Healthy AF | Healthy After 50

Zane Griggs: Health Tips
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Healthy AF, the podcast dedicated to helping you live a healthier life after the age of 50, hosted by health and longevity expert Zane Griggs. This show is your guide to achieving optimal health, both physically and mentally. Whether you're in your 20s and want to plan for a healthy future or in your 50s and seeking to catch up, this show could help you improve your nutrition, fitness, and overall well-being. Each week, we'll dive into the latest research and expert advice on topics such as exercise, stress management, and more. We'll discuss practical strategies for maintaining a healthy lifestyle, including how to balance your diet and stay active as you age. Remember, it's never too late to prioritize your health and become Healthy AF! (Hit play to learn more)

  1. 1d ago ·  Video

    54. Why Am I Always Hungry? The Mitochondrial Connection to Hunger, Cravings & Seed Oils Part 2 VIDEO

    You just ate a full meal. You consumed enough calories. So why are you hungry again 45 minutes later? Or maybe it's 3 PM—you've eaten plenty, but you're running on fumes, struggling to focus, and craving something sweet or starchy. Most people blame willpower, blood sugar, or a lack of protein. In Part 2 of Zane Griggs' series on seed oils and mitochondrial health, he explores a different possibility: what if the problem isn't how much energy you're eating, but how efficiently your cells are converting that food into ATP? In this episode, Zane breaks down the difference between food energy and cellular energy, how your mitochondria convert calories into ATP, and why inefficient energy production may contribute to hunger, cravings, fatigue, brain fog, poor recovery, and stubborn body composition. He also continues the mitochondrial story from Episode 1, exploring how PUFA-rich mitochondrial membranes may contribute to proton leak and cardiolipin damage, how lipid oxidation products such as 4-HNE and MDA can interact with mitochondrial DNA, and why these processes may become increasingly relevant as we age. Zane also explains what these issues can look like in everyday life: feeling unsatisfied after meals, afternoon cravings, energy crashes, poor exercise recovery, and body composition that doesn't seem to respond proportionately to your diet and training. This is Part 2 of the Healthy AF series examining seed oils, mitochondrial function, and metabolic health. Episode Timestamps: 0:00 Why Are You Hungry Again After Eating? 1:00 Food Energy vs. Cellular Energy 2:00 Calories Have to Be Converted Into ATP 3:00 Why Low ATP Can Trigger Hunger & Cravings 4:00 How Mitochondrial Inefficiency Changes the Equation 5:00 Proton Leak: Losing Energy as Heat 6:00 Cardiolipin Damage & the Electron Transport Chain 7:00 Why Your Cells Signal You to Eat More 8:00 Hunger Isn't Always a Willpower Problem 9:00 4-HNE, MDA & Oxidative Damage 10:00 How Oxidation Can Reach Mitochondrial DNA 11:00 Why Mitochondrial DNA Damage Matters After 40 12:00 Hunger & Fatigue as Early Warning Signs 13:00 Cravings, Energy Crashes & Poor Recovery 14:00 How Much Linoleic Acid Are We Eating? 15:00 Where Seed Oils Hide in the Modern Diet 16:00 Why Some People Seem Fine Eating Seed Oils 17:00 Metabolic Problems Can Develop Over Decades 18:00 Next: Blood Sugar, Glucagon + Free Fit Over 40 Plan   Connect with Zane Griggs: 🧠 Free Plan: free40plan.com 📲 Instagram: @zanegriggsfitness 🌐 Website: zanegriggs.com Research Referenced Hulbert et al. (2007) — Membrane Composition & Lifespan Seebacher et al. (2010) — Oxidative Metabolism & Proton Leak Paradies et al. (2009) — Cardiolipin Peroxidation & Mitochondrial Dysfunction Chicco & Sparagna (2007) — Cardiolipin & Mitochondrial Disease Stanley et al. (2012) — Dietary Fat & Mitochondrial Function Khairallah et al. (2012) — Membrane Fatty Acids & Mitochondrial Function Penzo et al. (2002) — Fatty Acids & Mitochondrial Function Hulbert et al. (2006) — Peroxidation-Resistant Membranes & Longevity Pamplona et al. (2004) — Fatty Acid Unsaturation & Mitochondrial DNA Damage Porter, Hulbert & Brand (1996) — Mitochondrial Proton Leak

  2. Aug 17

    53. What Happens to Seed Oils After You Eat Them?

    What actually happens to seed oils once they enter your body? In this first episode of a new Healthy AF series, Zane Griggs breaks down the metabolic chain reaction he argues can begin when dietary polyunsaturated fats become incorporated into the membranes of your mitochondria. Your mitochondria produce the ATP that powers your cells—but the fats you eat can become part of the physical structure of the mitochondrial membrane. Zane explores research around membrane composition, polyunsaturated fats, oxidative vulnerability, proton leak, mitochondrial uncoupling, and cardiolipin. You'll learn why Zane believes the conversation around seed oils needs to go much deeper than calories or inflammation—and why mitochondrial health may be an important piece of understanding metabolic health, energy production, and longevity. Zane also discusses research suggesting mitochondrial membrane composition can change in response to dietary fat composition, meaning what your mitochondria are built from isn't necessarily fixed. This is Part 1 of Zane's deep dive into seed oils, mitochondria, and metabolic health. In the next episode, he'll explore how this chain of events may connect to hunger and why you can feel hungry even when you're consuming plenty of food. Get Zane's FREE Fit Over 40 Plan: Free40Plan.com Research & Resources Want to dig into the research behind this episode? Here are some of the studies and reviews referenced in Zane's deep dive into dietary fats, mitochondrial membranes, oxidation, and longevity: Life and Death: Metabolic Rate, Membrane Composition, and Life Span of Animals — Hulbert et al. (2007) https://pubmed.ncbi.nlm.nih.gov/17928583/ Role of Cardiolipin Peroxidation and Ca²⁺ in Mitochondrial Dysfunction and Disease — Paradies et al. (2009) https://pubmed.ncbi.nlm.nih.gov/19368971/ Role of Cardiolipin Alterations in Mitochondrial Dysfunction and Disease — Chicco & Sparagna (2007) https://pubmed.ncbi.nlm.nih.gov/16899548/ Improved Mitochondrial Function with Diet-Induced Increase in DHA or Arachidonic Acid in Membrane Phospholipids — Khairallah et al. (2012) https://pmc.ncbi.nlm.nih.gov/articles/PMC3316678/ Effects of Fatty Acids on Mitochondria: Implications for Cell Death — Penzo et al. (2002) https://pubmed.ncbi.nlm.nih.gov/12206909/ Extended Longevity of Wild-Derived Mice Is Associated with Peroxidation-Resistant Membranes — Hulbert et al. (2006) https://pubmed.ncbi.nlm.nih.gov/16620917/ Modification of Fatty Acid Unsaturation, Oxidative Damage & Longevity — Pamplona et al. (2004) https://pubmed.ncbi.nlm.nih.gov/15130667/ Allometry of Mitochondrial Proton Leak: Membrane Surface Area & Fatty Acid Composition — Porter, Hulbert & Brand (1996) https://pubmed.ncbi.nlm.nih.gov/8997352/ YouTube Chapters 0:00 What Happens to Seed Oils After You Eat Them? 2:15 How Your Mitochondria Produce Energy 3:25 The Fats You Eat Become Part of Your Mitochondria 4:20 Why Polyunsaturated Fats Are More Vulnerable to Oxidation 6:40 Mitochondrial Membranes and the "Pacemaker of Aging" 8:00 How Seed Oils May Contribute to Proton Leak 10:40 Cardiolipin and the Mitochondrial Damage Cycle 14:00 What Long-Lived Species Can Teach Us About Membrane Fat 15:20 How This May Connect to Metabolic Disease 16:05 Can You Rebuild Your Mitochondrial Membranes? 17:00 What's Coming Next + Free Fit Over 40 Plan

  3. Jul 20

    52. The Truth About Alcohol Nobody Wants to Hear | Sam Lander

    Can you be Healthy AF if you still drink alcohol? In this episode of Healthy AF (Healthy After 50), I sit down with functional diagnostic nutritionist, peptide educator, and My Peptide University faculty member Sam Lander for one of the most honest conversations we've had on the podcast. Sam opens up about her incredible journey—from addiction, prison, and rebuilding her life—to becoming one of the most respected educators in functional medicine and peptide therapy. We dive into why so many people are doing everything "right" but still don't feel well, how functional lab testing uncovers hidden problems, and why alcohol may be the single biggest obstacle standing between you and optimal health. If you're focused on building muscle after 40, increasing energy, improving your gut, optimizing hormones, or extending your healthspan, this is an episode you don't want to miss. In this episode we discuss: • Sam's journey from addiction and prison to functional medicine • Why functional lab testing changes everything • The hidden connection between gut health and chronic symptoms • Why peptides require individualized protocols • The truth about "mommy wine culture" • How alcohol affects metabolism, inflammation and longevity • Why quitting alcohol is the biggest health hack most people ignore • Building resilience physically and mentally • Creating lasting health after 40 Connect with Sam Lander https://seefitliving.com https://www.instagram.com/seefitliving 0:00 Introduction: Meet functional diagnostic nutritionist Sam Lander 1:25 What functional diagnostic nutrition really is 2:05 Sam's childhood health struggles 3:20 Addiction begins at a young age 6:10 Prison, rock bottom, and rebuilding her life 10:45 Becoming a personal trainer after prison 15:30 Why doing "everything right" still wasn't enough 16:40 Discovering functional medicine through gut health 18:00 Why alcohol is the biggest health hack people ignore 22:30 The truth about mommy wine culture 27:40 How alcohol affects hormones, weight loss, and longevity 33:15 Peptides: why certification and protocols matter 38:20 Creating personalized health strategies instead of one-size-fits-all advice 43:10 Recovery, resilience, and building a healthier future 48:10 Final thoughts and where to connect with Sam

  4. Jun 4

    51. The Seed Oil Studies Are Measuring the Wrong Thing

    A new seed oil study may look reassuring at first glance — but what did it actually measure? In this episode, Zane Griggs breaks down a 2025 review of clinical studies on seed oils and explains why short-term improvements in blood markers do not necessarily tell us what is happening inside the mitochondria. You'll learn why the real concern is not only what shows up in a blood draw, but what happens when polyunsaturated fats become incorporated into mitochondrial membranes over time. Zane walks through: what the seed oil review actually found why flaxseed and sesame oil are not the same as soybean or corn oil the difference between blood markers and mitochondrial damage cardiolipin, ATP production, and oxidative stress why 4-HNE and other aldehydes matter how cooking oils change when heated why stored linoleic acid can remain in the body for years why a short-term study may miss a long-term mitochondrial problem how soybean oil consumption has changed over the last century why stable fats may matter more than most people realize Studies: Laurindo et al. Frontiers in Nutrition. 2025;12:1502815 Hulbert AJ et al. Physiological Reviews. 87:1175–1213, 2007 Seebacher F, Brand MD, Else PL, Guderley H, Hulbert AJ, Moyes CD. Physiological and Biochemical Zoology. 83(5):721–732, 2010 UC Riverside / Journal of Lipid Research, November 2025 SNI Global soybean oil consumption data The point is not to ignore studies that show short-term improvements. The point is to understand their limitations and ask whether they are measuring the outcome that actually matters. Download Zane's Free Fit Over 40 Plan: https://free40plan.com   00:00 The seed oil study everyone is going to cite 01:00 What the 2025 review actually measured 02:00 Why flaxseed and sesame oil are different 03:30 The short-term benefits are real — but limited 04:00 The problem with relying on blood markers 05:00 What happens inside the mitochondria 06:00 Cardiolipin and ATP production explained 07:00 The damage the studies did not measure 08:00 Why higher antioxidant activity can be misleading 09:00 The researchers admitted a major limitation 10:00 They did not verify the oil composition 11:00 Why processing, heat, and storage matter 12:00 Fast-food fryer oil is not the same intervention 13:00 How stored linoleic acid remains in the body 15:00 Why the control groups were not truly low-PUFA 16:00 The washout problem no short-term study solves 17:00 Comparing two versions of excess exposure 18:00 How much soybean oil Americans consume 19:00 Physiological need vs modern consumption 21:00 Why the baseline recommendation may already be too high 22:00 The UC Riverside soybean oil research 23:00 Oxylipins, liver health, and mitochondrial function 25:00 Why standard blood tests may miss the damage 26:00 The peroxidation index explained 27:00 Omega-3 vs omega-6 vs monounsaturated fats 28:00 Why more fish oil may not solve the problem 29:00 Saturated fat and mitochondrial membrane stability 31:00 What membrane fluidity actually requires 32:00 Why longer-lived species matter 33:00 What the pro-seed-oil literature can and cannot prove 35:00 Short-term blood improvements vs long-term membrane loading 36:00 What fats Zane recommends using instead 38:00 Why ingredient labels matter 39:00 Final takeaway: read the studies carefully

  5. Jun 2

    50. Your Body Is Stuck Burning Fat — And It's Making You Sick (Part 2)

    What happens when your body gets stuck burning fat and can't switch back to glucose? In Part 2, Zane breaks down metabolic inflexibility and explains why being locked into fat-dominant metabolism is not the same as being metabolically healthy. You'll learn how this pattern affects the muscle, heart, and liver — and how elevated fatty acids can impair glucose oxidation, disrupt insulin signaling, and contribute to insulin resistance, fatty liver disease, and heart failure. Start with Part 1 first for the ATP and glucose-efficiency breakdown. 01:00 The metabolic signature of insulin resistance 03:30 Why your body should switch between fat and glucose 06:00 The 3 tissues that reveal metabolic inflexibility 08:30 Why Zane changed his mind about low carb 13:30 The real definition of metabolic inflexibility 15:00 Why elevated blood sugar can happen on keto or carnivore 20:00 Heart failure and metabolic disease 22:00 Why failing hearts become more dependent on fat 25:00 Why glucose is not the problem 29:00 The liver and fatty liver disease 33:00 Fatty liver is a metabolic inflexibility problem 34:00 Why the liver starts producing more glucose 40:00 How liver disease progresses 41:00 The muscle, heart, and liver connection 46:00 How to restore glucose oxidation 47:00 Why high-fat, low-carb can mimic metabolic disease   Kelley, D.E. (2005) "Skeletal muscle fat oxidation: timing and flexibility are everything" Journal of Clinical Investigation — JCI25758 / PMC1159159 Used for: Definition of metabolic inflexibility; experimental elevation of plasma FFAs recreating T2D metabolic signature in skeletal muscle; blunted insulin-stimulated glucose oxidation; impaired suppression of lipid oxidation Ukropcova, B. et al. (2005) "Dynamic changes in fat oxidation in human primary myocytes mirror metabolic characteristics of the donor" Journal of Clinical Investigation — JCI24332 Used for: Formal definition of metabolic inflexibility — insulin-resistant muscle characterized by lower fasting lipid utilization and failure to switch to carbohydrate oxidation in response to insulin Sun, Q., Lopaschuk, G.D. et al. (2024) "Mitochondrial fatty acid oxidation is the major source of cardiac ATP production in heart failure with preserved ejection fraction" Cardiovascular Research, Volume 120 — PMID 38193548 Used for: Direct radiolabeled substrate measurements in HFpEF; suppressed insulin-stimulated glucose oxidation; increased FAO; decreased PDH phosphorylation confirmed in human heart samples; disrupted glucose/fat ATP balance Sun, Q., Karwi, Q.G., Wong, N., Lopaschuk, G.D. (2024) "Advances in myocardial energy metabolism: metabolic remodelling in heart failure and beyond" Cardiovascular Research — PMC11646102 Used for: Comprehensive synthesis — decreased glucose oxidation as universal defect across HFpEF, HFrEF, and diabetic cardiomyopathy; uncoupling of glycolysis from glucose oxidation; FAO increases in HFpEF and diabetic cardiomyopathies Lopaschuk, G.D., Ussher, J.R., Folmes, C.D.L., Jaswal, J.S., Stanley, W.C. (2010) "Myocardial Fatty Acid Metabolism in Health and Disease" Physiological Reviews — PMC3976623 Used for: Fat oxidation dominance in HF, ischemia, and diabetes; uncoupling of glycolysis from glucose oxidation; therapeutic case for reducing FAO and increasing glucose oxidation (quotes carried over from Video 1 for context) Fillmore, N., Jaswal, J.S., Lopaschuk, G.D. (2011) "Uncoupling of glycolysis from glucose oxidation accompanies the development of heart failure" Journal of Molecular and Cellular Cardiology — ScienceDirect Used for: Pharmacological shifting from fat to glucose oxidation improving ATP efficiency; cardiac ischemia and heart failure therapeutic mechanism (context reference from Video 1) Satapati, S. et al. (2011) "Excessive hepatic mitochondrial TCA cycle and gluconeogenesis in humans with nonalcoholic fatty liver disease" Cell Metabolism — PMC3658280 Used for: 50% higher lipolysis in NAFLD; 30% higher gluconeogenesis; 2-fold increase in TCA cycle flux correlated with intrahepatic triglyceride content; increased FFA delivery and oxidation driving gluconeogenesis and oxidative stress Donnelly, K.L., Smith, C.I., Schwarzenberg, S.J., Jessurun, J., Boldt, M.D., Parks, E.J. (2005) "Sources of fatty acids stored in liver and secreted via lipoproteins in patients with nonalcoholic fatty liver disease" Journal of Clinical Investigation — JCI23621 Used for: Fat source breakdown in NAFLD — ~60% from plasma NEFA/adipose lipolysis, ~26% from de novo lipogenesis, ~15% dietary fat; stable isotope methodology confirming adipose lipolysis as primary driver Kolwicz, S.C. Jr. (2021) "Ketone Body Metabolism in the Ischemic Heart" Frontiers in Cardiovascular Medicine — DOI 10.3389/fcvm.2021.789458 Used for: Supporting context on cardiac metabolic flexibility; KD association with worse ischemic outcomes in some models; ketone-glucose suppression dynamic in the ischemic heart

  6. May 29

    50. Glucose Is the Most Efficient Fuel | The ATP & Metabolism Science Explained (Part 1)

    What if the most efficient fuel for the human body isn't fat… but glucose? In this episode, Zane Griggs breaks down the actual biochemistry behind ATP production, mitochondrial efficiency, and why cardiologists actively try to shift failing hearts away from fat oxidation and back toward glucose oxidation. This conversation dives deep into the P/O ratio, oxygen efficiency, insulin resistance, heart failure, ketones, metabolic flexibility, and the misunderstood role of glucose in human metabolism. If you've been told that fat is always the superior fuel source, this episode may completely change how you think about metabolism, performance, and energy production. In this episode: Why glucose produces more ATP per oxygen molecule The truth about fat oxidation vs glucose oxidation Why the heart becomes "stuck" burning fat in heart failure The real meaning of metabolic flexibility Why insulin is not the villain it's been made out to be The difference between glycolysis and glucose oxidation Why ketones are not the "super fuel" many claim How mitochondrial inefficiency impacts metabolic disease The connection between diabetes, heart disease, and fuel selection This is Part 1 of a deeper metabolic series exploring insulin resistance, ATP production, glucose metabolism, and how the body actually creates energy. Feeling "off" despite doing everything right? Download Zane's free Metabolic Stress Marker Guide to learn: ✔ what your labs may actually be telling you ✔ why "normal" doesn't always mean optimal ✔ the hidden hormone, thyroid, and metabolic markers most people overlook 👉 Get the free guide: https://zanegriggs.com/freeguide Ready to learn more? Get Zane's Free Over 40 Performance Plan: https://free40plan.com 00:00 Why fuel efficiency matters 01:00 What is ATP and the P/O ratio? 02:00 Why oxygen efficiency changes everything 03:00 Calories vs mitochondrial efficiency 05:00 The engine analogy explained 06:00 The studies comparing glucose, fat, and ketones 08:00 Why glucose creates more ATP than fat 09:00 What happens in heart failure 11:00 Are ketones really a "super fuel"? 13:00 Ketones and mitochondrial uncoupling 14:00 How cardiologists use glucose therapeutically 16:00 Fat oxidation and heart dysfunction 18:00 Diabetes, heart disease, and blocked glucose oxidation 20:00 Why doctors shift patients toward glucose oxidation 22:00 The metabolic flexibility explanation 24:00 Fat oxidation blocking glucose oxidation 25:00 Why insulin is NOT the enemy 27:00 The real driver of insulin resistance 28:00 Key takeaways on glucose vs fat burning 30:00 Preview of Part 2   Mookerjee et al. (2017) "Quantifying intracellular rates of glycolytic and oxidative ATP production and consumption using extracellular flux measurements" Journal of Biological Chemistry — PMC5409486 Used for: Glucose P/O ratio of 2.79; updated theoretical maximum ATP yields Agilent Technologies / Seahorse Bioscience (white paper) "Quantifying ATP Production Rate Using the Seahorse XF Real-Time ATP Rate Assay" Agilent application note 5991-9303EN Used for: P/O ratio range — palmitate 2.45, glucose 2.79–2.86; average cellular P/O of 2.75 Lopaschuk, Ussher, Folmes, Jaswal, Stanley (2010) "Myocardial Fatty Acid Metabolism in Health and Disease" Physiological Reviews — PMC3976623 Used for: All four extended quotes on fat oxidation dominance in heart failure, ischemia, and diabetes; therapeutic strategy of reducing fat oxidation and increasing glucose oxidation Fillmore, Jaswal, Lopaschuk (2011) "Uncoupling of glycolysis from glucose oxidation accompanies the development of heart failure" ScienceDirect / Journal of Molecular and Cellular Cardiology Used for: Quote on pharmacological shifting from fat to glucose oxidation improving ATP efficiency; cardiac ischemia and heart failure Sun, Lopaschuk et al. (2024) "Mitochondrial fatty acid oxidation is the major source of cardiac ATP production in heart failure with preserved ejection fraction" Cardiovascular Research, Volume 120 — PMID 38193548 Used for: HFpEF data — suppressed insulin-stimulated glucose oxidation, increased FAO, decreased PDH phosphorylation in mouse and human samples Kolwicz (2021) "Ketone Body Metabolism in the Ischemic Heart" Frontiers in Cardiovascular Medicine — DOI 10.3389/fcvm.2021.789458 Used for: Ketone P/O ratio ~2.50 vs glucose ~2.58 vs fat ~2.33; ischemic heart disease ketone data; KD associated with worse outcomes post-MI in some models MDPI / Koutnik et al. (2020) "Ketones Elicit Distinct Alterations in Adipose Mitochondrial Bioenergetics" International Journal of Molecular Sciences — DOI 10.3390/ijms21176255 Used for: β-hydroxybutyrate increases respiration without commensurate ATP production; elevated O2:ATP ratio confirming uncoupling; UCP1 and PGC1α upregulation Sullivan et al. / ResearchGate (2004) "The Ketogenic Diet Increases Mitochondrial Uncoupling Protein Levels and Activity" Used for: Ketogenic diet increases hippocampal uncoupling proteins; decreased ROS but at cost of coupling efficiency

  7. Mar 24

    49. Fix Your Blood Sugar Without Cutting Carbs With Isaac Pohlman

    In this episode, Zane sits down with registered dietitian and Type 1 diabetic Isaac Pohlman to challenge one of the biggest misconceptions in modern health: that carbs are the problem. Isaac shares his powerful personal journey—from a high-level athlete dealing with chronic fatigue, hormonal issues, and gut dysfunction to being diagnosed with Type 1 diabetes in grad school. What followed wasn't just managing symptoms, but completely rethinking metabolism, energy production, and how the body actually uses fuel. Together, Zane and Isaac break down why the fear around carbohydrates is not only misguided—but often making blood sugar issues worse. They unpack the real drivers of insulin resistance, including stress, circadian rhythm disruption, ultra-processed foods, and loss of muscle mass. This conversation goes far beyond "carbs vs. no carbs." It reframes metabolic health as a system—one that includes lifestyle, light exposure, recovery, food quality, and nervous system regulation. If you've been told to cut carbs to fix your blood sugar… this episode will challenge everything you thought you kne 👇 Download Zane's Free Plan https://free40plan.com/ Follow Zane IG: https://www.instagram.com/zanegriggsfitness Guest: https://www.thepohlmaninstitute.com https://www.facebook.com/isaacpohlmannutrition https://www.instagram.com/isaacpohlman https://www.youtube.com/@isaacpohlman Where to learn more about the Pohlman Institute's work and protocols Carb Sweet Spot Masterclass [FREE] https://programs.isaacpohlman.com/offers/FoFv4San Have Your Carbs and Eat 'Em Too Book https://book.isaacpohlman.com/book-sales-page The Pohlman Method - 1:1 Coaching: https://www.thepohlmaninstitute.com/the-pohlman-method 00:00 – Intro: Why cardio & diet aren't working anymore 01:00 – Isaac's background & metabolic health approach 03:00 – Athlete to chronic fatigue: early warning signs 05:00 – Stress, trauma & the link to autoimmune conditions 07:00 – The moment metabolism changed everything 10:00 – Type 1 diabetes diagnosis & symptoms 13:00 – Why carbs are misunderstood 15:00 – Fear of carbs & blood sugar spikes explained 17:00 – Why blood sugar SHOULD rise after meals 19:00 – Insulin, thyroid & energy production connection 21:00 – The real cause of insulin resistance 23:00 – Why low-carb can backfire 26:00 – Stress hormones, muscle loss & metabolism 29:00 – How to actually reverse pre-diabetes 31:00 – Lifestyle before diet (what most people miss) 34:00 – Food density & why your meals aren't satisfying 37:00 – What's REALLY causing the diabetes epidemic 40:00 – Light exposure, circadian rhythm & blood sugar 42:00 – Ultra-processed foods & fat storage 44:00 – Personal fat threshold explained 47:00 – Getting off medication naturally 50:00 – Reintroducing carbs safely 54:00 – Best carbs for blood sugar control

  8. Mar 17

    48. The Real Reason Your Metabolism Slows After 40 It's Not Age

    Most people believe your metabolism automatically slows down after 40. But the science says something very different. In this episode of Healthy AF, Zane Griggs breaks down the truth about metabolism, aging, and why fat loss gets harder for many people after 40. You'll learn why muscle loss, lifestyle habits, and hormone changes play a much bigger role than age itself — and what you can do to keep your metabolism strong for decades. If you want better energy, improved body composition, and long-term metabolic health, this episode is a must watch. Download Zane's Free Fit Over 40 Plan: https://free40plan.com 00:00 Why metabolism doesn't actually slow after 40 02:10 The metabolism myth most people believe 04:45 What really causes weight gain after 40 08:10 Muscle loss and its impact on metabolism 12:00 Why strength training becomes critical 16:15 Hormones and metabolic health 21:40 Lifestyle habits that slow metabolism 27:20 The role of sleep and stress 32:45 Nutrition strategies for metabolic health 38:30 How to support metabolism as you age 43:15 Practical habits to improve fat loss 47:30 Key takeaways for staying metabolically healthy

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Healthy AF, the podcast dedicated to helping you live a healthier life after the age of 50, hosted by health and longevity expert Zane Griggs. This show is your guide to achieving optimal health, both physically and mentally. Whether you're in your 20s and want to plan for a healthy future or in your 50s and seeking to catch up, this show could help you improve your nutrition, fitness, and overall well-being. Each week, we'll dive into the latest research and expert advice on topics such as exercise, stress management, and more. We'll discuss practical strategies for maintaining a healthy lifestyle, including how to balance your diet and stay active as you age. Remember, it's never too late to prioritize your health and become Healthy AF! (Hit play to learn more)

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