Diabetes The Basics: The Body In and Out of Balance

from Dr. Bernstein’s book “Diabetes Solution”
© 2007 by Richard K. Bernstein, M.D.


Diabetes is the breakdown or partial breakdown of one of the more important of the body’s autonomic (self-regulating) mechanisms, and its breakdown throws many other self-regulating systems into imbalance. There is probably not a tissue in the body that escapes the effects of the high blood sugars of diabetes. People with high blood sugars tend to have osteoporosis, or fragile bones; they tend to have tight skin; they tend to have inflammation and tightness at their joints; they tend to have many other complications that affect every part of their body, including the brain, with impaired short-term memory.

Insulin: What It Is, What It Does

At the center of diabetes is the pancreas, a large gland about the size of your hand, which is located toward the back of the abdominal cavity and is responsible for manufacturing, storing, and releasing the hormone insulin. The pancreas also makes several other hormones, as well as digestive enzymes. Even if you don’t know much about diabetes, in all likelihood you’ve heard of insulin and probably know that we all have to have insulin to survive. What you might not realize is that only a small percentage of diabetics must have insulin shots.

Insulin is a hormone produced by the beta cells of the pancreas. Insulin’s major function is to regulate the level of glucose in the bloodstream, which it does primarily by facilitating the transport of blood glucose into most of the billions of cells that make up the body. The presence of insulin stimulates glucose transporters to move to the surface of cells to facilitate glucose entry into the cells. Insulin also stimulates centers in the brain responsible for feeding behavior. Indeed, there is some insulin response even as one begins to eat, before glucose hits the bloodstream. Insulin also instructs fat cells to convert glucose and fatty acids from the blood into fat, which the fat cells then store until needed. Insulin is an anabolic hormone, which is to say that it is essential for the growth of many tissues and organs.* In excess, it can cause excessive growth—as, for example, of body fat and of cells that line blood vessels. Finally, insulin helps to regulate, or counterregulate, the balance of certain other hormones in the body. More about those later. One of the ways insulin maintains the narrow range of normal levels of glucose in the blood is by regulation of the liver and muscles, directing them to manufacture and store glycogen, a starchy substance the body uses when blood sugar falls too low. If blood sugar does fall even slightly too low—as may occur after strenuous exercise or fasting— the alpha cells of the pancreas release glucagon, another hormone involved in the regulation of blood sugar levels. Glucagon signals the muscles and liver to convert their stored glycogen back into glucose (a process called glycogenolysis), which raises blood sugar. When the body’s stores of glucose and glycogen have been exhausted, the liver, and to a lesser extent the kidneys and small intestines, can transform some of the body’s protein stores—muscle mass and vital organs— into glucose.

Insulin and Type 1 Diabetes

As recently as eighty years ago, before the clinical availability of insulin, the diagnosis of type 1 diabetes—which involves a severely diminished or absent capacity to produce insulin—was a death sentence. Most people died within a few months of diagnosis. Without insulin, glucose accumulates in the blood to extremely high toxic levels; yet since it cannot be utilized by the cells, many cell types will starve. Absent or lowered fasting (basal) levels of insulin also lead the liver, kidneys, and intestines to perform gluconeogenesis, turning the body’s protein store—the muscles and vital organs—into even more glucose that the body cannot utilize. Meanwhile, the kidneys, the filters of the blood, try to rid the body of inappropriately high levels of sugar. Frequent urination causes insatiable thirst and dehydration. Eventually, the starving body turns more and more protein to sugar.

The ancient Greeks described diabetes as a disease that causes the body to melt into sugar water. When tissues cannot utilize glucose, they will metabolize fat for energy, generating by-products called ketones, which are toxic at high levels and cause further water loss as the kidneys try to eliminate them (see the discussion of ketoacidosis and hyperosmolar coma, in Chapter 21,“How to Cope with Dehydration, Dehydrating Illness, and Infection”).

* Anabolic and catabolic hormones normally work in harmony, building up and breaking down tissues, respectively.

Today type 1 diabetes is still a very serious disease, and still eventually fatal if not properly treated with insulin. It can kill you rapidly when your blood glucose level is too low—through impaired judgment or loss of consciousness while driving, for example—or it can kill you slowly, by heart or kidney disease, which are commonly associated with long-term blood sugar elevation. Until I brought my blood sugars under control, I had numerous automobile accidents due to hypoglycemia, and it’s only through sheer luck that I’m here to talk about it. The causes of type 1 diabetes have not yet been fully unraveled. Research indicates that it’s an autoimmune disorder in which the body’s immune system attacks the pancreatic beta cells that produce insulin. Whatever causes type 1 diabetes, its deleterious effects can absolutely be prevented. The earlier it’s diagnosed, and the earlier blood sugars are normalized, the better off you will be.

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 insulin producing 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.

Insulin Overeating
Hereditary Craving
for Carbohydrate Foods
High Dietary High
Carbohydrate Blood Hunger
by Reduced
Number of
Beta Cells
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.*

Type 2 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 2, however, can through chronically but less dramatically elevated blood sugars be much more insidious. Because so many more people are affected, it probably causes more heart attacks, strokes, and amputations than the more serious type 1 disease. Type 2 is a major cause of hypertension, heart disease, kidney failure, blindness, and erectile dysfunction. That these serious complications of type 2 diabetes can progress is no doubt because it is initially milder and is often left untreated or treated more poorly.

Individuals with type 2 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 overweight type 2 diabetics actually make more insulin than slim nondiabetics.

* A common early sign of mild chronic blood sugar elevation in women is recurrent vaginal yeast infections that cause itching or burning.