u/stubborn_batchlist_maybe

Incretin-based agents stimulate insulin secretion in a glucose-dependent manner, which is why hypoglycaemia risk with them alone is low. Risk rises with agents that act independently of glycaemia.

On hypoglycaemia, because the risk gets attributed to the wrong thing constantly.

Incretin-based agents stimulate insulin secretion in a glucose-dependent way: the effect scales with glycaemia rather than acting unconditionally. That is why monotherapy risk is low. Where risk rises substantially is in combination with agents that lower glucose independently of the current level.

Which means the question "does this cause hypos" is not answerable without knowing the rest of the regimen — and that the person who can answer it is the one who wrote the regimen. Nothing on this board is a substitute for that conversation, and the good threads here end by saying so.

A1c, CGM, or fingersticks — which are we discussing?

I would not compare your numbers to that population. Different baseline, different regimen, different trial.

Continuous monitoring shows the shape: postprandial excursions, overnight behaviour and time in range. Two people with identical A1c can have very different distributions.

Have you taken this to whoever manages your diabetes?

How long between the two A1c measurements?

Disagreeing with this line: that endpoint is from the obesity programme and does not answer the question.

Yes — time in range tells you about variability, which the average deliberately hides.