Diabetes: The Basics
At the time they are diagnosed, many type 1 diabetics still produce a small amount of insulin. It’s important to recognize that if they are treated early enough and treated properly, what’s left of their insulinproducing capability frequently can be preserved. Type 1 diabetes typically occurs before the age of forty-five and usually makes itself apparent quite suddenly, with such symptoms as dramatic weight loss and frequent thirst and urination. We now know, however, that as sudden as its appearance may be, its onset is actually quite slow. Routine commercial laboratory studies are available that can detect it earlier, and it may be possible to arrest it in these early stages by aggressive treatment. My own body no longer produces any insulin at all. The high blood sugars I experienced during my first year with diabetes burned out, or exhausted, the ability of my pancreas to produce insulin. I must have insulin shots or I will rapidly die. I firmly believe— and know from experience with my patients—that if the kind of diet and medical regimen I prescribe for my patients had been utilized when I was diagnosed, the insulin-producing capability left to me at diagnosis would have been preserved. My requirements for injected insulin would have been lessened, and it would have been much easier for me to keep my blood sugars normal.
Blood Sugar Normalization: Restoring the Balance
According to the NIH, nearly 200,000 people die annually from both type 1 and type 2 diabetes and their long-term complications—and it is the NIH’s contention that diabetes is grossly underreported on death certificates. (Is a diabetic’s death from heart disease, kidney disease, or stroke, for example, really a death from diabetes?) Certainly everyone has to die of something, but you needn’t die the slow, torturous death of diabetic complications, which often include blindness and amputations. My history and that of my patients support this.
The Diabetes Control and Complication Trial (DCCT), conducted by the NIH’s National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), began in 1983 as a ten-year study of type 1 diabetics to gauge the effects of improved control of blood sugar levels. Patients whose blood sugars were nearly “normalized” (my patients’ blood sugars are usually closer to normal than were those in the intensive care arm of the trial because of our low-carbohydrate diet) had dramatic reductions of long-term complications. Researchers began the DCCT trying to see if they could, for example, lessen the frequency of diabetic retinopathy by at least 33.5 percent.
Instead of a one-third reduction in retinopathy, they found more than a 75 percent reduction in the progression of early retinopathy. They found similarly dramatic results in other diabetic complications and announced the results of the study early in order to make the good
news immediately available to all. They found a 50 percent reduction of risk for kidney disease, a 60 percent reduction of risk for nerve damage, and a 35 percent reduction of risk for cardiovascular disease. I believe that with truly normal blood sugars, which many of my patients have, these reductions can be 100 percent.
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 remotely as high as was suggested in the DCCT’s findings.
The Insulin-Resistant Diabetic: Type 2
Different from type 1 diabetes is what is officially known as type 2. This is by far the more prevalent form of the disease.According to statistics from the American Diabetes Association, 90–95 percent of diabetics are type 2. Furthermore, as many as a quarter of Americans between the ages of sixty-five and seventy-four have type 2 diabetes. A recent study, published by Yale University, discovered that 25 percent of obese teenagers now have type 2 diabetes.
(A new category of “pre-diabetes” has been recently called latent autoimmune diabetes, or LADA. This category applies to mild diabetes with onset after the age of thirty-five, in which the patient has been found to produce an antibody to the pancreatic beta cell protein called GADA, just as in type 1 diabetes. Eventually these people may develop overt diabetes and require insulin.)
Approximately 80 percent of those with type 2 diabetes are overweight and are affected by a particular form of obesity variously known as abdominal, truncal, or visceral obesity. It is quite possible that the 20 percent of the so-called type 2 diabetics who do not have visceral obesity actually suffer from a mild form of type 1 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 true type 2 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 1 diabetes may still be somewhat mysterious, the cause of type 2 is less so. As noted previously, another designation for type 2 diabetes is insulin-resistant diabetes. Obesity, particularly visceral obesity, and insulin resistance—the inability to fully utilize the glucose-transporting effects of insulin—are interlinked. For reasons related to genetics (see Chapter 12, “Weight Loss—If You’re Overweight”), 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 released from abdominal fat—in the branch of the bloodstream that feeds the liver. (Transient insulin resistance can be created in laboratory animals by injecting triglycerides—fat—directly into their liver’s blood supply.)* Insulin resistance by its very nature increases the body’s need 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.
* New evidence demonstrates a role for fat contained in muscle cells (intramyocyte fat) as another important factor in causing insulin resistance.
High levels of insulin in the blood down-regulate the affinity for insulin that insulin receptors all over the body have naturally. This “tolerance” to insulin causes even greater insulin resistance.
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.
for Carbohydrate Foods
High Dietary High
Carbohydrate Blood Hunger
Beta Cell Burnout
If that sounds circular, it is. But note that the fat that is the culprit here is not dietary fat.
Triglycerides are in circulation at some level in the bloodstream at all times. High triglyceride levels 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 actually 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 obese individuals and especially those 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 adverse effects of elevated blood sugar are the same—type 2 diabetes differs from type 1 in several important ways.
The onset of type 2 diabetes is slower and more stealthy, but even in its earliest stages the abnormal blood sugar levels, though not skyhigh, can cause damage to nerves, blood vessels, heart, eyes, and more. Type 2 diabetes is often called the silent killer, and it is quite frequently discovered through one of its complications, such as hypertension, visual changes, or recurrent infection.*