAR1, so that it didn’t work very well. The findings suggest that Z-DNA forms during fear then, during fear extinction, ADAR1 binds to that Z-DNA and carries out two important jobs: it rapidly increases RNA editing and then flips Z-DNA back into B-DNA. “It seems that the more easily you can switch between DNA structures, the more plastic your memory is,” says Dr Marshall. “Flexibility of DNA structure, flexibility of memory.” Plastic Fear Memories This enables an agile response to our environment, he adds. “Fear memories need to be plastic. They can be very useful for survival, but they can also get in the way of normal functioning.” The balance between fear and fear-extinction is critical to cognitive flexibility, says Professor Bredy. Indeed, the impairment of fear extinction is a key feature of PTSD and phobias. The more we understand about how fear extinction works, the more chance we have of finding better treatments for those conditions. To read the original article click here.

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DNA Discovery Can Lead to New Types of Cancer Drugs

AHA Publisher — Sat, 07 Mar 2020 08:00:46 +0000

University of Copenhagen the Faculty of Health and Medical Sciences via EurekAlert – Cells can both survive and multiply under more stress than previously thought, shows research from the Faculty of Health and Medical Sciences. This was found by inhibiting the essential gene DNA polymerase alpha, or POLA1, which initiates DNA replication during cell division. The discovery gives researchers new insights into DNA replication and may potentially be used for a new type of cancer treatment. Research Leader and Associate Professor Luis Toledo of the Center for Chromosome Stability at the Department of Cellular and Molecular Medicine states as follows: ‘If we are visionaries, I would say that we might be at the birth of a whole new set of molecules that could be used in fighting cancer’, adding: ‘Basically, if we turn the finding on its head, this novel strategy aims at exploiting an in-built weakness in cancer cells and make them crash while they divide.’ Loose Zippers When a cell divides, the double DNA strand is opened lengthwise like a zipper that is unzipped. The new double strands are built at each of the separated strands, so that you gradually end up with two new “zippers”. Before the new halfs of the zipper are made, a bit of DNA is temporally exposed in single stranded form. This process is required for the new zippers to form. Nevertheless, large amounts of single-stranded DNA have traditionally been considered by researchers to be a sign of pathological stress during cell proliferation. However, the researchers behind the new study discovered that DNA unzippers act more loosely than expected. This can generate large amounts of single-stranded DNA, which the researchers now show is no more than a form of natural stress that cells can actually tolerate in high quantities. Still, for this tolerance to exist, cells require a sufficient amount of the protective protein RPA to cover the single-stranded DNA parts. ‘We have seen that cells can duplicate their genome, even with large amounts of single stranded DNA. They can divide and go on living healthily because they have a large excess of RPA molecules that acts as a protective umbrella.’ says the study’s first author and former postdoc at the University of Copenhagen Amaia Ercilla, adding: ‘But there is a flip side of the coin. When we make the cells generate single strand DNA faster than what they can protect, chromosomes literally shatter in hundreds of pieces, a phenomenon we call replication catastrophe. We always thought that we could use this for instance to kill cancer cells,’ she adds. Weapon Against Cancer Both Amaia Ercilla and Luis Toledo explain that under normal circumstances it is extremely difficult to deplete a cell’s reserve of RPA. The same was true in the new study, when researchers used different types of chemotherapy to increase the amount of single-stranded DNA. Even when using the best compounds available so far it took around one hour to deplete the RPA reserve in a cell, provoking a replication catastrophe and the associated cell death. However, the researchers behind the new study believe to have found what Luis Toledo calls ‘the ultimate single-stranded DNA generator’: When the researchers used a so-called POLA1 inhibitor, the cells met their final destiny after just five minutes. ‘Although no new DNA can be made when we inhibit POLA1, the DNA unzippers keep advancing and generate single-stranded DNA at very high speed,’ says the Associate Professor, adding: ‘All cells can be sensitive to POLA1 inhibitors, including cancer cells, and we might speculate that the strategy could be especially useful against very aggressive forms of cancer that proliferate at a high pace’. The next step of the research group is to find more molecules that biologically inhibits the POLA1 gene and which, in combination with other substances, may be used in the treatment of cancer patients. To read the original article click here.

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