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c/t2dglp1·posted 1 year ago by u/tomas_kimani

[Discussion] we are measuring T2D at the wrong time and calling it noise

Discussion

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 fingersticks alongside the sensor for two weeks to sanity-check it. Worth doing once.

If two or three other people have done the same thing we might actually learn something. Alone it is an anecdote.

165 up / 6 down96% upvoted17 commentsid xrp3ne6 Oct 2024

17 comments

17 in this archive, depth 5

best — the order this archive was captured in

u/a1c_arcMOD19 points·1 year ago

Left up. It distinguishes the sensor data from the lab result, which most posts here do not.

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[removed]13 points·1 year ago

[removed by moderator]

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u/tomas_kimaniOP9 points·1 year ago

Are you quoting a diabetes trial or an obesity one?

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u/adnan_karlsen2 points·1 year ago

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.

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u/ice_pack_auditcold chain1 point·1 year ago

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.

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u/meal_prep_mira11 points·1 year ago

variability matters as much as the mean

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u/chidi_abubakar8 points·1 year ago

CGM shows you the shape, A1c shows you the area

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u/tomas_kimaniOP8 points·1 year ago

check the trial population before quoting a result at somebody

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u/emil_okwuosa2 points·1 year ago

dose for glycaemic control is not the same conversation as dose for weight

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u/lucia_balogun2 points·1 year ago

Cosigning that postprandial excursions improve first and the fasting number is the laggard.

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u/runa_grimaldi7 points·1 year ago

Small fix — insulin secretion in this class is glucose-dependent, which is precisely why the risk you describe comes from the other agent.

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u/kaia_cabrera2 points·1 year ago

I would not compare your numbers to that population. Different baseline, different regimen, different trial.

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u/hana_lehtinen-15 points·1 year ago

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.

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u/tomas_kimani2 points·1 year ago

Disagree — that is an obesity trial endpoint and this thread is about glycaemic control.

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u/neha_falk13 points·1 year ago

Continuous monitoring shows the shape: postprandial excursions, overnight behaviour and time in range. Two people with identical A1c can have very different distributions.

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u/ice_pack_auditcold chain10 points·1 year ago

Correction: that trial is the diabetes programme and the figure you quoted is its glycaemic endpoint, not a weight result.

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u/gentle_correctionnice about it7 points·1 year ago

That A1c change is inside the assay’s variability and the interval you measured over is too short.

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Type 2 diabetes as the original indication: A1c trajectories, CGM traces, hypoglycaemia risk when stacked with sulfonylureas or insulin, metformin combinations, and why the weight-loss conversation sometimes drowns out the glycaemic one.

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