Prescribed on cardiovascular grounds rather than for weight, and almost everything written for patients assumes the opposite.
Relative versus absolute is the distinction that gets lost: a 20% relative reduction on a high baseline risk is a large absolute benefit, and the same relative figure on a low baseline risk is a small one.
The narrow version of the question is how much of the SELECT benefit is plausibly independent of the weight loss, and whether that distinction changes anything practical.
If the honest answer is that nobody knows, that is a useful answer and I would rather have it.
nick_newbie said:Prescribed on cardiovascular grounds rather than for weight, and almost everything written for patients assumes the opposite.
CRP reduction on cardiovascular risk — this is the lab result that excites me most:
Baseline hsCRP: 6.0 mg/L (high cardiovascular risk)
Month 6 hsCRP: 2.5 mg/L (moderate risk)
Month 12 hsCRP: 0.3 mg/L (low risk)
This level of inflammatory marker reduction is comparable to what you'd see with statin therapy. Combined with the weight loss, my 10-year ASCVD risk score dropped from 13% to 5%. My cardiologist is genuinely impressed.
amsterdam_pete said:CRP reduction on cardiovascular risk — this is the lab result that excites me most: Baseline hsCRP: 6.0 mg/L (high cardiovascular risk) Month 6 hsCRP:…
Vitamin deficiency cascade with cardiovascular risk: after 6+ months of reduced food intake, I developed a subtle but important pattern: low B12 → elevated homocysteine → increased cardiovascular risk marker.
The connection: B12 is a cofactor for homocysteine metabolism. Without adequate B12, homocysteine accumulates. This is ironic — taking a CV-protective medication while developing a CV risk factor from reduced nutrition.
Solution: comprehensive vitamin supplementation and regular lab monitoring. Don't let the medication's benefits be undermined by nutritional deficiencies.
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View Resultsnick_newbie said:Prescribed on cardiovascular grounds rather than for weight, and almost everything written for patients assumes the opposite.
Mine went the same way, slower. Nothing to add that would improve it.
Adding the clinical framing, because it changes how the question reads.
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.