• 57. The Future of Personalized Medicine: Genetics, Biomarkers & Longevity| LIVE with Dr. Anil Bajnath at Mindshare
    19 Oct 2026

    I sat down LIVE at Mindshare with Dr. Anil Bajnath to talk about where medicine is headed next: precision medicine, advanced biomarkers, genetics, chronic illness, longevity, and regenerative health.

    Dr. Bajnath is a family physician with additional training in anti-aging, regenerative, functional, and precision medicine. He founded the Institute for Human Optimization and the American Board of Precision Medicine, and his approach is built around connecting what he calls the molecular dots—from your genome to your phenotype—to understand what is actually driving an individual's health.

    In this conversation, we get into why two people can be exposed to the same environment and respond completely differently, how genetics and environmental exposures can interact, and why advanced testing can reveal patterns that standard labs may miss.

    We also talk about:

    • Whole genome sequencing and individualized risk
    • Chronic inflammatory response syndrome and complex illness
    • Mold, Lyme, viral illness, and environmental exposures
    • Detoxification pathways and pharmacogenomics
    • Advanced biomarker testing
    • Alzheimer's and neurodegenerative disease
    • Therapeutic plasma exchange
    • Hyperbaric oxygen and photobiomodulation
    • Environmental toxicants and microplastics
    • Ozone therapies
    • Regenerative medicine, stem cells, and exosomes
    • Why I like Dr. Bajnath's philosophy of letting the data drive the treatment, rather than chasing whatever health trend happens to be popular

    One of my favorite concepts from this conversation is his approach to P4 medicine: personalized, predictive, preventative, and participatory.

    This is what the future of individualized health care looks like to me: understanding the person in front of you first, then choosing the intervention.

    Huge thanks to Dr. Anil Bajnath for sitting down with me at Mindshare.

    Learn more about Dr. Bajnath:
    Institute for Human Optimization: https://www.ifho.org/
    American Board of Precision Medicine: https://theabopm.org/ Transcript(20261019-002329)

    YouTube Chapters

    0:00 The Future of Personalized Medicine
    1:00 Inside the Institute for Human Optimization
    2:00 Chronic Complex Illness & CIRS
    3:00 Genetics, Environment & Chronic Inflammation
    5:00 Transcriptomics: Which Genes Are Being Turned On?
    6:00 Whole Genome Sequencing & Precision Medicine
    8:00 Testing Beyond Standard Labs
    9:00 Advanced Treatments for Complex Disease
    10:00 Therapeutic Plasma Exchange & Neurodegeneration
    11:00 Environmental Toxins, Microplastics & Detoxification
    12:00 Ozone Therapy, NRF2 & Advanced Interventions
    13:00 "Weed, Seed & Feed" Before Regenerative Medicine
    14:00 Health Optimization for Executives & High Performers
    15:00 P4 Medicine: Personalized, Predictive & Preventative
    16:00 Stem Cells, Exosomes & Regenerative Medicine
    17:00 The Future of Stem Cell Access
    18:00 Where to Find Dr. Anil Bajnath

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    20 dk.
  • 56. The Overlooked Hormone Behind Fasting Blood Sugar | Glucagon, Cortisol & Mitochondria (Part 3)
    28 Sep 2026
    Why is your fasting blood sugar high even when you're eating clean, training consistently, cutting sugar, or even following a low-carb diet? That's what I'm breaking down in Part 3 of this series. I've dealt with this myself. There was a period where I was eating low carb, doing intermittent fasting, training fasted, and still waking up with fasting glucose in the 90s and sometimes higher. At first glance, that doesn't make much sense. But once I started looking deeper into glucagon, cortisol, adrenaline, liver glucose production, and what happens when your cells aren't producing enough ATP, the picture changed. Your fasting blood sugar isn't just about what you ate the night before. Your liver is making glucose all night long, and hormones like glucagon, cortisol, and adrenaline help control how much gets released into the bloodstream. In this episode, I break down: Why low ATP can create a stress responseHow adrenaline raises blood sugar and free fatty acidsHow cortisol can keep gluconeogenesis runningWhy glucagon may be one of the most overlooked hormones in metabolic healthHow insulin and glucagon are supposed to regulate each otherWhy fasting glucose can stay elevated even on a low-carb dietHow the Randle cycle can interfere with glucose oxidationWhy simply cutting more carbs may lower the number without fixing the underlying issueThe labs I look at beyond fasting glucose alone This connects directly back to Parts 1 and 2, where I explained how mitochondrial dysfunction can reduce ATP production even when enough calories are coming in. When that energy deficit keeps happening, your body responds like there's an emergency. And over time, that hormonal response can start showing up in your labs. If you haven't watched the first two episodes yet, go back and start there. It'll make this one much easier to follow. In Part 4, I'm going to zoom out and show how this same underlying metabolic dysfunction can show up as several different problems across the body. Subscribe and turn on notifications so you don't miss it. Stay Healthy AF, Zane Episode Timestamps: 0:00 The Overlooked Hormone Behind Fasting Blood Sugar0:45 Zane's Own Experience With Elevated Fasting Glucose2:00 When You're "Doing Everything Right" But Glucose Is Still High3:00 How Seed Oils & Mitochondrial Dysfunction Fit Into the Story5:00 Adrenaline: The First Stress Response6:20 How Adrenaline Raises Fat & Glucose in the Blood8:00 Why Stored Linoleic Acid Matters8:45 Cortisol Takes Over When the Stress Doesn't Stop10:00 Gluconeogenesis & Chronically Elevated Cortisol12:00 Cortisol, PGC-1α & Mitochondrial Repair13:00 Glucagon: The Overlooked Hormone14:00 Why Low ATP Can Drive Glucagon Higher15:00 When Insulin & Glucagon Stop Regulating Each Other16:00 Why Your Liver Makes Glucose Overnight17:30 The Randle Cycle Explained19:00 Why Glucose Can Back Up in the Bloodstream20:00 Why Cutting More Carbs May Not Fix the Problem21:00 What Your Fasting Glucose Number Doesn't Tell You21:40 Labs Zane Looks At22:40 What's Coming in Part 423:20 Looking at the Whole Metabolic Pattern Connect with Zane Griggs: 📲 Instagram: @zanegriggsfitness 🌐 Website: zanegriggs.com Research Referenced in This Series Hulbert et al. (2007) — Membrane Composition & Lifespan — https://pubmed.ncbi.nlm.nih.gov/17928583/ Seebacher et al. (2010) — Oxidative Metabolism & Proton Leak — https://pubmed.ncbi.nlm.nih.gov/20586603/ Paradies et al. (2009) — Cardiolipin & Mitochondrial Dysfunction — https://pubmed.ncbi.nlm.nih.gov/19368971/ Chicco & Sparagna (2007) — Cardiolipin Alterations — https://pubmed.ncbi.nlm.nih.gov/16899548/ Stanley et al. (2012) — Dietary Fat & Mitochondrial Function — https://pmc.ncbi.nlm.nih.gov/articles/PMC4067133/ Khairallah et al. (2012) — Membrane Fatty Acids & Mitochondrial Function — https://pmc.ncbi.nlm.nih.gov/articles/PMC3316678/ Penzo et al. (2002) — Fatty Acids & Mitochondria — https://pubmed.ncbi.nlm.nih.gov/12206909/ Hulbert et al. (2006) — Peroxidation-Resistant Membranes & Longevity — https://pubmed.ncbi.nlm.nih.gov/16620917/ Pamplona et al. (2004) — Fatty Acids & Mitochondrial DNA Damage — https://pubmed.ncbi.nlm.nih.gov/15130667/ Porter, Hulbert & Brand (1996) — Mitochondrial Proton Leak — https://pubmed.ncbi.nlm.nih.gov/8997352/
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    26 dk.
  • 55. Your Vision Is Trainable: How to Improve Eyesight, Focus & Brain Performance | Dr. Bryce Appelbaum
    7 Sep 2026

    What if declining vision, eye strain, headaches, brain fog, and difficulty focusing weren't simply things you had to accept as you get older?

    In this episode of Healthy AF, Zane Griggs sits down with neuro-optometrist Dr. Bryce Appelbaum to explore the connection between your eyes and your brain—and why he believes vision should be trained just like the rest of your body.

    Dr. Appelbaum explains the important difference between eyesight and vision, how hours of daily screen time can place the visual system under stress, and why functional vision problems can sometimes produce symptoms that overlap with problems involving attention, reading, and learning.

    They also dive into vision after 40, reading glasses, screen-related eye strain, concussion recovery, and how Dr. Appelbaum works with professional and Olympic-level athletes to improve visual processing, peripheral awareness, reaction time, depth perception, and performance.

    Plus, Dr. Appelbaum walks Zane through a simple "eye push-up" exercise designed to train the focusing system and shares the 20-20-20 rule you can start using during screen-heavy days.

    In this episode:

    • Eyesight vs. vision: why they're not the same thing

    • How screen time affects the eye-brain connection

    • Vision, attention, reading, and focus

    • Why your distance vision may change with heavy near work

    • The 20-20-20 rule for screen breaks

    • Vision training for professional athletes

    • Vision changes after concussion and head injuries

    • Why vision matters for balance and fall prevention as we age

    • What happens to near vision after 40

    • How to perform Dr. Appelbaum's eye push-ups

    • Reading glasses and the focusing system

    • Digital performance lenses and screen stress

    • How to start training your vision

    Connect with Zane Griggs:
    • 🧠 Free Plan: free40plan.com

    • 📲 Instagram: @zanegriggsfitness

    • 🌐 Website: zanegriggs.com

    Guest Links:

    ScreenFit: ScreenFit.com — use code ZANE for $200 off / 40% off

    My Vision First: MyVisionFirst.com

    Digital Performance Lenses: use code ZANE for 10% off

    https://myvisionfirst.com

    0:00 Meet Dr. Bryce Appelbaum

    1:42 Vision Problems, ADHD & Dyslexia Symptoms

    2:33 Eyesight vs. Vision: What's the Difference?

    3:45 Why Your Eyesight May Change With Screen Time

    5:48 Can You Actually Exercise Your Vision?

    6:41 What Screens Are Doing to Your Visual System

    8:39 The Problem With 7+ Hours of Screen Time

    10:55 How Vision Can Affect Your Stress Response

    12:29 Adding "Vision Snacks" to Your Day

    13:43 The 20-20-20 Rule

    16:19 ScreenFit & Vision Performance Training

    17:34 How Elite Athletes Train Their Vision

    20:34 Concussions, Head Injuries & Vision

    23:47 How Vision Training Changed an MLB Player's Performance

    25:09 Does Vision Have to Decline With Age?

    43:58 Why Reading Gets Harder After 40

    45:53 How to Do Eye Push-Ups

    50:02 The Problem With Monovision

    52:26 Vision Training for Longevity

    53:21 ScreenFit + Special Offer

    55:02 Digital Performance Lenses

    58:44 Where to Find Dr. Bryce Appelbaum

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    59 dk.
  • 53. What Happens to Seed Oils After You Eat Them?
    17 Aug 2026

    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

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    19 dk.
  • 52. The Truth About Alcohol Nobody Wants to Hear | Sam Lander
    20 Jul 2026

    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
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    49 dk.
  • 51. The Seed Oil Studies Are Measuring the Wrong Thing
    4 Jun 2026

    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

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    41 dk.
  • 50. Your Body Is Stuck Burning Fat — And It's Making You Sick (Part 2)
    2 Jun 2026
    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 resistance03:30 Why your body should switch between fat and glucose06:00 The 3 tissues that reveal metabolic inflexibility08:30 Why Zane changed his mind about low carb13:30 The real definition of metabolic inflexibility15:00 Why elevated blood sugar can happen on keto or carnivore20:00 Heart failure and metabolic disease22:00 Why failing hearts become more dependent on fat25:00 Why glucose is not the problem29:00 The liver and fatty liver disease33:00 Fatty liver is a metabolic inflexibility problem34:00 Why the liver starts producing more glucose40:00 How liver disease progresses41:00 The muscle, heart, and liver connection46:00 How to restore glucose oxidation47:00 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
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    59 dk.
  • 50. Glucose Is the Most Efficient Fuel | The ATP & Metabolism Science Explained (Part 1)
    29 May 2026
    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 moleculeThe truth about fat oxidation vs glucose oxidationWhy the heart becomes "stuck" burning fat in heart failureThe real meaning of metabolic flexibilityWhy insulin is not the villain it's been made out to beThe difference between glycolysis and glucose oxidationWhy ketones are not the "super fuel" many claimHow mitochondrial inefficiency impacts metabolic diseaseThe 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 ...
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    32 dk.