[Discussion] we are measuring T2D at the wrong time and calling it noise
Thinking out loud about this: we are measuring T2D at the wrong time and calling it noise. Assumed the weight endpoints from the obesity trials applied to my situation. They are different programmes. Variability dropped before the average did, which was visible on the sensor and invisible on the lab result. Kept…
Left up. It distinguishes the sensor data from the lab result, which most posts here do not.
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Are you quoting a diabetes trial or an obesity one?
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.
Sensor accuracy varies across wear, and readings on the first day are the least reliable.
Adding the obvious one — bring the export, not the single number, to whoever manages this.
variability matters as much as the mean
CGM shows you the shape, A1c shows you the area
check the trial population before quoting a result at somebody
dose for glycaemic control is not the same conversation as dose for weight
Cosigning that postprandial excursions improve first and the fasting number is the laggard.
Small fix — insulin secretion in this class is glucose-dependent, which is precisely why the risk you describe comes from the other agent.
I would not compare your numbers to that population. Different baseline, different regimen, different trial.
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.
Disagree — that is an obesity trial endpoint and this thread is about glycaemic control.