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Arousal-induced eating: A response to Robbins and Fray
Appetite 1980. 1.343-348
Arousal-induced Eating: A Response to Robbins and Fray LYNN SPITZER, JANICE MARCUS and JUDITH RODIN Department of Psychology, Yale University
Robbins and Fray's (1980) consideration of arousal-induced eating is intriguing and we applaud their efforts to grapple with this significant question and to serve as another point of departure for much-needed empirical work in this area. They are suggesting that eating can be elicited by non-specific stimuli, especially those that have an arousing or activating component, and with this we strongly agree. As we have stated many times, arousal probably energizes a prepotent response; if this is eating and food cues are present, the organism will most likely eat (e.g. Rodin, 1977, in press-a). Whether arousal also increases the salience of external cues, however, remains an open question (Rodin, 1978, in press-a). While we suspect that this is likely and will be demonstrated under certain conditions, Marques, Fisher, Okrutny and Rowland (1979) have shown that tail-pinched animals do not drink less quinine, a finding that is inconsistent with the notion of increased reactivity to salient stimulus properties under arousal. We believe that the next step is to seek good empirical support for the Robbins and Fray proposition that the non-specific factors they list do, in reality, have the physiological consequences they are presumed to ha ve. l Confirmation of this assumption is crucial if the "activation" construct is to have more than illusory explanatory power (cf. Blundell, 1979). This will require, among other things, an explicit description of the nature of the physiological responses that are presumed to occur. This is especially important since terms such as "activation", "arousal", "stress", and "anxiety" all have very distinctive histories, have been examined in dissimilar contexts and have been associated with very different operational definitions. We believe that empirical tests oftheir proposals, and our own as well, require more explicit attention to the similarities and differences among these motivational states. Robbins and Fray suggest that activation should be assessed by inference from rate or vigor of behavioral output. However, if one infers "activation" from behavior and is interested in the effects of activation on eating, then the same class of behavioral measures (i.e. general hyperresponsiveness) must be used to assess both the proposed causal agent and the dependent variable. As a result, the construct may wind up having little predictive value. As an alternative, we suggest that direct physiological measurement of arousal and/or activation may be more promising. 'One might argue that many of the non-specific factors examined by Robbins and Fray have been shown elsewhere to increase measures of "activation". However, one must be very cautious in attributing a uniform "activating" effect to any of these non-specific stimuli since the nature of their activating effects has been shown to vary depending on the context in which they are presented as well as the present state of the organism (e.g. Dews. 1958; Heffner, Drawbaugh & Zigmond, 1974). Requests for reprints should be sent to Judith Rodin, Department of Psychology, Yale University, Box II A Yale Station, New Haven, Connecticut 06520, U.S.A. 0195-6663/80/040343+ 06 $02'00/0
(. 1980 Academic Press Inc. (London) Limited
344
L. SPITZER, J. MARCUS AND J. RODIN
One conclusion from the demonstration that non-specific stimuli can elicit eating, which Robbins and Fray draw, is that these stimuli therefore can be viewed as sharing the same interoceptive cues "which are sufficiently indiscriminable to the response selection mechanism that they" elicit the same response, which is a response "apparently irrelevant to the particular" elicitor. We urge that this point, if it is shown to be true, does not obscure the fact that the cues might nonetheless be experienced as discriminably different. Although electrical brain stimulation, tail-pinch and deprivation may all induce the same behavior, i.e. eating, this is not proof that these stimuli are all experienced as similar and/or are indiscriminable. We may cry when we are joyful, when gravely distressed or when peeling onions, yet be perfectly capable of differentially experiencing the interoceptive cues eliciting this identical response. A second conclusion from the demonstration that non-specific stimuli elicit eating, drawn by Robbins and Fray, is that they do so because they come to produce a state functionally equivalent to hunger. Thus, they argue that "hunger" is not specific to food deprivation but rather can be learned in response to any stimulus that is regularly paired with food. As a result, any state induced by activation that predicts food is said to elicit both a subjective experience of "hunger" and eating behaviors that are "indistinguishable" from those elicited by food deprivation. It appears to us that the use of the concept of "hunger" as a mediating variable between conditioned metabolic responses and eating behavior lacks heuristic value in this context. First, it may not be possible to provide an explicit description of the parameters governing the relationship between hunger and either conditioned metabolic responses or eating behavior. Thus, the use of the concept provides no benefits in terms of additional explanatory or predictive value. This becomes obvious in examining the animal literature since "hunger" elicited by non-specific activating stimuli can only be inferred from behavioral measures of eating behavior. Furthermore, in the human literature, there is little evidence that self-report of hunger correlates highly with actual eating behavior (McKenna, 1972; Nisbett, 1968; Singh, 1973) and, as a result, one cannot readily assume that "hunger" will elicit "( over)eating". In addition, the suggestion that the subjective desire for food elicited by food deprivation and other non-specific activating stimuli are "indistinguishable" is simply not supported by clinical data, although more rigorous empirical studies are greatly needed. Bruch (1973), for example, upon whose arguments many of the Robbins and Fray hypotheses rely, asserts that the subjective sensations accompanying deprivationinduced physiological changes and activation-induced physiological changes are not identical. She states that people "experience neither hunger nor pleasure, nor satiation during this kind of eating ... (that occurs with) ... anxious and depressive feelings" (p. 45). Thus, although one might infer that an individual who eats in response to arousal, does, at some level, "desire" food, it is not accurate to assume that this desire for food is subjectively equivalent to the desire felt during deprivation. Most important, other aspects of the Robbins and Fray hypothesis themselves suggest that one should not expect the states induced by non-specific activating stimuli and food-deprivation to be indistinguishable. For example, if we assume that Robbins and Fray are correct in their assertion that eating is not stess-reducing, then eating in response to stress cannot be expected to remove the non-specific activating stimulus nor the internal state that is produced. However, eating should be expected to remove deprivation-induced states. Thus, after one has eaten, it should be possible to differentiate between activation-induced "hunger" and deprivation-induced "hunger". Furthermore, if different external stimuli are associated with these two types of
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"hunger", as might reasonably be expected, then, with experience, assoCiative conditioning processes should allow one to differentiate between them even before food is ingested. Another major issue to be raised in commenting upon the Robbins and Fray paper, and one that greatly needs direct investigation, is the differentiation among eating, overeating and obesity as responses to arousal. Their review has shown, at least for animals and sometimes for people, that arousal-induced eating occurs and can be elicited by a variety of non-specific activators. One cannot go directly, however, from this demonstration to assertions about overeating and obesity. First, there is no strong evidence at present that arousal leads to overeating, relative to normative data or the individual's own baseline. Steritt's (1962) data, reviewed by Robbins and Fray, in fact suggest the opposite showing that "overall, there was greater eating in the no-shock group" than in the shock group. Even more problemmatic are Strongman's (1965) data showing that the more aroused animals had a slight reduction in intake, relative to unshocked controls. Eating here took place in the home cages for 1 h after the shock experience, so it would be hard to argue that behavioral responses to the shock interfered with eating behavior. Only the most minimally aroused animals (receiving one 3-sec shock) overate relative to controls. The association between arousal and obesity is even less well-documented than the association between arousal and overeating. Robbins and Fray suggest that arousalinduced eating may be a causal mechanism in the development and maintenance of obesity. They state that "the obese may be seen as that class of people that learn to eat inappropriately in response to a variety of activating events". However, there is a lack of good evidence in humans that arousal does lead to overeating, rather than to eating that is later compensated for in another meal. Even if it does, amount ingested during short-term observations cannot be presumed to be the sole determinant of the levels of body weight that are maintained over the long-term (cf. Van Itallie, Smith & Quartermain, 1977). For example, Rodin and Slochower (1976) measured individual differences in the extent to which normal weight girls responded to salient environmental food cues. These girls were then followed during their attendance at an eightweek summer camp where they actually lived away from home and where food was highly palatable and plentiful. The girls who were hyperresponsive to external cues were those who gained the most weight when exposed to a major change in their foodrelevant environment. However, of these externally responsive normal weight campers who had gained weight during the summer, 70% had reached their highest weights before the final week of the eight-week summer program, and then began to lose weight. While the final weighing showed that they still weighed more at the end of the summer than they had at the beginning, these data suggest that other factors may become more important than hyperresponsiveness to salient external cues in their influence on the final levels of body weight maintained. It is now clear that obesity is not a homogeneous disorder and that even the same types of obesity are most likely multiply-determined. We hope that suggesting that heightened emotional reactivity to stimuli and its pairing with ingestion "may be a sufficient factor in the mechanism of production of obesity", will not cause us to overlook considerable evidence that the etiology and maintenance of obesity is far more complex, depending on important genetic and metabolic parameters as wel1. 2 Nonetheless, we do believe that there may be individual differences with respect to 2 The same criticism can be lodged against the earlier assertion by Rowland and Antelman (1976) that tail-pinch-induced eating is a model for obesity in humans.
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basal levels of arousal or arousability (Rodin, 1977, 1978) that may make foods appear more palatable, thereby increasing consumption. For example, in our own studies (Spitzer & Rodin, unpubl. obs.), people who showed greater GSR reactivity (as measured by amplitude of specific GSR responses) found a novel food (mango sherbet) more palatable when paired with arousal than less arousable subjects. They also consumed more of the sherbet (in a two-sherbet choice test) on a subsequent occasion. None of these subjects was obese, however. If obese subjects are selected, they too can be divided into those who are more or less arousable. Thus, without more empirical work, we should be especially cautious about imputing causal significance for obesity to the relationship between arousal and eating. Furthermore, many correlates of obesity have been shown to be consequences of obesity rather than causes (see Rodin, 1977, in press-b for review). Thus, even if we assume that there is a reliable correlation between arousal-induced eating or overeating and obesity, it is imperative to address the possibility that this behavior may be the result of being overweight before assuming that it is a causal factor. As a final point regarding the Robbins and Fray paper, we would like to consider the hypothesis that they set out to discount, namely, that stress-induced eating has instrumental value. Robbins and Fray assert that "eating cannot produce a reduction in the aversiveness of the eliciting stimulus since the eating behavior would not be strengthened and maintained". Eating should be viewed as an escape response, however, and not an avoidance response since eating does not prevent the appearance of the aversive stimulus (which is often unsignalled) in any of the experiments they reviewed. While we have argued against using stress-induced eating as an explanation for obesity per se, this escape response may serve as a useful model for understanding instances of eating disorders, for example, binge eating. Let us consider how, but emphasizing once more that we are speculating about binge eating specifically and not about obesity. The most reinforcing response in the presence of an aversive stimulus is direct removal of that stimulus. Assuming that this response is often unavailable, we propose that the aroused organism next performs another prepotent response under arousal. Eating is a likely candidate, especially because of the high reinforcing value that food has acquired in other contexts. Once initiated, eating behavior may be maintained by negative reinforcement (decreased attention to the aversive stimulus) and/or the positive reinforcement value offood. If eating distracts one's attention from the aversive stimulus, then the cessation of eating should be met with renewed awareness of that stimulus. Therefore, "stopping eating" would be punished and less likely to occur. Furthermore, food, or the particular food available, which acquired reinforcement value independently of the aversive situation, should increase in value because of its association with distraction and/or its presentation during arousal. Therefore, eating may be strengthened by its function as a positive reinforcer as well. It would be intriguing to speculate that eating under these circumstances will only stop when it becomes more stressful than the aversive stimulus or when the latter is removed. Eating may become aversive, for example, when the organism experiences discomfort from extreme fullness. This must remain a post hoc explanation, however, until it is possible to predict a priori the point of physical or psychological discomfort at which this should occur. The postulated mechanism can also explain the pattern ofbinging and then fasting seen in many compulsive eaters. At the start of a binge the cues of an empty stomach,
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full plates of food and so on, become associated with the positive aspects of eating (namely its good taste and ability to distract from aversive stimuli). However, cues that are present at the end of the binge, such as a full stomach and crumbs of food, are associated with discomfort due to an expanded stomach, allisthesia and renewed attention to possible aversive stimuli. Eating in the presence of early cues is reinforcing, but because eating precedes and predicts punishment in the presence ofthe later cues, it is no longer reinforcing in their presence. Therefore, cues associated with the start of a binge will elicit eating and those at the end will elicit fasting. Robbins and Fray dismiss an anxiety-reduction hypothesis of eating partly on the basis of subjective reports of increased anxiety after eating in humans . Our hypothesis, however, makes just this prediction. Since eating is not anxiety-reducing and does not remove a stressor but only temporarily distracts from the aversive stimulus, the discomfort that decreases while eating will return to a pre-eating level upon its cessation. Since the individual may not stop eating until that behavior is more aversive than the eliciting state, there will be additional discomfort due to overeating. So, in sum, the discomfort experienced after eating may actually exceed that which preceded it. This is especially true since in real life, as well as in the laboratory studies in this area, the aversive stimulus is not eliminated as a consequence of eating (e.g. Abramson & Wunderlich, 1972; McKenna, 1972; Schachter, Goldman & Gordon, 1968). Subjects are usually presented with, or threatened with, an aversive stimulus, food intake is measured, and then anxiety is reported after food is removed, but before the stressor is removed. Thus, they will undoubtedly still experience the aversiveness of the stressor (because the distractor has been removed and the stressor has not). This leads us to point to a crucial difference in human and animal paradigms for studying eating in response to "stress" or "arousal". In animal studies, the aversive stimulus is applied (e.g. tail-pinch, shock, ESB), food intake is measured during this stimulus, and then both the eliciting stimulus and the food are removed. In human studies, the "stressor" (e.g. threat of shock, noise, predictions of social failure) is presented, food intake is measured, food is removed and anxiety reports may be taken, and finally debriefing occurs, which only then leads to elimination of the stressor. Thus, in the studies with humans, and most often in the real world, food presentation and/ or eating do not come to reliably predict removal of the stressor. Indeed, the failure of human laboratory studies to show arousal-induced eating comparable to that shown in animals may have to do with the nature of the experimental paradigm, rather than with the fact that the eliciting arousing stimulus is "labeled" rather than "unlabeled". If the analogy between animal and human studies is to have any heuristic value, important methodological differences such as these demand careful consideration . The important question of how arousing stimuli come to elicit eating, and the significance of this relationship for our understanding of overeating and obesity continue to concern us and we commend Robbins and Fray's efforts to evaluate the extant data and put forth several working hypotheses. We hope that our comments will be seen, not as discouraging, but rather as encouraging of further considerations of this problem, especially further empirical study. REFERENCES
Abramson, E. D., & Wunderlich, R. A. Anxiety, fear and eating: a test of the psychosomatic concept of obesity. Journal of Abnormal Psychology, 1972,79,317-321. Blundell, J. Hunger, appetite and satiety: constructs in search of identities. In M . Turner (Ed.), Nutrition and Lifestyles . London: Applied Science Publishers, 1979.
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Bruch, H. Eating Disorders. New York: Basic Books, 1973. Dews. P. B. Studies on behavior: IV. Stimulant actions of methamphetamine. JOl/mal of P/wrlllacologr aI/(/ Experimental Therapellfics. 1958.122.137-147. Heffner, T. G., Drawbaugh, R. B., & Zigmond, M. J. Amphetamine and operant behavior in rats: relationship between drug effect and control response rate. Journal of Comparatire and Physiological Psychology, 1974,86,1031-1043. Marques, D. N., Fisher. A. E., Okrutny, M. S., & Rowland, N. E. Tail-pinch induced fluid ingestion: interactions of taste and deprivation. Physiology and Behavior, 1979, 22, 37-41. McKenna, R. J. Some effects of anxiety level and food cues on the eating behavior of obese and normal subjects. Journal of Personality and Social Psychology, 1972,221,311-319. Nisbett, R. E. Taste, deprivation and weight determinants of eating behavior. Journal of Personality and Social Psychology, 1968, 10, 107-116. Robbins, T., & Fray, P. Stress-induced eating: fact, fiction or misunderstanding. Appetite, 1980. 1, 103-133. Rodin, J. Obesity: why the losing battle'? Washington, D.C.: American Psychological Association, Master Lecture, 1977. Rodin, J. Has the distinction between internal versus external control of feeding outlived its usefulness? In G. A. Bray (Ed.), Recent Advances ill Obesity Research (Vol. 2). London: Newman Publishing, 1978. Rodin, J. The current status of the internal-external obesity hypothesis: what went wrong? American Psychologist, in press. (a) Rodin, J. Exploding the Weight Myths. Multimedia Publications, in press. (b) Rodin, J., & Siochower, J. Externality in the non-obese: the effects of environmental responsiveness on weight. Journal of Personality and Social Psychology, 1976,33,338-344. Rowland, N. E., & Antelman, S. M. Stress-induced hyperphagia and obesity in rats: a possible model for understanding human obesity. Science, 1976,191,310-312. Schachter, S., Goldman, R., & Gordon, A. Effects offear, food-deprivation and obesity on eating. Journal of Personality and Social Psychology, 1968, 10,91-97. Singh, D. Role of response habits and cognitive factors in determination of behavior of obese humans. Journal of Personality and Social Psychology, 1973,27, 220-238. Sterritt, G. M. Inhibition and facilitation of eating by electric shock. Journal of Com par alive and Physiological Psychology, 1962,55, 226-229. Strongman, K. T. The effect of anxiety on food intake in the rat. Quarterly Journal of Experimental Psychology, 1965, 17, 225-260. Van Itallie, T. B., Smith, N. S., & Quartermain, D. Short-term and long-term components in the regulation of food intake: evidence for a modulatory role of carbohydrate status. The American Journal of Clinical Nutrition, 1977,30, 742-757.
Received 31 July, 1980
Arousal-induced Eating: A Response to Robbins and Fray LYNN SPITZER, JANICE MARCUS and JUDITH RODIN Department of Psychology, Yale University
Robbins and Fray's (1980) consideration of arousal-induced eating is intriguing and we applaud their efforts to grapple with this significant question and to serve as another point of departure for much-needed empirical work in this area. They are suggesting that eating can be elicited by non-specific stimuli, especially those that have an arousing or activating component, and with this we strongly agree. As we have stated many times, arousal probably energizes a prepotent response; if this is eating and food cues are present, the organism will most likely eat (e.g. Rodin, 1977, in press-a). Whether arousal also increases the salience of external cues, however, remains an open question (Rodin, 1978, in press-a). While we suspect that this is likely and will be demonstrated under certain conditions, Marques, Fisher, Okrutny and Rowland (1979) have shown that tail-pinched animals do not drink less quinine, a finding that is inconsistent with the notion of increased reactivity to salient stimulus properties under arousal. We believe that the next step is to seek good empirical support for the Robbins and Fray proposition that the non-specific factors they list do, in reality, have the physiological consequences they are presumed to ha ve. l Confirmation of this assumption is crucial if the "activation" construct is to have more than illusory explanatory power (cf. Blundell, 1979). This will require, among other things, an explicit description of the nature of the physiological responses that are presumed to occur. This is especially important since terms such as "activation", "arousal", "stress", and "anxiety" all have very distinctive histories, have been examined in dissimilar contexts and have been associated with very different operational definitions. We believe that empirical tests oftheir proposals, and our own as well, require more explicit attention to the similarities and differences among these motivational states. Robbins and Fray suggest that activation should be assessed by inference from rate or vigor of behavioral output. However, if one infers "activation" from behavior and is interested in the effects of activation on eating, then the same class of behavioral measures (i.e. general hyperresponsiveness) must be used to assess both the proposed causal agent and the dependent variable. As a result, the construct may wind up having little predictive value. As an alternative, we suggest that direct physiological measurement of arousal and/or activation may be more promising. 'One might argue that many of the non-specific factors examined by Robbins and Fray have been shown elsewhere to increase measures of "activation". However, one must be very cautious in attributing a uniform "activating" effect to any of these non-specific stimuli since the nature of their activating effects has been shown to vary depending on the context in which they are presented as well as the present state of the organism (e.g. Dews. 1958; Heffner, Drawbaugh & Zigmond, 1974). Requests for reprints should be sent to Judith Rodin, Department of Psychology, Yale University, Box II A Yale Station, New Haven, Connecticut 06520, U.S.A. 0195-6663/80/040343+ 06 $02'00/0
(. 1980 Academic Press Inc. (London) Limited
344
L. SPITZER, J. MARCUS AND J. RODIN
One conclusion from the demonstration that non-specific stimuli can elicit eating, which Robbins and Fray draw, is that these stimuli therefore can be viewed as sharing the same interoceptive cues "which are sufficiently indiscriminable to the response selection mechanism that they" elicit the same response, which is a response "apparently irrelevant to the particular" elicitor. We urge that this point, if it is shown to be true, does not obscure the fact that the cues might nonetheless be experienced as discriminably different. Although electrical brain stimulation, tail-pinch and deprivation may all induce the same behavior, i.e. eating, this is not proof that these stimuli are all experienced as similar and/or are indiscriminable. We may cry when we are joyful, when gravely distressed or when peeling onions, yet be perfectly capable of differentially experiencing the interoceptive cues eliciting this identical response. A second conclusion from the demonstration that non-specific stimuli elicit eating, drawn by Robbins and Fray, is that they do so because they come to produce a state functionally equivalent to hunger. Thus, they argue that "hunger" is not specific to food deprivation but rather can be learned in response to any stimulus that is regularly paired with food. As a result, any state induced by activation that predicts food is said to elicit both a subjective experience of "hunger" and eating behaviors that are "indistinguishable" from those elicited by food deprivation. It appears to us that the use of the concept of "hunger" as a mediating variable between conditioned metabolic responses and eating behavior lacks heuristic value in this context. First, it may not be possible to provide an explicit description of the parameters governing the relationship between hunger and either conditioned metabolic responses or eating behavior. Thus, the use of the concept provides no benefits in terms of additional explanatory or predictive value. This becomes obvious in examining the animal literature since "hunger" elicited by non-specific activating stimuli can only be inferred from behavioral measures of eating behavior. Furthermore, in the human literature, there is little evidence that self-report of hunger correlates highly with actual eating behavior (McKenna, 1972; Nisbett, 1968; Singh, 1973) and, as a result, one cannot readily assume that "hunger" will elicit "( over)eating". In addition, the suggestion that the subjective desire for food elicited by food deprivation and other non-specific activating stimuli are "indistinguishable" is simply not supported by clinical data, although more rigorous empirical studies are greatly needed. Bruch (1973), for example, upon whose arguments many of the Robbins and Fray hypotheses rely, asserts that the subjective sensations accompanying deprivationinduced physiological changes and activation-induced physiological changes are not identical. She states that people "experience neither hunger nor pleasure, nor satiation during this kind of eating ... (that occurs with) ... anxious and depressive feelings" (p. 45). Thus, although one might infer that an individual who eats in response to arousal, does, at some level, "desire" food, it is not accurate to assume that this desire for food is subjectively equivalent to the desire felt during deprivation. Most important, other aspects of the Robbins and Fray hypothesis themselves suggest that one should not expect the states induced by non-specific activating stimuli and food-deprivation to be indistinguishable. For example, if we assume that Robbins and Fray are correct in their assertion that eating is not stess-reducing, then eating in response to stress cannot be expected to remove the non-specific activating stimulus nor the internal state that is produced. However, eating should be expected to remove deprivation-induced states. Thus, after one has eaten, it should be possible to differentiate between activation-induced "hunger" and deprivation-induced "hunger". Furthermore, if different external stimuli are associated with these two types of
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"hunger", as might reasonably be expected, then, with experience, assoCiative conditioning processes should allow one to differentiate between them even before food is ingested. Another major issue to be raised in commenting upon the Robbins and Fray paper, and one that greatly needs direct investigation, is the differentiation among eating, overeating and obesity as responses to arousal. Their review has shown, at least for animals and sometimes for people, that arousal-induced eating occurs and can be elicited by a variety of non-specific activators. One cannot go directly, however, from this demonstration to assertions about overeating and obesity. First, there is no strong evidence at present that arousal leads to overeating, relative to normative data or the individual's own baseline. Steritt's (1962) data, reviewed by Robbins and Fray, in fact suggest the opposite showing that "overall, there was greater eating in the no-shock group" than in the shock group. Even more problemmatic are Strongman's (1965) data showing that the more aroused animals had a slight reduction in intake, relative to unshocked controls. Eating here took place in the home cages for 1 h after the shock experience, so it would be hard to argue that behavioral responses to the shock interfered with eating behavior. Only the most minimally aroused animals (receiving one 3-sec shock) overate relative to controls. The association between arousal and obesity is even less well-documented than the association between arousal and overeating. Robbins and Fray suggest that arousalinduced eating may be a causal mechanism in the development and maintenance of obesity. They state that "the obese may be seen as that class of people that learn to eat inappropriately in response to a variety of activating events". However, there is a lack of good evidence in humans that arousal does lead to overeating, rather than to eating that is later compensated for in another meal. Even if it does, amount ingested during short-term observations cannot be presumed to be the sole determinant of the levels of body weight that are maintained over the long-term (cf. Van Itallie, Smith & Quartermain, 1977). For example, Rodin and Slochower (1976) measured individual differences in the extent to which normal weight girls responded to salient environmental food cues. These girls were then followed during their attendance at an eightweek summer camp where they actually lived away from home and where food was highly palatable and plentiful. The girls who were hyperresponsive to external cues were those who gained the most weight when exposed to a major change in their foodrelevant environment. However, of these externally responsive normal weight campers who had gained weight during the summer, 70% had reached their highest weights before the final week of the eight-week summer program, and then began to lose weight. While the final weighing showed that they still weighed more at the end of the summer than they had at the beginning, these data suggest that other factors may become more important than hyperresponsiveness to salient external cues in their influence on the final levels of body weight maintained. It is now clear that obesity is not a homogeneous disorder and that even the same types of obesity are most likely multiply-determined. We hope that suggesting that heightened emotional reactivity to stimuli and its pairing with ingestion "may be a sufficient factor in the mechanism of production of obesity", will not cause us to overlook considerable evidence that the etiology and maintenance of obesity is far more complex, depending on important genetic and metabolic parameters as wel1. 2 Nonetheless, we do believe that there may be individual differences with respect to 2 The same criticism can be lodged against the earlier assertion by Rowland and Antelman (1976) that tail-pinch-induced eating is a model for obesity in humans.
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basal levels of arousal or arousability (Rodin, 1977, 1978) that may make foods appear more palatable, thereby increasing consumption. For example, in our own studies (Spitzer & Rodin, unpubl. obs.), people who showed greater GSR reactivity (as measured by amplitude of specific GSR responses) found a novel food (mango sherbet) more palatable when paired with arousal than less arousable subjects. They also consumed more of the sherbet (in a two-sherbet choice test) on a subsequent occasion. None of these subjects was obese, however. If obese subjects are selected, they too can be divided into those who are more or less arousable. Thus, without more empirical work, we should be especially cautious about imputing causal significance for obesity to the relationship between arousal and eating. Furthermore, many correlates of obesity have been shown to be consequences of obesity rather than causes (see Rodin, 1977, in press-b for review). Thus, even if we assume that there is a reliable correlation between arousal-induced eating or overeating and obesity, it is imperative to address the possibility that this behavior may be the result of being overweight before assuming that it is a causal factor. As a final point regarding the Robbins and Fray paper, we would like to consider the hypothesis that they set out to discount, namely, that stress-induced eating has instrumental value. Robbins and Fray assert that "eating cannot produce a reduction in the aversiveness of the eliciting stimulus since the eating behavior would not be strengthened and maintained". Eating should be viewed as an escape response, however, and not an avoidance response since eating does not prevent the appearance of the aversive stimulus (which is often unsignalled) in any of the experiments they reviewed. While we have argued against using stress-induced eating as an explanation for obesity per se, this escape response may serve as a useful model for understanding instances of eating disorders, for example, binge eating. Let us consider how, but emphasizing once more that we are speculating about binge eating specifically and not about obesity. The most reinforcing response in the presence of an aversive stimulus is direct removal of that stimulus. Assuming that this response is often unavailable, we propose that the aroused organism next performs another prepotent response under arousal. Eating is a likely candidate, especially because of the high reinforcing value that food has acquired in other contexts. Once initiated, eating behavior may be maintained by negative reinforcement (decreased attention to the aversive stimulus) and/or the positive reinforcement value offood. If eating distracts one's attention from the aversive stimulus, then the cessation of eating should be met with renewed awareness of that stimulus. Therefore, "stopping eating" would be punished and less likely to occur. Furthermore, food, or the particular food available, which acquired reinforcement value independently of the aversive situation, should increase in value because of its association with distraction and/or its presentation during arousal. Therefore, eating may be strengthened by its function as a positive reinforcer as well. It would be intriguing to speculate that eating under these circumstances will only stop when it becomes more stressful than the aversive stimulus or when the latter is removed. Eating may become aversive, for example, when the organism experiences discomfort from extreme fullness. This must remain a post hoc explanation, however, until it is possible to predict a priori the point of physical or psychological discomfort at which this should occur. The postulated mechanism can also explain the pattern ofbinging and then fasting seen in many compulsive eaters. At the start of a binge the cues of an empty stomach,
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full plates of food and so on, become associated with the positive aspects of eating (namely its good taste and ability to distract from aversive stimuli). However, cues that are present at the end of the binge, such as a full stomach and crumbs of food, are associated with discomfort due to an expanded stomach, allisthesia and renewed attention to possible aversive stimuli. Eating in the presence of early cues is reinforcing, but because eating precedes and predicts punishment in the presence ofthe later cues, it is no longer reinforcing in their presence. Therefore, cues associated with the start of a binge will elicit eating and those at the end will elicit fasting. Robbins and Fray dismiss an anxiety-reduction hypothesis of eating partly on the basis of subjective reports of increased anxiety after eating in humans . Our hypothesis, however, makes just this prediction. Since eating is not anxiety-reducing and does not remove a stressor but only temporarily distracts from the aversive stimulus, the discomfort that decreases while eating will return to a pre-eating level upon its cessation. Since the individual may not stop eating until that behavior is more aversive than the eliciting state, there will be additional discomfort due to overeating. So, in sum, the discomfort experienced after eating may actually exceed that which preceded it. This is especially true since in real life, as well as in the laboratory studies in this area, the aversive stimulus is not eliminated as a consequence of eating (e.g. Abramson & Wunderlich, 1972; McKenna, 1972; Schachter, Goldman & Gordon, 1968). Subjects are usually presented with, or threatened with, an aversive stimulus, food intake is measured, and then anxiety is reported after food is removed, but before the stressor is removed. Thus, they will undoubtedly still experience the aversiveness of the stressor (because the distractor has been removed and the stressor has not). This leads us to point to a crucial difference in human and animal paradigms for studying eating in response to "stress" or "arousal". In animal studies, the aversive stimulus is applied (e.g. tail-pinch, shock, ESB), food intake is measured during this stimulus, and then both the eliciting stimulus and the food are removed. In human studies, the "stressor" (e.g. threat of shock, noise, predictions of social failure) is presented, food intake is measured, food is removed and anxiety reports may be taken, and finally debriefing occurs, which only then leads to elimination of the stressor. Thus, in the studies with humans, and most often in the real world, food presentation and/ or eating do not come to reliably predict removal of the stressor. Indeed, the failure of human laboratory studies to show arousal-induced eating comparable to that shown in animals may have to do with the nature of the experimental paradigm, rather than with the fact that the eliciting arousing stimulus is "labeled" rather than "unlabeled". If the analogy between animal and human studies is to have any heuristic value, important methodological differences such as these demand careful consideration . The important question of how arousing stimuli come to elicit eating, and the significance of this relationship for our understanding of overeating and obesity continue to concern us and we commend Robbins and Fray's efforts to evaluate the extant data and put forth several working hypotheses. We hope that our comments will be seen, not as discouraging, but rather as encouraging of further considerations of this problem, especially further empirical study. REFERENCES
Abramson, E. D., & Wunderlich, R. A. Anxiety, fear and eating: a test of the psychosomatic concept of obesity. Journal of Abnormal Psychology, 1972,79,317-321. Blundell, J. Hunger, appetite and satiety: constructs in search of identities. In M . Turner (Ed.), Nutrition and Lifestyles . London: Applied Science Publishers, 1979.
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Bruch, H. Eating Disorders. New York: Basic Books, 1973. Dews. P. B. Studies on behavior: IV. Stimulant actions of methamphetamine. JOl/mal of P/wrlllacologr aI/(/ Experimental Therapellfics. 1958.122.137-147. Heffner, T. G., Drawbaugh, R. B., & Zigmond, M. J. Amphetamine and operant behavior in rats: relationship between drug effect and control response rate. Journal of Comparatire and Physiological Psychology, 1974,86,1031-1043. Marques, D. N., Fisher. A. E., Okrutny, M. S., & Rowland, N. E. Tail-pinch induced fluid ingestion: interactions of taste and deprivation. Physiology and Behavior, 1979, 22, 37-41. McKenna, R. J. Some effects of anxiety level and food cues on the eating behavior of obese and normal subjects. Journal of Personality and Social Psychology, 1972,221,311-319. Nisbett, R. E. Taste, deprivation and weight determinants of eating behavior. Journal of Personality and Social Psychology, 1968, 10, 107-116. Robbins, T., & Fray, P. Stress-induced eating: fact, fiction or misunderstanding. Appetite, 1980. 1, 103-133. Rodin, J. Obesity: why the losing battle'? Washington, D.C.: American Psychological Association, Master Lecture, 1977. Rodin, J. Has the distinction between internal versus external control of feeding outlived its usefulness? In G. A. Bray (Ed.), Recent Advances ill Obesity Research (Vol. 2). London: Newman Publishing, 1978. Rodin, J. The current status of the internal-external obesity hypothesis: what went wrong? American Psychologist, in press. (a) Rodin, J. Exploding the Weight Myths. Multimedia Publications, in press. (b) Rodin, J., & Siochower, J. Externality in the non-obese: the effects of environmental responsiveness on weight. Journal of Personality and Social Psychology, 1976,33,338-344. Rowland, N. E., & Antelman, S. M. Stress-induced hyperphagia and obesity in rats: a possible model for understanding human obesity. Science, 1976,191,310-312. Schachter, S., Goldman, R., & Gordon, A. Effects offear, food-deprivation and obesity on eating. Journal of Personality and Social Psychology, 1968, 10,91-97. Singh, D. Role of response habits and cognitive factors in determination of behavior of obese humans. Journal of Personality and Social Psychology, 1973,27, 220-238. Sterritt, G. M. Inhibition and facilitation of eating by electric shock. Journal of Com par alive and Physiological Psychology, 1962,55, 226-229. Strongman, K. T. The effect of anxiety on food intake in the rat. Quarterly Journal of Experimental Psychology, 1965, 17, 225-260. Van Itallie, T. B., Smith, N. S., & Quartermain, D. Short-term and long-term components in the regulation of food intake: evidence for a modulatory role of carbohydrate status. The American Journal of Clinical Nutrition, 1977,30, 742-757.
Received 31 July, 1980