Good Calories, Bad Calories

except in this manner no one would attribute any such function to it…. Is a persistent [high blood sugar] a cause of arteriosclerosis in diabetes? It very likely is a cause because it is an abnormal condition and any abnormal state would tend to wear out the machine.

ELLIOTT JOSLIN, “Arteriosclerosis and Diabetes,” 1927

DESPITE NEARLY A CENTURY’S WORTH OF therapeutic innovations, the likelihood of a diabetic’s contracting coronary artery disease is no less today than it was in 1921, when insulin was first discovered. Type 2 diabetics can still expect to die five to ten years prematurely, with much of this difference due to atherosclerosis and what Joslin’s Diabetes Mellitus has called an “extraordinarily high incidence” of coronary disease.

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.

Consider Keys’s cholesterol hypothesis as an example of this logic. One reason we came to believe that high cholesterol is a cause of heart disease is that severe atherosclerosis is a common symptom of genetic disorders of cholesterol metabolism. If having a cholesterol level of 1,000 mg/dl—as these individuals often do—makes atherosclerosis seemingly inevitable, the logic goes, and if higher cholesterol seems to associate with higher risk of heart disease among the rest of us, then cholesterol is a cause of heart disease, and elevating cholesterol by any amount will increase risk. The higher the cholesterol, the greater the risk. If eating saturated fat elevates cholesterol, then that in turn causes heart disease. And this is supposedly true of diabetics as well. Keys oversimplified the science and was wrong about the true relationship of cholesterol and heart disease, but the logic itself is otherwise sound.

The same logic holds for blood pressure and heart disease. The higher the blood pressure, the greater the risk of heart disease. If salt supposedly raises blood pressure, even if only by a few percentage points, then salt is a nutritional cause of heart disease. This, too, is held to be true for diabetics. Thus, the atherogenic American diet, as now officially defined, the diet that clogs arteries and causes heart disease, is a diet high in saturated fat and salt.

Now let’s apply the same reasoning to metabolic syndrome and diabetes. Diabetics suffer more virulent atherosclerosis and die of heart disease more frequently than those with metabolic syndrome, and much more frequently than healthy individuals who manifest neither condition. Some aspect of the diabetic condition must be the cause—most likely, either high blood sugar, hyperinsulinemia, or insulin resistance, all three of which will tend to be worse in diabetics than in those with metabolic syndrome. Indeed, the existence of metabolic syndrome tells us that these same abnormalities exist in nondiabetics, although to a lesser extent, and though individuals with metabolic syndrome suffer an increased risk of heart disease, they do so to a lesser extent than diabetics. And because dietary carbohydrates and particularly refined carbohydrates elevate blood sugar and insulin and, presumably, induce insulin resistance, the implication is that eating these carbohydrates increases heart-disease risk not only in diabetics but in healthy individuals. By this reasoning, the atherogenic American diet is a carbohydrate-rich diet. Hence, cognitive dissonance.

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