Obesity and Diabetes

You are in your fifties. You haven't been eating that much more than earlier in life, but you're gaining weight all the same. On your last checkup, your doctor discovered that you had diabetes, and prescribed DiaBeta, Micronase, or something similar and instructed you to lose weight. You have been trying, but without success; the diabetes is getting worse; and now your doctor is talking about insulin injections.

This scenario repeats millions of times each year in this country. The link between age, obesity, and diabetes seems to be the "expression"—or actions—of two genes. We all know that obesity leads to diabetes, but diabetes doesn't develop in every obese individual. When diabetes is linked to obesity, the diabetic condition will often be dramatically improved—but usually not eliminated—by weight loss, a very low-fat and high-fiber diet, and exercise. 

However, there are some true breakthroughs on the horizon, and one is the recognition that DHEA (dehydroepiandrosterone), an extremely safe steroid-like hormone, reverses the expression of both the obesity gene and the diabetes gene in experimental animals.

Working at the Jackson Laboratory in Bar Harbor, Maine, researchers Douglas L. Coleman and Edward H. Leiter have found that adding DHEA in very large doses to (db/db) mice genetically bred to develop diabetes and to the (ob/ob) mice bred to develop obesity blocked the development of both conditions completely, and this occurred without any change in food consumption!

However, the effect was not that of DHEA; by itself, DHEA has no known function or toxicity. It is a "prohormone." That is, it can be converted by the body into estrogen, progesterone, cortisone, testosterone, and all the other sex and steroid hormones. It is the "mother steroid," so to speak, and in all animal experiments the effect of DHEA is brought on by the cascade of steroid and sex hormones produced by the animal once it is given DHEA.

Animals are able to take the extra DHEA and produce what they need to solve the problem under consideration. For instance, DHEA is the prohormone for both estrogen and testosterone. Estrogens are more potent than androgens in blocking the tendency toward diabetes and obesity in mice, and when DHEA is given to these animals, the amount of estrogens produced by the animals is far higher than the amount produced by lean mice, which produce more androgens.

In humans, the tendency to become obese and develop diabetes later in life likely requires not only the genes for obesity and diabetes, but also the dietary and other lifestyle changes that bring on the expression of these genes. Age-related obesity and diabetes runs rampant in cultures like ours, where we eat foods high in fat, simple sugars, and calories, and get very little physical activity.

For example, a tribe of Pima Indians living on the Gila River Reservoir in New Mexico are riddled with obesity and diabetes. However, an isolated tribe of the Pimas living in the mountains—and subsisting on a much lower calorie, more natural, high-fiber diet—do not have significant diabetes or obesity. As researchers point out, a "Coke and bun" diet is necessary for the genetic tendency toward obesity and diabetes to occur in the Pima Indians.

In humans, mechanisms similar to those found in experimental animals are likely present, and low DHEA levels have been associated with both diabetes and obesity. In 1964, it was found that DHEA was absent from the urine in 27 of 32 elderly obese diabetics. One year later, the same researchers found that obese people tended to excrete less DHEA than persons of normal weight.

Most of the anti-obesity and anti-diabetic actions of DHEA are thought to be due to its inhibition of the enzyme G6PD (glucose-6-phosphate dehydrogenase). Block that enzyme and you block fat production. In addition, DHEA has profound anti-tumor activity in experimental animals, and likely in humans as well. This, too, is thought to be due to the blockage of the G6PD enzyme.

In humans, DHEA has been shown to increase the sensitivity of cells to insulin. This is very important because age and obesity/diabetes are characterized by a loss of the sensitivity of the cells to insulin. In addition, DHEA tends to increase the body's sensitivity to thyroid hormone, and to increase the production in the liver of malic acid. Both of these changes block the development of obesity.

Your body produces more DHEA than any other steroid or sex hormone, and the levels of DHEA peak about age 20 in both men and women. It then falls in linear fashion in both sexes, and as it falls, age-related diseases, including obesity and diabetes, increase.

Common sense would dictate that since the hormone is remarkably safe, it could be used in individuals suffering with degenerative diseases to elevate their DHEA blood levels to those levels found in healthy, normal-functioning 20-year-olds. This would require about 50 mg to 100 mg of DHEA a day.

The most common drugs used for age-related diabetes, such as DiaBeta, Micronase, or Glucatrol, have been shown to increase the death rate from heart disease, and do very little if anything to stop the worsening of the diabetes. However, DHEA has been shown to reduce levels of the dangerous forms of cholesterol, and high serum levels of this safe hormone are associated with decreased death rate from heart disease.

DHEA is far safer and has fewer side effects than any of the other hormones used for physiologic replacement, and it is infinitely safer than the currently used diabetic drugs.
Why, then, isn't DHEA given to the millions with obesity and diabetes, particularly those with low blood levels of this hormone, just to elevate those levels to a healthier state?
Because the FDA, the most tyrannical bureaucracy in the so-called "free world," is standing, gun in hand, protecting the interests of the drug companies. Their mission is to make sure that doctors use only patented drugs like DiaBeta—drugs that increase the death rate from diabetes and do nothing to stop the progression of the disease—instead of DHEA, a cheap, unpatentable hormone that likely decreases the death rate of heart disease while it is correcting the obesity/diabetes connection.