『Healthy AF | Healthy After 50』のカバーアート

Healthy AF | Healthy After 50

Healthy AF | Healthy After 50

著者： 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)2023 衛生・健康的な生活
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  • 51. The Seed Oil Studies Are Measuring the Wrong Thing

    51. The Seed Oil Studies Are Measuring the Wrong Thing
    2026/06/04

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

    50. Your Body Is Stuck Burning Fat — And It's Making You Sick (Part 2)
    2026/06/02
    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 分
  • 50. Glucose Is the Most Efficient Fuel | The ATP & Metabolism Science Explained (Part 1)

    50. Glucose Is the Most Efficient Fuel | The ATP & Metabolism Science Explained (Part 1)
    2026/05/29
    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 分
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