how much of what we believe about CGM actually comes from T2D threads
how much of what we believe about CGM actually comes from T2D threads. I am not trying to be the "source?" guy. I would just like a source.
The three numbers, and what each one can and cannot tell you.
A1c is an average over about three months, weighted to the recent weeks. It cannot show variability and it lags change. Continuous monitoring shows the shape — excursions, overnight, time in range — and is where improvement usually becomes visible first. Fingersticks are point measurements, useful for sanity-checking a sensor and for specific questions.
Most of the frustrated posts here come from expecting one of the three to answer a question that belongs to another. And all three are inputs to a conversation with whoever manages your care, which is not this board.
The order things move in, since nobody explains it and it worries people.
Postprandial excursions generally respond earliest. Variability tends to narrow before the average does, which is visible on a sensor and invisible on a lab result. Fasting glucose is often the laggard, and A1c — being a three-month average — is the last thing to reflect anything.
So a month in which the sensor looks better and the fasting number has not moved is the ordinary sequence, not a contradiction. Knowing that in advance would have saved me a quarter of unnecessary worry, which is why it is worth writing down.
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.
Sceptical readings welcome. The confident ones are the ones I distrust.
best — the order this archive was captured in
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.
Yes — time in range tells you about variability, which the average deliberately hides.
This. Hypoglycaemia risk in this class is driven mostly by the other agents in the regimen.
This.
Adding the obvious one — bring the export, not the single number, to whoever manages this.
Yes — time in range tells you about variability, which the average deliberately hides.
Agreed, and the glucose-dependence point is the reason the risk profile reads the way it does.
Continuous monitoring shows the shape: postprandial excursions, overnight behaviour and time in range. Two people with identical A1c can have very different distributions.
Retitled — the original quoted an obesity endpoint as a glycaemic one.
That is a sensor value, not a plasma value, and the two are not interchangeable at that level of precision.
Agreed. A1c is an integrated average over roughly three months and treating it as a current reading causes a lot of unnecessary alarm.
Correction: that trial is the diabetes programme and the figure you quoted is its glycaemic endpoint, not a weight result.
Postprandial excursions typically respond earlier than fasting glucose, so the sequence people observe is not a sign that something is not working.
- 1Continuous monitoring shows the shape: postprandial excursions, overnight…6 comments in this branch · started by u/stubborn_batchlist_maybe