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[DOI] [PubMed] [Google Scholar] Meiser B., Wong W.K.T., Peate M., Julian-Reynier C., Kirk J., Mitchell G

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?

Hunger suppression remains stable throughout treatment as long as you continue therapy

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