Fat Science

This week on Fat Science, Dr. Emily Cooper, Mark Wright, and Andrea Taylor tackle a wide-ranging mailbag episode with listener questions from the U.S., UK, and Europe. Topics include unexpected weight regain on GLP-1s, post-meal sleepiness and hypoglycemia, metabolic dysfunction despite normal labs, GLP-1 dosing strategies, and why these medications are about metabolism, not appetite suppression.Key Questions AnsweredWhy can weight regain happen on GLP-1s even when habits haven’t changed?How do leptin, ghrelin, injury, stress, and under-fueling affect weight regulation?What does it mean if you get extremely sleepy after meals—is it hypoglycemia?Do GLP-1s increase insulin in a harmful way for non-diabetics?Can you have metabolic dysfunction with normal A1C, cholesterol, and blood pressure?Do GLP-1 medications “wear off,” and how should dosing be adjusted long term?Are GLP-1s just appetite suppressants—or true metabolic treatment?Is it possible to undo decades of calorie counting and restriction-based thinking?What are the risks of the return to extreme thinness in celebrity culture?Key TakeawaysCalories don’t explain metabolism. GLP-1 and GIP work across the brain and body—repairing signaling, not just reducing appetite.Leptin matters after dieting. Years of restriction and weight cycling can weaken leptin signaling, making the brain defend weight gain.Fueling is foundational. Medication can’t replace adequate food, sleep, and recovery.Post-meal fatigue is a clue. Reactive hypoglycemia is common and often misunderstood.Lowest effective dose wins. GLP-1 success is about pacing, not racing to the max dose.Chasing the “last 10 pounds” can backfire. Cosmetic restriction can create new metabolic problems.Dr. Cooper’s Actionable TipsIf weight gain appears after injury or stress, focus first on sleep, regular meals, and full fueling, not restriction.Suspected hypoglycemia? Ask about a mixed meal tolerance test to assess glucose and insulin response.Stay on the lowest GLP-1 dose that’s working and adjust only when progress truly stalls.Push back on “appetite suppressant” language—these meds amplify hormones your body already makes.Notable Quote“GLP-1s aren’t about eating less—they’re about strengthening metabolic signaling” — Dr. Emily CooperLinks & ResourcesPodcast Home: Fat Science Podcast Website – https://fatsciencepodcast.com/Podcast Episode References: https://fatsciencepodcast.com/wp-content/uploads/2025/06/Scientific-References-Fat-Science-Episodes.pdfCooper Center for Metabolism & Fat Science Episodes: https://coopermetabolic.com/podcast/Resources from Dr. Cooper: https://coopermetabolic.com/resources/Submit a Show Question: [email protected]. Cooper direct show email: [email protected] Science breaks diet myths and advances the science of real metabolic health. No diets, no agendas—just science that makes you feel better. This show is informational only and does not constitute medical advice.

This week on Fat Science, Dr. Emily Cooper, Mark Wright, and Andrea Taylor talk with pediatric eating disorder specialist Dr. Julie O’Toole (Kartini Clinic) and pediatric obesity expert Dr. Evan Nadler about what childhood obesity really is: a biologic, metabolic disease—not a willpower problem and not a failure of parenting.They explore how excess weight, constant hunger, and disordered eating in kids are often signs of underlying metabolic dysfunction and genetics—and why the old “eat less, move more” advice can do real harm, especially when children are shamed or restricted in the name of “health.”Key Questions AnsweredWhy is childhood obesity a metabolic disease, not a behavior problem?How are obesity and eating disorders deeply connected instead of opposite extremes?What role do GLP-1 medications play in children—and how do we protect against under-fueling?When should parents suspect genetic drivers like hyperphagia or MC4 mutations?How can medical treatment for obesity actually reduce disordered eating behaviors?When does excess weight become a medical issue requiring metabolic evaluation—not another diet?Key TakeawaysWeight is a symptom. Childhood obesity is often a sign of metabolic dysfunction, not overeating.Obesity & eating disorders overlap. Restriction can trigger disordered eating; disordered eating can worsen obesity.“Eat less, move more” harms. Shame-based approaches delay treatment and increase risk of eating disorders.GLP-1s work metabolically, not just through appetite suppression. Kids still need consistent fueling.Genetics matter. Single-gene differences can drive severe childhood hunger & rapid weight gain.Not treating is harm. Avoiding obesity care violates first, do no harm.Dr. Cooper’s Actionable TipsIf your child is gaining weight or constantly hungry, request metabolic labs (insulin, glucose, lipids, liver, hormones).If the doctor only says “eat less, move more,” ask: “How are we evaluating metabolism and genetics?”On GLP-1s? Monitor for under-fueling (skipped meals, low energy, food anxiety) and intervene promptly.Notable Quote“Not treating childhood obesity is doing harm. It’s a disease, not a lifestyle choice.” — Dr. Evan NadlerLinks & ResourcesPodcast Home: Fat Science WebsiteEpisodes & Show Archive: Cooper Center Podcast PageEducation & Metabolic Resources: coopermetabolic.com/resourcesSubmit a Show Question: [email protected] Dr. Cooper Directly: [email protected] with Our GuestsDr. Evan P. Nadler, MD, MBA – Founder, ProCare Consultants & ProCare TeleHealthWebsite: obesityexplained.comYouTube Channel: Obesity ExplainedDr. Julie K. O’Toole, M.D., M.P.H. – Chief Medical Officer & Founder, Kartini ClinicWebsite: kartiniclinic.comBooks: amazon.com/author/julieotoole*Fat Science breaks diet myths and advances the science of real metabolic health. No diets. No agendas. Just science that makes you feel better. This episode is informational only and not medical advice.

This week on Fat Science, Dr. Emily Cooper, Mark Wright, and Andrea Taylor talk with exercise physiologist Russell Cunningham and patient Becca Wert about a counterintuitive reality: for some people, exercise can actually slow metabolism, stall weight loss, and trigger weight gain—especially when the brain senses a threat to energy availability. Dr. Cooper explains how overtraining, under-fueling, and even thinking about workouts can activate famine signals in the brain and shut down key hormone pathways and what it takes to rebuild trust so movement becomes helpful instead of harmful.Key Questions AnsweredHow can exercise trigger metabolic slowdown and weight gain instead of weight loss?What lab markers (leptin, ghrelin, thyroid, cortisol, sex hormones) signal that your body is in “conservation mode”?Why did Becca lose more than 120 pounds after stopping intense workouts—and what did her COVID experience reveal about her metabolism?How did Russell’s overtraining syndrome develop, and what did his recovery teach him about fueling, rest, and nervous system regulation?How should fueling before, during, and after activity look different for people who are highly sensitive to energy deficits?When is it time to pull back on exercise, even if every message you’ve heard says “move more”?Key TakeawaysExercise is stress, not magic. When the brain perceives low energy or famine risk, it can respond to exercise by slowing metabolism, shutting down hormones, and defending body fat.Labs tell the story. Low leptin with high “famine signals,” along with thyroid, cortisol, and reproductive hormone suppression, are red flags that the body is conserving energy—not freely burning fuel.Fueling beats punishment. For sensitive metabolisms, you often “can’t overdo the fueling” around movement—sports drinks and carbs, even for short sessions, can help reassure the brain that it’s safe.Movement ≠ grind. Reframing exercise as enjoyable movement and nervous system regulation (walking, gentle climbing, yard work) helps break from all-or-nothing “training” mindsets that can backfire.Dr. Cooper’s Actionable TipsIf your weight climbs or stalls despite hard workouts and restricted eating, talk with a clinician about metabolic labs instead of just pushing harder.Cushion any exercise with real fuel: eat before, add carbs/electrolytes during, and refuel after—especially if you have a history of dieting, overtraining, or weight cycling.Consider starting with low-intensity, pleasant movement and always “leave gas in the tank” instead of chasing exhaustion as the goal.Notable Quote“Exercise should not be used as a weight loss tool. It should be used as a performance and a health tool.” — Dr. Emily CooperLinks & ResourcesPodcast Home: Fat Science Podcast Website – https://fatsciencepodcast.com/Cooper Center for Metabolism & Fat Science Episodes: https://coopermetabolic.com/podcast/Resources and education from Dr. Cooper: https://coopermetabolic.com/resources/Submit a Show Question: [email protected]. Cooper direct show email: [email protected] Science is your source for breaking diet myths and advancing the science of true metabolic health. No diets, no agendas—just science that makes you feel better. The show is informational only and does not constitute medical advice.

This week on Fat Science, Dr. Emily Cooper, Mark Wright, and Andrea Taylor unpack the biggest GLP-1 headlines from around the world—from the World Health Organization’s first-ever GLP-1 obesity guidelines to access battles, brain research, and the coming wave of generics and new meds.Dr. Cooper explains what the WHO’s move really means for patients, why long-term treatment matters, and how policy decisions in places like California and India could reshape who actually benefits from these breakthroughs. This isn’t hype—it’s metabolic medicine, health-system reality, and grounded hope.Key Questions AnsweredWhy is the WHO’s new guidance on GLP-1s for obesity such a historic turning point?What does it mean to treat obesity as a chronic, relapsing disease—not a willpower problem?Why do GLP-1s usually need to be taken long term, and how is that similar to blood pressure or cholesterol meds?How should GLP-1s be paired with metabolic care—fueling, sleep, movement, and real clinical oversight?What did the “stone cold negative” Alzheimer’s trials show—and why are addiction trials still promising?How could India’s launch of Ozempic and future generics impact global pricing and access?What new GLP-1 and metabolic drugs are on the horizon (like orforglipron, higher-dose oral semaglutide, and GLP-1/amylin combos)?Key TakeawaysWHO is catching up to the science. Obesity is affirmed as a chronic, relapsing disease that deserves pharmacologic treatment—not “eat less, move more” lectures or moral judgment.Long-term meds are the rule, not the exception. Stopping GLP-1s usually leads to weight and risk factors returning, just like stopping blood-pressure meds. That’s physiology, not failure.Behavior ≠ blame. WHO calls for pairing GLP-1s with “behavioral” care—but Dr. Cooper reframes this around fueling, sleep, and supported habits, not deprivation or diet culture.Access is the battleground. Even as WHO elevates GLP-1s, programs like California’s Medi-Cal are cutting coverage for obesity, a move Dr. Cooper calls penny-wise and pound-foolish given the downstream costs of diabetes and cardiovascular disease.Brain outcomes are nuanced. Large oral semaglutide trials failed to slow Alzheimer’s, but GLP-1s (and other obesity meds) still show promise for addiction by modulating reward pathways and the “internal drug factory” (POMC).Global markets are shifting. India’s huge population, looming Ozempic patent expirations, and emerging generics could eventually drive prices down—especially as more manufacturers compete.New meds may expand options. Orforglipron (a small-molecule oral GLP-1), higher-dose oral semaglutide, and a weekly GLP-1/amylin combo could bring more flexible, powerful, and potentially more affordable tools.Dr. Cooper’s Actionable TipsThink of obesity treatment like any chronic disease: long-term, medical, and individualized—not a short-term “diet.”If you’re using a GLP-1, pair it with real metabolic care: consistent fueling (not under-eating), good sleep, and appropriately fueled exercise.Be cautious with “cheap” or unsanctioned online GLP-1 options—especially if you’re being squeezed out of coverage. Safety and oversight matter.Remember there are other evidence-based obesity meds beyond GLP-1s; if you can’t tolerate or access one class, ask your clinician about alternatives.Notable Quote“Your metabolism is a lifelong issue. It’s not a headache.”— Andrea TaylorLinks & ResourcesPodcast Home: Fat Science Podcast Website – https://fatsciencepodcast.com/ Cooper Center for Metabolism & Fat Science Episodes: https://coopermetabolic.com/podcast/ Resources and education from Dr. Cooper: https://coopermetabolic.com/resources/ Submit a Show Question: [email protected]. Cooper direct show email: [email protected]*Fat Science is your source for breaking diet myths and advancing the science of true metabolic health. No diets, no agendas—just science that makes you feel better.

This week on Fat Science, Dr. Emily Cooper, Mark Wright, and Andrea Taylor answer listener questions about BMI cutoffs, weight cycling, metabolic adaptation, trauma, GLP-1 differences, and why some people gain weight on ultra-low calories. Dr. Cooper explains what’s really happening inside the metabolic system and why individualized treatment—not dieting—creates sustainable change.Key Questions AnsweredIf my BMI doesn’t “qualify” for GLP-1s, is Naltrexone + Bupropion helpful—and what labs matter first?Does being overweight always indicate metabolic dysfunction, and why are U.S. rates so high?If diets damage metabolism, what do you do when you’re already 80 pounds overweight?How long does it take for leptin and ghrelin to stabilize with mechanical eating?How can someone gain weight on 1,200 calories/day?After sleeve gastrectomy, how do you eat enough while on a GLP-1?Is set point theory real—and how does the melanocortin pathway influence it?If obesity runs in my family, will I need meds like Zepbound for life?How do trauma and stress alter long-term metabolic health?Can GLP-1s offset weight gain from steroids, mood meds, or hormones?Why might Ozempic work well while Mounjaro causes weight gain?Key Takeaways1. BMI rules don’t reflect metabolic truth.A mid-20s BMI can still mask significant dysfunction, especially with weight cycling.2. Weight cycling is metabolically stressful.Repeated losses/regains increase visceral fat, insulin abnormalities, and cardiovascular risk.3. Obesity is a multi-hormonal disease.Most people need pharmacology plus sleep, fueling, and movement—not restrictive dieting.4. Metabolic adaptation is powerful.Under-fueling lowers thyroid output, suppresses fat-burning, and slows metabolism dramatically.5. After bariatric surgery or on GLP-1s, frequency matters.Frequent, nutrient-dense snacks protect muscle, metabolism, and energy.6. Set point changes with better signaling.GLP-1s and related therapies help the brain accurately detect weight and lower the defended level.7. Genetics often mean lifelong support.Family patterns of obesity usually indicate long-term need for metabolic medication.8. Trauma amplifies metabolic risk.Childhood trauma disrupts IGF-1, sleep, stress hormones, insulin, leptin, and ghrelin.9. Medications can cause weight gain—GLP-1s can help counteract it.Steroids, mood meds, hormonal agents, and more can be metabolically unfriendly.10. “Newer” isn’t always better.Some people respond poorly to the GIP component in Mounjaro/Zepbound. Individual physiology rules.Dr. Cooper’s Actionable TipsRequest deeper evaluation: DEXA, visceral fat, fasting insulin/glucose, leptin, reproductive hormones.Stop restrictive dieting permanently—mechanical eating protects metabolic stability.Work with a fueling-focused dietitian (often ED-trained).Review your medication list for drugs known to cause weight gain.Don’t switch GLP-1s or chase higher doses if your current regimen works.Notable Quote“Obesity isn’t a willpower problem. It’s a metabolic disease, and when the underlying system is supported, the body finally has permission to change.” — Dr. Emily CooperLinks & ResourcesPodcast Home: Fat Science Podcast WebsiteSubmit a Show Question: [email protected] or [email protected]. Emily Cooper on LinkedInMark Wright on LinkedInAndrea Taylor on InstagramFat Science is your source for breaking diet myths and advancing the science of true metabolic health. No diets, no agendas—just science that makes you feel better. The show is informational only and does not constitute medical advice.