One concrete data point for the thread. 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 or a sulfonylurea, which usually need reducing.
Worth separating that from glycaemic control, which this thread keeps folding into the same question. They behave differently and the advice does not transfer.
A narrower follow-up, since the general answer is now clear:
Why A1C lags the way it does, and what to look at in the meantime if you want to know sooner?
jason_paloalto 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…
There is a second half to this that has not been said yet. HbA1c reflects roughly three months of average glycaemia weighted toward the most recent weeks, which is why repeating it at six weeks tells you very little. The improvement on this class comes from two directions — direct glucose-dependent insulin secretion and glucagon suppression, plus the indirect effect of weight loss on insulin sensitivity — and the second continues after the first has plateaued.
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Update — I was wrong in the opening post, specifically about the direction. Correcting it here rather than editing it away.
james_edin said:HbA1c reflects roughly three months of average glycaemia weighted toward the most recent weeks, which is why repeating it at six weeks tells you very…
True, with the qualification that this is a self-selected group. The people for whom it did not work post less, and that shapes everything we think we know.