Podcasts about clinical endocrinology

Credits: 0.25 AMA PRA Category 1 Credit™   CME/CE Information and Claim Credit: https://www.pri-med.com/online-education/podcast/frankly-speaking-cme-486 Overview: Optimizing diabetes management starts with choosing the right medication for the patient. Listen in as we discuss current prescribing recommendations, empowering you to confidently compare medication classes and select therapies that best fit individual patient needs—while prioritizing kidney protection to reduce the risk of long-term complications. Episode resource links: Jensen SK, Heide-Jørgensen U, Andersen IT, et al. SGLT2 Inhibitors vs GLP-1 Receptor Agonists for Kidney Outcomes in Individuals With Type 2 Diabetes. JAMA Intern Med. Published online January 20, 2026. doi:10.1001/jamainternmed.2025.7409 Samson SL, et al. American Association of Clinical Endocrinology consensus statement: comprehensive type 2 diabetes management algorithm—2023 update. Endocr Pract. 2023;29(5):305-340. Guest: Jillian Joseph, MPAS, PA-C   Music Credit: Matthew Bugos Thoughts? Suggestions? Email us at FranklySpeaking@pri-med.com  The views expressed in this podcast are those of Dr. Domino and his guests and do not necessarily reflect the views of Pri-Med.

Credits: 0.25 AMA PRA Category 1 Credit™   CME/CE Information and Claim Credit: https://www.pri-med.com/online-education/podcast/frankly-speaking-cme-486 Overview: Optimizing diabetes management starts with choosing the right medication for the patient. Listen in as we discuss current prescribing recommendations, empowering you to confidently compare medication classes and select therapies that best fit individual patient needs—while prioritizing kidney protection to reduce the risk of long-term complications. Episode resource links: Jensen SK, Heide-Jørgensen U, Andersen IT, et al. SGLT2 Inhibitors vs GLP-1 Receptor Agonists for Kidney Outcomes in Individuals With Type 2 Diabetes. JAMA Intern Med. Published online January 20, 2026. doi:10.1001/jamainternmed.2025.7409 Samson SL, et al. American Association of Clinical Endocrinology consensus statement: comprehensive type 2 diabetes management algorithm—2023 update. Endocr Pract. 2023;29(5):305-340. Guest: Jillian Joseph, MPAS, PA-C   Music Credit: Matthew Bugos Thoughts? Suggestions? Email us at FranklySpeaking@pri-med.com  The views expressed in this podcast are those of Dr. Domino and his guests and do not necessarily reflect the views of Pri-Med.

  In March of 2026, the International Olympic Committee released a new policy on the Protection of the Female (Women's) Category in Olympic Sports. This new policy is applicable to the 2028 Olympic Games to be hosted in Los Angeles and onward and is not being applied retroactively or to any grassroots or recreational sports programs.  But what does this new policy address and how what should we think about this. I have a longtime friend and mentor as my guest today who will help us work through this topic.    Connect with The Host! Subscribe to This Podcast Now!     The ultimate success for every podcaster – is FEEDBACK! Be sure to take just a few minutes to tell the hosts of this podcast what YOU think over at Apple Podcasts! It takes only a few minutes but helps the hosts of this program pave the way to future greatness! Not an Apple Podcasts user? No problem! Be sure to check out any of the other many growing podcast directories online to find this and many other podcasts via The Podcaster Matrix!     Housekeeping -- Get the whole story about Dr. Mark and his launch into this program, by listing to his "101" episode that'll get you educated, caught up and in tune with the Doctor that's in the podcast house! Listen Now! -- Interested in being a Guest on The Pediatric Sports Medicine Podcast? Connect with Mark today!   Links from this Episode: -- Dr. Mark Halstead: On the Web -- On X  -- David Allen, MD Profile https://www.uwhealth.org/providers/david-b-allen-md Publications/Milestones https://www.pediatrics.wisc.edu/staff/allen-david/ IOC New 2026 Policy on Protection of Female (Women) Category in Olympic Sports https://www.olympics.com/ioc/news/international-olympic-committee-announces-new-policy-on-the-protection-of-the-female-women-s-category-in-olympic-sport Rupert JL. Genitals to genes: the history and biology of gender verification in the Olympics. Can Bull Med Hist. 2011;28(2):339-65. doi: 10.3138/cbmh.28.2.339. PMID: 22164600. https://pubmed.ncbi.nlm.nih.gov/22164600/   Calls to the Audience Inside this Episode: -- Be sure to interact with the host, send detailed feedback via our customized form and connect via ALL of our social media platforms! Do that over here now! -- Interested in being a guest inside The Pediatric Sports Medicine Podcast with Dr. Mark? Tell us now! -- Ready to share your business, organization or efforts message with Dr. Mark's focused audience? Let's have a chat! -- Do you have feedback you'd like to share with Dr. Mark from this episode? Share YOUR perspective!   Be an Advertiser/Sponsor for This Program!     Tell Us What You Think! Feedback is the cornerstone and engine of all great podcast. Be sure to chime in with your thoughts, perspective sand more.  Share your insight and experiences with Dr. Mark by clicking here!   The Host of this Program: Mark Halstead:  Dr. Mark Halstead received his medical degree from the University of Wisconsin Medical School. He stayed at the University of Wisconsin for his pediatric residency, followed by a year as the chief resident. Following residency, he completed a pediatric and adult sports medicine fellowship at Vanderbilt University. He has been an elected member to the American Academy of Pediatrics (AAP) Council on Sports Medicine and Fitness and the Board of Directors of the American Medical Society for Sports Medicine (AMSSM). He has served as a team physician or medical consultant to numerous high schools, Vanderbilt University, Belmont University, Washington University, St. Louis Cardinals, St. Louis Blues, St. Louis Athletica, and St. Louis Rams. He serves and has served on many local, regional and national committees as an advisor for sports medicine and concussions. Dr. Halstead is a national recognized expert in sport-related concussions and pediatric sports medicine. — Dr. Mark Halstead on Facebook — Dr. Mark Halstead on LinkedIn — Dr. Mark Halstead on X — Learn Why The Pediatric Sports Medicine Podcast Exists...   The Guest Featured Inside this Program: David Allen David B. Allen, MD, is Professor of Pediatrics at the University of Wisconsin School of Medicine and Public Health, and Head of Endocrinology and Diabetes and Director of the Endocrinology and Diabetes Fellowship Program at the University of Wisconsin American Family Children's Hospital in Madison.  He graduated from Stanford University with honors in humanities and biology, obtained his MD degree from Duke University School of Medicine, and completed pediatric residency, chief residency, and a fellowship training at the University of Wisconsin. He is the recipient of numerous awards for excellence in education, clinical care, and academic leadership, most notably the ACGME Parker Palmer “Courage to Teach” national award, the University of Wisconsin Presidential Physician Leadership Award, the Wisconsin Medical Alumni Association Career Citation Award, the University of Wisconsin Clinical Educator Award, and the Judson Van Wyk Prize for outstanding career achievement given by the Pediatric Endocrine Society. Dr. Allen served as Director of the UW Pediatric Residency Program from 1993-2007 and as Program Director of the UW Pediatric Endocrinology and Diabetes Fellowship since 2003.  On the national level, Dr. Allen was elected Director (2000-2003) and then President (2010-2011) of the Pediatric Endocrine Society.  He served as Chair of the Wisconsin Endocrine Newborn Screening Committee from 1991-2015, and as member of the American Board of Pediatrics sub-board for Pediatric Endocrinology 2010-2015.  He is an editorial reviewer for numerous peer-reviewed journals, served as editorial board member for the Journal of Clinical Endocrinology and Metabolism and Associate Editor for the International Journal of Pediatric Endocrinology.  On the international level, Dr. Allen was selected to Chair the Organizing Committee for and then serve as President of the 2017 10th International Meeting of Pediatric Endocrinology. His research interests have included innovative use of human growth hormone to restore normal growth and increase physical function in children with glucocorticoid-induced growth suppression and with Prader-Willi syndrome. He has also led studies of childhood adipose organ development and dysfunction, improving fitness and insulin sensitivity to prevent diabetes onset in children, improving newborn screening programs for endocrine disorders, and preventing and assessing systemic effects of inhaled corticosteroids.  Throughout his career, Dr. Allen has also spoken and published extensively about issues of ethics and cost-effectiveness in the treatment of disorders of childhood growth.  He has written more than 240 articles, letters, monographs, and book chapters, edited 4 textbooks, and has presented at more than 180 regional, national, and international meetings. Dr. Allen's personal interests include improvisational jazz piano and providing philanthropic music for local charities and missions.  He is an avid cyclist, skier, and runner (two-time US Olympic Marathon trials qualifier with a PR of 2 hours 17 minutes) and most importantly, a doting grandfather.

Woran merkst du eigentlich, dass du zu wenig isst? In dieser Folge sprechen wir darüber, warum eine zu geringe Energiezufuhr oft lange unbemerkt bleibt und sich nicht nur über Hunger oder Gewichtsverlust zeigt. Es geht um typische körperliche und mentale Warnsignale, Veränderungen im Training, hormonelle und metabolische Folgen sowie die Frage, warum „gesund essen“ nicht automatisch bedeutet, dass der Körper auch wirklich ausreichend versorgt ist. Außerdem besprechen wir, welche Gruppen besonders gefährdet sind, wie du Unterversorgung im Alltag erkennen und was du konkret tun kannst, wenn du den Verdacht hast, dauerhaft zu wenig zu essen. ------------------------------------------------------------------------ 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 ------------------------------------------------------------------------ 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 ------------------------------------------------------------------------ Quellen: Fahrenholtz, I. L., Sjödin, A., Benardot, D., Tornberg, Å. B., Skouby, S. O., Faber, J., Sundgot-Borgen, J. K., & Melin, A. K. (2018). Within-day energy deficiency and reproductive function in female endurance athletes. Scandinavian Journal of Medicine & Science in Sports, 28(3), 1139–1146. Ihle, R., & Loucks, A. B. (2004). Dose-response relationships between energy availability and bone turnover in young exercising women. Journal of Bone and Mineral Research, 19(8), 1231–1240. Lieberman, H. R., Bukhari, A. S., Caldwell, J. A., Wilson, M. A., Mahoney, C. R., Pasiakos, S. M., McClung, J. P., & Smith, T. J. (2017). Two days of calorie deprivation induced by underfeeding and aerobic exercise degrades mood and lowers interstitial glucose but does not impair cognitive function in young adults. The Journal of Nutrition, 147(1), 110–116. Longland, T. M., Oikawa, S. Y., Mitchell, C. J., Devries, M. C., & Phillips, S. M. (2016). Higher compared with lower dietary protein during an energy deficit combined with intense exercise promotes greater lean mass gain and fat mass loss: A randomized trial. The American Journal of Clinical Nutrition, 103(3), 738–746. Loucks, A. B., & Thuma, J. R. (2003). Luteinizing hormone pulsatility is disrupted at a threshold of energy availability in regularly menstruating women. The Journal of Clinical Endocrinology & Metabolism, 88(1), 297–311. Loucks, A. B., Verdun, M., & Heath, E. M. (1998). Low energy availability, not stress of exercise, alters LH pulsatility in exercising women. Journal of Applied Physiology, 84(1), 37–46. Melin, A. K., Tornberg, Å. B., Skouby, S. O., Møller, S. S., Sundgot-Borgen, J., Faber, J., Sidelmann, J. J., Aziz, M., & Sjödin, A. M. (2015). Energy availability and the female athlete triad in elite endurance athletes. Scandinavian Journal of Medicine & Science in Sports, 25(5), 610–622. Mettler, S., Mitchell, N., & Tipton, K. D. (2010). Increased protein intake reduces lean body mass loss during weight loss in athletes. Medicine & Science in Sports & Exercise, 42(2), 326–337. Murphy, C., Bilek, L. D., & Koehler, K. (2021). Low energy availability with and without a high-protein diet suppresses bone formation and increases bone resorption in men: A randomized controlled pilot study. Nutrients, 13(3), 802. Murphy, C., & Koehler, K. (2020). Caloric restriction induces anabolic resistance to resistance exercise. European Journal of Applied Physiology, 120(5), 1155–1164. Staal, S., Sjödin, A. M., Fahrenholtz, I. L., Bonnesen, K., & Melin, A. K. (2018). Low RMR ratio as a surrogate marker for energy deficiency, the choice of predictive equation vital for correctly identifying male and female ballet dancers at risk. International Journal of Sport Nutrition and Exercise Metabolism, 28(4), 412–418. Torstveit, M. K., Fahrenholtz, I., Stenqvist, T. B., Sylta, Ø., & Melin, A. (2018). Within-day energy deficiency and metabolic perturbation in male endurance athletes. International Journal of Sport Nutrition and Exercise Metabolism, 28(4), 419–427.    

Die meisten Ratgeber beruhen auf Stress-Forschung aus den 90ern – und wurden für 30-Jährige geschrieben. Kein Wunder, dass die alte Cortisol-Formel ab 40 nicht mehr zu funktionieren scheint.In dieser Folge erfährst Du, wie chronischer Stress Dein Hormonsystem ab 40 aus dem Takt bringt, warum Östrogen und Testosteron als natürliche Stresspuffer schwächer werden – und warum die gleiche Belastung Dich mit 45 messbar härter trifft als mit 30.Dazu bekommst Du fünf evidenzbasierte Werkzeuge, die Du noch diese Woche umsetzen kannst. Eins davon kostet Dich fünf Minuten am Tag. Eins brauchst Du nur, wenn Du in der Mittagspause ohnehin essen willst. Und eins ist das am besten dokumentierte Anti-Stress-Werkzeug der letzten zehn Jahre – obwohl es fast nie in Stress-Ratgebern auftaucht.Diese Folge ist für Dich, wenn Du wissen willst, was sich an Deinem Körper ab 40 wirklich verändert – und was konkret dagegen hilft.____________*WERBUNG: Infos zum Werbepartner dieser Folge und allen weiteren Werbepartnern findest Du hier.____________

Modern medicine has come a long way in its fight against diabetes. We now have continuous glucose monitors (CGM) and automated insulin delivery (AIDs) systems. These have revolutionized patient care. The FDA has approved devices for use in pregnancy as “nonadjunctive use” (meaning they may be used alone), although capillary finger stick assessments are currently still considered the Gold Standard. While the most robust data in support of CGMs is for preexisting Type 1 DM (Class B or beyond) and Type 2, there is recent growing support for CGM use in GDM patients, although some limitations still apply. Listen in for details.1. Feig DS, et al; CONCEPTT Collaborative Group. Continuous glucose monitoring in pregnant women with type 1 diabetes (CONCEPTT): a multicentre international randomised controlled trial. Lancet. 2017 Nov 25;390(10110):2347-2359. doi: 10.1016/S0140-6736(17)32400-5. Epub 2017 Sep 15. Erratum in: Lancet. 2017 Nov 25;390(10110):2346. 2. Benhalima K, Durnwald C, Sweeting A et al.Application of continuous glucose monitoring and automated insulin delivery technologies for pregnant women with type 1, type 2, or gestational diabetes: an international consensus statementThe Lancet Diabetes & Endocrinology, 2025; 14, 157-1773. Salmen BM, Reurean-Pintilei D, Salmen T, Bohîlțea RE. Exploring Continuous Glucose Monitoring in Gestational Diabetes: A Systematic Review. Life (Basel). 2025 Aug 28;15(9):1369. doi: 10.3390/life15091369. PMID: 41010309; PMCID: PMC12470761.4. Wyckoff JA, Lapolla A, Asias-Dinh BD, et al.Preexisting Diabetes and Pregnancy: An Endocrine Society and European Society of Endocrinology Joint Clinical Practice Guideline. The Journal of Clinical Endocrinology and Metabolism. 20255. American Diabetes Association Professional Practice Committee for Diabetes*; 15. Management of Diabetes in Pregnancy: Standards of Care in Diabetes—2026. Diabetes Care 1 January 2026; 49 (Supplement_1): S321–S338. https://doi.org/10.2337/dc26-S0156. Burk J, Ross GP, Hernandez TL, Colagiuri S, Sweeting A. Evidence for improved glucose metrics and perinatal outcomes with continuous glucose monitoring compared to self-monitoring in diabetes during pregnancy. Am J Obstet Gynecol. 2025 Sep;233(3):162-175. doi: 10.1016/j.ajog.2025.04.010. Epub 2025 Apr 10. PMID: 40216177.7. Linder T, et al; GRACE study collaborative group. Glycaemic control and pregnancy outcomes with real-time continuous glucose monitoring in gestational diabetes (GRACE): an open-label, multicentre, multinational, randomised controlled trial. Lancet Diabetes Endocrinol. 2026 Jan;14(1):50-61. doi: 10.1016/S2213-8587(25)00288-8. Epub 2025 Nov 24. PMID: 41308662.8. Valent AM, et al. Real-Time Continuous Glucose Monitoring in Pregnancies With Gestational Diabetes Mellitus: A Randomized Controlled Trial. Diabetes Care. 2025 Sep 1;48(9):1581-1588. doi: 10.2337/dc25-0115. PMID: 40730104; PMCID: PMC12368369.9. Kusinski LC, et al. Continuous Glucose Monitoring Metrics and Pregnancy Outcomes in Women With Gestational Diabetes Mellitus: A Secondary Analysis of the DiGest Trial. Diabetes Care. 2025 Aug 19:dc250452. doi: 10.2337/dc25-0452. Epub ahead of print. PMID: 40828742; PMCID: PMC7618813.10. García-Moreno RM, et al. Efficacy of continuous glucose monitoring on maternal and neonatal outcomes in gestational diabetes mellitus: a systematic review and meta-analysis of randomized clinical trials. Diabet Med. 2022 Jan;39(1):e14703. doi: 10.1111/dme.14703. Epub 2021 Oct 13. PMID: 34564868.11. Amylidi-Mohr Set,.et al (DipGluMo): an open-label, single-centre, randomised, controlled trial. Lancet Diabetes Endocrinol. 2025 Jul;13(7):591-599. doi: 10.1016/S2213-8587(25)00063-4. Epub 2025 May 26. Erratum in: Lancet Diabetes Endocrinol. 2026 Mar;14(3):e6. doi: 10.1016/S2213-8587(25)00403-6. PMID: 40441173.

Deb (00:03.606)Within the next seven months, up to 1.5 million Americans could lose access to a medication that they’ve relied on for decades. Not because it’s dangerous, but because a pharmaceutical giant may have lobbied the FDA to eliminate their competition. And if you’re one of them, your doctor may already have told you about this issue and stopped prescribing it.This isn’t a conspiracy theory. This is documented in federal court filings. This is happening right now. And the company that stands to profit, well, they’re the same ones manufacturing the only product that might survive.Today on Let’s Talk Wellness Now, we’re exposing the desiccated thyroid extract crisis, the corporate manipulation behind it, and what you need to do right now to protect your health. Stay with me because I’m about to share what could save your access to the medication keeping you alive.Welcome back to Let’s Talk Wellness Now, the show where we uncover the root causes of chronic illness, expose regulatory capture in healthcare, and empower you with the tools to advocate for yourself. I’m Dr. Deb, naturopathic doctor, your medical detective, and today we’re diving into one of the most consequential and corrupt healthcare decisions affecting patients right now. If you or someone you love takes Armour thyroid, NP thyroid, or any desiccated thyroid extract,for hypothyroidism or if you’ve struggled to find a thyroid medication that actually works for your body, this episode is absolutely critical. And if you have celiac disease, gluten sensitivity or corn allergies, what I’m about to reveal will make your blood boil. Now grab your cup of coffee, don’t forget your notebook and settle in because what’s happening to this medication right now is a masterclass in how pharmaceutical companies use regular Deb (02:06.544)agencies to eliminate competition, control markets, and price gouge patients. And I have all the receipts. Deb (02:20.982)Let me start with what might surprise you. Desiccated thyroid extract, or DTE as we call it, is actually one of the most oldest thyroid medications in the world. And I mean old. From the 1890s through 1970, this was the standard treatment for hypothyroidism.Now let’s really dive into that. From the 1890s to the 1970s, this was standard hypothyroidism treatment.In 1965 alone, and this is documented in peer-reviewed literature published in the Journal of Clinical Endocrinology and Metabolism, approximately four out of every five prescriptions for thyroid hormone in the United States were of natural desiccated thyroid preparations.The Journal of Clinical Endocrinology and Metabolism is a very high-end journal. Now think about that. This wasn’t some fringe therapy. This was mainstream medicine. Armour Thyroid, the most recognizable brand name, has been manufactured since the early 1900s, well over a century ago.and this is cited again in NIH bookshelf. When the FDA was officially established in 1938, Arbor thyroid was already on the market. And this is important and I want you to understand why. Under the federal Food, Drug and Cosmetic Act, any drug that was already being marketed before 1938 was automatically grandfathered into the system. That means it didn’t have to Deb (04:08.112)go through the formal FDA approval process. And this again is cited under the Federal Food, Drug and Cosmetic Act, grandfathered drugs and exemptions. And this is crucial to understanding what happens next. By the 1970s, synthetic levothyroxine, brand name Synthroid and generics became the preferred treatment. Hmm, wonder why?It was easier to standardize, came into consistent doses, and worked well for most patients, and could be mass manufactured. By the 1980s, levothyroxine had largely replaced desiccated thyroid in clinical practice, according to the American Thyroid Association 2014 guidelines for the treatment of hypothyroidism. But here’s what matters. Some patients…a very significant minority of them, never felt right on levothyroxine alone. Despite their lab work looking normal, they still had fatigue, brain fog, weight gain, cold intolerance, and depression.These patients often found relief when they switched back to their desiccated thyroid, which contains both T4 and T3 hormones, the way human thyroid naturally produces them. And this is not anecdotal. This is documented in randomized double-blind crossover studies published in Endocrine Practice.For decades, that was fine. Their doctors prescribed it, insurance sometimes covered it, patients were getting better, and the system worked really well. Until August 6th of 2025, just a short time ago, everything changed. On that date, the FDA sent letters to manufacturers, importers, and distributors of desiccated thyroid extract products stating that these medications would need an approval. Deb (06:04.654)a biologics licensed application, a BLA, to remain legally on the market. And this is cited in the FDA’s official statement, FDA’s actions to address unapproved thyroid medications. understand it says unapproved thyroid medications. However, desiccated thyroid, specifically Armour, has been approved since 1938. And this was dated August 6th through 7th, 2025.This wasn’t a guideline. This wasn’t a suggestion. It was an endorsement of action. And the timeline they gave them? Well, just 12 months to transition patients to another medication before enforcement action could begin.This was also cited by an FDA notice to the industry, animal derived thyroid products notice to industry, August 6th, 2025. Now do the math, that means August 2026, seven months from now, 1.5 million Americans currently taking this medication. And this number comes from the FDA official statement, citing that it’s an estimation of 1.5 million patients receiving prescriptions for these medications.could potentially lose their thyroid access. Now, here’s where it gets interesting. The FDA didn’t wake up in August of 2025 and decide to regulate desiccated thyroid after a century. This decision has a much longer backstory. And understanding that backstory is critical to understanding what’s really happening in this industry.The shift started in 2022. Back in September of 2022, over three years ago, an FDA branch chief sent a letter to the National Associations of Boards of Pharmacy noting that the agency had decided to designate DTE as a biological product, which would affect its eligibility for compounding. Deb (08:13.972)This also is cited in an FDA letter to the National Association of Boards of Pharmacy September 2022.Then two months later, in November of 2022, the FDA’s Office of Compounding Quality and Compliance sent a softer letter acknowledging that many Americans take medication to treat hypothyroidism and some choose to take DTE products. The letter stated that the FDA would focus enforcement on cases that pose the greatest public health risks, such as serious adverse offense or serious product quality or adulteration.also is cited by an FDA letter from Francis G. Bromel, the director, Office of Compounding Quality and Compliance, November of 2022. Now, let me just think about this for a second. If this drug has been on the market since the 1800s, been FDA approved since 1938, would we not have seen a health crisis long before 2022?I honestly don’t know of any other drug that’s been around this long that’s used by this many people. Now granted, I haven’t done the research on it either, which I can do for you guys, but I’m just thinking if a drug is on the market today and it causes harm, it doesn’t make it three years, five years before you see lawsuits everywhere. Why are there no lawsuits on this drug? Why are there no major reactions that people are seen having?Hmm, just thought. But here’s the pattern. The FDA was already laying the groundwork back in 2022, testing the waters, signaling where this was headed. The August 2025 action. Then this came down. Deb (10:09.806)August 6, 2025, the FDA announced its position publicly and sent formal letters to all DTE manufacturers, importers, and distributors. This was cited by the FDA Enforcement Action August 6, 2025, letters to manufacturers, importers, distributions of DTE products. The agency stated several concerns. First, DTE products have experienced quality and dosing issues.The FDA cited, and I’m quoting directly from their statement, over 500 adverse events reported associated with DTE products from 1968 to 2025. From 1968 to 2025, we had 500 adverse reactions? What is that math equate to?A couple a year? Come on guys, this is insane! With a substantial increase, you, between 2019 and 2020 that the agency suggested was related to voluntary recalls of sub-potent or super-potent products.This was cited in the FDA statement, over 500 adverse events reported associated with ADT products from 1968 through 2025.Second, the agency expressed concern about batch inconsistency. According to the FDA’s official statements, tablets made from the same manufacturing batches may not always provide the same thyroid hormone levels. Okay, this was cited in the FDA statement, tablets made from the same manufacturing batches may not always provide the same thyroid hormone levels. Thirdly, and I want to actually let’s back up. I want you to remember I said that Deb (12:11.216)because further down in this podcast, we’re going to talk about this. This is an important point to remember. Thirdly, the agency raised concerns about potential impurities from animal source material, including potential for viral contamination due to the animal source and supraphysiological levels of T3.the FDA statement on impurities, viral contamination and super physiological T3 levels. Now I will tell you, I’ve been prescribing armarithograde for 20 years. I’ve rarely seen a super physiological dose given of T3 in lab results, unless the patient takes their medication like four or five hours before you do the blood test, then you’ll see a false rise because you’re actually seeing the medication. You’re not seeing people walking aroundsuperphysiological T3 levels. Nobody would like that feeling. So anyway, I digress. Now let me pause here because this is where I need to give you some context that the FDA hasn’t quite emphasized yet. Of course, we have another connection and it is the China connection.So the FDA’s concerns about contaminated drugs and quality issues don’t exist in a vacuum. In 2024, the U.S. over 828,000 metric tons of pharmaceuticals, seven times the level from 2000. And here’s the kicker. China and India supply the majority of active pharmaceutical ingredients. APIs for U.S. generics accounting for 70 to 80 % of the total genericdrug supply. According to Reuters industry report in 2024, they state that China supplies 82 % of the APIs for critical drugs. Deb (14:08.204)Got to question that, right? Why are we giving all of our drug formulas to China and allowing them to import them into our country? In fact, roughly 20 % of the critical drugs have APIs exclusively sourced from China. And China controls 80 to 90 % of the global production for antibiotics and other key compounds. This was also cited by Reuters industry data thatcontrols 80 to 90 percent of the global production for antibiotics and other key compounds. Now just think about this. They control 80 to 90 percent of our medication. They control 20 percent of our critical drugs and we just put what kind of tariff on them? Hmm.In 2025 alone, the FDA issued multiple warning letters to foreign manufacturers for contamination issues and failure to follow good manufacturing practices. This is also cited by the FDA warning letters 2024 through 2025 and multiple citations to foreign manufacturing facilities. This is a systematic problem affecting the entire US drug supply, not just desiccated thyroid.So when the FDA suddenly became concerned about DTE quality and contamination, part of that concern was legitimate. But this is crucial. The same inconsistencies and contamination issues exist across the entire generic drug supply. And the FDA has not taken the same enforcement action against them. Let that sink in.They have not taken the same enforcement action against the other drug companies. So what’s behind all of this? Where is this all coming from? Hmm. Let’s address something directly, because you deserve to know it. And I’m going to cite my sources precisely so that when the medical boards have something to say about this, and they might, I have a documentation for every single word that I am about to speak. Deb (16:24.878)According to the court documents filed in October 2025, in the case ofa urine, a urine. I’m going to say that wrong. Pharmaceuticals versus Dr. George Tidmarsh from ABBV, the multinational pharmaceutical company that manufactures armor thyroid, reportedly petitioned the FDA in 2024, asking the agency to reclassify DTE as a biologic and to prohibit other manufacturers from selling unlicensed DTE products unless they havehad an investigational new drug application, we call this an IND, and a clinical development program aimed at eventual approval. This is cited in the court filing a Urena pharmaceuticals lawsuit versus Dr. George Tidmarsh, October 2025, reported by Fierce Pharma. Now let me explain why this matters and why this is one of the most brazen examples of regulatory capture I’ve ever seen in my career.AbbeVee is one of the world’s largest pharmaceutical companies. In 2024, they reported over $54 billion in revenue. Drop the mic on that one.They have the resources, the regulatory expertise, the legal teams, and the financial capacity to navigate a biologics license application process that costs between $500 million and $1 billion. Let that sink in. Deb (18:07.882)A drug that’s been on the market since the 1800s that was grandfathered in 1938 that’s making plenty of money right now. They’re going to spend 500 million to $1 billion to get a biologics license application. Why would they do that? Well, we’re about to find out. Most otherDTE manufacturers, smaller companies like Acela Pharmaceuticals, which makes NP-thyroid, and RLC Labs, which made WP-thyroid, do not have those same resources. And this is cited in Pharma Voice in 2025. Why a treatment older than the FDA is getting new regulatory scrutiny. So when you petition the FDA to reclassify a drug in a way that requires this type of expensivetime-consuming biological approval, you’re not just asking for safety. You’re asking to eliminate your competitors from the marketplace. Now, I want to be very precise here. These allegations are documented in federal court filings, and it hasn’t been approved in court. It’s also been reported by multiple industry sources, including Fierce Pharma. But I’m telling you,what has been reported in legal proceedings, not stating it as an absolute fact because you deserve to know the difference and because I have to protect my license. Now, what do we know for certain?AbbeVee is working on a biologics license application for Armour thyroid through clinical trials called Avantia. This is cited by the AbbeVee corporate statement 2025 Avantia clinical trial for Armour thyroid. A cell of pharmaceuticals has been pursuing BLA approval for NP thyroid for seven years since 2017 and it completed its phase two trials successfully in 2025. They’re now moving Deb (20:15.448)into Phase 3 trials. This is also cited by the Acela Pharmaceuticals CEO statement 2025 seven-year pursuit for BLA approval completed Phase 2 trials moving to Phase 3.RLC Labs, which manufactured WP thyroid, has made no public announcement about pursuing BLA approval and really probably don’t have a plan to do this since they’ve been off the market for some time now. About five years, I think maybe a little longer. Here’s the market manipulation.If only ABBV is successful and obtains a BLA approval for Armour thyroid, that company would effectively have a monopoly on the DDT market. And in pharmaceutical markets, monopolies historically lead to price increases.We’ve seen this pattern over and over again when turning pharmaceuticals acquired Daraprim and raised their price from $13.50 to $750 per tablet overnight. When Myelin raised EpiPen increased prices by 400 % when insulin manufacturers colluded to raise prices in lockstep. This is the playbook.use regulatory barriers to eliminate your competition and then exploit pricing power. For a drug that’s been on the market since the 1800s, guess corporate greed is everywhere. They’re not making enough money on this product already and they’re taking advantage of the rules that they can manipulate their competition by. And here’s what really makes me furious. The American Thyroid Association, the professional organization Deb (22:06.672)representing endocrinologists sent letters to the FDA commissioner on October 8th of 2025 and September 18th of 2025.advocating for continued patient access to DTEs. This is cited in the American Thyroid Association statement and letter to the FDA commissioner dated October 8th, 2025 and September 18th, 2025. The American Association of Clinical Endocrinologists issued a statement on September 9th of 2025 supporting equitable access and personalized medicine for DTE. This was also cited in the American AssociationAssociation of Clinical Endocrinologists, AACE, statement dated September 9th, 2025. Even the medical establishment, which has historically favored levothyroxine, is saying, wait, this is going too far. Patients need access to this medication. But the FDA is moving forward anyway. Why? Well, where does it always lead us? Follow the money trail.Okay, so I need to explain what a biologics license application actually is because this is where the rubber meets the road for what’s going to happen to pricing and availability. What is a BLA?A BLA is a biologics license application. It’s a formal request submitted to the FDA to market a biologic product in the United States. A biologic is defined under the Public Health Service Act section 351 as a product derived from or made using living material, in this case, animal thyroid glands. And this is cited in the FDA definition for biologic products. So they’re putting armor thyroid right Deb (23:57.377)right up with stem cells and exosomes. Think about that. Stem cells and exosomes cost thousands of dollars per application because of how they have to be harvested, stored, freezed, all of that. But we’re talking about a thyroid gland. Good Lord, people.Unlike regular drug applications for synthetic medications which follow a simpler pathway, the BLA process is designed for complex biological products like monoclonal antibodies, vaccines, and gene therapy products. It’s a much more expensive, much more time-consuming process. The BLA processis what manufacturers have to do. And we’re going to talk about that. So according to Reprocell and Forge Biologics analysis of the FDA’s BLA process, here’s what companies need to submit. First, they need to complete a clinical trial data, phase one, two, and three trials, proving safety and efficacy for desiccated thyroid. Haven’t we done that since it’s been on the market since the 1800s? Just saying.This means they have to conduct large randomized controlled trials comparing it to levothyroxine, measuring safety outcomes, efficacy outcomes, and quality of life metrics. Second,Chemistry, Manufacturing and Controls, CMC’s data. Detailed information about how the product is manufactured, quality control measures, stability testing and specifications that must be met for every batch. Third, preclinical and animal safety data. Fourth, labeling and product information. Now, I think we have labeling and product information. Deb (25:53.717)since the 1800s? But just saying. Fifth, they need Pharma Covigilance Plan, a detailed plan for monitoring safety after the product is on the market. Haven’t they had to do that since the 1800s? And they have to have a timeline. And this is the critical part. The FDA’s standard review time for a BLA is 10 months.That’s after the application is deemed complete and accepted for filing. So this is cited by the FDA standard review timeline, BLA submission, and FDA review.Now, before you even get to filing, you need to conduct the clinical trials and compile all the data that’s typically several years of work. How are you going to prove safety and effectiveness in a large clinical trial long term? What do they consider? What do they deem long term? Three months, six months, a year, two years. These companies had 10 months.Well, maybe 12. They did it a year in advance. But unless you knew this was coming, how are you going to put together a trial, enroll the people, have all the trial components set up and ready to go in less than 12 months unless you knew it was coming beforehand? Even ifhad started all their clinical trials in 2024, completing them, compiling the data, and getting a complete application ready for submission, this would likely take you through mid-2026, then add another 10 months for FDA review. We’re looking at 2027 at the earliest for most of these companies to receive a BLA application. Deb (27:54.319)But the FDA gave the manufacturers until August of 2026. That’s approximately 19 months from when the August 2025 letters were sent. Most companies cannot reasonably complete the BLA approval in that timeframe. And when I’m talking about the 19 months, I’m talking about the information they would have had earlier. Now the cost.This gets me even more frustrated. Why are we spending this kind of money? The BLL process is extraordinarily expensive. The current FDA user fee for a BLA submission is approximately $483,560 just for the filing fee. And this is cited at the FDA user fees prescription drug user fee rates for 2025.The full cost of conducting clinical trials, CMC studies, and all the supporting documentation typically ranges from $500 million to over $1 billion, depending on the scope of the trials and the complexity. And this is cited in JAMA’s network, Open2023. A cell of pharmaceuticals has been pursuing the BLA approval since 2017. That’s eight years. And it’s just now.moving into phase three trials with a planned enrollment of approximately 300 patients. This is cited by the Acela Pharmacies CEO statement of 2025. Now that’s unusual. That’s typical for this process. This is not unusual. This is typical for this process to take seven, 10 years to get approval for this. So if Abby’s the one that requested this,Abby V. And Acela started this in 2017. Was Abby V threatened by Acela that Acela might get this approval and it would be quietly done without anybody seeing it? And maybe Abby V would be left out of the market after a century? Who knows? It’s possible. Deb (30:13.112)But for smaller manufacturers without billions in revenue, this cost is completely prohibitive. And this is why this matters. When you push an old established medication through an extraordinary, expensive approval process with a compromised timeline, one of three things happen. First, only the largest companies can afford it, creating a monopoly. And when that happens, the company that holds the only approved product can set pricing withminimal competitive pressures. Two, smaller manufacturers can’t afford it and their products disappear and the market shrinks and access decreases. Three, we see a combination of both and who pays the price? Literally, patients do. Now here’s whereThere’s something I want you to really think about because this is where the regulatory argument falls apart when you look at it carefully. The FDA’s concern about DTE is that, and I’m quoting their official statement, tablets from the same manufacturing batches may not always provide the same thyroid hormone levels. This is from their FDA statement.And that’s a legitimate quality concern, right? It is. Thyroid medications have a narrow therapeutic window like any other hormone, meaning the difference between an effective dose and the dose that causes problems can be quite small. But here’s what the FDA doesn’t emphasize. Generic drugs have the exact same dosing inconsistency issue, and it’s considered acceptable and has been since we allowed generics on the market.So how does a generic drug dose work anyway? Well, for generic drugs to be approved as bioequivalent to a brand name medication, the FDA requires that the generic drugs bioavailability fall within 80 to 125 % of the brand name product. Isn’t that a dose inconsistency? Deb (32:22.894)from the brand name medication? 800 or sorry, 80 to 125%. According to the pharmacy times analysis of the FDA’s bioequivalent standards, the 80 to 125 % bioequivalence rule means that a generic drug can have 20 to 45 % variability compared to the original brand product.Now, most generics are much closer than that. The FDA study data shows that the mean difference for an AUC value between generic and reference products is about three and a half percent in the two year post-Waxman hatch period, and 80 % of the generics fall within a five percent range. But the FDA’s regulations allow for that much higher variability. And this is cited in an FDA study data mean difference for AUC.Now, let me put this in plain language. A patient could take a generic levothyroxine tablet where one batch provides, say, 75 micrograms of an active thyroid hormone. And the next batch from a different manufacturer, a different generic manufacturer, could provide up to 93.75 micrograms, 125 % of that 75. That’s an 18 microgram difference.in the same prescribed dose. Now, this is considered acceptable and patients tolerate it and this system works.Yet the FDA’s argument against DTE is that batch-to-batch inconsistency is unacceptable and requires this expensive biologic approval? That’s a double standard. So why is batch inconsistency acceptable for generic levothyroxine, but supposedly unacceptable for desiccated thyroid? I’ll give you the regulatory answer. Deb (34:29.366)because DDT is a biological product derived from an animal tissue and the FDA considers biological products to require more rigorous control. That’s the regulatory answer, but I’ll give you the real answer.because there’s no billion dollar pharmaceutical company with a patent pending on generic levothyroxine who petitioned the FDA to regulate their competitors more strictly. The inconsistency argument is legitimate, but it’s selectively applied. And that matters when you’re trying to understand whether this is really about patient safety or whether it’s about market control.Now I want to talk about something that hasn’t gotten nearly enough attention in this discussion and it’s something that makes me absolutely furious. What is Armour Thyroid? According to the official prescribing information published by AbbeV and available through rxabbev.com and the FDA’s daily med database, Armour Thyroid contains the following inactive ingredients. Calcium steroid,dextrose derived from corn, mycocrystalline cellulose,sodium starch glycolate and a opadri white coating. Now let’s talk about dextrose. Dextrose is a sugar derived from corn and while manufacturers claim that the corn derived dextrose in armor thyroid is gluten free, here’s the problem. Cross contamination during corn processing can introduce gluten proteins especially if the corn is processed in facilities that also handle Deb (36:18.808)wheat, barley, or rye. Corn sensitivity is extremely common in patients with celiac disease and non-celiac gluten sensitivity, and studies show that up to 50 % of the celiac patients react to corn proteins due to molecular mimicry, and the corn proteins look similar enough to gluten that the immune system attacks them. And this is cited by RestartMD.com.And here’s what’s documented in peer-reviewed medical literature in a 2023 case report published in Case Reports in Endocrinology. These researchers documented five patients with gluten intolerance or celiac who were taking natural desiccated thyroid. Three of those patients also reported lactose intolerance. Now these patients had to switch from DTE to liquid levothyroxine formulations to avoid the inactiveSo here’s my question. If AbbeV becomes the only manufacturer with an approved DTE product and their formulations contain corn-derived dextrose that triggers reactions in celiac patients, what are those patients supposed to do? They can’t take armor because of the corn. They can’t take compounded DTE because the FDA is banning compounding of these biologics. They can’t take NPKsor WP thyroid because those companies may not survive the BLA process. So they’re left with a synthetic version of levothyroxine which may not work for them.Now the NP thyroid and WP thyroid difference. Now here’s what’s interesting according to drugs.com comparison of inactive ingredients and P thyroid and P thyroid has calcium steroid dextrose also derived from corn, mineral oil, multi-crystalline cellulose. Deb (38:19.31)cross carmelicin sodium and a opadri to white. So NP thyroid also has corn-derived dextrose. WP thyroid on the other hand was specifically formulated to be hypoallergenic according to ROC labs, but it’s no longer available and its ingredients were inulin from chicory root and medium chain triglycerides. No corn, no gluten, no common allergies. So todayWe do not have a glandular thyroid, a DTE, that is not potentially contaminated with gluten. Yet, patients with autoimmune thyroid disease are supposed to avoid gluten.Now, some of these people can handle a DTE and many cannot, so that argument could be a mute point. But at the end of the day, the one product that we had that was designated for patients with multiple chemical sensitivities, celiac disease and coron allergies, has been off the market for a long time already.We have a monopoly problem. So if ABBV becomes the only approved manufacturer, patients with these celiac diseases and corn allergies will either be forced to take a medicine that makes them sick and triggers their immune reaction or switch to a synthetic that doesn’t adequately treat their hypothyroidism or choose to go without treatment. This is not hypothetical. This is real patients with real medical needs who are about to lose accessto the only formulation that works for their body. And the FDA’s response is silence. Deb (40:07.69)Now I want to highlight something that hasn’t gotten nearly enough attention in this discussion. Compounding pharmacies. What is a compounding pharmacy? Compounded medications are custom made by licensed pharmacists to meet a patient’s specific needs. Maybe you need a different strength that was commercially available, but you have an allergy to a filler or a dye in the commercial product. Maybe you need a liquid formulation or instead of a tablet or you need a capsule. That’s when compoundingin. And the FDA’s, this is the FDA’s definition of compounding. And for decades, compounding pharmacies have been making desiccated thyroid extract for patients who needed customization. Some patients couldn’t take the commercial products because of the dyes and the fillers, and some needed strengths that were not available. And these compounding pharmacies filled the gap.But reclassification changes everything. When the FDA reclassified DTE as a biologic in 2022 and reinforced that decision in August of 2025, explicitly stated, and I’m quoting directly from the FDA’s official statement, these unapproved animal-derived thyroid medications are not eligible for compounding because these products are regulated as biologic products under the Public Health Service Act.How can that be? These products have been approved since 1938 and the Biologics Act didn’t go into effect or doesn’t go into effect until August of 2026.So how in 2022 were they able to say that the compounding pharmacies could not make these products? Anyway, what this means is after August 2026, compounding pharmacies will no longer be permitted to compound a desiccated thyroid extract, even for patients with specific medical needs. Now, compounding pharmacies can still compound T4 and T3 separately, synthetic versions of levothyroxine and liothyronine, according to Deb (42:12.728)healing dose compounding pharmacy. These pharmacists can create custom ratios of these two synthetic hormones to approximate what a patient was receiving from a DTE. But that’s not the same thing. Some patients respond better to the whole DTE preparation than to a compounded synthetic combination. And for patients with specific allergies to standard fillers like your celiac patients that I just talked about, losing the ability to get a compounded DTE alternative isreal hardship. This is going to be a ripple effect. For a subset of patients, maybe 5 to 10 percent of those on DTE compounding was their lifeline and it was their way to get a medication formulation that worked for their unique body. When compounding goes away, these patients lose that option as well and for some it will be a significant problem. Now let’s talk about what this likely means for your wallet.The current pricing right now, according to SingleCare and GoodRx, Armour Thyroid costs approximately $150 to $157 for a 90-day supply of 60-milligram tablets, about $1.67 per tablet. With discount cards, some patients can get it down to $101 to $152 for a 90-day supply.Generic levon thyroxine costs about $70 for a 90 day supply, less than half that price. And p-thyroid costs approximately $133 for a 90 day supply of 60 milligrams with a discount card about $83 to $101.What happens after we get BLA approval? Well, here’s the pharmaceuticals pricing model. When a company spends 500 million to $1 billion to bring a product to market, including conducting massive clinical trials, the cost tens of millions of dollars they recoup in that investment through pricing power. And this is cited in the pharmaceutical pricing models. If ABBIEV is the only company with an approved BLA of DTE, Deb (44:18.248)They have pricing power. They don’t have competitors. They can set their price, whatever they want. And historically, when drugs transition from grandfather status, which is basically unregulated to formal formally approved status, prices often increase significantly, not always, but often. And typically they have to get re-approval for insurance. SoTouring Pharmaceuticals acquired DARPM and raised the price again from $1,350 to $750 overnight, a 5,000 % increase. This is the playbook.Let’s talk about insurance coverage. This is the other consideration. Insurance companies sometimes have different coverage policies for approved versions versus unapproved drugs. And right now, many insurance plans cover armor thyroid or NP thyroid, even though they’re technically unapproved because they’ve been on the market for decades and patients are on them. Once a drug becomes formally approved, insurance companies may have new contractual relationships, prior authorization requirements, or preferred drugs.list that could affect your coverage. If 1.5 million people have to get a prior auth for their insurance to cover this new medication, this is going to drive the doctor’s offices crazy. We do not have the staff to man this. We do not have the manpower. We do not have the time. This is going to interrupt people’s ability to get their medications. This is going to create chaos within the system. And some patients might see better coverage, but manymost likely are going to see worse coverage and some might find themselves in a situation where they need to try to get the drug approved first or get an approval for something else like levothyroxine and they’re going to have to document that it didn’t work and the documentation that they had from 20 years ago is probably not going to be enough because it’s not documented anywhere. It’s lost in the system after 10 years. So for patients the practical takeaway is expect Deb (46:25.774)a price increase. I would say possible, but I don’t think that’s true. think you’re going to see a price increase if they get approved. Expect possible insurance complexities, budget accordingly, talk to your insurance company now about what your coverage is going to look like in 2027 if they even know. And if you want my honest assessment of what is likely to happen,I’ll give you a scenario, 30 % likelihood. The FDA enforces the August 26 deadline and DTE products not approved by then are pulled from the market. Patients will have 30 to 90 days to transition to other medications. Some patients suffer significant symptom relapse. Compounding for DTE becomes illegal and this disruptiveness of the system creates a real hardship. Scenario two.which is 50 % likely. This is actually what the FDA commissioner, Marty McCreary suggested on August 13th of 2025 when he posted on social media. The FDA is committed to pursuing the first ever approval of desiccated thyroid access pending results of the ongoing clinical trials. In the meantime, we’ll ensure access for all Americans. Hopefully that continues. What this likely means is the FDA uses enforcement discretion to allow continuedsales while approvals are being pursued and the deadline gets extended. Maybe patients get access for another two to three years while companies work on a BLA approval. This would be the least disruptive scenario, but it’s also legally uncertain because the enforcement letters have been formally rescinded. And scenario three, which is 20 % likelihood, one or two companies get BLA approval. Those products stay on the market at higher product prices and companies, products, other companiescompanies, products are pulled, the market shrinks, availability is limited, prices are higher, but patients can still get something. This is likely if a seller successfully completes phase three trials for NP-thyroid. And my assessment is based on the regulatory language and the enforcement letters that have not been rescinded yet, that the pattern of FDA enforcement, I believe scenario two enforcement discretion with an extended time frame is most likely what we’re going to see. Deb (48:49.488)doesn’t mean patients should sit back and do nothing. It means you should be prepared for change while advocating for access. If you want to keep Arm or Thigh Right on the market, 1.5 million people need to start talking about this publicly and flooding our Congress people, Bobby Kennedy, the FDA, with what you want to see happen. We have the ability to shape this and to change this with our voice. But if we sit back on our laurels and we do absolutelynothing. What is going to happen is what the FDA wants to have happen and ABV wants to have happen because they’re going to simply think people don’t give a shit. And if the American people are going to be lazy and not want to step forward and actually start using their voice for some good and instead of just going to social media and bitching and hoping something is going to happen, well, then we’re going to get what we deserve. But if you start taking someaction and you start advocating for the things that you want. Contacting your representatives, contacting your U.S. tell them the FDA has done this. Many of them may not know this, may not be on their radar. Tell them what you want. Start going after this. Start writing to the FDA Commissioner’s Office. They have a website. They have a Commissioner’s Office at fda.hhs.gov. Be responsible.respectful, but be firm. Explain your scenario. How long you’ve been on DTE. Why levothyroxine doesn’t work. What symptoms you experience when not adequately treated. How this decision will affect your quality of life and your pocketbook. Let’s do something proactive. So let’s consider this. Moving forward, work with your provider who understands the regulatory landscape around DTE. You can discuss the evidence for and against combination therapy.You can monitor for thyroid function with free T3 and free T4 testing, not just TSH. If you’re willing to try individualized approaches, you can do that. If you need help finding a functional medicine provider who understands this issue, come to serenityhealthcarecenter.com or explorethevanari.com. It’s a self-directed functional medicine support group. And right now what is happening is going to shape how history Deb (51:19.024)is made with not just armor thyroid, but many drugs to come. And it is important for you to take action. So I want to thank you for joining me today on Let’s Talk Wellness Now. This episode is about far more than thyroid medication. It’s about your right to personalized medical treatment. It’s about your regulatory capture and corporate influence. And it’s about what happens when billion dollar companies shape healthcare policy in ways that reduce patient choice and increase their profits.this episode resonates with you or you know somebody who’s going to be affected by desiccated thyroid, please share it. Post it on social media, send it to your doctor, email it to your representatives, tag AbbeVee, tag FDA. Make noise because the only way we stop this is if we make it too politically costly for them to continue. Your voice truly matters. Your health truly matters and you deserve access to treatments that work best for your unique body.If you’re ready to explore comprehensive personalized health care that puts you in control, visit us at SerenityHealthCareCenter.com. Learn more about functional medicine approaches to thyroid and beyond and explore my new platform, Venari.com, which is a self-directed functional medicine tool. Thank you for joining me today. Until next time, I’m Dr. Deb reminding you, your health is your responsibility, your choice, and your right. Be well, stay informed, fight back.and I’ll see you in the next episode. And if you’re looking for a full citation list of this episode, you can head over to letstalkwellnessnow.com and I will post all the citations for you so you have them in your arsenal as well. Thank you again.The post Episode 259 – The Desiccated Thyroid Crisis: FDA's Unseen Impact & Corporate Manipulation first appeared on Let's Talk Wellness Now.

This episode is sponsored by LMNT. LMNT - Get a free 8-count Sample Pack of LMNT's most popular drink mix flavors with any purchase at https://drinklmnt.com/FLIPPING50. Connect with Flipping 50: Facebook Group - Flipping50 Insiders Instagram - @Flipping50TV YouTube - @Flipping50TV More Episodes - Flipping 50 The Stronger Way References: The Journal of Clinical Endocrinology and Metabolism. 2007, PMID: 17200169. The American Journal of Clinical Nutrition. 2009, PMID: 19056590. Nutrients. 2021, PMID: 33652669. Front Public Health. 2026, PMID: 41668861. Sleep Medicine Clinics. 2018, PMID: 30098758. The American Journal of Clinical Nutrition. 2016, PMID: 27385608. BMC Women's Health. 2013, PMID: 24228934. Other Episodes You Might Like: Previous Episode - GLP-1 Medications for Weight Loss: A 42-Year Fitness Professional's Honest Take Next Episode - Beyond Hot Flashes: How Heat Impacts Health & Longevity More Like This - Does Hormonal Phase and Training Intensity Change How Hard You Can Train? New Science Finally Tested It Resources: Don't know where to start? Book your Discovery Call with Debra. Leave this session with insight into exactly what to do right now to make small changes, smart decisions about your exercise time and energy. Use Flipping 50 Scorecard & Guide to measure what matters with an easy at-home self-assessment test you can do in minutes. This episode breaks down the science-backed mistakes sabotaging your metabolism, especially for women in perimenopause and postmenopause. You're eating less. You're moving more. You're trying to “be disciplined.” And your metabolism? Slower. Hungrier. More stubborn. I'm giving you the 6 common strategies to lose weight that are hurting your metabolism in menopause — with real data on muscle loss, metabolic adaptation, sleep disruption, and hormone shifts. No fear mongering tactics. No arguing.  Just physiology. Then, it's up to you to test to know if it's working or not. If this episode made you flip your workout routine — share it!

Dr Deb Muth 00:03Well, welcome back to Let’s Talk Wellness Now. I am your host, Dr. Deb. And what is the most talked-about peptides in functional medicine? aren’t actually FDA approved. Not because they don’t work, but because no one’s funded the research to prove it yet. The truth is, some of the compounds that dominate wellness forums, BPC-157, TB-500, thymosin beta-4, epitalin, occupy a fascinating space between breakthrough science and unregulated experimentation. In today’s episode, we’re stepping into that grey zone, the world of investigational peptides, to separate mechanism from marketing. I’m going to walk you through the science that actually shows and where it stops, how to evaluate claims when human data don’t yet exist, and the quality, purity, and safety red flags that you need to recognise. Dr Deb Muth 01:06I created it in a previous episode, so go check that one out. And why honesty is the most important prescription in peptide medicine. If you’ve ever wondered whether these research-only peptides are the frontier of healing or the next functional medicine fad, this episode is for you. So grab your cup of tea or coffee, get comfortable, and let’s talk about what it really means to use peptides that are promising but still under investigation. So we’re going to break just for a second here and have a word from our sponsor. It is because of them that we stay on the air. So thank you for this. And we will be right back. Did you know sweating can literally heal your cells? Infrared saunas don’t just relax you. They detox your body, balance hormones, and boost mitochondrial energy. I’m obsessed with my Health Tech sauna. And right now, you can save $500 with my code at healthtechhealth.com slash dr-muth-req-25. Dr. Deb Muth 02:15All right, guys, welcome back. Let’s dive into investigational peptides, the evidence gap. So the following peptides we’re about ready to discuss are extensively in integrative, functional, and regenerative medicine circles. They may have intriguing mechanisms and promising preclinical data. However, they lack FDA approval, and the evidence quality varies dramatically. from interesting preliminary research to essentially no human data at all. And this distinction is really critical for maintaining scientific integrity. So let’s talk about immune-modulating peptides. There’s thymus and alpha-1, and this is an international story on the thymic peptides. Thymusin alpha-1, known as TA1, is marketed internationally as zidaxin. Dr. Deb Muth 03:16It’s a 28-amino acid polypeptide originally isolated from thymusin fraction 5, which was extracted from bovine thymus tissue. Modern production uses synthetic peptide synthesis. The thymus gland is located behind the sternum and is the primary site for T cell maturation, and thymic peptides like TA1 play roles in human system development and regulation. Now, I love thymus peptides. I love thymus glandular products. I’ve used thymus glandular products for decades. Ground-up animal thymus gland is basically what it is. There are a couple of different supplement companies that I’ve used over the years that are amazing with this. And they do a fantastic job, and they really do help to support the immune system. So when thymus peptides came out, it was really exciting because it took the whole idea of thymus support to a new level. Dr. Deb Muth 04:17The mechanism actually behind the thymus in alpha-1 is complex and involves multiple aspects of immune function. At the cellular level, TA1 enhances T cell maturation and differentiation, particularly the development of helper T cells and cytotoxic T cells. It modulates T cell receptor expression and can influence the balance between Th1 cell-mediated immunity and Th2 humoral immunity responses. And it also enhances the natural killer cell activity and modulates dendritic cell function, which are critical for antigen presentation. and initiation of adaptive immune responses. And on the cytokine level, TA1 influences production of interleukin-2, IL-2, interferon gamma, IFN-γ, and interleukin-10, IL-10. Dr. Deb Muth 05:19These create immune modulatory rather than simple immune stimulatory effects. This is a very important distinction because TA1 appears to help balance the immune system rather than simply ramping this up, which theoretically makes it safer in conditions where immune overstimulation would be a problem, such as an autoimmune disease. Hashimoto’s, autoimmune, lupus, Sjogren’s, any of those autoimmune diseases, we don’t want to overstimulate their immune system. So you want to use a product like this that’s non-stimulating. Now, the regulatory status on TA1 is geographically variable and represents one of the challenges in discussing this peptide with patients. It is not FDA-approved in the United States. However, it is approved in several other countries for specific conditions. Dr. Deb Muth 06:19In Italy, it’s approved for the treatment of chronic hepatitis B and hepatitis C. In China, it’s approved for chronic hepatitis B and adjunct immune compromised patients receiving vaccinations or suffering from certain infections. It has an orphan drug designation in the United States for certain cancer indications, but its designation does not constitute approval. It simply provides regulatory incentives for further development. So the evidence base for thymosin alpha-1 is substantial in some areas but comes primarily from non-US populations and research groups, which creates challenges in evaluating quality and generalizable information. So in hepatitis B and C, multiple clinical trials, many conducted in China and Italy, have examined TA1 as an adjunct to antiviral therapy. Dr. Deb Muth 07:21A meta-analysis by Wu and colleagues published in the Journal of Viral Hepatitis in 2013 examined 23 randomized controlled trials, including over 2,000 patients with chronic hepatitis B. The analysis found that combining TA1 with nucleoside analogs like LAMVDUDE or an and TCAVAR improved the hepatitis antigen seroconversion rates by HBV DNA clearance compared to its nucleoside analogs alone. And the effect sizes were modest but statistically significant, with the HBE-AG seroconversion rates improving from about 24% with antivirals alone to 38% in combined therapy. Now in hepatitis C, early trials before the development of direct-acting antivirals showed that TA1 combined with interferon alpha improved sustained virological responses, and compared to interferon alpha, Dr. Deb Muth 08:30Furon alone, particularly in difficult-to-treat populations like those with a genotype one or a high viral load. However, the advent of highly effective direct acting antivirals that achieve SRV rates, sorry, SVR rates exceeding 95%, the role of TA1 in hepatitis C has become less clear. Now in sepsis and critical illness, more recent interest has focused on TA1 in severe cases of sepsis and septic shock. Ren and colleagues published a systematic review and meta-analysis in the Frontiers of Immunology in 2022, analyzing 18 randomized controlled trials, including 1787 patients with severe sepsis or septic shock the pooled analysis showed that ta1 administration was associated with reduced 28-day mortality relative risk at 0.70 meaning a 30 reduction in mortality compared to the standard care alone and the effect appeared Dr. Deb Muth 09:39most pronounced in patients with sepsis-induced immunosuppression measured by HLA-DR expression in monocytes. Now, this is amazing because going forward, we’re going to talk about something that’s commonly known as cytokine storm. Now, cytokine storm really became apparent since 2020 with the viral infection that we’re dealing with in the world today. But they were already looking at this kind of cytokine storm produced by sepsis or sepsis-induced immunosuppression. And it triggered this hyperinflammatory response called the cytokine storm. And many patients who survived the initial phase of the immune suppressed stata, characterized by a T cell exhaustion, reduced antigen presentation, and increased susceptibility to secondary infections. Thymusin alpha-1, TA1, may help restore this immune competence in this phase. However, it’s important to note that patient selection and timing are critical. Dr. Deb Muth 10:43Giving this immune stimulant during a hyperinflammatory phase could theoretically worsen outcomes. So you don’t want to give it to them while they’re in the flare up or the sepsis or the infection, but given to them during the immunosuppression phase afterwards might be beneficial. Now there is also some cancer immunotherapy that we see with TA1 and has been studied as an adjunct in cancer treatment with the hypothesis that it could enhance immune surveillance and response to tumors. And a comprehensive review of Garci and colleagues published in Expert Opinion on Biological Therapy in 2007 examined multiple trials in melanoma, lung cancer, hepatocellular carcinoma, and other malignancies. And the results were mixed. Some trials showed improvement in the immune parameters, increased CD4 in T-cells. improved lymphocyte proliferation responses and some actually showed trends toward improved progression free survival but overall survival benefits were inconsistent and the heterogeneity of the cancer types treatment protocols and outcome measures makes a definitive conclusion difficult as a vaccine adjunct several studies particularly from china have examined ta1 as an adjunct to enhance vaccine responses Dr. Deb Muth 12:11in immune-compromised populations, including the elderly, dialysis patients, and transplant recipients. The rationale is sound. These populations often mount suboptimal antibody responses to vaccines, and TA1’s immune-enhancing effects might improve protection. There are small trials. They have shown improvement in seroconversion rates of hepatitis B vaccines and influenza vaccine in these populations. And though large-scale confirmatory studies are limited, there is a possibility here. Now, on their safety profile, one of the appealing aspects of thymusin alpha-A TA1 is that it’s apparently favorable safety profile in clinical trials. There are some injection site reactions with a little redness, a mild discomfort, and most commonly reported adverse effects. is that their severe adverse events attributable to TA1 have been rare in published trials. However, comprehensive long-term safety data are limited Dr. Deb Muth 13:13And theoretically, concern exists that immune modulation could potentially trigger or exasperate autoimmune conditions in susceptible individuals. Though this hasn’t been clearly demonstrated in clinical trials, integrative medicine considerations for integrative practitioners concerning the thymus and alpha-1, several factors require careful thought. First, sourcing and quality control are critical concerns. Since it’s not FDA approved, TA1 available in the United States typically will come from a compounding pharmacy or an international supplier with variable quality assurance. And pharmaceutical grade product with certificates of analysis showing purity, sterility, and endotoxin testing is essential, but it is readily available from many of these companies. Second, patient selection matters immensely. TA1 should be considered in complex cases where conventional approaches have been insufficient, such as chronic viral infections not responding adequately Dr. Deb Muth 14:21to standard antivirals, post-viral syndromes with evidence of immune dysfunction, cancer patients with immune suppression in consultation with oncology, and it should generally be avoided in active autoimmune disease unless there’s a compelling rationale and close monitoring. Now, TA1 is not a standalone therapy. In cases of chronic viral infection, Comprehensive immune support includes addressing nutritional deficiencies, optimizing vitamin D levels to be between 50 and 80, adequate zinc, selenium, and vitamin A, optimizing gut health since 80% of our immune function is in the gut, you need to optimize gut function. Managing stress from the HPA access dysfunction, chronic cortisol elevation, suppression, and immunity, ensuring adequate sleep, immune memory consolidations during sleep, addressing any metabolic dysfunction, insulin resistance, repairs in the immune function, and the bottom line on thymus and alpha-1 is Dr. Deb Muth 15:26is that it represents legitimate medicine in other countries with a substantial evidence base in specific contexts, but it remains experimental in the U.S., and practitioners using it should provide comprehensive, informed consent about its regulatory status, evidence quality, and source verification. while ensuring it’s part of comprehensive protocols. It is not a magic bullet. And again, what you’re gonna hear me say quite often here is that many of these peptides should be used in conjunction with something else. They should not be used alone. And can peptides be stacked? The answer is yes, they can. So if somebody has an insulin resistance, or a metabolic dysfunction, they can tier TA1 with a GLP-1 like terzepatide or semiglutide. That is not a problem to do that. You need to just work with a practitioner that understands how to do that effectively. So let’s look at BPC-157. Dr. Deb Muth 16:26This is a phenomenon I love BPC-157. Let’s separate it from marketing to actual mechanism of actions here. So BPC-157 stands for Body Protection Compound 157. It is a chain of 15 amino acids that are described as a partial sequence of body protection compound, a protein found in human gastric juice. It has become one of the most hyped peptides in regenerative medicine inside the athletic performance and biohacking communities with claims ranging from healing tendons and ligaments to repairing gut lining or reversing organ damage. The challenge is separating the legitimate mechanisms of science from the marketing hype. The proposed mechanism of BPC-157 are biologically plausible and intriguing. The research suggests that it may influence several growth factor pathways, including vascular endothelial growth factor, VEGF, which promotes new blood vessel formation and has improved better supply of blood flow to injured tissues, theoretically accelerating healing. Dr. Deb Muth 17:40It may also affect fibrous blast growth factor, FGF, and transforming growth factor beta, TGF beta pathways. both involved in tissue repair and remodeling. And some studies actually suggest that BPC-157 modulates inflammatory cascades, potentially reducing excessive inflammation while promoting the resolution phase that allows tissue rebuilding. Now I want to talk just a few moments here about these different tests that we’re talking about tgf beta veg f for those of you who are in our mold world you are very familiar with these uh lab tests we do this to see if you have a mold exposure what’s happening to your body and it’s been very challenging to try to heal this part of the mold illness and manipulate these VEGFs and TGF betas. And so with the fact that BPC helps us modulate this inflammatory cascade, BPC can be very helpful in the world of mold or mycotoxin illness in repairing those parts of the body that have been damaged by the mycotoxins. Dr. Deb Muth 18:48Now there is animal research on BPC-157. It is extensive and primarily from a research group led by pre-drag, oh, I can never say these names, Cyrek at the University of Zagreb in Croatia. Published studies in animal models have shown accelerated healing in a remarkable variety of injury types. A 2011 paper by Chang and colleagues in the Journal of Applied Physiology demonstrated that BPC-157 improved therapy tendon healing in rats with Achilles tendon injuries, and the treated rats showed increased tendon outgrowth, better cell survival in the injured area, enhanced cell migration to the injury site, and improved biochemical strength of the healed tendon compared to controls. Multiple other animal studies have shown similar promising effects. Ligament tears, healing faster in rabbits, muscle damage recovering more quickly in rodent models, gastric ulcers healing in rats given experimental induced ulcerations, inflammatory bowel lesions improving in mouse models of colitis, and even bone to tendon healing showing enhancement in animal studies. Dr. Deb Muth 20:02The breadth of injury types showing benefit in preclinical models explains the enthusiasm of this peptide. However, this is critical. These animal studies, primarily in rodents and rabbits, animal models of injury healing don’t reliably translate to human clinical outcomes. And the doses used in these animal studies when converted to human equivalent doses vary widely. And optimal human dosing is completely unknown at this point. it is all considered experimental and perhaps most importantly there are essentially no peer-reviewed controlled clinical trials in human published in humans published in major medical journals in a 2001 review of arthroscopy and the journal of arthroscopic and related surgery specifically examined in the evidence of bpc 157 and other peptides in musculoskeletal medicine The authors concluded bluntly that BPC-157 lacks evidence from randomized controlled trials and has an unknown safety profile in humans. Dr. Deb Muth 21:09 They emphasized that the jump from animal data to recommending peptides for humans use bypasses the fundamental requirement for Phase I safety studies, Phase II dose-finding studies, and Phase III efficacy trials that would establish whether BPC-157 actually works in humans and whether or not it’s safe. The absence of human safety data is particularly concerning given BPC-157’s proposed mechanisms. Peptides that influence growth factor signaling and angiogenesis could theoretically have off-target effects. Uncontrolled angiogenesis, for instance, is a hallmark of cancer progression. Tumors require blood vessel formation to grow beyond a certain size. And while there’s no evidence that BPC 157 promotes cancer, The complete absence of long term human safety studies means we simply don’t know. This isn’t fear mongering. It’s acknowledging uncertainty and uncertainty exists and understanding that if you’re choosing to use peptides like BPC 157, you are doing it in an experimental model. Dr. Deb Muth 22:17We’re experimenting with the doses that are being used. And there is potential for it to cause cancer cells in your body to grow. And you need to be aware of this and understand the risks that you’re taking when you’re using an investigational or off label use peptide. Now, quality control issues with BPC also exist. It’s not FDA approved for any indication in the US. It’s not approved in any major regulatory jurisdiction worldwide. It’s marketed as a research chemical explicitly to bypass FDA oversight. And commercial sources selling BPC-157 range from compounding pharmacies, which have some quality standards but are not FDA inspected. You can take that for what you want to believe on that one. to overseas suppliers operating with absolutely no quality assurance whatsoever. If you are choosing to use BPC-157, you have to understand who’s manufacturing it for you, where you are getting it from, how pure it is. Dr. Deb Muth 23:26You want to make sure that you have the certificate of analysis and that it does not contain bacterial endotoxins that can contaminate the peptide or degrade the peptide and cause other issues for you. So when you talk about peptides with patients regarding BPC-157 or if you’re listening to this and you’re already using BPC-157 or other peptides, that are quote-unquote not for human consumption, an evidence-based response acknowledges both the appeal and the limitations. And you want to talk about the animal data that’s definitely showing some progress and some potential, but we don’t know what we don’t know in humans. If people are willing to take that risk, that is up to them to do that. But using BPC right now is experimental and people need to be aware of that. Are there evidence-based alternatives for patients with tendon or ligament injuries? Dr. Deb Muth 24:26And there are. There’s PRP, which has been studied in multiple randomized controlled trials. for conditions like lateral epicondylitis, tennis elbow, Achilles issues, patellar issues, knee issues. However, I want to caution you on this too. So the study that was done by Cox and colleagues in muscles, ligaments, and tendons in the Journal of 2014 showed modest benefits in pain and function compared to controls. And though the effects vary by injury type, PRP preparations can be helpful. You have to understand that a lot of times when people are doing PRP injections in their office, they are not doing it exactly the same way it was done in the study. And not to mention, if you’re using your own PRP to heal a ligament or a tendon or help your arthritis and you’re 60 or 70 years old, That is not good quality protein rich plasma. It is old protein rich plasma. And you’re not going to see necessarily the same benefits that you would see if you were using placental tissue or umbilical tissue. Dr. Deb Muth 25:33You also want to address the nutritional deficiencies or support that’s needed for connective tissue healing. And these are collagen peptides dosed at 15 grams a day. And this has been shown in a study by Shaw and colleagues in the American Journal of Clinical Nutrition in 2017 to augment collagen synthesis when combined with intermittent loading. Vitamin C is also an essential cofactor for collagen production and stabilization of collagen structure at a dose of around 500 to 1000 milligrams a day to support this process. You also need to have good adequate intake of copper and zinc. These are cofactors in collagen. Silica is also important. This comes from horsetail extract. This provides additional support as well. So more importantly, I think remembering that rehabilitation matters as well. Doing these protocols without doing some rehab is not going to get you where you want to go. Dr. Deb Muth 26:33There’s a research study by Alfredson and others for Achilles tendinopathy using the control lengthening of muscle tendon units under load to promote tendon remodeling and healing. These protocols have solid evidence and cost nothing beyond professional guidance from a physical therapist. They are important for patients seeking cutting edge regenerative approaches. Stem cell therapies, growth factors, concentrates derived from patients’ own tissues like PRP. These have a lot of good endogenous materials and they have good safety profiles. BPC-157 represents the perfect example of how promising Preclinical science gets marketed far beyond the evidence and it may eventually prove to be valuable. I think it will. But right now that determination does require some human studies and hopefully with the administration that we have right now and Bobby Kennedy, we will actually start to see some of that occur. Now the next peptide I want to talk about is TB4, thymus and beta-4. Dr. Deb Muth 27:36This is a wound healing peptide. It is a 43 amino acid peptide that’s naturally present in virtually all human cells except red blood cells. It’s actually one of the most abundant peptides in the human body, particularly concentrated in blood platelets, wound fluid, and many tissues. It’s naturally ubiquity makes it mechanistically interesting. The body wouldn’t produce it in such abundance if it didn’t serve a function. So the primary role of TB4 involves building G-actin. It’s a form of monomeric actin. And it’s structural protein that forms the microfilaments within the cells, providing cellular structure and enabling cell movement. TB4 prevents from F-actin filaments. I’m not going to talk too much about this. It’s really critical for wound healing as cells need to migrate into the injury sites. Dr. Deb Muth 28:37so the cell shape changes and the cellular response to the injury. So think of this as though you tore your meniscus and the body created all this TB4 to come to that injury to try to heal that site. That’s exactly what the TB4 is doing inside the body when there’s an injury. It’s been shown in research to help produce new blood vessel formation, promote endothelial cells, It helps modulate inflammatory cytokines, potentially reducing TNF-alpha, IL-1, and possibly protecting in programmed cell death, which we call apoptosis. And some studies suggest that it is cardioprotective in its effects in animal models of myocardial infarction, so heart attack, and neuroprotective in other models for brain injury. Now, these remain to be preliminary, but they are being seen. So the regulatory status on TB4 can create some confusion. Dr. Deb Muth 29:40The natural TB4 molecule itself is not FDA approved as a drug. However, TB4 based drug candidates called RGN259, formerly TB4, has been in the development by regen tree for corneal injuries of the dry eye disease. And as of recent updates, this drug is completed phase three trials for its neurotrophic keratopathy, severe corneal condition. But the FDA approval is still pending. So that means that the most advanced TB4-based pharmaceuticals hasn’t yet crossed the finish line for approval. The commercial peptide market further muddies the picture with TB500, which is often described as the synthetic fragment of TB4. However, this extract’s relationship between TB500 and TB4 varies depending on the source. Dr. Deb Muth 30:41So some claim that TB500 is identical to TB4, but positions 1 through 4 suggest it’s a different fragment. and the quality control across suppliers is not existent. So this confusion is part of why recommending TB500 becomes problematic for practitioners and patients, often because they aren’t certain what molecule they’re actually getting. The evidence base for TB4 in humans is limited, primarily to eye research, and the studies from Sohn’s and colleagues published in journals like Vitamins and Hormones in 2016 have examined topical TB4 for corneal injuries and neurotrophic keratopathy, dry eye, and other surface diseases. Now, these studies showed some promise in promoting this, and there is, however, a topical application to the cornea that is vastly different from a systemic injection. So for systemic use in wound healing, musculoskeletal issues, Dr. Deb Muth 31:42cardiac protection, neuroprotection, human clinical trials. There is scarce to non-existent evidence in humans. Most of the evidence remains in animal models or cell culture studies. And a review by Flip and colleagues in the Journal of Investigational Dermatology in 2006 detailed TB4’s effects on the matrix remodeling during wound repair in animal models, showing effects on collagen disposition, granulation, tissue reformation, and wound contraction. Another review by Ho and colleagues in expert opinion on biological therapy in 2007 discussed TB4’s potential in tissue regeneration and regenerative medicine, but noted the field remained largely blank. preclinical. So this is really important again to understand that there is just not enough human data. So there is a concern with cell division and migration. This theoretically exists Dr. Deb Muth 32:45for the potential effects on cancer cells, which would also rely on migration and division and other intended consequences of disrupting normal cellular architecture. These aren’t proven risks, but they are unexplored questions that we need to be aware of when we’re using peptides. This can cause cancerous tissue to grow. Very similar to what we talked about with BPC-157. These are also sold as research chemicals. There is no FDA oversight. So purity, potency, contaminations all still exist for these peptides. Now from an integrative perspective, the natural presence of TB4 in wound fluid and its biological roles in healing are legitimate science. in presence does not equal therapeutic utility. The body tightly regulates where and when and how much TB4 is present through natural production and bypassing that regulation with external dosing may or may not cause us to have beneficial or introduce risk. Dr. Deb Muth 33:49So we need to know that this is experimental use. Those people who are seeking wound healing and tissue repair the evidence-based approach of the body’s own capacity to heal is huge definitely want to be increasing your protein intake optimizing your zinc copper vitamin c and vitamin a and then managing glucose is really important during this time as well so let’s talk about a fun topic now and that’s growth hormone secretagogues this is the anti-aging hype machine these peptides in this category are things like semoralin ipameralin cjc 1220 1295 and others and among the most aggressively marketed in anti-aging and longevity medicine they all share a common goal stimulating the pituitary gland to release more growth hormone and the appeal is understandable. GH levels decline with age, and this decline is associated with increased fat mass, decreased lean muscle, reduced bone density, and other aspects of aging. Dr. Deb Muth 34:55The other times we’ll see growth hormone levels decline significantly is with chronic illness, and the logic is to restore youthful GH levels and youthful physiology. Now, semirelin from an FDA approved diagnostic to compound anti-aging product. Semirelin is a 29 amino acid peptide representing the first 29 amino acids of the full 44 amino acid human growth releasing hormone, GHRH. We talked about this on another episode of the podcast. And you can go back and listen to that one a little bit if you want. This fragment contains the complete biological activity of the full GHRH molecule and it binds to GHRH receptors in the anterior pituitary and stimulates growth releasing peptides, growth hormone releasing peptides. Semirelin was previously FDA approved as diagnostic testing of growth hormone secretion, essentially, to determine if the pituitary could still respond to GHRH stimulation in patients being evaluated for growth hormone deficiency. Dr. Deb Muth 36:06However, the manufacturer was discontinued and there was no longer an FDA approved semirelin product on the market in the United States. What exists now is semirelin available from compounding pharmacies used off label for anti-aging, body composition, and general growth hormone optimization purposes. This represents a significant gray area. Again, compounding medications serve a very important role, but they need to meet certain recommendations and regulations, as we’ve talked about in the past. You want to make sure that your compounding pharmacy that you’re obtaining semirelin from is qualified to do that, that they are doing best practices, and that you’re getting a good product. The theoretical advantage to semirelin over direct growth hormone administration is that it preserves more of the physiological growth hormone secretion patterns. Natural GH is released in pulses, primarily during sleep, not as a continuous elevation. Dr. Deb Muth 37:07So semirelin stimulates the pulses rather than providing a constant super physiological growth hormone level. And that pulsatile pattern is thought to reduce some of the side effects and metabolic concerns that we have with continuous growth hormone exposure. However, the evidence supporting semirelin for anti-aging and body composition in healthy adults is minimal. Most of the data comes from studies conducted in the 1990s when the FDA approved product existed. Not that that means it’s bad. We have drugs that have been in the market for over a hundred years that are still there, that still have the research and are still being used successfully and safely today. So we don’t want to let that really make us think that this product isn’t safe. So a 2006 review from Walker in Clinical Interventions of Aging suggested that semirelin might be a better approach than direct GH for adult onset growth hormone insufficiency, but they do acknowledge that the evidence was limited. Dr. Deb Muth 38:12And although we don’t have any large scale trials that we can examine for semirelin’s efficacy, it is now commonly prescribed. And the optimal dosing for anti-aging purposes is still unknown. It is considered experimental and it does vary from person to person, but it is still unstudied. The effects on cancer risk, cardiovascular disease, metabolic dysfunction over long time periods are also still unknown. I would argue that the side effects or the risk factors of not having growth hormone are equally as bad as the unknowns that we have here. We’re not looking to try to get super physiological doses. We’re trying to restore youthful GH levels. Typically, we’re not trying to restore back to a 20-year-old. We’re trying to restore back maybe 10 years. That is a better way of doing this. And I think that’s important for people to understand. Now, ipamirelin is the ghrelin mimicker. Dr. Deb Muth 39:12Ipamirelin is a pent-up peptide, five amino acid, that acts as a growth hormone secretagogue receptor, a GHS-R agonist. It mimics the action of ghrelin, the hunger hormone, that also stimulates growth hormone release. The proposed advantage over earlier secretagogues is that ipamirelin stimulates growth hormone release without significantly affecting cortisol, prolactin, or other glucose things, which can be increased by growth hormone secretagogues. The regulatory status is clear. Ipamirelin is not FDA approved for any indication. It’s sold as a research chemical. Human evidence is thin. It’s limited to single dose studies examining how quickly it’s absorbed and metabolized with minimal data on dosing and clinical outcomes. Now there are marketing claims for ipamirelin and they are extensive. Dr. Deb Muth 40:13It increases lean muscle mass, it decreases body fat, it improves sleep quality, faster recovery from workouts, enhanced injury healing, better skin quality. The evidence supporting these claims in humans is not available we don’t have it these are claims that are made by the effects that we know from growth hormone so it’s not necessarily a bad thing we know what growth hormone does we know growth hormone does all of these things if ipamorelin is a precursor to that it will obviously help improve those things making that correlation of what growth hormone does So there are safety concerns that mirror the same as any other growth hormone elevating therapy. It can cause fluid retention, joint pain, carpal tunnel syndrome, insulin resistance, glucose intolerance, and theoretically, can it increase calcium? cancer risks? It can because IGF-1 promotes cell proliferation and can inhibit apoptosis in cancer cells. Now remember, your body makes IGF-1. Dr. Deb Muth 41:15If it’s not making enough of it, that’s a problem. If it’s making too much of it, That’s a problem. So just understand that if you are adding these things, and especially in elevated doses, you are taking a potential risk. So there is also now CJC 1295 is a modified GHRH analog of 30 amino acid peptide based on GHRH structure, but with modifications. So it includes the addition of drug affinity complex, DACC, DAC, which involves conjugation with a small albumin binding molecule, dramatically extends the peptide’s half-life from minutes to as much as potentially a week or more. And this creates sustained growth hormone elevation rather than that pulsatile release. There are actually two versions of this. There’s CJC 1295 with DAC, longer acting version, and CJC 1295 without DAC, which is essentially a shorter duration of semirelin. Dr. Deb Muth 42:19And so when we’re comparing products, it is… only the difference between long acting and short acting. The human evidence for CJC 1295 is limited to a single published phase one study by Techman and colleagues in the Journal of Clinical Nutrition and Metabolism in 2006. And the study involves 18 healthy young adults showed that CJC 1295 with DAC produced a sustained elevation of GH and IGF-1 lasting several days after the injection. That’s essentially the entire published human evidence of this peptide. There are no phase two studies examining optimal dose. So that is all considered experimental. And there is no phase three studies examining clinical efficacy. So the sustained GH levels created by CJC 1295 with DAC raises specific concerns because the natural GH secretion It goes up and down, up and down, up and down. Dr. Deb Muth 43:19And that constant elevation may have a different metabolic and cellular effect. And we just really don’t know what that’s going to be yet. So we can understand that elevated IGF-1 levels can theoretically increase cancer concerns and metabolic risks. So rather than always injecting peptides, which are very expensive… You can do other things. And there was a study by Hartman and colleagues in the Journal of Clinical Endocrinology and Metabolism in 1992 that demonstrated the 48-hour fast increased integrated growth hormone secretion five-fold through increased GH levels. Now, the problem with this is fasting for 48 hours is a challenge. And how long is it going to increase the growth hormone secretion without causing issues? Or in general, how long is it going to go up? Dr. Deb Muth 44:19So we have to be cautious about that as well. Sleep optimization is non-negotiable. The majority of growth hormone secretion occurs during sleep, slow wave sleep, typically the first sleep cycle, and poor sleep quality or insufficient sleep typically. can dramatically affect your growth hormone levels. And then high intensity interval training, HIIT resistance training can stimulate growth hormone as well. This was seen in a study by Godfrey and colleagues in sports medicine in 2003 and was examined in exercise-induced growth hormone responses to athletes. So we definitely see these kinds of things. So let’s talk about some longevity peptides now. These expand the telomere. So there’s epitalin and epithalamin and when these are used in anti-aging they can produce some amazing results. Dr. Deb Muth 45:22So epitalin is a synthetic terapeptide, just four amino acids. It was originally synthesized as a simplified version of epithalamine. a pineal gland extract containing multiple peptides. The synthetic four amino acid version was created to isolate what researchers believed might be the active anti-aging component. The mechanism produced for epitalin centers on telomere and telomerase, Telomeres are protective caps at the end of the chromosomes consisting of repetitive DNA sequencing. And every time a cell divides, telomeres shorten slightly because DNA polymers cannot fully replicate the ends of the linear chromosomes. So this progressive shortening acts as a molecular clock. After 50 or 70 divisions, the telomeres become critically short, triggering a cellular senescence. Dr. Deb Muth 46:22This telomere shortening is one mechanism of cellular aging and telomeres in the enzyme that can rebuild telomeres by adding these caps back onto the end of the chromosome. It’s active in stem cells, germ cells, and unfortunately in about 85 to 90% of the cancer cells. In most adult somatic cells, telomerase is inactive or present at very low levels, allowing the telomeres to shorten with division. The research on epitalin suggests it might activate this telomeres act telomeres process primarily from a research group led by Vladimir in Russia. Vladimir Kavasan in Russia. He is a huge peptide researcher or was he passed away with publications dating back to the early 2000s and a study published in bio gerontology in 2000 by Kavasan Dr. Deb Muth 47:25and colleagues examined the effect of epitalin on the lifespan of fruit flies, and they treated fruit flies that showed a modest increase in mean and maximum lifespan compared to its controls by approximately 10 to 15% lifespan extension in some experimental groups. And there were other studies in 2003 that examined epitalamine in a female Swiss-derived mouse. This was done by Ann Simove and colleagues. And the researchers reported that epitalin treatment was associated with increased lifespan as well. And the most cited mechanistic work comes from cell culture studies. And that is also Cavason’s group that published this research in 2003, showing increased telomeres activity in cultured somatic cells again. More recently, between 20 and 25, the series of publications have continued to explore epithelial effects on telomere dynamics in cell cultures. Dr. Deb Muth 48:32So there is a lot of research that’s been done. The mass majority has been done on epithelin. And most of it has been done by a single research group in Russia. There is some restrictions on some of the cell culture data that we’re seeing. And it does show that epithelin sometimes can be described as a regulating hormone. Carcadian rhythm for melatonin production, which is derived by the penile extracts. And however the evidence for this affects minimally and mechanistically unclear, the pineal gland primarily functions as melatonin secretion in that light-dark cycles. So Epithalin or epitalin is not FDA approved. It is not approved for any major regulatory jurisdiction. It is sold as a research chemical only. Dr. Deb Muth 49:33So you need to follow the same safety profiles that we’ve talked about in other episodes and in today’s episodes. And when we’re talking about epithalin, and we’re excited about it being an anti-aging science, we should balance this with the honesty and the evidence of the quality of that evidence. We don’t know its safety effect. We don’t know if it’s going to increase the risk of cancer. We can’t verify that. And we need to be using it in an experimental use of unknown risks only. Of course, diet, physical activity, stress management, sleep quality, all of those things are important for us to be looking at when we’re looking at these peptides. Now, I want to get into some of the brain peptides. This is the nootrophic frontier. C-Max and C-Lank, there is Russian pharmacology that’s done. C-Max and C-Lank represent an interesting case study in how different regulatory environments and research traditions Dr. Deb Muth 50:36create challenges in evaluating this evidence. Both peptides were developed in Russia, are approved for their specific indications and have substantial Russian language and literature supporting their use. However, the FDA approval in the United States is still not there. C-Max is a seven amino acid. It’s a synthetic analog. It is a fragment, particularly ACTH 4 through 10. It’s sometimes called the melanocortin effects because it involves the melanocortin receptors of the central nervous system. CMAX was developed by the Institute of Molecular Genetics of Russia Academy of Sciences and is approved in Russia for several indications, including acute stroke, transient ischemic attacks, cognitive disorders. It has Russian approval and is based on clinical trials primarily in Russia. Dr. Deb Muth 51:39It does help to increase brain-derived neurotrophic factor, BDNF, a protein critical for neuroplasticity, the brain’s ability to form new connections and adapt to the challenges. BDNF supports neuronal survival and promotes growth of these new neurons. C-Max also influences neurotransmitter systems, particularly dopamine and serotonin, and there is some research that suggests it affects on metabolism as well, and endogenous opioid peptides that involve pain reception and mood regulation. So it has some good potentials there. There is also C-Link, which is a hepatopeptide structurally similar to Tufts’ and an immune modulatory peptide. It was also developed in Russia and was approved for anxiety disorders as a neurotropic. Its effects involve anxiolytic effects, possibly through the GABAnergic system or the GABA system of the brain, and immune modulation. Dr. Deb Muth 52:44The Russian research is examined by C-Link for anxiety disorders. and finding reductions in anxiety without sedation. There is a dependency potential or cognitive impairment does not exist like it does with benzodiazepines with C-Link. So that is really good. And they do report attention and memory improvement using C-Link. There is a study that was done in neuroscience and behavioral psychology in 2018 that examined C-Linx effects and proposed that it exerts cytoprotective effects through BDNF pathways similar to C-Max. So both of these are Russian research-based They’re not wrong or fraudulent. It’s just that they are from Russia and we all have our concerns with Russia. However, that does not necessarily mean their research doesn’t hold quality. Dr. Deb Muth 53:49Neither peptide is approved by the FDA, and so you are using this off-label. The same rules apply for all of the other peptides that we’ve talked about that are produced off label. You want to do the same things that you would do with anything else. Good protein, omegas, B vitamins, acetylcarnitine, exercise, sleep, all of that still applies when we’re using these peptides. So I want to talk briefly about clinical decision and framework when we’re looking at this. First and foremost, we always want to go to FDA-approved peptides. Secondly, we would look at international approval with peptides that are established in other countries but lack FDA approval. And then preclinical evidence only or experimental peptides. These can be used, but they are not ethically recommended in the traditional medicine world. Dr. Deb Muth 54:50 If patients use them, we need to have appropriate counseling about the evidence surrounding them, the safety, and where to find them. how to find them and how to ask for these certificates of analysis. So I think it’s really good that we were exploring all these peptides and understanding what they are. There’s a lot of controversy out there. There’s a lot of concern out there. And what we can say with confidence is that peptides are powerful biological signaling molecules. Some peptide based medications, semi-glutide, triseptide, PT 141, Lupron that are all FDA approved. can dramatically improve outcomes in patients that are obviously selected for the correct ones. There are many other peptides that we address that are integrative and longevity space in the regenerative medicine. These peptides are all experimental. That does not automatically make them wrong. Dr. Deb Muth 55:50It just means that we need to be honest about what we’re doing with them and we need to be cautious with the patients so that they can make a decision to be part of an experimental study. in looking at how to use these peptides. So peptides are tools like any other tools. They work best in the hands of skilled people, and they are applied to appropriate situations, integrating into comprehensive approaches that address root causes. The most powerful peptide administered to a patient with untreated inflammation, hormonal chaos, nutritional deficiencies, and disorders of sleep will disappoint. The simplest evidence-based interventions apply. to a patient whose foundational physiology has been optimized. And this is the art of the science of peptide, right? If done right, respecting both the power of these molecules and the complexity of human beings that we are privileged to serve can make a difference in their lives. So thank you for listening to this episode. Dr. Deb Muth 56:52I hope this was helpful. If you can know of somebody that might benefit from this, please like, share, and subscribe. It means a lot to us. And I hope you join us for our next episode of Let’s Talk Wellness Now. Welcome to Let’s Talk Wellness Now, where we bring expert insights directly to you. Please note that the views and information shared by our guests are their own and do not necessarily reflect those of Let’s Talk Wellness Now, its management, or our partners. Each affiliate, sponsor, and partner is an independent entity with its own perspectives. Today’s content is provided for informational and educational purposes only and should not be considered specific advice, whether financial, medical, or legal. While we strive to present accurate and useful information, we cannot guarantee its completeness or relevance to your unique circumstances. We encourage you to consult with a qualified professional to address your individual needs. Dr. Deb Muth 57:54Your use of information from this broadcast is entirely at your own risk. By continuing to listen, you agree to indemnify and hold Let’s Talk Wellness Now and its associates harmless from any claims or damages arising from the use of this content. We may update this disclaimer at any time and changes will take effect immediately upon posting or broadcast. Thank you for tuning in. We hope you find this episode both insightful and thought-provoking. Listener discretion is advised.The post Episode 258 – Investigational Peptides: What's Promising, What's Hype & What You Must Know first appeared on Let's Talk Wellness Now.

Is fasted running sabotaging your performance? Are you accidentally under-eating on your hardest training days? This week, we break down the seven most common nutrition mistakes runners make, from calorie restriction at the wrong time to blindly copying elite protocols, and explain why the science says you probably need to eat more, not less.We cover why your gut issues might actually be a training problem, not a food problem. We talk about why "clean eating" is often just restriction in disguise. And we explain why doing what Kipchoge does probably isn't what you should be doing.Plus, we answer listener questions on accountability and whether high-carb fueling causes diabetes (spoiler: it doesn't). And Coach James Nance joins to talk about coaching multi-sport athletes, helping runners recover from overtraining, and his TrainingPeaks hot take that might surprise you.In this episode:Why restricting calories on training days backfiresThe truth about fasted running and morning workoutsHow to actually fix gut issues during exerciseWhy "clean eating" can become problematicWhat 90-120g of carbs per hour actually means for recreational runnersHow to evaluate nutrition advice and follow the moneyStudies and resources mentioned are linked below.Get involved: Join our Foothills coaching community—one-on-one coach access, twice-monthly roundtables, and a supportive crew of runners. $10/month with code FOOTHILLS10 at microcosm-coaching.com.Questions? microcosmcoaching@gmail.comREFERENCES:Burke, L. M., Ross, M. L., Garvican-Lewis, L. A., Welvaert, M., Heikura, I. A., Forbes, S. G., Mirtschin, J. G., Cato, L. E., Strobel, N., Sharma, A. P., & Hawley, J. A. (2017). Low carbohydrate, high fat diet impairs exercise economy and negates the performance benefit from intensified training in elite race walkers. Journal of Physiology, 595(9), 2785–2807.Costa, R. J. S., Hoffman, M. D., & Stellingwerff, T. (2019). Considerations for ultra-endurance activities: Part 1 – Nutrition. Research in Sports Medicine, 27(2), 166–181.Cox, G. R., Clark, S. A., Cox, A. J., Halson, S. L., Hargreaves, M., Hawley, J. A., Jeacocke, N., Snow, R. J., Yeo, W. K., & Burke, L. M. (2010). Daily training with high carbohydrate availability increases exogenous carbohydrate oxidation during endurance cycling. Journal of Applied Physiology, 109(1), 126–134.Loucks, A. B., & Thuma, J. R. (2003). Luteinizing hormone pulsatility is disrupted at a threshold of energy availability in regularly menstruating women. Journal of Clinical Endocrinology & Metabolism, 88(1), 297–311.Melin, A. K., Heikura, I. A., Tenforde, A., & Mountjoy, M. (2019). Energy availability in athletics: Health, performance, and physique. International Journal of Sport Nutrition and Exercise Metabolism, 29(2), 152–164.Mountjoy, M., Ackerman, K. E., Bailey, D. M., Burke, L. M., Constantini, N., Hackney, A. C., Heikura, I. A., Melin, A., Pensgaard, A. M., Stellingwerff, T., Sundgot-Borgen, J. K., Torstveit, M. K., Jacobsen, A. U., Verhagen, E., Budgett, R., Engebretsen, L., & Erdener, U. (2023). 2023 International Olympic Committee's (IOC) consensus statement on Relative Energy Deficiency in Sport (REDs). British Journal of Sports Medicine, 57(17), 1073–1098.

Send us a textThis week we're heading into week three of the challenge, and I want to talk about something subtle that can quietly make everything feel harder—your energy, your focus, your patience, even your progress. I've been thinking a lot about how often we push through discomfort without ever stopping to ask why it's there. And how, as women who manage full lives and full calendars, we're incredibly skilled at overriding ourselves instead of listening.In today's shorty episode, I invite you to slow down just enough to notice what your body has been trying to tell you all along. This is about strength without force, awareness without judgment, and learning how to trust yourself again in a world that constantly asks you not to. If you've ever felt like something was “off” but couldn't quite put your finger on it, this conversation is for you.Quote of the Week:“The body is your instrument. Learn to play it well.” — Martha GrahamReferencesSkypala, I. J., & Venter, C. (2019). Food intolerance: Clinical perspectives and management. Nutrients, 11(7), 1684. https://doi.org/10.3390/nu11071684Turner, P. J., & Campbell, D. E. (2019). Epidemiology of food allergy. Journal of Allergy and Clinical Immunology, 143(1), 37–44. https://doi.org/10.1016/j.jaci.2018.11.003Fletcher, J., & Adolphus, K. (2021). Food intolerance and mental health: Associations with anxiety and depression. Nutrients, 13(12), 4386. https://doi.org/10.3390/nu13124386Phillips, C. M., Chen, L. W., Heude, B., Bernard, J. Y., Harvey, N. C., Duijts, L., … Godfrey, K. M. (2019). Dietary inflammatory index and metabolic health. Journal of Clinical Endocrinology & Metabolism, 104(12), 6118–6128. https://doi.org/10.1210/jc.2019-00294Esposito, K., Kastorini, C. M., Panagiotakos, D. B., & Giugliano, D. (2011). Mediterranean diet and metabolic syndrome. Journal of the American College of Cardiology, 57(11), 1299–1313. https://doi.org/10.1016/j.jacc.2010.09.073Hotamisligil, G. S. (2006). Inflammation and metabolic disorders. Nature, 444, 860–867. https://doi.org/10.1038/nature05485Saltiel, A. R., & Olefsky, J. M. (2017). Inflammatory mechanisms linking obesity and metabolic disease. Journal of Clinical Investigation, 127(1), 1–4. https://doi.org/10.1172/JCI92035Oddy, W. H., Allen, K. L., Trapp, G. S., Ambrosini, G. L., Black, L. J., Huang, R. C., … Mori, T. A. (2018). Dietary inflammatory index and mental health. British Journal of Nutrition, 119(8), 1–10. https://doi.org/10.1017/S0007114518000218 Let's go, let's get it done. Get more information at: http://projectweightloss.org

Send us a textDr. Christie M. Ballantyne, MD is a Cardiologist and is one of the nation's foremost experts on lipids, atherosclerosis and heart disease prevention. He holds many leadership positions at Baylor College of Medicine ( https://www.bcm.edu/people-search/christie-ballantyne-17846 ), including director of the Center for Cardiometabolic Disease Prevention, co-director of the Lipid Metabolism and Atherosclerosis Clinic, and chief of the Section of Cardiology. With over 1000 publications in the area of atherosclerosis, lipids, and inflammation, Dr. Ballantyne's research on heart disease prevention has led him to become an established investigator for the American Heart Association and the recipient of continuous funding from the National Institutes of Health with a core focus on in basic research of leukocyte–endothelial interactions, translational research in biomarkers, and clinical trials.Dr. Ballantyne's many accomplishments have included being elected as Fellow of the American Association for the Advancement of Science, the American Society of Clinical Investigation, and the Association of American Physicians. In 2012, he received the American College of Cardiology Distinguished Scientist Award (Basic Domain). In 2014 and 2015, Thomson Reuters recognized Dr. Ballantyne as one of “The World's Most Influential Scientific Minds.” Clarivate Analytics, Web of Science, named Dr. Ballantyne as a “Highly Cited Researcher” 2017-2022 in the top 1% of researchers most cited. In 2019, Dr. Ballantyne was awarded the Baylor College of Medicine Michael E. DeBakey, M.D., Excellence in Research Award. His research in biomarkers has led to the FDA approval of 2 biomarkers for cardiovascular risk prediction, and he has played a prominent role in the development and FDA approval of new therapies for treatment of lipids.Dr. Ballantyne also serves on the Editorial Board for Circulation and the Journal of the American College of Cardiology. He received his MD from Baylor College of Medicine with internal medicine residency at The University of Texas Southwestern Medical School and cardiology fellowship at Baylor College of Medicine and an AHA fellowship at the Howard Hughes Medical Institute and Institute for Molecular Genetics at Baylor.Dr. Alexander Tal, MD is an accomplished and recently retired board-certified Endocrinologist ( https://www.doximity.com/pub/alexander-tal-md ) with extensive training from institutions like Baylor College of Medicine, East Tennessee State University/Quillen College of Medicine, Mount Sinai Hospital Medical Center of Chicago and Tel Aviv University Sackler, where he specialized in Diabetes, Metabolism, and Geriatric Medicine, and held Fellow status with the American Association of Clinical Endocrinology, treating various hormonal conditions.Important Episode Link - Merck's Enlicitide Decanoate, an Investigational Oral PCSK9 Inhibitor, Significantly Reduced LDL-C in Phase 3 CORALreef Lipids Trial - https://www.merck.com/news/mercks-enlicitide-decanoate-an-investigational-oral-pcsk9-inhibitor-significantly-reduced-ldl-c-in-phase-3-coralreef-lipids-trial/#ChristieBallantyne #Cardiologist #Lipids #Atherosclerosis #HeartDiseasePrevention #BaylorCollegeOfMedicine #CardiometabolicDisease #LipidMetabolism #Cardiology #AlexanderTal #Endocrinologist #Diabetes #Metabolism #GeriatricMedicine #Merck #Enlicitide #OralPCSK9Inhibitor #Statins #Ezetimibe #Hypercholesterolemia #apoB #Lpa #Lipoproteins #Healthspan #Longevity #Aging #STEM #Innovation #Science #Technology #Research #ProgressPotentialAndPossibilities #IraPastor #Podcast #Podcaster #Podcasting #ViralPodcastSupport the show

Testosterone is everywhere in menopause conversations right now, often framed as a solution for everything from low energy and brain fog to bone health and longevity. In this episode, Dr. Sarah Court breaks down what actually matters when it comes to testosterone for menopausal women, separating social media hype from clinical evidence. The real questions are not whether women have testosterone or whether levels change with age, but whether testosterone should be prescribed, for whom, and what the data truly supports.Using current consensus guidelines, this episode explains why testosterone has one narrow, evidence-based indication, hypoactive sexual desire disorder, and why claims about mood, energy, cognition, bone health, and longevity are not supported by high-quality research. Dr. Court also walks through how testosterone is prescribed in the real world, why the lack of FDA-approved products for women creates problems, and what the safety data does and does not tell us about long-term risks. If you have heard confident claims about testosterone as a menopause cure-all, this episode provides the context you need to evaluate those messages with clarity and skepticism.FOLLOW @MovementLogicTutorials on InstagramMovement Logic: Free Barbell Mini CourseInstagram: Professor Susan DavisInstagram: Dr. Kelly CaspersonGlobal Consensus Position Statement on the Use of Testosterone Therapy for Women — Davis et al., 2019, Journal of Clinical Endocrinology & MetabolismISSWSH Clinical Practice Guideline on Systemic Testosterone for Women — Parish et al., 2021Testosterone Therapy for Women, Systematic Review & Meta-analysis(Lancet Review) — Islam et al., 2019Androgen Therapy in Women, A Reappraisal — Davis & Wahlin-Jacobsen, 2015Kelly Casperson blog post — Testosterone Can Help With Libido, Energy, Focus, & More During MenopauseYou Are Not Broken Podcast — Kelly Casperson, MDYouTube Short: Testosterone and Bone HealthYouTube Short: Testosterone, Motivation & Vitality

In today's episode, I'm opening the first chapter of what I believe is the most important series I've ever created — a deep dive into progesterone and why it became the heart of my medical practice. For more than 20 years, I've watched this “simple, humble hormone” transform women's lives in ways most conventional medicine overlooks. What started in two small treatment rooms has grown into a 25,000 sq ft facility, and the core of our success comes down to understanding progesterone's impact on the female brain, stress response, and emotional resilience. In this episode, I break down: Why progesterone is far more than a reproductive hormone How it regulates the female stress response (amygdala, hippocampus, prefrontal cortex) Why anxiety, insomnia, irritability, and emotional overwhelm often map directly to progesterone decline Why so many women feel “unraveled” in their 40s — and why it's not their fault The science behind oral vs. sublingual progesterone (and why I use troches) How conventional medicine often misses the root cause The importance of physicians showing their work, their data, and their citations The lived stories and clinical outcomes that changed how I practice medicine If you've ever felt dismissed, unseen, or told that your anxiety or mood changes are “just stress,” this episode is for you. This is the beginning of a 7-part series where I break down the neurobiology, endocrinology, testing, dosing, delivery methods, breast health, perimenopause, and more.   Citations: Brinton, Roberta Diaz, et al. “Neurosteroids and Brain Function.” Steroids, vol. 81, 2014, pp. 61–78. Epperson, C. Neill, et al. “New Insights into Perimenopausal Depression: A Neuroendocrine Vulnerability Framework.” The Lancet Psychiatry, vol. 9, no. 2, 2022, pp. 110–118. Frye, Cheryl A. “Neurosteroids—Endogenous Modulators of GABA_A Receptors.” Pharmacology & Therapeutics, vol. 116, no. 1, 2007, pp. 58–76. Genazzani, Andrea R., et al. “Progesterone, Stress, and the Brain.” Human Reproduction Update, vol. 16, no. 6, 2010, pp. 641–655. Meeker, John D., et al. “Environmental Endocrine Disruptors: Their Effects on Human Reproduction and Development.” Reproductive Toxicology, vol. 25, 2008, pp. 1–7. Mellon, Stanley H. “Neurosteroid Regulation of Central Nervous System Development.” Pharmacology & Therapeutics, vol. 116, 2007, pp. 107–124. Mizrahi, Romy, et al. “The Role of Allopregnanolone in Stress, Mood, and Trauma.” Neurobiology of Stress, vol. 11, 2019, 100198. Paul, Steven M., and Graziano Pinna. “Allopregnanolone: From Molecular Pathways to Therapeutic Applications.” Current Opinion in Neurobiology, vol. 48, 2018, pp. 90–96. Pluchino, Nicoletta, et al. “Progesterone and Allopregnanolone: Effects on the Central Nervous System in the Luteal Phase and in Perimenopause.” Gynecological Endocrinology, vol. 36, no. 6, 2020, pp. 441–445. Rasgon, Natalie L., et al. “Perimenopausal Changes in the Brain and Mood: A Review.” Journal of Clinical Endocrinology and Metabolism, vol. 107, no. 4, 2022, pp. 1120–1134. Reddy, Doodipala Samba. “The Neurosteroid Allopregnanolone and GABA-A Receptor Modulation in Epilepsy and Mood Disorders.” Frontiers in Neuroscience, vol. 12, 2018, 933. Schiller, Crystal E., et al. “The Neuroendocrinology of Perimenopausal Depression.” Trends in Neurosciences, vol. 44, no. 2, 2021, pp. 119–135. Schumacher, Michael, et al. “Neuroprotective Effects of Progesterone and Its Metabolites.” Frontiers in Neuroendocrinology, vol. 33, 2012, pp. 415–439. Selye, Hans. “The General Adaptation Syndrome and the Diseases of Adaptation.” Journal of Clinical Endocrinology, vol. 6, no. 2, 1946, pp. 117–230. Sheng, Jun, and György Buzsáki. “Neuronal Firing and Theta Oscillations in the Amygdala During Fear Conditioning.” Neuron, vol. 53, 2007, pp. 653–667. Smith, Sheryl S. “Progesterone Withdrawal Increases Neuronal Excitability in the Hippocampus: A GABA_A Mechanism.” Journal of Neuroscience, vol. 28, 2008, pp. 10171–10179. Snyder, Jonathan S., et al. “Adult Hippocampal Neurogenesis and Stress Regulation.” Nature Reviews Neuroscience, vol. 12, 2011, pp. 1–9. Stanczyk, Frank Z., and Jerilynn C. Prior. “Progesterone and Progestins: A Review of Pharmacology, PK, and Clinical Use.” Steroids, vol. 82, 2014, pp. 1–8. Tu, Ming-Je, et al. “Oral, Vaginal, and Transdermal Progesterone: PK, Metabolism, and Tissue Distribution.” Drug Metabolism Reviews, vol. 52, no. 2, 2020, pp. 1–28. Wang, Jun, et al. “Stress, Amygdala Plasticity, and the Neuroendocrine Interface.” Nature Neuroscience, vol. 10, 2007, pp. 1093–1100. Weinstock, Marta. “The Hippocampus and Chronic Stress.” Neurochemical Research, vol. 42, 2017, pp. 1–12. World Health Organization. Progesterone and Reproductive Function: Clinical Perspectives. WHO, 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.  

Send us a message with this link, we would love to hear from you. Standard message rates may apply.We discuss a clear, practical guide to menopause, explaining what it is, why it happens, and how to manage the most common symptoms with everyday steps and evidence-based options. We set up next week's deep dive on hormone therap. • Defining menopause and typical timing• Why estrogen declines and bodywide effects• Common symptoms across sleep, mood, and metabolism• Hot flashes and night sweats frequency and duration• Vaginal and urinary symptoms that mimic UTIs• Bone density loss and changing heart risk• Lifestyle tactics that actually help• When to ask about hormonal and non-hormonal treatments• Teaser for hormone therapy update next weekSend us an email at yourcheckuppod@gmail.comReferences1. Menopause-Biology, Consequences, Supportive Care, and Therapeutic Options. Davis SR, Pinkerton J, Santoro N, Simoncini T. Cell. 2023;186(19):4038-4058. doi:10.1016/j.cell.2023.08.016.2. The Menopause Transition: Signs, Symptoms, and Management Options. Santoro N, Roeca C, Peters BA, Neal-Perry G. The Journal of Clinical Endocrinology and Metabolism. 2021;106(1):1-15. doi:10.1210/clinem/dgaa764.3. Management of Menopausal Symptoms: A Review. Crandall CJ, Mehta JM, Manson JE. JAMA. 2023;329(5):405-420. doi:10.1001/jama.2022.24140.4. Menopause. Davis SR, Lambrinoudaki I, Lumsden M, et al. Nature Reviews. Disease Primers. 2015;1:15004. doi:10.1038/nrdp.2015.4.5. Menopause: Physiology, Definitions, and Symptoms. Gatenby C, Simpson P. Best Practice & Research. Clinical Endocrinology & Metabolism. 2024;38(1):101855. doi:10.1016/j.beem.2023.101855.6. Reproductive Aging in Biological Females: Mechanisms and Immediate Consequences. Muhammad YA. Frontiers in Endocrinology. 2025;16:1658592. doi:10.3389/fendo.2025.1658592.7. Treating Menopause - MHT and Beyond. Davis SR, Baber RJ. Nature Reviews. Endocrinology. 2022;18(8):490-502. doi:10.1038/s41574-022-00685-4.8. Management of Perimenopausal and Menopausal Symptoms. Duralde ER, Sobel TH, Manson JE. BMJ (Clinical Research Ed.). 2023;382:e072612. doi:10.1136/bmj-2022-072612.9. Hormone Therapy for Postmenopausal Women. Pinkerton JV. The New England Journal of Medicine. 2020;382(5):446-455. doi:10.1056/NEJMcp1714787.10. An Empowerment Model for Managing Menopause. Hickey M, LaCroix AZ, Doust J, et al. Lancet (London, England). 2024;403(10430):947-957. doi:10.1016/S0140-6736(23)02799-X.11. Menopause. Carter AE, Merriam S. The Medical Clinics of North America. 2023;107(2):199-212. doi:10.1016/j.mcna.2022.10.003.Support the showSubscribe to Our Newsletter! Production and Content: Edward Delesky, MD & Nicole Aruffo, RNArtwork: Olivia Pawlowski

This episode's guests:Tatsiana Thomson, Brome Bird Care.John Barentine, Dark Sky Consulting.Lynne Peeples, Author of the Inner Clock.Bill's News Picks:Environmental Commission applauds progress on bird-safe buildings, Amy Smith, Austin Monitor. Great River Bridge goes dark for birds, Hawk Eye.Puffins, petrels, and places: Understanding human perceptions to prevent seabird mortality due to light pollution, Ornithological Applications.Light does not phase shift the circadian clock of subcutaneous adipose tissue in vitro, Biological Timing and Sleep. Brighter bedroom light at night predicts risk for earlier pubertal onset: a two-year longitudinal study, The Journal of Clinical Endocrinology & Metabolism. Send Feedback Text to the Show!Support the showA hearty thank you to all of our paid supporters out there. You make this show possible. For only the cost of one coffee each month you can help us to continue to grow. That's $3 a month. If you like what we're doing, if you think this adds value in any way, why not say thank you by becoming a supporter! Why Support Light Pollution News? Receive quarterly invite to join as live audience member for recordings with special Q&A session post recording with guests. Receive all of the news for that month via a special Supporter monthly mailer. Satisfaction that your support helps further critical discourse on this topic. About Light Pollution News: The path to sustainable starry night solutions begin with being a more informed you. Light Pollution, once thought to be solely detrimental to astronomers, has proven to be an impactful issue across many disciplines of society including ecology, crime, technology, health, and much more! But not all is lost! There are simple solutions that provide for big impacts. Each month, Bill McGeeney, is joined by upwards of three guests to help you grow your awareness and understanding of both the challenges and the road to recovering our disappearing nighttime ecosystem.

In this episode, Dr. Brendan McCarthy, Chief Medical Officer of Protea Medical Center, dives deep into estrone, one of the three key estrogens, and explains why understanding it is crucial for women's health. Learn about: The differences between estradiol, estriol, and estrone How estrone levels shift during perimenopause and menopause Why oral estrogen can dramatically increase estrone The impact of lifestyle factors like diet, body fat, stress, alcohol, and sedentary behavior on estrogen balance Practical tips to support healthy estrogen metabolism naturally Dr. McCarthy breaks down complex biochemistry in a clear, actionable way so you can take charge of your hormonal health.   Citations: 1. Bulun, Serdar E., et al. “Aromatase and Estrogen Biosynthesis in Adipose Tissue.” Endocrine Reviews, vol. 23, no. 3, 2002, pp. 305–342. 2. Labrie, Fernand, et al. “Importance of the Intracrinology of Estrogen Synthesis in Peripheral Tissues in Postmenopausal Women.” Journal of Steroid Biochemistry and Molecular Biology, vol. 118, nos. 4–5, 2010, pp. 273–279. 3. Sasano, Hironobu, and Toshihiko Harada. “Differential Expression of Aromatase and 17β-Hydroxysteroid Dehydrogenase Isoenzymes in Human Tissues.” Journal of Steroid Biochemistry and Molecular Biology, vol. 86, no. 3–5, 2003, pp. 327–333. 4. Yager, James D., and Nancy E. Davidson. “Estrogen Carcinogenesis in Breast Cancer.” New England Journal of Medicine, vol. 354, no. 3, 2006, pp. 270–282. 5. Cavalieri, Ercole L., and Eleanor G. Rogan. “Depurinating Estrogen-DNA Adducts, Mechanisms of Formation, and Prevention.” Clinical Cancer Research, vol. 16, no. 3, 2010, pp. 596–602. 6. Suba, Zsuzsanna. “Circulating Estrogens and Estrogen Metabolism in Obese Women.” Journal of Clinical Endocrinology and Metabolism, vol. 98, no. 11, 2013, pp. 4336–4344. 7. Simpson, Evan R., and Konstanze C. Pike. “Aromatase Expression in Adipose Tissue: Relationship to Obesity and Insulin Resistance.” Endocrinology, vol. 156, no. 9, 2015, pp. 3422–3435. 8. Key, Timothy J., et al. “Circulating Sex Hormones and Breast Cancer Risk Factors in Postmenopausal Women: Reanalysis of 13 Studies.” British Journal of Cancer, vol. 105, no. 5, 2011, pp. 709–722. 9. Stanczyk, Frank Z., et al. “Oral, Transdermal and Injectable Hormone Therapy: Pharmacokinetics and Effects on Estrone/Estradiol Ratios.” Menopause, vol. 24, no. 9, 2017, pp. 1080–1090. 10. Santen, Richard J., et al. “Estrogen Bioidentical Hormone Therapy: Route of Administration and Risk.” Journal of Clinical Endocrinology and Metabolism, vol. 105, no. 7, 2020, pp. 2062–2074. 11. Zeleniuch-Jacquotte, Anne, et al. “Postmenopausal Levels of Estrone, Estradiol, and Estrone Sulfate and Breast Cancer Risk.” Cancer Epidemiology, Biomarkers & Prevention, vol. 23, no. 8, 2014, pp. 1531–1539. 12. Dall, Gabriella V., and Christine L. Clarke. “Local Estrogen Biosynthesis and Signaling in Breast Cancer Progression.” Steroids, vol. 78, no. 7, 2013, pp. 639–646. 13. Heald, Anthony H., et al. “Relationships Between Serum Estrone, Insulin Resistance, and Adiposity in Postmenopausal Women.” Clinical Endocrinology, vol. 67, no. 3, 2007, pp. 340–345. 14. Kuiper, George G. J. M., et al. “Estrogen Receptor β Selectivity of Estriol and Implications for Tissue-Specific Effects.” PNAS, vol. 94, no. 17, 1997, pp. 9105–9110. 15. Michnovicz, Joseph J., et al. “Dietary Indoles and Estrogen Metabolism: Effects of Cruciferous Vegetable Intake.” Journal of Nutrition, vol. 134, no. 12, 2004, pp. 3479S–   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.  

La croissance humaine ne s'arrête pas à un âge fixe, mais dépend d'un processus biologique précis : la fermeture des plaques de croissance, aussi appelées cartilages de conjugaison. Ces plaques, situées à l'extrémité des os longs (comme le fémur ou le tibia), produisent du nouveau tissu osseux pendant l'enfance et l'adolescence. Tant qu'elles restent ouvertes, on peut continuer à grandir. Lorsqu'elles se ferment sous l'effet des hormones sexuelles, la taille devient définitive.Chez la plupart des filles, cette fermeture intervient entre 15 et 17 ans ; chez les garçons, un peu plus tard, entre 17 et 19 ans. Mais ces moyennes cachent une grande variabilité individuelle. Certains adolescents continuent à grandir légèrement jusqu'à 21 ans, voire exceptionnellement jusqu'à 22 ou 23 ans, si la maturation osseuse est plus lente.Une étude publiée en 2013 dans le Journal of Clinical Endocrinology & Metabolism (R. Rogol et al.) a précisément mesuré ces différences à partir de radiographies des poignets et des genoux. Les chercheurs y montrent que l'âge osseux — c'est-à-dire le degré de maturation du squelette — varie parfois de 2 à 3 ans par rapport à l'âge chronologique. En clair : deux adolescents de 17 ans peuvent être à des stades de croissance très différents, selon leurs gènes, leur nutrition ou leurs taux hormonaux.Le principal moteur de la croissance reste la hormone de croissance (GH), produite par l'hypophyse. Elle agit de concert avec les hormones sexuelles (œstrogènes et testostérone), qui stimulent d'abord la poussée de croissance pubertaire avant de provoquer, paradoxalement, la fermeture des plaques. C'est pourquoi les garçons, dont la puberté commence plus tard, grandissent souvent plus longtemps et finissent plus grands.L'environnement joue aussi un rôle : une alimentation suffisante en protéines, calcium et vitamine D, un sommeil de qualité et une bonne santé générale favorisent la croissance. À l'inverse, des troubles hormonaux, une carence nutritionnelle ou un stress chronique peuvent la freiner.Passé 21 ans, la taille ne change généralement plus, car les cartilages sont ossifiés. Les variations observées ensuite (le fameux “je mesure un centimètre de moins à 40 ans”) ne traduisent pas une perte osseuse, mais un tassement naturel de la colonne vertébrale au fil du temps.En résumé, on grandit en moyenne jusqu'à 17 ans chez les filles et 19 ans chez les garçons, mais la biologie, plus que l'âge civil, dicte la fin de la croissance — et c'est le squelette, pas le calendrier, qui a le dernier mot. Hébergé par Acast. Visitez acast.com/privacy pour plus d'informations.

You've been told your metabolism is broken. That carbs are the enemy. That your hormones are making fat loss impossible. Let's cut the crap.In this episode, I break down the only scientifically proven way to lose body fat—and why most women are spinning their wheels on all the wrong things. We cover what an energy deficit really is, what it isn't, and how to actually apply this in your life in a sustainable way (without gimmicks, shame, or extremes). If you've ever felt like you're doing everything “right” and still not seeing results, this episode will help you stop second-guessing your body—and finally take action that works.Here's what you'll learn:Why carbs, hormones, and metabolism aren't the problemThe truth about exercise and why it's not a magic fixHow your body stores and uses energy (and what to do about it)Why sustainable deficits beat extreme dieting every time5 no-BS steps you can take today to make real progressFat loss is simple—but not always easy. You don't need to be perfect, you just need a plan that actually respects how your body works.Get Weekly Health Tips:  thrivehealthcoachllc.comLet's Connect:@‌ashleythrivehealthcoach or via email: ashley@thrivehealthcoachingllc.comPodcast Produced by Virtually You!Sources:The Lancet, 373(9678), 829–835. https://doi.org/10.1016/S0140-6736(09)60484-2Proceedings of the National Academy of Sciences, 112(4), 1232–1237. Evening use of light-emitting eReaders negatively affects sleep, circadian timing, and next-morning alertness | PNASThe Journal of Clinical Endocrinology & Metabolism, 95(6), 2963–2968. A Single Night of Partial Sleep Deprivation Induces Insulin Resistance in Multiple Metabolic Pathways in Healthy SubjectsAnnual Review of Psychology, 66, 143–172. Why Sleep Is Important for Health: A Psychoneuroimmunology PerspectiveJAMA, 305(21), 2173–2174. Effect of 1 Week of Sleep Restriction on Testosterone Levels in Young Healthy MenAnnals of Internal Medicine, 141(11), 846–850. Brief Communication: Sleep Curtailment in Healthy Young Men Is Associated with Decreased Leptin Levels, Elevated Ghrelin Levels, and Increased Hunger and Appetite | Annals of Internal MedicineThe Journal of Clinical Investigation, 47(9), 2079–2090. Effects of Adrenergic Receptor Activation and Blockade on the Systolic Preejection Period, Heart Rate, and Arterial Pressure in ManAnnals of the New York Academy of Sciences, 896(1), 254–261. https://doi.org/10.1111/j.1749-6632.1999.tb08117.xAnnual Review of Psychology, 57, 139–166. Sleep, Memory, and PlasticityOccupational and Environmental Medicine, 57(10), 649–655. https://doi.org/10.1136/oem.57.10.649Science, 342(6156), 373–377. Sleep Drives Metabolite Clearance from the Adult Brain

Mit den kürzeren Tagen sinkt bei vielen Menschen nicht nur die Energie, sondern auch ihr Vitamin-D-Spiegel. Rutscht er zu sehr ab, hat das Folgen für Leistungsfähigkeit, Immunsystem und Stimmung.Eine neue Studie deutet darauf hin, dass Indoor-Training den im Winter üblichen Vitamin-D-Abfall messbar ausbremst. Kann Deine Fitness-Routine also das Vitamin-D-Supplement ersetzen? Am Ende der Folge bist Du auf Stand und weißt, was das für Dich und Deinen Vitamin-D-Haushalt bedeutet.Außerdem bekommst Du eine klare Strategie an die Hand, um die dunklen Monate von Oktober bis März energiegeladen (und mit vollen Vitamin-D-Speichern) zu überbrücken – statt im Wintermodus auf Reserve zu laufen.____________*WERBUNG: Infos zum Werbepartner dieser Folge und allen weiteren Werbepartnern findest Du hier.____________Tools (Marks Empfehlungen):Vitamin-D-Selbsttest von Medivere.Vitamin-D-Präparat mit 2.000 IE von FormMed (vegane Variante).Weiterführende Inhalte:Download: Ratgeber NahrungsergänzungFolge 502: "Brauchen Sportler Nahrungsergänzung, Herr Ernährungsmediziner?" Mit Niels Schulz-RuhtenbergWissenschaftliche Literatur:Perkin OJ, Davies SE, Hewison M, et al. Exercise without weight loss prevents seasonal decline in vitamin D metabolites: The VitaDEx randomized controlled trial. Advanced Science. 2025;12(22):e2416312.Bikle DD. Vitamin D metabolism, mechanism of action, and clinical applications. Chemistry & Biology. 2014;21(3):319-329.Webb AR, Kazantzidis A, Kift RC, Farrar MD, Wilkinson J, Rhodes LE. Meeting vitamin D requirements in white Caucasians at UK latitudes: Providing a choice. Nutrients. 2018;10(4):497.Lin LY, Smeeth L, Langan S, Warren-Gash C. Distribution of vitamin D status in the UK: a cross-sectional analysis of UK Biobank. BMJ Open. 2021;11(1):e038503.de Oliveira LF, de Azevedo LG, da Mota Santana J, de Sales LPC, Pereira-Santos M. Obesity and overweight decreases the effect of vitamin D supplementation in adults: Systematic review and meta-analysis of randomized controlled trials. Reviews in Endocrine and Metabolic Disorders. 2020;21(1):67-76.Wortsman J, Matsuoka LY, Chen TC, Lu Z, Holick MF. Decreased bioavailability of vitamin D in obesity. Am J Clin Nutr. 2000;72(3):690-693.Drincic AT, Armas LAG, Van Diest EE, Heaney RP. Volumetric dilution, rather than sequestration best explains the low vitamin D status of obesity. Obesity (Silver Spring). 2012;20(7):1444-1448.Ekwaru JP, Zwicker JD, Holick MF, Giovannucci E, Veugelers PJ. The importance of body weight for the dose response relationship of oral vitamin D supplementation and serum 25-hydroxyvitamin D in healthy volunteers. PLoS One. 2014;9(11):e111265.Sun X, Cao ZB, Taniguchi H, Tanisawa K, Higuchi M. Effect of an acute bout of endurance exercise on serum 25(OH)D concentrations in young adults. Journal of Clinical Endocrinology & Metabolism. 2017;102(11):3937-3944.____________Shownotes und Übersicht aller Folgen.Trag Dich in Marks Dranbleiber Newsletter ein.Entdecke Marks Bücher.Folge Mark auf Instagram, Facebook, Strava, LinkedIn. Hosted on Acast. See acast.com/privacy for more information.

This week on Fat Science, Dr. Emily Cooper, Andrea Taylor, and Mark Wright break down five eye-opening research studies from 2025 that challenge everything you thought you knew about obesity, dieting, and metabolism. The hosts explore surprising new evidence on fitness trackers, the metabolic power of joy (and dessert!), the risks of intermittent fasting, how yo-yo dieting can damage kidney health, and the permanent impact of dieting on your brain-gut connection.Dr. Cooper shares clinical insights and explains why simple fixes—strict diets, calorie counting, and food restriction—can actually backfire, causing more harm than good. From the science of hormone signaling to the pitfalls of diet culture, the conversation reveals powerful new reasons to embrace flexibility, balance, and self-kindness on the journey to metabolic health.Key Takeaways:Fitness trackers can dramatically underestimate calorie burn—errors can reach 93%, especially for people with higher body weight. Companies rarely test enough real-world diversity and may fudge numbers for marketing.Including dessert and “forbidden foods” in your diet leads to better metabolic outcomes, greater mental stability, and less risk of binge eating or weight regain. Joyful eating helps regulate critical hormones like leptin and ghrelin.Intermittent fasting is linked to hair loss. Energy deficits force the body to use fatty acids as fuel, which can damage hair follicle stem cells. Long-term fasting negatively disrupts glucose/insulin balance and destabilizes metabolism.Yo-yo dieting (weight cycling) now shows a direct connection with kidney damage—even in those at normal weight. Rapid weight shifts restrict kidney blood flow, raise cortisol, and cause irreversible damage.Dieting creates lasting changes in the microbiome and brain-gut signaling that promote weight regain and appetite dysregulation. Even a single round of weight cycling can create stubborn metabolic obstacles.Personal Stories & Practical Advice:Andrea shares why dessert is a staple of her happiness—and how mental restriction backfires. Dr. Cooper gives real-world examples from patients: eating favorite foods can unlock better weight results, while “diet damage” often lingers until medical treatment repairs it. Resources from the episode:Fat Science is a podcast on a mission to explain where our fat really comes from and why it won't go and stay away. We are committed to creating a world where people are empowered with accurate information about metabolism and recognize that fat isn't a failure. This podcast is for informational purposes only and is not intended to replace professional medical advice.Check out our new website where you can ask a mailbag question. If you have a question for Dr. Cooper, a show idea, feedback, or just want to connect, email us at questions@fatsciencepodcast.com or dr.c@fatsciencepodcast.com.Connect with Dr. Emily Cooper on LinkedIn.Connect with Mark Wright on LinkedIn.Connect with Andrea Taylor on Instagram.REFERENCES FOR THIS EPISODEAlshurafa, N., et al. (2025). “More accurate fitness tracking for people with obesity.” *Scientific Reports*, Northwestern University Feinberg School of Medicine.Alfouzan, N.W., & Nakamura, M.T. (2025). “Reduced food cravings correlated with a 24-month period of weight loss and weight maintenance.” *Physiology & Behavior*, Vol. 291.Chen, H., Liu, C., Cui, S., et al. (2025). “Intermittent fasting triggers interorgan communication to suppress hair follicle regeneration.” *Cell*, Vol. 188.The Endocrine Society (2025). “Yo-yo dieting may significantly increase kidney disease risk in people with type 1 diabetes.” *Journal of Clinical Endocrinology & Metabolism*, February 2025.Fouesnard, M., et al. (2025). “Weight cycling deregulates eating behavior via the induction of durable gut dysbiosis.” *Advanced Science*, 2025

Send us a message with this link, we would love to hear from you. Standard message rates may apply.The DASH diet offers a powerful, evidence-based approach to lowering blood pressure through nutritional changes rather than medication.• Stands for Dietary Approaches to Stop Hypertension• Focuses on fruits, vegetables, whole grains, lean proteins, and low-fat dairy• Limits sodium, saturated fat, added sugars, and processed meats• Can lower systolic blood pressure by 5-6 points and diastolic by 3 points• Recommends 4-5 servings each of fruits and vegetables daily• Suggests 6-8 servings of whole grains per day• Advises limiting sodium to 1,500mg daily for those with hypertension• Provides numerous meal ideas including oatmeal with berries, turkey sandwiches, and grilled salmon• Encourages using herbs and spices instead of salt for flavoring• Benefits extend beyond blood pressure to include improved cholesterol and weight managementFor more information about hypertension management, check out our previous episodes: episode 4 (explaining hypertension), episode 5 (lifestyle changes), episode 14 (common medications), and episode 33 (measuring blood pressure at home).References1. Diets. Yannakoulia M, Scarmeas N. The New England Journal of Medicine. 2024;390(22):2098-2106. doi:10.1056/NEJMra2211889.2. Treatment of Hypertension: A Review. Carey RM, Moran AE, Whelton PK. JAMA. 2022;328(18):1849-1861. doi:10.1001/jama.2022.19590.3. DASH Dietary Pattern and Cardiometabolic Outcomes: An Umbrella Review of Systematic Reviews and Meta-Analyses. Chiavaroli L, Viguiliouk E, Nishi SK, et al. Nutrients. 2019;11(2):E338. doi:10.3390/nu11020338.4. Primary Prevention of ASCVD and T2DM in Patients at Metabolic Risk: An Endocrine Society* Clinical Practice Guideline. Rosenzweig JL, Bakris GL, Berglund LF, et al. The Journal of Clinical Endocrinology and Metabolism. 2019;104(9):3939-3985. doi:10.1210/jc.2019-01338.5. Recommended Dietary Pattern to Achieve Adherence to the American Heart Association/American College of Cardiology (AHA/ACC) Guidelines: A Scientific Statement From the American Heart Association. Van Horn L, Carson JA, Appel LJ, et al. Circulation. 2016;134(22):e505-e529. doi:10.1161/CIR.0000000000000462.6. Dietary Approaches to Stop Hypertension (DASH) for the Primary and Secondary Prevention of Cardiovascular Diseases. Bensaaud A, Seery S, Gibson I, et al. The Cochrane Database of Systematic Reviews. 2025;5:CD013729. doi:10.1002/14651858.CD013729.pub2.7. Popular Dietary Patterns: Alignment With American Heart Association 2021 Dietary Guidance: A Scientific Statement From the American Heart Association. Gardner CD, Vadiveloo MK, Petersen KS, et al. Circulation. 2023;147(22):1715-1730. doi:10.1161/CIR.0000000000001146.8. Dietary Approaches to Prevent and Treat Hypertension: A Scientific Statement From the American Heart Association. Appel LJ, Brands MW, Daniels SR, et al. Hypertension (Dallas, Tex. : 1979). 2006;47(2):296-308. doi:10.1161/01.HYP.0000202568.01167.B6.9. Dietary Approaches to Stop Hypertension (DASH): Potential Mechanisms of Action Against Risk Factors of the Metabolic Syndrome. Akhlaghi M. Nutrition Research Reviews. 2020;33(1):1-18. doi:10.1017/S0954422419000155.10. The Effects of the Dietary Approaches to Stop Hypertension (DASH) Diet on Metabolic Risk Factors in Patients With Chronic Disease: Support the showSubscribe to Our Newsletter! Production and Content: Edward Delesky, MD & Nicole Aruffo, RNArtwork: Olivia Pawlowski

The lads spoke to Emma Duncan about genetic testing in bone medicine. Have you ever wondered how your genes determine your bone mass or response to bone medicines? Tune in to find out and how genetic research is going to improve your care.Emma Duncan is Professor of Clinical Endocrinology at Kings College London.

This week on Fat Science, Dr. Emily Cooper, Andrea Taylor, and Mark Wright answer listener questions from around the world about metabolic health. This mailbag episode explores widely-debated topics like “starvation mode,” weight loss plateaus, the relationship between metabolism and cognitive health, cannabis and metabolism, metabolic effects of liposuction, and the latest on GLP-1 medications.Key Takeaways:Dr. Cooper dispels myths around “starvation mode,” citing research on the long-term metabolic impact of dieting and caloric restriction.Weight loss plateaus are often misunderstood—Dr. Cooper explains the natural adaptations behind them and how to assess true progress.Metabolic health plays a major role in brain function, cognitive decline, depression, and dementia prevention.Cannabis affects metabolic pathways in complex ways, with regular use potentially causing negative metabolic effects.Liposuction can trigger metabolic rebound and rapid fat regain for some patients, especially when leptin levels are low.Updates on GLP-1 meds: Liraglutide is available in generic form, but costs fluctuate. New oral and combination therapies are on the horizon.Personal Stories & Practical Advice:Andrea and Mark reflect on their own journeys with dieting, weight plateaus, and medication.Dr. Cooper shares clinical experiences with metabolic rebound after liposuction and ways to navigate pharmacologic treatments.Correction: Lilly has a lower cash pay for Medicare and Medicaid, but Novo Nordisk is not yet.References related to diet-induced metabolic adaptation, also called biological adaptation and defense of body weight. 1. Keys, A., Brozek, J., Henschel, A., Mickelsen, O., & Taylor, H. L. (1950). The Biology of Human Starvation. University of Minnesota Press.2. Dulloo, A. G. (2021). Physiology of weight regain: Lessons from the classic Minnesota Starvation Experiment on human body composition regulation. Obesity Reviews, 22, e13189.3. Müller, M. J., & Bosy-Westphal, A. (2013). Adaptive thermogenesis with weight loss in humans. Obesity, 21(2), 218-228.4. Rosenbaum, M., & Leibel, R. L. (2010). Adaptive thermogenesis in humans. International Journal of Obesity, 34(S1), S47-S55.5. Fothergill, E., Guo, J., Howard, L., Kerns, J. C., Knuth, N. D., Brychta, R., ... & Hall, K. D. (2016). Persistent metabolic adaptation 6 years after "The Biggest Loser" competition. Obesity, 24(8), 1612-1619.6. Johanssen, D. L., Knuth, N. D., Huizenga, R., Rood, J., Ravussin, E., & Hall, K. D. (2012). Metabolic slowing with massive weight loss despite preservation of fat-free mass. Journal of Clinical Endocrinology & Metabolism, 97(7), 2489-2496.7. Sumithran, P., Prendergast, L. A., Delbridge, E., Purcell, K., Shulkes, A., Kriketos, A., & Proietto, J. (2011). Long-term persistence of hormonal adaptations to weight loss. New England Journal of Medicine, 365(17), 1597-1604.8. MacLean, P. S., Bergouignan, A., Cornier, M. A., & Jackman, M. R. (2011). Biology's response to dieting: the impetus for weight regain. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 301(3), R581-R600Resources:Connect with Dr. Emily Cooper on LinkedIn.Connect with Mark Wright on LinkedIn.Connect with Andrea Taylor on Instagram.Fat Science is a podcast on a mission to explain where our fat really comes from and why it won't go and stay away. We are committed to creating a world where people are empowered with accurate information about metabolism and recognize that fat isn't a failure. This podcast is for informational purposes only and is not intended to replace professional medical advice.If you have a question for Dr. Cooper, email us at info@diabesityinstitute.org or dr.c@fatsciencepodcast.com.Fat Science is supported by the non-profit Diabesity Institute which is on a mission to increase access to effective, science-based medical care for those suffering from or at risk for diabesity. https://diabesityresearchfoundation.org/

A captivating conversation between Sonya and Jo explores the rapidly evolving landscape of menopause healthcare, research, and politics in Australia. In this episode we begin by unpacking the viral podcast between Dr. Rachel Rubin and Dr. Peter Attia – a two-and-a-half hour deep dive into menopause, vaginal health and GSM that's being celebrated as "the best podcast that has been recorded to date on this topic." What makes it exceptional isn't just the content but the peer-to-peer dynamic between two medical professionals sharing both evidence-based information and clinical experience.The conversation takes a powerful turn when journalist Jamila Rizvi's health journey is discussed. At just 31, a missed period led to the discovery of a rare brain tumour affecting her hormone production – a sobering reminder that health changes should never be dismissed without proper investigation. This naturally leads us to a discussion of exciting new research published in Clinical Endocrinology that examines the relationship between sex hormones and dementia risk.Politics takes centre stage as we celebrate Australia's increasingly female Parliament, with two major parties now led by women and gender equality achieved in the Labor cabinet. The shift in ministerial portfolios sees Rebecca White stepping into the Assistant Minister for Health role. We wrap up with news of an Australian company developing the first new estrogen patch in 22 years, potentially addressing supply issues and skin irritation problems plaguing current options.Links:ABC Conversations with Jamila RizviDr Rachel Rubin and Dr Peter Attia Podcast - Apple PodcastsDr Rachel Rubin and Dr Peter Attia Podcast - YouTubeSex Hormones and Risk of Incident Dementia in Men and Postmenopausal Women - Clinical Endocrinology ArticleThank you for listening to my show! Join the conversation on Instagram

Told it's impossible? Let's change that.In this episode, I break down what your AMH (Anti-Müllerian Hormone) levels really mean for your fertility — and why a low AMH is not the final word on your chances of getting pregnant.➡️ What you'll learn in this episode:✅ What AMH actually measures (and what it doesn't)✅ The surprising role of AMH as a “dam” in your ovarian function✅ Why are many women being misled by this one number✅ The difference between egg quantity vs. quality✅ Natural, research-backed strategies to support your fertility — even with low AMH

Von Hormonproduktion über Verdauung bis hin zur Energieverwertung: Der circadiane Rhythmus beeinflusst fast alle physiologischen Funktionen. Wenn wir im Einklang mit unserer inneren Uhr leben, funktioniert unser Körper effizienter und Verdauungsprobleme können besser gelöst werden. ShownotesIn dieser Folge dreht sich alles um den Zusammenhang von Stoffwechsel und zirkadianem Rhythmus. Ich teile meine wichtigsten Erkenntnisse, die dir helfen können, Verdauungsprobleme gezielt anzugehen, deine Ernährung in Einklang mit natürlichen Rhythmen zu bringen und kleine Veränderungen stressfrei in deinen Alltag zu integrieren - auch, wenn du zum Beispiel im Schichtdienst arbeitest. Dafür werfen wir einen Blick auf moderne wissenschaftliche Erkenntnisse und verbinden diese mit dem individuellen Ansatz des Ayurveda, um mit statt gegen unseren Körper zu arbeiten.In dieser Folge erfährst duWie der zirkadiane Rhythmus auf biologischer Ebene funktioniertWie dieser Rhythmus sich auf deine (Verdauungs-)hormone und deinen Stoffwechsel auswirktWie der Ayurveda und die aktuelle wissenschaftliche Studienlage die Relevanz des zirkadianen Rhythmus für unsere Essenszeiten bewertenWelche gesundheitlichen Folgen es haben kann, wenn wir gegen unsere innere Uhr lebenWelche Essenszeiten ideal sind und wie du deinen Stoffwechsel mit der idealen Mahlzeitenzusammensetzung unterstützen kannst (das geht auch, wenn du z. B. im Schichtdienst arbeitest)Konntest du etwas für dich mitnehmen? Dann würde ich mich riesig über deinen Like freuen.

On this episode we review the 2025 Clinical Practice Guideline for the Pharmacologic Management of Adults with Dyslipidemia published by the American Association of Clinical Endocrinology. We compare and contrast the common medications used in the management of dyslipidemia and examine how these can be utilized based on the 13 updated recommendations found in the 2025 guidelines.  Cole and I are happy to share that our listeners can claim ACPE-accredited continuing education for listening to this podcast episode! We have continued to partner with freeCE.com to provide listeners with the opportunity to claim 1-hour of continuing education credit for select episodes. For existing Unlimited (Gold) freeCE members, this CE option is included in your membership benefits at no additional cost! A password, which will be given at some point during this episode, is required to access the post-activity test. To earn credit for this episode, visit the following link below to go to freeCE's website: https://www.freece.com/ If you're not currently a freeCE member, we definitely suggest you explore all the benefits of their Unlimited Membership on their website and earn CE for listening to this podcast. Thanks for listening! If you want to support the podcast, check out our Patreon account. Subscribers will have access to all previous and new pharmacotherapy lectures as well as downloadable PowerPoint slides for each lecture. If you purchase an annual membership, you'll also get a free digital copy of High-Powered Medicine 3rd edition by Dr. Alex Poppen, PharmD. HPM is a book/website database of summaries for over 150 landmark clinical trials.You can visit our Patreon page at the website below:  www.patreon.com/corconsultrx We want to give a big thanks to Dr. Alex Poppen, PharmD and High-Powered Medicine for sponsoring the podcast..  You can get a copy of HPM at the links below:  Purchase a subscription or PDF copy - https://highpoweredmedicine.com/ Purchase the paperback and hardcover - Barnes and Noble website We want to say thank you to our sponsor, Pyrls. Try out their drug information app today. Visit the website below for a free trial: www.pyrls.com/corconsultrx We also want to thank our sponsor Freed AI. Freed is an AI scribe that listens, prepares your SOAP notes, and writes patient instructions. Charting is done before your patient walks out of the room. You can try 10 notes for free and after that it only costs $99/month. Visit the website below for more information: https://www.getfreed.ai/  If you have any questions for Cole or me, reach out to us via e-mail: Mike - mcorvino@corconsultrx.com Cole - cswanson@corconsultrx.com

Von Hormonproduktion über Verdauung bis hin zur Energieverwertung: Der circadiane Rhythmus beeinflusst fast alle physiologischen Funktionen. Wenn wir im Einklang mit unserer inneren Uhr leben, funktioniert unser Körper effizienter und Verdauungsprobleme können besser gelöst werden. ShownotesIn dieser Folge dreht sich alles um den Zusammenhang von Stoffwechsel und zirkadianem Rhythmus. Ich teile meine wichtigsten Erkenntnisse, die dir helfen können, Verdauungsprobleme gezielt anzugehen, deine Ernährung in Einklang mit natürlichen Rhythmen zu bringen und kleine Veränderungen stressfrei in deinen Alltag zu integrieren - auch, wenn du zum Beispiel im Schichtdienst arbeitest. Dafür werfen wir einen Blick auf moderne wissenschaftliche Erkenntnisse und verbinden diese mit dem individuellen Ansatz des Ayurveda, um mit statt gegen unseren Körper zu arbeiten.In dieser Folge erfährst duWie der zirkadiane Rhythmus auf biologischer Ebene funktioniertWie dieser Rhythmus sich auf deine (Verdauungs-)hormone und deinen Stoffwechsel auswirktWie der Ayurveda und die aktuelle wissenschaftliche Studienlage die Relevanz des zirkadianen Rhythmus für unsere Essenszeiten bewertenWelche gesundheitlichen Folgen es haben kann, wenn wir gegen unsere innere Uhr lebenWelche Essenszeiten ideal sind und wie du deinen Stoffwechsel mit der idealen Mahlzeitenzusammensetzung unterstützen kannst (das geht auch, wenn du z. B. im Schichtdienst arbeitest)Konntest du etwas für dich mitnehmen? Dann würde ich mich riesig über deinen Like freuen.

Credits: 0.25 AMA PRA Category 1 Credit™   CME/CE Information and Claim Credit: https://www.pri-med.com/online-education/podcast/frankly-speaking-cme-426 Overview: Drinking coffee offers potential health benefits—but does timing affect outcomes? This episode dives into new research on how morning vs. all-day coffee consumption impacts cardiovascular disease and all-cause mortality risk. Gain practical insights to optimize patient recommendations based on the latest evidence. Episode resource links: European Heart Journal (2025) 00, 1–11 https://doi.org/10.1093/eurheartj/ehae871 The Journal of Clinical Endocrinology & Metabolism, 2024, 00, 1–11 https://doi.org/10.1210/clinem/dgae552 Guest: Jillian Joseph, MPAS, PA-C   Music Credit: Matthew Bugos Thoughts? Suggestions? Email us at FranklySpeaking@pri-med.com  

Credits: 0.25 AMA PRA Category 1 Credit™   CME/CE Information and Claim Credit: https://www.pri-med.com/online-education/podcast/frankly-speaking-cme-426 Overview: Drinking coffee offers potential health benefits—but does timing affect outcomes? This episode dives into new research on how morning vs. all-day coffee consumption impacts cardiovascular disease and all-cause mortality risk. Gain practical insights to optimize patient recommendations based on the latest evidence. Episode resource links: European Heart Journal (2025) 00, 1–11 https://doi.org/10.1093/eurheartj/ehae871 The Journal of Clinical Endocrinology & Metabolism, 2024, 00, 1–11 https://doi.org/10.1210/clinem/dgae552 Guest: Jillian Joseph, MPAS, PA-C   Music Credit: Matthew Bugos Thoughts? Suggestions? Email us at FranklySpeaking@pri-med.com  

Mándanos un mensaje¿Alguna vez has sentido que sigues todas las reglas pero tu cuerpo no responde como esperabas? La respuesta podría estar en tus biomarcadores, esas pequeñas señales químicas que revelan la verdad sobre tu salud mucho antes que cualquier síntoma visible.Organizaciones de saludAmerican Diabetes Association (ADA): https://diabetes.org/American Heart Association (AHA): https://www.heart.org/World Health Organization (WHO): https://www.who.int/National Institutes of Health (NIH): https://www.nih.gov/Centers for Disease Control and Prevention (CDC): https://www.cdc.gov/Endocrine Society: https://www.endocrine.org/American College of Rheumatology: https://www.rheumatology.org/American Association for the Study of Liver Diseases: https://www.aasld.org/Estudios científicos específicosHemoglobina A1C: American Diabetes Association. (2021). Glycemic Targets: Standards of Medical Care in Diabetes. Diabetes Care, 44(Supplement 1): S73-S84.Ferritina y rendimiento: Sim, M., et al. (2019). Iron considerations for the athlete: a narrative review. European Journal of Applied Physiology, 119(7): 1463-1478.Miocinas: Pedersen, B. K. (2019). Physical activity and muscle-brain crosstalk. Nature Reviews Endocrinology, 15(7): 383-392.Perfil lipídico y riesgo cardiovascular: Grundy, S. M., et al. (2019). 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol. Journal of the American College of Cardiology, 73(24): e285-e350.Vitamina D: Holick, M. F., et al. (2011). Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society clinical practice guideline. The Journal of Clinical Endocrinology & Metabolism, 96(7): 1911-1930.Enzimas hepáticas: Kwo, P. Y., et al. (2017). ACG Clinical Guideline: Evaluation of Abnormal Liver Chemistries. The American Journal of Gastroenterology, 112(1): 18-35.Ácido úrico y enfermedad cardiovascular: Borghi, C., et al. (2020). Expert consensus for the diagnosis and treatment of patient with hyperuricemia and high cardiovascular risk. Cardiology, 145(1): 1-10.Variabilidad de frecuencia cardíaca: Shaffer, F., & Ginsberg, J. P. (2017). An Overview of Heart Rate Variability Metrics and Norms. Frontiers in Public Health, 5: 258.Support the showInstagram: andieillanesPágina web: andieillanes.com.mx

Coffee consumption is increasing in the United States, with 67% of adults drinking coffee, according to the National Coffee Association.Researchers suggest that moderate coffee consumption can offer health benefits, including a reduced risk of type 2 diabetes, coronary heart disease, and stroke.A recent study published in the Journal of Clinical Endocrinology and Metabolism found that the benefits of coffee were highest for those who drank a moderate amount, defined as three cups or 200 to 300 milligrams of caffeine per day.The Mayo Clinic also states that coffee can lower the risk of Alzheimer's, Parkinson's, liver disease, certain cancers, and kidney stones. However, dietitians warn that excessive caffeine intake can increase anxiety and disrupt sleep.It's also important to consider the amount of sugar, cream, and other additives in each cup of coffee.See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

What is the difference between Germ Theory and Terrain Theory? Where did each way of thinking come from, how do they differ in terms of key principles, and how do they impact treatment of disease? Tune in to hear us compare and contrast and give our two cents on what each one has gotten right or wrong.    In this episode, we unpack the historical origins of both Germ Theory and Terrain Theory. We discuss how each one has impacted medicine, from hygiene and sanitation to pharmaceutical intervention and beyond. Plus we discuss key aspects of how you can best support your body's individual terrain and immune system and share our Strep Throat Protocol.    Also in this episode:  Free Detox Class 1/8/25 Sign Up Here Free Keto Masterclass 1/15/25 Sign Up Here Save the Date, next LIVE Keto Reset starts 1/29 Buy 3 Get 1 Free Tea with code FREETEA What is Germ Theory? Historical Origins Shortcomings What is Terrain Theory? Nutrient Deficiency Vitamin D Balanced Blend Bio-C Plus Cellular Antiox Sugar Consumption Naturally Nourished Episode 262 The Keto-Immune Connection Gut Microbiome Beat the Bloat Cleanse Rebuild Spectrum Probiotic GI Immune Builder Stress Stress Manager Bundle Relax and Regulate Sleep Support Detox 10 Day Detox Branch Basics use code ALIMILLERRD on a starter kit Air Quality Air Doctor use code ALIMILLERRD Strep Throat Protocol References Wang, T., et al. (2014). The role of vitamin D in immunity and inflammation. Journal of Nutritional Biochemistry, 25(5), 499–505. Martineau, A. R., et al. (2017). Vitamin D supplementation to prevent acute respiratory tract infections: Systematic review and meta-analysis of individual participant data. The Lancet Infectious Diseases, 17(8), 810–818. Johnson, R. J., et al. (2014). Consumption of sugar-sweetened beverages and reduced immune function: An examination of leukocyte function and inflammation. The American Journal of Clinical Nutrition, 100(4), 1141-1146. Cranford, R. R., et al. (2002). The effects of dietary sugar on neutrophil function. The American Journal of Clinical Nutrition, 75(4), 781-785. Adkins, Y., et al. (2006). Acute intake of sugar-sweetened beverages decreases immune function. The Journal of Clinical Endocrinology & Metabolism, 91(2), 615–618. Shin, N. R., et al. (2015). The gut microbiota and its implications for health and disease. Frontiers in Immunology, 6, 121. Belkaid, Y., & Hand, T. (2014). Role of the microbiota in immunity and inflammation. Nature Reviews Immunology, 16(6), 390–400. Segerstrom, S. C., & Miller, G. E. (2004). Psychological stress and the human immune system: A meta-analytic study of 30 years of research. Psychoneuroendocrinology, 30(10), 1023–1039. Black, P. H., & Garbutt, L. D. (2002). Stress, inflammation, and cardiovascular disease. Brain, Behavior, and Immunity, 16(3), 331–338. Bryant, P. A., et al. (2004). Sleep and immune function. Journal of Immunology, 173(4), 2149–2156. Prather, A. A., et al. (2015). Sleep and C-reactive protein: A systematic review and meta-analysis. Sleep, 38(6), 827–835. Source: Saito, H., et al. (2014). Liver detoxification and its importance for health. Hepatology International, 8(1), 15–20. Brook, R. D., et al. (2010). Particulate matter air pollution and cardiovascular disease: An update to the scientific statement from the American Heart Association. Environmental Health Perspectives, 118(8), 1150–1156. Nieman, D. C. (2013). Exercise immunology: An introduction. Exercise Immunology Review, 19, 8–20. Sponsors for this episode:  According to extensive research by the Environmental Working Group, virtually every home in America has harmful contaminants in its tap water. That's why you've got to check out AquaTru. AquaTru purifiers use a 4-stage reverse osmosis purification process, and their countertop purifiers work with NO installation or plumbing. It removes 15x more contaminants than ordinary pitcher filters and are specifically designed to combat chemicals like PFAS in your water supply. Naturally Nourished Podcast listeners can use code ALIMILLERRD at AquaTru.com to save 20% off. 

Credits: 0.25 AMA PRA Category 1 Credit™   CME/CE Information and Claim Credit: https://www.pri-med.com/online-education/podcast/frankly-speaking-cme-410 Overview: In this episode, we discuss the latest updates on vitamin D. Learn about its link to common disorders, when to consider supplementation, and what the most recent practice guideline says about vitamin D and disease prevention—empowering you to make informed decisions and improve patient care without unnecessary screenings or treatments. Episode resource links: Marie B Demay, Anastassios G Pittas, Daniel D Bikle, Dima L Diab, Mairead E Kiely, Marise Lazaretti-Castro, Paul Lips, Deborah M Mitchell, M Hassan Murad, Shelley Powers, Sudhaker D Rao, Robert Scragg, John A Tayek, Amy M Valent, Judith M E Walsh, Christopher R McCartney, Vitamin D for the Prevention of Disease: An Endocrine Society Clinical Practice Guideline, The Journal of Clinical Endocrinology & Metabolism, Volume 109, Issue 8, August 2024, Pages 1907–1947, https://doi.org/10.1210/clinem/dgae290 Michael F. Holick, Neil C. Binkley, Heike A. Bischoff-Ferrari, Catherine M. Gordon, David A. Hanley, Robert P. Heaney, M. Hassan Murad, Connie M. Weaver, Evaluation, Treatment, and Prevention of Vitamin D Deficiency: an Endocrine Society Clinical Practice Guideline, The Journal of Clinical Endocrinology & Metabolism, Volume 96, Issue 7, 1 July 2011, Pages 1911–1930, https://doi.org/10.1210/jc.2011-0385 Guest: Jillian Joseph, PA-C   Music Credit: Matthew Bugos Thoughts? Suggestions? Email us at FranklySpeaking@pri-med.com  

Credits: 0.25 AMA PRA Category 1 Credit™   CME/CE Information and Claim Credit: https://www.pri-med.com/online-education/podcast/frankly-speaking-cme-410 Overview: In this episode, we discuss the latest updates on vitamin D. Learn about its link to common disorders, when to consider supplementation, and what the most recent practice guideline says about vitamin D and disease prevention—empowering you to make informed decisions and improve patient care without unnecessary screenings or treatments. Episode resource links: Marie B Demay, Anastassios G Pittas, Daniel D Bikle, Dima L Diab, Mairead E Kiely, Marise Lazaretti-Castro, Paul Lips, Deborah M Mitchell, M Hassan Murad, Shelley Powers, Sudhaker D Rao, Robert Scragg, John A Tayek, Amy M Valent, Judith M E Walsh, Christopher R McCartney, Vitamin D for the Prevention of Disease: An Endocrine Society Clinical Practice Guideline, The Journal of Clinical Endocrinology & Metabolism, Volume 109, Issue 8, August 2024, Pages 1907–1947, https://doi.org/10.1210/clinem/dgae290 Michael F. Holick, Neil C. Binkley, Heike A. Bischoff-Ferrari, Catherine M. Gordon, David A. Hanley, Robert P. Heaney, M. Hassan Murad, Connie M. Weaver, Evaluation, Treatment, and Prevention of Vitamin D Deficiency: an Endocrine Society Clinical Practice Guideline, The Journal of Clinical Endocrinology & Metabolism, Volume 96, Issue 7, 1 July 2011, Pages 1911–1930, https://doi.org/10.1210/jc.2011-0385 Guest: Jillian Joseph, PA-C   Music Credit: Matthew Bugos Thoughts? Suggestions? Email us at FranklySpeaking@pri-med.com  

En vieillissant, la qualité et la quantité de sommeil tendent à diminuer, un phénomène bien documenté par la recherche scientifique. Plusieurs facteurs physiologiques et neurologiques contribuent à ces changements. Changements dans les cycles du sommeilLe sommeil se compose de plusieurs cycles, dont le sommeil lent profond, qui est le plus réparateur. Avec l'âge, la proportion de sommeil profond diminue, tandis que les phases de sommeil léger augmentent. Une étude de *Sleep Medicine Reviews* en 2017 a montré que les personnes âgées passent moins de temps en sommeil profond, ce qui rend leur sommeil plus facilement interrompu. Cela signifie qu'ils se réveillent plus fréquemment durant la nuit et ressentent souvent un sommeil moins reposant. Modification de l'horloge biologiqueL'horloge interne, ou rythme circadien, qui régule le cycle veille-sommeil, devient moins stable avec l'âge. Les personnes âgées ressentent souvent une tendance à s'endormir plus tôt le soir et à se réveiller plus tôt le matin, un phénomène appelé « avancement de phase ». Une étude publiée dans *Chronobiology International* en 2018 a montré que ce changement dans l'horloge biologique est dû à une réduction de la sensibilité à la lumière et à des modifications dans la production de mélatonine, une hormone régulatrice du sommeil. Réduction de la production de mélatonineLa mélatonine, souvent appelée « hormone du sommeil », aide à induire le sommeil et à maintenir un rythme de sommeil régulier. En vieillissant, le corps produit moins de mélatonine, ce qui peut rendre l'endormissement plus difficile et le sommeil moins profond. Une recherche dans *Journal of Clinical Endocrinology & Metabolism* a révélé que les niveaux de mélatonine baissent progressivement avec l'âge, ce qui explique en partie pourquoi les personnes âgées peuvent avoir des difficultés à dormir aussi longtemps ou aussi profondément. Facteurs de santé et médicamentsLes troubles de santé chroniques, comme les douleurs articulaires, l'arthrite, ou les problèmes urinaires, peuvent également perturber le sommeil. Par ailleurs, de nombreux médicaments prescrits aux personnes âgées, comme les traitements pour la tension artérielle ou les diurétiques, peuvent avoir des effets secondaires qui nuisent au sommeil. Selon une étude publiée en 2015 dans *Sleep Health*, plus de la moitié des personnes âgées rapportent des interruptions de sommeil dues à des douleurs ou des besoins fréquents d'uriner la nuit. En somme, le vieillissement affecte le sommeil à plusieurs niveaux, de la structure même des cycles de sommeil à la régulation hormonale. Ces changements sont une combinaison de facteurs biologiques, de modifications de l'horloge biologique, et d'effets liés aux conditions de santé, ce qui explique pourquoi le sommeil devient moins profond et plus interrompu avec l'âge. Hébergé par Acast. Visitez acast.com/privacy pour plus d'informations.

Episode hosted by Dr. Julie Foucher of the Pursuing Health Podcast, on Sep 17, 2024: #PursuingHealth Tony Nader, MD, PhD is a medical doctor trained at Harvard University and Massachusetts Institute of Technology (Ph.D. in neuroscience) and a globally recognized expert in the science of Consciousness and human development. Dr. Nader, whose training includes internal medicine, psychiatry, and neurology, is a bestselling author (One Unbounded Ocean of Consciousness), with his book Consciousness is All There Is recently released on August 6 (Penguin/Hay House). He is the successor to Maharishi Mahesh Yogi and the head of the Transcendental Meditation organizations globally. Dr Nader conducted research on neurochemistry, neuroendocrinology, and the relationship between diet, age, behavior, mood, seasonal influences, and neurotransmitter and hormonal activity, and on the role of neurotransmitter precursors in medicine. Dr. Nader's interest to explore the full potential of the human physiology, and the human mind led him to also study and conduct research on ancient and modern techniques of self-development. For many years, Dr. Nader worked closely with Maharishi Mahesh Yogi, who first introduced Transcendental Meditation or TM® to the world in 1958, and who emphasized the scientific understanding and validation of Transcendental Meditation. Dr. Nader has discussed his expertise at academic institutions such as Harvard Business School on The Neuroscience of Transcendence, Stanford University, where he gave talks in a series entitled "Hacking Consciousness" as well as the keynote speaker for a number of conferences at the House of Commons, British Parliament. His research has been published in Neurology, Journal of Clinical Endocrinology and Metabolism, Journal of Gerontology, Progress in Brain Research, and many other journals. Dr. Nader has been awarded many time for his outstanding contribution in human development, environment, education, and health. You can connect with Dr. Nader via Instagram @drtonynader https://www.instagram.com/drtonynader If you like this episode, please subscribe to Pursuing Health on iTunes and give it a rating or share your feedback on social media using the hashtag #PursuingHealth. I look forward to bringing you future episodes with inspiring individuals and ideas about health. Disclaimer: This podcast is for general information only, and does not provide medical advice. I recommend that you seek assistance from your personal physician for any health conditions or concerns. iTunes: https://goo.gl/UFjY0q | Stitcher: http://goo.gl/xKMmiR | Spotify: https://spoti.fi/3aiTnBg | Google Play: http://bit.ly/2vrlTSD To order Dr Tony Nader's book Consciousness Is All There Is: https://www.drnaderbooks.com or use your favorite bookseller. Website https://www.drtonynader.com Instagram https://instagram.com/drtonynader Facebook https://facebook.com/DrTonyNader YouTube https://youtube.com/@DrTonyNader X https://x.com/DrTonyNader TikTok https://tiktok.com/@drtonynader Original podcast episode link https://youtu.be/V4QecGh3lNQ?si=wP7VzRkYHSlqz0wm To learn Transcendental Meditation https://www.tm.org To view the Meditate America event https://live.meditateamerica.org Maharishi International University https://www.miu.edu

Was man teilweise über Vitamin D hört, klingt fast zu schön, um wahr zu sein. Andererseits deuten hunderte verschiedener Forschungsarbeiten darauf hin, dass Vitamin D zur Vorbeugung einer Reihe von Krankheiten beitragen kann – darunter Osteoporose, Depression, Autoimmun- und Herz-Kreislauf-Erkrankungen. Ärzte empfehlen es. Gesundheits- und Fitnesspodcaster sprechen darüber. Vielleicht geht Dir sogar Deine Lieblingstante damit auf die Nerven. Bei all dem Hype ist die Frage berechtigt: "Solltest Du Vitamin D einnehmen?" Hier sind die Antworten – und die neuesten Fakten über ein faszinierendes Vitamin, das ein wahrer Verwandlungskünstler ist. ____________ *WERBUNG: KoRoDrogerie.de: 5% Ermäßigung auf alles mit dem Code „FMM“ beim Checkout. ____________ Ressourcen zur Folge: Literatur: Ratgeber Nahrungsergänzung – Mark Maslow (kostenlos auf MarathonFitness) Blut: Die Geheimnisse unseres flüssigen Organs* – Ulrich Strunz (Heyne) Vitamin D* – Uwe Gröber, Michael F. Holick (Wissenschaftl. Verlagsgesellschaft) Blutuntersuchung (Selbsttest): Vitamin D Test* von Medivere Präparate: D-Form 2.000 K2+* von FormMed D-Form 2.000 K2+ vegan* von FormMed ____________

Host Aaron Lohr talks with Rita Kalyani, MD, professor of medicine at Johns Hopkins University School of Medicine and president-elect of medicine and science at the American Diabetes Association. Earlier this year, Dr. Kalyani and colleagues published a position statement in The Journal of Clinical Endocrinology & Metabolism titled, “Prioritizing Patient Experiences in the Management of Diabetes and Its Complications: An Endocrine Society Position Statement.” Show notes are available at https://www.endocrine.org/podcast/enp93-patience-experience-in-managing-diabetes — for helpful links or to hear more podcast episodes, visit https://www.endocrine.org/podcast

Join Dr. Lonnie Lowery in this enlightening episode as he reveals groundbreaking research from the International Space Station about a new anabolic agent from green tomatoes, potentially combating age-related muscle loss. Dr. Mike also discusses a recent study linking caffeine consumption to reduced cardiometabolic disease risk. Dive into this exploration of health, strength sports, and nutrition, and stay updated on upcoming changes and expert discussions. Don't miss insights from the Journal of Clinical Endocrinology and Metabolism and future episodes on dietary supplements regulation.00:30 Exploring Muscle Loss in Microgravity02:54 Green Tomato Extract: A Potential Muscle Loss Drug07:08 Caffeine: Is It Healthy?07:23 Iron Radio Updates and Announcements08:35 Dr. Mike T. Nelson's Daily Newsletter09:07 Exclusive Newsletter and Free Information09:45 Exploring Caffeine and Cardiac Health10:18 Study Insights: Coffee and Cardiometabolic Diseases13:10 Caffeine's Potential Benefits and Mechanisms Donate to the show via PayPal HERE.You can also join Dr Mike's Insider Newsletter for more info on how to add muscle, improve your performance and body comp - all without destroying your health, go to www.ironradiodrmike.com Thank you!Phil, Jerrell, Mike T, and Lonnie

In today's episode of Daily Value, we look at the protective effects of coffee, tea, and caffeine consumption on cardiometabolic health. A recent study published in the Journal of Clinical Endocrinology & Metabolism (doi:10.1210/clinem/dgae552) reveals how moderate caffeine intake—equivalent to a specific amount of caffeine—is related to the reduced risk of cardiometabolic multimorbidity, which includes coexistence of conditions like type 2 diabetes, coronary heart disease, and stroke.Episode Talking Points:*The link between caffeine intake and reduced risk of developing cardiometabolic diseases.*Potential mechanisms of protection, including antioxidant and anti-inflammatory effects, improved lipid metabolism, and the role of specific compounds like chlorogenic acid and catechins.*Practical takeaways for incorporating moderate coffee or tea consumption into your daily routine for long-term heart health.https://academic.oup.com/jcem/advance-article-abstract/doi/10.1210/clinem/dgae552/7754545?redirectedFrom=fulltextSupport the show

Ready to ditch calorie counting and unlock the secrets to sustainable weight loss? In this episode of Weight Loss Made Simple, Dr. Stacy Heimburger dives into the multi-pronged approach to holistic weight loss. Discover why focusing on more than just calories is essential for long-term success. We explore the impact of psychological stress, the role of quality sleep, the importance of nutrient-dense foods, effective physical activity, and building a supportive network. Tune in to learn how integrating these lifestyle changes can transform your weight loss journey and overall wellness.References:Psychological Stress and Obesity - A. M. C. Farrow, E. E. White, A. M. Jacobs, Physiology & Behavior, October 2003Sleep and Obesity - M. G. Knutson, L. L. Van Cauter, Current Diabetes Reports, April 2006Nutrient-Dense Foods and Weight Management - K. L. Hlebowicz, E. D. Solomon, M. M. Mitchell, Nutrients, August 2019Physical Activity and Weight Loss - C. S. Albright, R. D. Thompson, G. T. Wright, Journal of Clinical Endocrinology & Metabolism, August 2008Stress Management and Weight Loss - J. K. Smith, R. S. Peterson, L. T. Morgan, Journal of Behavioral Medicine, April 2011Free 2-Pound Plan Call!Want to jump start your weight loss? Schedule a free call where Dr. Stacy Heimburger will work with you to create a personalized plan to lose 2 pounds in one week, factoring in your unique circumstances, challenges, and aspirations. Schedule now! www.sugarfreemd.com/2poundThis episode was produced by The Podcast Teacher.

Tony Nader, MD, PhD is a medical doctor trained at Harvard University and Massachusetts Institute of Technology (Ph.D. in neuroscience) and a globally recognized expert in the science of Consciousness and human development. Dr. Nader, whose training includes internal medicine, psychiatry, and neurology, is a bestselling author (One Unbounded Ocean of Consciousness), with his book Consciousness is All There Is recently released on August 6 (Penguin/Hay House). He is the successor to Maharishi Mahesh Yogi and the head of the Transcendental Meditation organizations globally.   Dr Nader conducted research on neurochemistry, neuroendocrinology, and the relationship between diet, age, behavior, mood, seasonal influences, and neurotransmitter and hormonal activity, and on the role of neurotransmitter precursors in medicine.   Dr. Nader's interest to explore the full potential of the human physiology, and the human mind led him to also study and conduct research on ancient and modern techniques of self-development.   For many years, Dr. Nader worked closely with Maharishi Mahesh Yogi, who first introduced Transcendental Meditation or TM® to the world in 1958, and who emphasized the scientific understanding and validation of Transcendental Meditation.   Dr. Nader has discussed his expertise at academic institutions such as Harvard Business School on The Neuroscience of Transcendence, Stanford University, where he gave talks in a series entitled "Hacking Consciousness" as well as the keynote speaker for a number of conferences at the House of Commons, British Parliament. His research has been published in Neurology, Journal of Clinical Endocrinology and Metabolism, Journal of Gerontology, Progress in Brain Research, and many other journals. Dr. Nader has been awarded  many time for his outstanding contribution in human development, environment, education, and health.   You can connect with Dr. Nader via Instagram @drtonynader Related Episodes: Ep 223 - Tapping to Reduce Stress with Nick Ortner Ep 277 - The Science of Spirituality and Mental Health with Dr. Lisa Miller If you like this episode, please subscribe to Pursuing Health on iTunes and give it a rating or share your feedback on social media using the hashtag #PursuingHealth. I look forward to bringing you future episodes with inspiring individuals and ideas about health. Disclaimer: This podcast is for general information only, and does not provide medical advice.  I recommend that you seek assistance from your personal physician for any health conditions or concerns.

Credits: 0.25 AMA PRA Category 1 Credit™   CME/CE Information and Claim Credit: https://www.pri-med.com/online-education/podcast/frankly-speaking-cme-397 Overview: In this episode, we review the T Trials—a coordinated set of 7 research trials that assessed the efficacy of testosterone gel treatment in 7 functional domains for men aged 65 years or older. Hear best practices for determining testosterone levels and how to balance the benefits and risks of testosterone replacement therapy during patient discussions. Episode resource links: Matsumoto AM. Testosterone Replacement in Men with Age-Related Low Testosterone: What Did We Learn From The Testosterone Trials? Curr Opin Endocr Metab Res. 2019 Jun;6:34-41. doi: 10.1016/j.coemr.2019.04.004. Epub 2019 Apr 25. PMID: 32043015; PMCID: PMC7009797.  The Journal of Clinical Endocrinology & Metabolism, 2024, 00, 1–10 https://doi.org/10.1210/clinem/dgae085 Guest: Robert A. Baldor MD, FAAFP Music Credit: Richard Onorato Thoughts? Suggestions? Email us at FranklySpeaking@pri-med.com  

Credits: 0.25 AMA PRA Category 1 Credit™   CME/CE Information and Claim Credit: https://www.pri-med.com/online-education/podcast/frankly-speaking-cme-397 Overview: In this episode, we review the T Trials—a coordinated set of 7 research trials that assessed the efficacy of testosterone gel treatment in 7 functional domains for men aged 65 years or older. Hear best practices for determining testosterone levels and how to balance the benefits and risks of testosterone replacement therapy during patient discussions. Episode resource links: Matsumoto AM. Testosterone Replacement in Men with Age-Related Low Testosterone: What Did We Learn From The Testosterone Trials? Curr Opin Endocr Metab Res. 2019 Jun;6:34-41. doi: 10.1016/j.coemr.2019.04.004. Epub 2019 Apr 25. PMID: 32043015; PMCID: PMC7009797.  The Journal of Clinical Endocrinology & Metabolism, 2024, 00, 1–10 https://doi.org/10.1210/clinem/dgae085 Guest: Robert A. Baldor MD, FAAFP Music Credit: Richard Onorato Thoughts? Suggestions? Email us at FranklySpeaking@pri-med.com  

Half of the world's population will go through menopause. Yet research shows that a large proportion of women do not feel informed and equipped for menopause. In this episode, we reveal the results of a brand new study that highlight the impact of diet on menopause symptoms. Davina McCall is a British household name and much-loved TV presenter on a mission to change this. Her 2022 book Menopausing provided a roadmap for women to be fearless in tackling this stage of life. She has her own very personal menopause story and today, she shares it with us. Together with ZOE's Chief Scientist Dr. Sarah Berry, we're having an honest and open conversation about perimenopause and menopause.

There has long since been a knowledge gap in medical education regarding care of LGBTQIA+ patients. This has manifested itself in health disparities that detrimentally affect the LGBTQIA+ population. This podcast serves as a way to start bridging the gap on order to mitigate the effects of bias, discrimination, and prejudice that queer patients often face in health care. Research has shown that consistent, early exposure in medical education to patients from the queer community has been beneficial in preparing future practitioners for gender inclusive care. We must also do our parts as pediatricians to make sure our queer youth grow into confident, thriving queer adults.  Join Dr. Farrah-Amoy Fullerton, a recent graduate of the pediatric residency program at MCG, and Professor of Pediatrics, Dr. Lisa Leggio, as they introduce LGBTQIA+ health care disparities and describe ways to bridge the gap for eager general practitioners who would like to know more. CME Credit (requires free sign up): Link Coming Soon! References: Bonvicini, K. A. (2017). LGBT healthcare disparities: What progress have we made? Patient Education and Counseling, 100(12), 2357–2361. https://doi.org/10.1016/j.pec.2017.06.003 Fish, J. N. (2020). Future directions in understanding and addressing mental health among LGBTQ youth. Journal of Clinical Child & Adolescent Psychology, 49(6), 943–956. https://doi.org/10.1080/15374416.2020.1815207 Nowaskie, D. Z., & Patel, A. U. (2020). How much is needed? patient exposure and curricular education on medical students' LGBT cultural competency. BMC Medical Education, 20(1). https://doi.org/10.1186/s12909-020-02381-1 Ormiston, C. K., & Williams, F. (2021). LGBTQ youth mental health during COVID-19: Unmet needs in public health and policy. The Lancet, 399(10324), 501–503. https://doi.org/10.1016/s0140-6736(21)02872-5 Reisman, T., & Goldstein, Z. (2018). Case report: Induced lactation in a transgender woman. Transgender Health, 3(1), 24–26. https://doi.org/10.1089/trgh.2017.0044 Reisner, S. L., Bradford, J., Hopwood, R., Gonzalez, A., Makadon, H., Todisco, D., Cavanaugh, T., VanDerwarker, R., Grasso, C., Zaslow, S., Boswell, S. L., & Mayer, K. (2015). Comprehensive Transgender Healthcare: The gender affirming clinical and public health model of Fenway Health. Journal of Urban Health, 92(3), 584–592. https://doi.org/10.1007/s11524-015-9947-2 Underman, K., Giffort, D., Hyderi, A., & Hirshfield, L. E. (2016). Transgender Health: A standardized patient case for advanced clerkship students. MedEdPORTAL. https://doi.org/10.15766/mep_2374-8265.10518 Wamboldt, R., Shuster, S., & Sidhu, B. S. (2021). Lactation induction in a transgender woman wanting to breastfeed: Case report. The Journal of Clinical Endocrinology & Metabolism, 106(5). https://doi.org/10.1210/clinem/dgaa976 Wylie, K., Knudson, G., Khan, S. I., Bonierbale, M., Watanyusakul, S., & Baral, S. (2016). Serving transgender people: Clinical Care Considerations and Service Delivery Models in transgender health. The Lancet, 388(10042), 401–411. https://doi.org/10.1016/s0140-6736(16)00682-6 The Williams Institute at UCLA School of Law. (2023, July 10). How many adults and youth identify as transgender in the United States? - Williams Institute. Williams Institute. https://williamsinstitute.law.ucla.edu/publications/trans-adults-united-states/ https://implicit.harvard.edu/implicit/takeatest.html Coleman E, Radix AE, Bouman WP, et al. Standards of Care for the Health of Transgender and Gender Diverse People, Version 8. Int J Transgend Health. 2022;23(Suppl 1):S1-S259. Published 2022 Sep 6. doi:10.1080/26895269.2022.2100644 https://pflag.org/ thetrevorproject.org

On episode 488 of The Nurse Keith Show nursing and healthcare career podcast, Keith interviews Thomas George, DNP, APRN, FNP-C, NASM-CPT, a family nurse practitioner specializing in the treatment of obesity. In the course of their conversation, Keith and Dr. George discuss obesity as a chronic disease of pandemic proportions, current treatment strategies, the concept of "food noise", the latest scientific evidence, and much more. Excellent resources shared by Dr. George include the Consensus Statement on Obesity as a Disease by the Stop Obesity Alliance; the consensus statement by the the American Association of Clinical Endocrinology; an informative article about "food noise"; the Obesity Action Coalition, and the Obesity Medicine Association. Dr. Thomas George is a family nurse practitioner and assistant professor at Frontier Nursing University, and the Clinic Director and obesity specialist and business consultant for Wellspring Weight and Wellness, a new startup in rural SE Idaho. Dr. George chairs the Obesity Medicine Association's CME Committee, and holds a certificate and advanced education in obesity medicine from the Obesity Medicine Association, and a certificate in primary care obesity management from the Obesity Society. He is a certified personal trainer and weight loss specialist with the National Academy of Sports Medicine, and he himself is a person living with obesity. Connect with Thomas George: Wellspring Weight and Wellness LinkedIn Contact Nurse Keith about holistic career coaching to elevate your nursing and healthcare career at NurseKeith.com. Keith also offers services as a motivational and keynote speaker and freelance nurse writer. You can always find Keith on LinkedIn. Are you looking for a novel way to empower your career and move forward in life? Keith's wife, Shada McKenzie, is a gifted astrologer and reader of the tarot who combines ancient and modern techniques to provide valuable insights into your motivations, aspirations, and life trajectory, and she offers listeners of The Nurse Keith Show a 10% discount on their first consultation. Contact Shada at TheCircelandtheDot.com or shada@thecircleandthedot.com.

High Fructose Corn Syrup's Profits over Health:  Richard Gale & Gary Null PhD Progressive Radio Network, July 24, 2024 There is an unseen culprit hiding in the shadows. It is a toxic poison contained in many of the foods and beverages that we commonly eat. A toxin that has been implicated in causing cancer, diabetes, heart disease, lowered cognitive function, addiction, depression, and obesity. The magicians and alchemists of the corporate food industry have cleverly disguised this ingredient and sing its praises.  If you are waiting for mainstream media to undertake an in-depth investigative report on this topic you will be waiting a long time. Back in 2015 Tufts University's department of nutritional sciences conducted a study published by the American Heart Association that documented the annual rates of global deaths directly due to over-consumption of beverages with high sugar content. The results estimated that 184,000 adults die annually from sugary drinks.  Dr. Gitanjali at Tufts analyzed data documenting sugar-related deaths across 51 countries between 1980 and 2010.  Deaths were compiled according to cardiovascular disease, diabetes and various cancers. Based upon the data, the study concluded that sugar contributed to 45,000 annual deaths from cardiovascular disease, 13,000 deaths from diabetic complications, and 6,450 deaths related to cancer.  Credit Suisse's Research Institute published a scathing report that brought sugar's health risks into sharper focus.  The study revealed that upward to 40% of American healthcare expenditures could be directly tied to overconsumption of sugar in the average American diet.  Today, the US' national addiction to sugar contributes to $1 trillion in healthcare costs annually, which includes coronary heart disease, diabetes and metabolic syndrome. There are numerous studies published in reliable peer-reviewed medical journals associating sugar with each of these life threatening diseases. As far back as 1971, I began writing about the hazards of sugar. In 2002, my documentary Seven Steps to Perfect Health was premiered on PBS stations. During a special appearance on one station's fund drive, I poured sugar out of a bag. The amount I poured equaled the number of teaspoons that an average American teenager consumes daily. My general counsel, David Slater, verified the quantity by proper measurement according to scientific food and diet data.  After the initial airing of this special, I was informed by the station's program director that they could not rebroadcast the performance, even though it was the most successful program during the fund drive. I was informed that the station had received harsh criticism from the sugar industry. The program director explained that the information I presented about sugar's dangers, even though I provided full scientific verification of the facts, ran up against the president of the station board Sharon Rockefeller. I was told she had received a phone call from a sugar-lobbying group representing soft drink makers and sugar manufacturers.  Therefore the station made the decision to pull my program. I was never asked to return to the station. Not surprisingly, a subsequent investigation revealed Sharon Rockefeller sat on Pepsi's board at the time, one of America's largest manufacturers of sweetened soft drinks.    That was my first personal encounter with the political forces supporting sugar. I wrote letters to the sugar industry, the station board and Sharon Rockefeller contesting their suppression of my program and their claim that sugar was unrelated to the declining health of Americans. They were presented with dozens of peer-reviewed studies. However in recent decades, the sweetener industry has undergone a dramatic transformation with the introduction and widespread adoption of high fructose corn syrup (HFCS) throughout our food system. This shift from traditional cane sugar, which dominated my criticism earlier, to fructose corn sugars has led to deep human health and environmental concerns due to its economic benefits for food manufacturers.  High fructose corn syrup was developed in the late 1960s by Japanese scientists who discovered a method to convert glucose from cornstarch into fructose using enzymes. This innovation was spurred by the need to find a cheaper and more versatile sweetener as an alternative to the more labor-intensive production of traditional cane sugar. HFCS is made by milling corn to produce cornstarch. The starch is then hydrolyzed into glucose by adding the enzyme alpha-amylase. Finally the glucose is further processed into fructose. The result is a syrup that typically contains 42-55 percent fructose, with the rest being glucose. Some methods can produce fructose as high as 90 percent.  Today, HFCS production has been so optimized that it has become the most cost-effective and efficient means to produce sweeteners. Monsanto's genetically modified Round-Up Ready corn, enabling the use of more toxic herbicides and pesticides, has now made HFCS the cornerstone of the sugar industry.  However, the shift to HFCS has been fundamentally driven by economics and the agro-chemical industry and has absolutely nothing to do with creating a healthier sugar.  Since corn is one of the most extensively cultivated crops in the United States, which is heavily subsidized by the government, it has provided an enormous, inexpensive supply of the raw material needed for HFCS production. In addition, the enzymatic conversion process can result in a high yield of sweetener from a relatively small amount of corn.  HFCS is now a ubiquitous ingredient that permeates our entire modern food supply. Starting in the 1980s, the introduction of HFCS has gradually displaced traditional sweeteners such as natural cane sugar, glucose and honey. According to the USDA, HFCS can cost up to 50% less than cane and other traditional sugars. This cost differential is particularly significant in industries where sweeteners constitute a major portion of production costs such as in soft drinks, artificial fruit juices, sweet baked goods, snack foods and candy, breakfast cereals, condiments and sauces, sweetened dairy products such as yoghurt and ice cream, and a large variety of processed canned and prepared meals. A study published in American Journal of Clinical Nutrition found that HFCS accounts for over 40% increase of caloric sweeteners added to foods and beverages. Having a purview of the distribution of different sugars in the American diet helps to illustrate the dominance of HFCS in the food system. Approximately 45 percent of added sugars in the American diet come from HFCS and an additional 2 percent from pure fructose. Between 35-40 percent of sweeteners derive from sucrose, the common table sugar made from sugarcane and sugar beets -- the latter now being genetically modified. The production process involves crushing the plant material to extract the juice, which is then purified, concentrated, and crystallized to produce table sugar.  Not to be confused with HFCS, corn syrup is largely glucose and represents about 10-15 percent of the nation's sugar intake. It is the most common sugar used in baked goods and candy. Lactose and galactose each account for about 4-5 percent of consumed sugars. However they are typically not added sugars to foods but naturally present in all dairy products.  Finally, honey, which at one time was a common food ingredient, today only accounts for about 1-2 percent of sweeteners.  Moreover, according to FDA testing, a lot of commercial honey found in grocery stores has been adulterated with HFCS and other sweeteners, such sucrose derived from cane and GMO beet sugars and artificial honey-flavored imitators.  A general estimate is that 20-30 percent of honey sold is impure.  Back in the 1970s and 1980s when I frequently railed publicly against the sugar industry and the health risks of processed table sugar that then completely dominated the food industry, I would never have imagined that sucrose would be gradually replaced by HFCS. This replacement accelerated after the emergence of genetically modified (GM) corn. As noted above, the vast majority of HFCS produced in the United States, the world's larger corn producer globally, is derived from genetically modified (GM) corn. Estimates suggest that around 85-90% of the corn grown in the U.S. is genetically modified. Therefore it is reasonable to infer that approximately 85-90% of HFCS is derived from GM corn. As many court cases and exposes of corruption in the agro-chemical industry have cone to light, GM corn has dire implications for the production and consumption of HFCS, especially considering the associated health risks linked to the use of toxic herbicides such as glyphosate. Research has linked glyphosate to various health issues, including cancer. A decade ago, the International Agency for Research on Cancer (IARC) classified glyphosate as a "probable human carcinogen"; today, it is no longer probable but a medical fact. Several studies have detected glyphosate residues in food products containing HFCS. A study published in Environmental Health found glyphosate residues in a variety of food products, highlighting the widespread contamination of the food supply with this herbicide. In addition to glyphosate's carcinogenic potential, the toxin has also been shown to disrupt endocrine function and it has been implicated in gut dysbiosis, an imbalance in the gut microbiome. This disruption can lead to a range of health problems, including inflammatory bowel disease (IBD) and other gastrointestinal disorders. Research published in Current Microbiology indicates that glyphosate exposure can alter the composition of the gut microbiota, leading to adverse health outcomes. HFCS and traditional sugars like table sugar differ significantly in their composition and metabolic effects. Sucrose is a disaccharide composed of equal parts glucose and fructose, while HFCS is a mixture of free glucose and fructose, with the fructose content higher than that in sucrose. This difference in composition affects how the body metabolizes these sugars. Briefly, HFCS poses more serious health risks than sucrose. The free fructose in HFCS is absorbed more rapidly than the bound fructose in sucrose, leading to quicker spikes in blood sugar and insulin levels. In addition, the high fructose content in HFCS places a greater burden on the liver, leading to increased fat production and storage, contributing to fatty liver disease and metabolic disorders. In contrast, the balanced glucose-fructose composition of sucrose is metabolized more evenly, posing lower risks. However, it is crucial to realize that excessive or even moderate consumption of any form of sugar can be detrimental to health. Extensive research has linked the consumption of HFCS to a range of adverse health effects. Key among these is metabolic disorders and cardiovascular diseases. A study published in the Journal of Clinical Endocrinology & Metabolism found that high consumption of HFCS is associated with an increased risk of developing metabolic syndrome, which includes conditions such as obesity, insulin resistance, hypertension, and dyslipidemia. These conditions collectively elevate the risk of heart disease and stroke. HFCS has been directly implicated in America's obesity epidemic due to its high fructose content, which is metabolized differently than glucose. Fructose is primarily processed in the liver, where it can be converted into fat more readily than glucose. This process can lead to increased fat accumulation and insulin resistance, both of which are risk factors for obesity and type 2 diabetes. A study in the American Journal of Clinical Nutrition highlighted that high HFCS consumption is correlated with an increased risk of obesity and diabetes, particularly in children and adolescents. HFCS intake also leads to non-alcoholic fatty liver disease (NAFLD). Unlike glucose, which is metabolized by all cells in the body, fructose is metabolized almost entirely in the liver. High levels of fructose overwhelms the liver's capacity to process it, leading to fat accumulation and liver damage. Research published in Hepatology has shown a strong correlation between HFCS consumption and the progression to more severe liver diseases, such as cirrhosis and liver cancer. Recent evidence reveals that HFCS has detrimental effects on cognitive function and mental health. Studies indicate that fructose impairs insulin signaling in the brain, which is crucial for maintaining cognitive functions. A study in the Journal of Physiology found that high-fructose diets can lead to insulin resistance in the brain, potentially increasing the risk of neurodegenerative diseases like Alzheimer's. Additionally, high sugar diets, including those high in HFCS, have been linked to mood disorders, such as depression and anxiety, as detailed in a review in Nature Reviews Neuroscience. HFCS and other fructose-rich sugars can have profound adverse effects on the gut and digestive system. These sugars are known to disrupt the normal functioning of the gastrointestinal tract, contributing to various digestive disorders and altering the gut microbiome. Fructose, unlike glucose, is not directly absorbed by the body. It requires a specific transporter, GLUT5, to be taken up by the intestinal cells. Fructose interferes with these transporters, leading to malabsorption. Unabsorbed fructose travels to the large intestine, where it undergoes fermentation by gut bacteria. This process produces gases such as hydrogen, carbon dioxide, and methane, which cause bloating, gas, and abdominal pain leading to malabsorption and the intestine's inability to absorb fructose efficiently. The gut microbiome, a complex community of trillions of microorganisms living in the digestive tract, is crucial for maintaining digestive health, immune function, and overall well-being. High intake of fructose negatively affects this delicate balance. Studies have shown that diets high in fructose can lead to an imbalance in the gut microbiota composition. This imbalance is characterized by a decrease in beneficial bacteria such as Bifidobacteria and Lactobacilli and an increase in harmful bacteria like Clostridia and Enterobacteria.  A study published in The American Journal of Clinical Nutrition found that high fructose levels increase intestinal permeability, also known as "leaky gut." This condition allows harmful substances, such as toxins and bacteria, to pass from the gut into the bloodstream, triggering inflammation and contributing to the development of various diseases, including inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS). Inflammatory bowel disease, which includes conditions like Crohn's disease and ulcerative colitis, is exacerbated by promoting inflammation and altering the gut microbiota. A study in the journal Gut reported that reducing fructose intake improved symptoms in individuals with IBS, suggesting a direct link between fructose consumption and IBS symptom severity. Finally we need to also consider the catastrophic effects of HFCS on children. Children are particularly vulnerable to the health risks associated with HFCS due to their higher consumption levels relative to their body weight. According to data from the CDC, the average American child consumes approximately 12-16 teaspoons of added sugars per day, a significant portion of which comes from HFCS. This high intake is largely driven by the consumption of sweetened beverages, snacks, and processed foods that are marketed specifically to children. The high consumption of HFCS among children is a major contributor to the rising rates of childhood obesity and metabolic disorders. Studies have shown that children who consume high levels of sugary beverages and snacks are more likely to develop obesity, insulin resistance, and type 2 diabetes. A study published in Pediatrics found that children who consume sugary drinks daily are at a significantly higher risk of developing obesity compared to those who consume them less frequently. There is also growing concern about the impact of HFCS on children's cognitive development and behavior. High sugar diets have been linked to attention deficit hyperactivity disorder (ADHD) and other behavioral issues in children. A study in the Journal of Attention Disorders found that excessive sugar consumption, including HFCS, exacerbates symptoms of ADHD and impair cognitive functions such as memory and learning. A deeper look at the politics of the sugar industry reveals that huge sums are being doled out by the government to support and subsidize sugar companies. Writing for the Wall Street Journal, health journalist Alexandra Wexler explains that American taxpayers are currently responsible for shelling out $280 million to cover the cost of loans from the USDA which sugar producers are unable to pay back. Given the undeniable evidence demonstrating the toxicity of HFCS and other commercial sugars and their enormous toll on the wellbeing of Americans, why is it that our health agencies and elected officials are not calling for an urgent overhaul of existing policies, which graciously support the domestic sugar industry to poison the population? Where is the outrage over bailing out the purveyors of what is likely the most dangerous staple in the American diet? For our answers we must follow the money-trail.