Owing to the thermic effect of eating and metabolism, eating should be expected to provide warmth. This is certainly the case. "Food has a marked effect on body temperature; the temperature difference between a fed animal and an unfed one in the same cage, in the same room, at the same time can vary as much as one full degree F. This difference is due to the specific dynamic action of food" (Beller, 1977). This effect extends fully to humans; for example, Dallosso and James (1984) found that a 50 percent increase in caloric intake by the addition of fat to the diet produced a 47 percent increase in the thermic effects of eating. Eating ground beefsteak and stewed tomatoes to satiety raised skin temperature an average of 2°C about 1 hour after the meal (Booth and Strang, 1936).
Experimental demonstrations of increased metabolic rate, oxygen consumption, and thermogenesis are now so well established that research focuses mainly on subtleties of the response. For instance, LeBlanc and Cabanac (1989) recently demonstrated that the postprandial thermogenic effect has both a cephalic and a gastrointestinal phase; remarkably, the cephalic effect—which was evident in subjects who did not even swallow the food but who merely chewed and spit it out—was even stronger than was the subsequent gastrointestinal effect in subjects who consumed the food. In dogs, a large thermic effect was obtained when the animals were exposed only to the sight and smell of food for 3 minutes (LeBlanc and Diamond, 1986). Thus, eating produces heat, as was known all along; and even sensory exposure to food may produce conditioned or anticipatory thermogenesis or both. One possibly remote implication of this research is that in order to prevent thermogenetic increases in body heat, one may be required to avoid not only eating but all the sensory trappings of food.
Hypothalamic disturbances that produce substantial weight gain may do so at least partially by suppressing the heat dissipation by brown adipose tissue (BAT) that normally follows a meal (Hogan et al., 1986), although medially lesioned rats continue to show BAT activation during cold exposure (Hogan et al., 1982). This finding suggests that the lesioned rat, in defending an artificially higher BW set-point, will store whatever additional calories it can but not if its thermoregulation is threatened. Numerous studies (for example, Booth and Strang, 1936; Segal et al., 1987) have found a blunted thermogenic response to eating in obese humans.
If the suppression of appetite observed during heat exposure drives BW levels below set-point, this heat-induced appetite suppression might be expected to be accompanied by greater metabolic efficiency. A reduced intake, accordingly, should not be cause for concern. And if heat-induced appetite suppression is accompanied or caused by a lowering of the BW set-point, then there is all the more reason to avoid forced feeding, because such