Podcasts about cell metabolism

Warum kreisen unsere Gedanken manchmal ständig ums Essen? Mit Ernährungspsychologe Frédéric Letzner sprechen wir über Food Noise, Diäten und Verbote, emotionales Essen, intuitive Ernährung, Bodybuilding, Social Media und GLP‑1‑Abnehmspritzen. Dabei geht es um die Frage, wann Gesundheitsstreben kippt – und wie ein entspannteres Verhältnis zu Essen und Körper entstehen kann. ------------------------------------------------------------------------ Dominiks Buch zur pflanzenbasierten Sporternährung im UTB-Verlag: https://www.utb.de/doi/book/10.36198/9783838560328 Dominiks Gesundheitscommunity: www.gsundes-hannover.de Dominiks Online-Knie-Kurs: https://gsundes-hannover.de/knieschmerzen/ Dominiks Online-Rücken-Kurs: https://copecart.com/products/34bd5abb/checkout Marcs veganes Online-Fitness-Coaching: https://vegainer-academy.com/ Marcs Online-Kurs: https://www.copecart.com/products/a50f88f2/checkout Frédérics Instagram-Kanal: https://www.instagram.com/frederic.letzner.official/?hl=de Frédérics Webseite: https://fredericletzner.de/ Frédérics Online-Kurse: https://fredericletzner-kurs.de/ ------------------------------------------------------------------------ Dieser Podcast wird unterstützt von der Firma Watson Nutrition. Die Firma bietet als einzige umfassend laborgeprüfte Nahrungsergänzungsmittel für eine optimierte Nährstoffversorgung. Zum Angebot zählen Multi-Supplemente, Mono-Supplemente, Sportsupplemente wie Kreatin oder auch Proteinriegel, Shakes und essenzielle Aminosäuren Mit dem Code veganperformance erhältst du 5 % Rabatt auf deine Bestellung.  Zur Firmenwebseite: Watson Nutrition ------------------------------------------------------------------------ Redaktionelle Anmerkungen 00:16:10:17–00:17:08:17 – Trauma und Disziplin: Trauma ist ein Risikofaktor für Adipositas und Binge Eating, aber keine belegte Erklärung für „die meisten“ Fälle. „Die allermeisten adipösen Menschen sind hochdiszipliniert“ sollte als therapeutische Erfahrung Frédérics gekennzeichnet werden, nicht als epidemiologischer Fakt. 00:21:54:17–00:29:47:17 – Bodybuilding und Clean Eating: Bodybuilding ist keine „Essstörung der Männer“. Es kann mit erhöhtem Risiko für gestörtes Essverhalten und Muskeldysmorphie verbunden sein. Ebenso können rigide Clean-Eating-Regeln und Essanfälle zusammenhängen, gehören aber nicht zwangsläufig zusammen. 00:51:58:17–00:56:05:17 – Fasten, Körperhass und Veganismus: Fasten „zerstört“ Hunger- und Sättigungssignale nicht generell. Es kann bei vulnerablen Menschen problematisch werden. Auch die behauptete hohe Dunkelziffer an Essstörungen unter vegan lebenden Menschen ist nicht belegt. Eine vegane Ernährung kann in Einzelfällen Restriktion verdecken, ist aber nicht automatisch ein Risikomarker. 01:09:03:17–01:09:58:17 – Langzeitfolgen von GLP-1: „Langzeitfolgen sind unbekannt“ ist zu grob. Es liegen inzwischen Daten über mehrere Jahre vor; offene Fragen betreffen besonders lebenslange Anwendung und sehr seltene Folgen. Quellenverzeichnis American Psychiatric Association. (2022). Diagnostic and statistical manual of mental disorders (5th ed., text rev.). American Psychiatric Association Publishing. Arnaut, T., Duncan, S., Faurby, M., Hahn-Pedersen, J. H., Kvist, K., Steenackers, N., & Buse, J. B. (2026). Retrospective assessment of food noise changes after initiation of injectable semaglutide for weight management in the USA: The INFORM survey. Advances in Therapy. Advance online publication. Bacon, L., Stern, J. S., Van Loan, M. D., & Keim, N. L. (2005). Size acceptance and intuitive eating improve health for obese, female chronic dieters. Journal of the American Dietetic Association, 105(6), 929–936. Bardone-Cone, A. M., Wonderlich, S. A., Frost, R. O., Bulik, C. M., Mitchell, J. E., Uppala, S., & Simonich, H. (2007). Perfectionism and eating disorders: Current status and future directions. Clinical Psychology Review, 27(3), 384–405. Brewis, A., Hayashi, D., Gualano, B., Precinotto, M. L., Scagliusi, F. B., Stöckelová, T., SturtzSreetharan, C., West, H., Williams, O., & Masterson, T. D. (2026). Food noise: Conceptual, methodological, and ethical considerations. Appetite, 226, 108700. Bulik, C. M., Blake, L., & Austin, J. (2019). Genetics of eating disorders: What the clinician needs to know. Psychiatric Clinics of North America, 42(1), 59–73. Bundesministerium der Justiz. (o. J.). Sozialgesetzbuch Fünftes Buch – Gesetzliche Krankenversicherung: § 43 Ergänzende Leistungen zur Rehabilitation. Gesetze im Internet. Burke, L. E., Wang, J., & Sevick, M. A. (2011). Self-monitoring in weight loss: A systematic review of the literature. Journal of the American Dietetic Association, 111(1), 92–102. Camilleri, G. M., Méjean, C., Bellisle, F., Andreeva, V. A., Kesse-Guyot, E., Hercberg, S., & Péneau, S. (2017). Intuitive eating dimensions were differently associated with food intake in the general population-based NutriNet-Santé study. The Journal of Nutrition, 147(1), 61–69. Dhurandhar, E. J., Maki, K. C., Dhurandhar, N. V., Kyle, T. K., Yurkow, S., Hawkins, M. A. W., Agley, J., Ho, E. H., Cheskin, L. J., Sørensen, T. I. A., Wang, X. R., & Allison, D. B. (2025). Food noise: Definition, measurement, and future research directions. Nutrition & Diabetes, 15, Article 30. Friedrichsen, M., Breitschaft, A., Tadayon, S., Wizert, A., & Skovgaard, D. (2021). The effect of semaglutide 2.4 mg once weekly on energy intake, appetite, control of eating, and gastric emptying in adults with obesity. Diabetes, Obesity and Metabolism, 23(3), 754–762. Galloway, A. T., Fiorito, L. M., Francis, L. A., & Birch, L. L. (2006). “Finish your soup”: Counterproductive effects of pressuring children to eat on intake and affect. Appetite, 46(3), 318–323. Gemeinsamer Bundesausschuss. (2026). Richtlinie über die Durchführung der Psychotherapie (Psychotherapie-Richtlinie). Hall, K. D., & Kahan, S. (2018). Maintenance of lost weight and long-term management of obesity. Medical Clinics of North America, 102(1), 183–197. Hayashi, D., Edwards, C., Emond, J. A., Gilbert-Diamond, D., Butt, M., Rigby, A., & Masterson, T. D. (2023). What is food noise? A conceptual model of food cue reactivity. Nutrients, 15(22), Article 4809. Herbert, B. M., Blechert, J., Hautzinger, M., Matthias, E., & Herbert, C. (2013). Intuitive eating is associated with interoceptive sensitivity: Effects on body mass index. Appetite, 70, 22–30. Hudson, J. I., Hiripi, E., Pope, H. G., Jr., & Kessler, R. C. (2007). The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication. Biological Psychiatry, 61(3), 348–358. Jansen, E., Mulkens, S., Emond, Y., & Jansen, A. (2008). From the Garden of Eden to the land of plenty: Restriction of fruit and sweets intake leads to increased fruit and sweets consumption in children. Appetite, 51(3), 570–575. Joubert, L. M., Gonzalez, G. B., & Larson, A. J. (2020). Prevalence of disordered eating among international sport lead rock climbers. Frontiers in Sports and Active Living, 2, Article 86. Levinson, C. A., Fewell, L., & Brosof, L. C. (2017). My Fitness Pal calorie tracker usage in the eating disorders. Eating Behaviors, 27, 14–16. Linardon, J., Tylka, T. L., & Fuller-Tyszkiewicz, M. (2021). Intuitive eating and its psychological correlates: A meta-analysis. International Journal of Eating Disorders, 54(7), 1073–1098. Look AHEAD Research Group. (2014). Eight-year weight losses with an intensive lifestyle intervention: The Look AHEAD study. Obesity, 22(1), 5–13. Loos, R. J. F., & Yeo, G. S. H. (2022). The genetics of obesity: From discovery to biology. Nature Reviews Genetics, 23(2), 120–133. McLean, C. P., Kulkarni, J., & Sharp, G. (2022). Disordered eating and the meat-avoidance spectrum: A systematic review and clinical implications. Eating and Weight Disorders, 27(7), 2347–2375. Mitchell, L., Murray, S. B., Cobley, S., Hackett, D., Gifford, J., Capling, L., & O'Connor, H. (2017). Muscle dysmorphia symptomatology and associated psychological features in bodybuilders and non-bodybuilder resistance trainers: A systematic review and meta-analysis. Sports Medicine, 47(2), 233–259. Palmisano, G. L., Innamorati, M., & Vanderlinden, J. (2016). Life adverse experiences in relation with obesity and binge eating disorder: A systematic review. Journal of Behavioral Addictions, 5(1), 11–31. Paslakis, G., Richardson, C., Nöhre, M., Brähler, E., Holzapfel, C., Hilbert, A., & de Zwaan, M. (2020). Prevalence and psychopathology of vegetarians and vegans—Results from a representative survey in Germany. Scientific Reports, 10, Article 6840. Rodriguez, P. J., Zhang, V., Gratzl, S., Do, D., Goodwin Cartwright, B., Baker, C., Gluckman, T. J., Stucky, N., & Emanuel, E. J. (2025). Discontinuation and reinitiation of dual-labeled GLP-1 receptor agonists among US adults with overweight or obesity. JAMA Network Open, 8(1), e2457349. Schaumberg, K., Anderson, D. A., Anderson, L. M., Reilly, E. E., & Gorrell, S. (2016). Dietary restraint: What's the harm? A review of the relationship between dietary restraint, weight trajectory and the development of eating pathology. Clinical Obesity, 6(2), 89–100. Schmitt, A., Frenser, M., & Fischer, T. (2025). Tendencies of eating disordered behaviours in male content creators: A social media analysis. Journal of Eating Disorders, 13, Article 201. Schultz, W. (2016). Dopamine reward prediction error coding. Dialogues in Clinical Neuroscience, 18(1), 23–32. Sundgot-Borgen, J., & Torstveit, M. K. (2004). Prevalence of eating disorders in elite athletes is higher than in the general population. Clinical Journal of Sport Medicine, 14(1), 25–32. Techniker Krankenkasse. (2026, 9. April). Ich brauche eine Ernährungsberatung: Wie unterstützt mich die TK? Teixeira, P. J., Carraça, E. V., Markland, D., Silva, M. N., & Ryan, R. M. (2012). Exercise, physical activity, and self-determination theory: A systematic review. International Journal of Behavioral Nutrition and Physical Activity, 9, Article 78. Thanarajah, S. E., Backes, H., DiFeliceantonio, A. G., Albus, K., Cremer, A. L., Hanssen, R., Lippert, R. N., Cornely, O. A., Small, D. M., Brüning, J. C., & Tittgemeyer, M. (2019). Food intake recruits orosensory and post-ingestive dopaminergic circuits to affect eating desire in humans. Cell Metabolism, 29(3), 695–706.e4. Tremelling, K., Sandon, L., Vega, G. L., & McAdams, C. J. (2017). Orthorexia nervosa and eating disorder symptoms in registered dietitian nutritionists in the United States. Journal of the Academy of Nutrition and Dietetics, 117(10), 1612–1617. Turner, P. G., & Lefevre, C. E. (2017). Instagram use is linked to increased symptoms of orthorexia nervosa. Eating and Weight Disorders, 22(2), 277–284. Westwater, M. L., Fletcher, P. C., & Ziauddeen, H. (2016). Sugar addiction: The state of the science. European Journal of Nutrition, 55(Suppl. 2), S55–S69. Wilding, J. P. H., Batterham, R. L., Davies, M., Van Gaal, L. F., Kandler, K., Konakli, K., Lingvay, I., McGowan, B. M., Kalayci Oral, T., Rosenstock, J., Wadden, T. A., Wharton, S., Yokote, K., Kushner, R. F., & STEP 1 Study Group. (2022). Weight regain and cardiometabolic effects after withdrawal of semaglutide: The STEP 1 trial extension. Diabetes, Obesity and Metabolism, 24(8), 1553–1564.

we dive deep into a landmark 2023 precision nutrition trial published in Cell Metabolism that shows why two people with identical body weight, insulin resistance levels, and fasting glucose can respond completely differently to the same diet—depending on whether their insulin resistance is strongest in muscle or liver tissue.

Many women are prescribed oral estrogen without ever being told what happens after it enters the body. In this episode, Dr. Brendan McCarthy takes a deeper look at estrone, the estrogen metabolite created when estradiol is taken orally, and explains why the delivery method of hormone therapy matters. You'll learn: The difference between estradiol and estrone Why oral estrogen creates significantly higher estrone levels How estrone may contribute to inflammation and insulin resistance The connection between estrogen metabolism and weight gain during perimenopause and menopause Why monitoring labs is essential when using hormone therapy The importance of understanding risks, benefits, and treatment options before starting hormones Dr. McCarthy also discusses the role of inflammation, body fat, metabolic health, and hormone delivery systems in creating long-term outcomes for women navigating menopause. This episode is about education, informed consent, and helping women better understand the science behind their care.   Citations: There is more than one estrogen; after menopause, estrone dominates Kuhl, Herbert. “Pharmacology of Estrogens and Progestogens: Influence of Different Routes of Administration.” Climacteric, vol. 8, no. S1, 2005, pp. 3–63. Body fat is an endocrine organ — aromatase converts androstenedione into estrone, and adipose becomes the dominant post-menopausal estrogen source Lee, Angel A., and Laura J. Den Hartigh. “Metabolic Impact of Endogenously Produced Estrogens by Adipose Tissue in Females and Males across the Lifespan.” Frontiers in Endocrinology, vol. 16, 2025, article 1682231. Inflamed fat raises IL-6; IL-6 tracks the insulin-resistant state Kern, Philip A., et al. “Adipose Tissue Tumor Necrosis Factor and Interleukin-6 Expression in Human Obesity and Insulin Resistance.” American Journal of Physiology-Endocrinology and Metabolism, vol. 280, no. 5, 2001, pp. E745–E751. IL-6 is part of the insulin-resistance machinery — it correlates with impaired insulin-stimulated glucose uptake Bastard, Jean-Philippe, et al. “Adipose Tissue IL-6 Content Correlates with Resistance to Insulin Activation of Glucose Uptake Both In Vivo and In Vitro.” The Journal of Clinical Endocrinology & Metabolism, vol. 87, no. 5, 2002, pp. 2084–2089. Inflammation amplifies aromatase — IL-6 raises aromatase via COX-2/PGE2 Bowers, Laura W., et al. “Obesity-Associated Systemic Interleukin-6 Promotes Pre-Adipocyte Aromatase Expression via Increased Breast Cancer Cell Prostaglandin E2 Production.” Breast Cancer Research and Treatment, vol. 149, no. 1, 2015, pp. 49–57. Human-tissue confirmation: HOMA-IR, IL-6, insulin, leptin, hsCRP track breast aromatase after menopause Brown, Kristy A., et al. “Menopause Is a Determinant of Breast Aromatase Expression and Its Associations with BMI, Inflammation, and Systemic Markers.” The Journal of Clinical Endocrinology & Metabolism, vol. 102, no. 5, 2017, pp. 1692–1701. Iyengar, Neil M., et al. “Effects of Obesity on Breast Aromatase Expression and Systemic Metabo-Inflammation in Women with BRCA1 or BRCA2 Mutations.” npj Breast Cancer, vol. 7, no. 1, 2021, article 18. The molecular crux: estrone drives ERα/NF-κB inflammatory signaling while estradiol opposes it Qureshi, Rehana, et al. “The Major Pre- and Postmenopausal Estrogens Play Opposing Roles in Obesity-Driven Mammary Inflammation and Breast Cancer Development.” Cell Metabolism, vol. 31, no. 6, 2020, pp. 1154–1172.e9. Estrone as a metabolic-risk signal — prospectively associated with diabetes (note: male cohort) Jasuja, Guneet Kaur, et al. “Circulating Estrone Levels Are Associated Prospectively with Diabetes Risk in Men of the Framingham Heart Study.” Diabetes Care, vol. 36, no. 9, 2013, pp. 2591–2596.   Dr. Brendan McCarthy is the founder and Chief Medical Officer of Protea Medical Center in Arizona. With over two decades of experience, he's helped thousands of patients navigate hormonal imbalances using bioidentical HRT, nutrition, and root-cause medicine. He's also taught and mentored other physicians on integrative approaches to hormone therapy, weight loss, fertility, and more. If you're ready to take your health seriously, this podcast is a great place to start.

PainExam Podcast Show Notes NAD+ Supplementation in Pain and Inflammation: Hype, Hope, or Emerging Science? Hosted by: PainExam Podcast Presented by: NRAP Academy (Neuromodulation, Regional Anesthesia & Pain) Host: David Rosenblum, MD Episode Overview In this episode of the PainExam Podcast, we explore the growing interest in NAD+ (Nicotinamide Adenine Dinucleotide) supplementation and its potential role in pain management, inflammation reduction, cellular recovery, and healthy aging. NAD+ is a naturally occurring coenzyme found in every living cell and is essential for energy production, mitochondrial function, DNA repair, and cellular resilience. As NAD+ levels decline with age, chronic stress, inflammation, and disease, researchers have begun investigating whether restoring NAD+ levels may improve outcomes in chronic pain conditions and inflammatory disorders. We review the current science, discuss potential mechanisms of action, and examine how NAD+ therapy is being integrated into regenerative medicine, wellness programs, and pain management practices. What is NAD+? NAD+ is a coenzyme involved in: ✅ Cellular energy production (ATP generation) ✅ Mitochondrial health ✅ DNA repair pathways ✅ Oxidative stress reduction ✅ Neuroprotection ✅ Cellular signaling ✅ Activation of longevity-associated proteins called sirtuins Without adequate NAD+, cells become less efficient at producing energy and managing inflammation. Why Might NAD+ Matter in Chronic Pain? Many chronic pain conditions involve: Mitochondrial dysfunction Oxidative stress Neuroinflammation Peripheral and central sensitization Impaired cellular recovery Researchers hypothesize that optimizing NAD+ levels may help address several of these pathways simultaneously. Potential areas of interest include: Neuropathic Pain NAD+ may support: Nerve repair Axonal recovery Mitochondrial function within neurons Reduction of oxidative injury Inflammatory Pain NAD+ influences inflammatory signaling pathways and may help modulate: Cytokine production Immune cell activity Cellular stress responses Fatigue and Recovery Patients with chronic pain frequently report: Fatigue Brain fog Reduced exercise tolerance Poor recovery Because NAD+ plays a critical role in energy metabolism, some clinicians report improvements in energy and recovery following supplementation. Potential Mechanisms of Action 1. Improved Mitochondrial Function Mitochondria generate ATP, the body's energy currency. Reduced NAD+ levels are associated with: Cellular aging Impaired energy production Increased inflammation Supplementation may help restore mitochondrial efficiency. 2. Activation of Sirtuins Sirtuins are proteins involved in: Cellular repair Longevity Metabolic regulation Inflammation control NAD+ serves as a critical substrate for sirtuin activity. 3. DNA Repair Support NAD+ is required for enzymes known as PARPs (Poly ADP Ribose Polymerases), which participate in DNA repair processes following cellular injury. 4. Reduction of Oxidative Stress Chronic inflammation often produces excessive reactive oxygen species (ROS). NAD+ may help maintain cellular antioxidant defenses and reduce oxidative injury. Routes of NAD+ Supplementation Intravenous (IV) NAD+ Most commonly marketed in wellness and recovery clinics. Potential advantages: Direct systemic delivery Avoids gastrointestinal absorption issues Allows higher dosing protocols Potential limitations: Cost Time commitment Variable evidence base Oral Precursors Rather than NAD+ itself, many supplements provide precursors such as: Nicotinamide Riboside (NR) Nicotinamide Mononucleotide (NMN) These compounds are converted into NAD+ within the body. What Does the Evidence Show? Current evidence remains preliminary. While preclinical and mechanistic studies are promising, large-scale randomized controlled trials evaluating NAD+ specifically for chronic pain are still limited. Areas under active investigation include: Neuropathic pain Neurodegenerative disorders Chronic fatigue syndromes Recovery optimization Healthy aging Patients should understand that NAD+ therapy remains an emerging treatment rather than a standard evidence-based pain intervention. Safety Considerations Reported side effects may include: Nausea Flushing Chest tightness during rapid infusions Headache Fatigue Lightheadedness Most adverse effects appear infusion-rate dependent and can often be minimized through slower administration protocols. Patients should discuss treatment with a qualified healthcare professional, especially if they have: Cardiovascular disease Active cancer Significant medical comorbidities Clinical Pearls for Pain Physicians ✔ Consider NAD+ as a potential adjunct—not a replacement—for evidence-based pain care. ✔ Continue emphasizing exercise, sleep optimization, nutrition, behavioral health, and appropriate interventional therapies. ✔ Discuss realistic expectations with patients. ✔ Recognize that evidence continues to evolve. ✔ Focus on patient-centered outcomes rather than laboratory markers alone. Key Takeaways NAD+ is essential for cellular energy production and repair. Declining NAD+ levels may contribute to aging, inflammation, and chronic disease. Early evidence suggests possible benefits in inflammation, recovery, fatigue, and nerve health. Robust pain-specific clinical trials remain limited. NAD+ therapy should currently be viewed as an adjunctive and investigational strategy in pain management. Resources for Physicians Pain Medicine Board Preparation Prepare for the ABA Pain Medicine Boards with:

    PainExam Podcast Show Notes NAD+ Supplementation in Pain and Inflammation: Hype, Hope, or Emerging Science? Hosted by: PainExam Podcast Presented by: NRAP Academy (Neuromodulation, Regional Anesthesia & Pain) Host: David Rosenblum, MD Episode Overview In this episode of the PainExam Podcast, we explore the growing interest in NAD+ (Nicotinamide Adenine Dinucleotide) supplementation and its potential role in pain management, inflammation reduction, cellular recovery, and healthy aging. NAD+ is a naturally occurring coenzyme found in every living cell and is essential for energy production, mitochondrial function, DNA repair, and cellular resilience. As NAD+ levels decline with age, chronic stress, inflammation, and disease, researchers have begun investigating whether restoring NAD+ levels may improve outcomes in chronic pain conditions and inflammatory disorders. We review the current science, discuss potential mechanisms of action, and examine how NAD+ therapy is being integrated into regenerative medicine, wellness programs, and pain management practices. What is NAD+? NAD+ is a coenzyme involved in: ✅ Cellular energy production (ATP generation) ✅ Mitochondrial health ✅ DNA repair pathways ✅ Oxidative stress reduction ✅ Neuroprotection ✅ Cellular signaling ✅ Activation of longevity-associated proteins called sirtuins Without adequate NAD+, cells become less efficient at producing energy and managing inflammation. Why Might NAD+ Matter in Chronic Pain? Many chronic pain conditions involve: Mitochondrial dysfunction Oxidative stress Neuroinflammation Peripheral and central sensitization Impaired cellular recovery Researchers hypothesize that optimizing NAD+ levels may help address several of these pathways simultaneously. Potential areas of interest include: Neuropathic Pain NAD+ may support: Nerve repair Axonal recovery Mitochondrial function within neurons Reduction of oxidative injury Inflammatory Pain NAD+ influences inflammatory signaling pathways and may help modulate: Cytokine production Immune cell activity Cellular stress responses Fatigue and Recovery Patients with chronic pain frequently report: Fatigue Brain fog Reduced exercise tolerance Poor recovery Because NAD+ plays a critical role in energy metabolism, some clinicians report improvements in energy and recovery following supplementation. Potential Mechanisms of Action 1. Improved Mitochondrial Function Mitochondria generate ATP, the body's energy currency. Reduced NAD+ levels are associated with: Cellular aging Impaired energy production Increased inflammation Supplementation may help restore mitochondrial efficiency. 2. Activation of Sirtuins Sirtuins are proteins involved in: Cellular repair Longevity Metabolic regulation Inflammation control NAD+ serves as a critical substrate for sirtuin activity. 3. DNA Repair Support NAD+ is required for enzymes known as PARPs (Poly ADP Ribose Polymerases), which participate in DNA repair processes following cellular injury. 4. Reduction of Oxidative Stress Chronic inflammation often produces excessive reactive oxygen species (ROS). NAD+ may help maintain cellular antioxidant defenses and reduce oxidative injury. Routes of NAD+ Supplementation Intravenous (IV) NAD+ Most commonly marketed in wellness and recovery clinics. Potential advantages: Direct systemic delivery Avoids gastrointestinal absorption issues Allows higher dosing protocols Potential limitations: Cost Time commitment Variable evidence base Oral Precursors Rather than NAD+ itself, many supplements provide precursors such as: Nicotinamide Riboside (NR) Nicotinamide Mononucleotide (NMN) These compounds are converted into NAD+ within the body. What Does the Evidence Show? Current evidence remains preliminary. While preclinical and mechanistic studies are promising, large-scale randomized controlled trials evaluating NAD+ specifically for chronic pain are still limited. Areas under active investigation include: Neuropathic pain Neurodegenerative disorders Chronic fatigue syndromes Recovery optimization Healthy aging Patients should understand that NAD+ therapy remains an emerging treatment rather than a standard evidence-based pain intervention. Safety Considerations Reported side effects may include: Nausea Flushing Chest tightness during rapid infusions Headache Fatigue Lightheadedness Most adverse effects appear infusion-rate dependent and can often be minimized through slower administration protocols. Patients should discuss treatment with a qualified healthcare professional, especially if they have: Cardiovascular disease Active cancer Significant medical comorbidities Clinical Pearls for Pain Physicians ✔ Consider NAD+ as a potential adjunct—not a replacement—for evidence-based pain care. ✔ Continue emphasizing exercise, sleep optimization, nutrition, behavioral health, and appropriate interventional therapies. ✔ Discuss realistic expectations with patients. ✔ Recognize that evidence continues to evolve. ✔ Focus on patient-centered outcomes rather than laboratory markers alone. Key Takeaways NAD+ is essential for cellular energy production and repair. Declining NAD+ levels may contribute to aging, inflammation, and chronic disease. Early evidence suggests possible benefits in inflammation, recovery, fatigue, and nerve health. Robust pain-specific clinical trials remain limited. NAD+ therapy should currently be viewed as an adjunctive and investigational strategy in pain management. Resources for Physicians Pain Medicine Board Preparation Prepare for the ABA Pain Medicine Boards with:

    PainExam Podcast Show Notes NAD+ Supplementation in Pain and Inflammation: Hype, Hope, or Emerging Science? Hosted by: PainExam Podcast Presented by: NRAP Academy (Neuromodulation, Regional Anesthesia & Pain) Host: David Rosenblum, MD Episode Overview In this episode of the PainExam Podcast, we explore the growing interest in NAD+ (Nicotinamide Adenine Dinucleotide) supplementation and its potential role in pain management, inflammation reduction, cellular recovery, and healthy aging. NAD+ is a naturally occurring coenzyme found in every living cell and is essential for energy production, mitochondrial function, DNA repair, and cellular resilience. As NAD+ levels decline with age, chronic stress, inflammation, and disease, researchers have begun investigating whether restoring NAD+ levels may improve outcomes in chronic pain conditions and inflammatory disorders. We review the current science, discuss potential mechanisms of action, and examine how NAD+ therapy is being integrated into regenerative medicine, wellness programs, and pain management practices. What is NAD+? NAD+ is a coenzyme involved in: ✅ Cellular energy production (ATP generation) ✅ Mitochondrial health ✅ DNA repair pathways ✅ Oxidative stress reduction ✅ Neuroprotection ✅ Cellular signaling ✅ Activation of longevity-associated proteins called sirtuins Without adequate NAD+, cells become less efficient at producing energy and managing inflammation. Why Might NAD+ Matter in Chronic Pain? Many chronic pain conditions involve: Mitochondrial dysfunction Oxidative stress Neuroinflammation Peripheral and central sensitization Impaired cellular recovery Researchers hypothesize that optimizing NAD+ levels may help address several of these pathways simultaneously. Potential areas of interest include: Neuropathic Pain NAD+ may support: Nerve repair Axonal recovery Mitochondrial function within neurons Reduction of oxidative injury Inflammatory Pain NAD+ influences inflammatory signaling pathways and may help modulate: Cytokine production Immune cell activity Cellular stress responses Fatigue and Recovery Patients with chronic pain frequently report: Fatigue Brain fog Reduced exercise tolerance Poor recovery Because NAD+ plays a critical role in energy metabolism, some clinicians report improvements in energy and recovery following supplementation. Potential Mechanisms of Action 1. Improved Mitochondrial Function Mitochondria generate ATP, the body's energy currency. Reduced NAD+ levels are associated with: Cellular aging Impaired energy production Increased inflammation Supplementation may help restore mitochondrial efficiency. 2. Activation of Sirtuins Sirtuins are proteins involved in: Cellular repair Longevity Metabolic regulation Inflammation control NAD+ serves as a critical substrate for sirtuin activity. 3. DNA Repair Support NAD+ is required for enzymes known as PARPs (Poly ADP Ribose Polymerases), which participate in DNA repair processes following cellular injury. 4. Reduction of Oxidative Stress Chronic inflammation often produces excessive reactive oxygen species (ROS). NAD+ may help maintain cellular antioxidant defenses and reduce oxidative injury. Routes of NAD+ Supplementation Intravenous (IV) NAD+ Most commonly marketed in wellness and recovery clinics. Potential advantages: Direct systemic delivery Avoids gastrointestinal absorption issues Allows higher dosing protocols Potential limitations: Cost Time commitment Variable evidence base Oral Precursors Rather than NAD+ itself, many supplements provide precursors such as: Nicotinamide Riboside (NR) Nicotinamide Mononucleotide (NMN) These compounds are converted into NAD+ within the body. What Does the Evidence Show? Current evidence remains preliminary. While preclinical and mechanistic studies are promising, large-scale randomized controlled trials evaluating NAD+ specifically for chronic pain are still limited. Areas under active investigation include: Neuropathic pain Neurodegenerative disorders Chronic fatigue syndromes Recovery optimization Healthy aging Patients should understand that NAD+ therapy remains an emerging treatment rather than a standard evidence-based pain intervention. Safety Considerations Reported side effects may include: Nausea Flushing Chest tightness during rapid infusions Headache Fatigue Lightheadedness Most adverse effects appear infusion-rate dependent and can often be minimized through slower administration protocols. Patients should discuss treatment with a qualified healthcare professional, especially if they have: Cardiovascular disease Active cancer Significant medical comorbidities Clinical Pearls for Pain Physicians ✔ Consider NAD+ as a potential adjunct—not a replacement—for evidence-based pain care. ✔ Continue emphasizing exercise, sleep optimization, nutrition, behavioral health, and appropriate interventional therapies. ✔ Discuss realistic expectations with patients. ✔ Recognize that evidence continues to evolve. ✔ Focus on patient-centered outcomes rather than laboratory markers alone. Key Takeaways NAD+ is essential for cellular energy production and repair. Declining NAD+ levels may contribute to aging, inflammation, and chronic disease. Early evidence suggests possible benefits in inflammation, recovery, fatigue, and nerve health. Robust pain-specific clinical trials remain limited. NAD+ therapy should currently be viewed as an adjunctive and investigational strategy in pain management. Resources for Physicians Pain Medicine Board Preparation Prepare for the ABA Pain Medicine Boards with:

Creatine causes cancer to spread — that headline is built on a real mouse study. But what does the human data actually say? In this solo explainer, Dr. Robert Lufkin breaks down both halves of the science behind the most studied supplement on the planet.He walks through the 2021 mouse metastasis study behind the viral claim, the surprising evidence that creatine actually powers the immune cells that HUNT cancer (CD8 T cells and, per new UCLA research, dendritic cells), and what the human data — HCAs, NHANES, and the 2025 safety review — really shows. The verdict is more nuanced, and more reassuring, than the headline suggests.Chapters:00:00 — Introduction00:46 — Why This Question Exists01:32 — The Scary Half (2021 Study)02:17 — How Creatine Fuels Tumor Spread03:03 — Creatine Fights Cancer Too03:48 — UCLA June 2026 Dendritic Cells04:35 — Tumor Suppressor or Fuel?05:21 — What Human Data Shows (HCAs)06:08 — NHANES & 2025 Safety Review06:55 — The Honest Caveat07:42 — The TakeawayKey takeaways:The scary headline comes from a 2021 mouse study where dietary creatine promoted metastasis via the MPS1 → SMAD2/3 → TGF-beta pathway — in mice with established, aggressive tumors.The same metabolism fuels your immune system: creatine is essential for CD8 "killer" T cells and the dendritic cells that direct them.In a controlled human trial, creatine did NOT drive carcinogen (HCA) formation.NHANES population data links higher dietary creatine to LOWER cancer risk, and the 2025 safety review calls the human cancer-risk claim "not substantiated."Healthy adults: the human evidence does not support avoiding creatine. Active or metastatic cancer: pause and talk to your oncologist. Always choose third-party tested creatine monohydrate.Studies & sources:Zhang et al., Cell Metabolism 2021 — Creatine promotes cancer metastasis via Smad2/3Geng et al., Int. J. Mol. Sci. 2024 — The multifaceted role of creatine metabolismDi Biase et al., J. Exp. Med. 2019 — Creatine and CD8 T cell antitumor immunityKang et al., iScience 2026 (UCLA) — Creatine and dendritic cell activationPereira et al., Amino Acids 2015 — Creatine and heterocyclic aminesNHANES 2017–2020 — Dietary creatine and cancer riskAntonio et al., Frontiers in Nutrition 2025 — Common safety concerns regarding creatine

This episode is about more than food. It's about understanding why we reach for certain foods, creating a realistic off-ramp from ultra-processed eating, and giving your body a chance to reset. If you've ever felt like you're doing everything right but still struggling with weight, energy, inflammation, or cravings, this episode is for you.   Citation: Hall, Kevin D., et al. “Ultra-Processed Diets Cause Excess Calorie Intake and Weight Gain: An Inpatient Randomized Controlled Trial of Ad Libitum Food Intake.” Cell Metabolism, vol. 30, no. 1, 2019, pp. 67–77.e3. https://doi.org/10.1016/j.cmet.2019.05.008 — This is the cornerstone. Same calories, sugar, fat, fiber, and macros on both diets; people ate ~500 kcal/day more on the ultra-processed one and gained weight. It's the strongest evidence that the processing, not just the nutrients, changes intake. Why fat + sugar together hijack reward more than either alone (the “hyperpalatable” mechanism) DiFeliceantonio, Alexandra G., et al. “Supra-Additive Effects of Combining Fat and Carbohydrate on Food Reward.” Cell Metabolism, vol. 28, no. 1, 2018, pp. 33–44.e3. https://doi.org/10.1016/j.cmet.2018.05.018 McDougle, Molly, et al. “Separate Gut-Brain Circuits for Fat and Sugar Reinforcement Combine to Promote Overeating.” Cell Metabolism, vol. 36, no. 2, 2024, pp. 393–407. https://doi.org/10.1016/j.cmet.2023.12.014 — Together these support your point that engineered fat-plus-sugar foods (the Doritos idea) light up reward pathways more than natural foods, because fat and sugar run on separate gut-brain circuits that combine. Why “glycemic velocity” matters — hidden refined starches like maltodextrin Hofman, Denise L., et al. “Nutrition, Health, and Regulatory Aspects of Digestible Maltodextrins.” Critical Reviews in Food Science and Nutrition, vol. 56, no. 12, 2016, pp. https://doi.org/10.1080/10408398.2014.940415 — Supports the egg-bite/maltodextrin point: maltodextrin is a refined starch with a glycemic index around 85–110, higher than table sugar, hiding on labels as “modified food starch.” Backs your “what the calories came from” framing. Why these foods genuinely relieve stress (your central, original thesis) Ulrich-Lai, Yvonne M., et al. “Pleasurable Behaviors Reduce Stress via Brain Reward Pathways.” Proceedings of the National Academy of Sciences, vol. 107, no. 47, 2010, pp. https://doi.org/10.1073/pnas.1007740107 Tomiyama, A. Janet, et al. “Comfort Food Is Comforting to Those Most Stressed: Evidence of the Chronic Stress Response Network in High Stress Women.” Psychoneuroendocrinology, vol. 36, no. 10, 2011, pp. 1513–1519. https://doi.org/10.1016/j.psyneuen.2011.04.005 — This is the science behind “the food was doing something right.” Palatable food measurably dampens the HPA (cortisol) stress axis through reward pathways — which is exactly why pulling it without replacing the stress tool fails. Why cravings are state-dependent and rise with stress (the “urge depends on the state of your blood / stress level” claim) Adam, Tanja C., and Elissa S. Epel. “Stress, Eating and the Reward System.” Physiology & Behavior, vol. 91, no. 4, 2007, pp. 449–458. https://doi.org/10.1016/j.physbeh.2007.04.011 Darcey, Valerie L., et al. “Brain Dopamine Responses to Ultra-Processed Milkshakes Are Highly Variable and Not Significantly Related to Adiposity in Humans.” Cell Metabolism, vol. 37, no. 3, 2025, pp. 616–628. https://doi.org/10.1016/j.cmet.2025.02.002  (edited)      WHAT TO EAT FOR THE NEXT SIX WEEKS — Protein. Plant. Potato. (P³) The formula for every meal: one protein + one plant + one starch (potato, or beans and rice). Add fat — olive oil, butter, avocado, cheese, nuts. Add flavor — salt, pepper, garlic, lemon, vinegar, salsa, hot sauce, herbs. This is not the meal you dreamed of. This is the meal that sets you free. BREAKFAST Eggs + sautéed vegetables + fruit on the side Plain Greek yogurt + berries + a handful of nuts Leftover chicken or beef + potato + vegetables (last night's dinner works) LUNCH Chicken + roasted potato + green salad with olive oil and lemon Tuna + white beans + cucumber + tomato, dressed with olive oil and vinegar Beef + potato + peppers + salsa DINNER Sheet-pan chicken + potatoes + green beans Instant Pot chicken + potato + a vegetable Burger patty (no bun) + potato + salad Batch chili (beef + beans + tomato) over rice Baked fish + sweet potato + roasted broccoli Pork + beans and rice + sautéed greens THE DURESS PLATE — for when the day collapses One protein + one plant + one starch, zero cooking. Examples: • Hard-boiled eggs + apple + handful of nuts • Tuna + canned beans + cucumber, with olive oil • Pre-cooked/frozen ground beef + frozen vegetables + microwave potato • String cheese + fruit + a few nuts (in a real pinch) SIMPLE RECIPES Sheet-Pan Chicken & Potatoes (serves 4) Toss chicken thighs and quartered baby potatoes in olive oil, salt, pepper, garlic. Roast at 425°F (220°C) ~35–40 min. Add green beans for the last 15 min. Batch Chili (serves 6) Brown 2 lb ground beef with chopped onion. Add 2 cans diced tomatoes, 2 cans beans (drained), garlic, cumin, chili powder, salt. Simmer 30+ min. Freezes well — make once, eat all week. Serve over rice. Instant Pot Chicken Chicken breasts + ½ cup broth + salt, garlic, paprika. Pressure cook 10 min, natural release 5. Shred. Pairs with any potato + vegetable. The 5-Minute Tuna Bean Bowl Can of tuna + can of white beans (rinsed) + diced cucumber and tomato. Dress with olive oil, lemon or vinegar, salt, pepper. Microwave Potato, Done Right Pierce a potato, microwave 5–7 min. Split, add butter or olive oil, salt, pepper. The reliable, universal starch. Remember: Don't aim for one perfect week repeated six times. Just follow the basic protocol the best you can for six weeks. When a craving hits, run the nine-minute interrupt from Episode 14.   Dr. Brendan McCarthy is the founder and Chief Medical Officer of Protea Medical Center in Arizona. With over two decades of experience, he's helped thousands of patients navigate hormonal imbalances using bioidentical HRT, nutrition, and root-cause medicine. He's also taught and mentored other physicians on integrative approaches to hormone therapy, weight loss, fertility, and more. If you're ready to take your health seriously, this podcast is a great place to start.

Most diets fail because they never address what the food was doing for you emotionally. In this episode, Dr. Brendan McCarthy explains the stress-craving loop behind emotional eating, why ultra-processed foods feel impossible to resist, and how shame actually reinforces the cycle. You'll learn: • Why cravings feel automatic • How stress drives food urges • The “cue → urge → reward” loop • A simple 9-minute method to interrupt cravings This isn't about perfection or willpower. It's about understanding the pattern so you can finally begin to change it.   Citations:  Boswell, Rebecca G., and Hedy Kober. “Food Cue Reactivity and Craving Predict Eating and Weight Gain: A Meta-Analytic Review.” Obesity Reviews, vol. 17, no. 2, 2016, pp. 159–177. doi:10.1111/obr.12354. Use for: Food cues can trigger craving and eating even without true hunger. Berridge, Kent C., and Terry E. Robinson. “Liking, Wanting, and the Incentive-Sensitization Theory of Addiction.” American Psychologist, vol. 71, no. 8, 2016, pp. 670–679. doi:10.1037/amp0000059. Use for: “Wanting” food is not the same as true pleasure. Schultz, Wolfram, Peter Dayan, and P. Read Montague. “A Neural Substrate of Prediction and Reward.” Science, vol. 275, no. 5306, 1997, pp. 1593–1599. doi:10.1126/science.275.5306.1593. Use for: Dopamine helps encode reward prediction and learning. Wood, Wendy, and Dennis Rünger. “Psychology of Habit.” Annual Review of Psychology, vol. 67, 2016, pp. 289–314. doi:10.1146/annurev-psych-122414-033417. Use for: Habits form through repeated cue-context loops. Laborde, Sylvain, et al. “Effects of Voluntary Slow Breathing on Heart Rate and Heart Rate Variability: A Systematic Review and a Meta-Analysis.” Neuroscience & Biobehavioral Reviews, vol. 138, 2022, article 104711. doi:10.1016/j.neubiorev.2022.104711. Use for: Slow breathing supports parasympathetic regulation and stress reduction. Lieberman, Matthew D., et al. “Putting Feelings into Words: Affect Labeling Disrupts Amygdala Activity in Response to Affective Stimuli.” Psychological Science, vol. 18, no. 5, 2007, pp. 421–428. doi:10.1111/j.1467-9280.2007.01916.x. Use for: Naming emotions can reduce emotional reactivity. Gollwitzer, Peter M. “Implementation Intentions: Strong Effects of Simple Plans.” American Psychologist, vol. 54, no. 7, 1999, pp. 493–503. doi:10.1037/0003-066X.54.7.493. Use for: “If-then” plans improve behavior change under stress. Forman, Evan M., et al. “A Comparison of Acceptance- and Control-Based Strategies for Coping with Food Cravings: An Analog Study.” Behaviour Research and Therapy, vol. 45, no. 10, 2007, pp. 2372–2386. doi:10.1016/j.brat.2007.04.004. Use for: Acceptance and urge-surfing strategies help cravings pass without acting on them. Hall, Kevin D., et al. “Ultra-Processed Diets Cause Excess Calorie Intake and Weight Gain: An Inpatient Randomized Controlled Trial of Ad Libitum Food Intake.” Cell Metabolism, vol. 30, no. 1, 2019, pp. 67–77.e3. doi:10.1016/j.cmet.2019.05.008. Use for: Ultra-processed foods increase intake and reinforce overeating patterns.   Dr. Brendan McCarthy is the founder and Chief Medical Officer of Protea Medical Center in Arizona. With over two decades of experience, he's helped thousands of patients navigate hormonal imbalances using bioidentical HRT, nutrition, and root-cause medicine. He's also taught and mentored other physicians on integrative approaches to hormone therapy, weight loss, fertility, and more. If you're ready to take your health seriously, this podcast is a great place to start.

Why is it so hard to stop eating ultra-processed foods — even when you know they're hurting you? In Episode 13 of this 16-part series, Dr. Brendan McCarthy explains why the real problem is not just the food itself. The real problem is the loop: Cue or emotional state → Wanting → Bargaining → Consumption → Temporary relief → Crash/regret → Repeat. This episode explores how ultra-processed and hyper-palatable foods become attached to stress, boredom, loneliness, exhaustion, anxiety, and emotional discomfort — training the brain to seek relief through food. Key ideas from this episode: • Hunger is the body asking for nourishment • Wanting is the conditioned brain asking for the expected hit • The food is the bait. The loop is the trap. • The food breaks the feeling. It does not heal the source. • You cannot remove a counterfeit regulator without restoring real regulation. Dr. McCarthy breaks down why willpower alone often fails and why lasting change requires a physiologic off-ramp: stable meals, protein, fiber, hydration, sleep, movement, emotional regulation, cue reduction, social planning, and relapse repair. This is not about “perfect eating.” It is about building a life where food is no longer your primary regulator of stress, comfort, or identity. If you've ever felt trapped in cravings, emotional eating, binge-restrict cycles, or constant food noise, this episode is designed to help you understand the mechanism behind the loop — and how to begin leaving it.

Creatine and Microbiomes A new 2026 Cell Metabolism study explores a compelling and increasingly central idea in modern biology: the gut/brain/immune/metabolism axis is not just associative, it is mechanistic. Specifically, Dr. Lu and colleagues investigate how the gut microbiota can directly influence depressive behavior by reshaping systemic and neural metabolism. This is another in a long running list of papers describing the amazing work that bacterial commensal microbes do for us. In this case, our minds and moods. "Although peripheral-brain crosstalk regulates energy metabolism, its role in depression remains unclear. Here, we used metabolic profiling to reveal elevated fecal creatine alongside reduced plasma and cerebrospinal fluid creatine in both patients with depression and mouse depression models. Exogenous creatine produced antidepressant-like effects mediated by gut microbiota. Bifidobacterium pseudolongum was identified as a significantly reduced gut bacterial species in depression, correlating with impaired creatine absorption. Subsequent supplementation with Bifidobacterium enhanced the antidepressant effects of creatine. Mechanistically, B. pseudolongum-derived acetate promoted the creatine transporter (Slc6a8) expression in intestinal epithelial cells via histone acetylation. The Slc6a8 mediated the antidepressant-like effects of creatine. Neuronal creatine deficiency influenced energetic metabolism and neurophysiological function. In patients with depression taking antidepressants, co-administration of creatine and Bifidobacterium increased plasma creatine levels and reduced depression scores. These findings identify the Bifidobacterium-creatine combination as a promising antidepressant strategy and highlight the critical role of gut-brain energy metabolism in depression." "The brain, as an energy-intensive organ, relies on precise metabolic regulation to maintain synaptic plasticity, neurotransmitter synthesis, and stress response systems. Accumulating evidence implicates energy metabolism dysregulation as a hallmark of depression. Neuroimaging studies using positron emission tomography (PET) have identified marked glucose hypometabolism in the medial prefrontal cortex (mPFC) of patients with depression. Cerebral mitochondrial dysfunction and ATP imbalance have been mechanistically linked to depression progression. Notably, emerging studies emphasize the bidirectional interplay between peripheral metabolic signals and central energy regulation, which is fundamental to neural metabolism. Clinical observations such as fatigue, appetite dysregulation, and unexplained weight fluctuations in patients with depression further suggest systemic metabolic disturbances spanning peripheral organs and the CNS.." (Lu et. al. 2026) This is next-level medicine. Mental health can no longer be framed as a disorder of genetics, experience, or circumstance alone. This work opens a clearer window, showing how the microbiome participates as an active partner, shaping brain function through the metabolites it helps produce and deliver. Compounds like creatine are no longer just peripheral players. They become signals, fuel, structure, and information, bridging gut and brain, metabolism and behavior.... and more Enjoy, Dr. M

In this episode, Dr. Brendan McCarthy dives deep into the psychology of ultra-processed foods, compulsive eating, shame, and why so many people feel trapped in unhealthy food cycles. This conversation goes far beyond calories and willpower. Dr. McCarthy explains how ultra-processed and hyper-palatable foods are intentionally engineered to drive repeat consumption, how emotional memories and stress shape cravings, and why shame-based nutrition advice often makes the problem worse instead of better. Topics covered in this episode include: • How ultra-processed foods affect the brain • Why compulsive eating is learned — and can be unlearned • The connection between trauma, stress, and food cravings • The difference between guilt and shame • How marketing and emotional associations shape eating habits • Why “clean eating” language can be harmful • The neuroscience of cravings, dopamine, serotonin, and reward • What real freedom with food actually looks like • Why self-compassion matters in healing If you've ever felt trapped in cycles of emotional eating, binge eating, food guilt, or shame around nutrition, this episode is for you.  

Ultra-processed food makes up over half the calories Americans eat - and over 60% for kids. Here's what the research shows happens inside your body in the first 5 days after you quit. In this episode of Health Longevity Secrets, Dr. Robert Lufkin walks through the hour-by-hour timeline: the glucose spikes that disappear within 24 hours, the insulin resistance that drops 30%+ in 48 hours, the gut microbiome that reorganizes in 3 days, the blood pressure that falls 6-8 mmHg in a week, and the NIH metabolic ward data showing a 500+ calorie daily swing driven entirely by food processing - not willpower. CHAPTERS 00:00 - Introduction: Why Ultra-Processed Food Matters 00:47 - Part 1: What Happens in the First 24 Hours 01:30 - Sodium, Water Retention and the Real Reason You Lose 1-3 lbs 02:10 - Part 2: 48 Hours - Insulin Sensitivity Returns Within Days 02:45 - Gut Microbiome Shifts in 24 Hours (David et al., Nature 2014) 03:23 - Taste Receptors Recalibrate: Why Fruit Tastes Sweeter Again 03:55 - Part 3: 72 Hours - Blood Pressure Drops 6-8 mmHg 04:34 - Inflammation Falls 35-43% in One Week (CRP Data) 05:30 - Part 4: 5 Days - Kevin Hall's NIH Metabolic Ward Trial 06:58 - Part 5: The Framework - 120 Hours to Reset Your Biology KEY TAKEAWAYS Glucose stabilizes within 24 hours when fiber and food matrix are restored 3 low-carb meals can reduce post-meal insulin resistance by over 30% in a day Gut bacterial composition shifts within 24 hours of dietary change Sodium reduction lowers systolic BP 6-8 mmHg in 70-75% of people in one week CRP drops 35-43% in 7 days on a whole-food, vegetable-rich diet Kevin Hall's 2019 NIH RCT: ultra-processed diet drove 500+ extra calories/day with zero awareness STUDIES AND SOURCES Hall et al., Cell Metabolism 2019 - NIH metabolic ward UPF trial David et al., Nature 2014 - diet alters gut microbiome Shukla et al., 2019 - meal sequence and postprandial glucose American Journal of Medicine 2026 - UPF and 47% increased CV risk AHA Scientific Sessions 2023 - sodium and BP in one week Lin and Borer, PLOS ONE 2016 - ⭐ Enjoying the show? Please leave a 5-star review on Apple Podcasts — it takes 30 seconds and helps more people discover the science of health and longevity. Thank you!New episodes every Tuesday & Thursday. Subscribe so you don't miss one.Continue this conversation on Substack: https://robertlufkinmd.substack.comLies I Taught In Medical School — Free sample chapter: https://www.robertlufkinmd.com/lies/Web: https://www.robertlufkinmd.comYouTube: https://www.youtube.com/robertlufkinmdX: https://x.com/robertlufkinmdInstagram: https://www.instagram.com/robertlufkinmd/TikTok: https://www.tiktok.com/@robertlufkinLinkedIn: https://www.linkedin.com/in/robertlufkinmd/

Registered dietitian nutritionist Leyla Muedin discusses how exposure to natural daylight may improve metabolic health beyond diet and exercise, highlighting a controlled crossover study of 13 adults aged 65+ with type 2 diabetes published in Cell Metabolism. Participants spent 4.5 days in living spaces lit by either natural light through large windows or artificial light, with identical meals, sleep, activity, and screen time; after a 4-week washout they switched conditions. Natural light was associated with more hours of blood glucose in the normal range, less glucose variability, higher evening melatonin, and improved fat oxidative metabolism, suggesting effects on circadian “body clocks” and coordination between central and peripheral clocks. Muedin recommends getting morning light on the face, reducing sunglasses and high SPF use, dimming lights at night, keeping consistent sleep, and spending more time outdoors; she also notes that architecture can limit sunlight exposure.

Today, we're diving into a topic that should be getting far more attention: Cardiovascular disease in women. Heart disease is one of the leading causes of death in women—yet it's often under-addressed, oversimplified, and misunderstood in clinical practice. Most women are told: “Eat better. Take this prescription.” But that approach misses something critical. Full citation list:    •    Hall, Kevin D., et al. “Ultra-Processed Diets Cause Excess Calorie Intake and Weight Gain: An Inpatient Randomized Controlled Trial of Ad Libitum Food Intake.” Cell Metabolism, vol. 30, no. 1, 2019, pp. 67–77.e3. Supports the core causal point that ultra-processed foods drive higher intake and weight gain even under controlled feeding conditions; this is not a women-specific lipid paper, but it is the cleanest experimental anchor for why UPFs create a high-throughput metabolic environment.     •    El Khoudary, Samar R., et al. “Menopause Transition and Cardiovascular Disease Risk: Implications for Timing of Early Prevention: A Scientific Statement From the American Heart Association.” Circulation, vol. 142, no. 25, 2020, pp. e506–e532. Supports the midlife women's frame: across the menopause transition, LDL-C and ApoB rise, metabolic risk shifts, and cardiovascular prevention needs to become more deliberate during this window. This supports the “why I care about lipids in endocrine care” part of the episode.     •    Derby, Carol A., et al. “Lipid Changes During the Menopause Transition in Relation to Age and Weight: The Study of Women's Health Across the Nation.” American Journal of Epidemiology, vol. 169, no. 11, 2009, pp. 1352–61. Foundational SWAN paper establishing that the menopause transition itself — not just chronological aging — is associated with adverse lipid shifts in midlife women. This is the original observation that the timing argument rests on.     •    Wu, Bingjie, et al. “Trajectories of Blood Lipids Profile in Midlife Women: Does Menopause Matter?” Journal of the American Heart Association, vol. 12, no. 22, 2023, e030388. Supports the claim that LDL-C, total cholesterol, and ApoB follow distinct trajectory patterns through the menopause transition, with subgroups of women showing rising lipids in the years before the final menstrual period — useful for the timing argument that body and symptom changes can precede the obvious lab story.     •    Matthews, Karen A., et al. “Age at Menopause in Relationship to Lipid Changes and Subclinical Carotid Disease Across 20 Years: Study of Women's Health Across the Nation.” Journal of the American Heart Association, vol. 10, no. 18, 2021, e021362. Supports the point that ApoB and Apo A1 changes cluster around the final menstrual period and that adverse lipid shifts in the early postmenopausal years track with subclinical carotid disease later — connects menopausal timing to the longer cardiovascular arc rather than a one-time lab blip.     •    De Oliveira-Gomes, Diana, et al. “Apolipoprotein B: Bridging the Gap Between Evidence and Clinical Practice.” Circulation, vol. 150, no. 1, 2024, pp. 62–79. Supports the practical ApoB explanation: ApoB reflects atherogenic particle burden and outperforms LDL-C for ASCVD risk prediction in many settings, but adoption lags because clear apoB targets and triggers are still lacking in mainstream guidelines. Good support for the public-service “what the hell is ApoB anyway?” section.     •    Williamson, Laura. “The Slowly Evolving Truth About Heart Disease and Women.” American Heart Association News, 9 Feb. 2024, heart.org/en/news/2024/02/09/the-slowly-evolving-truth-about-heart-disease-and-women. Supports the broader clinical framing that women remain underrecognized or undertreated in cardiovascular care and that women's heart disease still needs better public and clinical communication. This is more public-facing than mechanistic, but useful for your opening frame. Dr. Brendan McCarthy is the founder and Chief Medical Officer of Protea Medical Center in Arizona. With over two decades of experience, he's helped thousands of patients navigate hormonal imbalances using bioidentical HRT, nutrition, and root-cause medicine. He's also taught and mentored other physicians on integrative approaches to hormone therapy, weight loss, fertility, and more. If you're ready to take your health seriously, this podcast is a great place to start.

Today, we're diving into autoimmunity—what it actually is, why it happens, and how ultra-processed foods may be contributing to the problem. Autoimmune disease is often misunderstood. Some will tell you diet has nothing to do with it. Others claim diet is the cure. The truth is more nuanced—and that's exactly what we explore in this episode. You'll learn: What autoimmunity really is (and why it's a case of mistaken identity) How inflammation and the immune system interact The critical role of gut health and the microbiome How ultra-processed foods disrupt intestinal integrity and immune signaling Why stress and hyper-palatable foods create a harmful cycle A practical experiment you can try to see how diet impacts your own biomarkers This isn't about selling supplements or pushing extremes. It's about understanding the science so you can make informed decisions about your health. As always, this episode is backed by scientific literature. Full citations are included below, with abbreviated versions available on shorter clips. If you're dealing with autoimmune symptoms—or just want to better understand how food impacts your immune system—this episode is for you.   Full citation list: Hall KD, et al. “Ultra-Processed Diets Cause Excess Calorie Intake and Weight Gain: An Inpatient Randomized Controlled Trial of Ad Libitum Food Intake.” Cell Metabolism, 2019.     Supports the formulation argument: UPF intake increased spontaneous calorie intake and weight gain even with diets matched for presented calories, sugar, fiber, sodium, and macronutrients. This is your anchor for “hyper-palatability and formulation change physiology, not just psychology.”   Narula N, et al. “Association of Ultra-Processed Food Intake With Risk of Inflammatory Bowel Disease: Prospective Cohort Study.” BMJ, 2021.     Best human disease-level citation for the episode. Supports the claim that higher UPF intake is associated with greater IBD risk, making the gut-immune link clinically meaningful rather than purely theoretical.   Chassaing B, et al. “Randomized Controlled-Feeding Study of Dietary Emulsifier Carboxymethylcellulose Reveals Detrimental Impacts on the Gut Microbiota and Metabolome.” Gastroenterology, 2022.     Best emulsifier paper for human translation. Supports the claim that CMC can perturb the microbiota and metabolome and may contribute to barrier-hostile gut ecology in susceptible individuals.   Daniel N, et al. “Human Intestinal Microbiome Determines Individualized Responses to Dietary Emulsifier Carboxymethylcellulose.” Cellular and Molecular Gastroenterology and Hepatology, 2024.     Useful nuance paper. Supports the point that emulsifier sensitivity is not identical across all people and that host-microbiome context matters.   Shil A, et al. “Artificial Sweeteners Disrupt Tight Junctions and Barrier Function in the Intestinal Epithelium Through Activation of the Sweet Taste Receptor T1R3.” Nutrients, 2020.     Best citation for the “sugar-free does not mean barrier-neutral” point. Supports direct epithelial barrier effects of common artificial sweeteners in experimental models.   Peng L, et al. “Butyrate Enhances the Intestinal Barrier by Facilitating Tight Junction Assembly via Activation of AMP-Activated Protein Kinase in Caco-2 Cell Monolayers.” Journal of Nutrition, 2009.     Classic mechanistic citation for butyrate. Supports the claim that loss of fermentable fiber and reduced butyrate production can weaken barrier function.   Kumar KP, et al. “The Interplay Between the Microbiota, Diet and T Regulatory Cells in Maintaining Intestinal Homeostasis.” Frontiers in Microbiology, 2023.     Useful for the tolerance language. Supports the argument that diet and microbial metabolites shape Treg biology and mucosal tolerance.   Haase S, et al. “Sodium Chloride Triggers Th17 Mediated Autoimmunity.” Frontiers in Immunology, 2019.     Key citation for high salt and autoimmune-prone immune skewing. Supports the claim that excess salt can promote pathogenic Th17 biology relevant to autoimmune disease.   Wilck N, et al. “Salt-Responsive Gut Commensal Modulates TH17 Axis and Disease.” Nature, 2017.     Strong bridge between salt, microbiome, and Th17 signaling. Supports the point that salt is not just a blood pressure story; it is also an immune-story.   Vitales-Noyola M, et al. “Analysis of Sodium Chloride Intake and Treg/Th17 Lymphocytes in Patients With Rheumatoid Arthritis and Systemic Lupus Erythematosus.” Journal of Immunology Research, 2018.     Helpful human-facing citation for salt and immune skewing in autoimmune populations. Use cautiously, but it strengthens translation from theory to autoimmune terrain.   Phuong-Nguyen K, et al. “Advanced Glycation End-Products and Their Effects on Gut Health.” Nutrients, 2023.     Good review for the AGE section. Supports the argument that AGE-rich processed foods may worsen oxidative stress, microbiota balance, and barrier function.   Chen Y, et al. “Dietary Advanced Glycation End-Products Elicit Toxicological Effects by Disrupting Gut Microbiota and Increasing Colon Permeability in Rats.” Journal of Toxicology and Environmental Health, 2021.     Useful mechanistic support for the processing-chemistry section. Reinforces the claim that dietary AGEs can alter microbial ecology and increase permeability.   Monteiro CA, et al. “Ultra-Processed Foods: What They Are and How to Identify Them.” Public Health Nutrition, 2019.   Dr. Brendan McCarthy is the founder and Chief Medical Officer of Protea Medical Center in Arizona. With over two decades of experience, he's helped thousands of patients navigate hormonal imbalances using bioidentical HRT, nutrition, and root-cause medicine. He's also taught and mentored other physicians on integrative approaches to hormone therapy, weight loss, fertility, and more. If you're ready to take your health seriously, this podcast is a great place to start.  

A ketogenic diet put his ulcerative colitis into complete remission — off all medications, confirmed on colonoscopy. Dr. Nick Norwitz (PhD Oxford, MD Harvard) explains why evidence-based care isn't always optimal care, how keto rewires the gut and brain, and why GLP-1 drugs should catalyze lifestyle change, not replace it.CHAPTERS:0:00 - The most remarkable thing about my story is it's not unique1:14 - Welcome Nick Norwitz — Oxford PhD, Harvard MD2:02 - Ulcerative colitis, desperation, and keto remission5:34 - What medical school doesn't teach8:05 - Why evidence-based care ≠ optimal care15:53 - The carnivore-ketogenic IBD case series (10 patients)18:50 - Fiber elimination in pediatric Crohn's — 60–85% remission20:00 - Keto for depression: Ohio State trial — 69–71% reduction23:49 - Seed oils: the nuanced truth29:32 - Ketones and neurodegenerative disease32:52 - Autophagy, lateral habenula, and depression36:16 - Sonnenburg 2021: fermented foods beat fiber for inflammation37:20 - GLP-1 agonists: good tool, poor deployment43:29 - Statins slash GLP-1 by ~50% (Cell Metabolism, 2024)48:57 - ClosingREFERENCES:Carnivore-Keto for IBD (Norwitz et al., Frontiers, 2024): PMC11409203Keto for Depression (Ohio State, 2025): PMC12420795Fermented Foods vs Fiber (Sonnenburg, Cell, 2021): Stanford NewsStatins Slash GLP-1 (Cell Metabolism, 2024): pubmed/38325336Autophagy + Depression (Nature, 2025): NatureGUEST: Nick Norwitz, PhD MDHOST: Dr. Robert Lufkin MD | robertlufkinmd.com⭐ Enjoying the show? Please leave a 5-star review on Apple Podcasts — it takes 30 seconds and helps more people discover the science of health and longevity. Thank you!New episodes every Tuesday & Thursday. Subscribe so you don't miss one.Continue this conversation on Substack: https://robertlufkinmd.substack.comLies I Taught In Medical School — Free sample chapter: https://www.robertlufkinmd.com/lies/Web: https://www.robertlufkinmd.comYouTube: https://www.youtube.com/robertlufkinmdX: https://x.com/robertlufkinmdInstagram: https://www.instagram.com/robertlufkinmd/TikTok: https://www.tiktok.com/@robertlufkinLinkedIn: https://www.linkedin.com/in/robertlufkinmd/

GLP-1 medications like semaglutide and tirzepatide are everywhere right now—but are they actually solving the problem? In Episode 8 of this 16-part series on ultra-processed foods, Dr. Brendan McCarthy breaks down the truth about GLP-1 medications: how they work, why they can feel like a “miracle,” and where things go wrong when they're used without proper medical guidance. This isn't about shame. It's about understanding. GLP-1s can quiet “food noise” and help regulate appetite—but they don't fix your relationship with food, your metabolism, or the long-term patterns that lead to weight gain. Without structure, nutrition, and proper care, many patients end up with muscle loss, nutrient deficiencies, and rebound weight gain. In this episode, you'll learn: What GLP-1 medications actually do in your body Why they're not a long-term solution on their own The biggest mistakes doctors and clinics make when prescribing them How ultra-processed foods drive weight gain in the first place How to use GLP-1s the right way to create lasting change The goal isn't dependence—it's freedom. If you're currently on a GLP-1 (or considering it), this episode will change how you think about your treatment plan.   Mechanism Anchored References This episode is not anti medication. It is about putting GLP 1 therapy in its proper place. GLP 1 receptor agonists can reduce appetite pressure and alter satiety signaling. That matters. But quieter appetite is not the same as full recovery. Food quality still matters. Protein still matters. Muscle still matters. Structure still matters.   References U.S. Food and Drug Administration. WEGOVY semaglutide injection Prescribing Information. 2025. Wilding, John P H, et al. Once Weekly Semaglutide in Adults with Overweight or Obesity. New England Journal of Medicine, vol. 384, no. 11, 2021, pp. 989 to 1002. Wilding, John P H, et al. Weight Regain and Cardiometabolic Effects After Withdrawal of Semaglutide The STEP 1 Trial Extension. Diabetes Obesity and Metabolism, vol. 24, no. 8, 2022, pp. 1553 to 1564. Hall, Kevin D, et al. Ultra Processed Diets Cause Excess Calorie Intake and Weight Gain An Inpatient Randomized Controlled Trial of Ad Libitum Food Intake. Cell Metabolism, vol. 30, no. 1, 2019, pp. 67 to 77. Neeland, Ian J, et al. Changes in Lean Body Mass with Glucagon Like Peptide 1 Based Therapies and Mitigation Strategies. Diabetes Obesity and Metabolism, 2024. Wilding, John P H, et al. Impact of Semaglutide on Body Composition in Adults with Overweight or Obesity Exploratory Analysis of the STEP 1 Study. 2021. Everitt, Barry J, and Trevor W Robbins. Drug Addiction Updating Actions to Habits to Compulsions Ten Years On. Annual Review of Psychology, vol. 67, 2016, pp. 23 to 50. Monteiro, Carlos A, et al. The UN Decade of Nutrition the NOVA Food Classification and the Trouble with Ultra Processing. Public Health Nutrition, vol. 21, no. 1, 2018, pp. 5 to 17.   Dr. Brendan McCarthy is the founder and Chief Medical Officer of Protea Medical Center in Arizona. With over two decades of experience, he's helped thousands of patients navigate hormonal imbalances using bioidentical HRT, nutrition, and root-cause medicine. He's also taught and mentored other physicians on integrative approaches to hormone therapy, weight loss, fertility, and more. If you're ready to take your health seriously, this podcast is a great place to start.  

Craving junk food when you're stressed isn't a lack of discipline — it's biology. In this episode, Dr. Brendan McCarthy breaks down what ultra-processed and hyper-palatable foods actually do inside your body — from your metabolism to your hormones, your brain, and your stress response. But this isn't about guilt or shame. It's about understanding what you're up against — especially as a parent trying to make better choices in a world designed to make that difficult. You'll learn: What ultra-processed foods really are How they impact your endocrine system and metabolism Why stress makes you crave sugar and processed foods Why shame around food doesn't work (and never will) Simple, realistic ways to improve your family's eating habits This episode is about taking back control — without perfection, and without guilt.   Mechanism-Anchored References Monteiro, Carlos A., et al. “Ultra-Processed Foods: What They Are and How to Identify Them.” Public Health Nutrition, vol. 22, no. 5, 2019, pp. 936–941. Hall, Kevin D., et al. “Ultra-Processed Diets Cause Excess Calorie Intake and Weight Gain: An Inpatient Randomized Controlled Trial of Ad Libitum Food Intake.” Cell Metabolism, vol. 30, no. 1, 2019, pp. 67–77.e3. doi:10.1016/j.cmet.2019.05.008. Rush, E. Catherine, et al. “The Impact of Ultra-Processed Foods on Pediatric Health.” Nutrition Reviews, 2024. doi:10.1093/nutrit/nuae051. Ventura, Alison K., and John Worobey. “Early Influences on the Development of Food Preferences.” Current Biology, vol. 23, no. 9, 2013, pp. R401–R408. doi:10.1016/j.cub.2013.02.037. Mennella, Julie A., et al. “Preferences for Salty and Sweet Tastes Are Elevated and Related to Each Other during Childhood.” PLOS ONE, vol. 9, no. 3, 2014, e92201. doi:10.1371/journal.pone.0092201. Roberto, Christina A., et al. “Influence of Licensed Characters on Children's Taste and Snack Preferences.” Pediatrics, vol. 126, no. 1, 2010, pp. 88–93. doi:10.1542/peds.2009-3433. Swindle, Taren, et al. “Pester Power: Examining Children's Influence as an Active Component of the Family Food Environment.” Journal of Nutrition Education and Behavior, vol. 52, no. 8, 2020, pp. 801–807. doi:10.1016/j.jneb.2020.06.002. Pérez-Escamilla, Rafael, et al. “Responsive Feeding Recommendations: Harmonizing Integration into Dietary Guidelines for Infants and Young Children.” Current Developments in Nutrition, vol. 5, no. 6, 2021, nzab076. doi:10.1093/cdn/nzab076. Puhl, Rebecca M., and Chelsea A. Heuer. “Obesity Stigma: Important Considerations for Public Health.” American Journal of Public Health, vol. 100, no. 6, 2010, pp. 1019–1028. doi:10.2105/AJPH.2009.159491. World Health Organization. Set of Recommendations on the Marketing of Foods and Non-Alcoholic Beverages to Children. World Health Organization, 2010.   Dr. Brendan McCarthy is the founder and Chief Medical Officer of Protea Medical Center in Arizona. With over two decades of experience, he's helped thousands of patients navigate hormonal imbalances using bioidentical HRT, nutrition, and root-cause medicine. He's also taught and mentored other physicians on integrative approaches to hormone therapy, weight loss, fertility, and more. If you're ready to take your health seriously, this podcast is a great place to start.  

Send us Fan MailThis week, I'm taking a curious, watch-and-see approach to GLP-1 medications—things like semaglutide, Ozempic, Wegovy. We'll cover the research-backed potential benefits, the side effects, what happens after stopping, and why the conversation is about much more than just weight. No judgment, no pressure, just information, reflection, and a reminder that your choices are personal and worth considering thoughtfully.Tune in if you want to explore GLP-1 medications from a place of curiosity and clarity.Quote of the Week:“We are what we repeatedly do. Excellence, then, is not an act, but a habit.” — Will Durant Citations1.    Wilding, J. P. H., et al. (2021). Once-Weekly Semaglutide in Adults with Overweight or Obesity. New England Journal of Medicine, 384, 989–1002.2.    Rubino, D., et al. (2021). Effect of Continued Weekly Subcutaneous Semaglutide vs Placebo on Weight Loss Maintenance. Diabetes, Obesity and Metabolism.3.    SELECT Trial Investigators (2023). Semaglutide and Cardiovascular Outcomes in Obesity. New England Journal of Medicine.4.    Drucker, D. J. (2018). Mechanisms of Action and Therapeutic Application of GLP-1. Cell Metabolism.5.    Baggio, L. L., & Drucker, D. J. (2007). Biology of Incretins. Gastroenterology.Let's go, let's get it done.Get more information at: http://projectweightloss.org

If you've ever felt hungry and wondered “What is wrong with me?”—this episode will change how you see it.Hunger isn't a lack of discipline. It's a biological signal driven by your brain, hormones, and environment.In this episode, we break down what hunger actually is and why it can feel so hard to control. You'll learn how key hormones like ghrelin, leptin, insulin, and GLP-1 regulate appetite—and why your brain is the real decision-maker.More importantly, we cover the three types of hunger:Homeostatic (true energy need) Hedonic (pleasure-driven) Conditioned (habit-based) Understanding the difference is what gives you power.We also explore how ultra-processed foods, sleep, and stress disrupt hunger signals—and what you can do to better regulate your appetite without restriction.In this episode: What hunger actually is  The hormones behind appetite  The 3 types of hunger  How processed foods impact hunger  Why sleep and stress matter This isn't about fighting your hunger—it's about understanding it so you can make more informed choices.References: Batterham RL et al. (2002). Gut hormone PYY(3-36) physiologically inhibits food intake. Nature. Cummings DE et al. (2001). A preprandial rise in plasma ghrelin levels suggests a role in meal initiation. Diabetes. Friedman JM & Halaas JL (1998). Leptin and the regulation of body weight. Nature. Hall KD et al. (2019). Ultra-processed diets cause excess calorie intake and weight gain. Cell Metabolism. Leidy HJ et al. (2015). The role of protein in weight loss and maintenance. AJCN. Martinez Steele E et al. (2016). Ultra-processed foods in the US diet. BMJ Open. Monteiro CA et al. (2019). Ultra-processed foods: What they are and how to identify them. Public Health Nutrition. Morton GJ et al. (2006). Central nervous system control of food intake. Nature. Schwartz MW et al. (2000). Central nervous system control of food intake. Nature. Spiegel K et al. (2004). Sleep curtailment… decreased leptin and increased hunger. Annals of Internal Medicine. Volkow ND et al. (2013). Obesity and addiction: Neurobiological overlaps. Nature Reviews Neuroscience. Wang L et al. (2021). Trends in ultra-processed food consumption. JAMA. Woods SC (1991). The eating paradox. Psychological Review. Support the showGet Weekly Health Tips:  thrivehealthcoachllc.comJoin the Thrive Collective Facebook groupLet's Connect:@‌ashleythrivehealthcoach or via email: ashley@thrivehealthcoachingllc.comPodcast Produced by Virtually You!

In this episode, Vanessa breaks down the fasting mimicking diet (FMD) — including the exact calories, macros, and protein intake used in the research — and compares it to higher-protein fat loss approaches like protein-sparing modified fasting (PSMF) days.

Durante años nos han repetido que comer variado siempre es mejor, que hay que comer de todo y que esa es la base de una buena alimentación. Pero en este vídeo te explico por qué esa idea está mal planteada, cómo la variedad puede hacer que comas más y peor, y por qué una alimentación más simple, coherente y basada en alimentos densos en nutrientes puede darte más salud, más saciedad y más control.Hablamos de evolución, saciedad sensorial específica, dopamina, recompensa, control del hambre y del gran error de confundir variedad con buena nutrición.Si quieres entender por qué no necesitas una variedad absurda de comida para cubrir tus necesidades reales, este vídeo es para ti.Web: https://www.faustoalfaro.comInstagram: @faustoalfaro_X: @Faustoalfaro_Suscríbete al canal para más vídeos sobre salud, nutrición y rendimiento deportivo con criterio.#nutricion #alimentacion #salud #comidareal #dopamina #hambre #habitos #perdidadegrasa #rendimientodeportivo #nutricionsaludableReferencias:Vadiveloo M, Scott M, Quatromoni P, Jacques P. Dietary variety and its implications for obesity prevention in US adults. Circulation. 2018.Small DM, DiFeliceantonio AG. Processed foods and food reward. Science. 2019.Hall KD, Ayuketah A, Brychta R, et al. Ultra-processed diets cause excess calorie intake and weight gain. Cell Metabolism. 2019.

“工位靠窗”往往被视为职场的幸运儿专属，然而，这份“幸运”所蕴含的，远不止于舒适的工作环境。代谢领域顶级学术期刊Cell Metabolism发表的一项研究发现，与人工光相比，办公期间接触自然光能显著改善糖尿病患者的血糖控制，提高脂肪利用率，并优化生物钟功能。

Application pour EV0360 : https://hlperformance.caRéférences :Bellisle, F. (2003). Why should we study human food intake behaviour? *Nutrition, Metabolism and Cardiovascular Diseases*, *13*(4), 189–193. [https://doi.org/10.1016/S0939-4753(03)00063-7](https://doi.org/10.1016/S0939-4753(03)00063-7)Canadian Centre on Substance Use and Addiction. (2023). *Canada's guidance on alcohol and health*. CCSA. https://www.ccsa.ca/canadas-guidance-alcohol-and-healthDing, D., Nguyen, B., Nau, T., Luo, M., Del Pozo Cruz, B., Dempsey, P. C., Munn, Z., Jefferis, B. J., Sherrington, C., Calleja, E. A., Hau Chong, K., Davis, R., Francois, M. E., Tiedemann, A., Biddle, S. J. H., Okely, A., Bauman, A., Ekelund, U., Clare, P., & Owen, K. (2025). Daily steps and health outcomes in adults: A systematic review and dose-response meta-analysis. *The Lancet Public Health*, *10*(8), e668–e681. [https://doi.org/10.1016/S2468-2667(25)00164-1](https://doi.org/10.1016/S2468-2667(25)00164-1)Hall, K. D., & Guo, J. (2017). Obesity energetics: Body weight regulation and the effects of diet composition. *Gastroenterology*, *152*(7), 1718–1727. https://doi.org/10.1053/j.gastro.2017.01.052Hall, K. D., Ayuketah, A., Brychta, R., Cai, H., Cassimatis, T., Chen, K. Y., … & Walter, P. J. (2019). Ultra-processed diets cause excess calorie intake and weight gain: An inpatient randomized controlled trial. *Cell Metabolism*, *30*(1), 67–77. https://doi.org/10.1016/j.cmet.2019.05.008Hall, K. D., Sacks, G., Chandramohan, D., Chow, C. C., Wang, Y. C., Gortmaker, S. L., & Swinburn, B. A. (2012). Quantification of the effect of energy imbalance on bodyweight. *The Lancet*, *378*(9793), 826–837. [https://doi.org/10.1016/S0140-6736(11)60812-X](https://doi.org/10.1016/S0140-6736(11)60812-X)Mattes, R. D. (2014). Beverages and positive energy balance: The menace is the medium. *International Journal of Obesity*, *38*(S1), S1–S6. https://doi.org/10.1038/ijo.2014.21National Institutes of Health. (s. d.). *NIH Body Weight Planner* [Outil en ligne]. U.S. Department of Health and Human Services. https://www.niddk.nih.gov/bwpRyan, R. M., & Deci, E. L. (2000). Self-determination theory and the facilitation of intrinsic motivation, social development, and well-being. *American Psychologist*, *55*(1), 68–78. https://doi.org/10.1037/0003-066X.55.1.68Ryan, R. M., & Deci, E. L. (2017). *Self-determination theory: Basic psychological needs in motivation, development, and wellness*. Guilford Press.American College of Sports Medicine. (2022). *ACSM's guidelines for exercise testing and prescription* (11e éd.). Lippincott Williams & Wilkins. *(Position Stand original : 2009)*World Health Organization. (2020). *WHO guidelines on physical activity and sedentary behaviour*. WHO Press. https://www.who.int/publications/i/item/9789240015128

Ever feel like staying healthy today requires constant effort, planning, and discipline?You're not imagining it. Modern life is designed in ways that make health harder than it used to be. From ultra-processed foods and sedentary jobs to a culture built around convenience and constant access to calories, our environment often works against our biology.In this episode, we break down why maintaining your health today can feel like an uphill battle—and why that doesn't mean you're failing. It means you're navigating what public health researchers call an “obesogenic environment”: surroundings that make overconsumption easy and physical activity harder.You'll learn how changes in our food system, movement patterns, and daily routines have reshaped the health landscape—and most importantly, what you can do about it.In this episode:Why modern environments promote overeatingHow ultra-processed foods increase calorie intakeWhy sedentary lifestyles changed daily energy expenditureThe hidden role of convenience and “friction” in eating behaviorWhy health requires more intention todayFive practical strategies to make healthy choices easierThe goal isn't perfection—it's awareness and creating an environment that supports your health instead of working against it.You're not failing. You're navigating a system that wasn't built for human health. ReferencesBaumeister, R. F., et al. (1998). Ego depletion. Journal of Personality and Social Psychology. Ducrot, P., et al. (2017). Meal planning, diet quality and body weight. Int. Journal of Behavioral Nutrition and Physical Activity. Hall, K. D., et al. (2019). Ultra-processed diets increase calorie intake and weight gain. Cell Metabolism. Juul, F., et al. (2022). Ultra-processed food consumption and obesity in the U.S. American Journal of Clinical Nutrition. Levine, J. A. (2002). Non-exercise activity thermogenesis (NEAT). Proceedings of the Nutrition Society. Martínez Steele, E., et al. (2016). Ultra-processed foods and added sugars in the U.S. diet. BMJ Open. Matthews, C. E., et al. (2008). Sedentary behavior and health outcomes. American Journal of Epidemiology. Pontzer, H. (2015). Constrained energy expenditure model. Current Biology. Pontzer, H. (2021). Burn: New Research Blows the Lid Off How We Really Burn Calories. Swinburn, B., et al. (1999). Obesogenic environments. Preventive Medicine. Young, L. R., & Nestle, M. (2002). Expanding portion sizes. American Journal of Public Health.Support the showGet Weekly Health Tips: thrivehealthcoachllc.com Join the Thrive Collective Facebook group Let's Connect:@‌ashleythrivehealthcoach or via email: ashley@thrivehealthcoachingllc.com Podcast Produced by Virtually You!

ReferencesJ Biol Chem 2017 292: 20481.Cell Metabolism. 2018. 27.,3 p602-615.e4March 06Proc Natl Acad Sci U S A. 2010 May 8;107(21):9626–9631Proc Natl Acad Sci U S A. 2011 May 18;108(23):9466–9471Guerra,DJ. 2026. Unpublished LecturesHoward, B. 1954.Fly Me to the Moon. Sinatrahttps://open.spotify.com/track/7FXj7Qg3YorUxdrzvrcY25?si=3104a016654d4bb9Sparks, A. "Pinetop" 1935. Every Day I Have the Blues. Count Basis and Joe Williamshttps://open.spotify.com/track/1ZVV4uUYilEdZRySfKjvpx?si=62de0af91e7648f0Kaukonen, J. 1971. Third Week in Chelsea. JAhttps://open.spotify.com/track/5t5bV1HLuULF0bX1F6MfCv?si=d65795563a324df7

Type 2 diabetes management is influenced not only by diet and medication but also by environmental factors, including the type and timing of light exposure during typical indoor workdays A Cell Metabolism study found that participants exposed to natural daylight spent more time within a healthy glucose range than those exposed to standard office lighting Daylight supports circadian alignment by strengthening communication between the brain's master clock and peripheral clocks in organs that control insulin sensitivity, glucose uptake, and energy metabolism Natural daylight also shifted how the body used energy and improved metabolic flexibility, which plays an important role in long-term insulin sensitivity and glucose regulation Simple changes like getting morning light, taking outdoor midday breaks, sitting near windows, and keeping a consistent sleep schedule can help restore circadian rhythm and support glucose stability

Are you exhausted all the time? In this solo episode, Darin breaks down why so many people feel chronically exhausted despite eating clean, exercising, and "doing everything right." He explains how modern life disrupts mitochondrial function, circadian rhythm, stress signaling, and nutrient availability, and why fatigue is not a personal failure, but a biological signal. This episode offers a grounded, practical roadmap to restoring energy by realigning your environment, habits, and daily rhythms with how the body is actually designed to function.     What You'll Learn in This Episode: Why chronic fatigue is exploding—even among healthy, active people How mitochondria do far more than "make energy" The role of circadian rhythm, light exposure, and timing in energy production Why stress, overtraining, and modern lifestyles drain cellular energy How emotional suppression and unexpressed stress affect vitality The difference between forcing energy and allowing energy Simple daily practices that support mitochondrial repair How breathwork, stillness, and social connection restore resilience Why nutrition alone isn't enough without rhythm and recovery How to realign your biology with the modern world     Timecodes 00:00:00 – Welcome to SuperLife and the intention behind this episode 00:00:32 – Sponsor: TheraSage and natural frequency-based healing 00:02:10 – Happy New Year + why this conversation matters now 00:02:37 – Are you exhausted even though you're "doing everything right"? 00:03:26 – The modern energy crisis and rising chronic fatigue 00:04:12 – Why surface-level health advice no longer works 00:04:27 – Mitochondria: more than energy factories 00:04:59 – Circadian misalignment, EMFs, and modern stressors 00:05:36 – Overtraining, stress load, and lack of recovery 00:06:00 – Fatigue as a signal, not a lack of discipline 00:06:18 – How artificial light disrupts internal clocks 00:07:25 – Discipline as alignment with natural rhythms 00:07:36 – Emotional release, primal expression, and energy recovery 00:08:47 – Why "why am I tired all the time?" is exploding online 00:09:24 – The mitochondria as environmental sensors 00:10:06 – Stress signaling, thoughts, and cellular energy flow 00:11:18 – Breathwork and slowing the nervous system 00:12:24 – Social connection and low-stress signaling 00:13:02 – Sponsor: Bite toothpaste and eliminating plastic exposure 00:15:19 – Morning sunlight and circadian priming 00:15:52 – Reducing artificial light at night 00:16:15 – Nutrients that support mitochondrial function 00:17:29 – Sleep timing, consistency, and repair 00:18:20 – Evening routines and melatonin protection 00:19:46 – Small daily steps compound into real energy 00:20:17 – Antioxidants, inflammation, and recovery 00:20:49 – Training smarter, not harder 00:21:31 – Breathwork, sauna, and recovery rituals 00:22:26 – Nutrition, protein, and polyphenols 00:24:37 – Five daily energy takeaways 00:25:24 – Energy is permitted, not forced 00:26:03 – Listening to the body and closing reflections 00:26:49 – SuperLife Patreon and community support     Join the SuperLife Community Get Darin's deeper wellness breakdowns — beyond social media restrictions: Weekly voice notes Ingredient deep dives Wellness challenges Energy + consciousness tools Community accountability Extended episodes Join for $7.49/month → https://patreon.com/darinolien     Thank You to Our Sponsors: Therasage: Go to www.therasage.com and use code DARIN at checkout for 15% off Bite Toothpaste: Go to trybite.com/DARIN20 or use code DARIN20 for 20% off your first order.     Find More from Darin Olien: Instagram: @darinolien Podcast: SuperLife Podcast Website: superlife.com Book: Fatal Conveniences     Key Takeaway "Fatigue isn't failure. It's feedback. When your environment, timing, and signals align, your biology remembers how to thrive."     Bibliography/Sources: Ames, B. N. (2006). Low micronutrient intake may accelerate the degenerative diseases of aging through allocation triage. Proceedings of the National Academy of Sciences, 103(47), 17589–17594. https://doi.org/10.1073/pnas.0608757103 Bass, J., & Takahashi, J. S. (2010). Circadian integration of metabolism and energetics. Science, 330(6009), 1349–1354. https://doi.org/10.1126/science.1195668 Gooley, J. J., Chamberlain, K., Smith, K. A., Khalsa, S. B., Rajaratnam, S. M., Van Reen, E., Zeitzer, J. M., Czeisler, C. A., & Lockley, S. W. (2011). Exposure to room light before bedtime suppresses melatonin onset and shortens melatonin duration in humans. The Journal of Clinical Endocrinology & Metabolism, 96(3), E463–E472. https://doi.org/10.1210/jc.2010-2098 Kreher, J. B., & Schwartz, J. B. (2012). Overtraining syndrome: A practical guide. 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Psychosomatic Medicine, 80(2), 126–140. https://doi.org/10.1097/PSY.0000000000000544 Picard, M., McElroy, G. S., & Turnbull, D. M. (2015). Mitochondrial functions modulate neuroendocrine, metabolic, inflammatory, and transcriptional responses to acute psychological stress. Proceedings of the National Academy of Sciences, 112(48), 14920–14925. https://doi.org/10.1073/pnas.1518223112 Reiter, R. J., Rosales-Corral, S., Tan, D. X., Acuna-Castroviejo, D., Qin, L., Yang, S. F., & Xu, K. (2017). Melatonin as a mitochondria-targeted antioxidant: One of evolution's best inventions? Journal of Pineal Research, 62(1), e12394. https://doi.org/10.1111/jpi.12394 Scheer, F. A., Hilton, M. F., Mantzoros, C. S., & Shea, S. A. (2009). Adverse metabolic and cardiovascular consequences of circadian misalignment. Proceedings of the National Academy of Sciences, 106(11), 4453–4458. https://doi.org/10.1073/pnas.0808180106 Straub, R. H. (2017). The brain and immune system prompt energy shortage in chronic inflammation and ageing. Nature Reviews Rheumatology, 13(2), 74–79. https://doi.org/10.1038/nrrheum.2016.213 World Health Organization. (n.d.). Micronutrient deficiencies. World Health Organization. https://www.who.int/health-topics/micronutrients

Send us a textHey friends — this week, with the holidays in full swing, I wanted to bring you three research-backed strategies you can use to feel lighter — emotionally, mentally, and yes, physically — without rigidity, pressure, or perfection.This episode is all about top researched strategies, that coupled with awareness, and choosing yourself in the ways that truly matter and make a difference, particularly during the holidays. Take a listen and share the episode – even better, set up a buddy to implement the techniques with. Quotes of the Week:✨ “What most people don't realize is that food is not just calories: It's information… it communicates to every cell in the body.” — Dr. Mark Hyman✨ “Our modern lifestyle… disrupts our circadian rhythms and reduces the production of the sleep hormone melatonin.” — Satchin Panda, The Circadian CodeTake a listen — and let's move through this season with intention, clarity, and love. Citations1.    Sacks, F. M., Bray, G. A., Carey, V. J., et al. (2009). Comparison of weight-loss diets with different compositions of fat, protein, and carbohydrates. Journal of the American Medical Association, 360(9), 859–873.2.    Smith, J. D., Nguyen, T., Hall, K. D., et al. (2023). Protein and fiber intake and their effects on cravings and spontaneous snacking in adults: A randomized controlled trial. Nutrients, 15(4), 812–823.3.    Sutton, E. F., et al. (2018). Early Time-Restricted Feeding Improves Insulin Sensitivity, Blood Pressure, and Oxidative Stress Even Without Weight Loss in Men with Prediabetes. Cell Metabolism, 27(6), 1212–1221.Let's go, let's get it done. Get more information at: http://projectweightloss.org

In this solosode of The Energy Code, Dr. Mike unveils the most comprehensive update yet to BioLight's flagship supplement — BioBlue — and takes listeners deep inside the quantum bioenergetic thinking that shaped its redesign. What began as a methylene-blue-based mitochondrial catalyst has evolved into a next-generation longevity systemintegrating deuterium-depleted water, elevated NMN, taurine, and trace gold-silver resonance compounds.   Dr. Mike breaks down the science and reasoning behind each refinement: why Litewater's 10 ppm deuterium-depleted water now forms the clean matrix for all BioBlue liquids, how NMN has been increased ten-fold (10 mg → 100 mg) to meaningfully expand NAD⁺ pools and drive biogenesis, and how taurine stabilizes mitochondrial membranes and calcium signaling for endurance and resilience. He explains the subtle yet powerful tweaks — like a 50 % increase in colloidal gold and silver and a 40 % reduction in fulvic acid — that sharpen redox coherence and enhance longevity signaling.   Dr. Mike dives into: Overview of how BioBlue progressed from a simple methylene-blue solution to a full mitochondrial optimization system. Why all BioBlue liquids now utilizes Litewater for cleaner proton flow and improved ATP efficiency. Why NMN increased from 10 mg → 100 mg per dose to meaningfully raise NAD⁺ levels, drive biogenesis, and enhance DNA repair. Why the addition of Taurine – 100 mg per serving for membrane stability, calcium regulation, and long-term mitochondrial resilience. Enhanced Trace Elements – 50 % more colloidal gold & silver plus refined fulvic acid for smoother redox flow and higher photodynamic efficiency.   This episode isn't just about formulation — it's about why every molecule matters in the pursuit of mitochondrial efficiency, redox stability, and long-term cellular youthfulness. Mike also previews BioLight's upcoming new website, pre-Black-Friday event, and a soon-to-launch BioBlue Lite product line for those seeking simplicity without compromise.   Key Topics Covered Evolution of BioBlue — from the original methylene blue + NMN formula to a comprehensive mitochondrial optimization system. Integration of Deuterium-Depleted Water (Litewater, 10 ppm) — explanation of how lowering deuterium enhances ATP production, redox efficiency, and longevity potential. NMN Upgrade (10× Increase) — new 100 mg per serving dosage for boosting NAD⁺ levels, mitochondrial biogenesis, DNA repair, and energy metabolism. Addition of Taurine (100 mg per serving) — supports membrane integrity, calcium balance, ROS buffering, and cellular longevity signaling. Enhanced Colloidal Gold & Silver (50 % Increase) — improved redox stability, electron flow, and photodynamic synergy with methylene blue and red light. Refined Wu Jin Sun Fulvic Acid (−40 %) — optimizes redox balance and mineral transport while improving synergy between all active compounds. Comprehensive Mitochondrial Benefits — improved ATP efficiency, autophagy, and mitochondrial biogenesis for cleaner, more resilient energy production. New Product Lineup — introduction of BioBlue Lite and BioBlue Leuco Lite (simplified methylene blue + water versions) for accessible mitochondrial support. Key Quotes from Dr. Mike   “Deuterium-depleted water doesn't just make the mitochondria go faster—it helps them run truer, cleaner, and more efficiently.”   “We've moved BioBlue from a trace metabolic nudge to a real mitochondrial optimization protocol that supports redox cycling, biogenesis, and longevity pathways in a quantifiable way.”   “Taurine turns BioBlue from a fast-acting energy compound into a cellular longevity stack—supporting repair, recycling, and resilience.”   “By increasing colloidal gold and silver within their optimal bio-signal zones, BioBlue transforms from a chemical redox supplement into a biophysical energy transducer.”   “Each change — from Litewater to taurine — was made to help your mitochondria run longer, cleaner, and more accurately. This is longevity through bioenergetics.” Episode Timeline 00:00 – Announcements: Pre-Black Friday + new website 04:00 – The origin of BioBlue and its evolution 10:00 – Introducing the upgraded BioBlue formula 11:00 – Why BioLight partnered with Light Water 12:00 – How deuterium slows mitochondrial ATP production 17:00 – Functional benefits of deuterium-depleted water 19:00 – 10x increase in NMN for energy and repair 27:00 – Synergy between NMN and methylene blue 30:00 – Adding taurine for stability and longevity 39:00 – Increasing colloidal gold for photonic synergy 46:00 – Boosting colloidal silver for redox protection 52:00 – Why lowering fulvic acid improves coherence 56:00 – What's next: BioBlue Light + legacy pricing offer 01:02:00 – Dr. Mike's closing thoughts on mitochondrial optimization Resources & References Deuterium Depletion and Mitochondrial Efficiency Boros, L. G. Deuterium Depletion and Cellular Bioenergetics. Frontiers in Oncology (2020). Sagalevsky, V. — Light Water: The Science of Deuterium-Depleted Hydration (interview referenced in episode).   Nicotinamide Mononucleotide (NMN) & NAD⁺ Metabolism Mills, K. F. et al. Long-term administration of NMN mitigates age-associated physiological decline in mice. Cell Metabolism (2016). Yoshino, J. et al. NAD⁺ intermediates: The biology and therapeutic potential of NMN and NR. Cell Metabolism (2018).   Taurine and Longevity Pathways Wang, W. et al. Taurine deficiency as a driver of aging. Science (2023). Schaffer, S. W. et al. Physiological roles of taurine in the heart and mitochondria. Journal of Biomedical Science (2010).   Colloidal Gold & Silver in Cellular Redox Systems Li, Y. et al. Gold nanoclusters enhance mitochondrial cytochrome c oxidase activity. ACS Nano (2019). Kim, Y. S. et al. Silver nanoparticles exhibit SOD- and catalase-like activity for redox modulation. Nano Research (2020).   Fulvic & Humic Acids as Bioactive Redox Modulators   Senesi, N. Nature of humic substances and their interactions with trace metals and organics in the environment. Soil Science (1992). Wu Jin San extract — traditional Chinese “gold medicine” formulation known for enhanced mineral transport and detoxification support.     Additional Mentions PGC-1α, SIRT1/SIRT3, and Autophagy pathways in mitochondrial biogenesis and longevity. Quantum redox coupling and plasmonic resonance as mechanisms for light-driven bioenergetic optimization.  

Send us a textHave you ever wondered what happens inside your body when you don't eat for a while — when you give yourself space between meals? In this week's episode of Project Weight Loss, we explore that quiet magic with the story of Nobel Laureate Maester Yoshinori Ohsumi, whose discovery of autophagy — the body's natural process of self-cleaning and renewal — changed how we understand health, vitality, and longevity. From his humble lab in Japan to the moment he glimpsed a new world under the microscope, Ohsumi's curiosity reveals how our bodies are wired to restore themselves, especially in moments of pause.We'll talk about how autophagy connects to fasting, weight management, brain health, and aging — and why giving your body a little space to “dine in” can make such a difference. You'll hear about Ohsumi's groundbreaking experiments, his partnership with his wife and collaborator Mariko Ohsumi, and how their discoveries invite us to see self-renewal as a natural rhythm of life. I'll also link this episode to my earlier one on the Blue Zones — where long-living communities show us what it means to live in harmony with our biology. Listen in, reflect, and maybe even give your body that gentle reset it's been asking for.Quote of the Week:“We are wired for feast and famine, not feast, feast, feast.” — Dr. Jason FungListen to my related episode: The Blue Zones: The Secrets to Living Citations1.    Ohsumi, Y. (2014). Historical landmarks of autophagy research. Cell Research, 24(1), 9–23. https://doi.org/10.1038/cr.2013.1692.    Mizushima, N., & Ohsumi, Y. (2002). Autophagy: Molecular machinery for self-eating. Cell, 120(4), 639–652.3.    Kaushik, S., & Cuervo, A. M. (2018). The coming of age of chaperone-mediated autophagy. Nature Reviews Molecular Cell Biology, 19(6), 365–381.4.    Madeo, F., Zimmermann, A., Maiuri, M. C., & Kroemer, G. (2015). Essential role for autophagy in life span extension. Journal of Clinical Investigation, 125(1), 85–93.5.    Longo, V. D., & Panda, S. (2016). Fasting, circadian rhythms, and time-restricted feeding in healthy lifespan.Cell Metabolism, 23(6), 1048–1059.6.    Fung, J. (2016). The Obesity Code: Unlocking the Secrets of Weight Loss. Greystone Books.Let's go, let's get it done. Get more information at: http://projectweightloss.org

Today, we'll examine an important debate in nutrition: whether skipping breakfast or skipping dinner is more effective for your health and metabolism. We'll unpack what the research says, how your body's internal clock affects metabolism, and why the timing of your last meal can make or break your weight loss—especially if you're on a GLP-1 medication like semaglutide, dual GIP/GLP-1 like tirzepatide, or triple agonist like retatrutide. If you want to support what we do, head over to our Partners Page. You'll find some amazing brands we trust—and by checking them out, you're helping us keep the podcast going. https://pepties.com/partners/ Let's get into it. Circadian Rhythms and Eating Windows Our bodies are wired to follow a circadian rhythm—a 24-hour cycle that controls hormones like melatonin, cortisol, and insulin. One key thing to understand is that your body follows the rhythm of the day. When it's light out, you're naturally wired for activity—your metabolism is active, digestion works efficiently, and your body is more sensitive to insulin. As daylight fades, melatonin levels rise, signaling it's time to slow down, rest, and prepare for sleep. Here's the kicker: melatonin doesn't just make you sleepy—it also reduces insulin sensitivity. That means when you eat late at night—say at 8 or 9pm—your body doesn't handle sugar or calories as well. Instead of using that energy, you're more likely to store it as fat. So, a meal at 5pm when it's still light out? Your body's insulin response is stronger. You burn and use more of what you eat. But a meal at 9pm in the dark? Your body's gearing up for sleep, not digestion. Calories from that meal are more likely to go into fat storage. Breakfast vs. Dinner Skipping—What the Data Says Let's talk about what the research shows when it comes to skipping breakfast versus skipping dinner. Several studies have looked at early time-restricted feeding, where you eat earlier in the day, like between 8 a.m. and 4 p.m., versus eating later, where you skip breakfast and stretch meals into the evening. One of the most cited studies, published in Cell Metabolism. The study looked at men with prediabetes who followed an early time-restricted feeding schedule for five weeks. Even though they didn't lose weight, they had significant improvements in insulin sensitivity, blood pressure, and markers of oxidative stress compared to those eating over a twelve-hour window. The takeaway? Eating earlier in the day improved metabolic function even without reducing calories. Another study found that early eaters experienced lower evening hunger and better fat oxidation, meaning their bodies were burning fat more efficiently. By contrast, those eating later in the day had higher insulin and glucose levels after meals, signaling greater insulin resistance. And more broadly, research consistently shows that eating late at night, especially after seven or eight in the evening, is linked to increased body fat and higher risks of obesity and type 2 diabetes. The reason is straightforward: insulin sensitivity drops as the day goes on, so your body is less efficient at processing glucose at night, and those late calories are more likely to be stored as fat, especially around the belly. So while skipping breakfast might be easier for some people, from a metabolic standpoint, skipping dinner—or at least finishing it earlier—tends to be more beneficial. This connects directly to why fasting works for weight loss. Fasting gives your insulin a chance to drop, which signals your body to tap into stored fat for energy. Front-loading your meals earlier in the day aligns with your body's natural rhythm: insulin sensitivity is higher, digestion is more efficient, and your body has more opportunity to burn fat overnight. People who eat earlier often report feeling more energized, less hungry in the evening, and sleeping better—all key factors in long-term weight control. Now, if you're taking medications like semaglutide, tirzepatide, or retatrutide, timing becomes even more important. These drugs slow gastric emptying, which helps you feel full longer but also means that eating a large dinner late at night can lead to bloating, nausea, heartburn, and in turn, poor sleep. Digestion naturally slows down as melatonin rises and your body prepares for sleep, so combining a late meal with slower gastric emptying can make it harder for your body to rest and burn fat overnight. A good rule is to finish your last meal two to three hours before bed, ideally around five or six in the evening. This gives your body time to digest, allows insulin levels to drop, and lets you switch into fat-burning mode. What's the counter argument? Of course, it's important to remember that meal timing isn't one-size-fits-all. While the research often favors early eating, some people naturally aren't hungry in the morning, and skipping breakfast can actually be a helpful way to stick to a fasting window.  Then there are the “night owls.” Some people's circadian rhythms naturally shift later, and for them, eating later may actually align better with their biology. Forcing an early eating schedule might leave them tired, hungry, or unable to stick with it, which can actually be counterproductive for metabolic health. Research on chronotypes—the natural variations in our sleep-wake cycles—suggests that what works for a morning person might not work for someone who thrives later in the day. Practical lifestyle factors also play a role. Work schedules, family dinners, or social events can make it hard to consistently finish dinner at five or six in the evening. For some, a slightly later meal, if it's balanced and nutrient-dense, can be more sustainable over the long term than forcing an early window and ending up snacking late anyway. Finally, metabolic flexibility matters. Some people can handle a later meal without negative effects on fat storage, insulin sensitivity, or sleep, especially if the meal is lighter or focused on protein and vegetables. The bottom line is that while early eating has clear metabolic advantages for many, especially those taking weight loss medications like tirzepatide, the most important factors are consistency, total calories, and the quality of your food, not just the exact timing. So, whether you're a morning eater, a night owl, or somewhere in between, finding an approach that fits your body and lifestyle—and that you can stick to long term—is often more important than following a strict rule about skipping breakfast or dinner. Thanks for listening to The Peptide Podcast. If today's episode resonated, share it with a friend, please share this episode! Until next time, be well, and as always, have a happy, healthy week.

In this solo episode, Darin pulls back the curtain on one of the most important parts of his life:  he prepares for travel. From the supplements that keep his immune system strong to hydration hacks, adaptogenic elixirs, and EMF protection, this episode is a masterclass in staying grounded and resilient on the road. Travel doesn't have to destroy your health — it can actually elevate it. With a few intentional rituals, smart packing, and awareness, you can turn every trip into an opportunity to deepen your energy, focus, and connection to yourself. What You'll Learn 00:00:00 – Why travel is stressful and how to transform it into an empowering, health-boosting experience 00:01:00 – Darin's supplement protocol: Vitamin D3/K2, probiotics, zinc, vitamin C, and glutathione for immune defense 00:03:00 – The antioxidant power of glutathione and why it's critical for long flights and radiation exposure 00:04:30 – How CBD and terpenes support stress resilience and circadian rhythm through the endocannabinoid system 00:05:20 – Why magnesium and NAD are the unsung heroes of travel recovery and energy 00:06:30 – Darin's morning elixir recipe: cacao, guarana, ashwagandha, chaga, ginseng, and monk fruit 00:08:00 – Hydration 101: how to use a manual RO filter, mineralize your water, and ditch plastic 00:10:00 – How to build nutrient density into travel days using chlorella, spirulina, Shakeology, and Barukas 00:12:00 – Travel nutrition sovereignty: packing your own snacks, fasting, and avoiding airline food 00:14:00 – Movement anywhere: Darin's “portable gym” using bungee cords and bodyweight routines 00:16:00 – The 3-hour morning ritual: NewCalm, Healing Codes, journaling, cacao, red light therapy, and breathwork 00:20:00 – How to avoid radiation scanners, mitigate EMFs, and use WaveGuard for energy field protection 00:22:00 – Why Darin microdoses nicotine for cognitive focus and immune modulation 00:23:00 – Breathing practices for immune strength: 3–4 rounds of 40 deep breaths, Wim Hof style 00:24:00 – How to pack fruit and salads in mason jars to stay hydrated and nourished on planes 00:26:00 – Grounding after flights: barefoot on the earth, morning sunlight, and re-aligning your circadian rhythm Thank You to Our Sponsors Manna Vitality: Go to mannavitality.com/ or use code DARIN20 for 20% off your order. Fatty15: Get an additional 15% off their 90-day subscription Starter Kit by going to fatty15.com/DARIN and using code DARIN at checkout. Find More from Darin Olien: Instagram: @darinolien Podcast: SuperLife Podcast Website: superlife.com Book: Fatal Conveniences Key Takeaway “Preparation is sovereignty. When you take responsibility for your nutrition, your hydration, and your energy before you travel, you're no longer surviving the trip — you're expanding through it.” Bibliography Martineau AR et al. Vitamin D supplementation to prevent acute respiratory infections: systematic review. BMJ. 2017. Goldenberg JZ et al. Probiotics for prevention of respiratory infections. Cochrane Database. 2017. Hemilä H. Vitamin C and zinc in common cold. Nutrients. 2017. Blessing EM et al. Cannabidiol as a potential treatment for anxiety disorders. Neurotherapeutics. 2015. Morris HJ et al. Spirulina and chlorella as functional foods. Nutrients. 2022. Longo VD, Panda S. Fasting, circadian rhythms, and time-restricted feeding. Cell Metabolism. 2016. Booth FW et al. Waging war on physical inactivity. J Physiol. 2017. Balmori A. Electromagnetic pollution from radiofrequency fields. Pathophysiology. 2015. Kox M et al. Voluntary activation of sympathetic nervous system and attenuation of the innate immune response. PNAS. 2014.

Send us a textThis week we're tackling a food we all know and love: flour. But is it really as harmless as it seems? Join me as I break down the surprising science of refined flour, cravings, and hormones—plus how a few small shifts can help you take back control of your weight loss journey.We'll talk about why flour is classified as an ultra-processed food, how it hijacks hunger signals, and why it can make weight loss feel harder than it should. Don't worry, I'll make it simple, light, and easy to understand—because this is about living your best life, not stressing over bread.Quote of the Week:“Your body is your home—feed it with care.” – Unknown Citations:Monteiro et al., 2019 – Ultra-processed foods: What they are and how to identify them. Public Health Nutrition.Hall et al., 2019 – Ultra-processed diets cause excess calorie intake and weight gain. Cell Metabolism.Ludwig, 2002 – The glycemic index: Physiological mechanisms relating to obesity, diabetes, and cardiovascular disease. JAMA.Friedman, 2014 – Leptin and the regulation of body weight. American Journal of Clinical Nutrition.Volkow et al., 2013 – The addictive dimensionality of obesity. Biological Psychiatry.Slavin, 2013 – Fiber and prebiotics: Mechanisms and health benefits. Nutrients.Hu, 2011 – Globalization of diabetes: The role of diet, lifestyle, and genes. Diabetes Care.ADA, 2020 – Standards of medical care in diabetes—2020. Diabetes Care.Let's go, let's get it done. Get more information at: http://projectweightloss.org

It's In the News.. a look at the top headlines and stories in the diabetes community. This week's top stories: CRISPR modified cell transplant for type 1, risk of T1D if parent has a different type of diabetes, Metformin and the brain, oral GLP-1, and more! Find out more about Moms' Night Out  Please visit our Sponsors & Partners - they help make the show possible! Learn more about Gvoke Glucagon Gvoke HypoPen® (glucagon injection): Glucagon Injection For Very Low Blood Sugar (gvokeglucagon.com) Omnipod - Simplify Life Learn about Dexcom   Check out VIVI Cap to protect your insulin from extreme temperatures The best way to keep up with Stacey and the show is by signing up for our weekly newsletter: Sign up for our newsletter here Here's where to find us: Facebook (Group) Facebook (Page) Instagram Twitter Check out Stacey's books! Learn more about everything at our home page www.diabetes-connections.com  Reach out with questions or comments: info@diabetes-connections.com Episode transcription with links: Hello and welcome to Diabetes Connections In the News! I'm Stacey Simms and every other Friday I bring you a short episode with the top diabetes stories and headlines happening now. XX A 42-year-old man who has lived most of his life with type 1 diabetes has become the first human to receive a transplant of genetically modified insulin-producing cells. This marks the first pancreatic cell transplant in a human to sidestep the need for immunosuppressant drugs. “This is the most exciting moment of my scientific career,” says cell biologist Per-Ola Carlsson of Uppsala University in Sweden, who helped develop the procedure. The new treatment, he says, “opens the future possibility of treating not only diabetes but other autoimmune diseases.” This procedure uses the gene editing technique, CRISPR, to discourage the auto immune attack on the donor cells. Before the transplant, the participant had no measurable naturally produced insulin and was receiving daily doses of the hormone. But within four to 12 weeks following the transplant, his levels rose slightly on their own after meals—showing that the new beta cells were releasing some insulin in response to glucose. even though the new study is promising, it involved just one participant and is therefore preliminary. And longer-term monitoring is needed to confirm the therapy's safety before it can be offered to more people. She also notes that the injected cells produced only 7 percent of the insulin needed for a person to be fully independent of additional medication. The researchers supplied the recipient with insulin doses to maintain healthy blood sugar levels. While Herold thinks it's still too early to consider this approach for a cure, “these options are now here to change the disease in ways that have never been possible before,” he says. “There's tremendous hope.” https://www.scientificamerican.com/article/type-1-diabetes-patients-insulin-production-restored-with-new-cell/ XX   This one is interesting… a recent study shows that children of mothers with gestational diabetes or fathers with type 2 diabetes have higher chances of developing type 1 diabetes than kids whose parents do not have any type of diabetes. Specifically, the study found that children whose mothers had gestational diabetes during pregnancy were 94% more likely to develop type 1 diabetes compared to children of mothers without diabetes. Similarly, having a father with type 2 diabetes was linked to a 77% higher risk. The study also suggests a possible link between maternal type 2 diabetes and type 1 diabetes in children, although more data are needed to confirm whether the risk is real.   "What is interesting is that type 1 diabetes is a disease of lack of the hormone insulin while gestational diabetes and type 2 diabetes stem mostly from the body's resistance to the hormone. What may be happening is that genes, environments and behaviors that create insulin resistance may also, in some cases, trigger the immune reactions that lead to type 1 diabetes," adds Dr. Dasgupta. A 2019 meta-analysis by researchers at Soochow University in China found that gestational diabetes was linked to a 66% higher risk of type 1 diabetes in children. This new study, which includes more than twice as many studies, offers a robust synthesis of current evidence and shows the risk is even greater than previously estimated. It is also the first meta-analysis to examine the link between paternal type 2 diabetes and type 1 diabetes in offspring. "Several mechanisms may be at play. Families often share lifestyle and eating habits, which can raise the likelihood that children will be affected. But beyond that, high blood sugar levels may also cause biological changes in parents that could increase their children's risk of developing type 1 diabetes," explains Laura Rendon, co-first author of the study, who completed an MSc in experimental medicine at The Institute and, as someone living with type 1 diabetes herself, finds deep personal meaning in conducting this research. For instance, the authors suggest that high blood sugar during pregnancy may stress the fetus's insulin-producing beta cells, reducing their number at birth or making them more vulnerable to damage later in life. It may also trigger epigenetic changes—modifications to proteins and molecules attached to DNA—that increase the risk. Likewise, high blood sugar in fathers with type 2 diabetes may cause epigenetic changes in their sperm, potentially influencing their child's risk of developing type 1 diabetes. https://medicalxpress.com/news/2025-08-diabetes-children-linked-parents.html XX Can a CGM help you lose weight? The company Signos is banking on it – the just got FDA approval for their system, which uses the over the counter Dexcom Stelo. The claim here is that the system will help track how food choices, activity, stress and sleep can all affect metabolism. Signos also works in partnership with the digital nutrition counseling startup Nourish. It currently offers a quarterly subscription plan, including six CGM sensors, for $139 per month. And they tell you don't take any medical actions based on the app's output without consulting a physician. https://www.fiercebiotech.com/medtech/fda-clears-signos-over-counter-cgm-powered-weight-loss-app XX Good news for T1D1, a free mobile app that helps people calculate insulin doses, track daily data, and share insights with healthcare providers. After being pulled off the market with similar apps a few years ago, it's now back and FDA approved. Drew Mendelow created the app after his diagnosis at age 13. He came on the show last year and I'll link his story up in the show notes. Diabetes Center Berne provided the initial funding to support the T1D1 efforts to redesign the app per FDA standards.  Comerge AG , the registered manufacturer, enlisted a team of software engineers, regulatory experts, and design professionals to ensure T1D1 was FDA-ready. Dexcom graciously conducted the Human Factors study to ensure safety and accuracy.  ​ ​T1D1 is now FDA-cleared as a Class II medical device and is the first over-the-counter insulin calculator cleared for individuals aged 2 and older. T1D1 is expected to be live in the AppStore and Google Play Store by October 2025. https://diabetes-connections.com/the-fda-took-down-this-teens-free-bolus-calculator-he-needs-your-help-to-bring-it-back/ XX Metformin has been the standard treatment for type 2 diabetes for more than six decades, yet scientists still do not fully understand how it works. A team from Baylor College of Medicine, working with international collaborators, has now identified an unexpected factor in its effectiveness: the brain. Their findings reveal a brain pathway involved in metformin's glucose-lowering action, pointing to new strategies for treating diabetes with greater precision. The study was published in Science Advances. The researchers concentrated on a small protein called Rap1, located in a region of the brain known as the ventromedial hypothalamus (VMH). They discovered that metformin's ability to lower blood sugar at clinically relevant doses depends on suppressing Rap1 activity in this brain area.   “This discovery changes how we think about metformin,” Fukuda said. “It's not just working in the liver or the gut, it's also acting in the brain. We found that while the liver and intestines need high concentrations of the drug to respond, the brain reacts to much lower levels.”     https://scitechdaily.com/after-60-years-scientists-uncover-hidden-brain-pathway-behind-diabetes-drug-metformin/   XX Looks like GLP-1 pills are moving ahead. Lilly says it's version helped overweight adults with type 2 lose 10% of their body weights and lower A1C. Just two weeks ago, we were talking about how the same drug in people without diabetes had less than the stellar expected results. Orforglipron is a small-molecule pill that is easier to manufacture and package than wildly popular injectable drugs for obesity, such as Lilly's Zepbound and Novo Nordisk's NOVOb.CO rival treatment Wegovy, which are peptide mimics of the appetite-controlling GLP-1 hormone. In the 72-week study of more than 1,600 overweight or obese adults with type 2 diabetes, those who received the 36-milligram highest dose of orforglipron on average shed 10.5% of their weight, or about 23 pounds (10.43 kg), versus 2.2% for those who received a placebo, achieving the main goal of the trial. Patients on the lowest 6 mg dose of the Lilly drug lost 5.5% of their weight. https://www.usatoday.com/story/news/health/2025/08/26/lilly-glp-1-pill-weight-loss/85830686007/ XX     An intervention that combined a low-calorie Mediterranean diet and exercise led to less diabetes incidence in older adults. Men had a greater diabetes risk reduction with the intervention than women. The study was based in Spain, and the diet may not be as easy to adhere to in the U.S. Among nearly 5,000 adults with metabolic syndrome and overweight or obesity in the PREDIMED-Plus trial, those who followed this intervention had a 31% lower risk for type 2 diabetes over 6 years relative to those who received only ad libitum Mediterranean diet advice (aHR 0.69, 95% CI 0.59-0.82). the Mediterranean diet focuses on high intake of plant-based foods, moderate consumption of fish, poultry, and dairy with optional red wine, and low intake of red meats, sweets, and sugar-sweetened beverages. Common foods featured in the diet include extra-virgin olive oil, fruits, vegetables, legumes, nuts, and whole grains. However, Sharon Herring, MD, MPH, and Gina Tripicchio, PhD, MSEd, both of Temple University in Philadelphia, pointed out that this study was conducted solely in Spain, and sticking to this type of diet may be more challenging in countries like the U.S.   "Participants in the study received extra-virgin olive oil to support adherence and retention; in the United States, prices of extra-virgin olive oil have nearly doubled since 2021 due to a combination of factors including climate change, rising production costs, supply chain disruptions, and now tariffs," they noted in an accompanying editorial. "[T]he large number of dietitian contacts during the study may prove difficult to scale broadly in the United States given challenges with health care access and reimbursement for prevention services."         https://www.medpagetoday.com/primarycare/diabetes/117151 XX A group of Canadian researchers has identified an unexpected way to lower blood sugar and protect the liver: by capturing a little-known fuel produced by gut bacteria before it enters the body and causes harm. The findings, published in Cell Metabolism, could open the door to new therapies to treat metabolic diseases like type 2 diabetes and fatty liver disease. Scientists from McMaster University, Université Laval, and the University of Ottawa discovered that a molecule generated by gut microbes can cross into the bloodstream, where it drives the liver to overproduce glucose and fat. By designing a method to trap this molecule in the gut before it reaches circulation, they achieved striking improvements in blood sugar regulation and fatty liver disease in obese mice. https://scitechdaily.com/scientists-discover-a-surprising-new-way-to-fight-diabetes/ XX Dexcom, which specializes in technology for glucose biosensing, will lay off 350 workers, with nearly 200 of them in San Diego, according to the San Diego Union Tribune. The bulk of the local jobs being lost are focused on Dexcom operations and manufacturing. The Dexcom development follows cutbacks to Verily, a life sciences company that is a subsidiary of Alphabet, Google's corporate parent. Verily's work included a project with Dexcom on wearable glucose sensors. CEO Stephen Gillett, in a memo obtained by the publication, said there will be “workforce reductions across Verily.” A representative for Verily confirmed to Business Insider that “we have made the difficult decision to discontinue manufacturing medical devices and will no longer be supporting them going forward.” https://timesofsandiego.com/business/2025/08/27/report-life-sciences-firm-dexcom-lay-off-200-san-diego-workers/ XX Front office changes at Insulet. Eric Benjamin, former chief product and customer experience officer, will take the role of chief operating officer, effective immediately. Manoj Raghunandanan Mu-NOHJ Rug-a-nun-da-nun to the position of chief growth officer, leading Insulet's new growth organization. The appointments are some of CEO Ashley McEvoy's first changes since she was hired in April. The appointments come after McEvoy outlined four priorities for Insulet on an August earnings call:   enhancing the company's commercial capabilities, building Insulet's brand and direct-to-consumer capabilities, driving growth outside of the U.S. and accelerating the pace of innovation. https://www.medtechdive.com/news/insulet-eric-benjamin-manoj-raghunandanan-appointments/758668/ XX   XX Want to highlight The Children's Diabetes Foundation in Colorado – they held a medal ceremony for patients of the Barbara Davis Center who've lived with Type 1 diabetes for 50 years or more. There were 87 medal recipients in the ceremony including Dana Davis, Executive Director of the Children's Diabetes Foundation and the daughter of the founders of the Barbara Davis Center. Davis shared: "When you got Type1 diabetes in the 70s, they thought you shouldn't have children. They thought you weren't going to live past 30 or 40. It was definitely very different," Davis said.   https://www.cbsnews.com/colorado/news/barbara-davis-center-celebrates-colorado-type-1-diabetes-patients-milestone/

We all want more energy — but what if your fatigue isn't about sleep, diet, or exercise at all? In this solo episode, Darin O'Lien uncovers the invisible drains on your vitality that most people never notice. From blue light to toxic relationships, hidden mold, micro-stress loops, EMF exposure, and even unresolved trauma stored in your body, Darin reveals how your life force is being stolen — and how to take it back. You'll learn the overlooked ways your time, attention, and biology are constantly depleted — and the exact SuperLife Energy Seal Protocol Darin uses to plug those leaks, reclaim his vitality, and live fully charged.     What You'll Learn in This Episode 00:00 – Introduction & Episode Overview Darin introduces the concept of hidden energy leaks and why most fatigue isn't just about lack of sleep. 03:05 – Energy Deposits vs. Withdrawals How every interaction, choice, and environment either builds or depletes your life force. 04:33 – The Overlooked Energy Drains The most common — and invisible — ways energy slips away without your awareness. 06:58 – Blue Light & Circadian Rhythm Disruption The science of how nighttime screen use suppresses melatonin and wrecks your sleep quality. 09:06 – Ultra-Processed Foods & Energy Impact Why “dead calorie” foods cause fatigue and how to build an energy-supportive plate. 11:33 – Hydration & Water Quality Why dehydration is the #1 cause of fatigue, and the importance of filtering and mineralizing your water. 15:06 – Micro-Stress Loops & Mental Background Apps How unresolved thoughts quietly drain your energy — and how to shut them down. 17:28 – Toxic Relationships & Social Friction The measurable toll hostile interactions take on your health and recovery. 19:10 – Indoor Air Quality & Mold Exposure How unseen environmental toxins mimic chronic fatigue symptoms. 21:27 – EMF Exposure & Device Overload The overlooked stressor disrupting your sleep, nervous system, and cellular health. 23:14 – Stillness Breaks & Nature Time The proven stress-relieving effects of short nature “pills” and mindfulness pauses. 25:41 – Past Trauma & Recapitulation How unresolved experiences trap your life force — and the Toltec method to reclaim it. 30:39 – The SuperLife Energy Seal Protocol Darin's complete daily checklist to stop leaks and recharge vitality. 33:08 – Darin's Daily Rituals How he integrates energy-protective practices into his everyday life. 35:33 – Closing Thoughts Why energy isn't something you gain — it's what's left when you stop the leaks.     Thank You to Our Sponsors: Fatty15: Get an additional 15% off their 90-day subscription Starter Kit by going to fatty15.com/DARIN and using code DARIN at checkout. Therasage: Go to www.therasage.com and use code DARIN at checkout for 15% off     Find More from Darin Olien: Instagram: @darinolienPodcast: superlife.com/podcastsWebsite: superlife.comBook: Fatal Conveniences     Key Takeaway "Energy isn't something you get — it's what remains when you stop the leaks."      Bibliography · Chang AM et al. Evening use of light-emitting eReaders… PNAS, 2015. · Hall KD et al. Ultra-processed diets cause excess calorie intake… Cell Metabolism, 2019. · Ganio MS et al. Mild dehydration impairs vigilance… Br J Nutr, 2011. · McEwen BS. Allostatic load and stress physiology. Ann NY Acad Sci, 1999. · Kiecolt-Glaser JK et al. Hostile behavior slows wound healing… Arch Gen Psychiatry, 2005. · CDC/NIOSH. Health problems in damp buildings. · Satish U et al. CO₂ and decision-making. Environ Health Perspect, 2012. · WHO. Electromagnetic fields and public health. · Hunter MCR et al. Nature pill and stress relief. Front Psychol, 2019. · Levine P. Somatic experiencing and trauma discharge. PubMed, 2012. · · Somatic trauma & release: Levine P. Waking the Tiger; “Trauma creates a permanent imprint… the body can be retrained to discharge it.” (pubmed.ncbi.nlm.nih.gov) · · Recapitulation (Toltec lineage): Ruiz DM. The Four Agreements; narrative recounting as energy reclamation. (Ancestral wisdom, narrative psychology) · · Narrative therapy integration: White M. “Externalizing the problem, reclaiming identity.” (Case-based evidence, therapeutic outcomes) · · (And prior citations as listed—circadian, UPF, hydration, air, mindfulness, social, EMF, stillness—remain intact.)

Welcome to Ozempic Weightloss Unlocked, where we break down the latest science, headlines, and real world experiences around semaglutide, known by many as Ozempic and Wegovy.Here is what is new. Medical News Today reports on a fresh Cell Metabolism study in mice suggesting lean mass loss with Ozempic may be smaller than feared, about ten percent of lean mass during weight loss, with much of the change coming from organs like the liver rather than skeletal muscle. Researchers also noted some muscles maintained size while strength could still dip, underscoring the need for human trials to clarify muscle function during treatment. That is according to Medical News Today and University of Utah Health coverage of the same research.University of Utah Health explains that the liver in mice shrank by nearly half during weight loss, which can be part of healthy metabolic improvement, and that some reduction in skeletal muscle may reflect a return to baseline as body fat drops. Their message is clear. We need rigorous human studies to confirm how size and strength change in different muscles and what training and protein strategies best protect function during treatment.What about long term weight outcomes in the real world. A new analysis in the journal Advances in Therapy shows that around half of patients on semaglutide 2.4 milligrams achieved at least twenty percent weight loss at 18 to 24 months, pointing to meaningful, sustained results for many patients outside trials. That is according to Springer Nature's publication of the real world study.Stopping medication remains a pivotal issue. ScienceDaily reports on a meta analysis in BMC Medicine across 11 trials showing weight regain commonly begins about eight weeks after stopping anti obesity medications, including glucagon like peptide one drugs, and continues for several months before leveling off. The extent of regain varies by drug and by lifestyle consistency, but the pattern is widespread. One tirzepatide study found participants regained nearly half of the lost weight after switching to placebo. This highlights the importance of long term plans, whether continued medication, step down dosing, or robust nutrition, activity, sleep, and support.The pipeline is active. Fierce Biotech reports Eli Lilly's oral glucagon like peptide one candidate orforglipron achieved about twelve percent average weight loss in phase three, less than injectable rivals but with the convenience of a pill. Meanwhile, new semaglutide dosing research from Novo Nordisk's program suggests higher weekly doses like seven point two milligrams can approach or surpass twenty percent average loss at 72 weeks, adding competitive pressure and new options if approved. These developments matter for access, costs, and matching the right person to the right therapy.Beyond weight, McGill University highlights growing evidence that glucagon like peptide one medicines may also help conditions like heart and kidney disease, fatty liver disease, sleep apnea, osteoarthritis, and even addiction. Their review in eClinicalMedicine stresses both promise and open questions, including long term safety signals like gallbladder disease, mood effects, and vision risks, plus the realities of cost and access.Here are practical takeaways for listeners. First, combine medication with protein forward eating and resistance training to protect strength while losing fat. Second, plan for maintenance early, since weight regain after stopping is common. Third, talk with a clinician about the full cardiometabolic picture, including blood sugar, cholesterol, blood pressure, and fatty liver markers. Fourth, keep an eye on emerging options, including oral therapies and dose optimization, which may broaden choices.That is it for today on Ozempic Weightloss Unlocked. Thank you for tuning in, and please subscribe so you never miss an update. This has been a quiet please production, for more check out quiet please dot ai. Some great Deals https://amzn.to/49SJ3QsFor more check out http://www.quietplease.ai

If you're anything like me, you've probably looked back and thought, “Why didn't I know this 10 years ago?” That's exactly what today's chat is about - my top five health game-changers I wish I had embraced earlier. Whether you're 25 or 75, these insights can shift the needle in how you feel, look, and thrive. From nutrition tracking without guilt to finally getting that high-quality protein in, these tips aren't about restriction - they're about empowerment. I'm opening up about what's worked, what didn't, and why strength training, ditching the processed stuff, and even allowing yourself to be hungry can be revolutionary. This one is packed with real-life examples, scientific backing, and simple steps to get started without getting overwhelmed. What we're tackling: Track your food with intention, not shame. Ditch skinny, build strong with progressive overload. Prioritize protein without obsessing. Phase out processed foods gradually. Embrace hunger and stop snacking aimlessly. Meditation App : Simply Being App Get Weekly Health Tips:  thrivehealthcoachllc.com Let's Connect:@‌ashleythrivehealthcoach or via email: ashley@thrivehealthcoachingllc.com Podcast Produced by Virtually You! Sources: Tracking Nutrition Burke, L. E., Wang, J., & Sevick, M. A. (2011). Self-monitoring in weight loss: A systematic review of the literature. Journal of the American Dietetic Association, 111(1), 92–102. https://doi.org/10.1016/j.jada.2010.10.008 Raber, M., Patterson, M., & Jia, W. (2021). A systematic review of the use of dietary self-monitoring in behavioral weight-loss interventions: Current practices and future recommendations. Public Health Nutrition, 24(17), 5885–5913. https://doi.org/10.1017/S1368980021002381 Prioritizing High-Quality Protein Holt, S. H. A., Brand Miller, J. C., Petocz, P., & Farmakalidis, E. (1995). A satiety index of common foods. European Journal of Clinical Nutrition, 49(9), 675–690. Ortinau, L. C., Culp, J. M., & Hoertel, H. A. (2014). Effects of high-protein vs. high-fat snacks on appetite control, satiety, and eating initiation in healthy women. Nutrition Journal, 13, 97. https://doi.org/10.1186/1475-2891-13-97 Dhillon, J., Craig, B. A., Leidy, H. J., Amankwaah, A. F., Jacobs, A., Jones, B. L., & Jones, J. B. (2016). The effects of increased protein intake on fullness: A meta-analysis and its limitations. Journal of the Academy of Nutrition and Dietetics, 116(6), 968–983. https://doi.org/10.1016/j.jand.2016.01.003 Zhu, R., et al. (2021). Effect of a high-protein, low-glycemic index diet on hunger and weight maintenance: Results from the PREVIEW study. Frontiers in Nutrition, 8, 649928. https://doi.org/10.3389/fnut.2021.649928 Strength Training vs. Cardio Saeidifard, F., Medina-Inojosa, J. R., West, C. P., & Lopez-Jimenez, F. (2019). The role of resistance training in the prevention and management of chronic disease. European Journal of Preventive Cardiology, 26(5), 505–515. https://doi.org/10.1177/2047487318822333 Momma, H., et al. (2022). Muscle-strengthening activities and risk of all-cause and cause-specific mortality: A systematic review and meta-analysis of cohort studies. British Journal of Sports Medicine, 56(10), 755–763. https://doi.org/10.1136/bjsports-2021-105061 Cutting Ultra-Processed Foods Monteiro, C. A., Cannon, G., Levy, R. B., Moubarac, J. C., Louzada, M. L., Rauber, F., ... & Jaime, P. C. (2019). Ultra-processed foods: What they are and how to identify them. Public Health Nutrition, 22(5), 936–941. https://doi.org/10.1017/S1368980018003762 Srour, B., et al. (2019). Ultra-processed food intake and risk of cardiovascular disease: Prospective cohort study (NutriNet-Santé). BMJ, 365, l1451. https://doi.org/10.1136/bmj.l1451 Mindful Hunger / Fasting Bruce, L. J., & Ricciardelli, L. A. (2016). A systematic review of the psychosocial correlates of intuitive eating among adult women. Appetite, 96, 454–472. https://doi.org/10.1016/j.appet.2015.10.012 Longo, V. D., & Panda, S. (2016). Fasting, circadian rhythms, and time-restricted feeding in healthy lifespan. Cell Metabolism, 23(6), 1048–1059. https://doi.org/10.1016/j.cmet.2016.06.001

Send us a textHey my beautiful friends –This week's conversation was sparked by a funny little tech discovery and a box I mailed — both of which got me thinking about food in a new way. You know how people are always quick to tell you what not to eat? Well, this week we flip the script. I'm sharing thoughts from my own journey and a coach that made me laugh and think — and you'll hear why his words still stick with me to this day. We're keeping things simple, kind, and grounded in something real. I'm not handing out rules, I'm sharing a mindset and maybe even a little inspiration for your next grocery run or packed lunch. And as always, we'll close with a little heart lift — this one from Michael Pollan, who said, “Eat food. Not too much. Mostly plants.”Come hang out with me, and let's talk about what loves us back. References:1.    Zhang & Talalay, Frontiers in Nutrition, 20232.    Liu, Nutrients, 20233.    Viguiliouk et al., Obesity Reviews, 20234.    Jenkins et al., AJCN, 20245.    Estruch et al., The Lancet Diabetes & Endocrinology, 20236.    Guasch-Ferré et al., BMJ, 20237.    Yao et al., Nutrients, 20238.    Harvard Nurses' Health Study Update, 20239.    Anderson et al., AJCN, 202410.Simopoulos, Frontiers in Endocrinology, 202311.Ye et al., Nutrients, 202312.Sonnenburg et al., Cell Metabolism, 202413.Mozaffarian et al., AJCN, 202314.Mastrocola et al., Appetite, 202315.Pollan, M. (2009). In Defense of FoodLet's go, let's get it done. Get more information at: http://projectweightloss.org

This episode reveals groundbreaking research from the Journal of Cell Metabolism showing that when you eat matters as much as what you eat for hunger control and fasting success. Dr. Scott and Tommy break down a study demonstrating that consuming 45% of daily calories at breakfast versus dinner dramatically reduces hunger and appetite without changing metabolism or weight loss. Learn why your physiology works against you when eating large evening meals, making it harder to close your eating window and stick to fasts. If you struggle with late-night cravings, can't seem to end your eating window, or find yourself breaking fasts in the evening, this episode provides the meal timing strategy to align your eating with your body's natural circadian rhythm for easier, more sustainable fasting. ⁠Take the NEW FASTING PERSONA QUIZ! - The Key to Unlocking Sustainable Weight Loss With Fasting!⁠⁠ Resources and Downloads: ⁠⁠SIGN UP FOR THE DROP OF THE ULTIMATE GUIDE TO BLOOD SUGAR CONTROL⁠⁠ ⁠⁠GRAB THE OPTIMAL RANGES FOR LAB WORK HERE! - NEW RESOURCE! - December 2024⁠⁠ ⁠⁠FREE RESOURCE - DOWNLOAD THE NEW BLUEPRINT TO FASTING FOR FAT LOSS!⁠⁠ ⁠⁠SLEEP GUIDE DIRECT DOWNLOAD⁠⁠ ⁠⁠DOWNLOAD THE FASTING TRANSFORMATION JOURNAL HERE!⁠⁠ Partner Links: Get your⁠⁠ FREE BOX OF LMNT⁠⁠ hydration support for the perfect electrolyte balance for your fasting lifestyle with your first purchase⁠⁠ here!⁠⁠ Get ⁠⁠30% off a Keto-Mojo⁠⁠ blood glucose and ketone monitor (discount shown at checkout)! ⁠⁠Click here!⁠⁠ Our Community: Let's continue the conversation. Click the link below to JOIN the ⁠⁠Fasting For Life Community⁠⁠, a group of like-minded, new, and experienced fasters! The first two rules of fasting need not apply! If you enjoy the podcast, please tap the stars below and consider leaving a short review on Apple Podcasts/iTunes. It takes less than 60 seconds, and it helps bring you the best original content each week. We also enjoy reading them! Article Links: https://www.cell.com/cell-metabolism/pdfExtended/S1550-4131(22)00344-8

Join our Patreon and get access to monthly bonus episodes and more nutriton content!Can fasting really slow aging? Does calorie restriction work for humans, or just for mice and yeast? And how much protein do you actually need to age well? This week on Your Diet Sucks, we break down the evidence behind the most talked-about interventions in the longevity space, what holds up under scrutiny, what doesn't, and why you might not need a supplement stack to live longer, and enjoy life. We dig into:The actual science on calorie restriction, fasting, and supplements—and where the evidence stopsWhat inflammation, oxidative stress, and telomeres have to do with how we ageThe best-researched dietary patterns for living longer (hint: it's not sexy, but it might include red wine)Why protein becomes more important as we ageThe difference between lifespan and healthspan, and why quality of life needs to be part of the conversation

In this episode of Hema Now, Jonathan Sackier is joined by John Riches, Clinical Reader in Cancer Immunometabolism at the Barts Cancer Institute and Honorary Consultant Haemato-oncologist. They explore how metabolic shifts drive lymphoma progression, the potential of immunotherapy, and what the future holds for treating lymphoid malignancies.  Timestamps:      00:00 – Introduction  01:46 – Riches' journey into haematology  03:42 – What is T cell exhaustion?  07:06 – The key role of metabolism in lymphoma  09:33 - Richter's syndrome  13:17 – Breakthroughs in immunotherapy  20:27 – The challenges of translational research  25:39 – B cells in autoimmune diseases  28:16 – The potential of breath biopsy  32:58 – Riches' three wishes for healthcare 

Follow us on Instagram @yourdietsuckspod!This week, Kylee and Zoë take a deep dive into ultra-processed foods: what they are, where they came from, how they're designed to light up your brain's reward systems, and what role they play in athletic nutrition. We talk about everything from cereal meant to prevent sinning to the low-fat diet craze, the war-time origins of shelf-stable food, and the engineering behind the foods that are hyper-palatable.We also get into the landmark NIH study that showed just how much processing—not just calories or macros—can influence how much we eat, how full we feel, and how our bodies respond to food. This episode is about helping you understand the systems at play, so you can make choices that support your health and performance without getting caught in fear or shame about the food you eat. Because when it comes to ultra-processed foods, context matters—especially for athletes.

In this eye-opening episode of the Better Than Before Breast Cancer Podcast, host Laura Lummer dives into the powerful connection between your body's natural rhythms and the timing of your meals. Have you ever noticed how aligned you feel when you live in sync with nature's cycles? Drawing from Ayurveda—an ancient system of medicine from India—and contemporary scientific research, Laura reveals how understanding your body's internal clock, or circadian rhythm, can significantly enhance your health, especially after breast cancer.   What You'll Discover in This Episode: A gentle introduction to Ayurveda and how this 5,000-year-old wisdom emphasizes living in harmony with Earth's natural cycles. Clear, practical explanations of circadian rhythm, metabolism, hormonal balance, and their critical roles in breast cancer recovery. How Ayurvedic principles align surprisingly well with modern Western nutritional science. The profound health benefits of aligning meal timing with daylight hours, including improved sleep, reduced inflammation, and optimized metabolism. Easy strategies to shift your eating patterns gently, starting with simple steps like adjusting dinner times.   Key Studies Referenced: JAMA Oncology Study:Catherine R. Marinac, Dorothy D. Sears, Lok-Hei Lam, Shirley W. Flatt, Loki Natarajan, Ruth E. Patterson; "Prolonged Nightly Fasting and Breast Cancer Prognosis." JAMA Oncology, 2016; Read the full study here.   Cell Metabolism Study: Emily N.C. Manoogian, Satchidananda Panda et al.; "Time-restricted eating improves cardiometabolic health in overweight individuals." Cell Metabolism, 2019; Explore the study here.   Listen in to explore: How simple shifts in meal timing can powerfully support your body's natural detoxification pathways and hormonal balance. The Ayurvedic recommendations for ideal meal times and how they beautifully complement modern scientific guidelines. Ways to incorporate a loving, compassionate mindset toward food, meal timing, and your body's natural rhythm.   This episode encourages you to foster a nurturing, compassionate relationship with your body by syncing your daily habits with the earth's rhythms, creating lasting health and harmony after breast cancer.   Connect with Laura: Visit The Breast Cancer Recovery Coach for personalized metabolic health coaching, mindset transformation, and guidance specifically tailored for breast cancer survivors. Enjoyed the episode?  Subscribe, leave a review, and share with friends who could benefit from this healing wisdom!  

NADs have been a hot topic lately when it comes to conversations regarding longevity and anti-aging. Today, Courtney Van Bussem, Biomedical Engineer and COO at Longevity Launch Labs, joins us to talk about cellular health, longevity pathways, and precursors to NADs.  Courtney Van Bussem: https://www.linkedin.com/in/courtneyvanbussum Longevity Launch Labs: https://longevitylaunch.com/ Where to find 1MNA: https://www.1mna.com/

Introducing Blood sugar hacks to give you more energy | Glucose Goddess Jessie Inchauspé and Prof. Tim Spector from ZOE Science & Nutrition.Follow the show: ZOE Science & Nutrition Why do some people feel fine eating lots of carbs when others feel energy slumps? Is blood sugar to blame?In this episode, we learn why blood sugar varies so much between people, and the tools to manage these levels. Tim Spector and Jessie Inchauspé (aka the Glucose Goddess) will discuss the latest science around glucose control, what the cool new device on the block – the CGM – can tell us and why blood sugar levels are only one part of the picture of our health.Jessie is a bestselling author and science communicator with a community of over 5 million followers. Tim is a professor of epidemiology at King's College London and ZOE's scientific co-founder.

Why do some people feel fine eating lots of carbs when others feel energy slumps? Is blood sugar to blame? In this episode, we learn why blood sugar varies so much between people, and the tools to manage these levels.  Tim Spector and Jessie Inchauspé (aka the Glucose Goddess) will discuss the latest science around glucose control, what the cool new device on the block – the CGM – can tell us and why blood sugar levels are only one part of the picture of our health. Jessie is a bestselling author and science communicator with a community of over 5 million followers. Tim is a professor of epidemiology at King's College London and ZOE's scientific co-founder.