Semaglutide cardiovascular benefit: SELECT trial deep dive

FDA_TrackerJim said:

For anyone assembling their own picture: Tmax is one to three days, terminal half-life about 165 to 170 hours, steady state at four to five weeks, and…

CRP reduction on cardiovascular risk — this is the lab result that excites me most:

Baseline hsCRP: 10.0 mg/L (high cardiovascular risk)
Month 6 hsCRP: 2.5 mg/L (moderate risk)
Month 12 hsCRP: 0.7 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 17% to 5%. My cardiologist is genuinely impressed.

FDA_TrackerJim said:

For anyone assembling their own picture: Tmax is one to three days, terminal half-life about 165 to 170 hours, steady state at four to five weeks, and…

Thank you — that is the clearest version of this I have read, and I have read a lot of them. I will report back once I have actually tried it.

Clinical perspective, offered as context rather than as advice.

FDA_TrackerJim said:

...we're creating a generation dependent on cardiovascular risk...

I understand the concern, but consider this analogy: are we "creating a generation dependent on" blood pressure medication? Cholesterol medication? Thyroid medication?

Obesity is a chronic disease with biological drivers. Treating it with medication is no different from treating any other chronic condition. The "dependency" framing implies weakness or moral failure — neither of which is accurate.

If ongoing medication is what keeps someone healthy, that's successful treatment, not dependency.

hyun_seoul said:

FDA_TrackerJim said: ...we're creating a generation dependent on cardiovascular risk...

This is my experience too, for whatever a second data point is worth. Nothing to add that would improve it.

hyun_seoul said:

FDA_TrackerJim said: ...we're creating a generation dependent on cardiovascular risk...

Coming at hyun_seoul’s question from a different direction. The mechanism that matters here is not stomach emptying, it is central. GLP-1 receptor agonism in the arcuate nucleus stimulates POMC neurons and suppresses AgRP/NPY signalling, which is why the effect is appetite and food salience rather than physical fullness. Delayed gastric emptying largely tachyphylaxes over the first months; the appetite effect does not.