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The patients followed in the DCCT averaged twenty-seven years of age at the beginning of the trial, so reductions could easily have been greater in areas such as cardiovascular disease if they had been older or followed for a longer period of time. The implication is that full normalization of blood sugar could totally prevent these complications. In any case, the results of the DCCT are good reason to begin aggressively to monitor and normalize blood sugar levels. The effort and dollar cost of doing so does not have to be so high as was suggested in the DCCT's findings.

The Insulin-Resistant Diabetic: Type II
Different from Type I diabetes is what is commonly known as Type II. This is by far the more prevalent form of the disease. According to ADA statistics, 90–95 percent of diabetics are Type II. Furthermore, as many as a quarter of Americans between the ages of sixty-five and seventy-four have Type II.

Approximately 80 percent of those with Type II diabetes are overweight and suffer from a particular form of obesity known as truncal, or visceral, obesity. It is quite possible that the 20 percent of the so-called Type II diabetics who do not have visceral obesity actually suffer from a form of Type I diabetes that causes only partial loss of the pancreatic beta cells that produce insulin. If this proves to be the case, then fully all of those who have Type II diabetes may be overweight. (Obesity is usually defined as being at least 20 percent over the ideal body weight for one's height, build, and sex.)

While the cause of Type I diabetes may still be somewhat mysterious, the cause of Type II is less so. As noted earlier, another name for Type II diabetes is insulin-resistant diabetes. Obesity, particularly visceral obesity, and insulin resistance—the inability to fully utilize the glucose-transporting qualities of insulin—are interlinked. For reasons related to genetics (see Chapter 12, "Weight Loss"), a substantial portion of the population has the potential when overweight to become sufficiently insulin-resistant that the increased demands on the pancreas burn out the beta cells that produce insulin. These people enter the vicious circle depicted in Figure 1-1. Note in the figure the crucial role of dietary carbohydrate in the development and progression of this disease. This is discussed in detail in Chapter 12.

Insulin resistance appears to be caused at least in part by inheritance and in part by high levels of fat—in the form of triglycerides—in the branch of the bloodstream that feeds the liver. (Transient insulin resistance can be created in laboratory animals by injecting triglycerides directly into their liver's blood supply.) Insulin resistance by its very nature increases the body's needs for insulin, which therefore causes the pancreas to work harder to produce elevated insulin levels (hyperinsulinemia), which can indirectly cause high blood pressure and damage the circulatory system. So, to simplify somewhat, fat in the blood feeding the liver causes insulin resistance, which causes elevated serum insulin levels, which cause the fat cells to build even more abdominal fat, which raises triglycerides in the liver's blood supply, which causes insulin levels to increase because of increased resistance to insulin.

If that sounds circular, it is. The fat that is the culprit here is not dietary fat. High levels of triglycerides in the blood—which are in circulation at some level in the bloodstream at all times—are not so much the result of intake of dietary fat as they are of carbohydrate consumption and existing body fat. (We will discuss carbohydrates, fat, and insulin resistance more in Chapter 9, "The Basic Food Groups.") The culprit is rather a particular kind of body fat. Visceral obesity is a type of obesity in which fat is concentrated around the middle of the body, particularly surrounding the intestines (the viscera). A man who is viscerally obese has a waist of greater circumference than his hips. A woman who is viscerally obese will have a waist at least 80 percent as big around as her hips. All individuals with visceral obesity are insulin-resistant. The ones who eventually become diabetic are those who cannot make enough extra insulin to keep their blood sugars normal.

Though treatment has many similar elements—and many of the effects are the same—Type II diabetes differs from Type I in several important ways.

The onset of Type II diabetes is slower and more stealthy, but even in its earliest stages, the abnormal blood sugar levels, though not sky-high, can cause damage to nerves, blood vessels, heart, eyes, and more. Type II diabetes is often called the silent killer, and it is quite frequently discovered through one of its complications, such as hypertension or a defect in vision.*

Type II diabetes is, at the beginning, a less serious disease—patients don't melt away into sugar water and die in a few months' time. Type II, however, can through chronically but less dramatically elevated blood sugars be much more insidious. It probably causes more heart attacks, strokes, and amputations than the more serious Type I disease. Type II is a major cause of hypertension, heart disease, blindness, and amputation due to impaired sensation (nerve damage) in feet with poor circulation that do not heal when injured. That these serious complications of Type II diabetes can proliferate is no doubt because it is initially milder and is often left untreated or treated poorly.

Individuals with Type II still make insulin, and most will never require injected insulin to survive, though if the disease is treated poorly, they can eventually burn out their pancreatic beta cells and require insulin shots. Because of their resistance to the blood sugar–lowering effects of insulin (though not its fat-building effects), many obese Type II diabetics actually make more insulin than nondiabetics.

Since high blood sugar is the hallmark of diabetes, and the cause of every long-term complication of the disease, it makes sense to discuss where blood sugar comes from and how it is used and not used.

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