The paper on proline restoring mitochondrial function in senescent cells is interesting for a reason I haven’t seen discussed: a lot of people are already getting several grams of proline incidentally from collagen supplements. Collagen peptides run roughly 10-15% proline by mass. If you’re taking 10-20g collagen daily for joint health or connective tissue, you’re getting ~1-2g proline without tracking it as the variable. So the question I keep coming back to: how much of the connective tissue benefit people attribute to collagen synthesis is actually downstream of what proline is doing in senescent cells? The mechanisms aren’t mutually exclusive, but they predict different dosing curves and probably different timing. “Restores mitochondrial function” is a different claim than “supports synthesis.” That framing is what makes me take this more seriously than the usual amino acid paper. And for perimenopausal women specifically, where senescent cell burden accelerates during the transition, the timing question becomes non-trivial. Not suggesting anyone buy standalone proline. Just wondering if the collagen supplement RCT data should be reanalyzed with this mechanism as a candidate explanation.