And “as low as 150/mo” for the lowest dose.
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When you stop GLP-1RA, everything goes bad (higher CAD and HF risks post-DC, while ACS, stroke, and mortality risks): One-year cardiovascular outcomes before and after GLP-1 ra discontinuation: a real-world retrospective cohort study 2025
Still, GLP-1RAs seem useless for atrial fibrilation:
- Effect of glucagon-like peptide-1 receptor agonists on atrial fibrillation incidence: a systematic review and meta-analysis 2025
- Tirzepatide and the risk of atrial fibrillation: an updated meta-analysis of randomized controlled trials 2025
For neurodegenerative diseases, mixed picture (great for dementia, useless for PD? and better with sema or lira or dula? they didn’t look at tirzepatide): Neurodegeneration onset with glucagon-like peptide-1 receptor agonists in people with type 2 diabetes: a real-world multinational cohort study 2025
The associations were separately observed among women (0.78 [0.72 to 0.84]) and men (0.90 [0.83 to 0.98]), individuals aged ≥ 65 years old (0.82 [0.78 to 0.87]) or < 65 years old (0.84 [0.70 to 1.00]), and in those initiating semaglutide (0.75 [0.67 to 0.84]), liraglutide (0.77 [0.70 to 0.84]), or dulaglutide (0.82 [0.77 to 0.88]). The hazard ratios for dementia, Alzheimer’s disease, vascular dementia, and Parkinson’s disease onset were 0.76 [0.72 to 0.81], 0.77 [0.68 to 0.87], 0.75 [0.67 to 0.85], and 1.04 [0.93 to 1.17] with GLP-1 RAs versus DPP4i, respectively.
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That first study about CV risk getting worse after discontinuing GLP1’s really missed a golden opportunity not checking if those patients gained weight back once they stopped so we can have a better idea of whether their CV risk got worse because they gained the weight back or just because they stopped the drug itself.
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You’re very right. They show the obesity % and the median, Q1 and Q3 BMI and they don’t look that different between the two groups.
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https://jitc.bmj.com/content/13/Suppl_2/A752
We previously demonstrated in preclinical models that the triple incretin agonist retatrutide (RETA, LY3437943) significantly reduced PDAC tumor burden, yielding a 14-fold reduction in tumor volume compared to a 4-fold reduction with the single GLP-1 receptor agonist semaglutide. Remarkably, the anti-tumor effects of RETA persisted after treatment discontinuation and weight regain, suggesting tumor-intrinsic or immunometabolic mechanisms independent of weight loss.1 Motivated by these findings, we investigated whether RETA administered at a subtherapeutic dose insufficient to induce weight loss could achieve anti-tumor efficacy comparable to anti-PD-1 therapy
Low-dose RETA significantly reduced tumor volume by 3-fold compared to vehicle, demonstrating efficacy comparable to anti-PD-1 monotherapy, which achieved a 5-fold reduction in tumor volume. With a 4-fold reduction in tumor volume, RETA + anti-PD-1 combination therapy did not demonstrate significant additional benefit beyond either monotherapy. Importantly, body weight remained stable across all groups, while blood glucose levels were significantly lowered by RETA treatment, indicating RETA’s anti-tumor effects occurred independently of weight loss and may involve metabolic modulation.
Results validated in mice only.
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This is very old, and inaccurate. Attia has since walked back these statements. Lean mass loss is a function of weight loss rate, it doesn’t have much to do with GLP1 use. You can expect to lose at least 66% of fat mass of on a GLP1 if you don’t go too crazy trying to lose more than 1% of your body weight. This is comparable to other weight loss methods.
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? did you mean 10%?
Oops, I meant 1% of your body weight weekly
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