Obesity is the storage of excess fat, and it can be classified according to the number and size of fat cells. The greater the amount of lipids stored in the fat cells, the larger their size. In hyperplastic obesity, there is a greater-than-normal number of fat cells that are also larger than normal. This type of obesity is associated with massive obesity and begins at an early age. In nonobese children, the number of fat cells triples or quadruples between birth and 2 years of age and then remains relatively stable until puberty, when there is a further increase in number. In obese children, however, between 2 years of age and puberty, there is also an increase in the number of fat cells. Hypertrophic obesity results from normal number of fat cells that have increased in size. This type of obesity is more common, is associated with moderate obesity or "overweight," and typically develops in adults. People who were thin or of average weight and quite active when they were young become less active as they become older. They begin to gain weight at age 20 to 40, and although they no longer use as many kilocalories, they still take in the same amount of food as when they were younger. The unused kilocalories are turned into fat, causing fat cells to increase in size. At one time it was believed that the number of fat cells did not increase after adulthood. It is now known that the number of fat cells can increase in adults. Apparently if all the existing fat cells are filled to capacity with lipids, new fat cells are formed to store the excess lipids. Once fat cells are formed, however, dieting and weight loss do not result in a decrease in the number of fat cells--instead, they become smaller in size as their lipid content decreases.

The distribution of fat in obese individuals can vary. Fat can be found mainly in the upper body, such as in the abdominal region, or it can be associated with the hips and buttocks. These distribution differences can be clinically significant because upper body obesity is associated with an increased likelihood of diabetes mellitus, cardiovascular disease, stroke and death.

In some cases, a specific cause of obesity can be identified. For example, a tumor in the hypothalamus can stimulate overeating. In most cases, however, no specific case can be recognized. In fact, obesity can occur for many reasons, and obesity in an individual can have more than one cause. There seems to be a genetic component for obesity, and, if one or both parents are obese, their children are more likely to also be obese. Environmental factors such as eating habits, however, can also play an important role. For example, adopted children can exhibit similarities in obesity to their adoptive parents. In addition, psychological factors such as overeating as a means for dealing with stress can contribute to obesity.

Regulation of body weight is actually a matter of regulating body fat because most changes in body weight reflect changes in the amount of fat in the body. According to the "set point" theory of weight control, the body maintains a certain amount of body fat. If the amount of body fat decreases below or increases above this level, mechanisms are activated to return the amount of body fat to its normal value.

The two factors that affect the amount of adipose tissue in the body are energy expenditure and energy intake. Energy expenditure occurs as a result of basal metabolic rate, the thermic effect of food, and muscular activity. At present there is no convincing evidence that these two factors are significantly different in lean or obese individuals at their usual weights. This does not mean, of course, that expenditure of energy through exercise cannot result in weight loss. Instead, it means that the amount of energy used to move a specific amount of weight is the same for lean and obese people.

The regulation of energy intake is poorly understood. Apparently appetite and food-seeking behaviors are continually and spontaneously stimulated by neurons originating in or passing through the hypothalamus. After food is consumed, several mechanisms can be responsible for decreasing further food intake. Neural mechanisms such as distension of the stomach are known to inhibit feeding, and a number of hormones released from the gastrointestinal tract or pancreas also decrease appetite. For example, somatostatin, cholecystokinin, glucagon, insulin, and other hormones have been shown to reduce food intake. The level of fatty acids, glucose, or amino acids in the blood can also provide the brain with information necessary to adjust appetite. Low levels of fatty acids, glucose, and amino acids stimulate appetite, whereas high levels of these substances inhibit appetite.

Some scientists believe that the number of fat cells in the body can also affect appetite. According to this line of reasoning, fat cells maintain their size, and, once a "fat plateau" is attained, the body stays at that plateau. Fat cells can accomplish this by effectively taking up triacylglycerols and converting them to fat. Consequently, there is less energy available for muscle and body organs and to compensate, appetite increases to provide needed energy. In support of this hypothesis, it is known that obese individuals have an increased amount of the enzyme lipoprotein lipase, which is responsible for the uptake and storage of triacylglycerols in fat cells. Furthermore, in obese individuals who have lost weight, the levels of lipoprotein lipase increase even more.

It is a common belief that the main cause of obesity is overeating. Certainly for obesity to occur, at some time energy intake must have exceeded energy expenditure. A comparison of the kilocaloric intake of obese and lean individual at their usual weights, however, reveals that on a per kilogram basis, obese people consume fewer kilocalories than lean people.

When people lose a large amount of weight their feeding behavior changes. They become hyper-responsive to external food cues, think of food often, and cannot get enough to eat without gaining weight. It is now understood that this behavior is typical of both lean and obese individuals who are below their relative set point for weight. Other changes such as a decrease in basal metabolic rate take place in a person who has lost a large amount of weight. Most of this decrease in BMR probably results from a decrease in muscle mass associated with weight loss. In addition, there is some evidence that energy lost through exercise and the thermic effect of food are also reduced. Thus a person who has lost a large amount of weight is a person with an increased appetite and a decreased ability to expend energy. It is no surprise that only a small percentage of obese people maintain weight loss on a long-term basis. Instead, the typical pattern is one of repeated cycles of weight loss followed by a rapid regain of the lost weight.