Podcasts about uk biobank

What happens when a company focused on drug discovery and life sciences encounters a data problem that nobody else seems able to solve? Recorded at the IT Press Tour in Boston, this episode explores the fascinating story behind Paradigm4 and how a challenge in large-scale biomedical research ultimately led to the creation of flexFS, a cloud-native filesystem designed to tackle some of today's biggest data infrastructure challenges. Joining me on the podcast is David Freund from Paradigm4, who shares how the company was originally founded to help scientists work with enormous datasets in fields such as genomics, bioinformatics, and precision medicine. As researchers began working with population-scale datasets such as the UK Biobank, the team discovered that existing storage technologies either couldn't deliver the performance they needed, lacked the functionality required, or became prohibitively expensive at scale. Our conversation explores the moment Paradigm4 realized it would need to build its own solution, why traditional approaches to cloud storage often struggle under modern analytics workloads, and how flexFS emerged from a real-world customer problem rather than a technology trend. David also explains why object storage has become such an attractive foundation for modern infrastructure, while discussing the challenges of latency, performance, and cost that still need to be addressed. We also discuss why many organizations investing heavily in AI infrastructure may be overlooking one of the biggest constraints on performance. While much of the industry conversation focuses on GPUs and compute power, David argues that data access, movement, and management are becoming equally important considerations as AI workloads continue to grow. Along the way, we touch on cloud independence, resilience, large-scale analytics, and why flexibility across cloud providers is becoming an increasingly important requirement for enterprise technology leaders. Whether you're working in AI, life sciences, cloud infrastructure, or enterprise data management, this episode offers an interesting perspective on how customer problems can sometimes lead to entirely new categories of technology. Could the next major AI bottleneck be data rather than compute? And are organizations paying enough attention to the infrastructure feeding their most important workloads? I'd love to hear your thoughts.

HEALTH NEWS   Study links low vitamin C levels in the blood plasma to reduced brain connectivity Study: Tart Cherry Supplementation Alters Muscle Protein Profile After Exercise Socioeconomic factors may leave more lasting imprint on children's brains than IQ or parenting style Fasting-mimicking diet reduces gum disease inflammation Low blood pressure shows strongest link to Alzheimer's disease   Study links low vitamin C levels in the blood plasma to reduced brain connectivity Hirosaki University (Japan), June 10 2026 (News-Medical) Previous research has uncovered associations between diets higher in vitamin C and lower risk of cognitive impairment in older adults. However, few studies have looked directly at vitamin C levels in blood plasma and potential associations with brain structure and connectivity within brain networks. To help fill that gap, Nagaya and colleagues analyzed magnetic resonance imaging (MRI) scans and plasma vitamin C levels of 2,044 adults over the age of 64. Specifically, they measured the volume of each participant's gray and white brain matter (accounting for individual differences in total brain volume between participants). They also evaluated connectivity within the default mode network, which is associated with several cognitive functions, such as attention and autobiographical memory. After statistically accounting for other factors the researchers found that participants with lower plasma vitamin C levels tended to have lower gray matter volume, as well as lower connectivity within the default mode network. These findings suggest the possibility that optimal levels of vitamin C in blood plasma could potentially support cognitive function and counteract cognitive decline. However, the findings do not confirm any such cause-effect relationship between vitamin C levels and brain health.   Study: Tart Cherry Supplementation Alters Muscle Protein Profile After Exercise University of Exeter (UK), June 11 2026 (Natural News) Researchers recruited 34 healthy, recreationally active young men and assigned them to receive either a placebo, a low-dose tart cherry concentrate, or a high-dose tart cherry supplement, according to the study report. Participants consumed their assigned supplement for seven days before completing a muscle-damaging workout and continued supplementation for three days afterward, for a total intervention of 10 days. The study found that tart cherry supplementation significantly altered the muscle's protein profile following exercise-induced damage. Changes were observed in proteins involved in muscle structure, contraction, cellular repair processes, and immune-cell activity within muscle tissue. These findings suggest that tart cherry polyphenols may influence the way muscles respond to and recover from the stress of exercise. Researchers also detected significant increases in hippuric acid, a compound produced when gut microbes break down polyphenols from tart cherries and other plant foods. Participants with higher levels of hippuric acid tended to maintain better muscle function following exercise-induced damage.   Socioeconomic factors may leave more lasting imprint on children's brains than IQ or parenting style Washington University in St. Louis, June 11 2026 (Medical Xpress) After analyzing hundreds of biological, psychological, social and environmental factors related to children's development, researchers at Washington University School of Medicine in St. Louis found that a family's financial situation and the resources and opportunities in a child's neighborhood had the strongest connection to brain development. Socioeconomic factors accounted for about 16% of the variability in measures of children's brain function—far more than IQ, parenting style and health history.  As part of the study, the researchers analyzed brain scans from nearly 12,000 children ages 9 to 10 to see how a child's environment, health and regular activities are related to brain development. Of the hundreds of factors examined, the team found that the socioeconomic status of a child's family had the strongest relationship with that child's brain structure and function. Further, the parts of the brain that reflect socioeconomic factors were the same areas most sensitive to sleep and stress, suggesting that socioeconomic disadvantage affects the brain indirectly through disrupted sleep and chronic stress. Of the top 40 variables linked to brain function, 37 were socioeconomic, and of the top 40 tied to structure, 35 were socioeconomic. These included the social and economic resources in the child's neighborhood, akin to the overall wealth of an area. Strong influences included family income, homeownership, poverty rates and access to transportation. The remaining top variables were related to sleep, screen time and stress.   Fasting-mimicking diet reduces gum disease inflammation Kings College London, June 11 2026 (Eurekalert) People who follow a short-term low-calorie diet may have reduced markers of inflammation associated with gum disease. A new study by King's College London highlights how lifestyle modifications could be important alongside plaque control in managing gum disease. The research included 28 patients from across hospitals in Spain, split into two groups – those who followed a five-day restrictive diet, versus a control group who continued their usual diet. Patients who fasted ate 1,100 calories for two days, then 750 calories for three days. The sixth day gently introduced more calories with soft foods – then their diets returned to normal by the seventh day. This was repeated three times in six months, with patients reporting the diet easy to stick to. After six months, samples were analysed from the patients' blood and gingival crevicular fluid – liquid that comes from the small space between your tooth and gum, which helps gums stay healthy and fight germs. Those who fasted had reduced markers of inflammation in samples from blood and gum tissue compared to those whose diets stayed the same, including lower levels of C-reactive protein, a general indicator of inflammation around the body. The fasting group also had reduced molecules linked to inflammation specifically in the gums, compared to controls.   Low blood pressure shows strongest link to Alzheimer's disease Michigan Technological University, Jun 10 2026 (News-Medical) Numerous types of cardiovascular disease and CVD risk factors were linked to a higher risk of Alzheimer's disease, with low blood pressure showing the strongest connection, according to a new analysis published today in the Journal of the American Heart Association What are the key findings of the analysis? Adults with hypotension (low blood pressure) were about three times more likely to develop Alzheimer's and nearly twice as likely in the All of Us study when compared to individuals who did not have low blood pressure. Across both datasets, adults with high blood pressure (hypertension) were 1.6 times more likely to have Alzheimer's disease, compared to people without hypertension. Participants who had a previous stroke had a 1.5 times higher risk for Alzheimer's disease in the UK Biobank and 1.85 times in All of Us. Those with irregular heartbeat (or atrial fibrillation, also called AFib) were about 1.5 times more likely to have Alzheimer's disease compared to those without AFib.    

Nutritionist Leyla Muedin discusses research showing simple strength tests—grip strength and a five-rep sit-to-stand chair test—predict longevity in older women. In a University at Buffalo study of over 5,000 women ages 63–99 followed for eight years, stronger grip and faster chair-stand times were linked to lower mortality; every additional 7 kg of grip strength corresponded to a 12% reduction in death risk, and faster chair-stands were also associated with improved survival, even after adjusting for activity, cardiovascular fitness, and inflammation. She emphasizes prioritizing muscle-strengthening alongside aerobic exercise and suggests accessible resistance options (weights, bodyweight moves, or household items) with professional guidance as needed. She then cites UK Biobank data linking long-term statin use to declines in grip strength and appendicular lean mass, urging discussion with physicians and added vigilance, especially for those also using GLP-1 drugs that may reduce protein intake and muscle mass.

In this conversation, Dr. Reza Ardalan sits down with Dr. Hugh Coyne, a London-based family medicine practitioner and the son of a pediatric dentist, who built Coyne Medical with his wife and clinical partner Dr. Lucy Coyne specifically to practice the kind of preventive medicine the NHS 10-minute appointment window does not allow. His training at Imperial College London and postgraduate work in obstetrics and gynecology, pediatric health, and sports medicine give him a panoramic view of the screening opportunities most dentists are sitting on without realizing it. Dr. Coyne walks through the short blood panel he would build into every dental practice: HbA1c for diabetes risk that directly changes wound healing and periodontal outcomes, highly sensitive CRP for the kind of cardiovascular inflammation a UK Biobank study of over 400,000 people linked to a 61% higher risk of cardiovascular death, vitamin D with the K2 pairing that keeps calcium out of arterial walls, renal function, and a full blood count. From there, Dr. Coyne and Dr. Ardalan move into the oral microbiome shift from pathogen elimination to ecosystem restoration, the role of P. gingivalis in rheumatoid arthritis through citrullinated protein antibodies, and the cardiometabolic markers most patients never get tested for, including apolipoprotein B and lipoprotein(a). The third act covers GLP-1 medications, the Gila monster origin story, the medieval cautionary tale of Sancho the Fat, and the dental-chair implications most patients will never volunteer on a health history form. In this Episode:  The short blood panel any dental practice can start with: HbA1c, highly sensitive CRP, vitamin D, renal function, and a full blood count Why vitamin D supplementation without vitamin K2 may direct calcium into the wrong tissues, including arterial walls How a UK Biobank study of more than 400,000 people linked elevated hs-CRP to a 61% higher risk of cardiovascular death in patients otherwise considered well What the 87% of patients open to in-chair screening tells you about how to introduce blood testing in your practice without losing trust The rule of halves for blood pressure, and why a 158 reading caught on a second visit can be profoundly consequential for a patient's long-term survival How the oral microbiome model has shifted from pathogen elimination to ecosystem restoration, and what that changes about prevention Why P. gingivalis turns up in rheumatoid arthritis tissue, and how oral pathogens correlate with colorectal, pancreatic, and esophageal cancers The bachelor-party analogy for apolipoprotein B and lipoprotein(a), and why every dentist should know their own Lp(a) number What every dental practice needs to know before sedating a patient on a GLP-1 medication   Dr. Hugh Coyne is a London-based GP and the co-founder, with his wife Dr. Lucy Coyne, of Coyne Medical, a family medicine practice focused on preventive care and the early detection of disease. Dr. Hugh Coyne trained at Imperial College London with postgraduate degrees in obstetrics and gynecology, pediatric health, and sports medicine, and is a featured speaker at the Wellness Dental Forum 2026. Find him on Instagram and TikTok at @drhughcoyne and the clinic at @coyne_medical. Want to go deeper on the oral–systemic connection? Dentistry & Whole-Body Health is a 3-part live CE series on reading the medical signals hiding in your patients' bloodwork — and knowing what to do with them. Session 1:  Hidden Signals · Saturday, November 7, 2026 The bloodwork your patients already have, read through a dentist's lens. HbA1c, hs-CRP, vitamin D, CBC — and when to monitor, pause, or refer. Session 2: Cardiovascular Clues · Saturday, November 21, 2026 The lipid markers most panels skip (ApoB, Lp(a)) and the oral–heart connection behind them. Yes — this is the bachelor-party one. Session 3: The New Weight Loss Era · Saturday, December 5, 2026 What GLP-1s are quietly doing to how your patients eat, metabolize, and heal — and the chairside adjustments that come with it. All 3-hour sessions run 8 AM PT / 11 AM ET / 4 PM UK, with 30-day recording access if you can't make it live. 9 AGD-PACE-approved CE credits across the series. Nothing here asks you to become a doctor — it gives you the medical layer that's already shaping your outcomes. Enrollment opens soon: $1,497 → Or try a single session — $625 More details coming soon!

Fresh Pressed Olive Oil Club (buy 2 bottles, get 1 free for Ben's community): https://freshpressolive.com/3RBPwdG  Pre-order Ben's new book KetoFlex Revised — Pre-order now and get free bonus chapters:  https://bit.ly/4wKG1sM  Kidney disease doesn't start with pain. It starts with nothing. By the time you feel it, you may have already lost half your kidney function. The National Kidney Foundation reports 90% of people with chronic kidney disease don't know they have it. In most cases, the damage begins 10 to 15 years before any diagnosis — while labs still look normal. THE 7 HABITS Blood Sugar Spikes. Post-meal glucose spikes damage the hair-thin filtration vessels inside the kidneys over time. A 2024 Nature Communications paper found cellular insulin resistance drives kidney damage before diabetes ever appears. Chronic Dehydration. Your kidneys filter 180 liters of plasma daily. Less water means concentrated waste and a higher workload. Coffee, soda, and energy drinks don't count. Drink clean spring water. Processed Food. Phosphate additives and industrial seed oils (soybean, corn, canola) create ongoing inflammation in the blood vessels kidneys depend on. Swap to butter, ghee, tallow, coconut oil, and high-quality olive oil.  Sugar and Fructose. Fructose overwhelms the liver, converts to uric acid, and lands on the kidneys. A 2024 UK Biobank study of 127,000+ adults found even one sugar-sweetened beverage daily significantly raises kidney disease risk. Diet soda is not a safe swap. Ignoring Blood Pressure. No symptoms doesn't mean no damage. Every heartbeat sends pressure through delicate kidney capillaries. Damaged kidneys then lose their ability to regulate pressure — creating a worsening feedback loop. Chronic Stress and Poor Sleep. Cortisol raises blood sugar, blood pressure, and insulin resistance. Sleeping under four hours raises kidney disease risk by 45%. Kidney repair happens at night. Ignoring Insulin Resistance. The root of everything. By the time labs flag it, you've likely been insulin resistant for 6 to 14 years. About 93% of American adults have some form of it. Find All The Ben Azadi Show Sponsorship Deals ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠https://www.ketokamp.com/sponsorship-deals Learn more about your ad choices. Visit megaphone.fm/adchoices

Send us Fan MailHow omega-3 fats in human health, including dietary intake needs, supplements, & omega fat testing.TOPICS DISCUSSED:ω-3 chemistry: EPA and DHA differ from plant ALA in chain length and double-bond count, making them structurally and biologically distinct — and largely irreplaceable by ALA conversion.ALA-to-EPA/DHA conversion: A small percentage of dietary ALA converts to EPA, and conversion to DHA is even lower; vegans rely on this inefficient pathway for all long-chain omega-3s.Cardiovascular mechanisms: ω-3s lower triglycerides, reduce platelet stickiness, improve endothelial function, and slow resting heart rate, reducing cardiovascular risk.ω-3 Index: Defined as red blood cell EPA+DHA as a percent of total fatty acids; 8–12% is the target range, while most Americans sit around 4–5%.Brain & dementia risk: Higher DHA blood levels are associated with significantly lower risk of dementia and Alzheimer's in large cohorts including the UK Biobank and Framingham.Linoleic acid nuance: Higher blood levels of dietary linoleic acid (omega-6) associate with lower dementia and cardiovascular risk; downstream omega-6 metabolites — not linoleic acid itself — associate with adverse outcomes.Supplementation practicalities: Most people need 1–2 g/day of EPA+DHA to reach an ω-3 Index >8%; oxidation concerns with fish oil supplements may be overstated.ABOUT THE GUEST: Bill Harris, PhD is founder of both OmegaQuant Laboratory and the Fatty Acid Research Institute (Sioux Falls, SD), where his work centers on blood fatty acid biomarkers as predictors of disease risk in large population cohort studies.KNOW YOURSELF:OmegaQuant: At-home blood testing to see fatty acid profiles, including omega-3 fatty acids. Use link to see options and support M&M.RELATED EPISODE:M&M 134: Omega Fats, Vegetable & Seed Oils, Sugar, Processed Food, Metabolic Health & Dietary Origins of Chronic Inflammatory DiSupport the showHealth Products by M&M Partners:AquaTru: Water filtration devices that remove microplastics, metals, bacteria, and more from your drinking water. Through link, $100 off AquaTru Carafe, Classic & Under Sink Units; $300 off Freestanding models.OmegaQuant: At-home blood testing to see fatty acid profiles, including omega-3 fatty acids. Use link to see options and support M&M.SiPhox Health: Comprehensive, cost-effective bloodwork from the comfort of home. Use code TRIKOMES for 20% off.KetoCitra—Ketone body BHB + electrolytes formulated for kidney health. Use code MIND20 for 20% off any subscription (cancel anytime)Seed Oil Scout: Find restaurants with seed oil-free options, scan food products to see what they're hiding, with this easy-to-use mobile app.SporesMD: Premium mushrooms products (gourmet mushrooms, nootropics, research). Use code 'nickjikomes' for 20% off.For all the ways you can support my efforts

Your doctor orders a lipid panel every year — but 3 cheap blood tests predict heart disease, diabetes, and even dementia far better than cholesterol, and most doctors never order them. In this episode, Robert Lufkin MD walks through fasting insulin + HOMA-IR, homocysteine, and high-sensitivity CRP — three tests that together cost about $60, take one blood draw, and catch the metabolic dysfunction a standard lipid panel systematically misses. CHAPTERS: 00:00 — The 3 Blood Tests Your Doctor Isn't Ordering 00:40 — Part 1: Fasting Insulin and HOMA-IR 01:15 — How Insulin Resistance Hides for 10–15 Years 01:45 — HOMA-IR vs Glucose: What 516,000 People Revealed 02:05 — 59% Higher Cardiovascular Risk in the 2023 ATVB Study 02:45 — Optimal Fasting Insulin: Why 5–8 Beats the Lab's "25" 03:05 — Part 2: Homocysteine and the MTHFR Connection 03:35 — How Homocysteine Damages Your Arteries (6 Mechanisms) 03:50 — 60% Higher Stroke Risk and 48% Alzheimer's Risk 04:35 — The Oxford VITACOG Trial: 53% Less Brain Atrophy 05:05 — Part 3: High-Sensitivity CRP and Inflammatory Plaque 05:40 — The JUPITER Trial: 44% Drop in Cardiac Events 06:15 — UK Biobank: Why hs-CRP Beats LDL Cholesterol 06:50 — AHA Risk Categories for hs-CRP Since 2003 07:15 — Part 4: The Metabolic Picture (Why Cholesterol Is the Wrong Target) 07:50 — 3 Tests, $60, One Blood Draw — The Full Framework KEY TAKEAWAYS: Fasting insulin + HOMA-IR catches insulin resistance a decade before glucose goes abnormal — optimal is below 5–8, not the lab's reference range of 25 Every 5 µmol/L rise in homocysteine raises coronary artery disease risk 20–30% and stroke risk 60%, independent of cholesterol hs-CRP predicted cardiovascular events better than LDL in a 322,000-person UK Biobank analysis — yet fewer than 10% of cardiac panels order it Cardiovascular disease, type 2 diabetes, and dementia share the same upstream driver: metabolic dysfunction, not cholesterol All three tests together cost roughly $60 and come from a single blood draw LINKS:

Welcome to episode 245 of the Financial Crime Weekly Podcast. I am Chris Kirkbride. In this episode, the US Treasury's extensive sanctions targeting Iran's "shadow banking" network and its global oil revenue streams, alongside the UK's announcement of upcoming sanctions updates and revised trade licensing procedures. A French national has been sentenced for laundering nearly half a billion dollars through an unlicensed cryptocurrency exchange, and the FCA has announced a crackdown on "finfluencer" promotions. A US soldier has been charged with using classified data to influence prediction-market bets and a court ruling lifts anonymity in an NCA unexplained wealth case. Finally, the BIS has published a paper on the prudential risks of crypto conglomerates and an investigation has commenced into the unauthorised sale of volunteer data from the UK Biobank.A transcript of this podcast, with links to the stories, will be available at www.crimes.financial.

An estimated 55 million people worldwide are living with dementia, of which Alzheimer's is the most common form. This number continues to rise as global populations age. Despite the scale of the problem and large amounts of funding, no one has been able to find a cure. Could it be that data science, rather than medicine, holds the answers to tackling this disease?In this episode of Tech Tomorrow, David Elliman speaks with Alejo Nevado-Holgado, Associate Professor of Psychiatry at the University of Oxford and member of the Big Data Institute. He leads AI research within the Computational and Molecular Neuroscience Laboratory, an interdisciplinary team spanning AI, biochemistry, and bioinformatics.The conversation explores how advanced computational methods are using vast biological and clinical datasets, including genomics, transcriptomics, proteomics, stem cell imaging, brain scans, and electronic health records. This integrated approach aims to uncover disease mechanisms, identify new drug targets, and advance more personalized treatments, all supported by high-performance computing.A key challenge in Alzheimer's research is the difficulty of accessing and studying the brain. The blood-brain barrier limits treatment delivery, while the disease develops over decades before symptoms appear. The discussion also highlights ongoing scientific uncertainty about whether hallmark features such as amyloid plaques and tau tangles are causes of the disease or downstream effects.The episode examines how AI can support early detection through blood-based biomarkers and why it is particularly effective in analysing complex, high-dimensional data such as molecular structures and genomic information. The importance of combining diverse datasets, such as population-scale biobanks and drug discovery data, is emphasised as essential for progress.However, challenges remain, including the need for explainable AI systems and more complete longitudinal health data. The conversation also touches on emerging techniques like AI-driven molecular simulations, which may help predict how drugs interact within the brain.Episode Highlights01:07 – The background of Alejo's project.02:25 – Why are Alzheimer's and dementia so hard to treat?05:50 – How can neurodegenerative brain diseases be prevented?07:05 – Drug discovery and machine learning.09:43 – David's Thoughts: Multi-modal data.10:29 – Why high-quality data is so hard to access.14:55 – Why AI explainability remains an issue.17:06 – David's Thoughts: A black box within a black box.19:23 – The UK Biobank and rich medical data.23:54 – Wrap up.About Zühlke:Zühlke is a global transformation partner, with engineering and innovation at its core. We help clients envision and build their businesses for the future – running smarter today while adapting for tomorrow's markets, customers, and communities.Our multidisciplinary teams specialise in technology strategy and business innovation, digital solutions and applications, and device and systems engineering. We thrive in complex, regulated sectors such as healthcare and finance, connecting strategy, implementation, and operations to help clients build more effective and resilient businesses.Links:Zühlke WebsiteZühlke on LinkedInDavid Elliman on LinkedInProf. Alejo Nevado-Holgado BioDementia Research Oxford WebsiteUK Biobank Website

This week, Mikki breaks down a major 2025 study using UK Biobank wearable data to challenge one of the most widely accepted rules in exercise science. For decades, we've been told that one minute of vigorous activity equals two minutes of moderate activity. But the data tells a very different story. Drawing from over 73,000 participants, this episode unpacks how vigorous movement may be four to ten times more effective depending on the health outcome. Mikki explains what actually counts as “vigorous” (it's more accessible than you think), the physiological mechanisms driving these benefits, and how small bursts of effort throughout your day can meaningfully impact long-term health. This is a practical, evidence-based rethink of how to approach movement for metabolic health, cardiovascular fitness, and longevity.Key Highlights: Why the long-standing 1:2 activity ratio doesn't hold up  What “vigorous” really means in real-world terms  How short bursts of effort impact cardiovascular and metabolic health  The surprising limits of light activity for disease risk reduction  Practical ways to incorporate high-value movement into daily life Contact Mikki:https://mikkiwilliden.com/https://www.facebook.com/mikkiwillidennutritionhttps://www.instagram.com/mikkiwilliden/https://linktr.ee/mikkiwillidenNZ listeners - save 10% off Calocurb by using the code Mikkipedia10 at www.calocurb.co.nzSave 20% on all Nuzest Products WORLDWIDE with the code MIKKI at www.nuzest.co.nz, www.nuzest.com.au or www.nuzest.comCurranz supplement: MIKKI saves you 25% at www.curranz.co.nz or www.curranz.co.uk off your first order

Indoor Epidemic: Prescribing Nature, Light, Air, and Movement with Dr. John La Puma, internist, chef, and regenerative farmer. His book, "Indoor Epidemic," argues that spending about 93% of life indoors undermines health through poor light timing, air quality, limited movement, and reduced nature exposure. La Puma cites data that outdoor morning light helps set circadian rhythms, while nighttime blue light can impair sleep quality and raise cardiovascular risks, referencing a large UK Biobank study. He discusses indoor pollutants and CO2 buildup affecting inflammation and cognition, recommends strategies like getting daylight early (even just a sky view), using circadian lighting, and taking brief outdoor breaks to reduce myopia risk. He describes measurable benefits of forest bathing and gardening (including immune and mood effects), notes hospital studies linking window views to shorter stays and less pain medication, and reviews his pioneering work in culinary medicine now taught widely in medical schools, emphasizing cooking and growing food as preventive and therapeutic tools.

Darshan H. Brahmbhatt, Podcast Editor of JACC: Advances, discusses a recently published original research paper on Associations of Socioeconomic Status With Cardiorenal Metabolic Multimorbidity: Evidence From the UK Biobank Cohort.

A special good morning to all the redheads listening. There's some new Harvard research that's come out about human evolution and it mentions you. I'll get to you in a sec. Conventional wisdom says that homo sapiens (us) basically stopped evolving when we emerged 300,000 years ago. We reached peak human. It took us about seven million years to evolve from looking more like Apes. It took us four million years to walk on two legs, which is one of things that makes humans. More recently we learnt how to use tools, language. But once we stopped hunter-gathering, roaming round looking for food, and settled down to farm our own and build cities and civilisations, natural selection wasn't such a big deal. But that's not true. They looked at DNA from 16,000 people over 10,000 years, some from ancient burial sites and modern ones from the UK Biobank. We used to think natural selection was changing just a dozen genes, they now reckon it's hundreds. Coeliac disease is now more common. You might think why? Who doesn't love pasta and oats? You'd think evolution would edit out coeliac diseases. No, because the gene actually increases your resistance to a bunch of germs and bacteria. So, you're less likely to die, more likely to live longer. The longer you live, the more likely you pass that gene onto your kids. That's how natural selection works. The gene for narrow waists have become more common because we didn't need to store as much fat post-hunter-gatherer days (though you wouldn't know it walking through the supermarket). And redheads, the red hair gene, MC1R, it's become more common in recent history. It's popular. More gingers than ever before. Congratulations. The only mystery is why as there's no obvious survival advantage, other than looking fabulous, I suppose.See omnystudio.com/listener for privacy information.

This week's stories: *Bartonella Hides in Cat Scratches — and It Might Be Why You Feel Like Garbage A stealth bacterial infection transmitted by everyday cat scratches and flea dirt has been quietly linked to chronic fatigue, brain fog, and neurological symptoms for decades. Dave breaks down how Bartonella slips past standard testing, why it's almost never on a conventional doctor's radar, and the specific PCR protocol you need to actually find it. Sources: https://pubmed.ncbi.nlm.nih.gov/ *High Tyrosine Levels May Be Cutting Years Off Men's Lives A Mendelian randomization study of 270,000 UK Biobank participants found that elevated tyrosine is causally linked to nearly a full year of lost lifespan in men — with zero effect in women. The culprit appears to be an inflammatory oxidation pathway that men metabolize very differently. Dave examines what this means for every guy stacking L-tyrosine nootropics or eating high-protein keto. Sources: https://pubmed.ncbi.nlm.nih.gov/41045493/ https://www.aging-us.com/news-room/high-tyrosine-levels-linked-to-shorter-lifespan-in-men https://www.usnews.com/news/health-news/articles/2026-02-27/study-suggests-one-common-amino-acid-may-affect-how-long-men-live *Blue Light Blocking Contact Lenses Are a Legitimate Vision Upgrade ALTIUS Vision's tinted contact lenses aren't just blue light filters — they cut chromatic aberration by 53% and improve motion tracking and contrast sensitivity in ways that software filters simply can't replicate. Dave covers the mechanism, who benefits most (screen workers, TBI recovery, gamers), and how to find a provider. Sources: https://altiusvision.com/chromatic-aberration/ https://altiusvision.com/science-of-altius/ https://www.westvalleyvision.com/-altius--performance-tinted-contact-lenses *Taurine Plus B Vitamins Actually Moves the Needle on Motivation A randomized crossover trial found that a daily stack of taurine, B6, folate, and B12 sustained effort-reward motivation and cut cognitive lapses significantly compared to placebo — and the mechanism runs through glutathione production in brain astrocytes. Dave breaks down why this combo works when either ingredient alone doesn't. Sources: https://pubmed.ncbi.nlm.nih.gov/41889717/ https://www.frontiersin.org/journals/nutrition/articles/10.3389/fnut.2026.1711478/full https://www.nutraingredients.com/Article/2026/03/23/taurine-and-b-vitamins-bost-motivation-and-focus/ *30 Seconds of Smelling Flowers Resets Your Nervous System Research out of the Monell Chemical Senses Center confirms what your grandmother knew: a slow, deep floral inhale measurably lowers heart rate and activates the parasympathetic nervous system — and it works because olfaction bypasses the cortex entirely and hits the limbic system directly. Dave makes the case for building a daily scent ritual. Sources: https://time.com/ https://www.southtabor.com/healthy-living-tip-stop-and-smell-the-flowers/ This episode is designed for biohackers, longevity seekers, and high-performance listeners who want mechanism-level clarity on infection-driven cognitive decline, amino acid optimization, sensory performance, and evidence-based supplementation. Host Dave Asprey connects emerging clinical research, Mendelian randomization data, and real-world protocols into actionable frameworks for extending healthspan and sharpening performance. New episodes every Tuesday, Thursday, Friday, and Sunday. Keywords: Bartonella cat scratch infection, Bartonella brain fog chronic fatigue, stealth bacterial infection biohacking, tyrosine lifespan men, L-tyrosine risk men longevity, Mendelian randomization amino acid aging, blue light blocking contacts, ALTIUS vision chromatic aberration, performance contact lenses TBI, taurine B vitamins motivation RCT, taurine folate brain health, glutathione astrocytes focus, smelling flowers heart rate stress, olfaction parasympathetic nervous system, floral scent limbic system, biohacking news, longevity research 2026 Thank you to our sponsors! - GOT MOLD? | Go to http://gotmold.com/shop and use DAVE10 to save 10% and see what's in your air. - MASA Chips | Go to https://www.masachips.com/DAVEASPREY and use code DAVEASPREY for 25% off your first order. - iRestore | Grow thicker, healthier hair back naturally. Use code DAVE at irestore.com. Resources: • Get My 2026 Clean Nicotine Roadmap | Enroll for free at https://daveasprey.com/2026-clean-nicotine-roadmap/ • Get My 2026 Biohacking Trends Report: https://daveasprey.com/2026-biohacking-trends-report/ • Dave Asprey's Latest News | Go to https://daveasprey.com/ to join Inside Track today. • Danger Coffee: https://dangercoffee.com/discount/dave15 • My Daily Supplements: SuppGrade Labs (15% Off) • Favorite Blue Light Blocking Glasses: TrueDark (15% Off) • Dave Asprey's BEYOND Conference: https://beyondconference.com • Dave Asprey's New Book – Heavily Meditated: https://daveasprey.com/heavily-meditated • Join My Substack (Live Access To Podcast Recordings): https://substack.daveasprey.com/ • Upgrade Labs: https://upgradelabs.com Timestamps: 00:00 – Intro 00:37 – Bartonella & Cat Scratch Disease 02:06 – Tyrosine & Lifespan in Men 03:37 – Tinted Contacts & Visual Processing 05:56 – Taurine & Motivation 07:25 – Floral Scent & Nervous System Reset See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

Your nose knows more than you think. Professor Leslie M. Kay joins Vasant Dhar to reveal how smell is wired directly into the brain's emotional core — and how every breath you take is quietly synchronising your mind. Useful Resources: 1. Leslie Kay2. GenBank3. National Library of Medicine4. Walter Jackson Freeman III5. Dynamical Systems6. Linda B. Buck and Richard Axel7. Dmitry Rinberg, Rinberg Lab8. S. Murray Sherman9. John Hopfield10. Christof Koch11. Joy Milne12. Aromha test13. Lucia F. Jacobs14. From chemotaxis to the cognitive map: The function of olfaction - Lucia F Jacobs 15. Patricia Churchland16. Andrew Sheriff, Northwestern Human Olfaction Lab17. Long-Range Respiratory and Theta Oscillation Networks Depend on Spatial Sensory Context - Andrew Sheriff, Guinevere Pandolfi,  Vivian S Nguyen and Leslie M. Kay18. Evidence for a Chromatographic Model of Olfaction - Maxwell Mozell 19. COVID-19 and olfactory dysfunction: a looming wave of dementia? - Leslie M. Kay 20. SARS-CoV-2 is associated with changes in brain structure - UK Biobank 21. Asifa Majid22. Human Olfaction at the Intersection of Language, Culture, and Biology - Asifa Majid Check out Vasant Dhar's newsletter on Substack. The subscription is free! Order Vasant Dhar's new book, Thinking With Machines

Leyla Muedin, a registered dietitian nutritionist, discusses a UK Biobank analysis published in the Journal of Cachexia, “Sarcopenia and Muscle” (Nov 2025) linking continuous long-term statin use (e.g., Lipitor, Zocor, Crestor) to accelerated declines in grip strength and appendicular lean mass compared with never-users. Among 35,557 with follow-up data, grip strength declined by a mean 0.315 kg/year and appendicular lean mass by 0.057 kg/year in statin users; findings persisted after adjustment for age, sex, BMI, comorbidities, and a pharmacogenomic statin-response score. Leyla notes possible mechanisms (CoQ10/mevalonate pathway effects, mitochondrial dysfunction, apoptosis, calcium disruption, insulin resistance) and advises monitoring musculoskeletal health, supporting diet and regular physical activity, while not interpreting results as a reason to stop prescribing statins.

Send us Fan MailSunlight has been framed as a problem to avoid, but the data keeps pointing in the opposite direction: people who get more natural light tend to live longer and carry a lower risk of chronic disease. We take a hard look at why this topic still feels controversial, and how fear based messaging can flatten a complex risk-benefit reality into a single command: stay out of the sun.We walk through a powerful new UK Biobank analysis on habitual ultraviolet exposure and mortality, using a detailed exposure model that captures real-world behavior, not just a lab estimate. The headline is difficult to ignore: higher UV exposure tracks with lower cardiovascular and non-skin cancer mortality, without a clear increase in skin cancer mortality in the findings. That forces a more balanced conversation about sunlight, all-cause mortality, and what “safe” actually means when heart disease and cancer remain the biggest killers.Then we go deeper than vitamin D. We talk nitric oxide, vascular function, clotting biology, inflammation markers, proteomic signals, circadian rhythm, and why morning light is one of the most underused tools for better sleep and mood. We also revisit the forgotten history of heliotherapy and how modern indoor living, artificial light, and aggressive sun avoidance can create a kind of paleo deficit disorder.If this changes how you think about sunlight and health, subscribe, share the episode with a friend, and leave a review. What belief about sun exposure do you want to recheck this spring?For video, slides and open-source references: www.thehealthedgepodcast.com

Join Digital Education Committee member and podcast host Melissa E. Middeldorp, MPH, PhD, along with this week's guest contributors, Joshua Silverstein MD, FHRS from Allegheny Health Network and Jonathan Ariyaratnam, BChir, MA, MB, CCDS, CEPS-A from the University of Adelaidefor this week's episode. This study by Vad and colleagues examined markers of atrial cardiomyopathy (AtCM) in 26,467 UK Biobank participants without prior atrial fibrillation (AF), heart failure (HF), or stroke, integrating cardiac MRI, ECG, clinical risk factors, and genetic data. AtCM was defined using four markers: left atrial dilation, reduced left atrial emptying fraction (120 ms), and abnormal P-wave terminal force and 15.7% of individuals had at least one marker, while 2.3% had two or more. Over a median follow-up of nearly five years, the presence of AtCM markers showed a dose–response relationship with incident AF, with a HR: 4.59 in those with ≥2 markers and was also strongly associated with HF and ischemic stroke. Adding AtCM markers to clinical and genetic risk models improved AF risk prediction, supporting the concept that atrial cardiomyopathy may represent a common substrate linking AF, HF, and stroke and may help refine future risk stratification strategies. Article for Discussion Learning Objectives Understand how imaging- and ECG-based markers of atrial cardiomyopathy are defined and how they relate to the risk of incident AF, heart failure, and stroke. Evaluate how integrating atrial cardiomyopathy markers with clinical and genetic risk scores may improve risk stratification for AF and related cardiovascular outcomes. Article Authors Oliver B Vad, Nick van Vreeswijk, Ahmed S Yassin, Yuri Blaauw, Christian Paludan-Müller, Jørgen K Kanters, Claus Graff, Ulrich Schotten, Emelia J Benjamin, Jesper H Svendsen, Michiel Rienstra Podcast Contributors Melissa E. Middeldorp, MPH, PhD Joshua R. Silverstein, MD, FHRS Jonathan Ariyaratnam, BChir, MA, MB, CCDS, CEPS-A Host and Contributor Disclosure(s): M. Middeldorp Nothing to disclose. J. Ariyaratnam  Nothing to disclose.   J. Silverstein Honoraria/Speaking/Consulting: Medical Device Business Services, Biosense Webster, Inc., Medtronic Stocks, Privately Held: Heart Rhythm Clinical Solutions/3PH Alliance Staff Disclosure(s) (note: HRS staff are NOT in control of educational content. Disclosures are provided solely for full transparency to the learner): S. Sailor: No relevant financial relationships with ineligible companies to disclose.

You may have seen headlines or social media posts claiming that ketones increase the risk of heart attacks and that this proves ketogenic diets are dangerous for heart health. But when you actually examine the study behind those claims, the data tell a very different story.In this video, Dr. Bret Scher takes a closer look at a recent paper published in the Journal of the American Heart Association that analyzed circulating ketone levels in participants from the UK Biobank. The study has been widely shared online as evidence against ketogenic diets. The issue? The participants weren't following a ketogenic diet at all.Instead, researchers measured very small baseline ketone levels in a general population that was consuming around 250 grams of carbohydrates per day, that's far from the levels associated with nutritional ketosis.In this video, you'll learn:Why this study was not a ketogenic diet studyThe difference between association and causation in epidemiologyWhy the measured ketone levels were far below nutritional ketosisHow metabolic stress, illness, or diabetes can raise ketone levels independently of dietWhy these findings don't tell us anything about ketogenic dietsUnderstanding the context behind nutrition research is critical. Misinterpreting observational data can easily lead to misleading headlines and unnecessary confusion about diet and health.

This week's stories: Healthy Diets That Offset "Bad Genes" A major UK Biobank study of over 100,000 people found that following any one of five healthy dietary patterns was associated with up to 3 extra years of life — and the benefit held regardless of genetic predisposition to longevity. Your DNA is not an excuse. The macro pattern matters more than the perfect protocol. • Sources: -https://www.science.org/doi/10.1126/sciadv.ads7559 -https://pmc.ncbi.nlm.nih.gov/articles/PMC12904179 -https://www.medicalnewstoday.com/articles/eat-well-live-longer-study-5-healthy-diet-plans-longevity Micro-Habits in Sleep, Activity, and Diet That Extend Life Researchers built a composite "SPAN" score combining sleep, movement, sedentary time, and diet quality and found that small improvements across all four — we're talking minutes per day — cut mortality risk by up to 64% when stacked together. The gains only showed up when behaviors improved in combination, not in isolation. • Sources: -https://pmc.ncbi.nlm.nih.gov/articles/PMC11863424 -https://theconversation.com/small-improvements-in-sleep-physical-activity-and-diet-are-linked-with-a-longer-life-273502 -https://www.lboro.ac.uk/news-events/news/2026/january/small-improvements-in-health-linked-to-longer-life Methionine and Cysteine Restriction: The Diet That Mimics Cold Exposure New research shows that reducing sulfur amino acids — methionine and cysteine, found heavily in certain animal proteins — triggers fat browning and thermogenesis in mice, mimicking the metabolic effects of cold exposure without the cold. Supporting human data from Nature Metabolism suggests this lever works in people too • Sources: -https://elifesciences.org/reviewed-preprints/108825v2 -https://www.nature.com/articles/s42255-025-01297-8 -https://topics.consensus.app/news/research-finds-low-methionine-and-cysteine-diet-increases-caloric-burn-in-mice-evidence-review Tyrosine and Lifespan: What the Data Says for Men A Mendelian randomization analysis of over 270,000 UK Biobank participants found that genetically higher tyrosine levels were associated with nearly one year shorter lifespan in men — with no significant effect in women. This reflects lifelong endogenous levels, not short-term supplementation, but it's a signal worth understanding if you're using tyrosine strategically • Sources: -https://www.news-medical.net/news/20260301/Higher-tyrosine-levels-linked-to-shorter-lifespan-in-major-UK-Biobank-analysis.aspx -https://www.eurekalert.org/news-releases/1105915 -https://www.aging-us.com/news-room/high-tyrosine-levels-linked-to-shorter-lifespan-in-men War Doomscrolling and WW3 Anxiety as a Stealth Aging Accelerator Compulsive consumption of conflict and war news is linked to PTSD-like symptoms, existential anxiety, and chronic stress — even in civilians far from any battlefield. Layered on top of cardiology data connecting chronic stress to heart disease and stroke, your news diet is now a legitimate healthspan variable. Subtractive biohacking is still biohacking. • Sources: -https://www.sciencedaily.com/releases/2024/07/240718124709.htm -https://www.theguardian.com/technology/article/2024/jul/19/doomscrolling-linked-to-existential-anxiety-distrust-suspicion-and-despair-study-finds -https://www.health.harvard.edu/mind-and-mood/doomscrolling-dangers -https://pmc.ncbi.nlm.nih.gov/articles/PMC9517387 All source links are provided for direct access to the original reporting and research. This episode is designed for biohackers, longevity seekers, and high-performance listeners who want mechanism-level clarity on circadian biology, neurodegeneration signals, cognitive training, caffeine strategy, and supplement regulation. Host Dave Asprey connects emerging science, behavioral data, and policy shifts into practical frameworks you can use to build a resilient, adaptable health stack. New episodes every Tuesday, Thursday, Friday, and Sunday. Keywords: healthy diet longevity genes, UK Biobank diet study, Mediterranean diet lifespan, DASH diet mortality, SPAN score sleep activity diet, micro habits longevity, mortality risk reduction, methionine restriction thermogenesis, cysteine restriction fat loss, sulfur amino acids metabolism, FGF21 fat browning, tyrosine lifespan men, Mendelian randomization amino acids, tyrosine supplement risk, doomscrolling aging, war news anxiety stress, chronic stress heart disease, psychosocial stress healthspan, biohacking news, longevity research 2026 Thank you to our sponsors! -AquaTru | Go to https://aquatruwater.com/daveasprey and save $100 on all AquaTru water purifiers.-BEYOND Biohacking Conference 2026 | Register with code DAVE300 for $300 off https://beyondconference.comResources: • Get My 2026 Clean Nicotine Roadmap | Enroll for free at https://daveasprey.com/2026-clean-nicotine-roadmap/ • Get My 2026 Biohacking Trends Report: https://daveasprey.com/2026-biohacking-trends-report/ • Dave Asprey's Latest News | Go to https://daveasprey.com/ to join Inside Track today. • Danger Coffee: https://dangercoffee.com/discount/dave15 • My Daily Supplements: SuppGrade Labs (15% Off) • Favorite Blue Light Blocking Glasses: TrueDark (15% Off) • Dave Asprey's BEYOND Conference: https://beyondconference.com • Dave Asprey's New Book – Heavily Meditated: https://daveasprey.com/heavily-meditated • Join My Substack (Live Access To Podcast Recordings): https://substack.daveasprey.com/ • Upgrade Labs: https://upgradelabs.com Timestamps: 0:00 - Introduction 0:18 - Story #1: Diet vs. Genetics 2:14 - Story #2: 1% Better Every Day 4:26 - Story #3: Sulfur Amino Acids & Fat Loss 5:55 - Story #4: Tyrosine & Longevity 7:58 - Story #5: Doomscrolling & Aging 10:00 - Weekly Roundup See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

 This episode's guests:Remi Bouche, Science Coordinator at Mont-Megantic.Jeremey Evans, Photographer - Filmmaker.Dashiell Leeds, Conservation Coordinator for the Sierra Club Loma Prieta Chapter.Bill's News Picks:Let there be light — but not in Maine, GREG WALCHER, The Daily Sentinel.Our state is the best place in the country to bring dreams to life: A second Sphere venue is coming to the US, Fraser Lewry, Louder.LED lighting undermines visual performance unless supplemented by wider spectra, Nature. Exposure to outdoor artificial light at night is associated with a higher risk of ulcerative colitis: a prospective cohort study from the UK Biobank, Frontiers in Public Health.Are You Afraid of the Dark? This Oregon Retreat Locks You in Total Darkness. For Days. On Purpose, Danielle Denham, That Oregon Life. Send Feedback Text to the Show!Support the showA hearty thank you to all of our paid supporters out there. You make this show possible. For only the cost of one coffee each month you can help us to continue to grow. That's $3 a month. If you like what we're doing, if you think this adds value in any way, why not say thank you by becoming a supporter! Why Support Light Pollution News? Receive quarterly invite to join as live audience member for recordings with special Q&A session post recording with guests. Receive all of the news for that month via a special Supporter monthly mailer. Satisfaction that your support helps further critical discourse on this topic. About Light Pollution News: Ever wonder why migrating birds crash into buildings? Or why you can't sleep at night? What about where you can still see the Milky Way? Light Pollution News explores how our 24/7 lit world affects everything from wildlife and human health to our understanding of the stars, travel, and the future of our cities. Host Bill McGeeney brings on rotating guests to help dig into the latest research, policy activity, and real-world solutions - from how irresponsible lighting degrades our health to the best dark sky destinations for your next trip. Whether you're a birder, conservationist, astrophotographer, or just someone who misses sleeping in darkness, this is the show that connects the dots between your...

We discuss three pivotal studies showing how natural light wavelengths positively influence health from all-cause mortality to visual perfomance to blood glucose control in Type II diabetics.Jonathan Jarecki is a biomedical science sophomore with an interest in light and health, and host of Whole Health Podcast. SUPPORT MY WORK

Roger Seheult, MD of MedCram examines a new UK BioBank study on sunlight comparing melanoma mortality risk with all cause mortality benefit. See all Dr. Seheult's videos at: https://www.medcram.com/ (This video was recorded on January 24th 2026) Roger Seheult, MD is the co-founder and lead professor at: www.medcram.com He is Board Certified in Internal Medicine, Pulmonary Disease, Critical Care, and Sleep Medicine and an Associate Professor at the University of California, Riverside School of Medicine. MEDCRAM WORKS WITH MEDICAL PROGRAMS AND HOSPITALS: MedCram offers group discounts for students and medical programs, hospitals, and other institutions. Contact us at customers@medcram.com if you are interested. MEDIA CONTACT:  Media Contact: customers@medcram.com Media contact info: https://www.medcram.com/pages/media-contact Video Produced by Kyle Allred Edited by Daphne Sprinkle of Sprinkle Media Consulting, LLC FOLLOW US ON SOCIAL MEDIA: Facebook:  www.facebook.com/MedCram Twitter/X: www.twitter.com/MedCramVideos Instagram: www.instagram.com/medcram DISCLAIMER: MedCram medical videos are for medical education and exam preparation, and NOT intended to replace recommendations from your doctor. #sunlight #melanoma #infrared

Senior Scientist Fedor Galkin from Insilico Medicine in Abu Dhabi, UAE, joins Dr. Evgeniy Galimov to discuss a research paper he co-authored in Volume 17, Issue 8 of Aging-US, titled “AI-driven toolset for IPF and aging research associates lung fibrosis with accelerated aging.” DOI - https://doi.org/10.18632/aging.206295 Corresponding author - Alex Zhavoronkov - alex@insilico.com Video interview - https://www.youtube.com/watch?v=PV6DyIV7X7U Abstract video - https://www.youtube.com/watch?v=24lX2lHbt7o Longevity & Aging Series - https://www.aging-us.com/longevity Abstract Idiopathic pulmonary fibrosis (IPF) is a condition predominantly affecting the elderly and leading to a decline in lung function. Our study investigates the aging-related mechanisms in IPF using artificial intelligence (AI) approaches. We developed a pathway-aware proteomic aging clock using UK Biobank data and applied it alongside a specialized version of Precious3GPT (ipf-P3GPT) to demonstrate an AI-driven mode of IPF research. The aging clock shows great performance in cross-validation (R2=0.84) and its utility is validated in an independent dataset to show that severe cases of COVID-19 are associated with an increased aging rate. Computational analysis using ipf-P3GPT revealed distinct but overlapping molecular signatures between aging and IPF, suggesting that IPF represents a dysregulation rather than mere acceleration of normal aging processes. Our findings establish novel connections between aging biology and IPF pathogenesis while demonstrating the potential of AI-guided approaches in therapeutic development for age-related diseases. Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206295 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, IPF, generative AI, transformer, proteomics To learn more about the journal, please visit our website at https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ YouTube - https://www.youtube.com/@Aging-US Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Sleep: we all know it's essential for function in everyday life, and plays an important role in recovery and managing musculoskeletal pain. How much did you learn about assessing and managing sleep dysfunction in your musculoskeletal degree program? Today, Dr Mark Shepherd (Bellin College) shares practical tips to help you assess sleep, identify common sleep disorders, and incorporate behavioural strategies into your musculoskeletal rehabilitation practice. ------------------------------ RESOURCES Clinician's guide to assessing and addressing sleep dysfunction in people with musculoskeletal pain: https://www.jospt.org/doi/10.2519/josptopen.2025.0198 Spine pain and sleep study: https://pubmed.ncbi.nlm.nih.gov/35642567/ UK Biobank study on predictors of persistent pain: https://pubmed.ncbi.nlm.nih.gov/37414898/ Systematic review on lack of sleep measures: https://pubmed.ncbi.nlm.nih.gov/37259893/ APTA position paper on the PT's role in sleep health: https://www.apta.org/apta-and-you/leadership-and-governance/policies/role-pt-apta-sleep-health DPT students and sleep behaviours: https://pubmed.ncbi.nlm.nih.gov/39425093/

Nutritionist Leyla Muedin discusses the crucial importance of Omega-3 fats, particularly emphasizing their role in mental and heart health. She highlights a recent UK Biobank study demonstrating that higher Omega-3 levels are linked to a significantly lower risk of self-harm and suicidal ideation. Additionally, another study in the Journal of the American Heart Association reveals that elevated Omega-3 levels correlate with a reduced risk of atrial fibrillation (AFib). Leyla underscores the necessity of a balanced diet rich in Omega-3 sources like fatty fish and grass-fed meats, arguing that these nutrients are crucial for optimal mental and heart health.

In this special end-of-year episode of Behind the Genes, host Sharon Jones is joined by Dr Rich Scott, Chief Executive Officer of Genomics England, to reflect on the past year at Genomics England, and to look ahead to what the future holds.  Together, they revisit standout conversations from across the year, exploring how genomics is increasingly embedded in national health strategy, from the NHS 10-Year Health Plan to the government's ambitions for the UK life sciences sector. Rich reflects on the real-world impact of research, including thousands of diagnoses returned to the NHS, progress in cancer and rare condition research, and the growing momentum of the Generation Study, which is exploring whether whole genome sequencing could be offered routinely at birth.  This episode offers a thoughtful reflection on how partnership, innovation, and public trust are shaping the future of genomic healthcare in the UK and why the years ahead promise to be even more exciting.  Below are the links to the podcasts mentioned in this episode, in order of appearance:  How are families and hospitals bringing the Generation Study to life? How can cross-sector collaborations drive responsible use of AI for genomic innovation? How can we enable ethical and inclusive research to thrive? How can parental insights transform care for rare genetic conditions? How can we unlock the potential of large-scale health datasets? Can patient collaboration shape the future of therapies for rare conditions? https://www.genomicsengland.co.uk/podcasts/what-can-we-learn-from-the-generation-study “There is this view set out there where as many as half of all health interactions by 2035 could be informed by genomics or other similar advanced analytics, and we think that is a really ambitious challenge, but also a really exciting one.”  You can download the transcript, or read it below. Sharon: Hello, and welcome to Behind the Genes.   Rich: This is about improving health outcomes, but it's also part of a broader benefit to the country because the UK is recognised already as a great place from a genomics perspective. We think playing our role in that won't just bring the health benefits, it also will secure the country's position as the best place in the world to discover, prove, and where proven roll out benefit from genomic innovations and we think it's so exciting to be part of that team effort.  Sharon: I'm Sharon Jones, and today I'll be joined by Rich Scott, Chief Executive Officer at Genomics England for this end of year special. We'll be reflecting on some of the conversations from this year's episodes, and Rich will be sharing his insights and thoughts for the year ahead. If you enjoyed this episode, we'd love your support, so please subscribe, rate, and share on your favourite podcast app. So, let's get started.  Thanks for joining me today, Rich. How are you?  Rich: Great, it's really good to be here.   Sharon: It's been a really exciting year for Genomics England. Can you tell us a bit about what's going on?  Rich: Yeah, it's been a really busy year, and we'll dive into a few bits of the components we've been working on really hard. One really big theme for us is it's been really fantastic to see genomics at the heart of the government's thinking. As we'll hear later, genomics is at the centre of the new NHS 10-year health plan, and the government's life sciences sector plan is really ambitious in terms of thinking about how genomics could play a role in routine everyday support of healthcare for many people across the population in the future and it shows a real continued commitment to support the building of the right infrastructure, generating the right evidence to inform that, and to do that in dialogue with the public and patients, and it's great to see us as a key part of that.  It's also been a really great year as we've been getting on with the various programmes that we've got, so our continued support of the NHS and our work with researchers accessing the National Genomic Research Library. It's so wonderful to see the continued stream of diagnoses and actionable findings going back to the NHS. It's been a really exciting year in terms of research, publications. In cancer, some really exciting publications on, for example, breast cancer and clinical trials. Really good partnership work with some industry partners, really supporting their work. For me, one of the figures we are always really pleased to see go up with time is the number of diagnoses that we can return thanks to research that's ongoing in the research library, so now we've just passed 5,000 diagnostic discoveries having gone back to the NHS, it really helps explain for me how working both with clinical care and with research and linking them really comes to life and why it's so vital.   And then, with our programmes, it's been great to see the Generation Study making good progress. So, working with people across the country, more than 25,000 families now recruited to the study, and we're beginning to hear about their experiences, including some of the families who've received findings from the programme. It's really nice to see and hear from Freddie's family, who talked to the press a bit about the finding that they received. Freddie was at increased risk of a rare eye cancer, and really pleasingly, it was possible to detect that early through the screening that was put in place. Again, it really brings to life why we're doing this, to make a difference and improve health outcomes.  Sharon: That's an incredible 12 months. Diving into that Generation Study piece and for listeners who don't know what that is, it's a research study in partnership with the NHS that aims to sequence the genomes of 100,000 newborn babies. On an episode from earlier in the year, we had mum, Rachel Peck, join the conversation, whose baby Amber is enrolled on a study. Let's year from Rachel now.  Rachel: From the parents' point of view, I guess that's the hardest thing to consent for in terms of you having to make a decision on behalf of your unborn child. But I think why we thought that was worthwhile was that could potentially benefit Amber personally herself or if not, there's the potential it could benefit other children.  Sharon: Consent has been such a big area of focus for us, Rich, and Rachel touches on that complexity, you know, making a decision on behalf of her unborn child. Can you talk a bit about our approach to consent in the Generation Study and what's evolving in that model?  Rich: Yeah. It's been for the whole study, really, starting out asking a really big question here, what we're aiming to do is generate evidence on whether and if so, how whole genome sequencing should be offered routinely at birth, and that's responding to a really ill need that we know that each year thousands of babies are born in the UK with treatable rare conditions. We will also need to see if whole genome sequencing can make a difference for those families, but we realise to do that, as with all screening, that involves testing more people than are going to benefit from it directly themselves. So, you have to approach it really sensitively. There's lots of complicated questions, lots of nuance in the study overall. One of them is thinking really carefully about that consent process so that families can understand the choices, they can understand the benefits and risks. This is still a research study. We're looking to understand whether we should offer this routinely. It's not part of routine care at this point. The evidence will help decision-makers, policymakers in the future decide that.  At the beginning of the programme, we spent a lot of time talking to families, talking to health professionals who understand the sorts of decisions that people are making at that time of life, but also are experts in helping think about how you balance that communication. That involved, as I say, a lot of conversations. We learnt a lot, lots of it practical stuff, about the stage of pregnancy that people are at when we first talk to them about the study, so that people aren't hurried and make this decision. What we've learnt in the study, right from the outset, is talking to people from midway through the pregnancy so that they really have time to engage in it and think about their choice. So, it's an important part of getting the study design right so that we run the study right. It's also a really crucial element of the evidence that will generate from the study so that we can understand if this is something that's adopted, how should we communicate about it to families. What would they want to know? What's the right level of information and how do we make that accessible in a way that is meaningful to people from different backgrounds, with different levels of interest, different accessibility in terms of digital and reading and so on. There's a lot that we've learnt along the way and there's a lot that we're still learning. And as I say, important things that we'll present as evidence later on.  Sharon: Thank you. It's fascinating there are so many moving parts and a lot to consider when you're building the design of a programme like this or study like this.  Earlier in the year you had a great conversation with Karim Beguir about the developments of AI in genomics. Let's revisit that moment.  Karim: We live in an extraordinary time. I want to emphasise the potential of scientific discovery in the next two or three years. AI is going to move, let's say, digital style technologies like coding and math towards more like science and biology. In particular, genomics is going to be a fascinating area in terms of potential.  Sharon: So, Karim talks about AI moving from maths and coding into biology. Why is genomics such a natural area for AI?  Rich: It's really fascinating. I think it links a lot to how we think about genomics and how you get the most value in terms of health benefit and sort of the progress that we can see could come through genomics more generally. So, your genome, which is your DNA code, written in 3 billion little letters across each one of us, one copied from mum, one copied from dad, even just our genomic code of one person is a large amount of data. That is just part of the story because we're not just interested in DNA for DNA's sake, this is about thinking about health and how we can improve health outcomes. So, it's also thinking about the other sorts of information that needs to link to genomic data to make a difference. Whether that's just to provide routine healthcare with today's knowledge, or whether it's about continuing to learn and discover.  As I mentioned at the beginning, I think a really important part of this whole picture is we've learnt a lot in the last 20/30/40 plus years about genomics. It's incredible how much progress has been made, and we're really just scratching the surface. Take rare disease and the progress that's been made there, it's wonderful how many more families we're able to help today. We know that many thousands of families we still can't find a diagnosis for when we know that there is one there for many of them. That theme of ongoing learning is at the centre of all of our work, and that will continue as we look about broader uses of genomics in other settings beyond rare conditions and cancer. It's also that ongoing learning, but also the amount of, at the moment, manual steps that are required in some of the processes that we need to, for example, find a diagnosis for someone or to make sure the tools that we use are the most up to date, the most up to date with the medical literature, for example. AI is a tool that we're, as the whole of the society, we're beginning to see how it can play a role. We see it as important today for some of the just really practical things. I mentioned it, staying up to date with the medical literature, making sure that we and our systems are aware of all of the knowledge that's coming in from around the world. It's got real potential there.  I think the biggest bottom line here is that it's got the potential to be a really important tool in terms of our ongoing learning and improvement. I'm a doctor by background, the human intelligence alone is fantastic, it's moved us a long way, but we know it also has tremendous blind spots. AI has the potential to complement us there. I guess another thing to really call out here, AI isn't a panacea, it's not suddenly going to answer all of the questions. And, just like human intelligence, it will have its own biases, have its own strong points, and less strong points.  One of the things we're really committed to is working with people like Karim, and many others, to understand where AI could make a difference, to test it, to generate evidence on how well it works and an understanding in all sorts of ways about how that might play out. And, make sure that as AI becomes a tool, that we in genomics, but also in other areas, we understand its strong points and where we need to be more careful and cautious with it. That's a really important part of what we're going to be doing in the coming years here, is making sure that we can maximise the impact of it, but also be confident, so that we can explain to people whose data we might use it on how we're doing it and what it's bringing.  Sharon: Thanks Rich. It's definitely a fast-moving conversation of which we really want to be part of. One of the things that's come up again and again this year is participation and co-production. Let's hear quote that really captures that.  Bobbie: In an earlier conversation with Paul, which you might find surprising that it's stuck with me so much, he used the word ‘extractive'. He said that he'd been involved in research before and looking back on it, he had felt at times it could be a little bit extractive. You come in, you ask questions, you take the data away and analyse it, and it might only be by chance that the participants ever know what became of things next. One of the real principles of this project was always going to be co-production and true collaboration with our participants.  Sharon: That was Professor Bobbie Farsides talking about moving away from extractive research towards true co-production. How are we making that shift in practice here at Genomics England?  Rich: It's a great question. It's one of the areas where I think we've learnt most as an organisation over the years about how really engaging from the beginning with potential participants in programmes, participants who join our programmes, people who are involved in delivering our programmes and healthcare is so important at the beginning. I mentioned earlier the work to think about the consent process for the Generation Study, and that's one of the areas where I think from our first programme, 100,000 Genomes Project, we learnt a lot about how to do that well, some of the pitfalls, some of the bits that are most challenging. And really, right from the start of our programmes, making sure that people who will potentially benefit from the programmes, potentially join them, can be part of that engagement process, and really part of the design and the shaping of the research questions, the parameters around research, but also the materials and how people will engage with them. And that's one of the key capabilities we have internally as an organisation, so we work with partners externally, but also it's a really key part of the team that we have at Genomics England.  Sharon: So, whilst Bobbie talked about moving away from research that can feel one-sided and towards true collaboration, in another episode, Lindsay, a parent of a child with a rare condition, reflected on what that change really means for families and how it's empowering to see their voices and experiences shaping future treatments.  Lindsay: Historically, there's been a significant absence of a patient voice in rare disease research and development. And knowing that that's changing, I think that's really empowering for families. To know that professionals and industry are actually listening to our stories and our needs and really trying to understand, that offers much greater impact on the care and treatments of patients in the future.  Sharon: So, what role do you see participants as partners in shaping the next phase of Genomics England's work?  Rich: So, as you probably detected from my last answer, we see it as absolutely vital. One of the really exciting things here at Genomics England, we've had a participant panel from very early in our life as an organisation. That's one really important route to us at the heart of our organisation, part of our governance, making sure that participants representing all sorts of parts of our programme, but rare conditions being a really large focus for us. And I think, what's so striking as someone with a medical and a research background can see how I think historically medics and researchers have sometimes not known, sort of maybe been a bit scared about knowing how to involve participants from the outset. Often, because they're worried that they might ask the wrong questions in the wrong way, they just don't have the tools.   One of the things I often say now to people we work with is one of the most empowering and positive experiences we have at Genomics England is the power of our participants helping to, right from the beginning, shape what the questions are that we should be asking. Realise some of the challenges that you can't possibly, if you're not in their shoes, understand are the most important to really shape how we prioritise our work internally, the problems that we need to solve first, how we think about some of the practical impacts on people's lives that, again, without hearing from their voice you just wouldn't know. And again, to help our researchers, people accessing data in the National Genomic Research Library, helping them make sure that they involve participants in their work and the confidence and tools to do that.  Sharon: That's great, thank you. Another big theme this year has been collaboration across the NHS, academia, and industry. Dr Raghib Ali puts this really well.  Raghib: There are areas where academia and the NHS are very strong, and there are areas where industry is very strong, and why working together, as we saw, you know, very good examples during the pandemic with the vaccine and diagnostic tests, etc., a collaboration between the NHS, academia, and industry leads to much more rapid and wider benefits for our patients and, hopefully, in the future for the population as a whole in terms of early detection and prevention of disease.  Sharon: So, how does collaboration fit into the 10-year health plan and what's next for 2026 in that space, Rich?  Rich: I think one of the most enjoyable parts of my role at Genomics England and our role as an organisation is the fact that we see ourselves very much as part of a, sort of team across the UK and in fact internationally in terms of delivering on the potential we see for genomics. So, we have a vision as an organisation, which has been the same the last 5 or so years, which is a world where everyone can benefit from genomic healthcare. In fact, that vision is now shared by the NHS from a genomics perspective, and really demonstrably, the 2 parts of the system absolutely pointing in the same direction. And when we've been thinking, looking forward with that 10-year lens on it, what we always like to do, and I think it's a real privilege to be able to do, because we're here in the UK, because we have a National Health Service, because there's been that long-term commitment from government on genomics and really taking a long-term investment view there, and because of so many other parts of the ecosystem, other experts who access data in the National Genomic Research Library, research organisations like Our Future Health, UK Biobank, all teaming together, and the expertise that's there in genomics more broadly. So we've, if you like, worked back from what the UK could do as whole, and in the 10-year health plan, as I said earlier, genomics is at the heart of that.  There's a double helix on the front cover and, in fact, on the watermark on almost every page. And, there's this view set out there where as many as half of all health interactions by 2035 could be informed by genomics or other similar advanced analytics. And we think that that's a really ambitious challenge. We see a really important role for us, as Genomics England, in contributing to that, but it's very much a team effort. Our role is around where we have the biggest capabilities, so around building and running digital infrastructure at a national scale for healthcare delivery and for research, to building evidence to inform future policies, so running programmes like the Generation Study to inform future policy. And really, as part of that, that evidence piece, being driven by engagement, ethics, and work on equity, to really make sure that evidence that future policy can be built on is informed by a fully rounded view. We think if we do that right that we could as a country with others, the NHS, research organisations, many others could live up to that ambition that's set out there in the 10-year plan.   And the 10-year plan is really clear, and government is really clear that this is about improving health outcomes. But it's also part of a broader benefit to the country because the UK is recognised already as a great place from a genomics perspective. We think playing our role in that won't just bring the health benefits, it also will secure the country's position as the best place in the world to discover, prove and where proven role out benefit from genomic innovations. And we think it's so exciting to be part of that team effort.  Sharon: So, Genomics England's refreshed mission and direction of travel is really setting out how we move from research to routine care, and how we embed genomics across the health system. Carlo Rinaldi captured the idea perfectly, imagining a future where diagnosis and hope arrive hand in hand.  Carlo: My dream is that in five to ten years' time an individual with a rare disease is identified in the clinic, perhaps even before symptoms have manifested. At that exact time the day of the diagnosis becomes also a day of hope, in a way, where immediately the researcher, the genetic labs, flags that specific variant, that specific mutation. We know exactly which is the best genetic therapy to go after.   Sharon: And Rich, what are your thoughts on that?  Rich: I think Carlo captures it really well. And for us, I think a really big theme is for that potential for genomics to make a difference, a continued and in fact increased difference for people with rare conditions and cancer, areas where it's already making a difference, but also with the potential to make a much broader impact for people across the population. The real theme is embedding genomics into routine care, making it something that you don't need to know that you're seeing an expert in genomics to benefit from it, really make sure that those benefits can be felt as just part of routine care. It's not something separate where we recognise that the best healthcare is healthcare that's supported by all sorts of inputs, with genomics being a key part of that, and that we can continue to learn as we do that. So that with people's consent, with their understanding of how their data is being used, we know that if we don't have the best answer for them today, we give the best answer we can today, and we can continue to learn, and they can benefit from that in the future.   I'm a rare disease doctor by background, and one of the really most enjoyable parts of my job is seeing that come to practice. In the last year or so I've had a number of families where I've been seeing the family for years, and a researcher accessing data in the National Genomic Research library has found an answer that we've not been able to find for maybe their child's whole life, and then finally we're able to feed it back. Seeing that come to life is just so wonderful, and I think gives us a bit of a blueprint for how things could work more generally.  Sharon: That's great. I mean, what a feeling for those families who do get those answers. As we look ahead to 2026 and beyond, the conversation is starting to include prevention, using genomics not just to diagnose conditions but to predict and treat and even prevent them. Alice Tuff-Lacey summarised this nicely in an episode about Generation Study.  Alice: This is quite an exciting shift in how we use whole genome sequencing, because what we're talking about is using it in a much more preventative way. Traditionally where we've been using it is diagnostically where we know someone's sick and they've got symptoms of rare condition, and we're looking to see what they might have. What we're actually talking about is screening babies from birth using their genome to see if they're at risk of a particular condition. And what this means is this raises quite a lot of complex ethical, operational, and scientific and clinical questions.  Sharon: Rich, when you think about 2026, what's your biggest hope for where we'll be this time next year?  Rich: I think it's a really exciting time. As you can tell from how we've been speaking, I'm really excited about the direction of travel and how over the next 5 and 10 years we can really make a transformational shift because of how well placed we are in the UK from a genomics perspective. Where we are with today's knowledge, where we could be because of the continued government and NHS commitment to genomics being at the heart of this, if we build the right infrastructure, if we generate the right evidence to inform what's adopted, I think we're in a really exciting place.  From a 2026 perspective, I think what we're really committed to is continuing to do the work, the day-by-day-by-day work that is to build that incrementally. So, a really big focus for us is continuing to support the NHS and making sure researchers can access data, so that flow of answers for families can continue and grow, accelerate, to continue delivering the Generation Study because it's a really important part of that wider jigsaw to generate the evidence that can inform future policy on whether this is something that's adopted and offered routinely to every child when they're born.  I think a really important time now that the government's provided the opportunity for us as a team, as a UK genomics and life sciences ecosystem, is to really put in place some of the next steps, the building blocks that can take us towards that 10-year vision. So for us also, a really important part of the year is beginning the design process for an adult population genomics programme, where we're looking at what evidence it's important that we can provide that's complementary to different work around by others in the ecosystem that needs to be there if we're going to think about that potential broader use of genomics.  Sharon: That's great. It sounds like another exciting year ahead. So, we're going to wrap up there. Thank you to Rich Scott for sharing your reflections on the key milestones this year, and for your thoughts on the year ahead. Thanks, Rich.  Rich: Thanks very much for having me.  Sharon: If you enjoyed today's episode, we'd love your support, so please subscribe, share, and rate us on wherever you listen to your podcasts. I've been your host, Sharon Jones. This podcast was produced by Deanna Barac and edited by Bill Griffin at Ventoux Digital. Thank you for listening. 

Popular media leverage weak study to criticize RFK Jr.'s rethink of standard recommendations for saturated fat avoidance; Poor quality plant-based diets hike cardio risk; A listener complains his lp(a) is going up with age despite his healthy diet, lifestyle; Scientists pinpoint cocoa ingredient that slows aging; Berry proanthocyanidins preserve brain power; Tattooing may promote inflammation, undermine immunity.

Send us a textA minute that leaves you breathless can rival eight minutes of comfortable effort. That's the eye-opening takeaway we unpack as we dive into fresh UK Biobank data showing how vigorous activity dramatically outperforms moderate and light movement for reducing all-cause mortality, cardiovascular events, diabetes, and even cancer risk. We strip away jargon and use the talk test—can you sing, speak, or barely get a sentence out?—so anyone can gauge intensity without a lab or a smartwatch.We explore why intensity pays off under the hood: stronger left ventricular function, bigger stroke volume, better oxygen delivery, improved lactate recycling, greater capillary and mitochondrial density, and faster glycogen turnover. Then we get practical. No fancy gear required—try telephone-pole intervals on a walk, short hill surges, a flight of stairs at speed, or breathless bursts during yardwork and shoveling. Keep light movement threaded through your day to counter the stress signals of sitting, but add slim, safe slices of intensity to unlock outsized benefits when time is tight.We also lay out a sane progression. Find a steady state before nudging harder, start with tiny intervals, and build toward an 80 percent moderate base with 10 to 20 percent vigorous effort. Fold in resistance training to protect muscle, strength, and glucose control. The goal isn't punishment; it's leverage—using a few honest minutes to gain more health per unit of time. If you've ever wondered how to make movement matter more, this conversation offers a clear path you can start today. If it helps, share it with a friend, subscribe for more science-backed self-care, and leave a review to tell us your first vigorous minute.For video, PowerPoint slide deck and reference studies go to www.thehealthedgepodcast.com

Text Dr. Lenz any feedback or questions New Breakthrough: The Neurobiological Basis of Fibromyalgia Pain RevealedAre you or a loved one struggling with widespread pain often dismissed as stress-induced? Dr. Michael Lenz uncovers groundbreaking data showing that such pain is linked to measurable changes in the brain's structure. This episode delves into a massive study involving over 40,000 participants from the UK Biobank, validating the fibromyalgia index (FMI) as a reliable marker for nociplastic pain, especially seen in fibromyalgia. Key findings spotlight the altered structural connectivity within brain regions like the periaqueductal gray and amygdala, elucidating the link between chronic pain and symptoms such as fatigue and depression. Tune in to grasp a deeper understanding of the biological underpinnings of nociplastic pain and its ramifications for targeted treatments.Watch on Youtube Here00:00 Introduction to Nociplastic Pain01:32 Groundbreaking Study on Fibromyalgia Index01:52 Understanding Nociplastic Pain and Fibromyalgia02:52 Brain Networks and Pain Modulation04:08 Key Findings on Structural Connectivity04:53 Specific Brain Circuits and Symptoms06:10 Mediation Models and Symptom Domains07:10 Specificity of the Fibromyalgia Index07:48 Conclusion and Key Takeaways08:16  Final Thoughts Support the showWhen I started this podcast and YouTube Channel—and the book that came before it—I had my patients in mind. Office visits are short, but understanding complex, often misunderstood conditions like fibromyalgia takes time. That's why I created this space: to offer education, validation, and hope. If you've been told fibromyalgia “isn't real” or that it's “all in your head,” know this—I see you. I believe you. This podcast aims to affirm your experience and explain the science behind it. Whether you live with fibromyalgia, care for someone who does, or are a healthcare professional looking to better support patients, you'll find trusted, evidence-based insights here, drawn from my 29+ years as an MD. Please remember to talk with your doctor about your symptoms and care. This content doesn't replace per...

How can you write science-based fiction without info-dumping your research? How can you use AI tools in a creative way, while still focusing on a human-first approach? Why is adapting to the fast pace of change so difficult and how can we make the most of this time? Jamie Metzl talks about Superconvergence and more. In the intro, How to avoid author scams [Written Word Media]; Spotify vs Audible audiobook strategy [The New Publishing Standard]; Thoughts on Author Nation and why constraints are important in your author life [Self-Publishing with ALLi]; Alchemical History And Beautiful Architecture: Prague with Lisa M Lilly on my Books and Travel Podcast. Today's show is sponsored by Draft2Digital, self-publishing with support, where you can get free formatting, free distribution to multiple stores, and a host of other benefits. Just go to www.draft2digital.com to get started. This show is also supported by my Patrons. Join my Community at Patreon.com/thecreativepenn Jamie Metzl is a technology futurist, professional speaker, entrepreneur, and the author of sci-fi thrillers and futurist nonfiction books, including the revised and updated edition of Superconvergence: How the Genetics, Biotech, and AI Revolutions Will Transform Our Lives, Work, and World. You can listen above or on your favorite podcast app or read the notes and links below. Here are the highlights and the full transcript is below. Show Notes How personal history shaped Jamie's fiction writing Writing science-based fiction without info-dumping The super convergence of three revolutions (genetics, biotech, AI) and why we need to understand them holistically Using fiction to explore the human side of genetic engineering, life extension, and robotics Collaborating with GPT-5 as a named co-author How to be a first-rate human rather than a second-rate machine You can find Jamie at JamieMetzl.com. Transcript of interview with Jamie Metzl Jo: Jamie Metzl is a technology futurist, professional speaker, entrepreneur, and the author of sci-fi thrillers and futurist nonfiction books, including the revised and updated edition of Superconvergence: How the Genetics, Biotech, and AI Revolutions Will Transform Our Lives, Work, and World. So welcome, Jamie. Jamie: Thank you so much, Jo. Very happy to be here with you. Jo: There is so much we could talk about, but let's start with you telling us a bit more about you and how you got into writing. From History PhD to First Novel Jamie: Well, I think like a lot of writers, I didn't know I was a writer. I was just a kid who loved writing. Actually, just last week I was going through a bunch of boxes from my parents' house and I found my autobiography, which I wrote when I was nine years old. So I've been writing my whole life and loving it. It was always something that was very important to me. When I finished my DPhil, my PhD at Oxford, and my dissertation came out, it just got scooped up by Macmillan in like two minutes. And I thought, “God, that was easy.” That got me started thinking about writing books. I wanted to write a novel based on the same historical period – my PhD was in Southeast Asian history – and I wanted to write a historical novel set in the same period as my dissertation, because I felt like the dissertation had missed the human element of the story I was telling, which was related to the Cambodian genocide and its aftermath. So I wrote what became my first novel, and I thought, “Wow, now I'm a writer.” I thought, “All right, I've already published one book. I'm gonna get this other book out into the world.” And then I ran into the brick wall of: it's really hard to be a writer. It's almost easier to write something than to get it published. I had to learn a ton, and it took nine years from when I started writing that first novel, The Depths of the Sea, to when it finally came out. But it was such a positive experience, especially to have something so personal to me as that story. I'd lived in Cambodia for two years, I'd worked on the Thai-Cambodian border, and I'm the child of a Holocaust survivor. So there was a whole lot that was very emotional for me. That set a pattern for the rest of my life as a writer, at least where, in my nonfiction books, I'm thinking about whatever the issues are that are most important to me. Whether it was that historical book, which was my first book, or Hacking Darwin on the future of human genetic engineering, which was my last book, or Superconvergence, which, as you mentioned in the intro, is my current book. But in every one of those stories, the human element is so deep and so profound. You can get at some of that in nonfiction, but I've also loved exploring those issues in deeper ways in my fiction. So in my more recent novels, Genesis Code and Eternal Sonata, I've looked at the human side of the story of genetic engineering and human life extension. And now my agent has just submitted my new novel, Virtuoso, about the intersection of AI, robotics, and classical music. With all of this, who knows what's the real difference between fiction and nonfiction? We're all humans trying to figure things out on many different levels. Shifting from History to Future Tech Jo: I knew that you were a polymath, someone who's interested in so many things, but the music angle with robotics and AI is fascinating. I do just want to ask you, because I was also at Oxford – what college were you at? Jamie: I was in St. Antony's. Jo: I was at Mansfield, so we were in that slightly smaller, less famous college group, if people don't know. Jamie: You know, but we're small but proud. Jo: Exactly. That's fantastic. You mentioned that you were on the historical side of things at the beginning and now you've moved into technology and also science, because this book Superconvergence has a lot of science. So how did you go from history and the past into science and the future? Biology and Seeing the Future Coming Jamie: It's a great question. I'll start at the end and then back up. A few years ago I was speaking at Lawrence Livermore National Laboratory, which is one of the big scientific labs here in the United States. I was a guest of the director and I was speaking to their 300 top scientists. I said to them, “I'm here to speak with you about the future of biology at the invitation of your director, and I'm really excited. But if you hear something wrong, please raise your hand and let me know, because I'm entirely self-taught. The last biology course I took was in 11th grade of high school in Kansas City.” Of course I wouldn't say that if I didn't have a lot of confidence in my process. But in many ways I'm self-taught in the sciences. As you know, Jo, and as all of your listeners know, the foundation of everything is curiosity and then a disciplined process for learning. Even our greatest super-specialists in the world now – whatever their background – the world is changing so fast that if anyone says, “Oh, I have a PhD in physics/chemistry/biology from 30 years ago,” the exact topic they learned 30 years ago is less significant than their process for continuous learning. More specifically, in the 1990s I was working on the National Security Council for President Clinton, which is the president's foreign policy staff. My then boss and now close friend, Richard Clarke – who became famous as the guy who had tragically predicted 9/11 – used to say that the key to efficacy in Washington and in life is to try to solve problems that other people can't see. For me, almost 30 years ago, I felt to my bones that this intersection of what we now call AI and the nascent genetics revolution and the nascent biotechnology revolution was going to have profound implications for humanity. So I just started obsessively educating myself. When I was ready, I started writing obscure national security articles. Those got a decent amount of attention, so I was invited to testify before the United States Congress. I was speaking out a lot, saying, “Hey, this is a really important story. A lot of people are missing it. Here are the things we should be thinking about for the future.” I wasn't getting the kind of traction that I wanted. I mentioned before that my first book had been this dry Oxford PhD dissertation, and that had led to my first novel. So I thought, why don't I try the same approach again – writing novels to tell this story about the genetics, biotech, and what later became known popularly as the AI revolution? That led to my two near-term sci-fi novels, Genesis Code and Eternal Sonata. On my book tours for those novels, when I explained the underlying science to people in my way, as someone who taught myself, I could see in their eyes that they were recognizing not just that something big was happening, but that they could understand it and feel like they were part of that story. That's what led me to write Hacking Darwin, as I mentioned. That book really unlocked a lot of things. I had essentially predicted the CRISPR babies that were born in China before it happened – down to the specific gene I thought would be targeted, which in fact was the case. After that book was published, Dr. Tedros, the Director-General of the World Health Organization, invited me to join the WHO Expert Advisory Committee on Human Genome Editing, which I did. It was a really great experience and got me thinking a lot about the upside of this revolution and the downside. The Birth of Superconvergence Jamie: I get a lot of wonderful invitations to speak, and I have two basic rules for speaking: Never use notes. Never ever. Never stand behind a podium. Never ever. Because of that, when I speak, my talks tend to migrate. I'd be speaking with people about the genetics revolution as it applied to humans, and I'd say, “Well, this is just a little piece of a much bigger story.” The bigger story is that after nearly four billion years of life on Earth, our one species has the increasing ability to engineer novel intelligence and re-engineer life. The big question for us, and frankly for the world, is whether we're going to be able to use that almost godlike superpower wisely. As that idea got bigger and bigger, it became this inevitable force. You write so many books, Jo, that I think it's second nature for you. Every time I finish a book, I think, “Wow, that was really hard. I'm never doing that again.” And then the books creep up on you. They call to you. At some point you say, “All right, now I'm going to do it.” So that was my current book, Superconvergence. Like everything, every journey you take a step, and that step inspires another step and another. That's why writing and living creatively is such a wonderfully exciting thing – there's always more to learn and always great opportunities to push ourselves in new ways. Balancing Deep Research with Good Storytelling Jo: Yeah, absolutely. I love that you've followed your curiosity and then done this disciplined process for learning. I completely understand that. But one of the big issues with people like us who love the research – and having read your Superconvergence, I know how deeply you go into this and how deeply you care that it's correct – is that with fiction, one of the big problems with too much research is the danger of brain-dumping. Readers go to fiction for escapism. They want the interesting side of it, but they want a story first. What are your tips for authors who might feel like, “Where's the line between putting in my research so that it's interesting for readers, but not going too far and turning it into a textbook?” How do you find that balance? Jamie: It's such a great question. I live in New York now, but I used to live in Washington when I was working for the U.S. government, and there were a number of people I served with who later wrote novels. Some of those novels felt like policy memos with a few sex scenes – and that's not what to do. To write something that's informed by science or really by anything, everything needs to be subservient to the story and the characters. The question is: what is the essential piece of information that can convey something that's both important to your story and your character development, and is also an accurate representation of the world as you want it to be? I certainly write novels that are set in the future – although some of them were a future that's now already happened because I wrote them a long time ago. You can make stuff up, but as an author you have to decide what your connection to existing science and existing technology and the existing world is going to be. I come at it from two angles. One: I read a huge number of scientific papers and think, “What does this mean for now, and if you extrapolate into the future, where might that go?” Two: I think about how to condense things. We've all read books where you're humming along because people read fiction for story and emotional connection, and then you hit a bit like: “I sat down in front of the president, and the president said, ‘Tell me what I need to know about the nuclear threat.'” And then it's like: insert memo. That's a deal-killer. It's like all things – how do you have a meaningful relationship with another person? It's not by just telling them your story. Even when you're telling them something about you, you need to be imagining yourself sitting in their shoes, hearing you. These are very different disciplines, fiction and nonfiction. But for the speculative nonfiction I write – “here's where things are now, and here's where the world is heading” – there's a lot of imagination that goes into that too. It feels in many ways like we're living in a sci-fi world because the rate of technological change has been accelerating continuously, certainly for the last 12,000 years since the dawn of agriculture. It's a balance. For me, I feel like I'm a better fiction writer because I write nonfiction, and I'm a better nonfiction writer because I write fiction. When I'm writing nonfiction, I don't want it to be boring either – I want people to feel like there's a story and characters and that they can feel themselves inside that story. Jo: Yeah, definitely. I think having some distance helps as well. If you're really deep into your topics, as you are, you have to leave that manuscript a little bit so you can go back with the eyes of the reader as opposed to your eyes as the expert. Then you can get their experience, which is great. Looking Beyond Author-Focused AI Fears Jo: I want to come to your technical knowledge, because AI is a big thing in the author and creative community, like everywhere else. One of the issues is that creators are focusing on just this tiny part of the impact of AI, and there's a much bigger picture. For example, in 2024, Demis Hassabis from Google DeepMind and his collaborative partner John Jumper won the Nobel Prize for Chemistry with AlphaFold. It feels to me like there's this massive world of what's happening with AI in health, climate, and other areas, and yet we are so focused on a lot of the negative stuff. Maybe you could give us a couple of things about what there is to be excited and optimistic about in terms of AI-powered science? Jamie: Sure. I'm so excited about all of the new opportunities that AI creates. But I also think there's a reason why evolution has preserved this very human feeling of anxiety: because there are real dangers. Anybody who's Pollyanna-ish and says, “Oh, the AI story is inevitably positive,” I'd be distrustful. And anyone who says, “We're absolutely doomed, this is the end of humanity,” I'd also be distrustful. So let me tell you the positives and the negatives, and maybe some thoughts about how we navigate toward the former and away from the latter. AI as the New Electricity Jamie: When people think of AI right now, they're thinking very narrowly about these AI tools and ChatGPT. But we don't think of electricity that way. Nobody says, “I know electricity – electricity is what happens at the power station.” We've internalised the idea that electricity is woven into not just our communication systems or our houses, but into our clothes, our glasses – it's woven into everything and has super-empowered almost everything in our modern lives. That's what AI is. In Superconvergence, the majority of the book is about positive opportunities: In healthcare, moving from generalised healthcare based on population averages to personalised or precision healthcare based on a molecular understanding of each person's individual biology. As we build these massive datasets like the UK Biobank, we can take a next jump toward predictive and preventive healthcare, where we're able to address health issues far earlier in the process, when interventions can be far more benign. I'm really excited about that, not to mention the incredible new kinds of treatments – gene therapies, or pharmaceuticals based on genetics and systems-biology analyses of patients. Then there's agriculture. Over the last hundred years, because of the technologies of the Green Revolution and synthetic fertilisers, we've had an incredible increase in agricultural productivity. That's what's allowed us to quadruple the global population. But if we just continue agriculture as it is, as we get towards ten billion wealthier, more empowered people wanting to eat like we eat, we're going to have to wipe out all the wild spaces on Earth to feed them. These technologies help provide different paths toward increasing agricultural productivity with fewer inputs of land, water, fertiliser, insecticides, and pesticides. That's really positive. I could go on and on about these positives – and I do – but there are very real negatives. I was a member of the WHO Expert Advisory Committee on Human Genome Editing after the first CRISPR babies were very unethically created in China. I'm extremely aware that these same capabilities have potentially incredible upsides and very real downsides. That's the same as every technology in the past, but this is happening so quickly that it's triggering a lot of anxieties. Governance, Responsibility, and Why Everyone Has a Role Jamie: The question now is: how do we optimise the benefits and minimise the harms? The short, unsexy word for that is governance. Governance is not just what governments do; it's what all of us do. That's why I try to write books, both fiction and nonfiction, to bring people into this story. If people “other” this story – if they say, “There's a technology revolution, it has nothing to do with me, I'm going to keep my head down” – I think that's dangerous. The way we're going to handle this as responsibly as possible is if everybody says, “I have some role. Maybe it's small, maybe it's big. The first step is I need to educate myself. Then I need to have conversations with people around me. I need to express my desires, wishes, and thoughts – with political leaders, organisations I'm part of, businesses.” That has to happen at every level. You're in the UK – you know the anti-slavery movement started with a handful of people in Cambridge and grew into a global movement. I really believe in the power of ideas, but ideas don't spread on their own. These are very human networks, and that's why writing, speaking, communicating – probably for every single person listening to this podcast – is so important. Jo: Mm, yeah. Fiction Like AI 2041 and Thinking Through the Issues Jo: Have you read AI 2041 by Kai-Fu Lee and Chen Qiufan? Jamie: No. I heard a bunch of their interviews when the book came out, but I haven't read it. Jo: I think that's another good one because it's fiction – a whole load of short stories. It came out a few years ago now, but the issues they cover in the stories, about different people in different countries – I remember one about deepfakes – make you think more about the topics and help you figure out where you stand. I think that's the issue right now: it's so complex, there are so many things. I'm generally positive about AI, but of course I don't want autonomous drone weapons, you know? The Messy Reality of “Bad” Technologies Jamie: Can I ask you about that? Because this is why it's so complicated. Like you, I think nobody wants autonomous killer drones anywhere in the world. But if you right now were the defence minister of Ukraine, and your children are being kidnapped, your country is being destroyed, you're fighting for your survival, you're getting attacked every night – and you're getting attacked by the Russians, who are investing more and more in autonomous killer robots – you kind of have two choices. You can say, “I'm going to surrender,” or, “I'm going to use what technology I have available to defend myself, and hopefully fight to either victory or some kind of stand-off.” That's what our societies did with nuclear weapons. Maybe not every American recognises that Churchill gave Britain's nuclear secrets to America as a way of greasing the wheels of the Anglo-American alliance during the Second World War – but that was our programme: we couldn't afford to lose that war, and we couldn't afford to let the Nazis get nuclear weapons before we did. So there's the abstract feeling of, “I'm against all war in the abstract. I'm against autonomous killer robots in the abstract.” But if I were the defence minister of Ukraine, I would say, “What will it take for us to build the weapons we can use to defend ourselves?” That's why all this stuff gets so complicated. And frankly, it's why the relationship between fiction and nonfiction is so important. If every novel had a situation where every character said, “Oh, I know exactly the right answer,” and then they just did the right answer and it was obviously right, it wouldn't make for great fiction. We're dealing with really complex humans. We have conflicting impulses. We're not perfect. Maybe there are no perfect answers – but how do we strive toward better rather than worse? That's the question. Jo: Absolutely. I don't want to get too political on things. How AI Is Changing the Writing Life Jo: Let's come back to authors. In terms of the creative process, the writing process, the research process, and the business of being an author – what are some of the ways that you already use AI tools, and some of the ways, given your futurist brain, that you think things are going to change for us? Jamie: Great question. I'll start with a little middle piece. I found you, Jo, through GPT-5. I asked ChatGPT, “I'm coming out with this book and I want to connect with podcasters who are a little different from the ones I've done in the past. I've been a guest on Joe Rogan twice and some of the bigger podcasts. Make me a list of really interesting people I can have great conversations with.” That's how I found you. So this is one reward of that process. Let me say that in the last year I've worked on three books, and I'll explain how my relationship with AI has changed over those books. Cleaning Up Citations (and Getting Burned) Jamie: First is the highly revised paperback edition of Superconvergence. When the hardback came out, I had – I don't normally work with research assistants because I like to dig into everything myself – but the one thing I do use a research assistant for is that I can't be bothered, when I'm writing something, to do the full Chicago-style footnote if I'm already referencing an academic paper. So I'd just put the URL as the footnote and then hire a research assistant and say, “Go to this URL and change it into a Chicago-style citation. That's it.” Unfortunately, my research assistant on the hardback used early-days ChatGPT for that work. He did the whole thing, came back, everything looked perfect. I said, “Wow, amazing job.” It was only later, as I was going through them, that I realised something like 50% of them were invented footnotes. It was very painful to go back and fix, and it took ten times more time. With the paperback edition, I didn't use AI that much, but I did say things like, “Here's all the information – generate a Chicago-style citation.” That was better. I noticed there were a few things where I stopped using the thesaurus function on Microsoft Word because I'd just put the whole paragraph into the AI and say, “Give me ten other options for this one word,” and it would be like a contextual thesaurus. That was pretty good. Talking to a Robot Pianist Character Jamie: Then, for my new novel Virtuoso, I was writing a character who is a futurist robot that plays the piano very beautifully – not just humanly, but almost finding new things in the music we've written and composing music that resonates with us. I described the actions of that robot in the novel, but I didn't describe the inner workings of the robot's mind. In thinking about that character, I realised I was the first science-fiction writer in history who could interrogate a machine about what it was “thinking” in a particular context. I had the most beautiful conversations with ChatGPT, where I would give scenarios and ask, “What are you thinking? What are you feeling in this context?” It was all background for that character, but it was truly profound. Co-Authoring The AI Ten Commandments with GPT-5 Jamie: Third, I have another book coming out in May in the United States. I gave a talk this summer at the Chautauqua Institution in upstate New York about AI and spirituality. I talked about the history of our human relationship with our technology, about how all our religious and spiritual traditions have deep technological underpinnings – certainly our Abrahamic religions are deeply connected to farming, and Protestantism to the printing press. Then I had a section about the role of AI in generating moral codes that would resonate with humans. Everybody went nuts for this talk, and I thought, “I think I'm going to write a book.” I decided to write it differently, with GPT-5 as my named co-author. The first thing I did was outline the entire book based on the talk, which I'd already spent a huge amount of time thinking about and organising. Then I did a full outline of the arguments and structures. Then I trained GPT-5 on my writing style. The way I did it – which I fully describe in the introduction to the book – was that I'd handle all the framing: the full introduction, the argument, the structure. But if there was a section where, for a few paragraphs, I was summarising a huge field of data, even something I knew well, I'd give GPT-5 the intro sentence and say, “In my writing style, prepare four paragraphs on this.” For example, I might write: “AI has the potential to see us humans like we humans see ant colonies.” Then I'd say, “Give me four paragraphs on the relationship between the individual and the collective in ant colonies.” I could have written those four paragraphs myself, but it would've taken a month to read the life's work of E.O. Wilson and then write them. GPT-5 wrote them in seconds or minutes, in its thinking mode. I'd then say, “It's not quite right – change this, change that,” and we'd go back and forth three or four times. Then I'd edit the whole thing and put it into the text. So this book that I could have written on my own in a year, I wrote a first draft of with GPT-5 as my named co-author in two days. The whole project will take about six months from start to finish, and I'm having massive human editing – multiple edits from me, plus a professional editor. It's not a magic AI button. But I feel strongly about listing GPT-5 as a co-author because I've written it differently than previous books. I'm a huge believer in the old-fashioned lone author struggling and suffering – that's in my novels, and in Virtuoso I explore that. But other forms are going to emerge, just like video games are a creative, artistic form deeply connected to technology. The novel hasn't been around forever – the current format is only a few centuries old – and forms are always changing. There are real opportunities for authors, and there will be so much crap flooding the market because everybody can write something and put it up on Amazon. But I think there will be a very special place for thoughtful human authors who have an idea of what humans do at our best, and who translate that into content other humans can enjoy. Traditional vs Indie: Why This Book Will Be Self-Published Jo: I'm interested – you mentioned that it's your named co-author. Is this book going through a traditional publisher, and what do they think about that? Or are you going to publish it yourself? Jamie: It's such a smart question. What I found quickly is that when you get to be an author later in your career, you have all the infrastructure – a track record, a fantastic agent, all of that. But there were two things that were really important to me here: I wanted to get this book out really fast – six months instead of a year and a half. It was essential to me to have GPT-5 listed as my co-author, because if it were just my name, I feel like it would be dishonest. Readers who are used to reading my books – I didn't want to present something different than what it was. I spoke with my agent, who I absolutely love, and she said that for this particular project it was going to be really hard in traditional publishing. So I did a huge amount of research, because I'd never done anything in the self-publishing world before. I looked at different models. There was one hybrid model that's basically the same as traditional, but you pay for the things the publisher would normally pay for. I ended up not doing that. Instead, I decided on a self-publishing route where I disaggregated the publishing process. I found three teams: one for producing the book, one for getting the book out into the world, and a smaller one for the audiobook. I still believe in traditional publishing – there's a lot of wonderful human value-add. But some works just don't lend themselves to traditional publishing. For this book, which is called The AI Ten Commandments, that's the path I've chosen. Jo: And when's that out? I think people will be interested. Jamie: April 26th. Those of us used to traditional publishing think, “I've finished the book, sold the proposal, it'll be out any day now,” and then it can be a year and a half. It's frustrating. With this, the process can be much faster because it's possible to control more of the variables. But the key – as I was saying – is to make sure it's as good a book as everything else you've written. It's great to speed up, but you don't want to compromise on quality. The Coming Flood of Excellent AI-Generated Work Jo: Yeah, absolutely. We're almost out of time, but I want to come back to your “flood of crap” and the “AI slop” idea that's going around. Because you are working with GPT-5 – and I do as well, and I work with Claude and Gemini – and right now there are still issues. Like you said about referencing, there are still hallucinations, though fewer. But fast-forward two, five years: it's not a flood of crap. It's a flood of excellent. It's a flood of stuff that's better than us. Jamie: We're humans. It's better than us in certain ways. If you have farm machinery, it's better than us at certain aspects of farming. I'm a true humanist. I think there will be lots of things machines do better than us, but there will be tons of things we do better than them. There's a reason humans still care about chess, even though machines can beat humans at chess. Some people are saying things I fully disagree with, like this concept of AGI – artificial general intelligence – where machines do everything better than humans. I've summarised my position in seven letters: “AGI is BS.” The only way you can believe in AGI in that sense is if your concept of what a human is and what a human mind is is so narrow that you think it's just a narrow range of analytical skills. We are so much more than that. Humans represent almost four billion years of embodied evolution. There's so much about ourselves that we don't know. As incredible as these machines are and will become, there will always be wonderful things humans can do that are different from machines. What I always tell people is: whatever you're doing, don't be a second-rate machine. Be a first-rate human. If you're doing something and a machine is doing that thing much better than you, then shift to something where your unique capacities as a human give you the opportunity to do something better. So yes, I totally agree that the quality of AI-generated stuff will get better. But I think the most creative and successful humans will be the ones who say, “I recognise that this is creating new opportunities, and I'm going to insert my core humanity to do something magical and new.” People are “othering” these technologies, but the technologies themselves are magnificent human-generated artefacts. They're not alien UFOs that landed here. It's a scary moment for creatives, no doubt, because there are things all of us did in the past that machines can now do really well. But this is the moment where the most creative people ask themselves, “What does it mean for me to be a great human?” The pat answers won't apply. In my Virtuoso novel I explore that a lot. The idea that “machines don't do creativity” – they will do incredible creativity; it just won't be exactly human creativity. We will be potentially huge beneficiaries of these capabilities, but we really have to believe in and invest in the magic of our core humanity. Where to Find Jamie and His Books Jo: Brilliant. So where can people find you and your books online? Jamie: Thank you so much for asking. My website is jamiemetzl.com – and my books are available everywhere. Jo: Fantastic. Thanks so much for your time, Jamie. That was great. Jamie: Thank you, Joanna.The post Writing The Future, And Being More Human In An Age of AI With Jamie Metzl first appeared on The Creative Penn.

In this solo episode, Darin reframes one of the most misunderstood forces in life — stress. Instead of seeing it as the enemy, he explores how stress is actually a messenger, guiding you back to alignment, safety, and awareness. Through science, spirituality, and lived experience, Darin breaks down how stress shows us where we're trying to control, where we're disconnected, and where our nervous system is calling for attention. He unpacks the layers of modern stress — from trauma and environment to community and purpose — and offers practical, embodied tools to restore calm, clarity, and resilience.     What You'll Learn 00:00:00 – Welcome to Super Life: Solutions for a Healthier Life and Better World 00:00:32 – Sponsor Spotlight: TheraSauna - Natural Healing Technologies (15% off with code Darrandai) 00:02:10 – The Super Life Podcast: Finding Contentment, Happiness, and Purpose 00:02:51 – Today's Topic: Stress - Reframing Stress as an Ally and Dashboard Light 00:04:54 – The "No Choice" Universe: Reconnecting to Infinite Possibilities 00:05:16 – The Reality of Stress: Statistics and the Impact of Chronic Stress 00:06:21 – Stress is Layered: Beyond a Single Cause, Addressing Chronic Stress 00:08:29 – Solutions for a Super Life: Safety over Calm and the Vagal Response 00:09:38 – The Inner Dialogue Layer: Trauma, Unconsciousness, and Spiritual Bypassing 00:11:47 – The Social Field Layer: Relationships, Community, and Finding Your Way Home 00:14:20 – Sponsor Spotlight: Bite Toothpaste - Sustainable, Non-Toxic Tabs (20% off with code Darin20) 00:16:35 – Creating Your Own Vision: Setting Boundaries with Media and Social Algorithms 00:17:29 – Finding Your Purpose: From Raising Children to Healing Injuries 00:18:35 – Environmental and Existential Stress Layers: Clutter, Noise, and Service 00:19:26 – Stress Load and Resiliency: Why Small Triggers Cause Blow-Ups 00:20:02 – Understanding the Dashboard Light: Acknowledging Unwillingness 00:20:35 – Safety as the Signal: Body Relaxation and Providing Inner Security 00:23:44 – Reframing Trauma: Was it the Protector You Needed at the Time? 00:25:00 – Releasing Trauma: Techniques, The Healing Code, and Waking the Tiger 00:26:06 – Finishing the Survival Response: Shaking, Crying, Screaming, and Stretching 00:26:38 – Stress as a Multiplier: Impact on Immune System, Heart, and Aging 00:28:10 – Stress Slows Repair: Inflammation, Cardiovascular Risk, and Cellular Aging 00:29:48 – The Integrative Approach: Changing Your Environments to Support Anti-Stress 00:30:07 – Actionable Stress Solutions: Circadian Rhythm, Nature, and Noise Reduction 00:30:44 – Actionable Stress Solutions: Gratitude, Conscious Breath, and Movement 00:31:32 – Energy Drains to Eliminate: Conflict, Clutter, Scrolling, and Late Caffeine 00:32:17 – Connecting to Greater Purpose: The Super Life Patreon Platform 00:32:54 – Morning/Night Questions: Letting Go, Creating, and Contributing 00:33:17 – Final Toolkit: Slow Breathing, Movement, Nature, Sauna, and Sleep 00:34:25 – The Invitation: Digging into all Layers of a Super Life on Patreon   Thank You to Our Sponsors Therasage: Go to www.therasage.com and use code DARIN at checkout for 15% off Bite Toothpaste: Go to trybite.com/DARIN20 or use code DARIN20 for 20% off your first order. Find More from Darin Olien: Instagram: @darinolien Podcast: SuperLife Podcast Website: superlife.com Book: Fatal Conveniences   Key Takeaway "Stress isn't your enemy — it's your compass. Every wave of tension points you back to what's asking for care, attention, and love. When you stop fighting stress and start listening to it, you don't just survive — you evolve."       Bibliography (selected, peer-reviewed) Sources: Gallup Global Emotions (2024); Gallup U.S. polling (2024); APA Stress in America (2023); Natarajan et al., Lancet Digital Health (2020); Orini et al., UK Biobank (2023); Martinez et al. (2022); Leiden University (2025). Cohen S, Tyrrell DA, Smith AP. Psychological stress and susceptibility to the common cold. N Engl J Med.1991;325(9):606–612. New England Journal of Medicine Cohen S, et al. Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk. Proc Natl Acad Sci USA. 2012;109(16):5995–5999. PNAS Kiecolt-Glaser JK, et al. Slowing of wound healing by psychological stress. Lancet. 1995;346(8984):1194–1196. The Lancet Kiecolt-Glaser JK, et al. Hostile marital interactions, proinflammatory cytokine production, and wound healing.Arch Gen Psychiatry. 2005;62(12):1377–1384. JAMA Network Tawakol A, et al. Relation between resting amygdalar activity and cardiovascular events. Lancet.2017;389(10071):834–845. The Lancet Epel ES, et al. Accelerated telomere shortening in response to life stress. Proc Natl Acad Sci USA.2004;101(49):17312–17315. PNAS McEwen BS, Stellar E. Stress and the individual: mechanisms leading to disease. Arch Intern Med.1993;153(18):2093–2101. PubMed McEwen BS, Wingfield JC. Allostasis and allostatic load. Ann N Y Acad Sci. 1998;840:33–44. PubMed Felitti VJ, et al. Relationship of childhood abuse and household dysfunction to many leading causes of death in adults (ACE Study). Am J Prev Med. 1998;14(4):245–258. AJP Mon Online Edmondson D, et al. PTSD and cardiovascular disease. Ann Behav Med. 2017;51(3):316–327. PMC Afari N, et al. Psychological trauma and functional somatic syndromes: a systematic review and meta-analysis.Psychosom Med. 2014;76(1):2–11. PMC Goyal M, et al. Meditation programs for psychological stress and well-being: a systematic review and meta-analysis. JAMA Intern Med. 2014;174(3):357–368. PMC Qiu Q, et al. Forest therapy: effects on blood pressure and salivary cortisol—a meta-analysis. Int J Environ Res Public Health. 2022;20(1):458. PMC Laukkanen T, et al. Sauna bathing and reduced fatal CVD and all-cause mortality. JAMA Intern Med.2015;175(4):542–548. JAMA Network Zureigat H, et al. Physical activity lowers CVD risk by reducing stress-related neural activity. J Am Coll Cardiol.2024;83(16):1532–1546. PMC Holt-Lunstad J, Smith TB, Layton JB. Social relationships and mortality risk: a meta-analytic review. PLoS Med.2010;7(7):e1000316. PMC Chen Y-R, Hung K-W. EMDR for PTSD: meta-analysis of RCTs. PLoS One. 2014;9(8):e103676. PLOS Hoppen TH, et al. Network/pairwise meta-analysis of PTSD psychotherapies—TF-CBT highest efficacy overall.Psychol Med. 2023;53(14):6360–6374. PubMed van der Kolk BA, et al. Yoga as an adjunctive treatment for PTSD: RCT. J Clin Psychiatry. 2014;75(6):e559–e565. PubMed Kelly U, et al. Trauma-center trauma-sensitive yoga vs CPT in women veterans: RCT. JAMA Netw Open.2023;6(11):e2342214. JAMA Network Bentley TGK, et al. Breathing practices for stress and anxiety reduction: components that matter. Behav Sci (Basel). 2023;13(9):756. 

I have hypothyroidism.  Do I need to be concerned about low ferritin levels?What are the benefits of lower-dose fish oil?Is there a connection between melatonin supplementation and depression?Can I take melatonin while on warfarin?What to do about the state of our healthcare system?

Are children's IQs going down?An overview of medical reversalsCan you comment on the melatonin and heart failure study?Result of a prostate artery embolization

BUFFALO, NY — November 13, 2025 — A new #research paper was #published in Volume 17, Issue 10 of Aging-US on October 3, 2025, titled “The role of phenylalanine and tyrosine in longevity: a cohort and Mendelian randomization study.” In this study led by Jie V. Zhao, Yitang Sun, Junmeng Zhang, and Kaixiong Ye from the University of Hong Kong and the University of Georgia, researchers investigated whether two amino acids, phenylalanine and tyrosine, affect how long people live (lifespan). The results suggest that higher levels of tyrosine are linked to shorter life expectancy in men, pointing to potential sex-specific approaches to promoting longevity. Phenylalanine and tyrosine are amino acids involved in metabolism and brain function. Both are found in protein-rich foods and dietary supplements, but their long-term effects on aging are not well understood. Tyrosine, in particular, is a building block of neurotransmitters such as dopamine, which regulate mood and cognitive function, making it a molecule of interest in aging research. The study analyzed data from more than 270,000 individuals in the UK Biobank. Using both observational and genetic methods, the researchers examined the associations between blood levels of phenylalanine and tyrosine with overall mortality and predicted lifespan. Although both amino acids were initially linked to higher mortality risk, only tyrosine showed a consistent and potentially causal association with reduced life expectancy in men. Genetic analyses estimated that elevated tyrosine levels could shorten men's lifespan by nearly one year. No significant effect was observed in women. These findings remained consistent even after adjusting for related factors, including the role of phenylalanine. This suggests that tyrosine may independently influence aging. The researchers also observed that men tend to have higher tyrosine levels than women, which could partly explain the gender gap in lifespan. “Phenylalanine showed no association with lifespan in either men or women after controlling for tyrosine.” The exact mechanisms behind this effect are still under investigation. However, tyrosine's involvement in insulin resistance and the production of stress-related neurotransmitters may be contributing factors. Insulin resistance is associated with many age-related diseases, and hormone-related pathways influenced by tyrosine may differ between men and women, potentially explaining the sex-specific outcomes. Although tyrosine is commonly marketed as a supplement for enhancing focus and mental performance, the study raises concerns about its long-term impact on lifespan. While the researchers did not directly study tyrosine supplementation, their findings suggest that people with high tyrosine levels may benefit from dietary adjustments. Strategies such as protein restriction could help reduce tyrosine levels and support healthier aging. Further studies are needed to confirm these findings and explore whether diet and lifestyle changes can safely lower tyrosine levels to promote longevity. DOI - https://doi.org/10.18632/aging.206326 Corresponding author - Jie V. Zhao - janezhao@hku.hk Abstract video - https://www.youtube.com/watch?v=rr0G44TD36M Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@Aging-US LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Nutritionist Leyla Muedin discusses the critical health impacts of visceral fat, which is the hidden fat around the organs, and its role in accelerating heart aging. Drawing from recent research conducted by the Medical Research Council and published in the European Heart Journal, she explains how visceral fat differs from subcutaneous fat and its association with inflammation, heart diseases, and premature aging. The episode also highlights the importance of exercise, diet, particularly low-carb intake, and hormone replacement therapy in managing visceral fat and reducing health risks. Leyla also shares practical dietary advice and underscores the significance of focusing on fat distribution over total body weight for better health outcomes.

Vidcast:  https://www.instagram.com/p/DPazFqDjUYF/If you have a problem with alcohol, so-called alcohol use disorder, you are at a more than 50% higher risk of developing dementia.  Epidemiologists from Britain's University of Oxford and Yale studied adults with data in the UK Biobank and the US Million Veteran Program.The tabulated case data revealed that heavy drinkers consuming more than 40 alcoholic drinks/week have 41% higher risk of dementia compared with non-drinkers and those with alcohol use disorder have a 41% higher risk. A genetic analysis shows that every standard deviation increase in the log transformed number of drinks/week is associated with 15% higher dementia risk.The researchers emphasize that those having an occasional drink need not worry about this dementia risk.  Again, moderation is the best policy.https://ebm.bmj.com/content/early/2025/09/16/bmjebm-2025-113913#alcohol #dementia 

Mit den kürzeren Tagen sinkt bei vielen Menschen nicht nur die Energie, sondern auch ihr Vitamin-D-Spiegel. Rutscht er zu sehr ab, hat das Folgen für Leistungsfähigkeit, Immunsystem und Stimmung.Eine neue Studie deutet darauf hin, dass Indoor-Training den im Winter üblichen Vitamin-D-Abfall messbar ausbremst. Kann Deine Fitness-Routine also das Vitamin-D-Supplement ersetzen? Am Ende der Folge bist Du auf Stand und weißt, was das für Dich und Deinen Vitamin-D-Haushalt bedeutet.Außerdem bekommst Du eine klare Strategie an die Hand, um die dunklen Monate von Oktober bis März energiegeladen (und mit vollen Vitamin-D-Speichern) zu überbrücken – statt im Wintermodus auf Reserve zu laufen.____________*WERBUNG: Infos zum Werbepartner dieser Folge und allen weiteren Werbepartnern findest Du hier.____________Tools (Marks Empfehlungen):Vitamin-D-Selbsttest von Medivere.Vitamin-D-Präparat mit 2.000 IE von FormMed (vegane Variante).Weiterführende Inhalte:Download: Ratgeber NahrungsergänzungFolge 502: "Brauchen Sportler Nahrungsergänzung, Herr Ernährungsmediziner?" Mit Niels Schulz-RuhtenbergWissenschaftliche Literatur:Perkin OJ, Davies SE, Hewison M, et al. Exercise without weight loss prevents seasonal decline in vitamin D metabolites: The VitaDEx randomized controlled trial. Advanced Science. 2025;12(22):e2416312.Bikle DD. Vitamin D metabolism, mechanism of action, and clinical applications. Chemistry & Biology. 2014;21(3):319-329.Webb AR, Kazantzidis A, Kift RC, Farrar MD, Wilkinson J, Rhodes LE. Meeting vitamin D requirements in white Caucasians at UK latitudes: Providing a choice. Nutrients. 2018;10(4):497.Lin LY, Smeeth L, Langan S, Warren-Gash C. Distribution of vitamin D status in the UK: a cross-sectional analysis of UK Biobank. BMJ Open. 2021;11(1):e038503.de Oliveira LF, de Azevedo LG, da Mota Santana J, de Sales LPC, Pereira-Santos M. Obesity and overweight decreases the effect of vitamin D supplementation in adults: Systematic review and meta-analysis of randomized controlled trials. Reviews in Endocrine and Metabolic Disorders. 2020;21(1):67-76.Wortsman J, Matsuoka LY, Chen TC, Lu Z, Holick MF. Decreased bioavailability of vitamin D in obesity. Am J Clin Nutr. 2000;72(3):690-693.Drincic AT, Armas LAG, Van Diest EE, Heaney RP. Volumetric dilution, rather than sequestration best explains the low vitamin D status of obesity. Obesity (Silver Spring). 2012;20(7):1444-1448.Ekwaru JP, Zwicker JD, Holick MF, Giovannucci E, Veugelers PJ. The importance of body weight for the dose response relationship of oral vitamin D supplementation and serum 25-hydroxyvitamin D in healthy volunteers. PLoS One. 2014;9(11):e111265.Sun X, Cao ZB, Taniguchi H, Tanisawa K, Higuchi M. Effect of an acute bout of endurance exercise on serum 25(OH)D concentrations in young adults. Journal of Clinical Endocrinology & Metabolism. 2017;102(11):3937-3944.____________Shownotes und Übersicht aller Folgen.Trag Dich in Marks Dranbleiber Newsletter ein.Entdecke Marks Bücher.Folge Mark auf Instagram, Facebook, Strava, LinkedIn. Hosted on Acast. See acast.com/privacy for more information.

Stress isn't just something to “manage” — it's a signal, a teacher, and often, an invitation to look deeper at our health, our choices, and our lives. In this solo episode, Darin reframes stress not as an enemy, but as a dashboard light pointing toward misalignments in our nervous system, environment, relationships, and purpose. Drawing on science, practical tools, and personal insight, Darin reveals how layered stress silently drains our vitality — and how to transform it into an ally for growth, healing, and deeper contentment. Whether it's hidden trauma, toxic environments, unresolved conflict, or the modern distractions constantly pulling at our attention, Darin lays out a roadmap to stop the leaks and reclaim the energy already within you. This episode is a powerful reminder: stress isn't the end of the story — it's the beginning of awareness, safety, and a super life.     What You'll Learn in This Episode [00:00] Introduction to the Super Life podcast [03:27] Why stress might not be your enemy [04:17] Stress as an ally: the signals it gives us about misalignment [04:32] The dashboard light metaphor: how stress reveals hidden issues [05:28] The illusion of “no choice” and the infinite possibilities always available [06:12] Global stress statistics and why most people underestimate their stress load [07:23] Hidden stress revealed through heart rate variability and physiology [08:23] Layered stress: how sleep, exercise, and poor choices compound each other [09:25] Safety vs. calm — why your nervous system craves safety first [10:15] Trauma and the unconscious mind: how old wounds drive our stress response [11:54] Inner narratives and negative self-talk as hidden stress multipliers [12:22] The role of community and your social field in stress and resilience [13:53] Relationships, honesty, and how your circle shapes your energy [14:55] Why boundaries around media and politics are vital for mental clarity [17:42] Finding micro-purpose when life feels overwhelming [18:52] Environmental layers of stress — light, air, and clutter [19:15] The existential layer: stress from living without service or purpose [20:12] Stress as a risk amplifier — how it undermines healing and health [20:55] The deeper truth of safety, connection, and higher power [23:00] Practical tools: breathing, grounding, nature, and conscious choices [24:01] Trauma reframed: not a problem, but a protector at the time [25:25] Lessons from Peter Levine and wild animals: releasing trauma physically [26:04] Questions to ask trauma: “What are you protecting me from?” [26:56] Stress as a multiplier of aging, disease, and poor outcomes [29:20] Why stress isn't a single cause — it's layered and chronic [30:18] Anti-stress strategies: circadian rhythm, nature, and gratitude [31:49] Energy leaks to avoid: clutter, poor food, scrolling, bad boundaries [32:22] What matters most: service, contribution, and alignment [33:28] Final toolkit: breathwork, movement, nature, sleep, and gratitude [34:38] The deeper invitation: step into sovereignty and live your SuperLife     Thank You to Our Sponsors: Manna Vitality: Go to mannavitality.com/  or use code DARIN20 for 20% off your order. Bite Toothpaste: Go to trybite.com/DARIN20 or use code DARIN20 for 20% off your first order.     Find More from Darin Olien: Instagram: @darinolien Podcast: SuperLife Podcast Website: superlife.com Book: Fatal Conveniences Check out my podcast with Dr. Amy Abbington     Key Takeaway “Stress is not the enemy. It's a dashboard light — a teacher showing you where you're out of alignment. When you reframe stress, you reclaim your energy and create space for healing, safety, and the joy of living a super life.”     Bibliography (selected, peer-reviewed) Sources: Gallup Global Emotions (2024); Gallup U.S. polling (2024); APA Stress in America (2023); Natarajan et al., Lancet Digital Health (2020); Orini et al., UK Biobank (2023); Martinez et al. (2022); Leiden University (2025). Cohen S, Tyrrell DA, Smith AP. Psychological stress and susceptibility to the common cold. N Engl J Med.1991;325(9):606–612. New England Journal of Medicine Cohen S, et al. Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk. Proc Natl Acad Sci USA. 2012;109(16):5995–5999. PNAS Kiecolt-Glaser JK, et al. Slowing of wound healing by psychological stress. Lancet. 1995;346(8984):1194–1196. The Lancet Kiecolt-Glaser JK, et al. Hostile marital interactions, proinflammatory cytokine production, and wound healing.Arch Gen Psychiatry. 2005;62(12):1377–1384. JAMA Network Tawakol A, et al. Relation between resting amygdalar activity and cardiovascular events. Lancet.2017;389(10071):834–845. The Lancet Epel ES, et al. Accelerated telomere shortening in response to life stress. Proc Natl Acad Sci USA.2004;101(49):17312–17315. PNAS McEwen BS, Stellar E. Stress and the individual: mechanisms leading to disease. Arch Intern Med.1993;153(18):2093–2101. PubMed McEwen BS, Wingfield JC. Allostasis and allostatic load. Ann N Y Acad Sci. 1998;840:33–44. PubMed Felitti VJ, et al. Relationship of childhood abuse and household dysfunction to many leading causes of death in adults (ACE Study). Am J Prev Med. 1998;14(4):245–258. AJP Mon Online Edmondson D, et al. PTSD and cardiovascular disease. Ann Behav Med. 2017;51(3):316–327. PMC Afari N, et al. Psychological trauma and functional somatic syndromes: a systematic review and meta-analysis.Psychosom Med. 2014;76(1):2–11. PMC Goyal M, et al. Meditation programs for psychological stress and well-being: a systematic review and meta-analysis. JAMA Intern Med. 2014;174(3):357–368. PMC Qiu Q, et al. Forest therapy: effects on blood pressure and salivary cortisol—a meta-analysis. Int J Environ Res Public Health. 2022;20(1):458. PMC Laukkanen T, et al. Sauna bathing and reduced fatal CVD and all-cause mortality. JAMA Intern Med.2015;175(4):542–548. JAMA Network Zureigat H, et al. Physical activity lowers CVD risk by reducing stress-related neural activity. J Am Coll Cardiol.2024;83(16):1532–1546. PMC Holt-Lunstad J, Smith TB, Layton JB. Social relationships and mortality risk: a meta-analytic review. PLoS Med.2010;7(7):e1000316. PMC Chen Y-R, Hung K-W. EMDR for PTSD: meta-analysis of RCTs. PLoS One. 2014;9(8):e103676. PLOS Hoppen TH, et al. Network/pairwise meta-analysis of PTSD psychotherapies—TF-CBT highest efficacy overall.Psychol Med. 2023;53(14):6360–6374. PubMed van der Kolk BA, et al. Yoga as an adjunctive treatment for PTSD: RCT. J Clin Psychiatry. 2014;75(6):e559–e565. PubMed Kelly U, et al. Trauma-center trauma-sensitive yoga vs CPT in women veterans: RCT. JAMA Netw Open.2023;6(11):e2342214. JAMA Network Bentley TGK, et al. Breathing practices for stress and anxiety reduction: components that matter. Behav Sci (Basel). 2023;13(9):756. 

00:50 The AI tool that predicts disease riskResearchers have developed an AI tool that can calculate a person's risk of developing over 1,000 different diseases, sometimes years in advance. The system, called Delphi-2M, was trained to identify patterns of disease progression using 400,000 people's health records from data repository the UK Biobank. This training allowed it to predict someone's future disease risks, based on their current medical record. While AI health prediction systems do exist, they typically only estimate risks for a single disease — the authors hope that their system could one day save healthcare professionals time and be used to calculate disease burdens at a population level.Research Article: Shmatko et al.News: What diseases will you have in 20 years? This AI makes predictions11:01 Research HighlightsEvidence that refugees hosted by local families integrate better into their adoptive country — plus, the squidgy shirt that can keep wearers cool.Research Highlight: How to help refugees thrive: have local families host themResearch Highlight: Jelly-filled garment keeps wearers cool when heat and humidity soar13:50 Give an AI a task and it may cheat for youUsing AI tools may make you more likely to cheat at tasks like tax reporting, according to a new study. Using a well-studied test of honesty, researchers looked to see if people were more likely to engage in unethical behaviour if given the option of delegating it to an AI. Including AIs seemed to increase the chance that someone would be dishonest, which raises concerns about the impacts of these tools on ethics.Research Article: Köbis et alNews and Views: People are more likely to cheat when they delegate tasks to AI24:54 Briefing ChatEurope has a new supercomputer, JUPITER, that could boost its AI ambitions, and a catalogue of octopus movement.Nature: World's most energy-efficient AI supercomputer comes onlineNew York Times: Building an Octopus Dictionary, One Arm Movement at a TimeSubscribe to Nature Briefing, an unmissable daily round-up of science news, opinion and analysis free in your inbox every weekday. Hosted on Acast. See acast.com/privacy for more information.

Welcome to the Olink® Proteomics in Proximity podcast!  Below are some useful resources mentioned in this episode:  Olink tools and software·       Olink® Explore HT, Olink's most advanced solution for high-throughput biomarker discovery, measuring 5400+ proteins simultaneously with a streamlined workflow and industry-leading specificity: https://olink.com/products-services/exploreht/  UK Biobank Pharma Proteomics Project (UKB-PPP), one of the world's largest scientific studies of blood protein biomarkers conducted to date, https://www.ukbiobank.ac.uk/learn-more-about-uk-biobank/news/uk-biobank-launches-one-of-the-largest-scientific-studies  World Health Organization (2003). Adherence to long-term therapies: evidence for action (PDF). Geneva: World Health Organisation. ISBN 978-92-4-154599-0 Research articles and news·       Thermo Fisher Scientific's Olink Platform Selected for World's Largest Human Proteome Studyhttps://ir.thermofisher.com/investors/news-events/news/news-details/2025/Thermo-Fisher-Scientifics-Olink-Platform-Selected-for-Worlds-Largest-Human-Proteome-Study/default.aspx·       Hamilton Se-Hwee Oh et al 2025. Plasma proteomics links brain and immune system aging with healthspan and longevityhttps://www.nature.com/articles/s41591-025-03798-1. Nature Medicine (2025)·       Song, Y., Abuduaini, B., Yang, X. et al. Identification of inflammatory protein biomarkers for predicting the different subtype of adult with tuberculosis: an Olink proteomic study. Inflamm. Res. 74, 60 (2025). https://doi.org/10.1007/s00011-025-02020-9·       Ferhan Qureshi et al 2023. Analytical validation of a multi-protein, serum-based assay for disease activity assessments in multiple sclerosis. Proteomics clinical application 2023·       Dhindsa, R.S., Burren, O.S., Sun, B.B. et al. Rare variant associations with plasma protein levels in the UK Biobank. 2023 Nature, DOI: 10.1038/s41586-023-06547-xhttps://www.nature.com/articles/s41586-023-06547-x·       Sun, B.B., Chiou, J., Traylor, M. et al.  Plasma proteomic associations with genetics and health in the UK Biobank. 2023 Nature, DOI: 10.1038/s41586-023-06592-6 https://www.nature.com/articles/s41586-023-06592-6 https://academic.oup.com/eurheartj/advance-article/doi/10.1093/eurheartj/ehac495/6676779·       Eldjarn GH, et al. Large-scale plasma proteomics comparisons through genetics and disease associations. Nature. 2023 Oct;622(7982):348-358. doi: 10.1038/s41586-023-06563-xhttps://www.nature.com/articles/s41586-023-06563-x#Sec44·        Carrasco-Zanini et al 2024 Proteomic prediction of common and rare diseases. https://www.nature.com/articles/s41591-024-03142-z . NatureMedicine volume 30,  pages2489–2498 (2024)·       Watanabe K, Wilmanski T, Diener C, et al. Multiomic signatures of body mass index identify heterogeneous health phenotypes and responses to a lifestyle intervention.https://www.nature.com/articles/s41591-023-02248-0·       Petrera A, von Toerne C, Behlr J, et al. Multiplatform Approach for Plasma Proteomics: Complementarity of Olink Proximity Extension Assay Technology to Mass Spectrometry-Based Protein Profiling. (2020) Journal of Proteome Research, https://pubs.acs.org/doi/pdf/10.1021/acs.jproteome.0c00641·       Multicenter Collaborative Study to Optimize Mass Spectrometry Workflows of Clinical Specimens. Kardell O, von Toerne C, Merl-Pham J, König AC, Blindert M, Barth TK, Mergner J, Ludwig C, Tüshaus J, Eckert S, Müller SA, Breimann S, Giesbertz P, Bernhardt AM, Schweizer L, Albrecht V, Teupser D, Imhof A, Kuster B, Lichtenthaler SF, Mann M, Cox J, Hauck SM. J Proteome Res. 2024 Jan 5;23(1):117-129. doi: 10.1021/acs.jproteome.3c00473. Epub 2023 Nov 28. PMID: 38015820 https://pubs.acs.org/doi/10.1021/acs.jproteome.3c00473·       Wei, S., Shen, R., Lu, X. et al. Integrative multi-omics investigation of sleep apnea: gut microbiome metabolomics, proteomics and phenome-wide association study. Nutr Metab (Lond) 22, 57 (2025). https://doi.org/10.1186/s12986-025-00925-0·       Liu, L., Li, M., Qin, Y. et al. Childhood obesity and insulin resistance is correlated with gut microbiome serum protein: an integrated metagenomic and proteomic analysis. Sci Rep 15, 21436 (2025). https://doi.org/10.1038/s41598-025-07357-z·       Zhang, Xiaotao et al.Modulating a prebiotic food source influences inflammation and immune-regulating gut microbes and metabolites: insights from the BE GONE trial. eBioMedicine, Volume 98, 104873 (2023.).  10.1016/j.ebiom.2023.104873·      &nb...

Credits: 0.25 AMA PRA Category 1 Credit™   CME/CE Information and Claim Credit: https://www.pri-med.com/online-education/podcast/frankly-speaking-cme-443 Overview: In this episode, we evaluate the correlation between an increase in physical activity and step count and a reduction in cancer risk. We break down new evidence, equipping you with practical guidance for counseling patients on simple, impactful behavior changes to support long-term health. Episode resource links: Shreves AH, Small SR, Walmsley R, et al. Amount and intensity of daily total physical activity, step count and risk of incident cancer in the UK Biobank. Br J Sports Med. Published online 2025. doi:10.1136/bjsports-2024-109360 Islami, F., Goding Sauer, A., Miller, K.D., Siegel, R.L., Fedewa, S.A., Jacobs, E.J., McCullough, M.L., Patel, A.V., Ma, J., Soerjomataram, I., Flanders, W.D., Brawley, O.W., Gapstur, S.M. and Jemal, A. (2018), Proportion and number of cancer cases and deaths attributable to potentially modifiable risk factors in the United States. CA: A Cancer Journal for Clinicians, 68: 31-54. https://doi.org/10.3322/caac.21440 Guest: Jillian Joseph, PA-C   Music Credit: Matthew Bugos Thoughts? Suggestions? Email us at FranklySpeaking@pri-med.com   

Credits: 0.25 AMA PRA Category 1 Credit™   CME/CE Information and Claim Credit: https://www.pri-med.com/online-education/podcast/frankly-speaking-cme-443 Overview: In this episode, we evaluate the correlation between an increase in physical activity and step count and a reduction in cancer risk. We break down new evidence, equipping you with practical guidance for counseling patients on simple, impactful behavior changes to support long-term health. Episode resource links: Shreves AH, Small SR, Walmsley R, et al. Amount and intensity of daily total physical activity, step count and risk of incident cancer in the UK Biobank. Br J Sports Med. Published online 2025. doi:10.1136/bjsports-2024-109360 Islami, F., Goding Sauer, A., Miller, K.D., Siegel, R.L., Fedewa, S.A., Jacobs, E.J., McCullough, M.L., Patel, A.V., Ma, J., Soerjomataram, I., Flanders, W.D., Brawley, O.W., Gapstur, S.M. and Jemal, A. (2018), Proportion and number of cancer cases and deaths attributable to potentially modifiable risk factors in the United States. CA: A Cancer Journal for Clinicians, 68: 31-54. https://doi.org/10.3322/caac.21440 Guest: Jillian Joseph, PA-C   Music Credit: Matthew Bugos Thoughts? Suggestions? Email us at FranklySpeaking@pri-med.com   

Omega-3 fatty acids have long been lauded for heart health benefits. Yet, emerging research now points to an even more profound impact, directly on our most complex organ: the brain. Today, we delve into the critical, often misunderstood, role of omega-3s in cognitive function, mental well-being, and even the prevention of neurodegenerative conditions like dementia. We are joined by Dr. Bill Harris, a globally recognised authority in omega-3 fatty acid research. Bill is a Professor at the University of South Dakota and has over 300 peer-reviewed publications. His foundational work includes pioneering studies on fish oil in the 1980s and shaping American Heart Association scientific statements. In this episode, Dr. Harris - along with ZOE's Chief Scientist Professor Sarah Berry - illuminate why most individuals may be operating with suboptimal omega-3 levels, and the tangible implications this has for mood regulation, anxiety, and long-term brain resilience. We navigate nuances between omega-3 types like EPA and DHA, debunk common misconceptions surrounding plant-based sources and mercury content in fish, and explore the precise methods for assessing and improving your own "Omega-3 Index." Unwrap the truth about your food

The Story So Far The mid-20th century was the golden age of nurture. Psychoanalysis, behaviorism, and the spirit of the ‘60s convinced most experts that parents, peers, and propaganda were the most important causes of adult personality. Starting in the 1970s, the pendulum swung the other way. Twin studies shocked the world by demonstrating that most behavioral traits - especially socially relevant traits like IQ - were substantially genetic. Typical estimates for adult IQ found it was about 60% genetic, 40% unpredictable, and barely related at all to parenting or family environment. By the early 2000s, genetic science reached a point where scientists could start pinpointing the particular genes behind any given trait. Early candidate gene studies, which hoped to find single genes with substantial contributions to IQ, depression, or crime, mostly failed. They were replaced with genome wide association studies, which accepted that most interesting traits were polygenic - controlled by hundreds or thousands of genes - and trawled the whole genome searching for variants that might explain 0.1% or even 0.01% of the pie. The goal shifted toward polygenic scores - algorithms that accepted thousands of genes as input and spit out predictions of IQ, heart disease risk, or some other outcome of interest. The failed candidate gene studies had sample sizes in the three or four digits. The new genome-wide studies needed five or six digits to even get started. It was prohibitively difficult for individual studies to gather so many subjects, genotype them, and test them for the outcome of interest, so work shifted to big centralized genome repositories - most of all the UK Biobank - and easy-to-measure traits. Among the easiest of all was educational attainment (EA), ie how far someone had gotten in school. Were they a high school dropout? A PhD? Somewhere in between? This correlated with all the spicy outcomes of interest people wanted to debate - IQ, wealth, social class - while being objective and easy to ask about on a survey. Twin studies suggested that IQ was about 60% genetic, and EA about 40%. This seemed to make sense at the time - how far someone gets in school depends partly on their intelligence, but partly on fuzzier social factors like class / culture / parenting. The first genome-wide studies and polygenic scores found enough genes to explain 2%pp1 of this 40% pie. The remaining 38%, which twin studies deemed genetic but where researchers couldn't find the genes - became known as “the missing heritability” or “the heritability gap”. Scientists came up with two hypothesis for the gap, which have been dueling ever since: Maybe twin studies are wrong. Maybe there are genes we haven't found yet For most of the 2010s, hypothesis 2 looked pretty good. Researchers gradually gathered bigger and bigger sample sizes, and found more and more of the missing heritability. A big 2018 study increased the predictive power of known genes from 2% to 10%. An even bigger 2022 study increased it to 14%, and current state of the art is around 17%. Seems like it was sample size after all! Once the samples get big enough we'll reach 40% and finally close the gap, right? This post is the story of how that didn't happen, of the people trying to rehabilitate the twin-studies-are-wrong hypothesis, and of the current status of the debate. Its most important influence/foil is Sasha Gusev, whose blog The Infintesimal introduced me to the new anti-hereditarian movement and got me to research it further, but it's also inspired by Eric Turkheimer, Alex Young (not himself an anti-hereditarian, but his research helped ignite interest in this area), and Awais Aftab. (while I was working on this draft, the East Hunter Substack wrote a similar post. Theirs is good and I recommend it, but I think this one adds enough that I'm publishing anyway) https://www.astralcodexten.com/p/missing-heritability-much-more-than

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