humanOS Radio

Why do we sleep? This is a question that has bedeviled researchers for decades. But we think one major reason may be to facilitate DNA repair. In this episode of humanOS Radio, Dan speaks with Lior Appelbaum. Dr. Appelbaum and colleagues have performed some elegant studies elucidating the molecular mechanisms that underlie sleep, using zebrafish as a model organism. In a recent study, the team engineered zebrafish larvae to express colorful tags on their chromosomes, making it easy to monitor them. They then followed the activity of the chromosomes in their neurons, as well as DNA damage and repair, and were surprised by what they observed. To learn about their findings, check out the interview!

On this episode of humanOS Radio, Dan welcomes Ben Miller to the show. Ben is a principal investigator in the aging and metabolism research program at the Oklahoma Medical Research Foundation. In his study, Miller and his team randomly assigned 53 participants to consume either placebo or metformin for 12-weeks, while completing a supervised aerobic exercise program. This exercise regimen elicited measurable improvements in blood sugar control, insulin sensitivity, and aerobic fitness for the volunteers, as you would obviously expect. But when the groups were compared, some meaningful - and troubling - differences emerged, suggesting that metformin was counteracting some of the benefits associated with exercise. Check out the interview to learn more!

On this episode of humanOS Radio, Dan speaks with Richard Lin. Like all too many of us, Richard became personally invested in his health when he developed a problem that failed to respond to conventional medical interventions. He eventually realized that a disruption in the gut microbiota was the likely cause of his illness. This inspired him to start Thryve Inside. Thryve helps consumers test and learn about their own microbiota by providing at-home microbiome test kits. But here's what sets Thryve apart: they don't just give you information, they also endeavor to provide solutions. Thryve offers monthly subscriptions of personalized probiotics to customers, which are formulated based on their microbiome and their individual health goals. To learn more about Thryve, and about the exciting future of microbiome testing and probiotics, please check out the interview!

We associate getting older with a loss of energy. On the molecular level, this is quite literally true, because one of the hallmarks of aging is mitochondrial dysfunction. Mitochondria are often referred to as “the powerhouse of the cell,” because they convert nutrients from the food we eat into usable energy, in the form of ATP. But as we age, mitochondria become less effective at generating the energy we need for various chemical processes. So why does this happen? As with most things in biology, there are definitely multiple factors at work here. But one likely reason is a failure of quality control. As we age, mitochondrial autophagy (aka mitophagy) declines, and our body starts to accumulate broken and dysfunctional mitochondria. This becomes most obvious in tissues that consume a lot of energy, like skeletal muscle. Hence, mitochondrial dysfunction is linked to poor muscular strength in older people. If we could find a way to ramp up mitophagy, perhaps we could retain excellent mitochondrial function throughout our golden years. In this episode of humanOS Radio, Dan welcomes Dr. Davide D’Amico to the show. Davide is a research scientist in the field of metabolism and aging. He was previously a post-doc at the Auwerx Laboratory of Integrative Systems Physiology at the École Polytechnique Fédérale de Lausanne (EPFL), where he investigated the role of mitochondrial function in health, disease, and the aging process. In this interview, we discuss a recently published study from his team, which revealed one of the molecular mechanisms through which defective mitochondria accumulate in cells. Additionally, Davide is a scientific project manager at Amazentis, where he is investigating a naturally derived bioactive from pomegranate, that has been shown in a new clinical trial to reverse age-related decline in mitochondrial function in the muscles of older people. Please check out the interview to learn more about this exciting research!

We tend to think of age in terms of the number of years we have been alive - meaning our chronological age. But the year that you were born is not necessarily an accurate measure of your health or your life expectancy. We are coming to realize that a better predictor is your biological age - and that can be quite different from your chronological age. So how do you learn your biological age? And what can you do with this information? In this episode of humanOS Radio, Dan speaks with Ken Raj. Ken is a Senior Scientific Group Leader at Public Health London, and has worked extensively with Dr. Steve Horvath of UCLA in developing and interpreting genomic biomarkers of aging. They are best known for developing the “epigenetic clock,” a tool that predicts life expectancy by examining age-related changes to DNA methylation, then using that information to calculate biological age in relation to chronological age. The epigenetic clock is able to predict life expectancy with remarkable accuracy, with a margin of error of plus or minus three years. In this podcast, we discuss: -How the epigenetic clock uses DNA methylation to compare biological to chronological age. -Whether DNA methylation changes are the “drivers” or the “passengers” of biological aging, and how direct a role they play in the aging process. -Whether or not epigenetic changes can be passed down from generation to generation. -Whether or not someone with a biological age greater than their chronological age is more likely to develop certain pathologies. -On the other hand, whether having a younger biological age than chronological age means greater health and a longer life. -What diet and lifestyle factors have been researched to show an impact on epigenetic aging. -Whether or not epigenetic drugs have the ability to modify this clock and slow aging. -The potential for extracting the exact mechanisms through which things like exercise and certain dietary interventions slow down epigenetic aging. -If the epigenetic clock can be used for earlier diagnosis of such age-related conditions as cancer, diabetes and neurodegenerative diseases, leading to better outcomes. To learn more, check out the blog!

In this episode of humanOS Radio, Dan speaks with John Newman. Dr. Newman is a geriatrician (a physician who specializes in the care of older people) at UCSF, as well as a professor at the Buck Institute for Research on Aging. He is chief investigator at the Newman Lab, where he is exploring ways to harness metabolic signals to promote health and resilience, particularly in older adults. Dr. Newman’s research focuses predominantly on ketone bodies - molecules produced in the liver when glucose is scarce, either due to restricted intake or prolonged physical activity. So we tend to think of them primarily as an alternative source of fuel, particularly in the context of a low carb diet. However, they are also intriguing with respect to aging, because of how they function as molecular signals, and how they influence gene expression.

Why do we age? The fundamental causes of aging at the molecular level are relatively well established. But the question of why aging happens in the first place is a more challenging one, one which has bedeviled evolutionary biologists and philosophers for years. You might think, intuitively, that the process of natural selection would gradually eliminate senescence. Aging increases mortality, and organisms that experience impaired function and ultimately die would not be able to produce as many offspring as one that was able to live (and to reproduce) indefinitely, or at least for a much longer timespan. So, you would assume that this would result in selection for organisms that live much longer, generate more offspring, and ultimately the causes of age-related deterioration would fade from the genome. Yet aging is very commonly observed. Why is that? Natural selection is strongest in early life. This makes sense - the natural environment is full of predators, disease, and other perils that often kill organisms when they are young and vulnerable. Consequently, genes and pathways that enhance survival and reproduction in early life are likely to be favored - even if they come at the cost of problems later in life, when selection is comparatively weak. But is aging inevitable? Can it be slowed, or postponed, or stopped altogether? In this installment of humanOS, Dan talks with Michael Rose. Dr. Rose is a Distinguished Professor of Ecology and Evolutionary Biology at UC Irvine. He is a prolific biologist whose research into the evolution of aging has effectively transformed that field. Rose’s laboratory has been testing the theory of antagonistic pleiotropy for nearly forty years, through artificial selection experiments in fruit flies. In what was perhaps his most famous experiment, Rose allowed flies to only reproduce successfully if they laid their eggs late in life. He discarded the eggs of any flies that laid eggs before they reached fifty years of age. Over a few generations, this population of flies evolved longer lifespans. Why might this be? Remember that natural selection is strongest early in life, and becomes weak later on. In theory, if adults reproduce when they are older, natural selection is apt to favor genes that enhance resilience (and reproduction) later into the lifespan. Dr. Rose's research into aging has also drawn him to some interesting (and possibly controversial) notions about evolutionary changes in the human diet, and how our age may influence how adapted we are to modern agricultural foods. To learn what that means, and its potential implications, check out the interview!

For the vast majority of human history, our species lived hunter-gatherer lifestyles. We can therefore learn much about how humans probably once lived by studying preindustrial societies. Research on preindustrial societies has consistently shown that these people have exemplary metabolic health. And when we consider that modern humans are succumbing to chronic diseases at an alarming rate, we clearly have much to learn from preindustrial people. In this episode of humanOS Radio, Greg Potter speaks with Professor Herman Pontzer about what Herman has learned from his research on hunter-gatherers. Herman's findings led him to develop the counterintuitive hypothesis that how physically active we are each day may scarcely affect how many calories we burn… … no, I’m not kidding. As he explains in the podcast, however, this hypothesis in no way discounts the importance of being physically active – far from it! Tune in for more on Herman’s fascinating research on physical activity, diet, and more.

Do smartphones really affect the timing and quality of your sleep? In this episode of humanOS Radio, Dan speaks with Dr. Jeanne Duffy from Harvard Medical School on her most recent research investigating this question.

Stress is something we all experience all too frequently. The effects of different stressors accumulate, and when the resultant load is excessive, we are at increased risk of a range of diseases. So, to avoid the amount of stress we experience exceeding our bodies’ capacities to cope, it would be useful to have a way to monitor how we’re responding to stressors. In the last few years, numerous wearable devices that claim to monitor how we’re responding to stress have become available, and most of these measure either heart rate variability (HRV) or pulse rate variability. In this episode of humanOS Radio, Professor Phyllis Stein explains what you need to know about HRV, including what it is, why people measure it, and whether you should measure your own HRV.