My reason for being on this is cardiovascular rather than cosmetic, which puts me in a small minority in most of these threads.
What would genuinely help is knowing how much of the SELECT benefit is plausibly independent of the weight loss, and whether that distinction changes anything practical.
Happy to be told the question itself is wrong.
MASHdoc_SA said:My reason for being on this is cardiovascular rather than cosmetic, which puts me in a small minority in most of these threads.
Metabolic syndrome resolution on cardiovascular risk: I went from meeting 5 of 5 diagnostic criteria to meeting ZERO after 13 months of treatment.
The 5 criteria (and my journey):
- Waist circumference: 52" → 36" ✅ Resolved
- Triglycerides: 266 → 96 ✅ Resolved
- HDL: 36 → 58 ✅ Resolved
- Blood pressure: 146/96 → 119/73 ✅ Resolved
- Fasting glucose: 116 → 88 ✅ Resolved
Metabolic syndrome reversal is, in my view, the most medically significant outcome of GLP-1 therapy.
NeuroNate said:Metabolic syndrome resolution on cardiovascular risk: I went from meeting 5 of 5 diagnostic criteria to meeting ZERO after 13 months of treatment.
NNT calculation for cardiovascular risk clinical endpoints: NNT = 1/ARR (absolute risk reduction).
From SELECT trial: MACE at 39 months — 6.5% semaglutide vs 8.0% placebo. ARR = 1.5%. NNT = 67 over 3.3 years.
Compare to established therapies:
| Intervention | NNT | Timeframe |
|---|---|---|
| Semaglutide (MACE) | 67 | 3.3 years |
| Statins primary prevention (MI) | ~100 | 5 years |
| Aspirin secondary prevention | ~77 | 2 years |
These NNTs are clinically meaningful and comparable to accepted cardiovascular interventions.
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View ResultsMASHdoc_SA said:My reason for being on this is cardiovascular rather than cosmetic, which puts me in a small minority in most of these threads.
This matches mine closely enough to be worth saying so out loud.
Clinical perspective, offered as context rather than as advice.
Mendelian randomization evidence supporting GLP-1 pathway modulation for cardiovascular risk: genetic variants in the GLP1R gene region associated with lower BMI also show associations with reduced cardiovascular risk, confirming a causal pathway[1].
This "natural experiment" (people born with genetically higher GLP-1 signaling being leaner and healthier) provides orthogonal evidence supporting the pharmacological approach. When genetic epidemiology, clinical trials, and mechanistic studies all converge, confidence in the therapeutic approach is high.
[1] Zheng SL, et al. Lancet Diabetes Endocrinol. 2023;11(12):869-879.