Anxiety, restraint, and eating behavior.

It was hypothesized that individual differences in eating behavior based on the distinction between obese and normal subjects could be demonstrated within a population of normal subjects classified as to the extent of restraint chronically exercised with respect to eating. Restrained subjects resembled the obese behaviorally, and unrestrained subjects resembled normals. This demonstration was effected in the context of a test .of the psychosomatic hypothesis of obesity. The results indicated that although some individuals may eat more when anxious, there is little empirical support for the notion that eating serves to reduce anxiety. An explanation for this apparent inconsistency was offered. The role of anxiety as a possible causal agent in obesity has recently been subjected to experimental analysis. Schachter, Goldman, and Gordon (1968) hypothesized that although anxiety would decrease eating in normal-weight subjects by inhibiting gastric contractions and releasing sugar into the bloodstream, it would have little if any effect on the obese, who do not eat on the basis of internal physiological state. These predictions were confirmed, with normal-weight subjects eating substantially less (34%) when anxious and the obese eating nonsignificantly more (15%). Schachter et al. (1968) concluded that the psychosomatic hypothesis of obesity —that the obese in effect confuse hunger with negative affect (Bruch, 1961) and thus overeat in response to aversive emotional states (Kaplan & Kaplan, 1957)— had failed to find confirmation. Obese subjects did not eat more when anxious and did not exhibit significant anxiety reduction as a consequence of eating.