General Principles Of Gain And Loss In Weight

In normal persons weight is stable because caloric intake is matched to caloric expenditure by the coordinated activity of “feeding” and “satiety” centers presumably located in the hypothalamus. The signals that regulate the interactions of these centers are not known; regulation is probably multifactorial, and both short- and long-term controls are thought to be operative. Whatever the mechanisms the system is normally efficient over periods of months to years.

Gain or loss in tissue mass is determined by the net balance between caloric intake and caloric expenditure. Caloric intake is determined by availability and attractiveness of food and by emotional and physical factors. The bulk of energy expenditure is due to basal metabolism and physical activity. The former is defined as the total caloric requirement when the body is in the supine position, motionless except for quiet respiration, e.g., the energy required to maintain structural and functional integrity of the organism in the absence of physical activity. About half the total daily caloric intake is normally consumed by basal processes. Active persons spend about 40 percent of calories in physical activity; athletes may utilize 50 percent or more of ingested energy in exercise. Persons sedentary because of habit, illness, or obesity may expend far less in activity. In nonobese, nonsedentary subjects 10 percent of ingested calories is released as heat associated with the absorption of food, a process called dietary thermogenesis. This fraction, previously designated specific dynamic action, is usually considered a separate component of energy costs. Heat generated during and after exercise and that released for maintenance of body temperature (regulatory thermogenesis) are included in the energy costs of physical activity and basal metabolism, respectively.

Change in body weight as a consequence of voluntary alteration in diet or exercise is never worrisome; change in weight that is not deliberately sought, on the other hand, is a frequent reason for consultation with the physician and often indicates the presence of disease. Changes in weight may reflect alteration in either tissue mass or body fluid content. Rapid swings usually indicate the latter. Even when tissue mass is changing, fluid loss or gain plays a major role in the measured change in weight, particularly over the short run. Where the composition of weight loss was estimated during a 24-day period of semi starvation in 13 normal men (daily intake, 1010 kcal). During the first 3 days 70 percent of the decrease in weight was due to water loss, while in subsequent stages a diminution of protein and fat accounted for essentially all the weight loss. This varying contribution of fluid explains why a fixed formula cannot be used for predicting weight loss or gain. It is frequently stated that a net change of 7700 kcal will be accompanied by a 1-kg change in body mass (3500 kcal/lb). While this estimate is reasonable for long-term changes in caloric intake, the apparent caloric cost per kilogram of weight lost or gained varies with the accompanying fluid shifts. In the experiment for example, a negative balance of only 2596 kcal resulted in the loss of a kilogram of weight between days 1 and 3, while between days 22 and 24, loss of a kilogram required a deficit of 8700 kcal. In general if weight loss or gain has occurred over a period of weeks or months, it is safe to assume that change in tissue mass has occurred; weight loss or gain limited to a several-day period may be due to fluid shifts alone. Occasionally true loss of tissue mass is obscured by fluid retention as in the case of the cirrhotic patient who develops ascites or the patient with anorexia nervosa who has significant edema.

While obesity is a major public health concern , its diagnosis is usually uncomplicated. Obese subjects often deny overeating, but the true situation can be assessed either by tabulating actual food intake and determining its caloric content from standard tables or by interviewing the patient’s family and friends.

Regardless of history, excess caloric intake is the cause of obesity in the majority of cases. Pathologic causes are rare. In the adult, Cushing’s syndrome can result in acquired obesity in a previously nonobese patient, but usually the diagnosis is suggested by the pattern of fat distribution and the clinical picture. Other endocrine diseases such as hypothyroidism, hypogonadism, and insulin-secreting tumors are frequently listed in the differential diagnosis of obesity but do not represent significant diagnostic problems. Congenital diseases that cause obesity such as the Prader-Willi, Laurence-Moon-Biedl, and Alstrom syndromes are readily recognizable and appear early in life. Rarely, a disease involving the hypothalamus, particularly craniopharyngioma, may cause acquired obesity. Extensive workup of the central nervous system in obesity is not indicated, however, in the absence of suspicious symptoms (headache, visual difficulties, vomiting, or endocrine changes).