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.
is that when we think about insulin resistance we're referring to the ability of insulin to signal for glucose uptake so glucose is central in that argument and the the conversation that you're bringing up and the perspective that you have on insulin sensitivity is independent of glucose or doesn't put glucose as the central figure in the insulin resistance equation is that right well it doesn't it it asks it it looks at hyperinsulinemia in addition to that glucose disposal
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really the problems with diabetes are related to hyperinsulinemia and insulin resistance
so the problem is not insulin resistance per se the problem is hyperinsulinemia that is in the first place it was all this insulin that put all this glucose into the cell but you're putting so much into the cell that it's too full
so the problem is not insulin resistance per se the problem is hyperinsulinemia that is in the first place it was all this insulin that put all this glucose into the cell but you're putting so much into the cell that it's too full
the problem is not insulin resistance per se it's actually the hyperinsulinemia so what your body is doing is taking all this fat and sort of storing it away so it doesn't cause a problem
hyperinsulinemia which is actually too much glucose too much insulin is gonna feed back and not let the glucose into the cell which is why the glucose stays outside and you have this so called insulin resistance
And then lastly of the primary fast causes of insulin resistance is too much insulin itself. So we know in humans, rodents and cells, I've published my own work on this topic that too much insulin will result in a resistance to the stimulus. So too much insulin can cause insulin resistance.