tried glycaemic control for 4 weeks. here is what happened.
The title is the argument: tried glycaemic control for 4 weeks. here is what happened. Here is the rest of it.
Since the title puts numbers in the shop window: 4 weeks.
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.
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.
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
Postprandial excursions typically respond earlier than fasting glucose, so the sequence people observe is not a sign that something is not working.
Postprandial excursions typically respond earlier than fasting glucose, so the sequence people observe is not a sign that something is not working.
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
Assumed the weight endpoints from the obesity trials applied to my situation. They are different programmes.
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.
My TSH moved and it turned out to have nothing to do with glucose at all.
Certain conditions affect A1c independently of glycaemia. If a result looks inconsistent with the sensor data, that is a question for whoever manages your care rather than for this board.
This. Hypoglycaemia risk in this class is driven mostly by the other agents in the regimen.