My reason for being on this is cardiovascular rather than cosmetic, which puts me in a small minority in most of these threads.
What I am after is how much of the SELECT benefit is plausibly independent of the weight loss, and whether that distinction changes anything practical.
Numbers rather than impressions, if you have them.
CanadaChris said:My reason for being on this is cardiovascular rather than cosmetic, which puts me in a small minority in most of these threads.
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 43 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.MetabolicMD said:Lp(a) and cardiovascular risk: a nuance that matters.
Dr.MetabolicMD said:...we don't know the long-term effects of cardiovascular risk...
This is a fair point, and I think intellectual honesty requires acknowledging it. GLP-1 agonists in their current form have ~8-10 years of human exposure data. That's not nothing, but it's not 30+ years either.
However: the risk-benefit calculation should also consider the KNOWN long-term effects of untreated obesity — diabetes, cardiovascular disease, cancer, joint destruction, reduced lifespan by 5-10 years.
Uncertainty about GLP-1 long-term safety vs certainty about obesity consequences. The calculus seems clear to me, but reasonable people can disagree.
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Browse GL BiochemCanadaChris said:My reason for being on this is cardiovascular rather than cosmetic, which puts me in a small minority in most of these threads.
Can confirm. Same sequence, different timescale.
Adding the clinical framing, because it changes how the question reads.
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.