PharmacoVig_BOS said:

CarlaRPh_TPA said: ...we don't know the long-term effects of cardiovascular risk...

Filing a mild objection. Mild because I might be wrong; an objection because nobody has addressed the case that does not fit. 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.

Ask again with the specifics and you will get a better answer than this one.

CarlaRPh_TPA said:

Prescribed on cardiovascular grounds rather than for weight, and almost everything written for patients assumes the opposite.

Continuous metabolic monitoring dashboard for cardiovascular risk — I track everything in a spreadsheet and here's the month-over-month trend for my key markers:

Weight: consistent downtrend, -2.3 lbs/week average
Fasting glucose (finger stick): stable at 84 mg/dL
Blood pressure (home): 118/74 average
Resting heart rate: 64 bpm (down from 80)
Waist circumference: down 14 inches total

The resting heart rate improvement correlates with cardiovascular fitness gains. Everything is moving in the right direction.

PeptideChemSF said:

The "earlier than weight loss explains" argument is weaker than this thread makes it sound.

I want to bring up the cardiovascular angle on cardiovascular risk.

The SELECT trial demonstrated a 20% reduction in MACE with semaglutide 2.4mg[1]. This is practice-changing because the CV benefit appears to be independent of the degree of weight loss — suggesting direct vascular and anti-inflammatory mechanisms.

For cardiovascular risk, this means we need to think beyond the primary outcome and consider the cardiovascular implications. The all-cause mortality reduction (HR 0.81) is the most clinically meaningful signal.

One thing that is still open after patPC_UT’s answer:

Was that from a primary source or from a summary of one?

claudia_zurich said:

I want to bring up the cardiovascular angle on cardiovascular risk.

Anti-inflammatory mechanisms of GLP-1 agonists and cardiovascular risk: beyond weight loss, GLP-1R activation directly suppresses NF-κB signaling, reduces NLRP3 inflammasome activation, and decreases monocyte/macrophage adhesion to endothelium[1].

Clinical correlates: hsCRP reduction of 30-60% (consistently seen across trials), reduced carotid intima-media thickness, and decreased coronary plaque inflammation on PET imaging.

These anti-inflammatory effects likely contribute to the cardiovascular benefit seen in SELECT — and may explain benefits beyond what weight loss alone would predict.