Dr.ReproEndo said:tane_welly said: ...we don't know the long-term effects of cardiovascular risk...
This is where I part company with the consensus forming above. The "earlier than weight loss explains" argument is weaker than this thread makes it sound. Blood pressure and inflammatory markers move fast and are downstream of early weight loss, so the mechanism is not as cleanly separable as the summaries imply.
tane_welly said:Prescribed on cardiovascular grounds rather than for weight, and almost everything written for patients assumes the opposite.
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.
Dr.MetabolicMD said:The "earlier than weight loss explains" argument is weaker than this thread makes it sound.
6 month update on cardiovascular risk: down 41 lbs, off blood pressure meds, A1C normalized. Genuinely life-changing.
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View ResultsDr.GastroMayo said:6 month update on cardiovascular risk: down 41 lbs, off blood pressure meds, A1C normalized.
Lp(a) and cardiovascular risk: a nuance that matters. Unlike most lipid markers, Lp(a) is 90%+ genetically determined and doesn't really change with weight loss or GLP-1 therapy.
My Lp(a) has remained at 60 nmol/L across all time points. If yours is elevated (>50 nmol/L), you need additional risk mitigation strategies regardless of your GLP-1 response. Don't assume your medication is covering all cardiovascular risk factors.