[Question] A1c 5.6 but CGM says otherwise. which do i believe.
A1c 5.6 but CGM says otherwise. which do i believe. I would rather ask a basic question now than get this wrong quietly for two months.
Postprandial excursions flattened out first and the fasting number took months to follow. Nobody had told me to expect that order.
Time in range told me far more than the average did. Two quarters with the same A1c looked completely different on the sensor.
Panicked over a first-day sensor reading and rebuilt my week around it. It was the sensor.
That is everything I have. The rest is opinion and I have tried to keep it out.
best — the order this archive was captured in
The diabetes and obesity programmes are separate, with different populations and different primary endpoints. Reading a result across from one to the other is not a comparison.
CGM shows you the shape, A1c shows you the area
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 can be affected by things that have nothing to do with glucose
postprandial excursions are where most of the improvement shows up first
A1c is a three-month average and it lags everything
glycaemic control and weight are two different endpoints
What else is in the regimen?
What else is in the regimen?
Adding the obvious one — bring the export, not the single number, to whoever manages this.
the diabetes trials report different endpoints from the obesity ones
Yes — time in range tells you about variability, which the average deliberately hides.
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.
This. Hypoglycaemia risk in this class is driven mostly by the other agents in the regimen.
Correction: that trial is the diabetes programme and the figure you quoted is its glycaemic endpoint, not a weight result.
check the trial population before quoting a result at somebody
Right, and the diabetes programmes report glycaemic endpoints. Quoting an obesity trial result here is answering a different question.
A1c, CGM, or fingersticks — which are we discussing?
Postprandial excursions typically respond earlier than fasting glucose, so the sequence people observe is not a sign that something is not working.
My hs-CRP moved and it turned out to have nothing to do with glucose at all.