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But if androgen receptor density is such a dominant driver of anabolic response, how do you reconcile this with the fact that chronic low-grade inflammation (particularly via IL-6/STAT3 and TNF-/NF-B signaling) can suppress AR nuclear translocation even when receptor count is high and that in some individuals this blunts hypertrophy more dramatically than CAG-repeat length or hormone levels themselves?

Conversely, Habif et al

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In recent years, GLP-1 medications have become a focal point in the medical community due to their innovative treatment mechanisms, significant therapeutic efficacy, and broad development prospects

It continues, albeit at a declining rate, for much longer

The nicotinamide acts as a feedback inhibitor of SARM1