Show Notes
Have you been told you have PCOS but nothing seems to help? In May 2024, after 14 years of global collaboration involving 56 organizations and 22,000 stakeholders, the medical community officially changed PCOS to PMOS - and the reason why reveals everything that's been wrong with how this condition has been understood and treated for decades. Dr. Cooper breaks down why this isn't just a name change, but a complete reframe that puts metabolic dysfunction at the center where it belongs. KEY TAKEAWAYS PCOS is now officially called PMOS - Polyendocrine Metabolic Ovarian Syndrome - shifting focus from ovarian problems to metabolic dysfunction 70 million women globally are affected during reproductive years, with 70% remaining undiagnosed The condition can occur at any weight and is driven by insulin resistance and other metabolic signals, not ovarian problems Treatment should focus on metabolic health rather than weight loss or ovarian interventions The name change parallels similar shifts in medicine like MASLD replacing non-alcoholic fatty liver disease NOTABLE QUOTE "Most patients with this label that they've had in the past, the PCOS label, feel a sense of hopelessness, and even join support groups and things like that, and thinking that this will be a condition they have forever. And what I try to do is explain, no, this is just a physical manifestation of the metabolic disruption that we treat all the time" — Dr. Emily Cooper Links & Resources Podcast Home: fatsciencepodcast.com Cooper Center for Metabolism: coopermetabolic.com Resources from Dr. Cooper: coopermetabolic.com/resources Join Our Community: patreon.com/cw/FatSciencePodcast Submit Your Question: [email protected] or [email protected]
Fat Science is supported by the Diabesity Institute, a nonprofit dedicated to increasing access to effective, science-based metabolic care. This podcast is for informational purposes only and is not intended as medical advice. Please consult with a qualified healthcare provider for personalized recommendations.
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Wondering why weight stalls on treatment? Dr. Emily Cooper explains how the brain defends set points and why eating less stops progress. Dr. Emily Cooper, Mark Wright, and Andrea Taylor answer listener letters from around the world. The conversation addresses why athletic men with a BMI of 27 can still show high visceral fat on a DEXA scan, how medications defend metabolic set points, and why intentional undereating triggers starvation responses. The team also examines global access to metabolic treatments, dual incretin agonists versus single agonists, artificial sweeteners, and how to interpret two-hour insulin and glucose tolerance curves. Key Takeaways Rapid weight reduction without adequate nutrition can cause lean mass loss and trigger metabolic defense mechanisms. Dual incretin therapies stimulate GIP receptors far more than GLP-1 receptors compared to natural human hormones, creating different patient responses. Intentional calorie restriction reduces natural incretin production and can impair metabolic signaling, making mechanical fueling essential. Fasting insulin suppression combined with pre-diabetes indicators can reflect the brain pulling glucose during periods of low carbohydrate intake. Resources Mentioned Diabesity Foundations Course Cooper Center for Metabolism Diabesity Institute Connect with Us Podcast Home:fatsciencepodcast.com Cooper Center for Metabolism:coopermetabolic.com Diabesity Institute: diabesityinstitute.org Resources from Dr. Cooper:coopermetabolic.com/resources Join Our Community:patreon.com/cw/FatSciencePodcast Submit Your Question: [email protected] or [email protected] Fat Science is supported by the Diabesity Institute, a nonprofit dedicated to increasing access to effective, science-based metabolic care. This podcast is for informational purposes only and is not intended as medical advice. Please consult with a qualified healthcare provider for personalized recommendations. Produced by: Podcast Impact Studio https://podcastimpactstudio.com
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