From the other side of the consultation, briefly. The honest answer is that the effect is real, the magnitude is contested, and the individual variation is larger than either. Those three things can all be true at once, and most arguments here are two people holding different parts of that.
I would rather be corrected than agreed with, if it comes to it.
bri_stats said:Because it is glucose-dependent, this class carries a low intrinsic hypoglycaemia risk on its own — the risk arrives when it is combined with insulin…
Adding the part of the answer the thread has not reached. It helps to ask what evidence would change your mind before you look at any. If nothing would, the discussion is not about evidence, and it is better to say so early than to spend nine posts discovering it.
The figures, for anyone assembling their own picture. The dose-response is real but shallow at the top. Across STEP 1 and STEP 4 the gap between 1.7mg and 2.4mg is a couple of percentage points of body weight on average, and the average is carrying a wide spread — plenty of people at 1.7mg sit above the 2.4mg mean. If a dose is working and tolerable, "working" is the relevant variable, not "maximal".
Worth separating that from glycaemic control, which this thread keeps folding into the same question. They behave differently and the advice does not transfer.
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Browse GL BiochemOne thing that is still open after bri_stats’s answer:
Whether anyone has held at a sub-maximal dose long term and kept the result, or whether the maintenance data only exists at 2.4mg?
Moderator note: good thread. Keeping it here rather than moving it, because the question is general enough to be useful. Tagging this one for the weekly digest.