I see these two approaches discussed in the same breath for body recomposition, but I’ve been thinking about how fundamentally different they are, not just in mechanism but in the kind of evidence we have for them. Before I get into it, the strongest version of the argument for both is compelling.
For GLP-1s like semaglutide, the data is overwhelming. The big cardiovascular outcome trials (the SELECT trial, for instance) and the weight loss trials (STEP program) show a massive, unambiguous effect on weight reduction
that “unambiguous effect on weight reduction” is true at the population level in the big trials like STEP, no question. but on the individual level, the lived experience feels anything but unambiguous. the user-to-user response variability is wild, and it’s the one thing the big trials don’t really capture.
two people can be on the exact same dose and have completely different outcomes on everything from nausea to lean mass retention. i’ve seen some early research floating the gut microbiome as a potential reason for that variability, which mechanistically makes a lot of sense. that’s not proof, but it tracks better than just calling some people non-responders and leaving it at that.
it’s also why tracking your own response is so critical, because you’re really just running an n=
weight reduction data is strong 📊
1 Like