In the article, insulin resistance is defined as:
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The risk factor that has been most consistently associated with CVD, type 2 diabetes and obesity is ‘insulin resistance’ — defined as an impaired biological response to insulin.
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, and contextually as:
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Excessive consumption of refined carbohydrates (especially sugar) and the resultant glycaemic load can overwhelm hepatic mechanisms that regulate the body’s blood glucose levels.
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In the first quote, the actual definition is always in the context of glucose-preferred-fuel, i.e. the standard test for insulin resistance is oral glucose tolerance (OGTT). From the result of this test - blood glucose level at a point in time post-test - insulin resistance is assessed by proxy, not directly, through the assumption that since glucose is the preferred fuel, and since blood glucose is not "cleared" quickly enough, and since insulin is the hormone that "pushes" glucose inside cells, then cells must be resistant to insulin. The term "cells" refers generally to all cells, not specific cells.
A more appropriate definition of insulin resistance needs a few corrections. For example, the bulk of glucose from the gut is "cleared" by the liver itself. This is done primarily through insulin, the bulk of which is also cleared (not in quotes here, because insulin is actually cleared by degradation, unlike glucose which is merely stored by conversion to glycogen) by the liver with insulin-degrading enzyme. This means that it's not all cells that are insulin resistant, as the case may be, it's just the liver cells. When that happens, the liver doesn't do its job, blood glucose lingers, until blood glucose is cleared by other organs like the brain for example.
But there's a big problem with the whole idea. The liver does not actually resist insulin at any point. On the contrary, even in the most extreme cases of diabetes type 2, the liver will continue to normally receive - and respond to - insulin, which will inhibit ketogenesis as its first act. Proof is in the blood - zero ketones. If the liver was truly resistant to insulin, there would be lots of ketones. In fact, "insulin resistance" is deemed to be akin to absence of insulin, and in this case - diabetes type 1 - there is no insulin, and there's tons of ketones.
Furthermore, an obscure experiment with dogs and insulin shows insulin causes atherosclerosis directly. We could be dealing with some misunderstood insulin resistance, but we're certainly dealing with hyperinsulinemia. This means the conclusion "there is not enough insulin" is patently false.
The point is there is an obvious lack of genuine expertise in the field when it comes to insulin, the liver and their interaction, and the effect of insulin on heart disease itself. I certainly agree that the standard model is horribly flawed, but I also question vague alternative hypotheses even when they come from respected people.