Biofeedback and Self-Regulation, VoL 1, No. 1, 1976
Ideas and Commentary
The Behavioral Treatment of Obesity: A Reconnaissance Michael J. Mahoney The Pennsylvania State University
Few areas of clinical research have enjoyed such rapid expansion and widespread application as the behavioral treatment of obesity. Recent reviews have suggested that behavior modification is often more successful than traditional obesity treatment strategies (Stunkard, 1972; Stunkard & Mahoney, in press; Abramson, 1973; Hall & Hall, 1974). Unfortunately, this consensus has sometimes encouraged a complacency regarding our current knowledge and technical skills in clinical weight management. This is particularly apparent in applied realms, where behavioral packages are employed almost pro forma. The generally recognized superiority of behavioral strategies is often accompanied by two illicit corollaries: (1) the assumption that behavioral strategies are very effective, and (2) the assumption that their effectiveness confirms the theoretical assumptions on which they are based. The first corollary is patently inaccurate. While it is true that behavior modification has yielded consistently better results than other approaches, this does not necessarily mean that it has shown good results. We remain a long way from any semblance of complete success in the treatment of obesity. Impressively large losses are still the exception rather than the rule, and long-term follow-ups remain couched in intervals of months rather than years. Moreover, there is tremendous variability in responsiveness to behavioral strategies. Individuals ostensibly receiving the same treatment may vary in their success by as much as a tenfold difference. The second corollary is perhaps more elusive. Even granting that the available data indicate that we are pursuing a fruitful research direction, knowing whether behavioral strategies work does not tell us why they work. The processes operative in these clinical endeavors remain very poorly understood. As I have pointed out elsewhere (Mahoney, 1975a,b), many o f 127 © 1976 Plenum Publishing Corporation, 227 West 17th Street, New Y o r k , N.Y. 10011. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, In any form or by any means, electronic, mechanical, photocopying, microfilming, recording, or otherwise, without written permission of the publisher.
Mahoney
128
the independent variables in behavioral obesity research have been inferred from outcome. Clients are instructed to change their eating habits and activity patterns. Their actual adherence to these instructions is seldom observed, however it is often inferred from their subsequent weight loss. Individuals who are more successful are presumed to have followed therapist directions more conscientiously. Without refining our understanding of the processes involved in successful weight management, we risk stagnation of our clinical packages and lose invaluable opportunities for their improvement. The continuing inadequacy of our knowledge is exacerbated by two broad areas of oversight. First, our assumptions about obesity have remained primarily wed to theory rather than data. Although basic physiological research has rapidly accumulated, the behavior therapist has generally overlooked its relevance for some of his clinical assumptions. Secondly, our research methodology has remained sorely inadequate for a precise analysis of the processes and parameters in effective weight management. REVIEWING OUR ASSUMPTIONS
The behavioral treatment of obesity seems to invoke at least 4 assumptions: (1) Obesity is a learning disorder, (2) The obese individual is an overeater, (3) There are critical differences in the "eating style" of obese and nonobese individuals, and (4) Training the obese person to eat like a nonobese person will result in weight loss. While many of these assumptions have remained implicit, their role in molding behavioral strategies can hardly be denied. What is their empirical status? The assertion that obesity is a learning disorder is probably an oversimplification, since most behavior therapists would not deny the role of at least some biochemical influences. Nevertheless, the relative importance of genetic and metabolic factors has usually been deemphasized. Recent developments in the physiology of obesity suggest that this theoretical bias may be a costly one in our understanding of clinical weight problems. For example, although obesity is not inherited, somatotype is genetically transmitted, and the latter may place restrictions on the reasonable lower limits for weight loss goals (Seltzer & Mayer, 1964). Likewise, metabolic differences between individuals may play a significant role in their relative abilities to tolerate excess calories (Stunkard & Mahoney, in press). While a pound may be equivalent to 3500 kcal on the average, individuals may vary
Behavioral Treatment of Obesity
129
by several hundred kcal in the actual exchange quantity. In some individuals, moreover, dietary restrictions may suppress metabolic rate (Bray, 1969). There also seems to be increasing evidence for a "ponderostat" (set point) theory of human obesity, although its clinical implications remain to be evaluated (Hirsch & Knittle, 1971; Jordan, 1973; Polivy, 1975; Wooley & Wooley, 1975). Forthcoming developments in basic physiological research may thus provide invaluable knowledge for the clinical management of obesity. They have already produced evidence relevant to two of the other assumptions. Is the obese individual an overeater? Usually, but not always. There is evidence to suggest that at least some overweight persons actually consume fewer calories than their normal weight peers (e.g., Hashim & Van Itallie, 1965; Mayer, 1968). In these cases, which are apparently more frequent in adolescent girls and housewives, excess adiposity appears to be a result of extremely sedentary life styles (Chirico & Stunkard, 1960; Bradfield & Jourdan, 1972). The pro forma clinical recommendation to reduce food calories may therefore merit reconsideration. Unless it has been determined that the client is an overeater, these recommendations may offer little assistance in therapy. Is there an "obese eating style"? This assumption has played a very important role in molding clinical recommendations. The obese eating style has generally included (a) rapid eating pace, (b) a few large bites, (c) short meal duration, and (d) a hypersensitivity to external food-related cues (cf. Ferster, Nurnberger, & Levitt, 1962; Schachter, 1971; Stuart & Davis, 1972). One would presume that such a cardinal theoretical element would have received substantial experimental scrutiny since it forms a critical part of the foundations for therapy. However, surprisingly little research has been devoted to examining the empirical validity of the obese eating style. What has been reported is relatively recent and generally nonsupportive. For example, one study has found that obese persons eat more slowly than those of normal weight (Meyer & Pudel, 1972), and three others failed to find any obese-nonobese differences (Mahoney, 1975b; Tabas & Jordan, 1973). The sparse evidence on number and size of bites, meal duration, and hypersensitivity to food-related cues is also predominantly nonsupportive (Gaul, Craighead, & Mahoney, in press; Stunkard & Levitz, 1973; Mahoney, 1975b; Tabas & Jordan, 1973; Wooley & Wooley, 1975). The above evidence of course raises serious questions about the theoretical foundations of some of the behavioral strategies, but does not necessarily question their potential efficacy. For example, even though obese individuals may not be faster eaters than the nonobese, both groups can apparently reduce total food consumption by slowing their eating pace (Wooley & Wooley, 1975). This effect may be moderated, however, by tern-
Mahoney
130
poral parameters and beliefs (Mahoney, 1975b). Likewise, even though there may be no obese-nonobese differences in sensitivity to food-related cues, strategies which alter cue salience may influence eating patterns in both groups (Stunkard & Levitz, 1973). As mentioned earlier, our understanding of the clinical processes in weight management remains very incomplete due to a variety of methodological inadequacies in the existing research. EVALUATING THE ADEQUACY OF OUR RESEARCH In addition to overlooking some of the basic research relevant to our theoretical assumptions, our clinical applications have not been of the highest methodological caliber. When compared to such areas as desensitization, the behavioral treatment of obesity is embarrassingly inadequate in both the extent and the quality of its empirical documentation. Among the most common inadequacies have been the following. 1. Frequent Absence of No-Treatment Controls. In both within-subject and between-subject designs, the use of adequate no-treatment control conditions has been far from universal (cf. Stunkard & Mahoney, in press). In fact, a clear majority of reported studies have failed to employ no-treatment, reversal, or multiple-baseline designs. There are, of course, some ethical and strategic considerations which have contributed to this pattern. Nevertheless, our confidence in the internal validity of the research must take these omissions into account. 2. Frequent Absence of Attention-Placebo Controls. More costly, perhaps, is the virtual nonexistence of controls for expectancy effects and other potential influences in clinical treatment. Obesity researchers often employ procedures which are generally known to be impotent in an effort to control for therapist attention, attendance, etc. These strategies do not, however, control for the client's expectancies for improvement. An adequate placebo control must "be shown to be equally credible (to the client) as the experimental strategy. If it is patently unpromising, it tells us very little about the therapeutic process. 3. Poor Procedural Descriptions. Experimenters often describe their procedures with very general labels, such as "self-monitoring" or "stimulus control." While these may offer some minimal information about the strategies employed, they are usually much too imprecise. The fact that researchers employing ostensibly identical strategies often report diametrically opposite outcomes suggests that these procedural descriptions may be very important. For example, experimenters often omit the details of their procedures, the expectancies of the therapists employed, and whether or not fees were collected. Seasonal parameters are likewise unspecified. A study
Behavioral Treatment of Obesity
131
begun in January and finished in July has a much higher likelihood of success than one which follows the reverse schedule. 4. Incomplete Reporting of Dependent Variables. Despite the fact that obesity is primarily viewed as a cardiovascular risk, behavioral researchers seldom report any direct cardiovascular indices (blood pressure, serum lipids, etc.). Moreover, their reporting of changes in body weight is often idiosyncratic, with a few researchers reporting pounds lost, others reporting percentage of body weight lost, and still others reporting a variety of reduction indices (e.g., percentage of excess pounds lost, pounds lost per week, and so on). Since body weight is a very poor index of body fat, simple skin-fold measurements would seem to be a meaningful supplementary index of therapy outcome. 5. Inadequate Follow-Ups. As in many other areas of clinical research, the treatment of obesity seems to be dominated by relatively brief studies which fail to report the durability of any therapeutic improvements. Not only have maintenance data been sparse, but evidence on auxiliary effects are virtually nonexistent. Do the skills developed in weight management transfer to other areas of personal functioning? Are there any longterm negative effects of treatment? What are the r~redictor variables for successful treatment and maintenance? 6. Unexplored Variables of Influence. Since its inception in the early 1960s, the behavioral treatment of obesity has primarily restricted its independent variables to those directly prescribed by the obesity assumptions and behavioral theory. As outlined above, even these variables have been poorly scrutinized. A large set of other variables has remained virtually unexamined. For example, despite the fact that beliefs about eating may tremendously influence food intake (cf. Mahoney, 1975b; Nisbett & Storms, in press; Wooley, 1972), very little applied research has been devoted to this class of variables. The possible contribution of spouses, vicarious learning procedures, and a variety of other potential influences has been" likewise ignored. In addition to methodological inadequacies, of course, we have paid very little research attention to such topics as prevention, pediatric treatment, and motivating the "unmotivated." Our research has thus been inadequate in both form and focus. One is tempted here to reiterate William James' (1890) observation that "this is no science, it is only the hope of a science," or that it is still a vast "darkness in which we grope." One hopes that the darkness can be at least partially "illuminated by a humility born of ignorance (Mahoney, 1974, p. 294)." We are a long way from any justified complacency about our knowledge or potency in the clinical treatment of obesity. As with so many other areas in the realm of clinical research, our science has hardly begun.
132
Mahoney REFERENCES
Abramson, E. E. A review of behavioral approaches to weight control. Behaviour Research and Therapy, 1973, 11, 547-556. Bradfield, R. B., & Jourdan, M. Energy expenditure of obese women during weight loss. American Journal of Clinical Nutrition, 1972, 25, 971-975. Bray, G. A. Effect of caloric restriction on energy expenditure in obese patients. Lancet, 1969, 2, 397. Chirico, A. M., & Stunkard, A. J. Physical activity and human obesity. New England Journal of Medicine, 1960, 263, 935-946. Ferster, C. B., Nurnberger, J. I., & Levitt, E. B. The control of eating. Journal of Mathetics, 1962, 1, 87-109. Gaul, D. J., Craighead, W. E., & Mahoney, M. J. The relationship between eating rates and obesity. Journal of Consulting and Clinical Psychology (in press). Hall, S. M., & Hall, R. G. Outcome and methodological considerations in behavioral treatment of obesity. Behavior Therapy, 1974, 5, 352-364. Hashim, S. A., & Van Itallie, T. B. Studies in normal and obese subjects using a monitored food-dispensing device. Annals of the New York Academy of Science, 1965, 131, 654-661. Hirsch, J., & Knittle, J. L. Cellularity of obese and nonobese human adipose tissue. Federation Proceedings, 1971, 29, 1516-1521. James, W. Principles of psychology. New York: Holt, 1890. Jordan, H. A. Physiological control of food intake in man. Paper presented at the Fogarty International Conference on Obesity, Washington, D.C., October, 1973. Mahoney, M. J. Cognition and behavior modification. Cambridge, Massachusetts: Ballinger, 1974. Mahoney, M. J. Fat fiction. Behavior Therapy, 1975, (in press) (a). Mahoney, M. J. The obese eating style: Bites, beliefs, and behavior modification. Addictive Behaviors, 1975, (in press) (b). Mayer, J. Overweight: Causes, cost, and control. Englewood Cliffs: Prentice-Hall, 1968. Meyer, J. E., & Pudel, V. Experimental studies on food-intake in obese and normal weight subjects. Journal of Psychosomatic Research, 1972, 16, 305-308. Nisbett, R. E., & Storms, M. D. Cognitive and social determinants of food intake. In London, H. S. and Nisbett, R. E. (Eds.) Cognitive alteration of feeling states, Chicago: Aldine (in press). Polivy, J. Perception of calories and regulation of intake in man and animals. Unpublished manuscript, Loyola University, 1975. Schachter, S. Some extraordinary facts about obese humans and rats. American Psychologist, 1971, 26, 129-146. Seltzer, C. C., & Mayer, J. Body build and obesity--Who are the obese? Journal of the American Medical Association, 1964, 189, 677-684. Stuart, R. B., & Davis, B. Slim chance in a fat world: Behavioral control of obesity. Champaign, Illinois: Research Press, 1972. Stunkard, A. J. New therapies for the eating disorders: Behavior modification of obesity and anorexia nervosa. Archives of General Psychiatry, 1972, 26, 391-398. Stunkard, A. J., & Levitz, L. S. The influence of caloric density and availability on the food selections of normal and obese subjects. Unpublished manuscript, University of Pennsylvania, 1973. Stunkard, A. J., & Mahoney, M. J. Behavioral treatment of the eating disorders. In H. Leitenberg (Ed.), Handbook of behavior modification. New York: Appleton-Century-Crofts, 1975 (in press). Tabas, L., & Jordan, H. A. Ingestive behavior of obese and thin humans eating in a restaurant. Unpublished manuscript, University of Pennsylvania, 1973. Wooley, S. C. Physiologic versus cognitive factors in short-term food regulation in the obese and nonobese. Psychosomatic Medicine, 1972, 34, 62-68.
Behavioral Treatment of Obesity
133
Wooley, O. W., & Wooley, S. C. The experimental psychology of obesity. In T. Silverstone & J. Fincham (Eds.), Obesity: Pathogenesis and management. Lancaster: Medical and Technical Publishing Company, 1975. (Original received February 10, 1975)
Ideas and Commentary
The Behavioral Treatment of Obesity: A Reconnaissance Michael J. Mahoney The Pennsylvania State University
Few areas of clinical research have enjoyed such rapid expansion and widespread application as the behavioral treatment of obesity. Recent reviews have suggested that behavior modification is often more successful than traditional obesity treatment strategies (Stunkard, 1972; Stunkard & Mahoney, in press; Abramson, 1973; Hall & Hall, 1974). Unfortunately, this consensus has sometimes encouraged a complacency regarding our current knowledge and technical skills in clinical weight management. This is particularly apparent in applied realms, where behavioral packages are employed almost pro forma. The generally recognized superiority of behavioral strategies is often accompanied by two illicit corollaries: (1) the assumption that behavioral strategies are very effective, and (2) the assumption that their effectiveness confirms the theoretical assumptions on which they are based. The first corollary is patently inaccurate. While it is true that behavior modification has yielded consistently better results than other approaches, this does not necessarily mean that it has shown good results. We remain a long way from any semblance of complete success in the treatment of obesity. Impressively large losses are still the exception rather than the rule, and long-term follow-ups remain couched in intervals of months rather than years. Moreover, there is tremendous variability in responsiveness to behavioral strategies. Individuals ostensibly receiving the same treatment may vary in their success by as much as a tenfold difference. The second corollary is perhaps more elusive. Even granting that the available data indicate that we are pursuing a fruitful research direction, knowing whether behavioral strategies work does not tell us why they work. The processes operative in these clinical endeavors remain very poorly understood. As I have pointed out elsewhere (Mahoney, 1975a,b), many o f 127 © 1976 Plenum Publishing Corporation, 227 West 17th Street, New Y o r k , N.Y. 10011. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, In any form or by any means, electronic, mechanical, photocopying, microfilming, recording, or otherwise, without written permission of the publisher.
Mahoney
128
the independent variables in behavioral obesity research have been inferred from outcome. Clients are instructed to change their eating habits and activity patterns. Their actual adherence to these instructions is seldom observed, however it is often inferred from their subsequent weight loss. Individuals who are more successful are presumed to have followed therapist directions more conscientiously. Without refining our understanding of the processes involved in successful weight management, we risk stagnation of our clinical packages and lose invaluable opportunities for their improvement. The continuing inadequacy of our knowledge is exacerbated by two broad areas of oversight. First, our assumptions about obesity have remained primarily wed to theory rather than data. Although basic physiological research has rapidly accumulated, the behavior therapist has generally overlooked its relevance for some of his clinical assumptions. Secondly, our research methodology has remained sorely inadequate for a precise analysis of the processes and parameters in effective weight management. REVIEWING OUR ASSUMPTIONS
The behavioral treatment of obesity seems to invoke at least 4 assumptions: (1) Obesity is a learning disorder, (2) The obese individual is an overeater, (3) There are critical differences in the "eating style" of obese and nonobese individuals, and (4) Training the obese person to eat like a nonobese person will result in weight loss. While many of these assumptions have remained implicit, their role in molding behavioral strategies can hardly be denied. What is their empirical status? The assertion that obesity is a learning disorder is probably an oversimplification, since most behavior therapists would not deny the role of at least some biochemical influences. Nevertheless, the relative importance of genetic and metabolic factors has usually been deemphasized. Recent developments in the physiology of obesity suggest that this theoretical bias may be a costly one in our understanding of clinical weight problems. For example, although obesity is not inherited, somatotype is genetically transmitted, and the latter may place restrictions on the reasonable lower limits for weight loss goals (Seltzer & Mayer, 1964). Likewise, metabolic differences between individuals may play a significant role in their relative abilities to tolerate excess calories (Stunkard & Mahoney, in press). While a pound may be equivalent to 3500 kcal on the average, individuals may vary
Behavioral Treatment of Obesity
129
by several hundred kcal in the actual exchange quantity. In some individuals, moreover, dietary restrictions may suppress metabolic rate (Bray, 1969). There also seems to be increasing evidence for a "ponderostat" (set point) theory of human obesity, although its clinical implications remain to be evaluated (Hirsch & Knittle, 1971; Jordan, 1973; Polivy, 1975; Wooley & Wooley, 1975). Forthcoming developments in basic physiological research may thus provide invaluable knowledge for the clinical management of obesity. They have already produced evidence relevant to two of the other assumptions. Is the obese individual an overeater? Usually, but not always. There is evidence to suggest that at least some overweight persons actually consume fewer calories than their normal weight peers (e.g., Hashim & Van Itallie, 1965; Mayer, 1968). In these cases, which are apparently more frequent in adolescent girls and housewives, excess adiposity appears to be a result of extremely sedentary life styles (Chirico & Stunkard, 1960; Bradfield & Jourdan, 1972). The pro forma clinical recommendation to reduce food calories may therefore merit reconsideration. Unless it has been determined that the client is an overeater, these recommendations may offer little assistance in therapy. Is there an "obese eating style"? This assumption has played a very important role in molding clinical recommendations. The obese eating style has generally included (a) rapid eating pace, (b) a few large bites, (c) short meal duration, and (d) a hypersensitivity to external food-related cues (cf. Ferster, Nurnberger, & Levitt, 1962; Schachter, 1971; Stuart & Davis, 1972). One would presume that such a cardinal theoretical element would have received substantial experimental scrutiny since it forms a critical part of the foundations for therapy. However, surprisingly little research has been devoted to examining the empirical validity of the obese eating style. What has been reported is relatively recent and generally nonsupportive. For example, one study has found that obese persons eat more slowly than those of normal weight (Meyer & Pudel, 1972), and three others failed to find any obese-nonobese differences (Mahoney, 1975b; Tabas & Jordan, 1973). The sparse evidence on number and size of bites, meal duration, and hypersensitivity to food-related cues is also predominantly nonsupportive (Gaul, Craighead, & Mahoney, in press; Stunkard & Levitz, 1973; Mahoney, 1975b; Tabas & Jordan, 1973; Wooley & Wooley, 1975). The above evidence of course raises serious questions about the theoretical foundations of some of the behavioral strategies, but does not necessarily question their potential efficacy. For example, even though obese individuals may not be faster eaters than the nonobese, both groups can apparently reduce total food consumption by slowing their eating pace (Wooley & Wooley, 1975). This effect may be moderated, however, by tern-
Mahoney
130
poral parameters and beliefs (Mahoney, 1975b). Likewise, even though there may be no obese-nonobese differences in sensitivity to food-related cues, strategies which alter cue salience may influence eating patterns in both groups (Stunkard & Levitz, 1973). As mentioned earlier, our understanding of the clinical processes in weight management remains very incomplete due to a variety of methodological inadequacies in the existing research. EVALUATING THE ADEQUACY OF OUR RESEARCH In addition to overlooking some of the basic research relevant to our theoretical assumptions, our clinical applications have not been of the highest methodological caliber. When compared to such areas as desensitization, the behavioral treatment of obesity is embarrassingly inadequate in both the extent and the quality of its empirical documentation. Among the most common inadequacies have been the following. 1. Frequent Absence of No-Treatment Controls. In both within-subject and between-subject designs, the use of adequate no-treatment control conditions has been far from universal (cf. Stunkard & Mahoney, in press). In fact, a clear majority of reported studies have failed to employ no-treatment, reversal, or multiple-baseline designs. There are, of course, some ethical and strategic considerations which have contributed to this pattern. Nevertheless, our confidence in the internal validity of the research must take these omissions into account. 2. Frequent Absence of Attention-Placebo Controls. More costly, perhaps, is the virtual nonexistence of controls for expectancy effects and other potential influences in clinical treatment. Obesity researchers often employ procedures which are generally known to be impotent in an effort to control for therapist attention, attendance, etc. These strategies do not, however, control for the client's expectancies for improvement. An adequate placebo control must "be shown to be equally credible (to the client) as the experimental strategy. If it is patently unpromising, it tells us very little about the therapeutic process. 3. Poor Procedural Descriptions. Experimenters often describe their procedures with very general labels, such as "self-monitoring" or "stimulus control." While these may offer some minimal information about the strategies employed, they are usually much too imprecise. The fact that researchers employing ostensibly identical strategies often report diametrically opposite outcomes suggests that these procedural descriptions may be very important. For example, experimenters often omit the details of their procedures, the expectancies of the therapists employed, and whether or not fees were collected. Seasonal parameters are likewise unspecified. A study
Behavioral Treatment of Obesity
131
begun in January and finished in July has a much higher likelihood of success than one which follows the reverse schedule. 4. Incomplete Reporting of Dependent Variables. Despite the fact that obesity is primarily viewed as a cardiovascular risk, behavioral researchers seldom report any direct cardiovascular indices (blood pressure, serum lipids, etc.). Moreover, their reporting of changes in body weight is often idiosyncratic, with a few researchers reporting pounds lost, others reporting percentage of body weight lost, and still others reporting a variety of reduction indices (e.g., percentage of excess pounds lost, pounds lost per week, and so on). Since body weight is a very poor index of body fat, simple skin-fold measurements would seem to be a meaningful supplementary index of therapy outcome. 5. Inadequate Follow-Ups. As in many other areas of clinical research, the treatment of obesity seems to be dominated by relatively brief studies which fail to report the durability of any therapeutic improvements. Not only have maintenance data been sparse, but evidence on auxiliary effects are virtually nonexistent. Do the skills developed in weight management transfer to other areas of personal functioning? Are there any longterm negative effects of treatment? What are the r~redictor variables for successful treatment and maintenance? 6. Unexplored Variables of Influence. Since its inception in the early 1960s, the behavioral treatment of obesity has primarily restricted its independent variables to those directly prescribed by the obesity assumptions and behavioral theory. As outlined above, even these variables have been poorly scrutinized. A large set of other variables has remained virtually unexamined. For example, despite the fact that beliefs about eating may tremendously influence food intake (cf. Mahoney, 1975b; Nisbett & Storms, in press; Wooley, 1972), very little applied research has been devoted to this class of variables. The possible contribution of spouses, vicarious learning procedures, and a variety of other potential influences has been" likewise ignored. In addition to methodological inadequacies, of course, we have paid very little research attention to such topics as prevention, pediatric treatment, and motivating the "unmotivated." Our research has thus been inadequate in both form and focus. One is tempted here to reiterate William James' (1890) observation that "this is no science, it is only the hope of a science," or that it is still a vast "darkness in which we grope." One hopes that the darkness can be at least partially "illuminated by a humility born of ignorance (Mahoney, 1974, p. 294)." We are a long way from any justified complacency about our knowledge or potency in the clinical treatment of obesity. As with so many other areas in the realm of clinical research, our science has hardly begun.
132
Mahoney REFERENCES
Abramson, E. E. A review of behavioral approaches to weight control. Behaviour Research and Therapy, 1973, 11, 547-556. Bradfield, R. B., & Jourdan, M. Energy expenditure of obese women during weight loss. American Journal of Clinical Nutrition, 1972, 25, 971-975. Bray, G. A. Effect of caloric restriction on energy expenditure in obese patients. Lancet, 1969, 2, 397. Chirico, A. M., & Stunkard, A. J. Physical activity and human obesity. New England Journal of Medicine, 1960, 263, 935-946. Ferster, C. B., Nurnberger, J. I., & Levitt, E. B. The control of eating. Journal of Mathetics, 1962, 1, 87-109. Gaul, D. J., Craighead, W. E., & Mahoney, M. J. The relationship between eating rates and obesity. Journal of Consulting and Clinical Psychology (in press). Hall, S. M., & Hall, R. G. Outcome and methodological considerations in behavioral treatment of obesity. Behavior Therapy, 1974, 5, 352-364. Hashim, S. A., & Van Itallie, T. B. Studies in normal and obese subjects using a monitored food-dispensing device. Annals of the New York Academy of Science, 1965, 131, 654-661. Hirsch, J., & Knittle, J. L. Cellularity of obese and nonobese human adipose tissue. Federation Proceedings, 1971, 29, 1516-1521. James, W. Principles of psychology. New York: Holt, 1890. Jordan, H. A. Physiological control of food intake in man. Paper presented at the Fogarty International Conference on Obesity, Washington, D.C., October, 1973. Mahoney, M. J. Cognition and behavior modification. Cambridge, Massachusetts: Ballinger, 1974. Mahoney, M. J. Fat fiction. Behavior Therapy, 1975, (in press) (a). Mahoney, M. J. The obese eating style: Bites, beliefs, and behavior modification. Addictive Behaviors, 1975, (in press) (b). Mayer, J. Overweight: Causes, cost, and control. Englewood Cliffs: Prentice-Hall, 1968. Meyer, J. E., & Pudel, V. Experimental studies on food-intake in obese and normal weight subjects. Journal of Psychosomatic Research, 1972, 16, 305-308. Nisbett, R. E., & Storms, M. D. Cognitive and social determinants of food intake. In London, H. S. and Nisbett, R. E. (Eds.) Cognitive alteration of feeling states, Chicago: Aldine (in press). Polivy, J. Perception of calories and regulation of intake in man and animals. Unpublished manuscript, Loyola University, 1975. Schachter, S. Some extraordinary facts about obese humans and rats. American Psychologist, 1971, 26, 129-146. Seltzer, C. C., & Mayer, J. Body build and obesity--Who are the obese? Journal of the American Medical Association, 1964, 189, 677-684. Stuart, R. B., & Davis, B. Slim chance in a fat world: Behavioral control of obesity. Champaign, Illinois: Research Press, 1972. Stunkard, A. J. New therapies for the eating disorders: Behavior modification of obesity and anorexia nervosa. Archives of General Psychiatry, 1972, 26, 391-398. Stunkard, A. J., & Levitz, L. S. The influence of caloric density and availability on the food selections of normal and obese subjects. Unpublished manuscript, University of Pennsylvania, 1973. Stunkard, A. J., & Mahoney, M. J. Behavioral treatment of the eating disorders. In H. Leitenberg (Ed.), Handbook of behavior modification. New York: Appleton-Century-Crofts, 1975 (in press). Tabas, L., & Jordan, H. A. Ingestive behavior of obese and thin humans eating in a restaurant. Unpublished manuscript, University of Pennsylvania, 1973. Wooley, S. C. Physiologic versus cognitive factors in short-term food regulation in the obese and nonobese. Psychosomatic Medicine, 1972, 34, 62-68.
Behavioral Treatment of Obesity
133
Wooley, O. W., & Wooley, S. C. The experimental psychology of obesity. In T. Silverstone & J. Fincham (Eds.), Obesity: Pathogenesis and management. Lancaster: Medical and Technical Publishing Company, 1975. (Original received February 10, 1975)
