Skin-fold thickness is occasionally used to estimate body fat in clinical practice, but more precise measures (e.g., underwater weighing) are rarely employed. Clinicians most frequently use body weight or preferably the body mass index (weight (kg)/height (m) 2) to judge if a patient is “overweight”. Very muscular individuals may be moderately overweight and not obese. Others with small frames and low muscle mass may be obese without fulfilling criteria for overweight. Nevertheless, most seriously overweight patients are also obese. An obesity classification scheme based on body mass index is presented in Table 1.
Table 1. Obesity classification based on body mass index (kg/m2)
Pathogenesis. Obesity and overweight are largely genetically determined and are strongly conditioned by available palatable food and sedentariness. A child of two obese parents has about an 80 per cent chance of becoming obese, whereas the risk is only 15 per cent for the offspring of two normal-weight parents. Moreover, a correlation between parental and child body mass index is found across a broad spectrum of values, suggesting both polygenic inheritance of obesity and several contributing metabolic mechanisms. The precise causative mechanisms remain unknown.
Fat accounts for 25 to 40 per cent of the weight of middle-aged men and women (Table 2). Body fat cells vary from 10 to 200 µ in diameter or about 8000 fold in total volume. Their numbers may vary between 2 × 1010 and 16 × 1010. Fat cell size generally increases (hypertrophy) with increasing adiposity until the body fat content is about 30 kg. There is little increase in size as more body fat accumulates. Fat cell number, in contrast, increases in a linear fashion (hyperplasia) as total body fat increases from 10 to 90 kg.
A remarkable feature of adiposity is its constancy. Small increases in adiposity occur regularly with age (Table 2), but these are slight relative to the differences in adiposity among individuals. The extent of adiposity is therefore carefully and unconsciously regulated. Intentional overfeeding to increase weight is very difficult for experimental subjects and is followed by spontaneous caloric restriction until body weight returns to baseline.
Table 2. Variation of fat and lean body mass (LBM) with age.
How then does obesity occur?
Fat people do not generally eat more than lean people, and many eat less. Since mass and energy are conserved, it is clear that at some time in life the obese individual consumed more calories than he expended. This temporary imbalance between energy intake and expenditure could be due to several factors (Table 3) involving the central nervous system or the adipocyte itself. Reduced sympathetic activity manifested by lower plasma norepinephrine and epinephrine levels, reduced fat mobilization, or low thermogenesis could reduce energy mobilization and expenditure. Enhanced parasympathetic activity, typical of ventromedial hypothalamic lesions, may augment food consumption. And at least in theory, the brain may be insensitive to normal neural or humoral satiety signals.
Table 3. Possible cause of obesity
Fat cells with enhanced lipoprotein lipase activity may have a competitive advantage in assimilating lipoprotein triglycerides. This occurs in the syndrome of multiple symmetric lipomatosis. The adipocyte itself may also resist lipolytic stimuli from nerves or circulating catechol amines. Gluteal fat in both men and women, for example, has a lower lipolytic response to α-adrenergic stimulation than does abdominal fat. Some fat depots may resist mobilization even when the rest of the body is starving, as in women with steatopygia who have massive accumulation of gluteal and femoral fat.
Dr. Afsaneh Jeddi