The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
And so, that that glucose is moving from your blood, where we're measuring it with a continuous glucose monitor, into the muscle, into the liver. And in states of insulin resistance, aka metabolic dysfunction, the actions of that insulin, the signaling of that insulin at the level of the liver and at the level of the muscle are deranged. And the insulin is knocking on the door, but it's the doors are not being opened. And the glucose is not getting taken up postprandially.
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Native comments, Twitter mentions, and Reddit threads about this claim — surfaced together so the conversation isn't fragmented across platforms.
Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.
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in the diabetic contrast is there's two processes that have gone awry one is that the liver is geared up to make more glucose than it should be through a process called gluconeogenesis the conversion of non-glucose precursors like amino acids alanine lactate to glucose and that process is accelerated so the liver is making twice the amount of glucose as it should and then you have a block in the periphery where the glucose same amount of insulin is not causing the glucose to be taken up by the muscle again in terms of flux what i care most about production is up and clearance or disappearance is down
the beta cell it fails insulin resistance in the muscle when you uh ingested a meal the muscle didn't take up the glucose cuz you're insulin resistant and insulin resistance in the liver when you ate a meal insulin didn't shut down uh the liver so that was the Triumph rate