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Endocrine dialogues

@EndoDialogues

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Joined November 2020
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@MWeintraubMD
Michael Weintraub, MD
1 month
Newly published treatment algorithm for the pharmacologic treatment of obesity and its complications, from the European Association for the Study of Obesity (EASO) ⚕️ Semaglutide and tirzepatide are recommended as first line to treat obesity AND to treat underlying
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@EndoDialogues
Endocrine dialogues
2 months
As always → more research is needed Want to know more? https://t.co/TeUIdGwI1s
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@EndoDialogues
Endocrine dialogues
2 months
Higher calorie intake Faster eating → less satiety Additives & packaging chemicals (like bisphenol-A, phthalates) linked to obesity ✅ Conclusion: Observational studies strongly associate UPF with obesity, and one RCT supports a causal link. +
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@EBF2033
eBibleFellowship - NewOpenForum.org
29 days
Wrong is Still Wrong – No Matter How Hard Man Tries to Make it Right
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@EndoDialogues
Endocrine dialogues
2 months
RCT evidence (only 1 so far): A 2-week inpatient crossover trial found that when 83% of calories came from UPF, participants ate >500 kcal/day more, ate faster, and gained ~0.9 kg, despite diets being matched as possible. 🔹 Why might UPF promote weight gain? +
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@EndoDialogues
Endocrine dialogues
2 months
🔹 What studies show: Cross-sectional: Most find higher UPF = more obesity. Some show differences by sex (e.g., linked to obesity in women in Switzerland & Korea; in men in Iran). Cohort studies: Consistently show UPF predicts higher obesity risk. +
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@EndoDialogues
Endocrine dialogues
2 months
🔹 What counts as UPF? Using the NOVA system, UPF includes foods with ≥5 industrial ingredients not found in minimally processed foods. Examples: ice cream, packaged milk drinks, fruit yogurts. ➡️ They’re cheap, shelf-stable, and loaded with fat, sugar, and salt. +
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@EndoDialogues
Endocrine dialogues
2 months
🍔🥤 Ultra-Processed Foods & Obesity: What’s the Evidence? Over recent decades, consumption of ultra-processed foods (UPF) has risen in parallel with obesity. Coincidence… or causality? 🤔 +
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@MWeintraubMD
Michael Weintraub, MD
2 months
Skeletal muscle 💪 should be viewed as a vital metabolic organ 🧬. Preserving lean mass during weight loss ⚖️ is essential for physical performance 🏃‍♂️ and long-term metabolic health ❤️‍🩹. The risks of muscle loss, from impaired gly-caemic control 🩸 to loss of independence 🧑‍🦽,
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@EndoDialogues
Endocrine dialogues
2 months
- Lean mass = fat free mass, which is different than muscle mass. Lean mass account for bone mineral content and organs beyond muscle mass. - Current data don’t rule out differences between GLP-1 RAs. +
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@EndoDialogues
Endocrine dialogues
2 months
- RCTs closely follow-up lifestyle interventions for protein intake and encourage physical activity (including strength training) — real-world patients may not, increasing risk of muscle loss. - Methods to measure lean vs. fat mass vary (DEXA, bioimpedance, indexes) +
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@EndoDialogues
Endocrine dialogues
2 months
⚠️ Caveats: - Most studies come from liraglutide, which has weaker weight-loss effects than semaglutide and tirzepatide. - Very limited data with tirzepatide, the most potent of the class. +
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@EndoDialogues
Endocrine dialogues
2 months
Key points: ✅ With potent GLP-1 RAs, about 25% of lost weight is lean mass. ✅ More total weight lost = more absolute lean mass lost, but the percentage of lean mass doesn’t drop. ❌ No evidence that GLP-1 RAs decrease lean mass vs. other weight loss methods. +
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@EndoDialogues
Endocrine dialogues
2 months
🔹 Karakasis et al. → Focused on RCTs. Lean mass ≈ 25% of total weight lost. One tirzepatide study included. Again, many liraglutide studies, fewer with semaglutide. +
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@EndoDialogues
Endocrine dialogues
2 months
🔹 Anyiam et al. → Minimal to no muscle mass loss. <20% of weight lost came from muscle. Most data from liraglutide (less potent, rarely used today). No data from tirzepatide. +
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@EndoDialogues
Endocrine dialogues
2 months
💪 Muscle mass loss & GLP-1 receptor agonists: what do we know? Muscle loss with GLP-1 RAs (like semaglutide and tirzepatide) has been debated. Two new meta-analyses shed more light: +
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@EndoDialogues
Endocrine dialogues
5 months
How do we learn? Life—and medicine—is built on automatic moves, as we're usually good at predicting what comes next. But consciousness arises from prediction errors. And only through consciousness can learning happen!
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@sniezenMD
Sebastian Niezen MD, MMSc
6 months
🚨 New in @AGA_CGH 🚨 Waist-to-height ratio (WHtR) >>> BMI/waist in predicting: 🔑 Severe hepatic steatosis (AUROC 0.79) 🔑Advanced fibrosis (AUROC 0.78) 🔑 Especially effective in Hispanics @ebtapper @EndoDialogues @PittIMChiefs @PittGIM @BIDMC_GI https://t.co/cWAeOhkkCj
cghjournal.org
Obesity is an important component of the pathophysiology of metabolic dysfunction–associated steatotic liver disease (MASLD). The diagnosis of obesity, however, is complex, and other anthropometric...
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@MWeintraubMD
Michael Weintraub, MD
7 months
Subcutaneous semaglutide demonstrated cardiovascular benefit in T2DM back in 2016 (SUSTAIN-6) with 26% MACE reduction. Oral semaglutide demonstrates cardiovascular risk reduction in T2DM and high CV risk in the newly published SOUL trial with 14% MACE reduction with albeit a
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