Surely that depends on the degree of insulin-resistance, no? “Insulin-resistant” means that it takes more insulin than it’s supposed to, to get our glucose under control. Just because our insulin is still able to make our blood sugar behave, it doesn’t mean we’re not insulin-resistant. At the beginning, glucose is still controled, even though it’s taking more and more insulin to make it happen. At some point, however, the glucose levels start to show signs of the breakdown of the control (increasing insulin-resistance), and finally, at some point, fasting glucose reaches the threshold for a diagnosis of Type II diabetes.
Our obsession with glucose is the result of historical accident. Type I diabetes has been with us forever. It’s an autoimmune disease. Type II diabetes was rare, and was only found in the rich, so long as sugar and flour were difficult and expensive to refine. The diabetes epidemic began with the advent of cheap refined sugar and cheap refined flour, which brought the price of those commodities within reach of everyone. And given that insulin hadn’t been discovered yet, all they had to focus on was the blood glucose.
And that focus on glucose is wrong in both cases. Type I diabetes is about an immune system run amok, the glucose in the urine is merely a result. In Type II diabetes, the usual glucose sinks—the muscles and the adipose tissue—are tired of having glucose foisted on them, so the insulin has to work harder and harder to make them behave. We should be diagnosing Type II as soon as insulin starts to have to work harder, not waiting until the glucose finally gets out of control. It’s like a classroom of teacher-resistant kids: a first, the teacher can should loud enough to make them behave, but eventually the kids will become so rowdy that the teacher can’t shout loud enough to force proper behaviour, and the kids will stop listening altogether. Do we really want to wait until that point to admit there’s a problem?