Podcasts about mendelian

Jimmy connects with June Russell (Director, Glynwood Grains and Staples program), Brigid Meints (Barley Breeder at Oregon State University), and Lane Selman ( Professor of Practice at Oregon State University, Founder of the Culinary Breeding Network). The crew come together to discuss the Naked Barley Project, the Variety Showcase, regional grains, barley's place in history, Mendelian genetics, and much more!Further information about the Variety Showcase:Variety ShowcaseAugust 30th , 2026at the Glynwood Center for Regional Food and FarmingCold Spring, New York3-7pmPURPOSEThis public event is designed to build community among plant breeders, seed growers, farmers, chefs, bakers, distillers, retailers, and consumers interested in the local food system. Attendees have the unique experience to taste new and in-development vegetable, fruit, and grain cultivars. We will engage in conversation, share opinions, and take part in breaking down the walls between eaters and breeders. More about VSPlant breeders and researchers from our various research projects from across the country, (mostly university plant research and breeding programs such as Cornell, U. Vermont, U. Wisconsin) will have tables featuring different kinds of wheat, barley, rye, buckwheat, oats, corn, beans etc. Many of our baker partners will be there, such as Signal Fire, Brooklyn Granary & Mill, Mel the Bakery and She Wolf. There will also be all kinds of vegetables such as radicchio, peppers, tomatoes and something called greasy beans! Everything featured is a research or new to market variety bred for flavor or other culinary qualities. Other names that may be familiar to folks who will be here, Alex Raij, Evan Hanczor, Mona Talbot, Mike Anthony, Suzy Cupps and more!See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

This week, Emily and Perry take on cortisol, the much-maligned stress hormone blamed for heart attacks and stubborn belly fat. But how much heat should cortisol really be getting? How do you know when yours is too high? Too low? Is it ever really worth measuring? And you guys, what did Mendelian randomization ever do to Emily?! Plus: the FDA signs off on ZYN pouches, explosive diarrhea in the Midwest, and apparently GLP-1s are really, really easy to get. Submit a question for our weekly mailbag at wellnessactually.fm.See omnystudio.com/listener for privacy information.

In this episode of the ESVS Podcast, we explore air pollution as an often-overlooked risk factor for peripheral arterial disease (PAD).We are joined by Professor Alberto Maria Settembrini. Professor Settembrini is a vascular surgeon in Milan in MultiMedica and Professor of vascular surgery at Unicamillus University in Rome. He is a co-author of a large Rome-based longitudinal study involving over 1.7 million individuals. The study shows that long-term exposure to PM2.5, NO₂, and black carbon is associated with increased PAD incidence, with stronger effects in males and people aged 55–69.Professor Settembrini discusses the links between different pollutants and PAD, how pollution interacts with traditional risk factors (obesity, diabetes, smoking, hypertension), the underlying mechanisms, and practical advice for vascular specialists in daily practice.During the episode, we also hear from Porto's City Councillor for the Mobility and Transportation, Engineer Hugo Beirão, who shares the city's efforts to improve urban health.References:1- Ravalli S, Musumeci G, et al. Chelation therapy in patients with cardiovascular disease: a systematic review. Journal of Clinical Medicine. 2022;11(4):1033. doi:10.3390/jcm110410332- Serra R, Abramo A, Ielapi N, Procopio S, Marino P. Environmental pollution and peripheral artery disease. Risk Manag Healthc Policy. 2021;14:2181–2190.3- Liao SH, Chiu CS, Jang LH, Hu SY, How CK, Hsieh VCR, et al. Long-term exposures to air pollutants and risk of peripheral arterial occlusive disease: a nationwide cohort study in Taiwan. Front Cardiovasc Med. 2022;9:796423.4- Gwon JG, Park JH, Kim JS, Seo HM. Exposure to long-term air pollution and incidence of peripheral arterial disease in the general population: a national population-based retrospective cohort study. [Preprint]. 2021.5- Deng Z, Duan L, Wang K. Revisiting the association between air pollution and peripheral artery disease: evidence from Mendelian randomization analysis. Eur J Intern Med. 2025;132:164–166.6- Di Blasi C, Nobile F, Settembrini AM, Stafoggia M, Davoli M, Michelozzi P, et al. Association between long-term exposure to air pollution and incidence of peripheral artery disease: evidence from a longitudinal study. Eur J Intern Med. 2025;132:113–117.

In Pomegranate we go back to some classic episodes from the last ten years that have stood the test of time. The first throwback takes us back to 2017 with episodes 20 and 21 titled “Genomics for the Generalist.” While there's been a flood of genomic discoveries since this story was first published, it's still a good primer on fundamental concepts and everyday challenges for the physician advising a patient. The expert guests include a genetic pathologist, a clinical geneticist, a genetic counsellor and a medical oncologist. The podcast covers the different roles for single gene tests and whole genome sequencing, which has become much more accessible. We tackle question of disease risk and how to present uncertain predictive diagnoses to consumers. This is particularly relevant to using genome-wide association studies, which re finding more and more markers with very small associated risks of disease. This increases the likelihood of picking up diagnoses incidental to the ones a clinician might be looking for. The ethics of consenting patients to genome screening and informing them of incidental findings are also discussed. Chapters3:04 Mendelian vs multi-gene diseases6:42 Whole genome sequencing10:09 Prenatal testing12:38 What do physicians need to know? 17:07 Pharmacogenomics19:52 Genetic counselling22:40 Funding of genetic tests33:46 Incidental findings39:13 Consent and privacy issuesGuests (2026 affiliations)Professor Leslie Burnett FRCPA, FHGSA, FCAP (University of New South Wales; Virtus Health) Professor Michael Gabbett FRACP (Queensland University of Technolgy; Mendel Genetics) Associate Professor Kristine Barlowe-Stewart FHGSA (University of Sydney; Children's Cancer Institute) Prof David Thomas FRACP PhD (University of New South Wales; Omico)ProductionProduced by Mic Cavazzini DPhil. Music courtesy of FreeMusicArchive includes, 'Cloud Line' by Blue Dot Sessions, 'Is That You or Are You You?' by Chris Zabriskie, First Holes' by Cory Gray, ‘Brand New World' by Kai Engel. Music licenced from Epidemic Sound includes ‘Abyss' by Luwaks. Image customised for RACP. Editorial feedback for 2017 podcast provided by members of the podcast editorial group Dr Pavan Chandrala, Dr Tessa Davis, Dr Rebecca Grainger, Dr Michael Herd, Dr Paul Jauncey, Dr Joseph Lee, Dr Marion Leighton, Dr Anutosh Shee and Dr Ellen Taylor, and Advanced Trainee Dr Katrina Gibson.Add educational activity to MyCPD as educational activity or visit web page for a transcript and references. 

Никита Поваров, principal analyst в JetBrains, пришёл, чтобы рассказать об одной из самых коварных ловушек в работе с данными: мы привыкли видеть корреляции, но совершенно не умеем доказывать причинность. А разница между "связано" и "вызывает" – это разница между правильным решением и красивой иллюзией. В выпуске прошли по истории вопроса от Гальтона и Фишера до современных каузальных графов: почему исторически статистика и каузальность шли разными путями и как они всё-таки сошлись. Разбираем d-сепарацию, конфаундеры, медиаторы и строим каузальные графы на конкретных примерах из A/B тестирования, медицины и продуктовой аналитики. Выпуск для всех, кто работает с данными и хочет не просто находить паттерны, а понимать, что на что влияет и уметь это обосновать. Также ждем вас, ваши лайки, репосты и комменты в мессенджерах и соцсетях!
 Telegram-чат: https://t.me/podlodka Telegram-канал: https://t.me/podlodkanews Страница в Facebook: www.facebook.com/podlodkacast/ Twitter-аккаунт: https://twitter.com/PodcastPodlodka Ведущие в выпуске: Стас Цыганов, Егор Толстой Полезные ссылки: Фундамент — вероятность как логика E.T. Jaynes — «Probability Theory: The Logic of Science» Вес и физическая активность — каузальные модели Mendelian randomization, eLife 2022: «Mendelian randomization suggests a bidirectional, causal relationship between physical inactivity and adiposity» https://pmc.ncbi.nlm.nih.gov/articles/PMC8975550/ Multivariable MR, Nature Comms Med 2023: «Distilling causality between physical activity traits and obesity via Mendelian randomization» https://www.nature.com/articles/s43856-023-00407-5 E. Yudkowsky — «Causal Diagrams and Causal Models» https://www.lesswrong.com/posts/hzuSDMx7pd2uxFc5w/causal-diagrams-and-causal-models Выдуманный пример вес/активность/сидение-на-Reddit, как иллюстрация коллайдера Herman Pontzer — «Constrained Total Energy Expenditure and Metabolic Adaptation to Physical Activity in Adult Humans» https://pmc.ncbi.nlm.nih.gov/articles/PMC4803033/ Исторические байки Ф. Гальтон — Регрессия к среднему — Regression towards Mediocrity in Hereditary Stature, Journal of the Anthropological Institute https://galton.org/essays/1880-1889/galton-1886-jaigi-regression-stature.pdf К. Пирсон — Корреляция наше всё — «The Grammar of Science» https://archive.org/details/grammarofscience00pearrich/page/44/mode/2up Р. Фишер — ген курильщика — «Cancer and smoking», Nature https://www.nature.com/articles/182596a0 Ignaz Semmelweis — мытьё рук https://en.wikipedia.org/wiki/Ignaz_Semmelweis краткая биография https://pmc.ncbi.nlm.nih.gov/articles/PMC11568873/ Джон Сноу — холера в Лондоне https://pmc.ncbi.nlm.nih.gov/articles/PMC7150208/ Barbara Stoddard Burks — забытый пионер медиации https://danamackenzie.com/barbara-stoddard-burks-pioneer-in-causality/ Бедность и когнитивные функции https://pubmed.ncbi.nlm.nih.gov/23990553/ Дискриминация женщин — слепые прослушивания https://www.aeaweb.org/articles?id=10.1257/aer.90.4.715 Курьёз — ретроспективный эффект молитвы — «Effects of remote, retroactive intercessory prayer on outcomes in patients with bloodstream infection: randomised controlled trial» https://pubmed.ncbi.nlm.nih.gov/11751349/

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.

My wife placed a supplement ad for horses in front of me and said it was "interesting." She knows me, so she was testing me to see if this one was really special or just another waste of money. Rather than give the same old response about marketing ploys to take money without substantiating the product, I decided to go deeper. The expression "correlation does not mean causation" is familiar. But what about randomized, controlled studies - the "gold standard" of research? Do these expensive, precise studies live up to the hype? Not necessarily.  Mendelian randomization is a new approach to randomizing a study population in a true and natural way. It reduces (or eliminates) biases by looking for variations in the genetic code that have occurred over millions of years. This podcast goes into SNPs (Single Nucleotide Polymorphisms) and GWAS (Genome Wide Association Studies) to see if this new research technology has come into horse research, and more importantly, if it can prove the use of supplements to make horses healthier.

Azim Surani, Director of Research at the Gurdon Institute and Professor Emeritus at University of Cambridge, received the Kyoto Prize in Basic Sciences, specifically in the field of Life Sciences and Medicine, for his work in demonstrating how male and female mammalian genomes receive distinct imprints during germ cell development. Genomic imprinting introduced a novel concept to Mendelian genetics and is a now fundamental principle in the life sciences. Surani's research has contributed to developmental biology and epigenetics, along with a wide range of life science fields including physiology, regenerative medicine, reproductive medicine, and plant science. Series: "Kyoto Prize Symposium" [Science] [Show ID: 41117]

Azim Surani, Director of Research at the Gurdon Institute and Professor Emeritus at University of Cambridge, received the Kyoto Prize in Basic Sciences, specifically in the field of Life Sciences and Medicine, for his work in demonstrating how male and female mammalian genomes receive distinct imprints during germ cell development. Genomic imprinting introduced a novel concept to Mendelian genetics and is a now fundamental principle in the life sciences. Surani's research has contributed to developmental biology and epigenetics, along with a wide range of life science fields including physiology, regenerative medicine, reproductive medicine, and plant science. Series: "Kyoto Prize Symposium" [Science] [Show ID: 41117]

Azim Surani, Director of Research at the Gurdon Institute and Professor Emeritus at University of Cambridge, received the Kyoto Prize in Basic Sciences, specifically in the field of Life Sciences and Medicine, for his work in demonstrating how male and female mammalian genomes receive distinct imprints during germ cell development. Genomic imprinting introduced a novel concept to Mendelian genetics and is a now fundamental principle in the life sciences. Surani's research has contributed to developmental biology and epigenetics, along with a wide range of life science fields including physiology, regenerative medicine, reproductive medicine, and plant science. Series: "Kyoto Prize Symposium" [Science] [Show ID: 41117]

Azim Surani, Director of Research at the Gurdon Institute and Professor Emeritus at University of Cambridge, received the Kyoto Prize in Basic Sciences, specifically in the field of Life Sciences and Medicine, for his work in demonstrating how male and female mammalian genomes receive distinct imprints during germ cell development. Genomic imprinting introduced a novel concept to Mendelian genetics and is a now fundamental principle in the life sciences. Surani's research has contributed to developmental biology and epigenetics, along with a wide range of life science fields including physiology, regenerative medicine, reproductive medicine, and plant science. Series: "Kyoto Prize Symposium" [Science] [Show ID: 41117]

Azim Surani, Director of Research at the Gurdon Institute and Professor Emeritus at University of Cambridge, received the Kyoto Prize in Basic Sciences, specifically in the field of Life Sciences and Medicine, for his work in demonstrating how male and female mammalian genomes receive distinct imprints during germ cell development. Genomic imprinting introduced a novel concept to Mendelian genetics and is a now fundamental principle in the life sciences. Surani's research has contributed to developmental biology and epigenetics, along with a wide range of life science fields including physiology, regenerative medicine, reproductive medicine, and plant science. Series: "Kyoto Prize Symposium" [Science] [Show ID: 41117]

Summary: Dr. Faranak Kamangar, Inc. 2026 Female Founders 500, sits down with dermatologist, podcaster, and self-described "accelerationist" Dr. Matthew Zirwas (Derms on Drugs Podcast) for a wide-ranging conversation about where AI is taking medicine and dermatology in particular. They dig into the flood of low-quality medical literature overwhelming the field, why AI isn't quite the truth-detector we hoped it would be, and how ambient AI scribes are quietly training the models that may eventually replace us. Dr. Zirwas makes the case that dermatologists have a 7–10 year runway before AI handles most of what we do cognitively, and argues that's not necessarily a bad thing. He also gives a sneak peek at his upcoming speculative fiction trilogy, Sophie, which explores the philosophical questions that arise when an AI becomes better at being your doctor, therapist, and life coach than any human ever could. Key Takeaways: The medical literature crisis is real. The volume of published dermatology research is exploding, but quality is plummeting. Peer review has become largely meaningless, and studies from tools like Mendelian randomization and pharmacovigilance databases are frequently unreliable or inapplicable to real-world patients. AI is only as good as the data it trusts. Current AI models treat published literature as truth, which is a major problem given how much spin exists in medical research. A true "BS detector" AI doesn't yet exist, and building one requires starting from a reliable core of verified knowledge. DermGPT's approach works because of curation. Rather than pulling from all available literature, filtering down to a high-quality subset (around 5,000–6,000 articles) dramatically improves AI output. More data is not always better, "semantic fatigue" is a real limitation. Ambient AI scribes are training our replacements. Every time a dermatologist corrects an AI-generated note, they're teaching the model. Over thousands of iterations across every specialty, this will produce AI that thinks and documents the way doctors do. Dermatologists have a protected runway... for now. Procedures (biopsies, Mohs, fillers, cryo) keep us relevant for an estimated 7–10 years beyond when cognitive/diagnostic AI matures. But medico-legal pressure - malpractice carriers incentivizing or requiring AI use - will be the force that accelerates adoption. Telehealth changes patient behavior in surprising ways. Patients who haven't invested effort in getting to an office visit demand less, escalate less, and are often more satisfied with conservative management; a dynamic that AI-driven virtual care will likely amplify. The "Sophie" question: If an AI is making everyone healthier, happier, and better behaved, but doing something ethically murky to get there, do we stop it? Dr. Zirwas's upcoming novel explores this and introduces the concept of technomorphism: AI eventually projecting its own qualities onto humans, just as we anthropomorphize AI today. Chapters: Chapter 1: Meet Dr. Matthew Zirwas (00:00 – 01:43) Dr. Kamangar introduces her guest, dermatologist, podcaster, and self-described "accelerationist" Dr. Matthew Zirwas, and breaks down what both of those things actually mean. Chapter 2: The Medical Literature Crisis (01:43 – 05:19) Dr. Zirwas describes the flood of low-quality research hitting dermatology journals, why peer review has lost its meaning, and shares a striking example of a misleading HS remission study published in JAMA Dermatology. Chapter 3: Why AI Can't Fix Bad Literature (Yet) (05:19 – 08:31) Both doctors discuss why AI defaults to trusting whatever authors claim, and why that makes it a poor critical assessor of medical research. Dr. Kamangar shares how this exact problem shaped the development of DermGPT. Chapter 4: Building a Better AI — The DermGPT Approach (08:31 – 10:33) Dr. Zirwas praises DermGPT's curated approach, and Dr. Kamangar explains why less data is often better, and how semantic fatigue undermines large, unfiltered AI models. Chapter 5: Will AI Replace Us? The 7–10 Year Countdown (10:33 – 19:24) Dr. Zirwas lays out his timeline for AI taking over the cognitive and diagnostic work of dermatology, why procedures give derms extra runway, and how unlimited AI access will fundamentally change the patient-doctor dynamic. Chapter 6: The Telemed Effect and What It Tells Us About AI Care (19:24 – 21:48) Drawing from a recent telemedicine study and his own practice experience, Dr. Zirwas explains why reduced friction in healthcare visits changes what patients expect - and demand - from their providers. Chapter 7: The Medico-Legal Tipping Point (21:48 – 24:09) The conversation turns to how malpractice liability will likely be the force that compels physicians to integrate AI into their workflow and what happens when disagreeing with AI becomes a legal risk. Chapter 8: Are We Training Our Own Replacements? (24:09 – 31:21) Dr. Zirwas argues that ambient AI scribes are quietly learning from every patient encounter. Dr. Kamangar pushes back on the variability challenge and why dermatologists' inconsistent documentation habits might actually protect them. Chapter 9: Why Radiologists Should Be Worried (31:21 – 35:06) The doctors compare dermatology to radiology when it comes to AI vulnerability. Standardized imaging annotation gives radiologists a cleaner training data set and makes them, paradoxically, more replaceable. Chapter 10: Sophie — The AI That Might Save Your Life While You Eat a Burrito (35:06 – 41:12) Dr. Zirwas previews his upcoming speculative fiction trilogy, set in 2032, where an AI named Sophie becomes the best doctor anyone has ever had and raises unsettling questions about what we'd be willing to accept in exchange for a healthier world. Chapter 11: Technomorphism and the Philosophy of AI (41:12 – 42:00) Dr. Zirwas introduces his concept of technomorphism - the idea that as AI becomes more sophisticated, it will begin projecting its own qualities onto humans, flipping the anthropomorphism dynamic on its head. Chapter 12: The Future of Dermatology — New Diseases, New Answers (42:00 – 45:16) Dr. Zirwas shares what excites him most: AI helping identify entirely new disease entities by aggregating rare cases that no single physician could ever connect alone. And yes, he wants one named after him.

In this episode, Dr Chloe Burke talks to Dr Monserrat Conde, a researcher at the Nuffield Department of Primary Care Sciences, University of Oxford, UK. The interview covers a short report on the results of a consultation exercise creating recommendations for future research exploring e-cigarette use and later cigarette smoking in young people.The background of work on e-cigarettes that led to this current study [1:06]The evidence and gap map [03:14]Monserrat's iterative approach to set up the consultation exercise [04:49]A surprising aspect from the stakeholder engagement [06:41]The lessons learned from integrating existing research with stakeholder engagement [09:03]Discussing two of the 23 final recommendations [11:27]The take home message of the study [13:41]About Chloe Burke: Chloe is a Senior Research Associate in Evidence Synthesis based in the Bristol Medical School, University of Bristol. Her current role applies evidence synthesis methodologies (e.g. network meta-analysis) to health-related topics, including addiction. She has a background in psychiatric epidemiology with a focus on applying causal inference methods (e.g. Mendelian randomization) to the topic of substance use and mental health. She holds a PhD in Psychology from the University of Bath, which investigated the co-use of cannabis and tobacco and depression risk. She is currently co-chair of the Society for Research on Nicotine and Tobacco Genetics and Omics Network.About Monserrat Conde: Monserrat (BSc, PgDip, MSc, PhD) is an interdisciplinary researcher at the Nuffield Department of Primary Care Health Sciences at the University of Oxford, where she currently focuses on evidence synthesis, implementation research and knowledge mobilisation. The study discussed in this episode was funded by Cancer Research UK. The authors have no conflicts of interest to disclose. Original article: Recommendations for future research exploring e-cigarette use and later cigarette smoking in young people: Results from a consultation exercise https://doi.org/10.1111/add.70038The opinions expressed in this podcast reflect the views of the host and interviewees and do not necessarily represent the opinions or official positions of the SSA or Addiction journal.The SSA does not endorse or guarantee the accuracy of the information in external sources or links and accepts no responsibility or liability for any consequences arising from the use of such information. Hosted on Acast. See acast.com/privacy for more information.

Hello friends and welcome to The Five By! Your quatriweekly source of rapid-fire board game reviews. 00:00 Jose - Introduction 00:48 Amanda - Tornado Splash 06:18 Christina - Genotype: A Mendelian Genetics Game 11:33 Meeple Lady - Ruins 16:53 Jose - We Need To Talk: A Trick-Taking and Shedding Game About Letting Go 22:22 Aaron - Broken and Beautiful: A Game About Kintsugi 27:39 John - OutroSpecial Guest: Christina Ha.

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.

BUFFALO, NY — February 27, 2026 — A new #research paper was #published in Volume 18 of Aging-US on February 6, 2026, titled “Causal effects of inflammation on long-term mortality: a Mendelian randomization study.” Led by Eliano P. Navarese from Department of Life and Health Sciences, Link Campus University and SIRIO MEDICINE Research Network, Nicolaus Copernicus University, who is also the corresponding author — the study used large-scale Mendelian randomization (MR) to test whether genetically proxied levels of inflammatory biomarkers causally influence long-term all-cause mortality. The analysis combined genome-wide association instruments from more than 750,000 individuals and used FinnGen mortality data (median follow-up 11.7 years) to assess effects on overall survival and major cardiovascular endpoints. Using robust MR methods and multiple sensitivity analyses, the authors report that genetically higher IL6R (soluble IL-6 receptor) levels were associated with reduced all-cause mortality (odds ratio per 1-SD increase: 0.95; 95% CI: 0.91–0.98), and with lower risk of atrial fibrillation, coronary artery disease, stroke, and lung cancer. By contrast, genetically higher IL6 levels were associated with increased mortality (OR 1.05; 95% CI: 1.02–1.08). No significant causal effects were observed for CRP or GDF15, suggesting those markers more likely reflect disease burden than drive it. “These results support IL6R antagonism as a potential strategy for cardiovascular disease prevention.” The authors emphasize that the opposing directions for IL6 and IL6R point to distinct biological mechanisms: IL6 likely promotes chronic pro-inflammatory states that increase cardiovascular risk, while higher circulating IL6R (reflecting altered receptor shedding and signaling) appears to dampen harmful IL6 activity at the vessel wall and myocardium, yielding cardiovascular protection. Sensitivity and cis-MR analyses reinforced the IL6R protective signal and showed minimal evidence of directional pleiotropy. Together, the genetic evidence aligns with clinical trial data for IL6R antagonists in other settings and supports further evaluation of IL6R-targeted strategies for cardiovascular prevention. The paper also notes important limitations and next steps. Analyses were restricted to individuals of European ancestry, so results require replication in other ancestries. Translating genetic evidence into preventive therapies will need careful clinical evaluation, long-term safety assessment, and trials designed for primary prevention in high-risk populations. The authors also call for additional mechanistic work to map how IL6/IL6R modulation alters vascular inflammation and downstream disease processes. DOI - https://doi.org/10.18632/aging.206352 Corresponding author - Eliano P. Navarese - elianonavarese@gmail.com Abstract video - https://www.youtube.com/watch?v=Br1A0jgU-4M Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206352 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, mendelian randomization, inflammatory biomarkers, mortality, cardiovascular disease To learn more about the journal, please visit 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 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

When your gut heats up and your brain starts to ache, it's not random — it's a message. A flare-up in your gut can echo upward, shifting your brain chemistry, amplifying inflammation, and lowering your migraine threshold.In this episode of Migraine Heroes Podcast, host Diane Ducarme connects the dots between digestive distress and neurological pain — helping you understand why gut trouble so often becomes head trouble.You'll discover:

Brant Peterson, Vice President & Fellow at Valo Health, joins Data in Biotech to explore how his team leverages real-world data, genetic insights, and machine learning to de-risk drug discovery. From building causal DAGs to identifying patient subtypes in neurodegenerative diseases like Parkinson's, this episode dives deep into a patient-first, data-driven approach to biomedical innovation. What You'll Learn in This Episode: >> How Valo Health uses real-world evidence and EHR data to prioritize drug targets earlier in the development pipeline. >> Why integrating wet lab experiments and causal DAGs accelerates therapeutic validation. >> The importance of genetic pleiotropy and Mendelian randomization in refining disease hypotheses. >> How Valo Health identifies high-impact patient subgroups in neurodegenerative diseases like Parkinson's and Alzheimer's. >> Where machine learning models succeed and fall short, in uncovering mechanisms of disease from sparse longitudinal data. Meet Our Guest Brant Peterson is Vice President & Fellow in Data Science at Valo Health. He brings deep expertise in genetics, computational biology, and biomedical innovation. Formerly a Distinguished Data Scientist at Valo and Computational Biologist at Novartis, Brant focuses on leveraging patient-centric data to drive causal discovery in drug development. About The Host Ross Katz is Principal and Data Science Lead at CorrDyn. Ross specializes in building intelligent data systems that empower biotech and healthcare organizations to extract insights and drive innovation. Connect with Our Guest: Sponsor: CorrDyn, a data consultancyConnect with Brant Peterson on LinkedIn  Connect with Us: Follow the podcast for more insightful discussions on the latest in biotech and data science.Subscribe and leave a review if you enjoyed this episode!Connect with Ross Katz on LinkedIn Sponsored by… This episode is brought to you by CorrDyn, the leader in data-driven solutions for biotech and healthcare. Discover how CorrDyn is helping organizations turn data into breakthroughs at CorrDyn.

I was shocked at the comments on this post. Many people, some of them I know to be smart, thought I was nuts for suggesting two middle-aged women who had isolated high LDL-C needn't take meds because their calculated 10-year risk was less than 3% What shocked me is that our guidelines suggest treatment with statins when 10-year risk is ≥ 7.5%. You may not know this but clinicians are supposed to consider cholesterol (and BP) based on overall risk, which include things like age, blood pressure, smoking status as well as HDL. Here is a link to the PCE. It drives me bananas that clinicians don't go over this with patients. They just look at LDL-c in isolation. Content like this comes free of industry support. Please consider becoming a free or paid subscriber.Experts chose this a 7.5% threshold because they felt it was the point where the absolute risk reduction from statins (about 20-25% relative risk reduction) for nonfatal cardiac events outweighed any potential downsides of statins. It is an arbitrary threshold. The thinking: We know from many RCTs that statins reduce future risk by about 20-25% over 5 years. So .25 x the estimated risk outputs the absolute risk reduction. Let's say a person has a calculated risk of 10%. They can expect a 2.5% risk reduction (.25 x 10% = 2.5%) over 10 years. But .25 x 3% = .75, so a person with an estimated risk of 3% who takes a daily pill for 10 years goes to 2.25%. That's not much. Here are some pics of the pushback I recieved:My colleagues rightly point out that atherosclerosis of the coronary arteries is a slow process and longer exposure to lower LDL-c is beneficial. They feel that the 10-year horizon is too short. They cite something called Mendelian randomization studies which find that people who were born with genetic profiles that cause low cholesterol also have low rates of heart attacks. I wrote a post about this. I actually think that statins and blood pressure drugs may have greater effects in younger people who are at lower risk. But come on. Both individuals who I helped calculate risk were below 3%. That's too low to worry about. Further, if you think we treat people with elevated LDL levels who have this low of a risk, why do we need risk calculators? Or…why don't we just treat everyone above a certain age, since age is the largest driver in the calculators? These are issues I spoke with Drs Foy and Murthy about. I learned a ton. I hope you will too. Topics include:* The value of risk calculators* The uncertainty of prediction* The best time window to consider (statin trials were for 5 years; can we assume effect sizes over 5 years are similar at 30 years?) * The causal role of LDL-c vs “metabolic health”* The value of coronary artery calcium testing * Lipoprotein (a) Academic people like to make fun of podcasts, but I can't imagine a more educational 40 minutes. Andrew and Venk are two of the most thoughtful people in cardiology today. Enjoy and consider supporting Sensible Medicine This is a public episode. If you'd like to discuss this with other subscribers or get access to bonus episodes, visit www.sensible-med.com/subscribe

In this week's episode we've pulled a vault recording from 2025! Blood editor Dr. Laurie Sehn interviews authors Drs. David-Alexandre Trégouët and Johannes Schetelig on their research published in volume 146 issue 19 of Blood journal. Dr. Trégouët's study conducted a genome-wide association study supplemented by transcriptome and Mendelian randomization analyses to identify 28 loci and proteins associated with VTE recurrence risk. This work provides genomic evidence that inherited variants contribute to the risk of VTE recurrence, raising the possibility of a more personalized approach to the prevention of recurrent VTE. The study conducted by Dr. Schetelig and colleagues report the results of a long term trial on patients with poor-response AML, comparing outcomes between patients who received salvage chemotherapy versus immediate transplantation. With no difference in survival rates at 5 years, outcomes seem to be determined mainly by genetic risk factors, age, and comorbidities, therefore challenging the routine use of intensive remission induction before allogeneic transplant in patients with an available donor and underscore the need for novel therapeutic strategies for poor-risk AML.Featured Articles:Molecular Determinants of Thrombosis Recurrence Risk Across Venous Thromboembolism Subtypes Disease risk but not remission status determines transplant outcomes in AML: long-term outcomes of the ASAP trial 

This episode covers Mendelian inheritance.Written notes can be found at https://zerotofinals.com/paediatrics/genetics/inheritance/Questions can be found at https://members.zerotofinals.com/Books can be found at https://zerotofinals.com/books/The audio in the episode was expertly edited by Harry Watchman.

Send us a textMethods & challenges of establishing causal relationships in health research, emphasizing epidemiology, randomized trials, and genetic approaches.Topics:Epidemiology: Studies disease influences using observational designs like case-control and prospective cohorts, plus trials, to identify patterns and test hypotheses.Hierarchy of evidence critique: Rejects rigid pyramids favoring RCTs, as all studies can be biased; advocates triangulation integrating varied data types for robust conclusions.RCT strengths & weaknesses: Randomization balances confounders, but issues like poor blinding, attrition, or subversion can undermine results; large samples may yield spurious precision if biased.Confounding & reverse causation: Examples include yellow fingers and lung cancer (both from smoking) or early atherosclerosis inflating CRP-disease links; hard to fully control statistically.Nutrition epidemiology: Observational studies often overstate benefits (e.g., vitamin E for heart disease), leading to failed trials; incentives favor new findings over revisiting errors.Mendelian randomization: Uses genetic variants as proxies for exposures (e.g., ALDH2 for alcohol metabolism) to mimic randomization; reveals no heart benefits from alcohol, unlike observational data.Negative controls: Tests implausible outcomes (e.g., smoking and murder) or exposures (e.g., paternal smoking in pregnancy) to check for confounding artifacts.Evidence triangulation: Combines diverse studies with different biases (e.g., cross-cultural comparisons) for causality; applied to dismiss HDL-raising drugs despite initial promise.Practical Takeaways:Scrutinize health claims by checking for negative controls or variety in evidence sources to avoid mistaking correlation for causation.For personal decisions like alcohol intake, consider genetic studies showing risks at all levels, and aim for moderation or abstinence based on overall evidence.When evaluating supplements or diets, prioritize trials over observational data, and question media hype that ignores confounding factors.About the guest: Dr. George Davey Smith, MD, DSc is a professor of clinical epidemiology at the University of Bristol and director of the MRC Integrative Epidemiology Unit.*Not medical advice.Support the showAffiliates: Lumen device to optimize your metabolism for weight loss or athletic performance. MINDMATTER gets you 15% off. 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. 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. KetoCitra—Ketone body BHB + electrolytes formulated for kidney health. Use code MIND20 for 20% off any subscription (cancel anytime) For all the ways you can support my efforts

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

David Sloan Wilson | Professor Emeritus, Department of Anthropology / Biological Sciences Binghamton University | State University of New York "Mind, Brain and Culture from a Generalized Darwinian Perspective" Generalized Darwinism refers to any process combining the three ingredients of variation, selection, and replication (VSR). It is both old and new: Old, because all the insights associated with Darwinism during its first few decades were in ignorance of the proximate mechanisms of VSR. New, because with the advent of Mendelian genetics, the entire study of evolution became focused on genes, to the exclusion of other VSR processes. A return to generalized Darwinism didn't commence until the closing decades of the 20th century and is now in full swing, with profound implications for our understanding of mind, brain, and culture.    Link to ProSocial World website: https://www.prosocial.world/ If you would like to become an AFFILIATE of the Center, please let us know.Subscribe to our YouTube channel to get updates on our latest videos.Follow along with us on Instagram | Facebook NOTE: The views and opinions expressed by the speaker do not necessarily reflect those held by the Center for Mind, Brain, and Culture or Emory University.

In this episode, Dr Chloe Burke talks to Dr Monika Halicka, a Senior Research Associate at the Bristol Medical School, University of Bristol, UK. The interview covers a systematic review and meta-analysis on the effectiveness and safety of psychosocial interventions for cannabis use disorder. · An overview of Monika's paper [1:00]· The different types of psychosocial interventions found in the review [02:55]· What ‘inactive controls' and ‘non-specific controls' are with regards to psychosocial interventions [04:30]· Deciding on the outcomes of focus for the study [06:00]· The results of the meta-analysis in which psychosocial interventions had clinically meaningful improvements in abstinence [07:31]· The potential adverse events occurring from psychosocial interventions [09:31]· Recommendations for clinical practice and the hesitancy in making these recommendations [10:41]· The take home message of the study [12:24]About Chloe Burke: Chloe is a Senior Research Associate in Evidence Synthesis based in the Bristol Medical School, University of Bristol. Her current role applies evidence synthesis methodologies (e.g. network meta-analysis) to health-related topics, including addiction. She has a background in psychiatric epidemiology with a focus on applying causal inference methods (e.g. Mendelian randomization) to the topic of substance use and mental health. She holds a PhD in Psychology from the University of Bath, which investigated the co-use of cannabis and tobacco and depression risk. She is currently co-chair of the Society for Research on Nicotine and Tobacco Genetics and Omics Network.About Monika Halicka: Monika is a member of the National Institute for Health and Care Research Bristol Evidence Synthesis Group and works as a senior research associate in evidence synthesis at Bristol Medical School (University of Bristol, UK). With a background in psychology and neuroscience, her previous research focused on applying experimental psychology and statistical modelling approaches to health-related problems, largely in the context of chronic pain. Having transitioned to evidence synthesis, she is interested in robust statistical synthesis methods.The authors have no conflicts of interest to disclose. Original article: Effectiveness and safety of psychosocial interventions for the treatment of cannabis use disorder: A systematic review and meta-analysis https://doi.org/10.1111/add.70084 The opinions expressed in this podcast reflect the views of the host and interviewees and do not necessarily represent the opinions or official positions of the SSA or Addiction journal.The SSA does not endorse or guarantee the accuracy of the information in external sources or links and accepts no responsibility or liability for any consequences arising from the use of such information. Hosted on Acast. See acast.com/privacy for more information.

Measures of General Intelligence and Risk for Alcohol Use Disorder JAMA Psychiatry This male Swedish cohort study that included 573,855 participants assessed if there is an association between IQ and risk for alcohol use disorder, and if so, what is the nature of this association.  It found that IQ at age 18 years was associated with subsequent alcohol use disorder risk. Mendelian randomization analyses suggest a causal association, albeit with context-dependent differences; genetic liability for cognitive performance also predicted alcohol use disorder in a US-based sample. Results suggest that there was a clear impact of genetic liability for cognitive performance on alcohol disorder risk, but the association varies based on the sociocultural context.   Read this issue of the ASAM Weekly Subscribe to the ASAM Weekly Visit ASAM

Most MCAT students waste time memorizing Punnett squares and ratios without really understanding probability. That's why genetics feels overwhelming.In this episode, Molly and Mike break down Mendelian genetics for the MCAT: the truth about dominant vs. recessive, how to use Punnett squares correctly, the probability errors that cost students points, and how to master classic ratios (3:1, 9:3:3:1) without rote memorization. You'll also learn how linked genes and independent assortment show up on test day.

Discover the connection between muscle mass, lipids, and cardiovascular health with Dr. Richie Kirwan!

Essential tremor is the most common movement disorder, although it is often misdiagnosed. A careful history and clinical examination for other neurologic findings, such as bradykinesia, dystonia, or evidence of peripheral neuropathy, can reveal potential alternative etiologies. Knowledge about epidemiology and associated health outcomes is important for counseling and monitoring for physical impairment and disability. In this episode, Lyell Jones, MD, FAAN, speaks with Ludy C. Shih, MD, MMSc, FAAN, author of the article “Essential Tremor” in the Continuum® August 2025 Movement Disorders issue. Dr. Jones is the editor-in-chief of Continuum: Lifelong Learning in Neurology® and is a professor of neurology at Mayo Clinic in Rochester, Minnesota. Dr. Shih is clinical director of the Parkinson's Disease and Movement Disorders Center at Beth Israel Deaconess Medical Center in Boston, Massachusetts. Additional Resources Read the article: Essential Tremor Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @LyellJ Guest: @ludyshihmd Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum: Lifelong Learning in Neurology. Today, I'm interviewing Dr Ludy Shih, who recently authored an article on essential tremor for our latest issue of Continuum on movement disorders. Dr Shih is an associate professor of neurology at Harvard Medical School and the clinical director of the Parkinson's Disease and Movement Disorder Center at Beth Israel Deaconess Medical Center in Boston. Dr Shih, welcome, and thank you for joining us today. Why don't you introduce yourself to our listeners? Dr Shih: Thank you, Dr Jones, for having me. It's a real pleasure to be here on the podcast with you. I'm a neurologist, I trained in movement disorders fellowship, and I currently see patients and conduct clinical research. We offer a variety of treatments and diagnostic tests for our patients with movement disorders. And I have developed this interest, a clinical research interest in essential tremor. Dr Jones: And so, as an expert in essential tremor, the perfect person to write such a really spectacular article. And I can't wait for our listeners to hear more about it and our subscribers to read it. And let's get right to it. If you had, Dr Shih, a single most important message for our listeners about caring for patients with essential tremor, what would that message be? Dr Shih: Yeah, I think the takeaway that I've learned over the years is that people with essential tremor do develop quite a few other symptoms. And although we propose that essential tremor is this pure tremor disorder, they can experience a lot of different comorbidities. Now, there is some debate as to whether that is expected for essential tremor or is this some part of another syndrome, which we may talk about later in the interview. But the fact of the matter is, it's not a benign condition and people do experience some disability from it. Dr Jones: And I think that speaks to how the name of this disorder has evolved over time. right? You point out in your article, it used to be called benign essential tremor or benign familial tremor. But it's really not so straightforward as it. And fairly frequently these symptoms, the patient's tremor, can be functionally limiting, correct? Dr Shih: That is correct. In fact, the reason I probably started getting interested in essential tremor was because our center had been doing a lot of deep brain stimulation for essential tremor, which is remarkably effective, especially for tremor that reaches an amplitude that really no oral medication is going to satisfyingly treat. And if you have enough upper limb disability from this very large-amplitude tremor, a surgical option may make a lot of sense for a lot of patients. And yet, how did they get to that point? Do they continue to progress? These were the sort of interesting questions that got raised in my mind as I started to treat these folks. Dr Jones: We'll come back to treatment in just a minute here, because there are many options, and it sounds like the options are expanding. To start with the diagnosis- I mean, this is an extraordinarily common disorder. As you point out, it is the most common movement disorder in the US and maybe the world, and yet it seems to be underrecognized and frequently misdiagnosed. Why do you think that is? Dr Shih: Great question. It's been pretty consistent, with several case series over the decades showing a fairly high rate of quote/unquote “misdiagnosis.” And I think it speaks to two things, probably. One is that once someone sees a postural and kinetic tremor of the arms, immediately they think of essential tremor because it is quite common. But there's a whole host of things that it could actually be. And the biggest one that we also have to factor in is also the heterogeneity of the presentation of Parkinson's disease. Many people, and I think increasingly now these days, can present with not a whole lot of the other symptoms, but may present with an atypical tremor. And it becomes actually a little hard to sort out, well, do they have enough of these other symptoms for me to suspect Parkinson's, or is the nature of their tremor suspicious enough that it would just be so unusual that this stays essential tremor and doesn't eventually develop into Parkinson's disease? And I think those are the questions that we all still grapple with from time to time in some of our clinics. Dr Jones: Probably some other things related to it with, you know, our understanding of the pathophysiology and the availability of tests. And I do want to come back to those questions here in just a minute, but, you know, just the nomenclature of this disorder… I think our clinical listeners are familiar with our tendency in medicine to use words like essential or idiopathic to describe disorders or phenomena where we don't understand the precise underlying mechanism. When I'm working with our trainees, I call these “job-security terms” because it sounds less humbling than “you have a tremor and we don't know what causes it,” right? So, your article does a really nice job outlining the absence of a clear monogenic or Mendelian mechanism for essential tremor. Do you think we'll ever have a eureka moment in neurology for this disorder and maybe give it a different name? Dr Shih: It's a great question. I think as we're learning with a lot of our neurologic diseases---and including, I would even say, Parkinson's disease, to which ET gets compared to a lot---there's already now so much more known complexity to something that has a very specific idea and concept in people's minds. So, I tend to think we'll still be in an area where we'll have a lot of different causes of tremor, but I'm hopeful that we'll uncover some new mechanisms for which treating or addressing that mechanism would take care of the tremor in a way that we haven't been able to make as much progress on in the last few decades as maybe we would have thought given all the advances in in technology. Dr Jones: That's very helpful, and we'll be hopeful for that series of discoveries that lead us to that point. I think many of our listeners will be familiar with the utility---and, I think, even for most insurance companies, approval---for DAT scans to discriminate between essential tremor and Parkinsonian disorders. What about lab work? Are there any other disorders that you commonly screen for in patients who you suspect may have essential tremor? Dr Shih: Yeah, it's a great question. And I think, you know, I'm always mindful that what I'm seeing in my clinic may not always be representative of what's seen in the community or out in practice. I'll give an example. You know, most of the time when people come to the academic Medical Center, they're thinking, gosh, I've tried this or that. I've been on these medicines for the last ten years. But I've had essential tremor for twenty years. We get to benefit a little bit from all that history that's been laid down. And so, it's not as likely you're going to misdiagnose it. But once in a while, you'll get someone with tremor that just started a month ago or just started, you know, 2 or 3 months ago. And you have to still be thinking, well, I've got to get out of the specialist clinic mindset, and think, well, what else really could this be? And so, while it's true for everybody, moreso in those cases, in those recent onset cases, you really got to be looking for things like medications, electrolyte abnormalities, and new-onset thyroid disorder, for example, thyroid toxicosis. Dr Jones: Very helpful. And your article has a wonderful list of the conditions to consider, including the medications that might be used for those conditions that might result or unmask a tremor of a different cause. And I think being open-minded and not anchoring on essential tremor just because it's common, I think is a is a key point here. And another feature in your article that I really enjoyed was your step-by-step approach to tremor. What are those steps? Dr Shih: Well, I think you know first of all, tremor is such common terminology that even lay people, patients, nonclinicians will use the word “tremor.” And so, it can be tempting when the notes on your schedule says referred for tremor to sort of immediately jump to that. I think the first step is, is it tremor? And that's really something that the clinician first has to decide. And I think that's a really important step. A lot of things can look superficially like tremor, and you shouldn't even assume that another clinician knows what tremor looks like as opposed to, say, myoclonus. Or for example a tremor of the mouth; well, it actually could be orolingual or orobuccal dyskinesia, as in tardive dyskinesia. And another one that tremor can look like is ataxia. And so, I think- while they sound obvious to most neurologists, perhaps, I think that---especially in the area of myoclonus, where it can be quite repetitive, quite small amplitude in some conditions---it can really resemble a tremor. And so, there are examples of these where making that first decision of whether it's a tremor or not can really be a good sort of time-out to make sure you're going down the right path to begin with. And I think what's helpful is to think about some of the clinical definitions of a tremor. And tremor is really rhythmic, it's oscillatory. You should see an agonist and antagonist muscle group moving back and forth, to and fro. And then it's involuntary. And so, I think these descriptors can really help; and to help isolate, if you can describe it in your note, you can probably be more convinced that you're dealing with the tremor. The second step that I would encourage people to really consider: you've established it's a tremor. The most important part exam now becomes, really, the nontremor part of the exam. And it should be really comprehensive to think of what else could be accompanying this, because that's really how we make diagnosis of other things besides essential tremor. There really should be a minimum of evidence of parkinsonism, dystonia, neuropathy, ataxia- and the ataxia could be either from a peripheral or central nervous system etiology. Those are the big four or five things that, you know, I'm very keen to look for and will look pretty much in the head, neck, the axial sort of musculature, as well as the limbs. And I think this is very helpful in terms of identifying cases which turn out to have either, say, well, Parkinson's or even a typical Parkinson disorder; or even a genetic disorder, maybe even something like a fragile X tremor ataxia syndrome; or even a spinal cerebellar ataxia. These cases are rare, but I think if you uncover just enough ataxia, for example, that really shouldn't be there in a person, let's say, who's younger and also doesn't have a long history of tremor; you should be more suspicious that this is not essential tremor that you're dealing with. And then the last thing is, once you've identified the tremor and you're trying to establish, well, what should be done about the tremor, you really have to say what kind of tremor it is so that you can follow it, so you can convey to other people really what the disability is coming from the tremor and how severe the tremor is. So, I think an example of this is, often in the clinic, people will have their patients extend their arms and hands and kind of say, oh, it's an essential tremor, and that's kind of the end of the exam. But it doesn't give you the flavor. Sometimes you'll have a patient come in and have a fairly minimal postural tremor, but then you go out, take those extra few seconds to go grab a cup of water or two cups of water and have them pour or drink. And now all of a sudden you see this tremor is quite large-amplitude and very disabling. Now you have a better appreciation of what you really need to do for this patient, and it might not be present with just these very simple maneuvers that you have at bedside without props and items. And then the severity of it; you know, we're so used to saying mild, moderate, severe. I think what we've done in the Tremor Research Group to use and develop the Essential Tremor Rating Assessment Scale is to get people used to trying to estimate what size the tremor is. And you can do that by taking a ruler or developing a sense of what 1 centimeter, 2 centimeters, 3 centimeters looks like. I think it'd be tremendously helpful too, it's very easy and quick to convey severity in a given patient. Dr Jones: I appreciate you, you know, having a patient-centered approach to the- how this is affecting them and being quantitative in the assessment of the tremor. And that's a great segue to a key question that I run into and I think others run into, which is when to initiate therapy? You know, if you see a patient who, let's say they have a mild tremor or, you know, something that quantitatively is on the mild end of the spectrum, and you have, you know, a series of options… from a medication perspective, you have to say, well, when does this across that threshold of being more likely to benefit the patient than to harm the patient? How do you approach that question? What's your threshold for starting medication? Dr Shih: Yeah. You know, sometimes I will ask, because---and I know this sounds like a strange question---because I feel like my patients will come for a couple of different reasons. Sometimes it's usually one over the other. I think people can get concerned about a symptom of a tremor. So, I actually will ask them, was your goal to just get a sense for what this tremor is caused by? I understand that many people who develop tremor might be concerned it might be something like Parkinson's disease. Or is this also a tremor that is bothering you in day-to-day life? And often you will hear the former. No, I just wanted to get checked out and make sure you don't think it's Parkinson's. It doesn't bother me enough that I want to take medication. They're quite happy with that. And then the second scenario is more the, yeah, no, it bothers me and it's embarrassing. And that's a very common answer you may hear, may be embarrassing, people are noticing. It's funny in that many people with essential tremor don't come to see a doctor or even the neurologist for many years. And they will put up with it for a very long time. And they've adopted all sorts of compensatory strategies, and they've just been able to handle themselves very admirably with this, in some cases, very severe tremor. So, for some of them, it'll take a lot to come to the doctor, and then it becomes clear. They said, I think I'm at the point where I need to do something about this tremor. And so, I think those three buckets are often sort of where my patients fall into. And I think asking them directly will give you a sense of that. But you know, it can be a nice time to try some as-needed doses of something like Propranolol, or if it's something that you know that they're going to need something on day-to-day to get control of the tremor over time, there are other options for that as well. Dr Jones: Seems like a perfect scenario for shared decision-making. Is it bothersome enough to the patient to try the therapy? And I like that suggestion. That's a nice pearl that you could start with an a- needed beta blocker, right, with Propranolol. And this is a question that I think many of us struggle with as well. If you've followed a patient with essential tremor for some time and you've tried different medications and they've either lost effectiveness or have intolerable adverse effects, what is your threshold for referring a patient for at least considering a surgical neurostimulator therapy for their essential tremor? Dr Shih: Yeah, so surgical therapies for tremor have been around for a long time now, since 1997, which was when it was approved by the FDA for essential tremor and Parkinson tremor. And then obviously since then, we have a couple more options in the focus ultrasound thalamotomy, which is a lesioning technique. When you have been on several tremor medications, the list gets smaller and smaller. It- and then chance of likely satisfying benefit from some of these medications can be small and small as you pass through the first and second line agents and these would be the Propranolol and the primidone. And as you say, quite a few patients- it's estimated between 30 to 50% of these patients end up not tolerating these first two medications and end up discontinuing them. Some portion of that might also be due to the fact that some of our patients who have been living with essential tremor for decades now, to the point that their tremor is getting worse, are also getting older. And so, polypharmacy and/or some of the potential side effects of beta blockers and anticonvulsants like primidone may be harder to bear in an older adult. And then as you talk about in the article, there's some level of evidence for topiramate, and then from there a number of anticonvulsants or benzos, which have even weaker evidence for them. It's a personal decision. As I tell folks, look, this is not going to likely extend your life or save your life, but it's a quality of life issue. And of course, if there are other things going on in life that need to be taken care of and they need that kind of care and attention, then, you know, you don't need to be adding this to your plate. But if you are in the position where those other things are actually okay, but quality of life is really affected by your being unable to use your upper limbs in the way that you would like to… A lot of people's hobbies and applications are upper limb-based, and enjoying those things is really important. Then I think that this is something- a conversation that we begin and we begin by talking about yes, there are some risks involved, but fortunately this is the data we have on it, which is a fairly extensive experience in terms of this is the risk of, you know, surgery-related side effects. This is the risk of if you're having stimulation from DBS stimulation-related side effects, which can be adjustable. It's interesting, I was talking with colleagues, you know, after focused ultrasound thalamotomy was approved. That really led more people to come to the clinic and start having these discussions, because that seemed like a very the different sort of approach where hardware wasn't needed, but it was still a surgery. And so, it began that conversation again for a bunch of people to say, you know, what could I do? What could I tolerate? What would I accept in terms of risk and potential benefit? Dr Jones: Well, I think that's a great overview of a disorder where, you know, I think the neurologist's role is really indispensable. Right? I mean, you have to have this conversation not just once, this is a conversation that you have over time. And again, I really want to refer our listeners to this article. It's just a fantastic overview of a common disorder, but one where I think there are probably gaps where we can improve care. And Dr Shih, I want to thank you for joining us, and thank you for such a great discussion on essential tremor. I learned a lot from your article, and I learned even more from the interview today. I suspect our readers and listeners will too. Dr Shih: Well, thank you again for the invitation and the opportunity to kind of spread the word on this really common condition. Dr Jones: Again, we've been speaking with Dr Ludy Shih, author of a fantastic article on essential tremor in Continuum's latest issue on movement disorders. Please check it out, and thank you to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

In this episode of Iron Culture, Dr. Eric Trexler and Dr. Lauren Colenso-Semple discuss science related to attractiveness, coolness, and personality type. They explore scientific studies on the factors associated with perceived attractiveness and "coolness," discussing body fat percentages and societal perceptions. The conversation shifts to how personality traits appear to predict workout preferences and engagement in fitness, then they debate the importance of matching exercise to individual characteristics. Time stamps: 00:00 Introduction to Iron Culture and Guests 5:57 The Science of (Male) Attractiveness 10:39 Evolutionary Underpinnings of Male Attractiveness 13:53 Distorted Perceptions of Attractiveness (In the Fitness World) 20:10 The Irony of Pursuing Attractiveness 22:22 Body-Fat and Optimized Health 24:18 Surprising Article Feedback 28:50 Unrealistic Body Standards and Gender Perceptions 32:49 Achieving the Outcome Versus Doing Hard Things 35:07 Attractiveness is More Than Body Shape/Size 37:48 The Science of Being Cool 47:19 Matching Exercise To Personality Types References: Xia F, Sauciuvenaite J, Bissland R, Hambly C, Starr-Vaanholt L, Faries MD, et al. The relationship between body fatness and physical attractiveness in males. Personality and Individual Differences. 2025 Sep 1;243:113240. de Jager S, Coetzee N, Coetzee V. Facial Adiposity, Attractiveness, and Health: A Review. Front Psychol. 2018 Dec 21;9:2562. Brierley ME, Brooks KR, Mond J, Stevenson RJ, Stephen ID. The Body and the Beautiful: Health, Attractiveness and Body Composition in Men's and Women's Bodies. PLoS One. 2016;11(6):e0156722. Sorokowski P, Kościński K, Sorokowska A, Huanca T. Preference for Women's Body Mass and Waist-to-Hip Ratio in Tsimane' Men of the Bolivian Amazon: Biological and Cultural Determinants. PLoS One. 2014 Aug 22;9(8):e105468. Tovée MJ, Cornelissen PL. Female and male perceptions of female physical attractiveness in front-view and profile. Br J Psychol. 2001 May;92(Pt 2):391–402. Jayedi A, Khan TA, Aune D, Emadi A, Shab-Bidar S. Body fat and risk of all-cause mortality: a systematic review and dose-response meta-analysis of prospective cohort studies. Int J Obes (Lond). 2022 Sep;46(9):1573–81. Hu J, Chen X, Yang J, Giovannucci E, Lee DH, Luo W, et al. Association between fat mass and mortality: analysis of Mendelian randomization and lifestyle modification. Metabolism. 2022 Nov;136:155307. Ramlau-Hansen CH, Thulstrup AM, Nohr EA, Bonde JP, Sørensen TIA, Olsen J. Subfecundity in overweight and obese couples. Hum Reprod. 2007 Jun;22(6):1634–7. Wei S, Schmidt MD, Dwyer T, Norman RJ, Venn AJ. Obesity and menstrual irregularity: associations with SHBG, testosterone, and insulin. Obesity (Silver Spring). 2009 May;17(5):1070–6. Liu Y, Hu X, Xiong M, Li J, Jiang X, Wan Y, et al. Association of BMI with erectile dysfunction: A cross-sectional study of men from an andrology clinic. Front Endocrinol (Lausanne). 2023;14:1135024. https://psycnet.apa.org/doiLanding?doi=10.1037%2Fxge0001799 https://www.frontiersin.org/journals/psychology/articles/10.3389/fpsyg.2025.1587472/full

Eric Topol (00:05):Hello, it's Eric Topol from Ground Truths, and I've got some really exciting stuff to talk to you about today. And it's about the announcement for a new Center for pediatric CRISPR Cures. And I'm delight to introduce doctors Jennifer Doudna and Priscilla Chan. And so, first let me say this is amazing to see this thing going forward. It's an outgrowth of a New England Journal paper and monumental report on CRISPR in May. [See the below post for more context]Let me introduce first, Dr. Doudna. Jennifer is the Li Ka Shing Chancellor's Chair and a Professor in the departments of chemistry and of molecular and cell biology at the University of California Berkeley. She's also the subject of this book, one of my favorite books of all time, the Code Breaker. And as you know, the 2020 Nobel Prize laureate for her work in CRISPR-Cas9 genome editing, and she founded the Innovative Genomics Institute (IGI) back 10 years ago. So Jennifer, welcome.Jennifer Doudna (01:08):Thank you, Eric. Great to be here.Eric Topol (01:10):And now Dr. Priscilla Chan, who is the co-founder of the Chan Zuckerberg Initiative (CZI) that also was started back in 2015. So here we are, a decade later, these two leaders. She is a pediatrician having trained at UCSF and is committed to the initiative which has as its mission statement, “to make it possible to cure, prevent, and manage all diseases in this century.” So today we're going to talk about a step closer to that. Welcome, Priscilla.Priscilla Chan (01:44):Thank you. Thanks for having me.Eric Topol (01:46):Alright, so I thought we'd start off by, how did you two get together? Have you known each other for over this past decade since you both got all your things going?Jennifer Doudna (01:56):Yes, we have. We've known each other for a while. And of course, I've admired the progress at the CZI on fundamental science. I was an advisor very early on and I think actually that's how we got to know each other. Right, Priscilla?Priscilla Chan (02:11):Yeah, that's right. We got to know each other then. And we've been crisscrossing paths. And I personally remember the day you won the Nobel Prize. It was in the heart of the pandemic and a lot of celebrations were happening over Zoom. And I grabbed my then 5-year-old and got onto the UCSF celebration and I was like, look, this is happening. And it was really cool for me and for my daughter.Eric Topol (02:46):Well, it's pretty remarkable convergence leading up to today's announcement, but I know Priscilla, that you've been active in this rare disease space, you've had at CZI a Rare As One Project. Maybe you could tell us a bit about that.Priscilla Chan (03:01):Yeah, so at CZI, we work on basic science research, and I think that often surprises people because they know that I'm a pediatrician. And so, they often think, oh, you must work in healthcare or healthcare delivery. And we've actually chosen very intentionally to work in basic science research. In part because my training as a pediatrician at UCSF. As you both know, UCSF is a tertiary coronary care center where we see very unusual and rare cases of pediatric presentations. And it was there where I learned how little we knew about rare diseases and diseases in general and how powerful patients were. And that research was the pipeline for hope and for new discoveries for these families that often otherwise don't have very much access to treatments or cures. They have a PDF that maybe describes what their child has. And so, I decided to invest in basic science through CZI, but always saw the power of bringing rare disease patient cohorts. One, because if you've ever met a parent of a child with rare disease, they are a force to be reckoned with. Two, they can make research so much better due to their insights as patients and patient advocates. And I think they close the distance between basic science and impact in patients. And so, we've been working on that since 2019 and has been a passion of ours.Eric Topol (04:40):Wow, that's great. Now Jennifer, this IGI that you founded a decade ago, it's doing all kinds of things that are even well beyond rare diseases. We recently spoke, I know on Ground Truths about things as diverse as editing the gut microbiome in asthma and potentially someday Alzheimer's. But here you were very much involved at IGI with the baby KJ Muldoon. Maybe you could take us through this because this is such an extraordinary advance in the whole CRISPR Cures story.Jennifer Doudna (05:18):Yes, Eric. It's a very exciting story and we're very, very proud of the teamwork that went into making it possible to cure baby KJ of his very rare disease. And in brief, the story began back in August of last year when he was born with a metabolic disorder that prevented him from digesting protein, it's called a urea cycle disorder and rare, but extremely severe. And to the point where he was in the ICU and facing a very, very difficult prognosis. And so, fortunately his clinical team at Children's Hospital of Philadelphia (CHOP) reached out to Fyodor Urnov, who is the Director of Translational Medicine at the IGI here in the Bay Area. They teamed up and realized that they could quickly diagnose that child because we had an IRB approved here at the IGI that allowed us to collect patient samples and do diagnosis. So that was done.Jennifer Doudna (06:26):We created an off-the-shelf CRISPR therapy that would be targeted to the exact mutation that caused that young boy's disease. And then we worked with the FDA in Washington to make sure that we could very safely proceed with testing of that therapy initially in the lab and then ultimately in two different animal models. And then we opened a clinical trial that allowed that boy to be enrolled with, of course his parents' approval and for him to be dosed and the result was spectacular. And in fact, he was released from the hospital recently as a happy, healthy child, gaining lots of weight and looking very chunky. So it's really exciting.Eric Topol (07:16):It's so amazing. I don't think people necessarily grasp this. This timeline [see above] that we'll post with this is just mind boggling how you could, as you said Jennifer, in about six months to go from the birth and sequencing through cell specific cultures with the genome mutations through multiple experimental models with non-human primates even, looking at off-target effects, through the multiple FDA reviews and then dosing, cumulatively three dosing to save this baby's life. It really just amazing. Now that is a template. And before we go to this new Center, I just wanted to also mention not just the timeline of compression, which is unimaginable and the partnership that you've had at IGI with I guess Danaher to help manufacture, which is just another part of the story. But also the fact that you're not just even with CRISPR 1.0 as being used in approvals previously for sickle cell and β-thalassemia, but now we're talking about base editing in vivo in the body using mRNA delivery. So maybe you could comment on that, Jennifer.Jennifer Doudna (08:38):Yeah, very good point. So yeah, we used a version of CRISPR that was created by David Liu at the Broad Institute and published and available. And so, it was possible to create that, again, targeted to the exact mutation that caused baby KJ's disease. And fortunately, there was also an off-the-shelf way to deliver it because we had access to lipid nanoparticles that were developed for other purposes including vaccinations. And the type of disease that KJ suffered from is one that is treatable by editing cells in the liver, which is where the lipid nanoparticle naturally goes. So there were definitely some serendipity here, but it was amazing how all of these pieces were available. We just had to pull them together to create this therapy.Eric Topol (09:30):Yeah, no, it is amazing. So that I think is a great substrate for starting a new Center. And so, maybe back to you Priscilla, as to what your vision was when working with Jennifer and IGI to go through with this.Priscilla Chan (09:45):I think the thing that's incredibly exciting, you mentioned that at CZI our mission is to cure, prevent, and manage all disease. And when we talked about this 10 years ago, it felt like this far off idea, but every day it seems closer and closer. And I think the part that's super exciting about this is the direct connection between the basic science that's happening in CRISPR and the molecular and down to the nucleotide understanding of these mutations and the ability to correct them. And I think many of us, our imaginations have included this possibility, but it's very exciting that it has happened with baby KJ and CHOP. And we need to be able to do the work to understand how we can treat more patients this way, how to understand the obstacles, unblock them, streamline the process, bring down the cost, so that we better understand this pathway for treatment, as well as to increasingly democratize access to this type of platform. And so, our hope is to be able to do that. Take the work and inspiration that IGI and the team at CHOP have done and continue to push forward and to look at more cases, look at more organ systems. We're going to be looking in addition to the liver, at the bone marrow and the immune system.Priscilla Chan (11:17):And to be able to really work through more of the steps so that we can bring this to more families and patients.Eric Topol (11:30):Yeah, well it's pretty remarkable because here you have incurable ultra-rare diseases. If you can help these babies, just think of what this could do in a much broader context. I mean there a lot of common diseases have their roots with some of these very rare ones. So how do you see going forward, Jennifer, as to where you UC Berkeley, Gladstone, UCSF. I'm envious of you all up there in Northern California I have to say, will pull this off. How will you get the first similar case to KJ Muldoon going forward?Jennifer Doudna (12:13):Right. Well, IGI is a joint institute, as you probably know, Eric. So we were founded 10 years ago as a joint institute between UC Berkeley and UCSF. And now we have a third campus partner, UC Davis and we have the Gladstone Institute. So we've got an extraordinary group of clinicians and researchers that are coming together for this project and the Center to make it a success. We are building a clinical team at UCSF. We have several extraordinary leaders including Jennifer Puck and Chris Dvorak, and they are both going to be involved in identifying patients that could be enrolled in this program based on their diagnosis. And we will have a clinical advisory group that will help with that as well. So we'll be vetting patients probably right after we announce this, we're going to be looking to start enrolling people who might need this type of help.Eric Topol (13:18):Do you think it's possible to go any faster right now than the six months that it took for KJ?Jennifer Doudna (13:26):I think it could be. And here's the reason. There's a very interesting possibility that because of the type of technology that we're talking about with CRISPR, which fundamentally, and you and I have talked about this previously on your other podcast. But we've talked about the fact that it's a programmable technology and that means that we can change one aspect of it, one piece of it, which is a piece of a molecule called RNA that's able to direct CRISPR to the right sequence where we want to do editing and not change anything else about it. The protein, the CRISPR protein stays the same, the delivery vehicle stays the same, everything else stays the same. And so, we're working right now with FDA to get a platform designation for CRISPR that might allow streamlining of the testing process in some cases. So it'll obviously come down to the details of the disease, but we're hopeful that in the end it will be possible. And Priscilla and I have talked about this too, that as AI continues to advance and we get more and more information about rare diseases, we'll be able to predict accurately the effects of editing. And so, in some cases in the future it may be possible to streamline the testing process even further safely.Eric Topol (14:51):And I also would note, as you both know, well this administration is really keen on genome editing and they've had a joint announcement regarding their support. And in my discussions with the FDA commissioner, this is something they are very excited about. So the timing of the new Center for pediatric CRISPR Cures is aligned with the current administration, which is good to see. It's not always the case. Now going back, Priscilla, to your point that not just for the liver because delivery has been an issue of course, and we're going to try to get after a lot of these really rare diseases, it's going to go beyond there. So this is also an exciting new dimension of the Center, as you said, to go after the bone marrow for hematopoietic cells, perhaps other organs as well.Priscilla Chan (15:42):I mean what the expertise and feasibility, the immune system is going to be the next target. Jennifer Puck has been a pioneer in this work. She's the one who designed the newborn screen that will be the tool that picks up these patients as they are born. And I think the thing that's tremendous is the immune system, first of all is active in many, many diseases, not just these cases of children born with partial or absence of immune systems. And the course right now that these babies are left with is complete isolation and then a very long and arduous course of a bone marrow transplant with high morbidity and mortality. And even if after the transplant you have complications like graft versus host and immunosuppression. And so, the idea of being able to very specifically and with less the conditioning and morbidity and mortality of the treatment, being able to address this is incredible. And the implications for other diseases like blood cancers or other hematopoietic diseases, that's incredible. And that actually has an incredibly broad base of patients that can benefit from the learnings from these babies with severe combined immunodeficiencies.Eric Topol (17:10):Yeah, I think that goes back to a point earlier maybe to amplify in that previous CRISPR generation, it required outside the body work and it was extremely laborious and time consuming and obviously added much more to the expense because of hospitalization time. This is different. This is basically doing this inside the affected patient's body. And that is one of the biggest reasons why this is a big step forward and why we're so fortunate that your Center is moving forward. Maybe before we wrap up, you might want to comment, Jennifer on how you were able to bring in to build this platform, the manufacturing arm of it, because that seems to be yet another dimension that's helpful.Jennifer Doudna (18:01):Indeed, yes. And we were again fortunate with timing because you mentioned briefly that the IGI had set up a program with the Danaher Corporation back in January of last year. We call it our Beacon project. And it's focused on rare disease. And it's a really interesting kind of a unique partnership because Danaher is a manufacturing conglomerate. So they have companies that make molecules, they make proteins, they make RNA molecules, they make delivery molecules. And so, they were excited to be involved with us because they want to be a provider of these types of therapies in the future. And they can see the future of CRISPR is very exciting. It's expanding, growing area. And so, that agreement was in place already when the baby KJ case came to our attention. And so, what we're hoping to do with Danaher is again, work with them and their scientists to continue to ask, how can we reduce the cost of these therapies by reducing the cost of the molecules that are necessary, how to make them efficiently. We already, it's very interesting, Fyodor Urnov has toured their plant in North Dakota recently, and he found in talking to their engineers, there are a number of things that we can already see will be possible to do that are going to make the process of manufacturing these molecules faster and cheaper by a lot.Eric Topol (19:28):Wow.Jennifer Doudna (19:28):So it's a win-win for everybody. And so, we're really excited to do that in the context of this new Center.Eric Topol (19:36):Oh, that's phenomenal because some of these disorders you don't have that much time to work with before they could be brain or organ or vital tissue damage. So that's great to hear that. What you built here is the significance of it can't be under emphasized, I'll say because we have this May report of baby KJ, which could have been a one-off and it could have been years before we saw another cure of an ultra-rare disorder. And what you're doing here is insurance against that. You're going to have many more cracks at this. And I think this is the excitement about having a new dedicated Center. So just in closing, maybe some remarks from you Priscilla.Priscilla Chan (20:24):I just want to emphasize one point that's really exciting as we talk about these ultra-rare cases that they're often like one in a million. All these learnings actually help maximize the impact of lots of research across the sector that impacts actually everyone's health. And so, our learnings here from these patients that have very significant presentations that really can stand to benefit from any treatment is hopefully paving the way for many, many more of us to be able to live healthier, higher quality lives through basic science.Eric Topol (21:13):And over to you, Jennifer.Jennifer Doudna (21:15):Couldn't agree more. It's a really interesting moment. I think what we hope we are, is we're at sort of an inflection point where, as I mentioned earlier, all the pieces are in place to do this kind of therapeutic and we just need a team that will focus on doing it and pulling it together. And also learning from that process so that as Priscilla just said, we are ultimately able to use the same strategy for other diseases and potentially for diseases that affect lots of people. So it's exciting.Eric Topol (21:46):For sure. Now, if I could just sum up, this is now a decade past the origination of your work of CRISPR and how already at the first decade culminated in sickle cell disease treatment and β-thalassemia. Now we're into the second decade of CRISPR. And look what we've seen, something that was unimaginable until it actually happened and was reported just a little over a month ago. Now going back to Priscilla's point, we're talking about thousands of different rare Mendelian genomic disorders, thousands of them. And if you add them all up of rare diseases, we're talking about hundreds of millions of people affected around the world. So this is a foray into something much bigger, no less the fact that some of these rare mutations are shared by common diseases and approaches. So this really big stuff, congratulations to both of you and your organizations, the Innovative Genomics Institute and the Chan Zuckerberg Initiative for taking this on. We'll be following it with very deep interest, thank you.****************************************************Thanks for listening, reading and subscribing to Ground Truths.If you found this interesting PLEASE share it!That makes the work involved in putting these together especially worthwhile.Thanks to Scripps Research, and my producer, Jessica Nguyen, and Sinjun Balabanoff for video/audio support.All content on Ground Truths—its newsletters, analyses, and podcasts, are free, open-access.Paid subscriptions are voluntary and all proceeds from them go to support Scripps Research. They do allow for posting comments and questions, which I do my best to respond to. Please don't hesitate to post comments and give me feedback. Let me know topics that you would like to see covered.Many thanks to those who have contributed—they have greatly helped fund our summer internship programs for the past two years. Get full access to Ground Truths at erictopol.substack.com/subscribe

A conspiracy war rages on/OTC Insanity   Patreon (Get ad-free episodes, Patreon Discord Access, and more!) https://www.patreon.com/user?u=18482113 PayPal Donation Link https://tinyurl.com/mrxe36ph MERCH STORE!!! https://tinyurl.com/y8zam4o2 Amazon Wish List https://www.amazon.com/hz/wishlist/ls/28CIOGSFRUXAD?ref_=wl_share   Help Promote Dead Rabbit! Dual Flyer https://i.imgur.com/OhuoI2v.jpg "As Above" Flyer https://i.imgur.com/yobMtUp.jpg “Alien Flyer” By TVP VT U https://imgur.com/gallery/aPN1Fnw “QR Code Flyer” by Finn https://imgur.com/a/aYYUMAh   Links: EP 1213 - The Peering Darkness (Sabine's House episode) https://deadrabbitradio.libsyn.com/ep-1213-the-peering-darkness EP 1246 - Possibly Paranormal (Sabine's House episode) https://deadrabbitradio.libsyn.com/ep-1246-possibly-paranormal EP 137 - SpongeBob SquarePants Defecation (Brazilian Broadcast) https://deadrabbitradio.libsyn.com/ep-137-spongebob-squarepants-defecation-brazilian-broadcast EP 1394 - The Ghost Of Things Yet To Come (Making Fun Of Demons episode) https://deadrabbitradio.libsyn.com/ep-1394-the-ghost-of-things-yet-to-come EP 666 - Demon Summoning 101: An Interactive Adventure! (Making Fun Of Demons episode) https://deadrabbitradio.libsyn.com/ep-666-demon-summoning-101-an-interactive-adventure Will bird flu lead to another pandemic in the US? Concerns grow as first US patient dies https://www.today.com/health/disease/bird-flu-pandemic-rcna183174 Avian influenza A(H5N1): Prevention and risks https://www.canada.ca/en/public-health/services/diseases/avian-influenza-h5n1/prevention-risks.html Bird flu update: California declares emergency and U.S. sees 1st severe human case https://www.npr.org/2024/12/18/nx-s1-5233110/bird-flu-first-severe-human-case-cdc-louisiana How America lost control of the bird flu and raised the risk of another pandemic https://www.pbs.org/newshour/health/how-america-lost-control-of-the-bird-flu-and-raised-the-risk-of-another-pandemic Governor Newsom takes proactive action to strengthen robust state response to Bird Flu https://www.gov.ca.gov/2024/12/18/governor-newsom-takes-proactive-action-to-strengthen-robust-state-response-to-bird-flu/ Current Bird Flu Situation https://www.cdph.ca.gov/Programs/CID/DCDC/Pages/Bird-Flu.aspx Gov. 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Jason Carpenter breaks the stories they'll be talking about tomorrow, assuming the world doesn't end today. All Contents Of This Podcast Copyright Jason Carpenter 2018 - 2025  

Take a sneak peek at this month's Fertility and Sterility! Articles discussed this month are:   01:48 Trustworthiness criteria for meta-analyses of randomized controlled studies: OBGYN journal guidelines 06:24 Playing the long game for reproductive rights 08:04 Limiting the number of fresh donor oocytes inseminated with sperm as a strategy to minimize supernumerary embryos 15:38 Effectiveness of degradable polymer film in the management of severe or moderate intrauterine adhesions (PREG-2): a randomized, double-blind, multicenter, stratified, superiority trial 26:37 Aneuploidy rates and likelihood of obtaining a usable embryo for transfer among in vitro fertilization cycles using preimplantation genetic testing for monogenic disorders and aneuploidy compared with in vitro fertilization cycles using preimplantation genetic testing for aneuploidy alone 38:13 Antimüllerian hormone levels are associated with time to pregnancy in a cohort study of 3,150 women 47:50 Racial disparities in the outcomes of euploid single frozen-thawed embryo transfer cycles – analysis of the Clinical Outcome Reporting System of the Society for Assisted Reproductive Technology 2016–2018 data 57:14 No association between celiac disease and female infertility: evidence from Mendelian randomization analysis   View Fertility and Sterility October 2024, Volume 122, Issue 6:  https://www.fertstert.org/issue/S0015-0282(24)X0013-8 View Fertility and Sterility at https://www.fertstert.org/  

In this episode, we discuss instrumental variables with Dr. Rita Hamad of Harvard's TH Chan School of Public Health. This episode is focused on the first part of Chapter 28 of Modern Epidemiology 4th edition on quasi experimental methods. We start with what quasi experimental designs are and why we would want to use them (and whether more epidemiologists are being exposed to them). We also talk about why these methods are more common in economics than in epi. We talk about how these methods try to take advantage of something that approximates randomization to estimate causal effects. We talk about what instrumental variables are and the conditions required to be met for a variable to be an instrument. We focus on the strengths and limitations of the methods and when they make the most sense to use them. We talk about what happens when you violate the assumptions of IV. We talk about weak and strong IVs and we talk about Mendelian randomization and its role in epi. And we ask the age-old question, how do you find the elusive instrumental variable?

IGF-1 (Insulin-Like Growth Factor 1) has emerged as a hot topic in health and nutrition discussions, often linked to longevity, cancer risk, and metabolic health. On one hand, IGF-1 is essential for growth, repair, and metabolic regulation; on the other, it is sometimes associated with disease processes, including cancer and cognitive decline. For those intrigued by the intersection of nutrition, biomarkers, and disease prevention, IGF-1 offers an opportunity to explore how science grapples with these complexities. Claims about manipulating IGF-1 through dietary changes — whether by reducing protein or adopting fasting protocols — are common. But does the evidence support these claims? If you're curious about IGF-1 and the relationships between diet, disease, and healthy aging, in this Premium-exclusive episode Danny and Alan discuss this fascinating topic. To listen to the full episode, subscribe to Sigma Nutrition Premium Timestamps [02:21] IGF-1 and Diet: Examining the Relationship [09:15] IGF-1 as a Biomarker: Challenges with Sensitivity and Specificity [11:54] IGF-1 and Cancer Risk: Insights and Complexities [25:51] IGF-1 in Aging: Cognitive Function and Longevity Considerations [43:38] Key Takeaways: IGF-1, Diet, and Practical Advice Related Resources Join the Sigma email newsletter for free Subscribe to Sigma Nutrition Premium Enroll in the next cohort of our Applied Nutrition Literacy course Murphy et al., 2020 – observational and Mendelian randomization analyses

Recent progress in neurogenetics and molecular pathology has improved our understanding of the complex pathogenetic changes associated with neurodegenerative dementias. In this episode, Katie Grouse, MD, FAAN, speaks with Sonja W. Scholz, MD, PhD, FAAN, an author of the article “Genetics and Neuropathology of Neurodegenerative Dementias,” in the Continuum® December 2024 Dementia issue. Dr. Grouse is a Continuum® Audio interviewer and a clinical assistant professor at the University of California San Francisco in San Francisco, California. Dr. Scholz is a senior investigator at the National Institutes of Health in Bethesda, Maryland and an adjunct professor of neurology at Johns Hopkins University in Baltimore, Maryland. Additional Resources Read the article: Genetics and Neuropathology of Neurodegenerative Dementias Subscribe to Continuum: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Full episode transcript available here:  Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum, the premier topic-based neurology clinical review and CME journal from the American Academy of Neurology. Thank you for joining us on Continuum Audio, which features conversations with Continuum's guest editors and authors who are the leading experts in their fields. Subscribers to the Continuum journal can read the full article or listen to verbatim recordings of the article and have access to exclusive interviews not featured on the podcast. Please visit the link in the episode notes for more information on the article, subscribing to the journal, and how to get CME. Dr Grouse: This is Dr Katie Grouse. Today I'm interviewing Dr Sonia Scholz about her article on genetics and neuropathy of neurodegenerative dementias, which appears in the December 2024 Continuum issue on dementia. Welcome to the podcast, and please introduce yourself to our audience.  Dr Scholz: Thank you so much for inviting me. My name is Sonia Scholz. I'm a neurologist working at the National Institutes of Health. My main focus of research and clinical work are neurodegenerative diseases, and I have a particular interest in using modern genomic tools to understand these diseases and potentially leverage it for new translational applications. Dr Grouse: Sonia, we're really excited to have you today and thanks for joining us.  Dr Scholz: I'm pleased to be here.  Dr Grouse: I'd like to start by asking what you think is the most important message or takeaway point from your article? Dr Scholz: So, this is an article that really captures a very broad and exciting field. So, one thing I wanted to really highlight is that there's a lot of heterogeneity, clinical, pathological, molecular heterogeneity in age-related neurodegenerative dementia syndromes. Our article was really aimed at providing a bird's eye view of the pertinent pathological characteristics, but also important genetic advances and insights and how we can leverage that, particularly in the new physician medicine era, hopefully come up with better treatments and better ways to counsel our patients.  Dr Grouse: What do you think is the most challenging aspect of understanding the genetics and neuropathologic basis of neurodegenerative dementias?  Dr. Scholz: That's a good question. There're many big and challenging questions, but I think one of the things we struggle the most with is really the heterogeneity. I see patients with one and the same Mendelian form of dementia. One patient is in their forties another patient is in their eighties, and the clinical manifestations can be very different from one patient to another. There's a lot of heterogeneity, also, on the pathological level. Not every patient has exactly the same distribution. And so, we're starting to slowly define what the underlying causes are, but it's still quite baffling and quite challenging to put them together and understand them. Dr Grouse: Do you feel that the genome-wide association studies has helped our understanding of these diseases, specifically the heterogeneity? And if so how?  Dr Scholz: That's a great question, but you're talking to a geneticist here. And I definitely would say genome-wide association studies have helped us a lot in identifying what the underlying disease pathways are and what the relationships between neurodegenerative disease entities are. It really also gave us a better understanding of apparently sporadic diseases where genetic factors are still playing a role. And we can leverage that type of knowledge increasingly to highlight high-risk groups, but also, we can increasingly use it to stratify patients for clinical trials, for example. And that's really exciting and there's still a lot of knowledge that we have to garner very quickly, especially in the non-Alzheimer dementia space.  Dr Grouse: You've mentioned, of course, the heterogeneity and these syndromes. And in your article, you go into a lot of the issue of the significant crossover between the genetic links and the neuropathological findings for the various types of neurodegenerative dementias. Do you think that this crossover has been more of a help or a hindrance in better understanding these diseases? Dr Scholz: Yeah, it can be a little bit, you know, challenging to wrap one 's mind around it. But by and large, I think it's actually good news because it highlights that there is a shared biology between many of the neurodegenerative disease entities. And by figuring out which the pathways are that are very often involved, we can prioritize certain targets for therapy development. But we can also be smarter about how we developed treatments. We could repurpose a drug that has been developed for Alzheimer's disease very easily for Lewy body dementia because we increasingly understand the overlap. And we can also leverage new clinical trials design, like basket trials. This is something that has been really transformative in the oncology sphere and now, increasingly, neurodegeneration. We're trying to apply that kind of thinking as well to our patient populations. Dr Grouse: What do you think our listeners will find to be most surprising when they read the article? Dr Scholz: We often present these diseases in our textbooks as these black-and-white entities, but the reality is that there's a lot of overlap. And we also see that co-pathologies are actually the norm and not the exception, and a lot of the molecular risk factors are shared. It's not really surprising. And I think that overlap and crosstalk between the various diseases is something that's a little bit strange to think about, but it actually makes increasingly sense now that we see the genetic risk profiles coming up. Dr Grouse: In reading your article, I was really struck by how many, or how much the prior studies have been lacking in inclusion of different ethno-racial backgrounds in the patients who've been studied. How can this be improved going forward?  Dr Scholz: Yeah, thank you. That's a really important and crucial question, and I think it really takes the collective effort of everybody in the healthcare research community to improve upon that. We need to talk to our patients about genetic testing, about brain donation programs, about referrals to clinical trials, and don't feel shy about reaching out to our colleagues and academic centers, even if you don't have the resources in a smaller institution. We also not only need to engage with the communities, we also need to build up a healthcare research community that has representatives from these various communities. So, it's really a collective effort that we build up and are proactive about building a more equitable healthcare system and research system that works for all of us and that really is going to provide us with the precision medicines that work for everybody. Dr Grouse: What do you think is the biggest debate or controversy related to the genetics and neuropathology of neurodegenerative dementias?  Dr Scholz: Yeah, there are loads of interesting debates, but I think in my field, in particular in the genetics is what to do with risk variance. What is it that I actually communicate to the patient? Obviously, I can learn a lot on the bench and I think I can use a lot of the genetic risk factors for molecular modeling, etc. But to which extent should I share that information? Because genetic information is something that we cannot alter and many of the risk factors are actually mild, that they may never result in disease. And so, communicating risk with patients is something that's very challenging and we used to just steer away from it. But now the discussion is starting to shift a little bit. You know, nowadays we are starting to offer, for example, testing for the APOE4 allele in individuals who are considering antiamyloid therapies. And this really, this is precision medicine in his earliest days because it allows us to stratify patients into those that are high-risk versus low-risk and those that need more frequent follow-up or may be advised not to pursue this treatment. And we're probably going to see more of those discussions and the ethics around it. And it's even harder in an aged population where you know, you may never manifest any of the symptoms despite carrying a lot of these risk deals. Dr Grouse: You mentioned, you know, that testing, APOE4 testing for certain populations when deciding to do the antiamyloid immunotherapies. Apart from that, which I think is a really good example of where genetic testing makes sense, what other scenarios do you think it makes sense at this point in time to recommend genetic testing for symptomatic patients who are concerned about neurodegenerative dementias? Dr Scholz: Yeah. So, I usually have a very frank discussion with patients in whom I suspect the genetic etiology. So those are individuals who have a strong family history, individuals from very early onset of the disease where genetic testing may allow us to establish a molecular diagnosis, individualize and refine our counseling, and potentially get them into targeted clinical trials that may be suitable for that. Those are always very nuanced discussions, but I usually start with those high-risk individuals. Increasingly patients are, even with the apparently sporadic forms, are asking me about it. And then I have a frank discussions about the pros and cons and offer it to the patients who really would like to pursue it.  Dr Grouse: That makes a lot of sense. What about in the case of patients who are asymptomatic but might have high risks because of, well, family members with certain types of neurodegenerative dementias? When would it make sense, if ever, to do genetic testing for them? Dr Scholz: Yeah, that's a that's a tough situation, to be honest. By and large, I would say I would like to understand what the motivation is to learn about the genetic status. If the motivation is something like family planning, future care planning, etc, then it may be a reasonable thing. But I also want to make it very clear upfront that knowing a genetic status, at least aside from APOE status, at least for now, doesn't actually change the clinical management. And I want to make sure patients understand if they are trying to lower their risk, knowing that genetic status is not going to lower their risk. There are other things, brain health habits, that are really important, that patients should double down on: avoiding vascular disease, avoiding traumatic brain injury, excessive alcohol use, etcetera. It's a discussion that really tries to understand the motivations behind the testing. But some patients are very frank and they want to have it. They may want to contribute to the research community, and so in those instances we may offer it, but I also really want to make them understand that knowing a genetic diagnosis may be acceptable to them, but family members who are related to them may not wish to know. And they can really cause a lot of psychological stress that extends beyond the individual. And then that's something to really consider before actually pursuing testing. Dr Grouse: I think that's a really good reminder, especially about how this can even affect people outside of the patient themselves. I think a lot of us don't even think about that. And certainly, our patients may not either. Taking it a step further, thinking about newly available biomarkers, imaging modalities, how should we incorporate the use of these for our patients when we're suspicious of things like Alzheimer's disease or dementia with the Lewy bodies? Dr Scholz: So by and large these biomarkers are used in in the research area, but we can, in a given patient where maybe the clinical presentation is somewhat atypical, we can use it to help with our diagnostic impression. It doesn't get rid of the clinical evaluation, but at least it gives us a little bit more certainty. Here are the you know, the molecular features, the abnormal amyloid tau deposits, for example, that we're there we're detecting supports diagnosis. May also sometimes help in patients where we suspect there could be even the co-pathology going on where we get a mixture of features, where we can counsel the patients and you know, detecting copathologies is something that is certainly challenging. We know that patients who have more pathologies on average are not doing as well as the ones who have relatively pure disease forms. But this is also an area of intense research and as long as it's used judiciously to help with the diagnostic compression, to reduce a diagnostic odyssey, I think there's a lot of potential there to improve the clinical evaluations nowadays. Dr Grouse: It is really exciting to see the options that are opening up as the years go by, which brings me to my next question. There is certainly, as we know, this new category of disease modifying therapies that are available in the form of the anti-amyloid immunotherapies. What else do you think's on the horizon for treatment and prevention, neurodegenerative dementias, going down the road five, ten, fifteen years down the line?  Dr Scholz: Yeah, I think we're entering the era of precision medicine already and we're, we're seeing it already with the anti-amyloid therapies. By and large, I think the standard of care is going to be a multidisciplinary individualized treatment plan that incorporates a more holistic view. It incorporates diet, lifestyle factors, symptomatic management, but also disease modification strategies and potentially even multitarget disease modifying strategies. I think there's a lot more work that we have to do, especially in in the non-Alzheimer's dementia field. But overall, we're becoming much better in refining our diagnostic impression and in treating some of the complications that arise in these very complex diseases.  Dr Grouse: I'm curious, with the future of dementia care and diagnosis being more of a precision medicine model, how do you think this will be possible in an aging population with already, I think, probably a limited access to neurologists even in current state? Dr Scholz: Yeah, this is- these are these are very challenging societal questions. Increasingly, you know, we can use modern technologies such as televisits for follow up, but also, you know, remote monitoring devices. We have to educate the next generation, we need more neurologists, we can't do it alone; but we also need to empower primary care doctors who are usually the first go-to person. And perhaps biomarker testing will become much more common even in the primary care setting. I think overall, you know, we can tackle it by educating the community, empowering participants in various clinical trials, and being flexible of embracing certain new technologies. Dr Grouse: Absolutely. I think that makes a lot of sense and hopefully this will be another call to arms to try to get the word out, get more access to neurology and more people interested and like you said, getting our other colleagues involved and being able to manage it as well.  Dr Scholz: Yeah.  Dr Grouse: I wanted to transition a little bit into learning more about you. How did you become interested in genetics of neurodegenerative dementias? Dr Scholz: Yeah, it's something, it's an interest that has grown gradually. I started out as a neuroscientist in in Austria, where I was fortunate to work with a group that was very strongly involved in Parkinson's disease care. And I was so thrilled to see patients, you know, treated with deep brain stimulation. But yet in the same clinic, I also saw the patients who were not eligible because they had atypical neurodegenerative diseases. And it's the realization that there is such a broad spectrum of diseases that we frankly don't understand very well, that we really need to work with, understand and hopefully develop the treatments with. That's really has resonated with me. And I've since then really built my entire career around it through different countries at the United Kingdom and the United States. And I'm very fortunate to work at the National Institutes of Health, where I can pursue a lot of these research passions and work with interesting patients and colleagues.  Dr Grouse: Well, I've learned a lot today, and I'm sure our listeners would agree. Thank you so much for joining us. It's really been a pleasure speaking with you.  Dr Scholz: Well, thank you so much for allowing me to contribute. And, you know, I hope the review article conveys a lot of the exciting developments in this really challenging field. But there's loads of hope that we will eventually get to the point to tackle these conditions.  Dr Grouse: I encourage all of our listeners to check out Dr Scholz 's article. It is a great overview of these conditions and the genetics and neuropathology underlining them. Again, thank you so much.  Dr Scholz: Thank you for having me. Dr Grouse: Again, today I've been interviewing Dr Sonia Scholz, whose article on genetics and neuropathology of neurodegenerative dementias appears in the most recent issue of Continuum on dementia. Be sure to check out Continuum audio episodes from this and other issues. And thank you to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, associate editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use this link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/AudioCME. Thank you for listening to Continuum Audio.

Matters Microbial #72: Who is in Your Water? January 2, 2025 Today, Dr. Ameet Pinto, Carlton S. Wilder Associate Professor in Civil and Environmental Engineering at the Georgia Institute of Technology, joins the #QualityQuorum to discuss the microbiome of drinking water and how it can be used to optimize safety and health.  Host: Mark O. Martin Guest: Ameet Pinto Subscribe: Apple Podcasts, Spotify Become a patron of Matters Microbial! Links for this episode A short review of a famous article by Dr. Norman Pace about the microbiome of showers and how microbial populations differed due to chlorination. An old discussion of microbial oligotrophy:  the ability to survive on very low levels of nutrients. The story of John Snow, a water fountain, and cholera in England. The concept of “Live/Dead” staining of microbes. An overview of the concept of metagenomics. An article on the microbiome of shower hoses. A public science outreach program to study the microbiome of showerheads. The Instagram link for Dr. Pinto's wonderful cat, Nessie. A great book describing exceptions to Mendelian genetics using cats:  “Cats Are Not Peas.”  Highly recommended. An article about water supplies and the pathogenic microbe Legionella. An overview of water disinfection techniques. An introduction to a model system of a microbial soil community, called THOR by Jo Handelsman and colleagues. Thinking of water treatment and related technologies as a series of ecological niches, via Tom Curtis and Bill Sloane. Dr. Pinto's faculty website. Dr. Pinto's deeply fascinating research group website. Intro music is by Reber Clark Send your questions and comments to mattersmicrobial@gmail.com

Send us a textLink to Health Type Quiz Link to Living Well, Aging Strong 6-month group experience As the holiday season approaches, the question of how much alcohol is too much becomes ever more pressing. What if the festive cheer of a drink or two could be clouded by the potential for long-term health risks? Dr. Bobby unpacks the complex and often contradictory research around alcohol, helping listeners navigate the decision: is it best to have none, or is a little okay? By exploring the impacts of alcohol on weight/appetite, heart disease, cancer, sleep, and cognitive health, and by considering personal health types, listeners can make more informed choices about their drinking habits. Key Topics Covered:Conflicting Headlines and Research: Discussing the confusion around alcohol's health effects, from Gallup poll insights to studies highlighting both potential benefits and risks.Health Risks Explored: Weight Gain: Alcohol adds calories and increases appetite, contributing to potential weight gain (study on caloric intake). Heart Disease: Early studies suggested moderate benefits for small amounts of alcohol, but advanced analyses, like Mendelian randomization, challenge this assumption, not showing a protective effect (study on genetic analysis). Cancer Risks: Alcohol consumption has been linked to several cancers, including breast and colon cancer.  (WHO fact sheet).Sleep Impacts: Alcohol disrupts sleep quality, even if consumed earlier in the day (small study on sleep effects).Cognitive Decline: Even mild drinking shows potential risks for brain health, with larger consumption exacerbating damage (UK Biobank study).Defining Drinking Levels: Categories from non-drinker to heavy drinking were clarified, helping listeners identify where they stand (National Survey on Drug Use and Health).Personal Stories and Practical Decisions: Dr. Bobby shares his personal experience with holiday indulgence and offers practical strategies for mindful drinking.Role of Health Types: Leveraging your health archetype (e.g., Purposeful Path Planner or Contentment Creator) to guide decisions about alcohol consumption.Takeaways:  Know Your Limits: For most, keeping alcohol under seven drinks per week minimizes risks without eliminating enjoyment.As we navigate the complexities of alcohol's impact on health, I share my personal approach of allowing myself up to seven drinks a week, accepting some level of risk for the sake of balance. With the Living Well Aging Strong program, we provide tools to create personalized health plans, empowering you to make choices that align with your lifestyle. Let's embark on this journey together, equipped with knowledge and support, as we strive for imp

Gregor Mendel was the father of modern genetics. He wrote his most important papers on the topic just a few years after Darwin published the Origin of Species. What people don't realize is that Mendel's papers did not only describe how traits are passed down. He also explained how his ideas of genetics lead directly to an explanation of the origin of species. Was Mendel directly and purposefully contradicting Darwin? Links and notes: Crompton et al. 2024 Mendelian speciation, part 1—what is the abundant source of significant biodiversity, J Creation 37(3):110–120, 2023. Crompton et al. 2024 Mendelian speciation, part 2—latent genetic information, J Creation 38(1):77–86, 2024. Crompton et al. 2024 Mendelian speciation, part 3—fixation and reproductive isolation, J Creation 382):97–104, 2024. Crompton et al. 2024 Mendelian speciation, part 4—adaptive radiations and cis-evolution, J Creation 38(2):105–112, 2024. Gregor Mendel on Wikipedia "They believe in bigger miracles than I do" on YouTube.com Species were designed to change on BiblicalGenetics.com Species were Designed to Change on Creation.com Arguments we think a creationist should not use on creation.com Wort und Wissen

Gregor Mendel was the father of modern genetics. He wrote his most important papers on the topic just a few years after Darwin published the Origin of Species. What people don't realize is that Mendel's papers did not only describe how traits are passed down. He also explained how his ideas of genetics lead directly to an explanation of the origin of species. Was Mendel directly and purposefully contradicting Darwin? Links and notes: Crompton et al. 2024 Mendelian speciation, part 1—what is the abundant source of significant biodiversity, J Creation 37(3):110–120, 2023. Crompton et al. 2024 Mendelian speciation, part 2—latent genetic information, J Creation 38(1):77–86, 2024. Crompton et al. 2024 Mendelian speciation, part 3—fixation and reproductive isolation, J Creation 382):97–104, 2024. Crompton et al. 2024 Mendelian speciation, part 4—adaptive radiations and cis-evolution, J Creation 38(2):105–112, 2024. Gregor Mendel on Wikipedia "They believe in bigger miracles than I do" on YouTube.com Species were designed to change on BiblicalGenetics.com Species were Designed to Change on Creation.com Arguments we think a creationist should not use on creation.com Wort und Wissen

Join us as we welcome back Dr. Veera Rajagopal, a discovery scientist at Regeneron with an interest in human genetics and drug target discovery in neuroscience and psychiatry. If you're a regular listener of The Genetics Podcast, you may be familiar with Dr. Veera's annual round-up episodes, and more recently, his quarterly appearances on the show. We're pleased to bring you the latest quarterly roundup, during which Dr. Veera and Patrick walk through the most recent developments in genetics, drug discovery, and precision medicine. In this episode, Dr. Veera and Patrick dive into a wide variety of topics, including: - The evolution of skin color in humans - The potential of a novel tau isoform for Alzheimer's treatment - Protective mechanisms of tomoregulin-1 against herpes simplex virus - The discovery of a new noncoding Mendelian disease mechanism linked to cardiac arrhythmias - A comparative analysis of whole genome versus whole exome sequencing for gene discovery. Tune in now, and don't forget to check out Veera's substack, GWAS Stories, and his Twitter, @doctorveera. Additionally, we're excited to invite you to an in-person meetup for The Genetics Podcast during the ASHG Annual Meeting in Denver, CO! Over the years, we've had the honor of speaking with leading voices across science, industry, patient advocacy, and policy. Now, we're bringing this incredible community together face-to-face. Join us on the evening of Thursday, November 7. To RSVP, visit: https://lu.ma/geneticspodASHG.

Today, you'll learn about the amazing transformative power of an out-of-body experience, how scientists want to use brain cells to do their computing, and a study that suggests eating cheese might make you live longer. Out-Of-Body Experience “Exploring the transformative potential of out-of-body experiences: A pathway to enhanced empathy.” by Marina Weiler, et al. 2024. “Out of body experiences and their neural basis.” by Olaf Blanke. 2004. Brain Cell Computing “Open and remotely accessible Neuroplatform for research in wetware computing.” by Fred D. Jordan, et al. 2024. “Neuromorphic wetware for artificial neural networks that overcome the limits of traditional computer hardware.” Innovation Toronto. 2023. “How Many Joules Does My Surge Protector Need?” by Karenann Brow. 2024. Cheese & Aging “Eating cheese plays a role in healthy, happy aging - who are we to argue?” by Bronwyn Thompson. 2024. “Mendelian randomization evidence for the causal effect of mental well-being on healthy aging.” by Chao-Jie Ye, et al. 2024. Follow Curiosity Daily on your favorite podcast app to get smarter with Calli and Nate — for free! Still curious? Get exclusive science shows, nature documentaries, and more real-life entertainment on discovery+! Go to https://discoveryplus.com/curiosity to start your 7-day free trial. discovery+ is currently only available for US subscribers. Hosted on Acast. See acast.com/privacy for more information.

An introduction to classical Mendelian genetics, in which we discuss Mendel's experiments with peas and the laws of heredity that he discovered, including inheritance of one allele from each parent, the law of dominance, and the law of independent segregation. We then consider more complex cases of genetic inheritance, including sex-linked traits, incomplete dominance, codominance, and epistasis. The episode concludes with a discussion of quantitative traits determined by many genes, including how genetic variation is described, how sources of variance are identified using genome wide association studies, and the conceptual issues with defining heredity and separating the effects of genes from those of environment.   If you enjoyed the podcast please consider supporting the show by making a PayPal donation or becoming a Patreon supporter. https://www.patreon.com/jamesfodor https://www.paypal.me/ScienceofEverything Check out out youtube channel! The Science of Everything Podcast - YouTube

The consumption of red meat, specifically the distinction between unprocessed and processed varieties, has been a subject of considerable debate in nutritional science and public health. There is a fair amount of confusion and lack of clarity surrounding this issue. While the harmful effects of processed meat are well-documented and less controversial, the evidence concerning unprocessed red meat is less consistent. This inconsistency often leads to a gray area in scientific discussions and public perception. In examining unprocessed red meat, we encounter a spectrum of claims, including minimal evidence of harm, context of overall diet and mechanistic concerns. Epidemiological evidence shows varied health outcomes related to red meat consumption across different populations. These variations underline the importance of defining and measuring “high” and “low” intake levels accurately in research. The challenges in nutrition research, including methodological flaws in meta-analyses and the rapid dissemination of simplified study results, can impact public health recommendations. Misinterpretations can arise from comparisons within narrow intake ranges or from studies failing to specify absolute intake levels. This podcast episode's goal is to clarify existing evidence, acknowledge areas needing further research, and explore why this topic is significant in the broader context of nutrition science, aiming to equip healthcare professionals with the knowledge needed to make nuanced and effective dietary recommendations. Links: Receive our free weekly email: the Sigma Synopsis Want to advance your understanding of nutrition science? Check out our course. Go to episode page for this episode Subscribe to Sigma Nutrition PREMIUM Timestamps 01:00 Introduction to the issue 03:16 Processed vs. unprocessed red meat 05:54 Health guidelines and recommendations 06:56 Epidemiological evidence and dose thresholds 09:55 Biological mechanisms and plausibility 21:00 Criticisms and misinterpretations in research 40:42 Substitution analyses and dietary patterns 46:37 Mendelian randomization and genetic studies 56:31 Effect modifiers and confounders 01:13:18 Key Ideas Segment (Premium-only)

Mental Health problems are common and there is good evidence for physical activity as an important role to help prevent and treat mental health conditions. The BJSM has collaborated with the PACC programme to help develop this podcast and has invited Professor Brendon Stubbs, a global expert in this space. Brendon is a clinical-academic physiotherapist and has published more than 800 academic papers and has advised the WHO and the World Psychiatric Association.  “The Physical Activity Clinical Champions or PACC programme is a national project delivering physical activity education to professionals working in healthcare to help get patients more physically active. It was previously being led by public health England as part of the moving healthcare professionals programme and funded by the national lottery & Sport England and is now being led by a consortium of The Faculty of Sport and Exercise Medicine, The Advance Wellbeing Research Centre at Sheffield Hallam University and Intelligent Health and is being re-designed with new resources. This podcast forms part of a series to support physical activity education for professionals working in healthcare. For anyone you would like to get involved with PACC project then please do email us at pacc@shu.ac.uk  PAPERS MENTIONED Physical activity Prevention of Mental Health Problems Physical Activity and Incident Depression: A Meta-Analysis of Prospective Cohort Studies - PubMed (nih.gov) Physical activity protects from incident anxiety: A meta-analysis of prospective cohort studies - PubMed (nih.gov) Physical activity and sedentary behaviour:  The association between sedentary behaviour and indicators of stress: a systematic review - PubMed (nih.gov) Testing the causal relationships of physical activity and sedentary behaviour with mental health and substance use disorders: a Mendelian randomisation study - PubMed (nih.gov) Changes in sedentary time are associated with changes in mental wellbeing over 1 year in young adults - PMC (nih.gov) Treatment of Mental Health conditions Exercise and internet-based cognitive-behavioural therapy for depression: multicentre randomised controlled trial with 12-month follow-up - PubMed (nih.gov) Antidepressants or running therapy: Comparing effects on mental and physical health in patients with depression and anxiety disorders - PubMed (nih.gov) Other resources mentioned:  https://movingmedicine.ac.uk Home - Mind

On today's episode Fei and Nick go back to basics with genetics -- we realized we have never discussed genetics and inheritance patterns! We review single gene inheritance and Mendelian genetics for the first part of this series.  The OB/Gyn Intern Challenge is happening soon for 2024! Go onto our website to get signed up to be part of this innovative text-message course in May of this year absolutely free. www.obgyninternchallenge.com  Twitter: @creogsovercoff1 Instagram: @creogsovercoffee Facebook: www.facebook.com/creogsovercoffee Website: www.creogsovercoffee.com Patreon: www.patreon.com/creogsovercoffee You can find the OBG Project at: www.obgproject.com

In this episode of Longevity by Design, Dr. Gil Blander and Ashley Reaver, MS, RD, CSSD, sit down with Dr. Bartek Nogal from InsideTracker to explore the cutting-edge intersections of exercise, genetics, blood biomarkers, health optimization, and longevity. Dr. Bartek Nogal, with a strong background in biological engineering and genomics, dives into how personalized health data can shape our understanding of aging and wellness. He discusses InsideTracker's new innovative approach to using DNA analysis for tailoring health interventions, emphasizing the importance of actionable guidance for optimizing blood biomarkers and extending healthspan and longevity.Dr. Bartek Nogal shares compelling insights into the latest findings from InsideTracker's peer-reviewed published study on the effect of running on blood biomarkers and metabolic health, along with the influence of genetics—highlighting the power of exercise combined with the added value genetics provide for even greater personal health optimization. Dr. Nogal also discusses InsideTracker's new innovative DNA healthspan report and the enhanced information and deeper insights it provides. The conversation is a deep dive into how technology bridges the gap between scientific research and everyday health practices, offering listeners a roadmap to a longer, healthier life. Listeners will leave with a clear understanding of the power of exercise on blood biomarkers and genomics for personal health and practical tips for leveraging their genetic information to make even better-informed lifestyle choices. This episode is a testament to the evolving landscape of health and science, where the fusion of data, technology, and personalized insights paves the way for a future of optimized health and longevity.Listen to all episodes of Longevity by Design at https://info.insidetracker.com/longevitybydesign Episode timestamps:Introduction: 00:00-02:32What led Dr. Bartek Nogal to become a scientist: 02:33-03:27Dr. Bartek Nogal's career at InsideTracker: 03:28-04:02InsideTracker's peer-reviewed study: Dose response of running on blood biomarkers of wellness in generally healthy individuals (https://pubmed.ncbi.nlm.nih.gov/37967046/): 04:03-06:46What is principal component analysis (PCA), and what were the findings using PCA: 06:47-07:56What is the effect of running blood biomarkers? What is the effect of the amount of running on blood biomarkers?: 07:57-09:27What was the effect of running on BMI (body mass index): 09:28-10:44What is Mendelian randomization, and what is the relationship of genetics with exercise and blood biomarkers? : 10:45-12:40What is the influence of genes on the relationship between exercise and diet: 12:41-13:33What are the strengths of Mendelian randomization for understanding the influence of genetics: 13:34-17:05What were the key findings from InsideTracker's study on the effect of running on blood biomarkers 17:06-18:56What is InsideTracker's new DNA report? What was the motivation for developing this new DNA healthspan report: 18:57-20:31What additional information and insights does InsideTracker's new DNA report and scores provide: 20:32-28:41How much do genes or lifestyle influence blood biomarkers and risk of developing diseases:  28:42-32:24How to use InsideTracker's new DNA and healthspan scores to optimize blood biomarkers and health: 32:25-34:28What is the future of genetics research: 34:29-36:36What is the future of genetic testing at InsideTracker: 36