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Fat Science

Fat Science

著者: Dr Emily Cooper
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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. In each episode, we share little-known facts and personal experiences to dispel misconceptions, reduce stigma, and instill hope. Fat Science is 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.Dr Emily Cooper 衛生・健康的な生活 身体的病い・疾患
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  • I’m Working Out—So Why Am I Getting Fatter?
    2025/12/22

    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 Answered

    • How 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 Takeaways

    • Exercise 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 Tips

    • If 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 Cooper

    Links & 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: questions@fatsciencepodcast.comDr. Cooper direct show email: dr.c@fatsciencepodcast.com

    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. The show is informational only and does not constitute medical advice.

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    1 時間 2 分
  • The Latest GLP-1 News
    2025/12/15
    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: questions@fatsciencepodcast.comDr. Cooper direct show email: dr.c@fatsciencepodcast.com*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.
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    40 分
  • Listener Mailbag: Set Point Theory, Trauma & Metabolism, and Why 1200 Calories Can Still Lead to Weight Gain
    2025/12/08

    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 Answered

    • If 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 Takeaways

    1. 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 Tips

    • Request 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 Cooper

    Links & Resources

    • Podcast Home: Fat Science Podcast Website
    • Submit a Show Question: questions@fatsciencepodcast.com or dr.c@fatsciencepodcast.com
    • Dr. Emily Cooper on LinkedIn
    • Mark Wright on LinkedIn
    • Andrea Taylor on Instagram


    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. The show is informational only and does not constitute medical advice.

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    47 分
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