The logic of this argument has to be taken one step further, however, even if the cognitive dissonance is elevated with it. Both diabetes and metabolic syndrome are associated with an elevated incidence of virtually every chronic disease, not just heart disease. Moreover, the diabetic condition is associated with a host of chronic blood-vessel-related problems known as vascular complications: stroke, a stroke-related dementia called vascular dementia, kidney disease, blindness, nerve damage in the extremities, and atheromatous disease in the legs that often leads to amputation. One obvious possibility is that the same metabolic and hormonal abnormalities that characterize the diabetic condition—in particular, elevated blood sugar, hyperinsulinemia, and insulin resistance—may also cause these complications and the associated chronic diseases. And otherwise healthy individuals, therefore, would be expected to increase their risk of all these conditions by the consumption of refined and easily digestible carbohydrates, which inflict their damage first through their effects on blood sugar and insulin, and then, indirectly, through triglycerides, lipoproteins, fat accumulation, and assuredly other factors as well.

This is a fundamental tenet of the carbohydrate hypothesis: If the risk of contracting any chronic disease or condition increases with metabolic syndrome and Type 2 diabetes, then it’s a reasonable hypothesis that insulin and/or blood sugar plays a role in the disease process. And if insulin and blood sugar do play a pathological role, then it’s a reasonable hypothesis that the same conditions can be caused or exacerbated in healthy individuals by the consumption of refined and easily digestible carbohydrates and sugars.

Among the immediate examples that follow from this logic is the particularly disconcerting possibility that insulin itself causes or exacerbates atherosclerosis. Since insulin resistance and hyperinsulinemia characterize Type 2 diabetes, it’s certainly possible that chronically elevated levels of insulin are the cause of the persistently high incidence of atherosclerosis in diabetics, quite aside from any other effects insulin might have on triglycerides, lipoproteins, or blood pressure. And if this is the case, then the excessive secretion of insulin—induced by the consumption of refined carbohydrates and sugars—might be responsible for causing or exacerbating atherosclerosis in those of us who are not diabetic.