Podcasts about ldl cholesterol

Mexico's first fatal H5N1 case involved a healthy child and highlights localized risk despite low global concern. Long-term antidepressant use was linked to higher sudden cardiac death risk, especially in younger adults. A U.S. study found 25% of adults with very high LDL cholesterol lacked statin treatment. These stories reveal persistent gaps in infection control, cardiac monitoring, and preventive care.

Do you know your “remnant cholesterol”? It could be better than LDL for predicting your risk of having a heart attack or stroke; Vagal nerve stimulation for seizures—could adding a keto diet help? Exoskeletons that help runners, hikers, and cyclists have hit the consumer marketplace for recreational athletes; RFK Jr's HHS launches program to improve infant formulas; Insurers bilk taxpayers for billions by double-charging Medicaid.

Let's be real—entrepreneurs love the grind. Late nights, early mornings, endless coffee, and pushing the limits to build the dream. But here's the catch: if your heart isn't in peak condition, all that hustle could be cutting your time short.So, how do you level up your business without sacrificing your health?In this episode of The Happy Hustle Podcast, I sat down with Dr. Stefan Waller, a cardiologist turned health coach, to break down real strategies for optimizing heart health—without the fluff. We're talking about preventing heart disease before it even starts, simple nutrition hacks, and the key health metrics every entrepreneur should track.Dr. Waller emphasizes the importance of knowing your numbers. If you don't track your business finances, you'll go broke, right? Same thing with your health—if you don't track your key metrics, your body might be running on borrowed time.Here are two critical numbers you should be checking regularly:1️⃣ LDL Cholesterol (The Silent Killer)

Let's break down key insights from a recent two-hour and 20-minute conversation between Dr. Peter Attia and renowned lipidologist Tom Dayspring. Support your Intermittent Fasting lifestyle with the Berberine Fasting Accelerator  by MYOXCIENCE: https://bit.ly/berberine-fasting-accelerator Use code podcast to save 12% Get the Blood Work Cheat Sheet: https://courses.highintensityhealth.com/blood-work-cheat-sheet Show Notes: https://bit.ly/4hrDc72 Time Stamps:  0:00 Intro 0:52 Cholesterol's Role in Atherosclerosis  1:51 Triglycerides & Insulin Resistance: The Overlooked Risk Markers  3:28 Lipoprotein Exchange & Insulin Resistance  7:18 Triglycerides to HDL Ratio as a Risk Indicator  8:36 Metabolically Healthy Phenotype & LDL: 9:20 Sauna Therapy for Cardiovascular Health: 11:00 Cholesterol, Endothelial Health & Plaque Formation: 14:53 Case Study: A 24-Year-Old Athlete with High LDL 21:00 Lipoprotein(a) (LP(a)) and Its Role in Cardiovascular Risk:

Thank you for joining us for another episode of the Low Carb MD Podcast. Dr. Austin Dudzinski is Board Certified clinical pharmacist with special interest in nutrition and lifestyle modification to address the root cause of chronic, cardiometabolic disease. He is a Board Certified ambulatory care clinical pharmacist at Think Whole Person Healthcare - an integrated medical home - where he works primarily with patients with chronic cardiometabolic disease with the main focus of de-prescribing and getting to the root cause of illness. In this episode, Drs. Tro, Brian, and Austin talk about… (00:00) Intro (05:02) De-prescribing and addressing the root cause of disease with diet/lifestyle (16:38) How Austin first became interested in nutrition and lifestyle interventions (19:16) Pushback from other medical professionals against Austin's new low carb ideas (21:28) GLP-1 drugs (25:30) Bringing the perspective of food addiction into the conversation with obese, metabolically unwell patients (28:19) How the average person should view GLP-1 use and compounding pharmacies (35:29) LDL Cholesterol and A1C (40:16) Cardiovascular risk assessment (44:42) What we know and what we suspect is true of cardiovascular disease (48:52) Rheumatological disease and cardiovascular risk (52:20) The gut microbiome and ketosis (59:12) Plaque reduction and coronary calcium reduction (01:07:34) An overview of drugs and supplements that reduce plaque and, in some cases, all cause mortality (01:11:19) Outro For more information, please see the links below. Thank you for listening! Links: Please consider supporting us on Patreon: https://www.lowcarbmd.com/ Resources Mentioned in this Episode: Nutrition and mental health: A review of current knowledge about the impact of diet on mental health: https://www.frontiersin.org/journals/nutrition/articles/10.3389/fnut.2022.943998/full The role of diet and nutrition on mental health and wellbeing: https://www.cambridge.org/core/journals/proceedings-of-the-nutrition-society/article/role-of-diet-and-nutrition-on-mental-healthandwellbeing/372284768DB78DB02EB199E277AABF79 Bottle of Lies (book by Katherine Eban): https://www.amazon.com/Bottle-Lies-Inside-Story-Generic/dp/0062338781 MESA Study: https://www.mesa-nhlbi.org/MESA_508TextOnly.htm Dr. Austin Dudzinski: Think Health Care: https://thinkhealthcare.org/providers/austin-dudzinski/ Linkedin: https://www.linkedin.com/in/austin-dudzinski-pharmd-bcacp-b1635098/ Dr. Brian Lenzkes:  Website: https://arizonametabolichealth.com/ Twitter: https://twitter.com/BrianLenzkes?ref_src=twsrc^google|twcamp^serp|twgr^author Dr. Tro Kalayjian:  Website: https://www.doctortro.com/ Twitter: https://twitter.com/DoctorTro Instagram: https://www.instagram.com/doctortro/ Toward Health App Join a growing community of individuals who are improving their metabolic health; together.  Get started at your own pace with a self-guided curriculum developed by Dr. Tro and his care team, community chat, weekly meetings, courses, challenges, message boards and more.  Apple: https://apps.apple.com/us/app/doctor-tro/id1588693888  Google: https://play.google.com/store/apps/details?id=uk.co.disciplemedia.doctortro&hl=en_US&gl=US Learn more: https://doctortro.com/community/ 

ไลฟ์ #90: หลักฐานทางคลินิคและพยาธิวิทยา ที่สนับสนุน “The zero-LDL Hypothesis”วันจันทร์ 24 ก.พ. 2568เวลา 20.00 น.✅ จากหลักฐาน A consensus statement from the European Atherosclerosis Society Consensus Panel“Low-density Lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic. Epidemiologic, and clinical studies.ตีพิมพ์ใน European Heart Journal 24 April, 2017 ซึ่งรวบรวมการติดตามคนไข้ไป 20 million person years พบความสัมพันธ์เชิงเส้นตรงระหว่างระดับ LDL-Cholesterol กับ ความเสี่ยงของโรคหลอดเลือดหัวใจ ยิ่งลดระดับ LDL-Cholesterol ได้ต่ำเท่าไหร่ ความเสี่ยงของโรคหลอดเลือดหัวใจก็ลดลงเท่านั้น✅ ถึงแม้ว่าจะมีหลักฐานทางคลินิกที่สนับสนุนผลลัพธ์ของการลดระดับ LDL-C ในการป้องกันการเกิดโรคหลอดเลือดหัวใจมากแค่ไหนก็ตาม มันก็ยังคงน่าสนใจเป็นอย่างยิ่งที่จะศึกษาว่า การลดระดับ LDL-C ให้ต่ำอย่างยิ่งยวด มีผลกระทบต่อภาวะธำรงดุลของไขมันในเลือด (Lipid Homeostasis) หรือไม่

What if everything you thought you knew about “heart-healthy” cooking oils was based on outdated science and clever marketing? In this episode, I've sat down once again with Max Lugavere, and we've had an amazing conversation about the metabolic chaos that modern seed oils are silently creating in our bodies, and why the food industry's favourite oils might be driving the global rise in chronic disease. We also uncovered some actionable steps that we hope to see prioritised with the new government, and especially with the Make America Healthy Again movement. Ready to transform your understanding of nutrition and take control of your overall health? Hit subscribe and share this video with someone who needs to hear this message. Join Gary Brecka's FREE 3-Day Morning Routine Challenge!

This week on FUELED, we're joined by renowned cardiologist Dr. Carl ‘Chip' Lavie to unravel the complexities of LDL cholesterol and its impact on our health and risk factors. We go beyond the basics, shedding light on what the numbers really mean. Dr. Lavie offers insights into the latest tests, treatments and potential benefits of supplements like Red Yeast Rice. Tune in to gain a deeper understanding of your cholesterol profile and how to best take charge of your heart health. LINKS + NOTES Red Yeast Rice extract - brand approved by Consumer Lab: HPF Cholestene™  ASCVD Cardiovascular Risk Calculator | https://bit.ly/3WuL8N0  Past episodes with cardiologist Dr. Lavie:  Fish Oil: A Masterclass in Omega-3s | https://bit.ly/4hhKk6m Heart Symptoms You Shouldn't Ignore | https://bit.ly/4jnUIex Learn more about your ad choices. Visit megaphone.fm/adchoices

Dr. Andrew Freeman reviews the latest evidence on the benefits of a plant-based lifestyle in 2024. Discover why living this way is essential for health, sustainability, and the future. #PlantBased2024 #HealthBenefits #SustainableLiving

Comprehensive Cardiovascular Health and Prevention with Jim LaValle: In this episode of the Intelligent Medicine Podcast, Jim LaValle, a clinical pharmacist and heart health expert discusses various aspects of cardiovascular health in honor of Heart Health Month. The discussion covers risk factors for heart disease, including metabolic health markers and lifestyle influences. They examine the pros and cons of statins, their impact on brain health, and the role of natural supplements like Kyolic Aged Garlic Extract in cardiovascular prevention. Specific criteria for an ideal cardiovascular risk assessment are provided, and practical advice on exercise and maintaining a balanced diet is shared. 

Dr. Hoffman continues his conversation with Jim LaValle, a Clinical Pharmacist, Author, Board Certified Clinical Nutritionist, and Heart Health Expert. 

Residents living in and around Floresville can learn about their risk for cardiovascular disease, osteoporosis, diabetes, and other chronic, serious conditions with affordable screenings by Life Line Screening. American Legion Post 38 will host this community event on Monday, Feb. 3, at 1412 Fourth St. in Floresville. Screenings can check for: •The level of plaque buildup in your arteries, related to risk for cardiovascular disease, stroke, and overall vascular health •HDL and LDL Cholesterol levels •Diabetes risk •Kidney and thyroid function, and more. Screenings are affordable and convenient. Free parking is also available. Special package pricing starts at 9, but...Article Link

Dave MacLeod is one of the best all-around climbers in the world. He returns to the podcast to talk about his new book, Moving the Needle. We discuss the simple decisions that led to his success, getting the basics right, how to climb harder in your 40s, the value of daydreaming, writing books, how diet affects mood, Paul Saladino's meat and fruit approach, how to thrive on a keto diet, metabolic health, LCL cholesterol, seed oils, alcohol, the state of scientific research, and much more. Mad Rock:madrock.comUse code “NUGGET10” at checkout for 10% off your next order.AG1:drinkAG1.com/NUGGETUse this link to get a free year's supply of vitamin D + 5 travel packs.Arc'teryx:Women's climbing clothingMen's climbing clothingCheck out the Psiphon and Serratus Alpine Kits launching January 15th.PhysiVantage:physivantage.com (link includes 15% off coupon)Use code "NUGGET15" at checkout for 15% off your next order.The NUG:frictitiousclimbing.com/products/the-nugCheck out my new portable hangboard.Tindeq:tindeq.comUse code “nugget” for $10 off your order. Become a Patron:patreon.com/thenuggetclimbingWe are supported by these amazing BIG GIVERS:Michael Roy, Mark and Julie Calhoun, and Yinan LiuShow Notes:  thenuggetclimbing.com/episodes/dave-macleod-returnsNuggets:(00:00:00) – Intro(00:02:34) – Themes for the today's podcast(00:04:59) – ‘Moving the Needle'(00:10:54) – How curiosity feeds consistency(00:17:44) – Simple decisions that move the needle(00:21:55) – Time x mileage x variety(00:34:09) – Balancing projecting & volume(00:41:08) – Tree crimping(00:43:50) – Almost daily training(00:49:08) – The basics(01:00:38) – When to end bouldering sessions(01:06:38) – Rolling with the punches(01:13:31) – Managing training load & staying in the game(01:24:43) – Finger training(01:30:09) – An unlikely breakthrough (FA of ‘Bultitude' V14)(01:37:09) – Finger strength PRs(01:43:42) – How to climb harder in your 40s(01:59:54) – Taking short breaks(02:02:56) – Daydreaming(02:05:30) – Making it hard to fail(02:13:27) – One thing at a time(02:17:19) – Writing books(02:25:25) – Factors that led to sending ‘Rhapsody' E11(02:32:16) – Books vs. podcasts(02:34:35) – Confidence & conflict(02:42:06) – Dave's experiment with a Western Diet(02:46:48) – How our diet can affect mood(02:52:26) – Paul Saladino, keto, fruit, & metabolic health(03:10:37) – Why Dave keeps coming back to keto(03:15:52) – How much protein Dave eats on keto(03:19:36) – Energy & weight management(03:26:40) – LDL Cholesterol(03:40:25) – Kitavan Islanders, heart disease, & lifestyle factors(03:46:51) – Seed oils & alcohol(03:49:25) – A need for unbiased scientific research(03:54:50)  Where to buy Dave's book

In this episode, we dive into the challenges of working with our changing hormones age 35 and beyond, aka perimenopause, and how to reclaim vibrant health through simple female-specific lifestyle, nutrition and fitness changes. Your host, Louise, a multi award-winning women's integrative health practitioner and performance scientist, shares her personal journey of overcoming hormonal imbalances, gut issues, and genetic challenges, offering practical tips to improve your health and fitness naturally.We break down how hormonal shifts, like declining estrogen, can affect cholesterol and heart health. We explore cutting-edge biomarkers, clinical findings and what we can do about it. This episode encourages women in their 30s and beyond to take charge of their well-being with regular lab checks, proactive holistic health and performance monitoring. Instead of counterproductive messaging that medication is the only solution, the focus is on strategic nutrition, smart supplementation, and female-specific exercise strategies to feel, look and perform your best.Another key takeaway is the importance of community. A supportive group of like-minded ambitious active women and runners can keep you motivated, share innovative tips, and empower you to stay on track during perimenopause's many ups and downs. You'll also learn actionable ways to lower LDL cholesterol, reduce inflammation, and use tools like the Function Health platform to understand your unique female physiology better.Whether you love fitness, endurance sports, or are looking to live a long, healthy and vibrant life, this episode offers simple, empowering strategies to take control of your holistic well-being.Join Function Health & own your health with 110+ biomarker insights with us here:  https://my.functionhealth.com/signup?code=LVALENTINE11&_saasquatch=LVALENTINE11Get our free nutrition guide, weekly newsletter & explore our industry-leading Badass Breakthrough Academy here: https://www.breakingthroughwellness.com/Save 20% off healthcare's best supplements & wellness products with Louise's curated picks in our Fullscript portal here: https://us.fullscript.com/welcome/breakingthroughwellness/store-startEpisode Highlights:(0:00) Intro(3:16) Louise's health journey: Overcoming hormone and fitness struggles(6:10) Advocating for health: Navigating traditional vs. functional medicine(7:28) Understanding LDL cholesterol: Impact of lifestyle and genetic factors(12:17) Hormonal changes and cardiovascular risks in perimenopause(19:13) Personalized health monitoring: Tools and platforms to try(25:06) Dietary strategies: Reducing inflammatory foods and optimizing nutrition(35:52) Targeted supplementation: Omega-3s, red yeast rice, and more(43:51) Importance of community: Sharing resources and experiences(1:02:21) OutroTune in weekly to "Maximizing Fitness, Physique, and Running Through Perimenopause" for a simple female-specific science-based revolution. Let's unlock our best with less stress!I'd love to connect!Instagram

Become a member of The Metabolic Initiative to access exclusive ad-free episodes and earn CMEs here. In this journal club episode, host Victoria Field is joined by Dr. Angela Poff and Dr. Dominic D'Agostino to dive into two groundbreaking studies shaping our understanding of metabolism and its role in health and disease. The team explores the nuances of a recent randomized controlled trial on ketogenic diets, free sugar restriction, and their effects on glucose tolerance, lipid metabolism, and the gut microbiome. Then, they tackle a cutting-edge study uncovering the molecular mechanisms of ketogenic diets in reshaping cancer metabolism through lysine beta-hydroxybutylaration.From the clinical implications of these findings to the potential of ketone supplementation, this episode is packed with insights for researchers, clinicians, and health enthusiasts. Don't miss the opportunity to learn how these discoveries could shape the future of precision medicine.

Dr. Philip Ovadia, a heart surgeon, discusses his personal journey from being an unhealthy surgeon to advocating for low-carb and carnivore diets. He emphasizes the importance of coronary artery calcium scans in assessing heart health, critiques the traditional reliance on LDL cholesterol as a primary risk factor for heart disease, and explores the implications of dietary choices, particularly the role of seed oils and inflammation in heart disease. Dr. Ovadia also addresses various heart conditions, including atrial fibrillation, and offers insights into effective dietary strategies for improving heart health. Chapters 00:00 Introduction to Dr. Philip Avadia 11:16 Challenging LDL Cholesterol Myths 19:05 Blood Thinners and Their Effectiveness 24:40 Debunking Saturated Fat Myths 31:53 Exploring the Carnivore Diet and Ketosis 36:48 Understanding Arrhythmias and Inflammation 46:10 Lipoprotein(a) and Its Impact on Cardiovascular Risk 51:54 Lean Mass Hyper Responder: A Unique Metabolic State 57:10 The Connection Between Seed Oils and Heart Disease

Ready to reverse your chronic disease? Dr. Ford and the PrevMed staff are currently accepting new patients for a limited time. Book an appointment here: https://prevmedhealth.com/To ensure quality of care there are limited openings available so act quickly.

A new study finds poor metabolic health and low HDL is a greater predictor of coronary artery calcium than LDL cholesterol.  Support your Intermittent Fasting lifestyle with the Berberine Fasting Accelerator  by MYOXCIENCE: https://bit.ly/berberine-fasting-accelerator  Use code podcast to save 12% Video & Links to study: https://bit.ly/3Zj56fA Time Stamps:  0:00 Intro 0:30 LDL does not correlate with the degree of coronary artery plaque. 1:02 HDL is protective against coronary artery disease and plaquing. 2:10 Triglycerides correlate with diabetes, coronary artery disease and plaquing. 3:45 HDL size is highly predictive. 5:15 LDL, vLDL, and IDL had no strong association. 8:00 LDL may be lower with prediabetes and diabetes, reflecting imbalance. 12:10 HDL is increased by lifestyle. 13:00 Plaquing is more common in diabetics. 15:47 High triglycerides increase odds of metabolic disease by 100%. 18:00 The smaller HDL particles become, the less protective they are. 19:13 Coronary artery calcium is associated with HDL size, concentration and composition. 21:20 High HDL with low triglycerides is linked with better metabolic health. 23:10 Exercise increases the size and number of your protective HDL.  

Welcome back to the show!Today we have a Q and A episode and I have my friend and former client Emma Becker joining me to help ask the questions. In this episode we cover the following:Are nitrates/nitrites in lunch meat harmful to our health?Does cheese impact LDL cholesterol?What are the benefits of strength training versus cardio and is one better than the other?Are there any health benefits of Kangen water?Tune in to the show to better understand these topics and gain practical tips and strategies to help you live the healthiest life possible!LinksWant to leave a question for the next Q and A episode? You can do so here. https://www.thenutritionsciencepodcast.com/contact/Join our Nutrition Mastery Blueprint Course for 50% off before December 1sthttps://www.dradrianchavez.com/BLUEPRINT Studies comparing cheese vs. butter on LDL cholesterol Podcast Episodes mentioned in this episode:Are Saturated Fats Harmful To Our Health? https://www.thenutritionsciencepodcast.com/are-saturated-fats-harmful-to-our-health/ Two Part Series on LDL CholesterolPart 1: Does LDL Cholesterol Cause Heart Disease?https://www.thenutritionsciencepodcast.com/does-ldl-cholesterol-cause-heart-disease/Part 2: Lifestyle Strategies to Lower Cholesterol Levelshttps://www.thenutritionsciencepodcast.com/lifestyle-strategies-to-lower-cholesterol-levels/How to Build a Simple, Effective Exercise Planhttps://www.thenutritionsciencepodcast.com/how-to-build-a-simple-effective-exercise-plan/Support the show. https://www.paypal.com/paypalme/drchavez  Enjoying the show or have a questions about a particular topic? Send us a message here. Support the show

In this episode, Dr. Reddy and Anna dive into the often misunderstood role of LDL cholesterol, revealing its surprising functions beyond the “bad” reputation. While commonly viewed as a villain in heart health, LDL actually serves important protective roles within the body, such as supporting the immune system and transporting essential cholesterol for hormone production. The conversation explores how LDL can act as a defense against toxins and certain infections, and what happens when it's damaged or oxidized, leading to potential cardiovascular issues. Listeners will learn practical tips on minimizing LDL oxidation through diet, lifestyle choices, and simple adjustments to support heart health and overall well-being.

When discussing cardiovascular health, few topics stir as much debate as cholesterol, particularly in relation to low-carb and ketogenic diets. Recently, there's been significant attention given to a proposed model that suggests high LDL cholesterol may not pose the same cardiovascular risk in certain individuals, specifically those labeled as “lean mass hyper-responders.” This raises important questions: Is it possible that high cholesterol might not be dangerous for everyone? Or are we witnessing a dangerous misinterpretation of the science? In this episode, we break down the ideas behind the “lipid energy model” and explore how it has been framed in the context of low-carbohydrate and ketogenic diets. While proponents claim this model sheds light on how some people can have elevated LDL without increasing heart disease risk, critics warn that miscommunication and oversimplification of these ideas are leading many down a dangerous path. With real-world health decisions hanging in the balance, it's crucial to carefully examine what the science truly says about cholesterol, inflammation, and heart disease. Join us as we dive into the evidence with Dr. Gary McGowan. We'll dissect what the current research supports, what remains speculative, and how social media has amplified both the promising and problematic aspects of this model. If you've ever wondered about the impact of high cholesterol on heart disease risk in the context of ketogenic or low-carb diets, this episode is essential listening. Timestamps 02:27 What are the “Lean Mass Hyper Responder” phenotype and the “Lipid Energy Model” 27:29 Looking at recent publications and the “KETO Trial” 47:06 Public communication and misinterpretation 51:18 Clinical implications of diet-induced dyslipidemia 55:14 Responsibility in scientific communication 57:30 Real-world examples of poor communication or misinterpretation 01:13:27 Ethical concerns with the promotion of the model 01:25:59 Final thoughts Related Resources Go to episode page Join the Sigma email newsletter for free Subscribe to Sigma Nutrition Premium Enroll in the next cohort of our Applied Nutrition Literacy course Find Dr. McGowan at: Triage Method Instagram: @drgarymcgowan Papers discussed in this episode: Norwitz et al., 2022 – The Lipid Energy Model: Reimagining Lipoprotein Function in the Context of Carbohydrate-Restricted Diets Norwitz et al., 2021 – Elevated LDL Cholesterol with a Carbohydrate-Restricted Diet: Evidence for a “Lean Mass Hyper-Responder” Phenotype KETO Trial: Budoff et al., 2024 – Carbohydrate Restriction-Induced Elevations in LDL-Cholesterol and Atherosclerosis

Thank you for tuning in for another episode of Life's Best Medicine. Dr. Adrian Soto-Mota, MD, PhD is a clinical researcher at the Metabolic Diseases Research Unit at The National Institute of Medical Sciences and Nutrition Salvador Zubirán (INCMNSZ). He obtained his M.D. at UNAM (2013) and specialized in Internal Medicine at (INCMNSZ). Afterward, he obtained his Ph.D. at the University of Oxford (2021) and his Professional Certificate in Data Science that same year. Currently, he also serves as an Internal Medicine Consultant at (INCMNSZ), and as a Clinical Sciences Lecturer at the Monterrey Institute of Technology and Higher Education. His research interests are Human Metabolism (focused on Ketone Metabolism), Data Analysis, and Evidence-Based Medicine. He is an active member of the American College of Physicians. In this conversation, Drs. Brian and Adrian talk about… The field of statistics and how it impacts peoples' perceptions/beliefs about nutrition What drew Dr. Adrian to the field of medicine and how he found his way into doing nutrition research Mental health and its relation to metabolic health The process of change in dominant scientific theories How psychology comes into play when helping patients LDL Cholesterol and heart health Lean Mass Hyper-responders For more information, please see the links below. Thank you for listening! Thank you for listening. Have a blessed day and stay healthy!   Links:   Dr. Adrian Soto-Mota: Twitter Linkedin   Dr. Brian Lenzkes:  Arizona Metabolic Health Low Carb MD Podcast   HLTH Code: HLTH Code Promo Code: METHEALTH HLTH Code Website   Keto Mojo: Keto Mojo

In this episode of Hart2Heart with Dr. Mike Hart is joined by Dr. Anish Koka to a cardiologist based in Pennsylvania. They dive deep into a range of topics related to cardiology, focusing on cardiac health, the impacts of the C19Vax on the heart, and the potential benefits of various blood markers in assessing heart disease risk. Dr. Koka shares his knowledge on the vaccine's long-term effects, the role of statins, aspirin use, and the relevance of markers like LDL, HDL, triglycerides, and Lp(a). Additionally, they discuss how these markers influence treatment decisions in practice and explore novel approaches to cardiovascular health. Guest Bio and Links: Dr. Anish Koka is a Philadelphia-based cardiologist with a passion for patient-centered care and personalized treatment plans. He runs a private practice and frequently writes and speaks on healthcare policy and cardiac health. Listeners can learn more about Dr. Anish Koka at his website and on substack @anishkokamd  Show Notes: (0:00) Welcome back to the Hart2Heart Podcast with Dr. Mike Hart    (0:15) Dr. Hart introduces Dr. Anish Koka to the listeners (0:50) Dr. Koka gives a brief introduction and background of himself  (4:00) Myocarditis and COVID-19 vaccines (6:00) No long-term rise in cardiac issues post-vaccine (9:00) Long-term cardiac complication (12:30) A closer look at triglyceride to HDL ratio (18:00) The history of LDL and its impact on heart health (22:30) The law of diminishing returns in cholesterol management (26:30) Role of CRP in cardiac risk assessment (31:00) Colchicine - a powerful anti-inflammatory drug (35:30) A possible new marker for cardiovascular risk - Lp(a) (44:00) Particle size testing - worth it? (47:30) High oxidized LDL (52:00) Aspirin - general approaches --- Dr. Mike Hart is a Cannabis Physician and Lifestyle Strategist. In April 2014, Dr. Hart became the first physician in London, Ontario to open a cannabis clinic. While Dr. Hart continues to treat patients at his clinic, his primary focus has shifted to correcting the medical cannabis educational gap that exists in the medical community.  Connect on social with Dr. Mike Hart: Social Links: Instagram: @drmikehart Twitter: @drmikehart Facebook: @drmikehart

In this special episode titled “Lipids – Beyond Statins and LDL Cholesterol”, our host, Dr. Neil Skolnik will discuss with two expert guests the details of treatment for LDL-Cholesterol, Triglycerides, and other lipid risk markers.  This special episode is supported by an independent educational grant from Amarin. Presented by: Neil Skolnik, M.D., Professor of Family and Community Medicine, Sidney Kimmel Medical College, Thomas Jefferson University; Associate Director, Family Medicine Residency Program, Abington Jefferson Health James Underberg, M.D. , Clinical Assistant Professor of Medicine at NYU School of Medicine and the NYU Center for Prevention of Cardiovascular Disease, Director of the Bellevue Hospital Lipid Clinic, and Past President of the National Lipid Association. Layla A. Abushamat, M.D., MPH, Assistant Professor, Department of Medicine in the Division of Atherosclerosis and Vascular Medicine, Baylor College of Medicine,  Houston, Texas   Selected references referred to the in the Podcast: 1.     Icosapent Ethyl: REDUCE-IT - N Engl J Med 2019; 380:11-22 2.     Omega-3 Fatty Acids: STRENGTH trial - JAMA. 2020;324(22):2268-2280 3.     Lipoprotein(a) Blood Levels and Cardiovascular Risk Reduction With Icosapent Ethyl. JACC. 2024 Apr, 83 (16) 1529–1539 4.     Icosapent ethyl following acute coronary syndrome. European Heart Journal 2024; 45:1173–1176 5.     Cardiovascular Disease and Risk Management: ADA Standards of Care in Diabetes—2024. Diabetes Care 2024;47(supp 1): S179–S218

In this interview, Dave Feldman, citizen scientist and founder of the Citizen Science Foundation, and Nick Norwitz, Oxford PhD and Harvard medical student, discuss their latest study, which challenges the traditional view of LDL cholesterol and its relationship to heart disease risk and metabolic health. Their research focuses on lean mass hyper-responders (LMHRs)—lean, metabolically healthy individuals on a low-carb, high-fat diet, also known as a ketogenic diet. Their findings suggest that LDL cholesterol levels may not contribute to plaque buildup in these individuals as is commonly believed in the general population. They also delve into the role of coronary CT angiograms as a powerful tool for more accurately diagnosing heart health and evaluating cardiovascular risk. This study provides new insights into the intersection of cholesterol, heart disease, and metabolic health, offering fresh perspectives on how we should rethink diet, cholesterol management, and long-term health outcomes. Watch as they break down the intersection of cholesterol levels, heart disease, and metabolic health, offering fresh perspectives on assessing cardiovascular risk in modern medicine and calling for further research. Don't miss this enlightening discussion that could change how we view diet, cholesterol, and long-term health outcomes! *Featured In This Video* Dave Feldman X: @realDaveFeldman LinkedIn: https://www.linkedin.com/in/dave-feldman/ https://citizensciencefoundation.org/ Nick Norwitz, PhD X: @nicknorwitz https://www.linkedin.com/in/nicknorwitz/ *Related Papers* _Elevated LDL Cholesterol with a Carbohydrate-Restricted Diet: Evidence for a "Lean Mass Hyper-Responder" Phenotype_ https://pubmed.ncbi.nlm.nih.gov/35106434/ _Carbohydrate Restriction-Induced Elevations in LDL-Cholesterol and Atherosclerosis: The KETO Trial_ https://www.jacc.org/doi/10.1016/j.jacadv.2024.101109 _Carbohydrate restriction-induced elevations in LDL-cholesterol and atherosclerosis: The KETO Trial_ https://www.metabolismjournal.com/article/S0026-0495(24)00080-5/abstract *Related Videos* https://youtu.be/cXwpYDWS0RE Resources: Metabolic Mind's Families & Peers page: https://www.metabolicmind.org/families-and-peers Clinician Directory: https://www.diagnosisdiet.com/directory Follow our channel for more information and education from Bret Scher, MD, FACC, including interviews with leading experts in Metabolic Psychiatry. Learn more about metabolic psychiatry and find helpful resources at https://metabolicmind.org/ About us: Metabolic Mind is a non-profit initiative of Baszucki Group working to transform the study and treatment of mental disorders by exploring the connection between metabolism and brain health. We leverage the science of metabolic psychiatry and personal stories to offer education, community, and hope to people struggling with mental health challenges and those who care for them. Our channel is for informational purposes only. We are not providing individual or group medical or healthcare advice nor establishing a provider-patient relationship. Many of the interventions we discuss can have dramatic or potentially dangerous effects if done without proper supervision. Consult your healthcare provider before changing your lifestyle or medications. #MetabolicMind #MetabolicNeuroscience #KetogenicMetabolicTherapy #NutritionalKetosis#AlternativeTreatment#Keto#KetogenicTherapy #MetabolicHealth#LDL#HeartHealth

In this episode of The Metabolic Classroom, Dr. Ben Bikman explores the topic of leaky gut syndrome, explaining how substances enter the body through the intestines and how the gut acts as a controlled gateway.While nutrients like amino acids, glucose, and fats are transported through the intestinal lining via a process called transcellular transport, problems arise when the tight junctions between the cells weaken. This can lead to harmful substances, including large molecules and microbes, passing into the bloodstream in a process known as paracellular transport.A key player in leaky gut syndrome is the molecule lipopolysaccharide (LPS), which comes from certain gut bacteria. Under normal conditions, LPS stays in the intestines and is expelled with waste, but when it enters the bloodstream due to leaky gut, it can trigger a chronic inflammatory response. This inflammation is linked to conditions like obesity, heart disease, and fatty liver disease. Bikman emphasized that even low levels of LPS in the blood can promote insulin resistance, further contributing to metabolic disorders.Several dietary and environmental factors can compromise the integrity of the gut barrier. Ben highlights the negative impact of fructose, which weakens tight junction proteins and promotes oxidative stress. Polyunsaturated fats from refined seed oils and gluten, especially in people with sensitivities, can also increase intestinal permeability. Additionally, chronic stress and alcohol consumption were identified as contributors to leaky gut.On a positive note, Dr. Bikman discusses strategies to improve gut health, such as consuming short-chain fatty acids (like butyrate), found in dairy and certain fibers. He also mentioned the potential benefits of saturated fats, particularly from dairy, which may promote gut healing. Lastly, Dr. Bikman shares the role of LDL cholesterol as a “scavenger” that helps remove harmful LPS from the blood, suggesting its misunderstood importance in immune health.https://www.insuliniq.com 00:00 Introduction to Leaky Gut01:52 How Substances Enter the Body Through the Gut03:58 Structure and Function of the Gut Lining07:07 Normal Transport vs. Leaky Gut Transport09:23 The Role of LPS in Leaky Gut and Inflammation11:41 How LPS Affects the Body12:45 Low-Grade Systemic Inflammation15:23 Cardiometabolic Consequences of Leaky Gut18:52 Dietary Triggers of Leaky Gut: Fructose and Seed Oils22:14 The Impact of Gluten and Stress on Gut Health24:05 Strategies to Improve Gut Health25:09 Short Chain Fatty Acids and Saturated Fats for Gut Healing28:08 The Role of LDL Cholesterol in Gut Health31:16 The Importance of Fiber and Probiotics33:32 The Rare Sugar Allulose and Gut Integrity35:23 Conclusion and Practical TakeawaysMy favorite meal-replacement shake: https://gethlth.com (discount: BEN10)My favorite electrolytes (and more): https://redmond.life (discount: BEN15)My favorite allulose source: https://rxsugar.com (discount: BEN20)Study references referred to are available upon request. Email: support@insuliniq.com Hosted on Acast. See acast.com/privacy for more information.

Please Subscribe and Review: Apple Podcasts | RSS Submit your questions for the podcast here News Topic: Convention of States Three Article V Convention Efforts RFK Jr Speech Show Notes: Carbohydrate Restriction-Induced Elevations in LDL-Cholesterol and Atherosclerosis: The KETO Trial Heart of the Matter: Higher LDL on Keto Does NOT Mean More Plaque. https://www.jacionline.org/article/S0091-6749(24)00129-5/fulltext Long-term risk of autoimmune diseases after mRNA-based SARS-CoV2 vaccination in a Korean, nationwide, population-based cohort study Questions:    Keto/Carnivore for Autoimmune Jacob writes: Hi Robb, I have been following you since 2009 in the CrossFit days and my entire diet has been based around Paleo since then. In 2020 I got very sick and couldn't recover fully, ending up finding out that I have post viral dysautonomia. Recently I heard you talk about how the low carb version of the Paleo autoimmune protocol is really an upgrade. In the time since getting sick my baseline became low carb Paleo, and that kept me doing pretty well. Now that I have been heavily supplementing with LMNT it's been even better! Can you try and get into the mechanics of why/how a keto-paleo diet makes such of a difference for these kinds of issues? Does it come down simply to inflammation? Really appreciate the podcast. Keep up the good work! Thank you Jacob   Cholesterol…again Shane writes: Hey Robb and Nicki, I know you get asked this all the time and I've gone down the rabbit hole on every related podcast I could find of yours regarding this topic, but there is just so much information out there on this topic I don't know what to think, and I'm hoping you can help. I'm 41, fit and healthy at least by any American standard. I've been involved with CrossFit (was even at one of Robb's Nutrition Seminars back in the day where I got to meet you both), coached for a decade, life happened and now I'm a Software Engineer. While my job is nowhere near as active, I still train 5-6 days a week but more of a mix of strength training, with some metcons, and regular doses of zone2. I still prescribe to CrossFit's nutrition in 100 words and so eat meat, vegetables, some fruit little starch and no sugar about 90% of the time. We're not financially set enough to be able to buy as much from the farm directly as we'd like, so meat is still typical feedlot stuff you can get at City Market etc. but I do try to hit 1.7g/lb of protein per day and fill in with the fruits and veggies. I haven't had a PCP in forever and so decided to get one so maybe it wouldn't take 3 months to get any kind of appointment when/if I did need one and of course they wanted to do a blood panel, and I was curious too so I did. My panel came back and it wasn't great. My total cholesterol is 298, HDL is 55, triglycerides are 76, LDL is 225, LDL particle number is 2022 nmol/L, LDL pattern is A, ApoB is 162 mg/dL, LipoProteinA is 101. My doctor immediately started talking about statins so I asked about a CAC and did that and got back a score of 0. With all of that data I'm just not sure how to proceed. I hear Dr. Attia talking about prioritizing apoB reduction, Layne Norton talking about the mendelian randomization studies showing the linear relationship between LDL and cardiac risk. But then I also hear Dr. Malhotra talking about statins and their misrepresented effect on cardiac disease along with Chris Kresser and obviously I want to believe what they say but I also want to make sure I'm not cutting the time my kids get with their father shorter than it had to be. I quit drinking 2+ years ago, I don't smoke, and I feel like I eat cleaner now that I ever have, so I'm thinking I'll just keep on keeping on, continue getting yearly bloodwork, and go back for another CAC in 3-5 years to make sure things aren't progressing, but I'd love to hear any thoughts you have on the matter. Thank you both so much for all the great info you put out there and please keep it salty. Shane   Crohn's Part II Fred writes:  Hi Robb and Nicki, You responded to my question re: Crohn's on Podcast #156 dated June 15, 2023. Thanks again for the information. I followed up on the resources you gave me and implemented a bunch of the recommendations. My stomach has been great but now dealing with sore tendons and joints which is a side effect of the biologic meds. Anyway, I wanted to provide you some additional information because you had wondered what the "precipitating event" could have been to get Crohn's at the age of 54. Again, until this point I was incredibly healthy with no issues at all. Back to the "potential" precipitating events. March 30, 2021 I got Covid (Delta) just before the vaccines came out in Canada. I was sick but nothing too serious and then because of the vaccine mandates I had to get my first vaccine on May 12, 2021, then second shot July 6, 2021, third vaccine January 8, 2022. In August 2022 my blood pressure went through the roof. I have never had high blood pressure then in January 2022 I had major stomach issues and was diagnosed with Crohn's in March 2022. Who knows if there is any connection but its interesting that this illness came about after getting Covid and then hitting my system with 3 vaccinations in less than a year. Anyway, thought you might find this interesting. Thanks again! Fred   Sponsor: The Healthy Rebellion Radio is sponsored by our electrolyte company, LMNT. Proper hydration is more than just drinking water. You need electrolytes too! Check out The Healthy Rebellion Radio sponsor LMNT for grab-and-go electrolyte drink mix packets and the new LMNT Sparkling electrolyte performance beverage! Click here to get your LMNT electrolytes   Transcript: Coming soon!

Darshan H. Brahmbhatt, Podcast Editor of JACC: Advances discusses a recently published original research paper on carbohydrate restriction-induced elevations in LDL-cholesterol and atherosclerosis in the KETO Trial

Hey guys, can you please do us a huge favour and head over and vote for our podcast for Listeners Choice for The Australian Podcast Awards...please! https://www.australianpodcastawards.com/voting   In this episode, Nic and Steve delve into the complex world of cholesterol, revealing why LDL might not be as bad as you think. They explore the different types of cholesterol, including the good, the bad, and their subfractions, and discuss their impact on heart disease. Topics include total cholesterol, LDL, HDL (and whether it can be too high), and lipoproteins like (a) and Apo-B. They also compare statins to natural remedies and examine how diet influences cholesterol levels. Tune in for an insightful breakdown of everything you need to know about cholesterol!   As always, this information is not designed to diagnose, treat, prevent, or cure any condition and is for information purposes only - please discuss any information in this podcast with your healthcare professional before making any changes to your current lifestyle. Check out ATP Science's range of products at our online store - https://bit.ly/3WlwFnr  

Send us a Text Message.Have you heard or seen anything about the carnivore diet lately? It's been making waves in the health and wellness world, but is it really all it's cracked up to be?Whether you're considering the carnivore diet or simply curious about its popularity, this episode offers a balanced and informative perspective. Discover the truth behind the claims, learn about the potential long-term consequences, and gain insights from me, a registered dietitian.Tune in to hear my review of the carnivore diet and make an informed decision about your health and nutrition. Resources Mentioned:ArticleCarnivore Cringe InstagramTOPICS COVERED

Dr. Nicholas Norwitz is a researcher-educator focused on Metabolic Health. He got his PhD from Oxford & is a Harvard med student. Show sponsors: Quicksilver Scientific

Pradeep is a brilliant geneticist and Director of Preventive Cardiology, holds the Paul & Phyllis Fireman Endowed Chair in Vascular Medicine at Mass General Hospital and on faculty at Harvard Medical School and the Broad Institute. His prolific research has been illuminating for the field of improving our approach to reduce the risk of heart disease. That's especially important because heart disease is the global (and US) #1 killer and is on the increase. We didn't get into lifestyle factors here since there was so much ground to cover on new tests. drugs, and strategies.A video snippet of our conversation on ApoB. Full videos of all Ground Truths podcasts can be seen on YouTube here. The audios are also available on Apple and Spotify.Transcript with links to key publications and audioEric Topol (00:06):Well, welcome to Ground Truths. I'm Eric Topol and with me is Pradeep Natarajan from Harvard. He's Director of Preventative Cardiology at the Mass General Brigham Health System and he has been lighting it up on the field of cardiovascular. We're going to get to lots of different parts of that story and so, Pradeep welcome.Pradeep Natarajan (00:31):Thanks Eric, really delighted and honored to be with you and have this discussion.Eric Topol (00:36):Well, for years I've been admiring your work and it's just accelerating and so there's so many things to get to. I thought maybe what we'd start off with is you recently wrote a New England Journal piece about two trials, two different drugs that could change the landscape of cardiovascular prevention in the future. I mean, that's one of the themes we're going to get to today is all these different markers and drugs that will change cardiology as we know it now. So maybe you could just give us a skinny on that New England Journal piece.Two New Lipid Targets With RNA DrugsPradeep Natarajan (01:16):Yeah, yeah, so these two agents, the trials were published at the same time. These phase two clinical trials for plozasiran, which is an siRNA against APOC3 and zodasiran, which is an siRNA against ANGPTL3. The reason why we have medicines against those targets are based on human genetics observations, that individuals with loss of function mutations and either of those genes have reduced lipids. For APOC3, it's reduced triglycerides for ANGPTL3 reduced LDL cholesterol and reduced triglycerides and also individuals that have those loss of function mutations also have lower risk for coronary artery disease. Now that's a very similar parallel to PCSK9. We have successful medicines that treat that target because people have found that carriers of loss of function mutations in PCSK9 lead to lower LDL cholesterol and lower coronary artery disease.(02:11):Now that suggests that therapeutic manipulation without significant side effects from the agents themselves for APOC3 and ANGPTL3 would be anticipated to also lower coronary artery disease risk potentially in complementary pathways to PCSK9. The interesting thing with those observations is that they all came from rare loss of function mutations that are enriched in populations of individuals. However, at least for PCSK9, has been demonstrated to have efficacy in large groups of individuals across different communities. So the theme of that piece was really just the need to study diverse populations because those insights are not always predictable about which communities are going to have those loss of function mutations and when you find them, they often have profound insights across much larger groups of individuals.Eric Topol (03:02):Well, there's a lot there that we can unpack a bit of it. One of them is the use of small interfering RNAs (siRNA) as drugs. We saw in the field of PCSK9, as you mentioned. First there were monoclonal antibodies directed against this target and then more recently, there's inclisiran which isn't an RNA play if you will, where you only have to take it twice a year and supposedly it's less expensive and I'm still having trouble in my practice getting patients covered on their insurance even though it's cheaper and much more convenient. But nonetheless, now we're seeing these RNA drugs and maybe you could comment about that part and then also the surprise that perhaps is unexplained is the glucose elevation.Pradeep Natarajan (03:53):Yeah, so for medicines and targets that have been discovered through human genetics, those I think are attractive for genetic-based therapies and longer interval dosing for the therapies, which is what siRNAs allow you to do because the individuals that have these perturbations, basically the naturally occurring loss of function mutations, they have these lifelong, so basically have had a one-time therapy and have lived, and so far, at least for these targets, have not had untoward side effects or untoward phenotypic consequences and only reduce lipids and reduce coronary artery disease. And so, instead of taking a pill daily, if we have conviction that that long amount of suppression may be beneficial, then longer interval dosing and not worrying about the pill burden is very attractive specifically for those specific therapeutics. And as you know, people continue to innovate on further prolonging as it relates to PCSK9.(04:57):Separately, some folks are also developing pills because many people do feel that there's still a market and comfort for daily pills. Now interestingly for the siRNA for zodasiran at the highest dose, actually for both of them at the highest doses, but particularly for zodasiran, there was an increase in insulin resistance parameters actually as it relates to hyperglycemia and less so as it relates to insulin resistance, that is not predicted based on the human genetics. Individuals with loss of function mutations do not have increased risks in hyperglycemia or type 2 diabetes, so that isolates it related to that specific platform or that specific technology. Now inclisiran, as you'd mentioned, Eric is out there. That's an siRNA against PCSK9 that's made by a different manufacturer. So far, the clinical trials have not shown hyperglycemia or type 2 diabetes as it relates inclisiran, so it may be related to the specific siRNAs that are used for those targets. That does merit further consideration. Now, the doses that the manufacturers do plan to use in the phase three clinical trials are at lower doses where there was not an increase in hyperglycemia, but that does merit further investigation to really understand why that's the case. Is that an expected generalized effect for siRNAs? Is it related to siRNAs for this specific target or is it just related to the platform used for these two agents which are made by the same manufacturer?Eric Topol (06:27):Right, and I think the fact that it's a mystery is intriguing at the least, and it may not come up at the doses that are used in the trials, but the fact that it did crop up at high doses is unexpected. Now that is part of a much bigger story is that up until now our armamentarium has been statins and ezetimibe to treat lipids, but it's rapidly expanding Lp(a), which for decades as a cardiologist we had nothing to offer. There may even be drugs to be able to lower people who are at high risk with high Lp(a). Maybe you could discuss that.What About Lp(a)?Pradeep Natarajan (07:13):Yeah, I mean, Eric, as you know, Lp(a) has been described as a cardiovascular disease risk factors for quite so many years and there are assays to detect lipoprotein(a) elevation and have been in widespread clinical practice increasing widespread clinical practice, but we don't yet have approved therapies. However, there is an abundance of literature preclinical data that suggests that it likely is a causal factor, meaning that if you lower lipoprotein(a) when elevated, you would reduce the risk related to lipoprotein(a). And a lot of this comes from similar human genetic studies. The major challenge of just relating a biomarker to an outcome is there are many different reasons why a biomarker might be elevated, and so if you detect a signal that correlates a biomarker, a concentration to a clinical outcome, it could be related to that biomarker, but it could be to the other reasons that the biomarker is elevated and sometimes it relates to the outcome itself.(08:10):Now human genetics is very attractive because if you find alleles that strongly relate to that exposure, you can test those alleles themselves with the clinical outcome. Now the allele assignment is established at birth. No other factor is going to change that assignment after conception, and so that provides a robust, strong causal test for that potential exposure in clinical outcome. Now, lipoprotein(a) is unique in that it is highly heritable and so there are lots of different alleles that relate to lipoprotein(a) and so in a well powered analysis can actually test the lipoprotein(a) SNPs with the clinical outcomes and similar to how there is a biomarker association with incident myocardial infarction and incident stroke, the SNPs related to lipoprotein(a) show the same. That is among the evidence that strongly supports that this might be causal. Now, fast forward to many years later, we have at least three phase three randomized clinical trials testing agents that have been shown to be very potent at lowering lipoprotein(a) that in the coming years we will know if that hypothesis is true. Importantly, we will have to understand what are the potential side effects of these medicines. There are antisense oligonucleotides and siRNAs that are primarily in investigation. Again, this is an example where there's a strong genetic observation, and so these genetic based longer interval dosing therapies may be attractive, but side effects will be a key thing as well too. Those things hard to anticipate really can anticipate based on the human genetics for off target effects, for example.(09:52):It's clearly a risk signal and hopefully in the near future we're going to have specific therapies.Eric Topol (09:57):Yeah, you did a great job of explaining Mendelian randomization and the fact the power of genetics, which we're going to get into deeper shortly, but the other point is that do you expect now that there's these multiple drugs that lower Lp(a) efficiently, would that be enough to get approval or will it have to be trials to demonstrate improved cardiovascular outcomes?Pradeep Natarajan (10:24):There is a great regulatory path at FDA for approval just for LDL cholesterol lowering and inclisiran is on the market and the phase three outcomes data has not yet been reported because there is a wide appreciation that LDL cholesterol lowering is a pretty good surrogate for cardiovascular disease risk lowering. The label will be restricted to LDL cholesterol lowering and then if demonstrated to have clinical outcomes, the label could be expanded. For other biomarkers including lipoprotein(a), even though we have strong conviction that it is likely a causal factor there hasn't met the bar yet to get approval just based on lipoprotein(a) lowering, and so we would need to see the outcomes effects and then we would also need to understand side effects. There is a body of literature of side effects for other therapies that have targeted using antisense oligonucleotides. We talked about potential side effects from some siRNA platforms and sometimes those effects could overtake potential benefits, so that really needs to be assessed and there is a literature and other examples.(11:31):The other thing I do want to note related to lipoprotein(a) is that the human genetics are modeled based on lifelong perturbations, really hard to understand what the effects are, how great of an effect there might be in different contexts, particularly when introduced in middle age. There's a lot of discussion about how high lipoprotein(a) should be to deliver these therapies because the conventional teaching is that one in five individuals has high lipoprotein(a), and that's basically greater than 75 nanomoles per liter. However, some studies some human genetic studies to say if you want to get an effect that is similar to the LDL cholesterol lowering medicines on the market, you need to start with actually higher lipoprotein(a) because you need larger amounts of lipoprotein(a) lowering. Those are studies and approaches that haven't been well validated. We don't know if that's a valid approach because that's modeling based on this sort of lifelong effect. So I'm very curious to see what the overall effect will be because to get approval, I think you need to demonstrate safety and efficacy, but most importantly, these manufacturers and we as clinicians are trying to find viable therapies in the market that it won't be hard for us to get approval because hopefully the clinical trial will have said this is the context where it works. It works really well and it works really well on top of the existing therapies, so there are multiple hurdles to actually getting it directly to our patients.How Low Do You Go with LDL Cholesterol?Eric Topol (13:02):Yeah, no question about that. I'm glad you've emphasized that. Just as you've emphasized the incredible lessons from the genetics of people that have helped guide this renaissance to better drugs to prevent cardiovascular disease. LDL, which is perhaps the most impressive surrogate in medicine, a lab test that you already touched on, one of the biggest questions is how low do you go? That is Eugene Braunwald, who we all know and love. They're in Boston. The last time I got together with him, he was getting his LDL down to close to zero with various tactics that might be extreme. But before we leave these markers, you're running preventive cardiology at man's greatest hospital. Could you tell us what is your recipe for how aggressive do you go with LDL?Pradeep Natarajan (14:04):Yeah, so when I talk to patients where we're newly getting lipid lowering therapies on, especially because many people don't have a readout of abnormal LDL cholesterol when we're prescribing these medicines, it's just giving them a sense of what we think an optimal LDL cholesterol might be. And a lot of this is based on just empirical observations. So one, the average LDL cholesterol in the modern human is about 100 to 110 mg/dL. However, if you look at contemporary hunter gatherers and non-human primates, their average LDL is about 40 to 50 and newborn babies have an LDL cholesterol of about 30. And the reason why people keep making LDL cholesterol lowering medicines because as you stack on therapies, cardiovascular disease events continue to reduce including down to these very low LDL cholesterol values. So the population mean for LDL cholesterol is high and everybody likely has hypercholesterolemia, and that's because over the last 10,000 years how we live our lives is so dramatically different and there has not been substantial evolution over that time to change many of these features related to metabolism.(15:16):And so, to achieve those really low LDL cholesterol values in today's society is almost impossible without pharmacotherapies. You could say, okay, maybe everybody should be on pharmacotherapies, and I think if you did that, you probably would reduce a lot of events. You'll also be treating a lot of individuals who likely would not get events. Cardiovascular disease is the leading killer, but there are many things that people suffer from and most of the times it still is not cardiovascular disease. So our practice is still rooted in better identifying the individuals who are at risk for cardiovascular disease. And so, far we target our therapies primarily in those who have already developed cardiovascular disease. Maybe we'll talk about better identifying those at risk, but for those individuals it makes lots of sense to get it as low as possible. And the field has continued to move to lower targets.(16:07):One, because we've all recognized, at least based on these empirical observations that lower is better. But now increasingly we have a lot of therapies to actually get there, and my hope is that with more and more options and the market forces that influence that the cost perspective will make sense as we continue to develop more. As an aside, related aside is if you look at the last cholesterol guidelines, this is 2018 in the US this is the first time PCSK9 inhibitors were introduced in the guidelines and all throughout that there was discussions of cost. There are a lot of concerns from the field that PCSK9 inhibitors would bankrupt the system because so many people were on statins. And you look at the prior one that was in 2013 and cost was mentioned once it's just the cost effectiveness of statins. So I think the field has that overall concern.(17:01):However, over time we've gotten comfortable with lower targets, there are more medicines and I think some of this competition hopefully will drive down some of the costs, but also the overall appreciation of the science related to LDL. So long-winded way of saying this is kind of the things that we discussed just to give reassurance that we can go to low LDL cholesterol values and that it's safe and then we think also very effective. Nobody knows what the lower limit is, whether zero is appropriate or not. We know that glucose can get too low. We know that blood pressure can be too low. We don't know yet that limit for LDL cholesterol. I mean increasingly with these trials we'll see it going down really low and then we'll better appreciate and understand, so we'll see 40 is probably the right range.Eric Topol (17:49):40, you said? Yeah, okay, I'll buy that. Of course, the other thing that we do know is that if you push to the highest dose statins to get there, you might in some people start to see the hyperglycemia issue, which is still not fully understood and whether that is, I mean it's not desirable, but whether or not it is an issue, I guess it's still out there dangling. Now the other thing that since we're on LDL, we covered Lp(a), PCSK9, the siRNA, is ApoB. Do you measure ApoB in all your patients? Should that be the norm?Measuring ApoBPradeep Natarajan (18:32):Yeah, so ApoB is another blood test. In the standard lipid panel, you get four things. What's measured is cholesterol and triglycerides, they're the lipids insoluble in blood to get to the different tissues that get packaged in lipoprotein molecules which will have the cholesterol, triglycerides and some other lipids and proteins. And so, they all have different names as you know, right? Low density lipoprotein, high density lipoprotein and some others. But also in the lipid panel you get the HDL cholesterol, the amount of cholesterol in an HDL particle, and then most labs will calculate LDL cholesterol and LDL cholesterol has a nice relationship with cardiovascular disease. You lower it with statins and others. Lower risk for cardiovascular disease, turns out a unifying feature of all of these atherogenic lipoproteins, all these lipoproteins that are measured and unmeasured that relate to cardiovascular disease, including lipoprotein(a), they all have an additional protein called ApoB. And ApoB, at least as it relates to LDL is a pretty good surrogate of the number of LDL particles.(19:37):Turns out that that is a bit better at the population level at predicting cardiovascular disease beyond LDL cholesterol itself. And where it can be particularly helpful is that there are some patients out there that have an unexpected ratio between ApoB and LDL. In general, the ratio between LDL cholesterol and ApoB is about 1.1 and most people will have that rough ratio. I verify that that is the expected, and then if that is the expected, then really there is no role to follow ApoB. However, primarily the patients that have features related to insulin resistance have obesity. They may often have adequate looking LDL cholesterols, but their ApoB is higher. They have more circulating LDL particles relative to the total amount of LDL cholesterol, so smaller particles themselves. However, the total number of particles may actually be too high for them.(20:34):And so, even if the LDL cholesterol is at target, if the ApoB is higher, then you need to reduce. So usually the times that I just kind of verify that I'm at appropriate target is I check the LDL cholesterol, if that looks good, verify with the ApoB because of this ratio, the ApoB target should be about 10% lower. So if we're aiming for about 40, that's like 36, so relatively similar, and if it's there, I'm good. If it's not and it's higher, then obviously increase the LDL cholesterol lowering medicines because lower the ApoB and then follow the ApoB with the lipids going forward. The European Society of Cardiology has more emphasis on measuring ApoB, that is not as strong in the US guidelines, but there are many folks in the field, preventive cardiologists and others that are advocating for the increasing use of ApoB because I think there are many folks that are not getting to the appropriate targets because we are not measuring ApoB.Why Aren't We Measuring and Treating Inflammation?Eric Topol (21:37):Yeah, I think you reviewed it so well. The problem here is it could be part of the standard lipid panel, it would make this easy, but what you've done is a prudent way of selecting out people who it becomes more important to measure and moderate subsequently. Now this gets us to the fact that we're lipid centric and we don't pay homage to inflammation. So I wrote a recent Substack on the big miss on inflammation, and here you get into things like the monoclonal antibody to interleukin-6, the trial that CANTOS that showed significant reduction in cardiovascular events and fatal cancers by the way. And then you get into these colchicine trials two pretty good size randomized trials, and here the entry was coronary disease with a high C-reactive protein. Now somehow or other we abandon measuring CRP or other inflammatory markers, and both of us have had patients who have low LDLs but have heart attacks or significant coronary disease. So why don't we embrace inflammation? Why don't we measure it? Why don't we have better markers? Why is this just sitting there where we could do so much better? Even agents that are basically cost pennies like colchicine at low doses, not having to use a proprietary version could be helpful. What are your thoughts about us upgrading our prevention with inflammation markers?Pradeep Natarajan (23:22):Yeah, I mean, Eric, there is an urgent need to address these other pathways. I say urgent need because heart disease has the dubious distinction of being the leading killer in the US and then over the last 20 years, the leading killer in the world as it takes over non-communicable diseases. And really since the early 1900s, there has been a focus on developing pharmacotherapies and approaches to address the traditional modifiable cardiovascular disease risk factors. That has done tremendous good, but still the curves are largely flattening out. But in the US and in many parts of the world, the deaths attributable to cardiovascular disease are starting to tick up, and that means there are many additional pathways, many of them that we have well recognized including inflammation. More recently, Lp(a) that are likely important for cardiovascular disease, for inflammation, as you have highlighted, has been validated in randomized controlled trials.(24:18):Really the key trial that has been more most specific is one on Canakinumab in the CANTOS trial IL-1β monoclonal antibody secondary prevention, so cardiovascular disease plus high C-reactive protein, about a 15% reduction in cardiovascular disease and also improvement in cancer related outcomes. Major issues, a couple of issues. One was increased risk for severe infections, and the other one is almost pragmatic or practical is that that medicine was on the market at a very high price point for rare autoinflammatory conditions. It still is. And so, to have for a broader indication like cardiovascular disease prevention would not make sense at that price point. And the manufacturer tried to go to the FDA and focus on the group that only had C-reactive protein lowering, but that's obviously like a backwards endpoint. How would you know that before you release the medicine? So that never made it to a broader indication.(25:14):However, that stuck a flag in the broader validation of that specific pathway in cardiovascular disease. That pathway has direct relevance to C-reactive protein. C-reactive protein is kind of a readout of that pathway that starts from the NLRP3 inflammasome, which then activates IL-1β and IL-6. C-reactive protein we think is just a non causal readout, but is a reliable test of many of these features and that's debatable. There may be other things like measuring IL-6, for example. So given that there is actually substantial ongoing drug development in that pathway, there are a handful of companies with NLRP3 inflammasome inhibitors, but small molecules that you can take as pills. There is a monoclonal antibody against IL-6 that's in development ziltivekimab that's directed at patients with chronic kidney disease who have lots of cardiovascular disease events despite addressing modifiable risk factors where inflammatory markers are through the roof.(26:16):But then you would also highlighted one anti-inflammatory that's out there that's pennies on the dollar, that's colchicine. Colchicine is believed to influence cardiovascular disease by inhibiting NLRP3, I say believed to. It does a lot of things. It is an old medicine, but empirically has been shown in at least two randomized controlled trials patients with coronary artery disease, actually they didn't measure C-reactive protein in the inclusion for these, but in those populations we did reduce major adverse cardiovascular disease events. The one thing that does give me pause with colchicine is that there is this odd signal for increased non-cardiovascular death. Nobody understands if that's real, if that's a fluke. The FDA just approved last year low dose colchicine, colchicine at 0.5 milligrams for secondary prevention given the overwhelming efficacy. Hasn't yet made it into prevention guidelines, but I think that's one part that does give me a little bit pause. I do really think about it particularly for patients who have had recurrent events. The people who market the medicine and do research do remind us that C-reactive protein was not required in the inclusion, but nobody has done that secondary assessment to see if measuring C-reactive protein would be helpful in identifying the beneficial patients. But I think there still could be more work done on better identifying who would benefit from colchicine because it's an available and cheap medicine. But I'm excited that there is a lot of development in this inflammation area.Eric Topol (27:48):Yeah, well, the development sounds great. It's probably some years away. Do you use colchicine in your practice?Pradeep Natarajan (27:56):I do. Again, for those folks who have had recurrent events, even though C-reactive protein isn't there, it does make me feel like I'm treating inflammation. If C-reactive protein is elevated and then I use it for those patients, if it's not elevated, it's a much harder sell from my standpoint, from the patient standpoint. At the lower dose for colchicine, people generally are okay as far as side effects. The manufacturer has it at 0.5 milligrams, which is technically not pennies on the dollar. That's not generic. The 0.6 milligrams is generic and they claim that there is less side effects at the 0.5 milligrams. So technically 0.6 milligrams is off label. So it is what it is.CHIP and Defining High Risk People for CV DiseaseEric Topol (28:40):It's a lot more practical, that's for sure. Now, before I leave that, I just want to mention when I reviewed the IL-1β trial, you mentioned the CANTOS trial and also the colchicine data. The numbers of absolute increases for infection with the antibody or the cancers with the colchicine are really small. So I mean the benefit was overriding, but I certainly agree with your concern that there's some things we don't understand there that need to be probed more. Now, one of the other themes, well before one other marker that before we get to polygenic risk scores, which is center stage here, defining high risk people. We've talked a lot about the conventional things and some of the newer ways, but you've been one of the leaders of study of clonal hematopoiesis of indeterminate potential known as CHIP. CHIP, not the chips set in your computer, but CHIP. And basically this is stem cell mutations that increase in people as we age and become exceptionally common with different mutations that account in these clones. So maybe you can tell us about CHIP and what I don't understand is that it has tremendous correlation association with cardiovascular outcomes adverse as well as other system outcomes, and we don't measure it and we could measure it. So please take us through what the hell is wrong there.Pradeep Natarajan (30:14):Yeah, I mean this is really exciting. I mean I'm a little bit biased, but this is observations that have been made only really over the last decade, but accelerating research. And this has been enabled by advances in genomic technologies. So about 10 years or plus ago, really getting into the early days of population-based next generation sequencing, primarily whole exome sequencing. And most of the DNA that we collect to do these population-based analyses come from the blood, red blood cells are anucleate, so they're coming from white blood cells. And so, at that time, primarily interrogating what is the germline genetic basis for coronary artery disease and early onset myocardial infarction. At the same time, colleagues at the Broad Institute were noticing that there are many additional features that you can get from the blood-based DNA that was being processed by the whole exome data. And there were actually three different groups that converged on that all in Boston that converged on the same observation that many well-established cancer causing mutations.(31:19):So mutations that are observed in cancers that have been described to drive the cancers themselves were being observed in these large population-based data sets that we were all generating to understand the relationship between loss of function mutations in cardiovascular disease. That's basically the intention of those data sets for being generated for other things. Strong correlation with age, but it was very common among individuals greater than 70; 10% of them would have these mutations and is very common because blood cancer is extremely, it's still pretty rare in the population. So to say 10% of people had cancer causing driver mutations but didn't have cancer, was much higher than anyone would've otherwise expected. In 2014, there were basically three main papers that described that, and they also observed that there is a greater risk of death. You'd say, okay, this is a precancerous lesion, so they're probably dying of cancer.(32:17):But as I said, the absolute incidence rate for blood cancer is really low and there's a relative increase for about tenfold, but pretty small as it relates to what could be related to death. And in one of the studies we did some exploratory analysis that suggested maybe it's actually the most common cause of death and that was cardiovascular disease. And so, a few years later we published a study that really in depth really looked at a bunch of different data sets that were ascertained to really understand the relationship between these mutations, these cancer causing mutations in cardiovascular disease, so observed it in enrichment and older individuals that had these mutations, CHIP mutations, younger individuals who had early onset MI as well too, and then also look prospectively and showed that it related to incident coronary artery disease. Now the major challenge for this kind of analysis as it relates to the germline genetic analysis is prevalence changes over time.(33:15):There are many things that could influence the presence of clonal hematopoiesis. Age is a key enriching factor and age is the best predictor for cardiovascular disease. So really important. So then we modeled it in mice. It was actually a parallel effort at Boston University (BU) that was doing the same thing really based on the 2014 studies. And so, at the same time we also observed when you modeled this in mice, you basically perturb introduce loss of function mutations in the bone marrow for these mice to recapitulate these driver mutations and those mice also have a greater burden of atherosclerosis. And Eric, you highlighted inflammation because basically the phenotype of these cells are hyper inflamed cells. Interestingly, C-reactive protein is only modestly elevated. So C-reactive protein is not fully capturing this, but many of the cytokines IL-1β, IL-6, they're all upregulated in mice and in humans when measured as well.(34:11):Now there've been a few key studies that have been really exciting about using anti-inflammatories in this pathway to address CHIP associated cardiovascular disease. So one that effort that I said in BU because they saw these cytokines increased, we already know that these cytokines have relationship with atherosclerosis. So they gave an NLRP3 inflammasome inhibitor to the mice and they showed that the mice with or without CHIP had a reduction in atherosclerosis, but there was a substantial delta among the mice that are modeled as having CHIP. Now, the investigators in CANTOS, the manufacturers, they actually went back and they survey where they had DNA in the CANTOS trial. They measured CHIP and particularly TET2 CHIP, which is the one that has the strongest signal for atherosclerosis. As I said, overall about 15% reduction in the primary outcome in CANTOS. Among the individuals who had TET2 CHIP, it was a 64% reduction in event.(35:08):I mean you don't see those in atherosclerosis related trials. Now this has the caveat of it being secondary post hoc exploratory, the two levels of evidence. And so, then we took a Mendelian randomization approach. Serendipitously, just so happens there is a coding mutation in the IL-6 receptor, a missense mutation that in 2012 was described that if you had this mutation, about 40% of people have it, you have a 5%, but statistically significant reduction in coronary artery disease. So we very simply said, if the pathway of this NLRP3 inflammasome, which includes IL-6, if you have decreased signaling in that pathway, might you have an even greater benefit from having that mutation if you had CHIP versus those who didn't have CHIP. So we looked in the UK Biobank, those who didn't have CHIP 5% reduction, who had that IL-6 receptor mutation, and then those who did have CHIP, if they had that mutation, it was about a 60% reduction in cardiovascular disease.(36:12):Again, three different lines of evidence that really show that this pathway has relevance in the general population, but the people who actually might benefit the most are those with CHIP. And I think as we get more and more data sets, we find that not all of the CHIP mutations are the same as it relates to cardiovascular disease risk. It does hone in on these key subsets like TET2 and JAK2, but this is pretty cool as a preventive cardiologist, new potential modifiable risk factor, but now it's almost like an oncologic paradigm that is being applied to coronary artery disease where we have specific driver mutations and then we're tailoring our therapies to those specific biological drivers for coronary artery disease. Hopefully, I did that justice. There's a lot there.Why Don't We Measure CHIP?Eric Topol (36:57):Well, actually, it's phenomenal how you've explained that, but I do want to review for our listeners or readers that prior to this point in our conversation, we were talking about germline mutations, the ones you're born with. With CHIP, we're talking about acquired somatic mutations, and these are our blood stem cells. And what is befuddling to me is that with all the data that you and others, you especially have been publishing and how easy it would be to measure this. I mean, we've seen that you can get it from sequencing no less other means. Why we don't measure this? I mean, why are we turning a blind eye to CHIP? I just don't get it. And we keep calling it of indeterminate potential, not indeterminate. It's definite potential.Pradeep Natarajan (37:51):Yeah, no, I think these are just overly cautious terms from the scientists. Lots of people have CHIP, a lot of people don't have clinical outcomes. And so, I think from the lens of a practicing hematologists that provide some reassurance on the spectrum for acquired mutation all the way over to leukemia, that is where it comes from. I don't love the acronym as well because every subfield in biomedicine has its own CHIP, so there's obviously lots of confusion there. CH or clinical hematopoiesis is often what I go, but I think continuing to be specific on these mutations. Now the question is why measure? Why aren't we measuring it? So there are some clinical assays out there. Now when patients get evaluated for cytopenias [low cell counts], there are next generation sequencing tests that look for these mutations in the process for evaluation. Now, technically by definition, CHIP means the presence of these driver mutations that have expanded because it's detectable by these assays, not a one-off cell because it can only be detected if it's in a number of cells.(38:55):So there has been some expansion, but there are no CBC abnormalities. Now, if there's a CBC abnormality and you see a CHIP mutation that's technically considered CCUS or clonal cytopenia of unknown significance, sometimes what is detected is myelodysplastic syndrome. In those scenarios still there is a cardiovascular disease signal, and so many of our patients who are seen in the cancer center who are being evaluated for these CBC abnormalities will be detected to have these mutations. They will have undergone some risk stratification to see what the malignancy potential is. Still pretty low for many of those individuals. And so, the major driver of health outcomes for this finding may be cardiovascular. So those patients then get referred to our program. Dana-Farber also has a similar program, and then my colleague Peter Libby at the Brigham often sees those patients as well. Now for prospective screening, so far, an insurance basically is who's going to pay for it.(39:51):So an insurance provider is not deemed that appropriate yet. You do need the prospective clinical trials because the medicines that we're talking about may have side effects as well too. And what is the yield? What is the diagnostic yield? Will there actually be a large effect estimate? But there has been more and more innovation, at least on the assay and the cost part of the assay because these initial studies, we've been using whole exome sequencing, which is continuing to come down, but is not a widely routine clinical test yet. And also because as you highlighted, these are acquired mutations. A single test is not necessarily one and done. This may be something that does require surveillance for particular high risk individuals. And we've described some risk factors for the prevalence of CHIP. So surveillance may be required, but because there are about 10 genes that are primarily implicated in CHIP, that can substantially decrease the cost of it. The cost for DNA extraction is going down, and so there are research tests that are kind of in the $10 to $20 range right now for CHIP. And if flipped over to the clinical side will also be reasonably low cost. And so, for the paradigm for clinical implementation, that cost part is necessary.Eric Topol (41:10):I don't know the $10 or $20 ones. Are there any I could order on patients that I'm worried about?Pradeep Natarajan (41:17):Not yet clinical. However, there is a company that makes the reagents for at least the cores that are developing this. They are commercializing that test so that many other cores, research cores can develop it. I think it's in short order that clinical labs will adopt it as well too.Eric Topol (41:36):That's great.Pradeep Natarajan (41:37):I will keep you apprised.What About Polygenic Risk Scores?Eric Topol (41:39):I think that's really good news because like I said, we're so darn lipid centric and we have to start to respect the body of data, the knowledge that you and others have built about CHIP. Now speaking of another one that drives me nuts is polygenic risk score (PRS) for about a decade, I've been saying we have coronary disease for most people is a polygenic trait. It's not just a familial hypercholesterolemia. And we progressively have gotten better and better of the hundreds of single variants that collectively without a parental history will be and independently predict who is at double, triple or whatever risk of getting heart disease, whereby you could then guide your statins at higher aggressive or pick a statin, use one or even go beyond that as we've been talking about. But we don't use that in practice, which is just incredible because it's can be done cheap.(42:45):You can get it through whether it's 23andMe or now many other entities. We have an app, MyGeneRank where we can process that Scripss does for free. And only recently, Mass General was the first to implement that in your patient population, and I'm sure you were a driver of that. What is the reluctance about using this as an orthogonal, if you will, separate way to assess a person's risk for heart disease? And we know validated very solidly about being aggressive about lipid lowering when you know this person's in the highest 5% polygenic risk score. Are we just deadheads in this field or what?Pradeep Natarajan (43:30):Yeah, I mean Eric, as you know, lots of inertia in medicine, but this one I think has a potential to make a large impact. Like CHIP mutations, I said news is about 10% in individuals greater than 70. The prospect here is to identify the risk much earlier in life because I think there is a very good argument that we're undertreating high risk individuals early on because we don't know how to identify them. As you highlighted, Dr. Braunwald about LDL cholesterol. The other part of that paradigm is LDL cholesterol lowering and the duration. And as we said, everybody would benefit from really low LDL cholesterol, but again, you might overtreat that if you just give that to everybody. But if you can better identify the folks very early in life, there is a low cost, low risk therapy, at least related to statins that you could have a profound benefit from the ones who have a greater conviction will have future risk for cardiovascular disease.(44:21):You highlighted the family history, and the family history has given the field of clues that genetics play a role. But as the genome-wide association studies have gotten larger, the polygenic risk scores have gotten better. We know that family history is imperfect. There are many reasons why a family member who is at risk may or may not have developed cardiovascular disease. A polygenic risk score will give a single number that will estimate the contribution of genetics to cardiovascular disease. And the thing that is really fascinating to me, which is I think some of a clinical implementation challenge is that the alleles for an individual are fixed. The genotyping is very cheap. That continues to be extremely cheap to do this test. But the weights and the interpretation of what the effects should be for each of the SNPs are continually being refined over time.(45:18):And so, given the exact same SNPs in the population, the ability to better predict cardiovascular diseases getting better. And so, you have things that get reported in the literature, but literally three years later that gets outdated and those hypotheses need to be reassessed. Today, I'll say we have a great relative to other things, but we have a great polygenic risk score was just reported last year that if you compare it to familial hypercholesterolemia, which has a diagnostic yield of about 1 in 300 individuals, but readily detectable by severe hypercholesterolemia that has about threefold risk for cardiovascular disease. By polygenic risk score, you can find 1 in 5 individuals with that same risk. Obviously you go higher than that, it'll be even higher risk related to that. And that is noble information very early in life. And most people develop risk factors later in life. It is happening earlier, but generally not in the 30s, 40s where there's an opportunity to make a substantial impact on the curve related to cardiovascular disease.(46:25):But there is a lot of momentum there. Lots of interest from NIH and others. The major challenge is though the US healthcare system is really not well set up to prevention, as you know, we practice healthcare after patient's developed disease and prevent the complications related to progression. The stakeholder incentives beyond the patient themselves are less well aligned. We've talked a lot here today about payers, but we don't have a single payer healthcare system. And patients at different times of their lives will have different insurers. They'll start early in life with their parents, their first employer, they'll move on to the next job and then ultimately Medicare. There's no entity beyond yourself that really cares about your longevity basically from the beginning and your overall wellness. That tension has been a major challenge in just driving the incentives and the push towards polygenic risk scores. But there are some innovative approaches like MassMutual Life Insurance actually did a pilot on polygenic risk scoring.(47:33):They're in the business of better understanding longevity. They get that this is important data. Major challenges, there are federal protections against non-discrimination in the workplace, health insurance, not necessarily life insurance. So I think that there are lots of things that have to be worked out. Everybody recognizes that this is important, but we really have to have all the incentives aligned for this to happen at a system-wide level in the US. So there's actually lots of investment in countries that have more nationalized healthcare systems, lots of development in clinical trials in the UK, for example. So it's possible that we in the US will not be the lead in that kind of evidence generation, but maybe we'll get there.The GLP-1 DrugsEric Topol (48:16):Yeah, it's frustrating though, Pradeep, because this has been incubating for some time and now we have multi ancestry, polygenic risk scores, particularly for heart disease and we're not using it, and it's not in my view, in the patient's best interest just because of these obstacles that you're mentioning, particularly here in the US. Well, the other thing I want to just get at with you today is the drugs that we were using for diabetes now blossoming for lots of other indications, particularly the glucagon-like peptide 1 (GLP-1) drugs. This has come onto the scene in recent years, not just obviously for obesity, but it's anti-inflammatory effects as we're learning, mediated not just through the brain but also T cells and having extraordinary impact in heart disease for people with obesity and also with those who have heart failure, about half of heart failure for preserved ejection fraction. So recently you and your colleagues recently published a paper with this signal of optic neuropathy. It was almost seven eightfold increase in a population. First, I wanted to get your sense about GLP-1. We're also going to get into the SGLT2 for a moment as well, but how do you use GLP-1? What's your prognosis for this drug class going forward?Pradeep Natarajan (49:55):As it relates to the paper, I can't claim credit as one of my former students who is now Mass Eye and Ear resident who participated, but we can talk about that. There's obviously some challenges for mining real world data, but this was related to anecdotes that they were observing at Mass Eye and Ear and then studied and observed an enrichment. In general though, I feel like every week I'm reading a new clinical trial about a new clinical outcome benefit as it relates to GLP-1 receptor agonists. This is kind of one thing that stands out that could be interrogated in these other clinical trials. So I would have that caveat before being cautious about ocular complications. But the data has been overwhelmingly beneficial, I think, because at minimum, obesity and inflammation are relayed to myriad of consequences, and I'm really excited that we have therapies that can address obesity that are safe.(50:52):There's a legacy of unsafe medicines for obesity, especially related to cardiovascular disease. So the fact that we have medicines that are safe and effective for lowering weight that also have real strong effects on clinical outcomes is tremendous. We in cardiology are increasingly using a range of diabetes medicines, including GLP-1 receptor agonists and SGLT2 inhibitors. I think that is also the secular changes of what influences cardiovascular disease over time. I talked about over the last 10 years or so with this increase in deaths attributable to cardiovascular disease. If you look at the influences of traditional clinical risk factors today, many of them have decreased in importance because when abnormal, we recognize them, in general we modify them when recognized. And so, many of the things that are unaddressed, especially the features related to insulin resistance, obesity, they start rising in importance. And so, there is a dramatic potential for these kinds of therapies in reducing the residual risks that we see related to cardiovascular disease. So I'm enthusiastic and excited. I think a lot more biology that needs to be understood of how much of this is being influenced specifically through this pathway versus a very effective weight loss medicine. But also interesting to see the insights on how the effect centrally on appetite suppression has profound influences on weight loss as well too. And hopefully that will lead to more innovations in weight management.The SGLT-2 DrugsEric Topol (52:25):And likewise, perhaps not getting near as much play, but when it came on the cardiovascular scene that an anti-diabetic drug SGLT2 was improving survival, that was big, and we still don't know why. I mean, there's some ideas that it might be a senolytic drug unknowingly, but this has become a big part of practice of cardiology in patients with diabetes or with preserved ejection fraction heart failure. Is that a fair summary for that drug?Pradeep Natarajan (53:00):Yeah, I totally agree. I mean, as there has been increased recognition for heart failure preserved ejection fraction, it has been almost disheartening over the last several years that we have not had very specific effective therapies to treat that condition. Now, it is a tremendous boon that we do have medicines interestingly focused on metabolism that are very helpful in that condition for heart failure with preserved ejection fraction. But there is still much more to be understood as far as that condition. I mean, the major challenge with heart failure, as you know, especially with heart failure preserved ejection fraction, it likely is a mix of a wide variety of different etiologies. So in parallel with developing effective therapies that get at some aspect is really understanding what are the individual drivers and then targeting those specific individual drivers. That requires a lot of unbiased discovery work and further profiling to be done. So lot more innovation, but relative to heart failure itself, it is not had widespread recognition as heart failure reduced ejection fraction. So much more to innovate on, for sure.Eric Topol (54:07):Right, right. Yeah, I am stunned by the recent progress in cardiovascular medicine. You have been center stage with a lot of it, and we've had a chance to review so much. And speaking of genetics, I wanted to just get a little insight because I recently came across the fact that your mother here at the City of Hope in Southern California is another famous researcher. And is that, I don't know what chromosome that is on regarding parental transmission of leading research. Maybe you can tell me about that.Pradeep Natarajan (54:41):Yeah, I mean, I guess it is a heritable trait when a parent has one profession that there is a higher likelihood that the offspring will have something similar. So both of my parents are PhDs, nonphysicians. There is a diabetes department at the City of Hope, so she's the chair of that department. So very active. We do overlap in some circles because she does investigate both vascular complications and renal complications. And then sometimes will ask my advice on some visualization. But she herself has just had a science translational medicine paper, for example, just a couple of months ago. So it's fun to talk about these things. To be honest, because my parents are researchers, I was not totally sure that I would be a researcher and kind of wanted to do something different in medicine. But many of my early observations and just how common cardiovascular disease is around me and in my community and wanting to do something useful is what got me specifically into cardiology.(55:45):But obviously there are numerous outstanding, important questions. And as I went through my career, really focused on more basic investigations of atherosclerosis and lipids. What got me excited sort of after my clinical training was the ability to ask many of these questions now in human populations with many new biological data sets, at least first centered on genetics. And the capabilities continue to expand, so now I teach first year Harvard medical students in their genetics curriculum. And when I talk to them just about my career arc, I do remind them they're all doing millions of things and they're exploring lots of things, but when they get to my shoes, the capabilities will be tremendously different. And so, I really advise them to take the different experiences, mainly in an exercise for asking questions, thoughtfully addressing questions, connecting it back to important clinical problems. And then once they start to understand that with a few different approaches, then they'll totally take off with what the opportunities are down the road.Eric Topol (56:51):No, it's great. I mean, how lucky somebody could be in the first year of med school with you as their teacher and model. Wow. Pradeep, we've really gone deep on this and it's been fun. I mean, if there's one person I'm going to talk to you about cardiovascular risk factors and the things that we've been into today, you would be the one. So thank you for taking the time and running through a lot of material here today, and all your work with great interest.Pradeep Natarajan (57:24):Thanks, Eric. I really appreciate it. It's tremendous honor. I'm a big fan, so I would be glad to talk about any of these things and more anytime.***************Thanks for listening, reading or watching!The Ground Truths newsletters and podcasts are all free, open-access, without ads.Please share this post/podcast with your friends and network if you found it informative!Voluntary paid subscriptions all go to support Scripps Research. Many thanks for that—they greatly helped fund our summer internship programs for 2023 and 2024.Thanks to my producer Jessica Nguyen and Sinjun Balabanoff for audio and video support at Scripps Research.Note: you can select preferences to receive emails about newsletters, podcasts, or all I don't want to bother you with an email for content that you're not interested in. Get full access to Ground Truths at erictopol.substack.com/subscribe

In episode 1091, Nick Norwitz, Mark Bell, Nsima Inyang, and Andrew Zaragoza talk about how Nick was able to massively drop his LDL Cholesterol by eating 12 Oreo Cookies a day.  Nick's Response to LAYNE Norton - https://youtu.be/yiq67wpUhIs Follow Nick on IG: https://www.instagram.com/nicknorwitz/ Official Power Project Website: https://powerproject.live Join The Power Project Discord: https://discord.gg/yYzthQX5qN Subscribe to the Power Project Clips Channel: https://youtube.com/channel/UC5Df31rlDXm0EJAcKsq1SUw Special perks for our listeners below!

In episode 1091, Nick Norwitz, Mark Bell, Nsima Inyang, and Andrew Zaragoza talk about how Nick was able to massively drop his LDL Cholesterol by eating 12 Oreo Cookies a day. Follow Nick on IG: https://www.instagram.com/nicknorwitz/   Official Power Project Website: https://powerproject.live Join The Power Project Discord: https://discord.gg/yYzthQX5qN Subscribe to the Power Project Clips Channel: https://youtube.com/channel/UC5Df31rlDXm0EJAcKsq1SUw   Special perks for our listeners below!  

Send us a Text Message.Today is part 1 of a 2 part series on lowering LDL cholesterol. In this episode we are going to cover what LDL cholesterol is and how it might contribute to the development of heart disease. In the next episode we are going to discuss nutrition and lifestyle strategies for lowering LDL. In this episode we cover:What cholesterol is and how it functions in our bodyWhy cholesterol has been thought to cause heart diseaseThe truth about cholesterol and heart disease The right cholesterol test to measure to identify risk How cholesterol fits with other risk factors as well to contribute to the development of heart disease Tune in to the episode to learn more. I discussed measuring APO on the show and this a place where you can purchase the lab test online if you are not able to order it through your doctor.APO B Test Online  Sources and Additional Reading Apo B as a Rik Factor for Cardiovascular Disease A Review of How Lipoproteins Contribute to Cardiovascular DiseaseCheck out some of products/supplements that I personally use and recommend. 

Today, Paul and Mike unpack their opinions about lipids. They talk about true risk for cardiovascular disease, primary versus secondary prevention, lipid lowering drugs, and share their thoughts on a recent podcast episode with Peter Attia. *Produced by Mountain Valley Media 00:06:08 Blood markers & imaging techniques of metabolic function  00:14:38 Gene mutations 00:20:28 LDL & Plaque burden 00:27:23 Money in statins 00:31:38 Downsides of lowering LDL 01:21:23 The downsides of popular cholesterol lowering drugs 01:41:07 Should we fear heart attacks? 01:45:23 PCSK9 Inhibitors 01:52:43 Risk profile of Statins  01:53:02 Risk vs. reward of Ezetimibe 02:04:02 Primary vs. secondary prevention Resources: Debunking Sugar Claims: What Dr. Lustig Got Wrong On The Huberman Podcast: https://www.youtube.com/watch?v=JcEmSgbMfco&t=2933s Work With Mike: https://mikefave.com/

For the past 60 years the medical community has obsessively focused on lowering LDL-cholesterol levels… Research shows these five preventable health conditions make LDL-Cholesterol more likely to cause artery plaque build-up, even if your LDL-Cholesterol levels are low. Sponsored: Crush your Workouts and stay hydrated this summer with the Electrolyte + Creatine Combo by MYOXCIENCE: https://bit.ly/electrolyte-stix *Save with code podcast at checkout Link to Video and Show Notes: https://bit.ly/3WfpI5R Research Mentioned: Zanoni, P., Velagapudi, S., Yalcinkaya, M., Rohrer, L. & Eckardstein, A. von. Endocytosis of lipoproteins. Atherosclerosis 275, 273–295 (2018). Ference, B. A., Braunwald, E. & Catapano, A. L. The LDL cumulative exposure hypothesis: evidence and practical applications. Nat. Rev. Cardiol. 1–16 (2024) doi:10.1038/s41569-024-01039-5. Time Stamps: 00:45 LDL's link with atherosclerosis is nuanced.  02:30 Initial damage to the arterial wall makes LDL levels problematic. 03:45 Increases risk of arterial wall damage: elevated blood pressure, insulin resistance/diabetes, smoking/vaping, obesity, elevated blood viscosity, consuming oxidizableoils. 08:40 High LDL and high triglycerides suggest insulin resistance and increased cardiovascular risk. 09:50 Start with diet and exercise together. 11:20 Statins have concerning side effects. 13:15 Plaque formation begins early in life. 13:50 High LDL is found in centenarians. 14:44 Centenarians are metabolically healthy. 15:40 Your liver makes LDL cholesterol. 16:10 Every cell in your body requires cholesterol. 18:00  Diets high in seed oils make your LDL more likely to be oxidized. 20:55 30-50% of people who have heart attacks have optimal serum cholesterol.

Prayers for safety, healing, and peace in the USA and beyond. This week, Dr. Kahn dives into two fascinating case studies from the Kahn Center. But that's just the beginning. He also covers a range of mini-topics, including the role of CoQ10 in combating fatty liver disease, the surprising prevalence of unknown leaky valves in people over 60, and the impact of sleep apnea in younger adults (psst, you can get a home sleep study mailed to you from the Kahn Center at 248-731-7412). Women with heart disease will find the discussion on the proper aspirin dose particularly insightful. Plus, if you're curious about weight loss options, Dr. Kahn breaks down why "Mounjaro" might be a better choice than "Ozempic" for diabetic patients. The main topic is a groundbreaking paper by the legendary Dr. Eugene Braunwald from Harvard. He introduces the concept of "plaque years," which measures the duration and levels of LDL cholesterol in your body, akin to calculating smoking "pack years." The gist? More plaque years mean a higher risk of developing atherosclerosis. Dr. Kahn recommends getting a coronary artery calcium scan and a carotid IMT ultrasound to get a clearer picture of your heart health.

In a clinical study of 100 people with dry eyes, 4 capsules daily of sea buckthorn significantly relieved dry eye symptoms, including redness and burning! Don't miss these other topics that Terry will discuss on this show: Low T (Testosterone) What is the difference between Ibuprofen and Acetaminophen? Is a Broken Hip Worse than Cancer? A Closer Look at: LDL Cholesterol

Audio Commentary by Dr. Valentin Fuster, Emeritus Editor in Chief

A 22-year follow-up study involving 177,000 individuals reveals that low LDL cholesterol is associated with higher cardiovascular-specific mortality. The authors of this study write, "...the lowest risk for long-term mortality appears to exist in the wide LDL-C range of 100–189 mg/dL, which is much higher than current recommendations." Support your Intermittent Fasting lifestyle with the Berberine Fasting Accelerator by MYOXCIENCE: bit.ly/berberine-fasting-accelerator Use code podcast at checkout to save Links to Research & Video: https://bit.ly/4asJ4t3 Key Takeaways:  0:00 Intro 0:04 22 Year Study 0:22 Study Title 0:52 Study Findings  1:52 Probability of survival  2:12 Counterintuitive Findings 3:42 High LDL and odds of death  3:59 U-Shaped Curve 5:50 Metabolic Health 6:34 Study of 177,000 people  8:09 Lowest risk of mortality  9:17 Watch this! 11:01 Lipid paradox

Dave Feldman is a returning guest on our show! Check out his first appearance on Boundless Body Radio on episode 109, where he was interviewed by our mutual friend, guest host Dr. Nick Norwitz! Dave Feldman is a senior software engineer, entrepreneur and a citizen scientist. After starting a low-carb diet in 2015, Dave found that his cholesterol numbers had increased considerably. He then began reverse-engineering the lipid system through self-experimentation and testing, finding the system to be very dynamic and fluid. He has now demonstrated this phenomenon multiple times by moving his cholesterol up and down substantially in a matter of days. He's discovered similar and reproducible patterns in others and has since researched a particular phenotype that he coined “lean mass hyper responder”, or LMHR for short.Dave is the creator of the popular blog Cholesterol Code, where he shares all of his knowledge and research. Dave is also the founder of the Citizen Science Foundation, a non-profit that has funded several incredible studies. Dave has recently hosted the incredible Collaborative Science Conference in his hometown of Las Vegas in March of 2024, which I was fortunate to attend. Find Dave at- TW- @realDaveFeldmanIG- @realdavefeldmanYT- @realDaveFeldmanhttps://citizensciencefoundation.org/https://ownyourlabs.com/https://cholesterolcode.com/Find Boundless Body at- myboundlessbody.com Book a session with us here!

Vitamin E might be one of the least thought about vitamins these days, but it does have some standout benefits that you should know about. On this episode of Vitality Radio, Jared breaks down those benefits, the different forms of Vitamin E found in nature, as well as the difference between tocopherols and tocotrienols. This episode is meant to help you to decide if supplementing Vitamin E is right for you.Jared also shares another Homeopathic Minute from his series of quick, easy to digest information on single homeopathic remedies. Today's remedy is Borax.Products:Solaray Bio Vitamin E Gamma PlexNatural Factors Clear Base Vitamin EDerma - E Vitamin E Skin OilVital 5 Ultimate Vitality MultiOllois BoraxAdditional Information:#332: Cholesterol Controversy - Jared's Interview on Inside The Aisle with Niki Wolfe***Be sure to listen to Wednesday's podcasts this year for Jared's Homeopathic Minute to learn more about specific remedies.#393: What Is Homeopathy and How Does It Work? With Guillaume LoisBe Healthy Utah discount code: vitality40BeHealtyUtah.comVibrant Living Wellness ConferenceVisit the podcast website here: VitalityRadio.comYou can follow @vitalityradio and @vitalitynutritionbountiful on Instagram, or Vitality Radio and Vitality Nutrition on Facebook. Join us also in the Vitality Radio Podcast Listener Community on Facebook. Shop the products that Jared mentions at vitalitynutrition.com. Let us know your thoughts about this episode using the hashtag #vitalityradio and please rate and review us on Apple Podcasts. Thank you!Please also join us on the Dearly Discarded Podcast with Jared St. Clair.Just a reminder that this podcast is for educational purposes only. The FDA has not evaluated the podcast. The information is not intended to diagnose, treat, cure, or prevent any disease. The advice given is not intended to replace the advice of your medical professional.

In this episode the ladies answer questions from listeners including one about how to lower LDL cholesterol on a high protein diet: what might be causing the high LDL reading; what other factors other than diet may be contributing; and their advice for some lifestyle factors and further research to address the potential issue. They also discuss how much is too much protein powder: what percentage of your daily protein amount ideally should come from whole foods, and how much is ok to get from supplements like protein powder? How can you best meal prep or plan when you have a job that keeps you on the road and yet doesn't allow much downtime for eating? Finally, Ashleigh dives into yet another social media trend that grinds her gears: the polarizing discussion online about "healthy versions of classic desserts." One side says we should avoid dessert unless we make it ourselves, while the other side says that these healthy versions are just an expression of orthorexia. What do you think? Let us know your thoughts, or pose more questions or topic ideas to Rachel and Ashleigh at musclescience4women@gmail.com Sign up for our new Strong & Sculpted Shoulders workshop: https://www.rgfit.com/shoulders Get fit with us in 2024 - sign up for the Grow Your Glutes Workshop: https://www.rgfit.com/glutes  Or our flagship strength training program, Muscle Science for Women: http://www.musclescienceforwomen.com  If you've always wanted to test some things out and try a CGM, Muscle Science for Women is partnering with NutriSense to help you!  Nutrisense combines cutting-edge technology and human expertise so you can see how your body responds to different food, exercise, stress, and sleep in real time. By pairing a CGM with their app and expert nutritionist guidance, you can help understand which foods impact your glucose levels and how you respond to foods, stress, exercise, and sleep changes. You simply pair a continuous glucose monitor with their Nutrisense app, where you can keep all your data around food, exercise and so on, and their subscription plan also includes a month of free nutritionist support.  Go to Nutrisenseio.com/MSW or use the code MSW at checkout to receive a $30 discount off your first month which includes 2 CGM sensors, free shipping, and a month of professional Nutritionist support.    

This is a special episode taken from a few attendees of the Collaborative Science Conference, held in Las Vegas on March 15-16, 2024. I attended this wonderful conference, had an amazing time, and met all of these new friends, who each had incredible stories to tell. Thank you to Les, Shari, Chip, and Mark for participating! This one was special!PLEASE. If you are trying low-carb, or want to try low-carb, reach out so we can help. You can always book a free session with us here, we are more than happy to help you get to a place of better health.Find the Collaborative Science Conference at-https://cosci.org/https://citizensciencefoundation.org/TW- @realCSFTW- @realDaveFeldmanFind Boundless Body at- myboundlessbody.com Book a session with us here!

Welcome to Protecting Your Nest with Dr. Tony Hampton. Nina Teicholz is an investigative science journalist, author, and thought leader in nutrition. She is also the founder of the Nutrition Coalition, an independent non-profit dedicated to ensuring that nutrition policy is evidence based. She is the author of the New York Times bestseller, The Big Fat Surprise, which upended the conventional wisdom on dietary fat–especially saturated fat—and spurred a new conversation about whether these fats in fact cause heart disease. Teicholz attended Yale and Stanford where she studied biology and majored in American Studies. She has a master's degree from Oxford University and served as associate director of the Center for Globalization and Sustainable Development at Columbia University. In this discussion, Dr. Tony and Nina talk about: (03:27) The lack of critical journalists in nutrition (09:56) The work and legacy of Dr. Sarah Hallberg (18:13) The serious issues with the recently released Stanford Twin Studies and the documentary that was inspired by it (26:39) How can the average person know who to trust on the subject of nutrition (31:38) LDL Cholesterol and whether measuring it is enough to accurately calculate cardiovascular risk (41: 05) How to make a documentary that people can feel confident trusting (46:52) Chris Gardener's mission and why diets backed by bad science are so popular (01:00:15) Nina's current projects Thank you for listening to Protecting Your Nest. For additional resources and information, please see the links below.   Links:   Virta Health Dr. Sarah Hallberg TED Talk Sarah Hallberg Legacy Virtual Course   Nina Teicholz: Website Twitter Facebook   Dr. Tony Hampton: Linktree Instagram Account LinkedIn Account Ritmos Negros Podcast Q Med Symposium for Metabolic Health Lectures How Waking Up Every Day at 4:30 Can Change Your Life

The current thoughts around LDL cholesterol center on the fact that there is no scenario in which high LDL numbers could occur in healthy individuals. Traditionally, the belief is high levels of LDL can lead to a greater risk of cardiovascular disease regardless of metabolic health. Today's guest is here to share his hypothesis and research on how higher cholesterol levels in metabolically fit individuals could be a physiological response rather than a pathological response that can lead to disease. Today on The Dhru Purohit Show, Dhru sits down with Dave Feldman to discuss high levels of LDL in metabolically healthy individuals. Dave shares the current research on high LDL and cardiovascular disease in individuals eating a ketogenic diet. He also shares his personal approach to focusing on metabolic health and the key markers critical to overall health. Dave discusses the process and findings of the Oreo experiment conducted by his colleague and explains why this experiment further proves their hypothesis on how LDL particles move through the body. Dave Feldman is a software and platform engineer, entrepreneur, and founder of the Citizen Science Foundation. Through a series of self-experiments and partnering with formal researchers, he has since published the "Lipid Energy Model," which may explain this phenomenon. In this episode, Dhru and Dave dive into (audio version / Apple Subscriber version):Dave's hypothesis on LDL (00:24 /00:24)Rethinking our approach to high LDL (2:17 / 2:17) The research on high LDL and cardiovascular disease (10:00 / 6:48) The Oreo experiment and what it shows about fat adaptation (17:23 / 13:45)The pushback to lean mass hyper responder (27:36 / 24:15) Soft plaque versus hard plaque and the risk of cardiovascular disease (37:50 / 35:04) Dave's personal approach in focusing on overall metabolic health (51:42 / 48:30) Fasting Insulin and Vitamin D (59:33 / 53:45) Endothelial health and cardiovascular health (1:03:28 / 57:45) The vegan's twin study and the correlation to LDL (1:21:17 / 1:15:49)Dhru's experience (1:32:17 / 1:26:36) Also mentioned in this episode:Citizen Science Foundation Oreo Cookie TreatmentNicolas Norwitz, PhD Twitter This episode is brought to you by LMNT, Momentous, and Lumebox. Right now, LMNT is offering my listeners a free sample pack with any purchase. Head over to DrinkLMNT.com/dhru today.Optimize your Omega-3 levels by choosing a quality fish oil made by and used by the best. Go to livemomentous.com and enter promo code DHRU to get 20% off any order. Lumebox is offering my community $260 off their FDA-approved portable Red Light device! That's over 50% off! Go to thelumebox.com/dhru and get your Red Light device. Hosted on Acast. See acast.com/privacy for more information.

Just from today's title, you know we'll be diving into some questionable material but it's important to understand what is passing as "information" that your clients might be consuming. In today's episode, we'll look at a recent study examining the effects of Oreo consumption, LDL cholesterol markers, the lipid energy model, and more. Topics include:   - Recent Study on Oreos and LDL - My Thoughts on Cholesterol Episode 386 - The Lipid Energy Model - Diving Into The Study - Takeaways From This Study - Metabolism School - Metabolism Made Simple ----------  Subscribe to My New Youtube Channel:  https://youtube.com/@sammillerscience?si=s1jcR6Im4GDHbw_1 ----------  My Live Program for Coaches: The Functional Nutrition and Metabolism Specialization  www.metabolismschool.com ----------     [Free] Metabolism School 101: The Video Series http://www.metabolismschool.com/metabolism-101     ----------     Grab a Copy of My New Book - Metabolism Made Simple     ----------   Stay Connected:     Instagram: @sammillerscience     Youtube: SamMillerScience     Facebook: The Nutrition Coaching Collaborative Community     TikTok: @sammillerscience       ---------- “This Podcast is for general informational purposes only and does not constitute the practice of medicine, nursing or other professional health care services, including the giving of medical advice, and no doctor/patient relationship is formed. The use of information on this podcast and the show notes or the reliance on the information provided is to be done at the user's own risk. The content of this podcast is not intended to be a substitute for professional medical advice, diagnosis, or treatment and is for educational purposes only. Always consult your physician before beginning any exercise program and users should not disregard, or delay in obtaining, medical advice for any medical condition they may have and should seek the assistance of their health care professionals for any such conditions. By accessing this Podcast, the listener acknowledges that the entire contents and design of this Podcast, are the property of Oracle Athletic Science LLC, or used by Oracle Athletic Science LLC with permission, and are protected under U.S. and international copyright and trademark laws. Except as otherwise provided herein, users of this Podcast may save and use information contained in the Podcast only for personal or other non-commercial, educational purposes. No other use, including, without limitation, reproduction, retransmission or editing, of this Podcast may be made without the prior written permission of Oracle Athletic Science LLC, which may be requested by contacting the Oracle Athletic Science LLC by email at team@sammillerscience.com. By accessing this Podcast, the listener acknowledges that Oracle Athletic Science LLC makes no warranty, guarantee, or representation as to the accuracy or sufficiency of the information featured in this Podcast."

Watch the full video interview on YouTube here: https://youtu.be/iOwfhFWUwhE Dr. Nadir Ali has worked as an interventional cardiologist in the Houston area for the last 26 years.  Since 2013 he has focused his efforts to improve heart disease, diabetes and obesity through diet and lifestyle interventions in his clinical practice.  In this episode, we discuss: Why LDL cholesterol goes up on a low-carb diet Phytosterols (aka plant cholesterols) are dangerous if you're on a statin drug Ketones and cholesterol Does the body ever stop making cholesterol? The benefits of LDL cholesterol Why do we fear LDL cholesterol? Is oxidized LDL a firefighter or an arsonist? What is the real cause of heart disease and strokes? The thrombogenic hypothesis Insulin resistance is a mitochondrial disease The side effects of statins What is the lean low-carb diet plan? How the reward centre of the brain works Daily steps to become metabolically healthy When to start including more fat in the diet How many carbs should you eat a day? Understanding the dopamine system in your brain What is intermittent positive reinforcement? Practical tips to help you sleep better The body does not need fiber Dr. Ali's typical day of eating Carbs and high intensity exercise Dr. Ali's thoughts on supplements Show Sponsor: BiOptimizers

Nick Norwitz is an MD student at Harvard, & holds a PhD from Oxford in metabolism and nutrition. JOIN THE PATREON FAMILY: https://patreon.com/dannyjones SPONSORS https://ver.so/danny - Use code DANNY to save 15% on your first order. https://ketobrainz.com/pages/djp - Use code "DANNY20" at checkout. EPISODE LINKS https://www.youtube.com/@nicknorwitzPhD https://twitter.com/nicknorwitz FOLLOW DANNY JONES https://www.instagram.com/jonesdanny https://twitter.com/jonesdanny OUTLINE 00:00 - Nick's medical situation 07:02 - Ketogenic diet science 10:49 - Health industry contradictions 15:03 - Nutrition documentaries 20:12 - 500 LDL on low carb diet 23:41 - Lean mass hyper responder 34:43 - Evidence carbohydrates reduce cholesterol 36:50 - Oreo VS Statin Experiment 49:15 - Backlash from medical community 53:34 - Oreos vs Statin test results 01:11:03 - Adding carbs to Ketogenic diet 01:14:08 - Seed oils; polyunsaturated fats 01:16:02 - Risk profiles for heart disease 01:22:47 - Arterial plaque in fit people with high cholesterol 01:26:49 - ApoB & LP(a) 01:29:29 - Misconceptions about Keto 01:33:29 - Expanding the LMHR study 01:35:37 - Harvard Medical school 01:37:47 - Broken medical system 01:39:40 - Misinformation in medical journals 01:53:59 - GLP-1 fat loss meds 01:59:29 - Weight lifting affects on LDL 02:07:20 - Cardio effects on LDL 02:08:06 - Neuro-protective effects of Keto 02:10:53 - DARPA's interest in Keto diet 02:14:39 - Allulose: Healthy sugar? 02:21:17 - Diet Coke