Has anyone dealt with pharmacogenomics of glp-1 response?

This one has a reasonably settled answer, so here it is. The gap between trial results and real-world results is consistent and it is not fraud. Trial participants get titration by protocol, scheduled contact, free drug and dietetic support; removing that infrastructure costs a few percentage points every time it has been measured. When your own curve sits below the published mean, that is the likeliest explanation before anything about you or your material.

TrialTracker_MD said:

The gap between trial results and real-world results is consistent and it is not fraud.

Propensity score matching studies and the trial evidence: when RCTs aren't available for a specific question, propensity score-matched observational studies can provide useful evidence.

A recent PSM study of 18,000 GLP-1 users vs matched controls showed reduced MI incidence (HR 0.78) over 4 years of follow-up[1].

These results complement the RCT data and suggest the benefits translate to real-world populations.

LarryQC_SD said:

My own curve sits about four points below the published mean and I spent two months assuming that meant something was wrong with me or with my…

This matches mine closely enough to be worth saying so. Read four things before the headline number. The population, because trial populations are selected and supported in ways that real cohorts are not. The comparator, because "better than placebo" and "better than the current standard" are different claims and get reported identically. The primary endpoint as pre-registered, because a secondary endpoint promoted after the fact is a hypothesis rather than a finding. And the completion rate, because a large effect in the half of participants who finished is a different result from a large effect in everybody enrolled.

From the other side of the consultation, briefly.

LarryQC_SD said:

...regarding the trial evidence...

I think this is an underappreciated point. To expand on it with some data:

A recent meta-analysis of 22 RCTs (n=18,900) found that the trial evidence was associated with a consistent effect size across diverse patient populations[1].

The NNT was 20, which is comparable to metformin for T2DM prevention. That's a strong clinical argument for this approach.