Appetite, 14, 105-109.
From Dietary Restraint to Binge Eating: Some Theoretical Considerations REINHARD
J. TUSCHL
Division of Psychoneuroendocrinology, Max- Planck- Institute for Psychiatry, Munich
A correlation between dietary restraint and the occurrence of binge eating has been convincingly shown in several investigations. However, the mediating mechanisms have not yet been elaborated in detail nor linked to empirical evidence. This theoretical gap is addressed in the following. After a short review of behavioral and metabolic correlates of dietary restraint, potential effects of restrained eating on the psychophysiological regulation of food intake are described. These effects may lead to the disruption of intake regulation and therefore can be regarded as direct causes of binge eating. The tendency to control food intake consciously in order to prevent weight gain or to promote weight loss can be labeled as “restrained eating”. This concept has its roots in laboratory experiments showing that individuals with chronic weight concern are likely to overeat under conditions antagonistic to self-control (for review see Ruderman, 1986; Herman & Polivy, 1988 a), a phenomenon referred to as “counterregulation” (Hibscher & Herman, 1977) and regarded as an experimental analog of binge eating (Wardle & Beinart, 1981). For this reason the concept of “dietary restraint” deserves great attention. It mediates between two events which appear at first glance to conflict. New sociocultural expectations concerning the desirable physical appearance of women, extreme slimness or even emaciation, have emerged over the past three decades (Rodin et al., 1985; Polivy et al., 1986). During the same period, bulimia, experienced as a loss of control over eating while consuming a large amount of food, has become increasingly common in young women (Connors & Johnson, 1987; Drewnowski et al., 1988). Many women start to diet with the aspiration of approaching a slim body shape, but in most cases this may be unattainable for biological reasons. A causal link between fasting and bingeing is well substantiated (for review see Polivy & Herman, 1985; Wardle, 1987). The available empirical evidence, however, rests upon extreme forms of dieting behavior, which are accompanied by weight loss and concomitant biological alterations (e.g. the semistarvation experiment of Keys et al., 1950). Restrained eating, on the other hand, which has never been defined by objective behavioral criteria, is originally a psychological concept describing the intention to restrict food intake and implicates neither actual weight loss nor any obligatory procedure for weight control. Yet, if it is causally connected to binge eating, restrained eating also should be linked to specific longstanding alterations in everyday eating behavior, which are responsible, once cognitive control has broken down, for the failure of intake regulation to terminate a meal in time-that is, for suffering a binge. Address reprint requests to: Reinhard Tuschl, Max-Planck-Institute D-8000 Miinchen 40, F.R.G. 0195-6663/90/020105 + 05 %03.00/O
for Psychiatry, Kraepelinstr. 2, 0 1990 Academic Press Limited
106
R. J. TUSCHL
It has already been shown that restrained eating is in fact comprised of various inconspicuous forms of permanent dieting. Young women who were classified as restrained eaters on the basis of questionnaires reported consumption of less energy than the complementarily defined unrestrained eaters (Wardle & Beales, 1987; Kirkley et al., 1988; Laessle et al., 1989; Tuschl et al., Note 1). Restrained eaters showed a great variability in energy intake, too. Days of high and low caloric consumption frequently alternated (Laessle et al., 1989). A constant energy supply suffered additional interruption by planned days of starvation several times a month (Tuschl et al., Note 1). In addition, qualitative alterations in the everyday eating behavior of restrained eaters were found (Tuschl et al., 1990). They showed a strong tendency to avoid fat and a large percentage of them was used to consuming artificial sweeteners and other caloriereduced foodstuffs. Weight history revealed that restrained eaters had more often been on weight-reducing diets, on which they had lost more than 4 kg of body weight (Laessle et al., 1989; Tuschl et al., Note 1). Yet both the actual relative weight (body mass index; BMI) and the maximal one since entering adulthood were higher in the restraint group. This indicates weight cycling to a great extent. The seeming contradiction that restrained eaters weighed more than unrestrained ones and at the same time reported consumption of less energy is explained by results concerning energy expenditure (Tuschl et al., Note 1). Restrained eaters do not underreport. When adjusted for individual differences in body composition and height, they expended about 620 kcal/day less energy than women with an unrestrained eating style. No biochemical indices of acute starvation, i.e. an elevated level of /?-hydroxybutyric acid or a decreased level of triiodothyronine (see Pirke & Ploog, 1987), were found. These results indicate that restrained eaters are dieters whose energy metabolism fits with a relatively low and inconsistent level of caloric intake. On the average, they meet their actual, diminished caloric requirements and therefore do not lose weight. Nevertheless, as pointed out by Laessle et al. (1989), short-term states of physiological deprivation due to intermittent caloric restrictions might be frequently present in restrained eaters and could precipitate binge eating (cf. Bellisle et al., 1984). One of the mechanisms by which the organism economizes energy has already been identified. Restrained eaters have impaired menstrual function. Schweiger et al. (1989) found a shortened luteal phase of the menstrual cycle with decreased progesterone secretion. Low caloric requirements may have biological and behavioral causes. Given the prevailing social ideal of feminine beauty, a biological predisposition to a low level of energy expenditure could induce chronic weight concern and therefore be the “prima causa” of dietary restraint. The existence of such a predisposition in restrained eaters is suggested by the relatively elevated maximal former BMI in this group. It can be concluded that, although their BMI is still higher than in the unrestrained group, restrained eaters presently regulate their weight below the level at which they would do without dietary restrictions. In this case, a restrained eating style should have led to compensatory changes in energy expenditure (Apfelbaum, 1978; Djazayery, 1987) and may therefore be the reason why metabolic rate has declined and balanced below the biologically given level. In addition, repeated cycles of weight loss and regain cause a heightened food efficiency persisting beyond the deprivation periods and making subsequent weight loss more difficult (Brownell et al., 1987; Blackburn et al., 1989). Since restrained eaters report multiple dieting episodes with weight fluctuations in the past and diet several times per month at present, their energy requirements may have decreased additionally. Thus, as a consequence of restrained eating, the sociocultural pressure to restrict caloric intake in order to at least approximately reach the aspired
FROM DIETARY RESTRAINT TO BINGE EATING
107
slim body shape or to prevent weight gain rises further. This interdependency between biological and behavioral determinants of energy expenditure might result in a vicious circle of mutually reinforced fasting and bingeing, explaining the presently observed frequency of bulimic behaviors in young women. The still unanswered question is how restrained eating affects the psychophysiological regulation of food intake. An impairment of the satiation process must be assumed to be a prerequisite of a binge. In addition, an exaggeration of the responsiveness to nutritional or food-related stimuli has been observed in restrained eaters (Klajner et al., 1981; LeGoff & Spigelman, 1987) and may be relevant to the “disinhibition” phenomenon, the breakdown of cognitive control. The hypothesis has been put forward that restrained eating enhances the attractiveness of palatable foodstuffs while at the same time progressively destroying the learned components of satiation, thus leaving the termination of a meal to relatively insensitive physiological mechanisms like gastric distension (Herman & Polivy, 1988 b; Tuschl et al., 1988). Several effects of restrained eating disarranging intake regulation in this way can be postulated. A dissociation between food selection and food preferences-not the liked, but the cognitively “allowed” foods are selected-may not only cause psychological frustration and deprivation (Herman & Polivy, 1988b), but also enhance the attractiveness of the “forbidden fruits” directly by nutritional preference conditioning (see Booth, 198 1). As a consequence, the microstructure of eating changes. Eating rate is accelerated and chewing activity is decreased (Bellisle et al., 1984). Eating in such a way produces large and long meals in its own right (Bellisle et al., 1984), at least when it is not cognitively inhibited. In addition, it is incompatible with the emergence of the feeling of satisfaction that is normally induced by eating (Spiegel & Jordan, 1978). This probably compounds the overeating, once cognitive control has broken down. Regarding the satiation process, restrained eaters by definition are wont to end meals not because the sensation of satiety has emerged but because a cognitively set limit has been reached; it can be assumed that this extinguishes conditioned satiety cues. High variability in intake such as skipping meals and more extreme forms of intermittent dieting may weaken learned satiating contingencies further. Also cephalic-phase reflexes may be affected, leading to an impairment of the metabolism of ingested food (see Nicolaidis, 1977). Oversized meals, ascribed to the processes discussed above and occurring from time to time after disinhibition, do not permit the calibration of sensory cues by the postingestional consequencies of food. Furthermore, large but poorly satiating meals may favor the development of “belly bulimia” (Booth, 1988), in which fulness is conditioned to elicit increased attractiveness of foods. Uncoupling the sensory characteristics of food from its caloric content, such as occurs with the use of artificial sweeteners and other calorie-reduced ingredients, may lead to paradoxical effects on the sensations of hunger and satiety (Blundell & Hill, 1986; Rogers et al., 1988) and to overcompensation for caloric dilution (Hill et al., 1987; Foltin et al., 1988; Mattes et al., 1988; Louis-Sylvestre et al., 1989). The combination of these potential consequences of restrained eating render an adequate control of meal size impossible. The considerations above exemplify the necessity to get more detailed information on the everyday eating behavior of restrained eaters in order to understand better the processes involved in the genesis of bulimic behaviors. One must not forget that restrained eaters, who had been defined by means of questionnaires, are far from being a homogeneous group with regard to their actual eating behavior. For example, only some of them used artificial sweeteners or calorie-reduced foodstuffs (Tuschl et al., 1990). Many restrained eaters, like unrestrained ones, totally abstained from
108
R. J. TUSCHL.
consuming such products. Secondly, a subgroup of restrained eaters who constantly maintain and have adapted to weights lower than their previous weights and who therefore were labeled as “successful dieters” or “weight suppressors” (Lowe & Kleifield, 1988), show no “counter regulation” in the laboratory (Lowe & Kleifield, 1988). It looks as if this group is able to adhere permanently to the self-imposed dietary restrictions and does not tend to develop bulimic behaviors. Obviously, some forms of dietary restraint are more apt to disarrange intake regulation than others. It can be hypothesized that the more chaotic the everyday eating behavior, the higher the risk of developing bulimia. A subclassification of “restrained eating” in behavioral terms is urgently needed.
REFERENCENOTE 1. Tuschl, R. J., Platte, P., Laessle, R. G., Stichler, W. & Pirke, K. M. (1990) Energy expenditure and everyday eating behavior in healthy young women. American Journal of Clinical Nutrition (in press).
REFERENCES Apfelbaum, M. (1978) Adaptation to changes in caloric intake. Progress in Food and Nutrition Sciences, 2, 543-559.
Bellisle, F., Lucas, F., Amrani, R. & Le Magnen, J. (1984) Deprivation, palatability and the microstructure of meals in human subjects. Appetite, 5, 85-94. Blackburn, G. L., Wilson, G. T., Kanders, B. S., Stein, L. J., Lavin, P. T., Adler, J. 8z Brownell, K. D. (1989) Weight cycling: the experience of human dieters. American Journal of Clinical Nutrition, 49, 1105-l 109. Blundell, J. E. & Hill, A. J. (1986) Paradoxical effects of an intense sweetener (aspartame) on appetite. Lancet, i, 1092-1093. Booth, D. A. (1981) Hunger and satiety as conditioned reflexes. In H. Weiner, M. A. Hofer &A. J. Stunkard (Eds.), Brain, behavior, and bodily disease. Pp. 143-160. New York: Raven Press. Booth, D. A. (1988) Culturally corralled into food abuse: the eating disorders as physiologically reinfored excessive appetites. In K. M. Pirke, W. Vandereycken & D. Ploog (Eds.), The psychobiology of bulimia nervosa. Pp. 18-32. Berlin: Springer. Brownell, K. D., Steen, S. N. & Wilmore, J. H. (1987) Weight regulation practices in athletes: analysis of metabolic and health effects. Medicine and Science in Sports and Exercise, 19, 546-556.
Connors,
M. E. & Johnson, C. L. (1987) Epidemiology
of bulimia and bulimic behaviors.
Addictive Behaviors, 12, 165-179.
Djazayery, A. (1987) Effects of total energy and individual nutrient intakes on energy balance. World Review of Nutrition and Dietetics, 52, 143-208.
Drewnowski, A., Yee, D. K. & Krahn, D. D. (1988) Bulimia in college women: incidence and recovery rates. American Journal of Psychiatry, 145, 753-755. Foltin, R. W., Fischman, M. W., Emurian, C. S. & Rachlinski, J. J. (1988) Compensation for caloric dilution in humans given unrestricted access to food in a residential laboratory. Appetite, IO, 13-24.
Herman, C. P. & Polivy, J. (1988 a) Studies of eating in normal dieters. In B. T. Walsh (Ed.), Eating behavior in eating disorders. Pp. 95-l 11. Washington: American Psychiatric Press. Herman, C. P. & Polivy, J. (1988 b) Restraint and excess in dieters and bulimics. In K. M. Pirke, W. Vandereycken & D. Ploog (Eds.), The psychobiology of bulimia nervosa. Pp. 3341. Berlin: Springer. Hibscher, J. A. & Herman, C. P. (1977) Obesity, dieting, and the expression of “obese” characteristics. Journal of Comparative and Physiological Psychology, 91, 374-380. Hill, A. J., Leathwood, P. D. & Blundell, J. E. (1987) Some evidence for short-term caloric compensation in normal weight human subjects: the effects of high- and low-energy meals on hunger, food preference and food intake. Human Nutrition: Applied Nutrition, 4lA, 244-257.
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109
Keys, A., Brozek, J., Henschel, A., Mickelson 0. & Taylor, H. L. (1950) The biology ofhuman starvation. Minneapolis: University of Minnesota Press. Kirkley, B. G., Burge, J. C. & Ammerman, A. (1988) Dietary restraint, binge eating, and dietary behavior patterns. International Journal of Eating Disorders, 7, 771-778. Klajner, F., Herman, C. P., Polivy, J. & Chhabra, R. (1981) Human obesity, dieting, and anticipatory salivation to food. Physiology and Behuoior, 27, 195-198. Laessle, R. G., Tuschl, R. J., Kotthaus, B. C. & Pirke, K. M. (1989) Behavioral and biological correlates of dietary restraint in normal life. Appetite, 12, 83-94. LeGoff, D. B. & Spigelman, M. N. (1987) Salivary response to olfactory food stimuli as a function of dietary restraint and body weight. Appetite, 8, 29-35. Louis-Sylvestre, J., Tournier, A., Verger, P., Chabert, M., Delorme, B. & Hossenhopp, J. (1989) Learned caloric adjustment of human intake. Appetite, 12, 95-103. Lowe, M. R. & Kleifield, E. I. (1988) Cognitive restraint, weight suppression, and the regulation of eating. Appetite, ZO, 159-168. Mattes, R. D., Pierce, C. B. & Friedman, M. I. (1988) Daily caloric intake of normal-weight adults: response to changes in dietary energy density of a luncheon meal. American Journal of Clinical Nutrition, 48, 214-219.
Nicolaidis, S. (1977) Sensory-neuroendocrine reflexes and their anticipatory and optimizing role on metabolism. In M. R. Kare & 0. Mailer (Eds.), The chemical senses and nutrition. Pp. 123-143. New York: Academic Press. Pirke, K. M. & Ploog, D. (1987) Biology of human starvation. In P. J. V. Beumont, G. D. Burrows & R. C. Casper (Eds.), Handbook of eating disorders (Part 1). Pp. 79-102. Amsterdam: Elsevier. Polivy, J. & Herman, C. P. (1985) Dieting and binging. A causal analysis. American Psychologist, 40, 193-201.
Polivy, J., Gamer, D. M. & Garfinkel, P. E. (1986) Causes and consequences of the current preference for thin female physiques. In C. P. Herman, M. P. Zanna & E. T. Higgins (Eds.), Physical appearance, stigma, and social behavior (The Ontario Symposium, Vol. 3). Pp. 89112. Hillsdale: Erlbaum. Rodin, J., Silberstein, L. & Striegel-Moore, R. (1985) Women and weight. A normative discontent. In T. B. Sonderegger (Ed.), Psychology and gender (Nebraska Symposium on Motivation 1984). Pp. 267-307. Lincoln: University of Nebraska Press. Rogers, P. J., Carlyle, I., Hill, A. J. & Blundell, J. E. (1988) Uncoupling sweet taste and calories: comparison of the effects of glucose and three intense sweeteners on hunger and food intake. Physiology and Behavior, 43, 547-552.
Ruderman,
A. J. (1986) Dietary restraint: a theoretical and empirical review. Psychological
Bulletin, 99, 247-262.
Schweiger, U., Tuschl, R. J., Laessle, R. G., Broocks, A. & Pirke, K. M. (1989) Consequences of dieting and exercise on menstrual function in normal weight young women. In K. M. Pirke, W. Wuttke & U. Schweiger (Eds.), The menstrual cycle and its disorders. Influences of nutrition, exercise and neurotransmitters. Pp. 142-149. Berlin: Springer. Spiegel, T. & Jordan, H. A. (1978) Effects of simultaneous oral-intragastric ingestion on meal patterns and satiety in humans. Journal of Comparative and Physiological Psychology, 92, 133-141.
Tuschl,.R. J., Laessl+R.. G., Kotthaus, B. & Pirke, K. M. (1988) Vom Schlankheitsideal zur Bulimie: Ursachen und FoIgen willkfirlfcher Einschrgnkungen der Nahrungsaufnahme bei jungen Frauen. Verhaltensmodijikation und Verhaltensmedizin, 9, 195-216. Tuschl, R. J., Laessle, R. G., Platte, P. & Pirke, K. M. (1990) Differences in food-choice frequencies between restrained and unrestrained eaters. Appetite, 14, 9-13. Wardle, J. (1987) Compulsive eating and dietary restraint. British Journal of Clinical Psychology, 26,41-55.
Wardle, J. & Beales, S. (1987) Restraint and food intake: an experimental study of eating patterns in the laboratory and in normal life. Behavior Research and Therapy, 25, 179-185. Wardle, J. & Beinart, H. (1981) Binge eating: a theoretical review. British Journal of Clinical Psychology, 20,97-109. Received
19 September
1989
From Dietary Restraint to Binge Eating: Some Theoretical Considerations REINHARD
J. TUSCHL
Division of Psychoneuroendocrinology, Max- Planck- Institute for Psychiatry, Munich
A correlation between dietary restraint and the occurrence of binge eating has been convincingly shown in several investigations. However, the mediating mechanisms have not yet been elaborated in detail nor linked to empirical evidence. This theoretical gap is addressed in the following. After a short review of behavioral and metabolic correlates of dietary restraint, potential effects of restrained eating on the psychophysiological regulation of food intake are described. These effects may lead to the disruption of intake regulation and therefore can be regarded as direct causes of binge eating. The tendency to control food intake consciously in order to prevent weight gain or to promote weight loss can be labeled as “restrained eating”. This concept has its roots in laboratory experiments showing that individuals with chronic weight concern are likely to overeat under conditions antagonistic to self-control (for review see Ruderman, 1986; Herman & Polivy, 1988 a), a phenomenon referred to as “counterregulation” (Hibscher & Herman, 1977) and regarded as an experimental analog of binge eating (Wardle & Beinart, 1981). For this reason the concept of “dietary restraint” deserves great attention. It mediates between two events which appear at first glance to conflict. New sociocultural expectations concerning the desirable physical appearance of women, extreme slimness or even emaciation, have emerged over the past three decades (Rodin et al., 1985; Polivy et al., 1986). During the same period, bulimia, experienced as a loss of control over eating while consuming a large amount of food, has become increasingly common in young women (Connors & Johnson, 1987; Drewnowski et al., 1988). Many women start to diet with the aspiration of approaching a slim body shape, but in most cases this may be unattainable for biological reasons. A causal link between fasting and bingeing is well substantiated (for review see Polivy & Herman, 1985; Wardle, 1987). The available empirical evidence, however, rests upon extreme forms of dieting behavior, which are accompanied by weight loss and concomitant biological alterations (e.g. the semistarvation experiment of Keys et al., 1950). Restrained eating, on the other hand, which has never been defined by objective behavioral criteria, is originally a psychological concept describing the intention to restrict food intake and implicates neither actual weight loss nor any obligatory procedure for weight control. Yet, if it is causally connected to binge eating, restrained eating also should be linked to specific longstanding alterations in everyday eating behavior, which are responsible, once cognitive control has broken down, for the failure of intake regulation to terminate a meal in time-that is, for suffering a binge. Address reprint requests to: Reinhard Tuschl, Max-Planck-Institute D-8000 Miinchen 40, F.R.G. 0195-6663/90/020105 + 05 %03.00/O
for Psychiatry, Kraepelinstr. 2, 0 1990 Academic Press Limited
106
R. J. TUSCHL
It has already been shown that restrained eating is in fact comprised of various inconspicuous forms of permanent dieting. Young women who were classified as restrained eaters on the basis of questionnaires reported consumption of less energy than the complementarily defined unrestrained eaters (Wardle & Beales, 1987; Kirkley et al., 1988; Laessle et al., 1989; Tuschl et al., Note 1). Restrained eaters showed a great variability in energy intake, too. Days of high and low caloric consumption frequently alternated (Laessle et al., 1989). A constant energy supply suffered additional interruption by planned days of starvation several times a month (Tuschl et al., Note 1). In addition, qualitative alterations in the everyday eating behavior of restrained eaters were found (Tuschl et al., 1990). They showed a strong tendency to avoid fat and a large percentage of them was used to consuming artificial sweeteners and other caloriereduced foodstuffs. Weight history revealed that restrained eaters had more often been on weight-reducing diets, on which they had lost more than 4 kg of body weight (Laessle et al., 1989; Tuschl et al., Note 1). Yet both the actual relative weight (body mass index; BMI) and the maximal one since entering adulthood were higher in the restraint group. This indicates weight cycling to a great extent. The seeming contradiction that restrained eaters weighed more than unrestrained ones and at the same time reported consumption of less energy is explained by results concerning energy expenditure (Tuschl et al., Note 1). Restrained eaters do not underreport. When adjusted for individual differences in body composition and height, they expended about 620 kcal/day less energy than women with an unrestrained eating style. No biochemical indices of acute starvation, i.e. an elevated level of /?-hydroxybutyric acid or a decreased level of triiodothyronine (see Pirke & Ploog, 1987), were found. These results indicate that restrained eaters are dieters whose energy metabolism fits with a relatively low and inconsistent level of caloric intake. On the average, they meet their actual, diminished caloric requirements and therefore do not lose weight. Nevertheless, as pointed out by Laessle et al. (1989), short-term states of physiological deprivation due to intermittent caloric restrictions might be frequently present in restrained eaters and could precipitate binge eating (cf. Bellisle et al., 1984). One of the mechanisms by which the organism economizes energy has already been identified. Restrained eaters have impaired menstrual function. Schweiger et al. (1989) found a shortened luteal phase of the menstrual cycle with decreased progesterone secretion. Low caloric requirements may have biological and behavioral causes. Given the prevailing social ideal of feminine beauty, a biological predisposition to a low level of energy expenditure could induce chronic weight concern and therefore be the “prima causa” of dietary restraint. The existence of such a predisposition in restrained eaters is suggested by the relatively elevated maximal former BMI in this group. It can be concluded that, although their BMI is still higher than in the unrestrained group, restrained eaters presently regulate their weight below the level at which they would do without dietary restrictions. In this case, a restrained eating style should have led to compensatory changes in energy expenditure (Apfelbaum, 1978; Djazayery, 1987) and may therefore be the reason why metabolic rate has declined and balanced below the biologically given level. In addition, repeated cycles of weight loss and regain cause a heightened food efficiency persisting beyond the deprivation periods and making subsequent weight loss more difficult (Brownell et al., 1987; Blackburn et al., 1989). Since restrained eaters report multiple dieting episodes with weight fluctuations in the past and diet several times per month at present, their energy requirements may have decreased additionally. Thus, as a consequence of restrained eating, the sociocultural pressure to restrict caloric intake in order to at least approximately reach the aspired
FROM DIETARY RESTRAINT TO BINGE EATING
107
slim body shape or to prevent weight gain rises further. This interdependency between biological and behavioral determinants of energy expenditure might result in a vicious circle of mutually reinforced fasting and bingeing, explaining the presently observed frequency of bulimic behaviors in young women. The still unanswered question is how restrained eating affects the psychophysiological regulation of food intake. An impairment of the satiation process must be assumed to be a prerequisite of a binge. In addition, an exaggeration of the responsiveness to nutritional or food-related stimuli has been observed in restrained eaters (Klajner et al., 1981; LeGoff & Spigelman, 1987) and may be relevant to the “disinhibition” phenomenon, the breakdown of cognitive control. The hypothesis has been put forward that restrained eating enhances the attractiveness of palatable foodstuffs while at the same time progressively destroying the learned components of satiation, thus leaving the termination of a meal to relatively insensitive physiological mechanisms like gastric distension (Herman & Polivy, 1988 b; Tuschl et al., 1988). Several effects of restrained eating disarranging intake regulation in this way can be postulated. A dissociation between food selection and food preferences-not the liked, but the cognitively “allowed” foods are selected-may not only cause psychological frustration and deprivation (Herman & Polivy, 1988b), but also enhance the attractiveness of the “forbidden fruits” directly by nutritional preference conditioning (see Booth, 198 1). As a consequence, the microstructure of eating changes. Eating rate is accelerated and chewing activity is decreased (Bellisle et al., 1984). Eating in such a way produces large and long meals in its own right (Bellisle et al., 1984), at least when it is not cognitively inhibited. In addition, it is incompatible with the emergence of the feeling of satisfaction that is normally induced by eating (Spiegel & Jordan, 1978). This probably compounds the overeating, once cognitive control has broken down. Regarding the satiation process, restrained eaters by definition are wont to end meals not because the sensation of satiety has emerged but because a cognitively set limit has been reached; it can be assumed that this extinguishes conditioned satiety cues. High variability in intake such as skipping meals and more extreme forms of intermittent dieting may weaken learned satiating contingencies further. Also cephalic-phase reflexes may be affected, leading to an impairment of the metabolism of ingested food (see Nicolaidis, 1977). Oversized meals, ascribed to the processes discussed above and occurring from time to time after disinhibition, do not permit the calibration of sensory cues by the postingestional consequencies of food. Furthermore, large but poorly satiating meals may favor the development of “belly bulimia” (Booth, 1988), in which fulness is conditioned to elicit increased attractiveness of foods. Uncoupling the sensory characteristics of food from its caloric content, such as occurs with the use of artificial sweeteners and other calorie-reduced ingredients, may lead to paradoxical effects on the sensations of hunger and satiety (Blundell & Hill, 1986; Rogers et al., 1988) and to overcompensation for caloric dilution (Hill et al., 1987; Foltin et al., 1988; Mattes et al., 1988; Louis-Sylvestre et al., 1989). The combination of these potential consequences of restrained eating render an adequate control of meal size impossible. The considerations above exemplify the necessity to get more detailed information on the everyday eating behavior of restrained eaters in order to understand better the processes involved in the genesis of bulimic behaviors. One must not forget that restrained eaters, who had been defined by means of questionnaires, are far from being a homogeneous group with regard to their actual eating behavior. For example, only some of them used artificial sweeteners or calorie-reduced foodstuffs (Tuschl et al., 1990). Many restrained eaters, like unrestrained ones, totally abstained from
108
R. J. TUSCHL.
consuming such products. Secondly, a subgroup of restrained eaters who constantly maintain and have adapted to weights lower than their previous weights and who therefore were labeled as “successful dieters” or “weight suppressors” (Lowe & Kleifield, 1988), show no “counter regulation” in the laboratory (Lowe & Kleifield, 1988). It looks as if this group is able to adhere permanently to the self-imposed dietary restrictions and does not tend to develop bulimic behaviors. Obviously, some forms of dietary restraint are more apt to disarrange intake regulation than others. It can be hypothesized that the more chaotic the everyday eating behavior, the higher the risk of developing bulimia. A subclassification of “restrained eating” in behavioral terms is urgently needed.
REFERENCENOTE 1. Tuschl, R. J., Platte, P., Laessle, R. G., Stichler, W. & Pirke, K. M. (1990) Energy expenditure and everyday eating behavior in healthy young women. American Journal of Clinical Nutrition (in press).
REFERENCES Apfelbaum, M. (1978) Adaptation to changes in caloric intake. Progress in Food and Nutrition Sciences, 2, 543-559.
Bellisle, F., Lucas, F., Amrani, R. & Le Magnen, J. (1984) Deprivation, palatability and the microstructure of meals in human subjects. Appetite, 5, 85-94. Blackburn, G. L., Wilson, G. T., Kanders, B. S., Stein, L. J., Lavin, P. T., Adler, J. 8z Brownell, K. D. (1989) Weight cycling: the experience of human dieters. American Journal of Clinical Nutrition, 49, 1105-l 109. Blundell, J. E. & Hill, A. J. (1986) Paradoxical effects of an intense sweetener (aspartame) on appetite. Lancet, i, 1092-1093. Booth, D. A. (1981) Hunger and satiety as conditioned reflexes. In H. Weiner, M. A. Hofer &A. J. Stunkard (Eds.), Brain, behavior, and bodily disease. Pp. 143-160. New York: Raven Press. Booth, D. A. (1988) Culturally corralled into food abuse: the eating disorders as physiologically reinfored excessive appetites. In K. M. Pirke, W. Vandereycken & D. Ploog (Eds.), The psychobiology of bulimia nervosa. Pp. 18-32. Berlin: Springer. Brownell, K. D., Steen, S. N. & Wilmore, J. H. (1987) Weight regulation practices in athletes: analysis of metabolic and health effects. Medicine and Science in Sports and Exercise, 19, 546-556.
Connors,
M. E. & Johnson, C. L. (1987) Epidemiology
of bulimia and bulimic behaviors.
Addictive Behaviors, 12, 165-179.
Djazayery, A. (1987) Effects of total energy and individual nutrient intakes on energy balance. World Review of Nutrition and Dietetics, 52, 143-208.
Drewnowski, A., Yee, D. K. & Krahn, D. D. (1988) Bulimia in college women: incidence and recovery rates. American Journal of Psychiatry, 145, 753-755. Foltin, R. W., Fischman, M. W., Emurian, C. S. & Rachlinski, J. J. (1988) Compensation for caloric dilution in humans given unrestricted access to food in a residential laboratory. Appetite, IO, 13-24.
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