Diabetes specialists have historically perceived this plague of atherosclerosis among their patients as though it has little relevance to the atherosclerosis and heart disease that affect the rest of us. Textbooks would note the importance of identifying and controlling the “numerous and as yet ill-defined factors generally involved in the pathogenesis of atherosclerosis,” as the 1971 edition of Joslin’s Diabetes Mellitus did, but the implication was that the requisite revelations would emerge, as they had in the past, from heart-disease researchers, as though the flow of knowledge about heart disease could proceed only from heart-disease research to diabetology and never the other way around.

The extreme example of this thinking has been the assumption that saturated fat is the nutritional agent of heart disease in diabetics, just as it supposedly is in everyone else. “The frequent cardiovascular complications seen in past years among persons with diabetes,” the 1988 Surgeon General’s Report on Nutrition and Health says, are caused by the “traditional restriction of carbohydrate intake in persons with diabetes” and thus an increased intake of fat, “usually, saturated.” This was the logic that led the American Diabetes Association, from the early 1970s, to recommend that diabetics eat more carbohydrates rather than less, despite a complete absence of clinical trials that might demonstrate that the benefits of doing so outweigh the risks, and the decades of clinical experience establishing carbohydrate restriction as an effective method of controlling blood sugar. If atherosclerosis was accelerated in diabetics, the thinking went, it was accelerated because they ate more saturated fat than nondiabetics. Diabetologists believed they could safely prescribe a carbohydrate-rich diet to their patients, because a diet that is low in fat will be high in carbohydrates.

But the research on metabolic syndrome suggests an entirely different scenario. If the risk of heart disease is elevated in metabolic syndrome and elevated still further with diabetes, then maybe the flow of knowledge about heart disease should proceed from diabetics, who suffer the most extreme manifestation of the disease, to the rest of us, and not the other way around. Maybe diabetics have such extreme atherosclerosis because there is something about the diabetic condition that causes the disease. Perhaps the metabolic abnormalities of the diabetic condition are the essential cause of atherosclerosis and coronary heart disease in everyone, only diabetics suffer to a greater extent.

Another way to look at this is to consider that metabolic syndrome and Type 2 diabetes lie on a continuum or a curve of physical degeneration. This curve is marked by ever-worsening disturbances of carbohydrate and fat metabolism—high insulin, insulin resistance, high blood sugar, high triglycerides, low HDL, and small, dense LDL. Atherosclerosis is one manifestation of this physical degeneration. In diabetes, the metabolic abnormalities are exacerbated—diabetics are further down the curve of physical degeneration—and the atherosclerotic process is accelerated. But we all live on the same curve. The mechanisms that cause atherosclerosis are the same in all of us; only the extent of damage differs.