Clinical perspective, offered as context rather than as advice.

marco_milano 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.

Dr.PainCLE said:

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

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 69 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.

Dr.PainCLE said:

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

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

Baseline hsCRP: 12.0 mg/L (high cardiovascular risk)
Month 6 hsCRP: 1.5 mg/L (moderate risk)
Month 12 hsCRP: 0.9 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 19% to 4%. My cardiologist is genuinely impressed.

Dr.PainCLE said:

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

This is exactly what I could not find anywhere else.

Moderator note: good thread. Keeping it here rather than moving it, because the question is general enough to be useful.