three years of metformin threads, summarised so you do not have to read them
The title is the argument: three years of metformin threads, summarised so you do not have to read them. Here is the rest of it.
Variability dropped before the average did, which was visible on the sensor and invisible on the lab result.
Assumed the weight endpoints from the obesity trials applied to my situation. They are different programmes.
Brought the whole CGM export to my appointment rather than one number. Entirely different conversation.
Not medical advice, obviously, and nothing here is approved for human use. One person with a spreadsheet.
best — the order this archive was captured in
Retitled — the original quoted an obesity endpoint as a glycaemic one.
Have you taken this to whoever manages your diabetes?
Sensor accuracy varies across wear, and readings on the first day are the least reliable. Calibration practice and compression artefacts explain many alarming single values.
Kept fingersticks alongside the sensor for two weeks to sanity-check it. Worth doing once.
Push back: one sensor reading is not a data point worth acting on, especially in the first day of wear.
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.
How long between the two A1c measurements?
Correcting myself: 23 weeks between those two A1c results, which is too short an interval to interpret.
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.
I would not compare your numbers to that population. Different baseline, different regimen, different trial.
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variability matters as much as the mean
Time in range told me far more than the average did. Two quarters with the same A1c looked completely different on the sensor.
Incretin-based agents stimulate insulin secretion in a glucose-dependent manner, which is why hypoglycaemia risk with them alone is low.
Disagreeing with this line: that endpoint is from the obesity programme and does not answer the question.
Panicked over a first-day sensor reading and rebuilt my week around it. It was the sensor.
- 1Retitled — the original quoted an obesity endpoint as a glycaemic one.6 comments in this branch · started by u/a1c_arc
- 2Incretin-based agents stimulate insulin secretion in a glucose-dependent…6 comments in this branch · started by u/teodor_duarte