The headline is broadly defensible, but the qualifications matter. Effect sizes vary by population, the strongest claims rest on shorter trials, and credible voices push back on how it's typically framed.
But that is it can be difficult because you could have a person on a ketogenic calorie deprived diet model who has an IGF-1 that is on the low end of the reference range be manually administering growth hormone and be using a higher dose than would otherwise be necessary to get to high normal optimal function put in quotation marks. Um, so it that's the best proxy we have as far as I'm aware is that serum biioarker IGF-1
Every Sunday: the week’s new conflicts and verdict changes — and nothing else.
Native comments, Twitter mentions, and Reddit threads about this claim — surfaced together so the conversation isn't fragmented across platforms.
Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.
Would love a "what would change this verdict" RSS feed. Sign me up if it exists.
the the waste basket term how do they know that you know because typically they're using about one to two units per day isn't that the typical dose yeah it depends largely on liver function too so some people with compromise function or type 1 diabetics for example they could have super high GH production but very low igf-1 from seemingly lack of insul ogenic signaling because it also has a positive relationship with igf-1 production but that is it can be difficult because you could have a person on a ketogenic calorie deprived diet model who has an igf-1 that is on the low end of the reference range be manually administering growth hormone and be using a higher dose than would otherwise be necessary to get to high normal optimal function put in quotation marks um so it that's the best proxy we have as far as I'm aware is that serum biomarker igf-1