Many of the experts call obesity a disease, say it is in the genes, is inherited, and that the body has a set point for weight that may destine you to fatness. But not all scientists agree on the theories on obesity. The Annals of the New York Academy of Sciences says that overweight itself, whatever its original cause, may be responsible for the changes in body chemistry: “The obese state, once established, may be stabilized by secondary metabolic changes that the obesity itself generates.”

Annals also questions the set point theory: “This Annal provides little evidence in support of either hypothesis.” Glandular problems are cited as causes of overweight, especially the thyroid, which has a major role in controlling metabolism. The point is raised by some, however, that its failure might be caused by overeating. Dr. Riggle of Texas comments on this: “The thyroid governs metabolism, as well as the pituitary. But we have to remember that people who get into poor nutritional habits cause these glands not to get the nutrients they need to manufacture their products. So the glandular problems can start with the dietary indiscretions.”

Overeating is the simple reason for obesity that so many people, including researchers on obesity, associate with it: “For most obese people, however, the accumulation of excess weight and adipose tissue most likely signifies a prolonged, and often, insidious process: excessive consumption of calories, during a sufficient number of days, above and beyond those used for muscular or metabolic work.” (Annals of the New York Academy of Sciences, 1987, page 343) The health hazards they thereby lay themselves open to are sobering indeed:

“Obesity is associated with a number of health hazards. It may impair both cardiac and pulmonary function, modify endocrine function, and cause emotional problems. Hypertension, impaired glucose tolerance, and hypercholesterolemia are more common in overweight individuals than in individuals of normal weight. Thus, it is not surprising that obesity may contribute to morbidity [disease] and mortality in individuals with hypertension, stroke, type II or non-insulin-dependent diabetes mellitus, some types of cancer, and gallbladder disease. Over the long term, obesity is also considered an independent risk factor for atherosclerotic heart disease.”​—Journal of the American Medical Association, November 4, 1988, page 2547.

Rather than weight alone being the basis for judgment, the percentage of fat in the body is considered by scientists to be a better guide. They define overweight as obesity when in men 20 to 25 percent of body weight is fat and in women when 25 to 30 percent is fat.

Certainly, specific weights given in tables based on height and weight alone are inadequate. As one researcher says: “What the tables don’t tell you, though, is that two people of the same weight and height can differ greatly in their degree of obesity and overall physical condition. Lean tissue and muscle weigh more per volume than fat, so weight alone is not a very good measure of health or fitness.” A more reliable guide​—though still imperfect—​are those tables that consider age, sex, and body type, and give a range of acceptable weights, such as the one on page 7.

Many persons assume that fat cells (called adipocytes) are very lazy things, just lying around in the body taking up space​—far too much space! Fat tissue (called adipose tissue) is more than a storage depot for triglycerides (fats). About 95 percent of adipose tissue is nonliving fat, but the remaining 5 percent is divided between structural material, blood and blood vessels, and living cells active in the body’s metabolism. These cells can be very greedy, grabbing on to and converting to fat the dietary nutrients from blood circulating through the capillaries that intersperse adipose tissue. Certain hormones promote either the synthesis of fat or its release as fatty acids into the blood to meet the body’s energy needs. Instead of being lazy, to the despair of some people, their fat cells work overtime!

In the past it was thought that once established in the body, fat cells did not increase in number, only in size. Later research has proved otherwise. As one scientific source says: “Enlargement of the storage capacity of adipose tissue is accomplished first by enlargement of the adipocyte contents of storage fat, triglyceride, and later on, when available adipocytes are filled to full capacity, by the formation of new fat cells.” When nearly empty, the adipocytes are very small, but as they add fat, they can increase their diameters tenfold, which means an increase in volume by a factor of about one thousand.

There are certain fat depots in the body where fat tends to collect. In men the waistline is one. In women it is the hips and thighs. Such persons may shed fat, but these locations are the last to release theirs. Researchers have discovered that fat cells have on their surfaces small molecules called alpha and beta receptors. Alpha receptors stimulate fat accumulation; beta receptors promote fat breakdown. Those favoring fat accumulation predominate on the fat cells of the hips and thighs of women and on the abdomen of men. One woman lost 15 percent of her body fat but virtually none from her hips and thighs. A man cut his weight drastically but kept his paunch.

Counting calories is not the simple solution to losing weight that many think. Calories are not equal. Eat 100 calories in carbohydrates and you may store 77 of them as body fat​—23 are burned in digesting the carbohydrates. But consume 100 calories in a pat of butter and 97 are stored as fat​—only three are consumed for digesting. The reason: Dietary fat is already chemically close to body fat, so it is stored as such much more easily. Counting calories is only part of the story. The source of those calories also counts. Calorie for calorie, fat foods are more fattening and less nourishing than carbohydrates. In one study, men overfed on a high-carbohydrate diet for seven months gained 30 pounds, but men overfed on a high-fat diet gained 30 pounds in three months.