A realistic approach to treating obesity

Clinical Psychology Rewew, Vol. 7, pp. 449-465, Printed iA the USA. .411 rights reserved.

1987 Copyright

0272.7358187 $3.00 + .OO @ 1987 Pergamon Journals Ltd.

A REALISTIC APPROACH TO TREATING OBESITY

Martha E. Smith William ). Fremouw

West Virginia

University

ABSTRACT. Num.erousbiological, psychological, and environmental factors contribute to the development and maintenance of obesity. Attempts to treat this weight disorakr have produced discouraging results in the weight loss literature. However, several studies have o!emonstratedthat weight loss successes a% occur. Five factors which predict favorable weight loss outcomes are identtfied. Instead of applying weight loss strategies indiscriminatey, researchers need to assess those variables that are predictive of successful weight loss. Obese individuals with a poor prognosis may then be more realistically treated by placing an emphasis on the rieuelopment of a healthy lifestyle and self-coruept while de-emphasizing weight loss as the primary goal.

Obesity has been recognized as one of the most serious and prevalent health problems in the United States (Gotto, Foreyt, & Scott, 1976). Approximately 35 % of the population is considered to be obese (Stunkard, 1984). The prevalence is even greater among some ethnic groups, and tends to increase as age increases and social class decreases (Stunkard, 1975). Approximately 90% of the obese population is mildly obese (20-40 % overweight), while 9 % and 0.5 % are moderately obese (41-100 % overweight) and severely obese ( > 100 % overweight), respectively (Stunkard, 1984). When describing this disorder, it is important to distinguish between the terms “obesity” and “overweight.” Obesity is defined as an excess

of body

fat.

Overweight,

on the other

which is higher than a desirable However, this latter definition can body composition (i.e., percentages ple, athletes who are very muscular the norm for body fat content. The determine

the percentage

hand,

is defined

as a body

weight

or appropriate weight in relation to height. be misleading because it does not consider of fat, muscle, and water content). For exammay be overweight for their height but below ideal way to diagnose obesity, therefore, is to

of body fat through

the methods

of hydrostatic

Reprint requests should be addressed to William J. Fremouw, Department West Virginia University, Morgantown, WV 26506. 449

weighing

of Psychology,

450

hf. E. Smith and W J. Fremouw

or by measuring skinfold thickness with calipers. Unfortunately, these procedures are expensive, technical, and time-consuming. Therefore, most people must rely on height-weight tables for defining obesity. Obesity and weight gain have long been associated with numerous conditions detrimental to health and longevity, including cardiovascular disease, diabetes mellitus, gallbladder disease, liver disorders, renal disease, and musculoskeletal disorders (Van Itallie, 1979). I n addition to serious health problems, many obese persons suffer adverse psychosocial consequences due to the pervasive negative attitudes towards obesity in our society (Allon, 1982). Millions of dollars each year are expended on low-calorie “diet” foods and liquid formulas, appetite supand a variety of other diet programs pressants, fad diets, surgical interventions, (Stuart & Davis, 1972). H owever, despite the multitude of attempts to discover a reliably effective treatment, the literature is replete with failures. Numerous biological and psychological factors which inhibit permanent weight change in many obese individuals may account for the modest success rate in treatment studies and a growing pessimism among researchers. In fact, Wooley and Wooley (1984) question whether obesity should be treated at all. Some studies suggest that repeated dieting, rather than obesity itself, is the cause of serious health problems (Division of Chronic Diseases, 1966). In addition, the continued efforts to eradicate obesity may be perpetuating society’s obsession with weight control and the stigma of obesity. Despite these important concerns, an increasing focus on treatment failures and their negative consequences may cause us to overlook numerous cases of successful weight reduction within the literature (e.g., Schacter, 1982; Strain, Strain, Zumoff, & Knittle, 1984). A s is true of many psychological and medical problems, a single successful treatment of obesity for a few individuals does not imply a successful treatment for all. Rather than ask which treatment is most effective, we need to ask which treatment is most effective for which individual. There appear to be a number of factors which are predictive of successful weight loss (e.g., high basal metabolic rate, history of exercise). Instead of abandoning efforts altogether or, at the other extreme, attempting to treat all obese similarly, researchers and clinicians should learn to identify these predictive variables so they can approach treatment in a more realistic manner. For those obese who have a low probability for weight loss, treatment may not be justified. Rather, these persons may need psychological support and therapy to learn to overcome a negative self-image and to better deal with society’s prejudices. On the other hand, obese persons who evidence the developmental, biological, and psychological criteria that are predictive of successful weight loss should not be denied the opportunity to reach this goal. The following review will examine the factors causing and maintaining obesity, weight loss failures and their negative physical consequences and social impact, and weight loss successes and variables which may be predictive of these successes. Finally, a realistic approach to treating obesity based on the identification of these variables will be presented. CAUSES

OF OBESITY

On the basis of what is presently known, only 5% of all obesity can be attributed to underlying physical disorders such as brain damage, endocrine dysfunction, and hereditary diseases (Van Itallie, 1977). The primary cause of the remaining

95% of obesity has not been conclusively established. However, various viewpoints on its pathogenesis have emerged. One school of thought holds that obesity develops from particular kinds of lifestyles, including inactivity and chronic overingestion of food (Van Itallie & Campbell, 1972). I n addition to the use of food for nutritive purposes, many individuals eat in response to various arousal states such 1982). Much overeating may also be as anger, anxiety, or boredom (Rodin, attributed to highly palatable foods, especially those high in fat and sugar content, which are readily accessible in our society. It is this combination of fat, sweetness, and variety in the diet that has been shown to create obesity in laboratory animals. Sclafani and Springer (1976) fed rats a diet of “supermarket” foods including chocolate chip cookies, salami, cheese, bananas, marshmallows, milk chocolate, and peanut butter. At least seven foods were available at any one time, and the food choices were changed frequently to maintain variety. After a 2-month period, these rats had gained 269% more weight than had control animals fed only Purina Chow. This “supermarket” diet may similarly contribute to the development of obesity in humans. Another variable contributing to the onset of obesity may be the low levels of physical activity often displayed by obese individuals. Chirico and Stunkard (1960) demonstrated that obese men and women walked less than normal-weight adults during their routine daily activities. Obese men walked, on the average, 4 miles/day, whereas men of normal weight walked 6 miles/day. Obese women walked, on the average, 2 miles/day, whereas those of normal weight walked 5 miles/day. Similarly, obese adolescent girls in summer camp were observed to swim and play tennis for less time than normal-weight girls during periods of mandatory physical activity (Bullen, Reed, & Mayer, 1964). Since it is often difficult for obese individuals to engage in physical activity given their large body size, they are not typically physically fit. Therefore, a vicious cycle is created. The more fat an individual gains, the less physically active he/she becomes, and the more weight he/she gains. Although it is often difficult to determine whether inactivity initially contributed to the obese state, the research findings suggest that inactivity at least plays a role in its maintenance. Another school of thought regarding the pathogenesis of obesity holds that obese individuals are biologically programmed to be fat. The amount of fat stored in the body is a product of the number and size of the fat cells. Nisbett (1972) postulated that the number of adipocytes in the body is determined by heredity and early nutritional experiences and is permanently fixed by the time of adolescence. Overfeeding during this critical period results in a permanent elevation in fat cell number. Weight loss or gain following this period results only in a change in size but not number of adipocytes. Hirsch and Knittle (1970) identified two possible subtypes of obesity from morphologic studies of adipose tissue. Early-onset obesity is characterized by an elevated fat cell number, whereas adult-onset obesity is characterized by an increase in cell size. While early-onset obesity may be attributed to excessive feeding in the early stages of human development, there is growing evidence to suggest an influence of genetic factors in the etiology of obesity (Foch & McClearn, 1980). Hereditary factors may influence the obese state through channels such as body size, number of fat cells, efficiency of fat storage, and metabolism. Perhaps the most convincing evidence for a genetic influence in obesity comes from an adoption study by Stunkard and his colleagues (Stunkard, S&-enson, Hanis, Teasdale, Chakraborty, Schull, & Schulsinger, 1986). They examined height and weight

452

M. E. Smith and W. J. Fremouw

data on the biologic and adoptive parents of 540 adult Danish adoptees who were divided into four weight classes: thin, median weight, overweight, and obese. Analyses revealed a clear relation between the weight class of the adoptees and the body-mass index (weight in kilograms divided by the square of the height in meters) of their biologic parents (for mothers, p
MAINTAINING

OBESITY

Once obesity is established in an individual, a variety of different mechanisms may operate to maintain the obese state. An intriguing fact is that the state of being fat is a characteristic that may perpetuate one’s fatness. This occurs because obesity itself alters body chemistry, size and number of fat cells, and metabolic activity, each contributing to the maintenance of obesity. As an individual accumulates fat in the body, the fat cells become larger and their capacity to store more fat becomes even greater (Salans, Knittle, & Hirsch, 1968). In addition, obese persons tend to have higher basal insulin levels than normal-weight individuals (Jahr, Ratzmann, Beckert, Besch, & Hahn, 1983). This condition of hyperinsulinemia enhances fat storage by accelerating the entry of sugar into the fat cell and converting the sugar into fat more rapidly (Rodin, 1981). The antilypolytic action of insulin is maintained to a larger extent in obese than in nonobese individuals, therefore maintaining fat deposition in the obese (Howard, Klimes, Vasquez, Brady, Nagulesparan, & Unger, 1984). J o h nson and Wildman (1983) found that exposure to both external and covert food stimuli produced a greater insulin secretion among obese than among normal-weight individuals. In addition, the obese displayed an increased poststimulus salivary output that was significantly higher than among normals. These data suggest that insulin may act as an appetite-inducing mechanism that can lead to a vicious cycle of hyperphagia and increasing obesity. As previously mentioned, early-onset obesity is characterized by an increase in fat cell number or hyperplasia, while adult-onset obesity is characterized by an increase in cell size or hypertrophy (Hirsch & Knittle, 1970). In a study examining the effect of a dietary regimen in relation to adipose tissue cellularity, 10 obese women identified as hyperplastic and 11 obese women identified as hypertrophic were placed on a 1,100 kcal/day diet until weight loss failure occurred. At failure of therapy, the enlarged fat cells had decreased to the size of the fat cells of controls. However, the fat cell number remained unchanged, suggesting that an increase in fat cell number is irreversible. While the hypertrophic obese subjects

Obesity

453

ended therapy with a normal body fat content, the hyperplastic subjects remained obese (Bjiirntorp, Carlgren, Isaksson, Krotkiewski, Larsson, & Sjijstriim, 1975). Although hyperplastic obesity is thought to develop early in life, there is some evidence to suggest that an increase in fat cell number may occur at any point in life. As an individual accumulates body fat, the size of the fat cell,s increases up to a certam weight past which an increase in fat cell number occurs (Bjorntorp cur Sjostrom, 1971). I n a laboratory study, adult rats became obese when they were fed a highly palatable diet for several months (Faust, Johnson, Stern, & Hirsch, 1978). Analysis of adipose tissue revealed that the weight gain was characterized by hypertrophic and hyperplastic fat cells. The return to an ordinary chow diet precipitated a period of weight loss in these animals. Fat cell size decreased to normal, but fat cell numbers remained at the increased levels achieved during weight gain. The diet-induced elevation in adipocyte numbers appeared to be due to a proliferation of the cells, rather than to an increase in lipid content of previously unobservable adipocytes. It is possible that a similar process occurs in adult humans such that an undetermined period of diet-induced weight gain irreversibly increases the number of fat cells in the body and maintains the obese state by creating an elevated boundary below which weight loss cannot occur. Fat accumulation also affects the metabolic activity of obese individuals. Since fat tissue is more metabolically inert than lean tissue, the metabolic rate is lowered if lean body tissue is replaced by fat. Bernstein, Thornton, Yang, Wang, Redmond, Pierson, Pi-Sunyer, & Van Itallie (1983) found that the contribution of fat-free mass to resting metabolic rate was 3 to 5 times greater per kg than that of body fat. When placed on very-low-calorie-diets, both obese and nonobese humans lose not only fat, but also a great deal of lean tissue. In one study, an adult obese male on a 670 kcal/day diet lost 22 % of his lean body mass over the course of 64 days (Yang, Barbosa-Saldivar, Pi-Sunyer, & Van Itallie, 1981). This change in body composition among severe restricters may be one reason why some obese people require fewer calories to maintain their elevated body weight than normals. Decreases in metabolic rate during restrictive dieting can be detected through different mechanisms. Several studies have shown that exposure to very restricted diets results in a decrease in the thermogenic hormone metabolite serum T3 (e.g., Jung, Shetty, &J ames, 1980; Palmblad, Levi, Burger, Melander, Westgren, von Schenck, & Skude, 1977). It has been suggested that the decrease of serum T3 concentration may be responsible for the lowered metabolic rate and resistance to dietary treatment among some obese individuals. Another metabolic adaptation to food restriction is a decrease in 0, consumption in the organism. Following periods of restricted food consumption in male rats, the resting rates of 0, consumption were significantly reduced below control levels. In addition, the thermogenic response to a meal was significantly less following a period of food restriction and during the early stages of refeeding (Boyle, Storlien, Harper, & Keesey, 1981). D uring this period of realimentation, food-restricted rats gain more weight per unit of food ingested than control animals (Boyle, Storlien, & Keesey, 1978). This increase in the efficiency of food utilization has obvious survival value for organisms during periods of food deprivation. A reduction in 0, consumption has also been demonstrated among dieting humans. A group of obese adults placed on a restricted diet (220 kcal/day) for 15

454

M. E. Smith and W J. Fremouw

days evidenced a 12% to 17% decrease in energy expenditure as measured by 0, consumption (Apfelbaum, Bostsarron, & Lacatis, 1971). Similarly, a 6-week reduction in food intake by 1,000 kcal/day in nine adults showed an average decline in sedentary energy expenditure by 12% (Webb & Abrams, 1983). This energysaving decrease in metabolic rate during food restriction makes dieting a very slow and difficult process for obese persons. Thus, dieting itself may be a critical factor in maintaining the obese state. To make matters worse, the reduction in energy expenditure may become more pronounced with each weight loss attempt. Garrow (1974) found that with longer periods of food restriction, the recovery of metabolic rate to baseline values took longer, and the metabolic rate declined more rapidly with repeated dieting than it did initially. It appears as if the body adapts to the previous episodes of food deprivation by becoming more efficient at minimizing energy expenditure, requiring the dieter to consume fewer and fewer calories to lose the same amount of weight. Concomitant with this restriction of food intake is a chronic hunger and a compelling drive to eat. When an individual develops a restrained eating pattern, he/she becomes extremely likely to binge. Pyle, Mitchell, and Eckert (1981) found that overeating began after a period of dieting in 30 out of 34 patients. Similarly, Hawkins and Clement (1980) found that degree of dietary restraint was significantly correlated with severity of binge eating. Ruderman and Wilson (1979) and Wardle (1980) found a similar relationship between dietary restraint and bingeing. Restrained eaters thus appear to be highly susceptible to bouts of overeating, repeatedly bringing their diets to an abrupt end. Dieting has long been associated with adverse emotional effects, including depression, anxiety, and irritability. In the general obese population, such responses occur in as many as half of all persons on reducing diets and are more common among persons with childhood-onset obesity and among the severely obese (Stunkard & Rush, 1974). Halmi, Stunkard, and Mason (1980) found that 41% of severely obese patients experienced moderate-to-severe depression, 53 % experienced moderate-to-severe anxiety, and 64% experienced moderate-to-severe irritability while dieting. Only a minority of these patients did not experience negative responses to weight loss attempts. The adverse reactions to dieting may become especially pronounced for those who eat to counteract loneliness, anxiety, or anger. In fact, negative emotional responses to dieting often play a key role in disinhibiting a person’s dietary restraint and facilitating an eating binge. Laboratory studies have demonstrated that obese individuals are more likely to overeat when aroused than are individuals of normal weight (Slochower, 1976; Slochower & Kaplan, 1980). These results have been extended to the natural environment, indicating that emotional eating occurs among obese individuals in response to distress aroused by naturally occurring events (Lowe & Fisher, 1983; Slochower, Kaplan, & Mann, 1981). The evidence indicates that dieting is associated with adverse biological and psychological reactions which predispose restrained eaters to overeat. Ironically, this fact suggests that the reducing diet itself, so frequently utilized by overweight persons, may be a critical factor in perpetuating their obese state. Obesity is maintained when calorie intake is equivalent to calorie expenditure at an elevated level of body fat. One way to tip the balance is to decrease the caloric intake. However, as mentioned, the slowdown of metabolism and the

Obesity

455

physical and emotional effects that lead to overeating make significant weight loss difficult. An alternative is to modify the other end of the equation by increasing calorie expenditure through physical activity. Numerous reports have shown that exercise increases calorie expenditure and facilitates weight loss in obese (e.g., Gwinup, 1975; Leon, Conrad, Hunninghake, & Serfan, 1979). Unfortunately, sedentariness is often associated with obesity (Stern, 1984). Excessive weight makes exercise more difficult and, as a result, less enjoyable than does normal weight. Since inactivity itself minimizes energy expenditure, a vicious cycle develops in which obesity produces inactivity which in turn enhances obesity. In conclusion, an overaccumulation of fat in the body creates a physiological state that is highly resistant to weight change. Once obesity has developed, a number of biological, psychological, and behavioral factors, including body chemistry, size and number of fat cells, metabolic activity, adverse emotional reactions, and sedentariness, all contribute to its maintenance. DISCOURAGING

RESULTS OF WEIGHT

LOSS STUDIES

Despite the variety of factors that have been found to produce and maintain obesity, it is still most commonly believed that obesity results from a period of overeating. However, whether or not obesity is caused by an increase in caloric intake, it can certainly be maintained without overeating (Wooley & Wooley, 1984). In fact, obese on the average do not eat any more than persons of normal weight (Garrow, 1974). Despite this finding, one of the most popular weight reduction techniques is behavior modification, which is based on the notion that eating patterns are maladaptive and need to be normalized. However, behavior modification has often yielded discouraging results. Although the majority of people can lose weight initially utilizing behavior modification techniques, very few can keep their weight off. Stunkard and Penick (1979) reviewed the results of follow-up studies and concluded that clinically important weight losses attained by behavioral treatments were rare, and those that occurred were not well maintained. In an attempt to prevent relapse and promote the maintenance of weight loss following the completion of treatment, booster sessions were provided in a number of studies. Results indicated that individuals participating in booster sessions initially achieved significantly greater weight losses than did those who did not attend these sessions. However, by the end of a l-year follow-up, these differences had disappeared (Hall, Bass, & Monroe, 1978; Kingsley & Wilson, 1977). Other studies have also failed to produce more enduring weight loss as a result of booster sessions or long-term contact (Ashby & Wilson, 1977; Beneke & Paulsen, 1979). A recent development in the treatment of obesity is the use of very-low-calorie diets. These diets can produce large weight losses, averaging 20 kg in 12 weeks (Wadden, Stunkard, & Brownell, 1983). Although early use of liquid protein diets was associated with numerous deaths (e.g., Sours, Frattali, Brand, Feldman, Forbes, Swanson, & Paris, 1981), the addition of a high-quality protein appears to make the diet safe if it is limited to 3 months or less. Despite this fairly safe and effective treatment for obesity, studies have reported that, as with behavior modification techniques, the weight losses achieved with very-low-calorie diets have been poorly maintained (Wadden, Stunkard, & Brownell, 1983). Although it has been suggested that the relinquishment of these weight loss techniques may con-

456

M. E. Smith and Vt?J. Fremouw

tribute to the regaining of weight, the specific variables predictive of relapse remain unclear (Abramson, 1982). Severely obese persons are likely to suffer medical complications as a result of their extreme fatness (Stunkard, 1984). Therefore, a number of surgical techniques, such as jejunoileal and gastric bypass, have been developed in an effort to treat this population. However, the surgical treatments themselves have caused severe medical problems and even death (see Symposium, 1980). A promising treatment of severe obesity is the implantation of a plastic bubble into the stomach. This bubble has the effect of producing a feeling of satiety and decreasing hunger between meals. One study showed that 100 morbidly obese patients had a mean weight loss of 76.5 lbs over a lo-month continuous treatment period (Garren, Garren, Garren, & Giordano, 1985). Although longer follow-up periods are needed to reveal whether the weight losses will be maintained, the gastric bubble appears to be a promising treatment for those persons suffering from morbid obesity. SHOULD

OBESITY

BE TREATED

AT ALL?

Despite the multitudinous attempts to discover a successful treatment for weight loss, the limited follow-up literature indicates that the weight losses are poorly maintained. As a result of these discouraging findings, Wooley and Wooley (1984) raise an important question, “Should obesity be treated at all?” Do the modest benefits of temporary weight loss outweigh the negative effects of repeated dieting and relapse? One report discovered that repeated dieting was a cause of atherosclerosis, leading to heart attacks and strokes (Division of Chronic Diseases, 1966, p. 40). In an important study of an Italian American community (Stout, Morrow, Brandt, & Wolf, 1964), a high incidence of obesity was associated with levels of heart disease and diabetes below the average for slender Americans. In this community, the majority of the people were obese as a result of an abundant consumption of calories, including high-fat foods and wine. Obesity was socially acceptable and the people were happy, supportive, and trusting. This study suggests that the strain of being fat and suffering persecution in a society that condemns fat people may contribute to the medical and psychological problems associated with obesity (Allon, 1982). Although overweight is generally considered to be a health risk, several studies suggest that becoming thinner does not necessarily make one healthier. Keys (1980) reviewed 13 prospective studies on obesity and mortality and concluded that weight increases the risk of mortality among women only at the extremes of the weight continuum, but has no effect on health in the middle 80 % . A second study found no relationship between fatness and mortality for women in the middle 60% of the weight range (Sorlie, Gordon, & Kannel, 1980). Nevertheless, we cannot conclude that obesity is risk-free. Many studies have demonstrated a link between severe obesity and disease. However, this relationship is not evidence of causation, but may be the result of a third factor. Frequent weight fluctuations that occur with dieting and relapse may be the actual cause of a disease. The stress of the stigma of being overweight may also contribute to the development of medical problems. Researchers have placed an emphasis on discovering effective weight loss techniques but have expended little energy on studying the physical and psychological

Obesity

457

effects of society’s negative attitudes towards fatness. The continuing efforts to eliminate obesity may actually be perpetuating people’s obsessions with the need to be thin. Perhaps a more worthwhile effort, especially for those obese who repeatedly fail with weight loss attempts, would be to help these individuals develop a healthy lifestyle and a greater self-concept independent of weight loss. As more overweight people learn to feel happy, attractive, and self-confident, less emphasis will be placed on the importance of being thin, and the prejudicial attitudes towards obesity in our society may diminish. OPTIMISM

IN THE WEIGHT

LOSS LITERATURE

Thus far, a pessimistic picture has been painted regarding the weight loss literature. The numerous incidences of weight loss failures have created a near-hopeless attitude among researchers and clinicians alike. Unfortunately, this attitude is defeating since it maintains the focus of attention on the dieting failures. A further examination of the literature shows that many successful weight loss attempts with long-term maintenance exist. Strain, Strain, Zumoff, and Knittle (1984) utilized a comprehensive psychosocial approach to treat 44 obese patients who were 49% to 332% above normal weight. The patients were classified according to fat cell 7 with predominant fat cell hypertrophy, 18 with predominant morphometrics: hyperplasia, and 19 with mixed fat cells. Treatment included psychological support and lifestyle alteration by nutrition education and behavior modification. Forty-five percent of the patients lost 18 to 52 kg and maintained the loss for 1 year. The success rate did not differ significantly for fat cell morphometrics. These results contradict earlier findings which suggest that patients with fat cell hypertrophy may be more successful in maintaining a weight change than those with hyperplasia (Bjorntorp et al., 1975). One factor typically not taken into consideration when reviewing the obesity treatment literature is that the obese subjects are self-selected, having made numerous unsuccessful attempts at weight loss and, as a last resort, actively seek professional help. By virtue of their repeated dieting failures, these persons have a for the majority of treatment failures in the poor prognosis, thus accounting weight loss literature. The use of this unrepresentative group of subjects in treatment studies creates a success rate that may be much lower than would be found in the general population. In fact, interviews with nontherapeutic populations have revealed that long-term self-cure of obesity is a relatively common event. Schacter (1982) interviewed 40 people with a history of obesity who had actively attempted to lose weight and found that 62.5% had lost substantial amounts of weight and were no longer fat. Sixty-seven percent of the men and 58% of the women were, on the average, 39.1 and 29.0 Ibs lighter after 13.4 and 8.3 years, respectively. Those subjects exceeding 30% overweight and averaging 56.1% overweight were, on the average, 46.7 Ibs lighter after 8.6 years, and 63.6 % were classified as “cured.” To determine the weight loss strategies utilized by individuals who have been highly successful in their efforts, Colvin and Olson (1983) performed a descriptive analysis of people who had lost at least 20% of their body weight and had maintained that loss for at least 2 years. The 13 male and 41 female subjects had lost an average of 76.2 and 53.2 lbs and had maintained the losses for an average of 5.8 and 6.0 years, respectively. The principal strategies used by the subjects to

458

M. E. Smith and M/: J. Fremouw

achieve and maintain their weight losses were vigorous exercise, better nutrition, and self-monitoring of weight. In addition, many of the women who had been housewives sought business or professional jobs and became more involved in other activities outside of the home. Although an emphasis has often been placed on the numerous weight loss failures in the obesity literature, the aforementioned studies demonstrate that successes do occur. The innovative studies by Schacter (1982) and Colvin and Olson (1983) suggest that the success rate for significant weight loss and maintenance is probably far higher in the general population than is indicated in the literature. This raises the important question of why some individuals are more successful at weight loss than others in this heterogeneous population. Rather than continue to indiscriminately apply behavioral or other weight loss strategies to all obese people, researchers should begin attempting to identify those factors which differentiate the weight loss successes and failures. For those individuals who are identified as having a high probability of failure, it may be more beneficial to their well-being to learn to live with their obese state, rather than continue to fail at dieting. FACTORS PREDICTING

SUCCESSFUL

WEIGHT

LOSS

In reviewing the obesity literature, a number of variables emerge which seem to be predictive of successful weight loss. In fact, the single most effective predictor of weight loss may be the rate of one’s metabolism. Garrow and his colleagues (Garrow, Durrant, Mann, Stalley, & Warwick, 1978) studied 37 obese women on a metabolic ward who were placed on an 800 kcal/day diet for 3 weeks. The single best predictor of weight loss under these strictly controlled conditions was the patient’s resting metabolic rate. In another study (Ashwell, Priest, Bondoux, & Garrow, 1975), obese subjects who believed they could lose weight on a negative energy balance were compared to a group who were particularly resistant to further weight reduction. After a 3week period on a 1,500 kcal/day diet, eight “good losers” (weight loss > 1.5 kg) from the first group and seven “poor losers” (weight loss < 1.5 kg) from the second group were identified. Other than average weight loss, the only significant difference between the good losers and poor losers was their resting metabolic rate. There were no differences with respect to age, relative weight, body fat, or adipose tissue cellularity. It appears that many obese have a lowered metabolic rate that makes a negative energy balance virtually impossible to achieve. Thus, regardless of how the obese state was attained, it can be maintained by the slowed metabolic rate alone. Although various drugs have been found to elevate metabolic rate and act as slimming agents in obese laboratory animals (e.g., Arch, DPhil, ,& Ainsworth, 1983; Yen, 1984), none, as yet, have proven to be safe and effective in humans. Until such a drug is discovered, obese persons are left with only “natural” methods by which to elevate their metabolic rate. The best method for facilitating weight loss by increasing metabolism is vigorous and consistent exercise. In fact, strict adherence to an exercise program may be another factor which is predictive of successful weight loss and maintenance. It has been well documented that caloric restriction produces 15 % to 30 % decreases in basal metabolic rate in obese and normal weight persons (e.g., Garrow, 1974).

Obesity

459

However, there is evidence to suggest that exercise counteracts this energy-saving slowdown during dieting by increasing metabolism to predieting levels (Schultz, Bernauer, Mole, Superko, & Stern, 1980). This effect of exercise on metabolism may even last for several hours after the physical activity is completed (Bradfield, Curtis, & Margen, 1968). Exercise also exerts its effects on metabolism by altering body composition. Dieters typically lose muscle tissue as well as fat when severely restricting their food intake. However, consistent exercise in addition to dieting will increase fat loss while maintaining lean tissue (Zuti & Golding, 1976). Since the contribution of fat-free mass to metabolic rate is 3 to 5 times greater per kg of body weight than that of fat (Bernstein et al., 1983), dieters can maximize their metabolic rate by maintaining or even gaining muscle tissue through physical activity. Furthermore, exercise does not increase hunger, as is often believed, and actually may decrease one’s appetite (Durrant, Royston, & Wloch, 1982). Exercise produces many positive effects and accelerates weight loss through a number of mechanisms. Obese persons who are motivated to adhere to a strenuous exercise program for an indefinite period of time may be the most successful in maintaining a clinically important weight loss. Present activity level and history of exercise may be the best predictors of those individuals who are likely to remain seriously involved in an exercise program and, as a result, maintain a significantly reduced weight. In addition to a relatively high basal metabolic rate and strict adherence to an exercise program, a third predictor of successful weight loss may be a very minimal history of repeated dieting attempts. Miller and Parsonage (1975) found that 29 women who claimed they could not lose weight and, in fact, maintained their weight on a 1,500 kcal/day diet over a 3-week period were characterized by a long previous history of dieting and a low metabolic rate. Obese patients who have a long history of dieting failures have a poor prognosis, making them unlikely candidates for future success. A fourth factor that may be predictive of an individual’s ability to lose weight is his/her developmental history. There is increasing evidence that obesity in humans may have a genetic component, though it is difficult to determine whether rapid weight gain in infancy is a result of heredity or environmental influences. One study demonstrated that normal-weight children of obese parents have a lower metabolic rate than children of nonobese parents (Griffiths & Payne, 1976). This may be a predisposing variable in the development of obesity among some children. Regardless of the cause of obesity, 80 % of obese children become obese adults (Abraham & Nordsieck, 1960). In fact, if obese children have not reduced by the end of adolescence, the odds against them becoming normal-weight adults are 28 to 1 (Stunkard & Burt, 1967). Perhaps the best defense against obesity, therefore, is prevention prior to the development of abnormal cellular and metabolic factors that predispose to this problem (Knittle, 1975). Interventions beginning at infancy and continuing through the “critical period” of fat cell development may help prevent the expression of these influences. Future research employing early interventions and follow-up into adulthood may provide significant insight into the prevention of obesity. Persons who remain in the normal weight range through adolescence but develop obesity as adults have a greater chance of losing that weight (Colvin & Olson, 1983). Adult-onset obesity may be a result of a lifestyle change, such as a decrease

460

M. E. Smith and W J. Fremouw

in activity level or a period of overeating. Given the previous history of appropriate eating habits and activity level, it is relatively easy to re-establish these behaviors to produce weight loss. Sims, Goldman, Gluck, Horton, Kelleher, and Rowe (1968) studied normal-weight subjects who ate an 8,000 kcal/day diet and gained an average of 25 % of their body weight. However, when the subjects were allowed to self-select their own diets, they all returned quickly and effortlessly to their previous weights. Thus, early-onset obesity, which may be indicative of a genetic influence, is much more resistant to change than is obesity acquired during adulthood. Consequently, clinicians should obtain a thorough weight history from their obese clients to determine age of onset and possible precipitating variables. The clinician can then decide whether to treat the obese state, or perhaps adopt a more realistic, therapeutic approach to dealing with the client’s body dissatisfaction. A final variable influencing weight loss is the nutritional makeup and caloric content of a diet. Although many factors contribute to obesity, numerous cases are ultimately due to an excessive caloric intake relative to the body’s energy requirements (Rodin, 1982). The most common strategy for losing weight is to reverse this process by restricting one’s food intake to produce a negative energy balance. Although this seems like a fairly simple task, the multitude of different diets which claim to produce rapid and effortless weight loss may only produce confusion and misconceptions about dieting. While most diets restrict calorie intake, all calories are not equal in terms of their uptake and usage by the body Diets consisting of various combinations of proteins, carbohydrates, and fats have differing physiological effects and, thus, may be differentially maintained. There is evidence to suggest that, through the involvement of brain serotonin, humans regulate the quantities of carbohydrates they consume (Wurtman & Wurtman, 1982183). When obese persons are placed on low-carbohydrate diets, they become carbohydrate-deprived and develop a craving for “starchy” foods. This process could contribute to the carbohydrate bingeing which is common among dieters. The obvious way to combat this problem is to increase the proportion of carbohydrates while decreasing the proportion of highly-caloric fats in the diet, thus minimizing the chances of relapse. While a low-carbohydrate diet may contribute to the maintenance of obesity by eliciting dietary relapse, a high-fat diet may promote obesity by improving the efficiency of food utilization. Laboratory rats fed a high-fat diet stored a greater proportion of their energy intake and gained more weight than rats fed a low-fat isocaloric diet. This has been attributed to the lower energy requirement of converting dietary fat to body fat (Wood & Reid, 1975). High-fat and low-fat diets have also produced differing effects in humans. Duncan, Bacon, and Weinsier (1983) compared the effects of a high-energydensity diet (high fat, low bulk) and a low-energy-density diet (low fat, high bulk) on satiety, energy intake, and eating time. Satiety was reached on the low-fat diet at a mean caloric intake one-half that of the high-fat diet. Eating time was 33 % longer on the diet low in energy density. A calorically-restricted diet that is low in fat and high in fiber-containing complex carbohydrates thus appears to enhance weight loss by minimizing the “carbohydrate craving,” decreasing the proportion of calories stored as fat, and accelerating the time to satiety on relatively low-calorie foods. In addition, a lowenergy-density diet may decrease the hunger and frustration and, most importantly, prevent the relapse that is so common in obese dieters.

461

ObesiCy

A REALISTIC

APPROACH TO TREATING

OBESITY

Obesity is a complex disorder that has been associated with serious pathological and psychological consequences. Genetic, biological, behavioral, and environmental factors appear to play interdependent roles in its development and maintenance. Although the remedy for obesity appears to be so simple, the treatment literature demonstrates that obesity is exceedingly recalcitrant. This has yielded a growing pessimism among researchers in the field (Wooley & Wooley, 1984). However, it is unfair to cease all efforts to help the millions of people who are overweight. A closer look at the literature proves that numerous people who had once been obese have successfully lost their excess weight and are maintaining a slimmer body (Colvin & Olson, 1983). Rather than continue to indiscriminately apply weight loss techniques to the obese, researchers need to examine the characteristics of these individuals who have successfully managed their weight problem. A number of factors that are predictive of weight loss and maintenance have been mentioned. A relatively high basal metabolic rate and thermogenic response, adherence to an exercise program and a low-fat, high-carbohydrate diet, obesity onset during adulthood, and a minimal history of previous dieting attempts are variables that have proven to maximize an individual’s potential for permanent weight loss. The most common approach to treating obesity has been to modify patients’ maladaptive eating patterns and caloric intakes. However, all obese bring to treatment different genetic, biological, and developmental backgrounds and, consequently, different probabilities for permanently maintaining a reduced weight. A more realistic approach to treating obesity would be to thoroughly assess each individual to determine his or her previous weight, exercise, and diet history; present lifestyle; and, if possible, metabolic rate. Based on this information, the clinician and patient can make an educated decision about the individual’s probability of success. If a favorable prognosis is indicated (e.g., adult-onset obesity that was precipitated by a recent change in lifestyle), the clinician can apply behavioral strategies presently utilized for treating obesity. In addition, the clinician can educate the patient on the importance of consistent exercise and adherence to a low-fat, high-bulk diet, while emphasizing the necessity of permanently adopting these behaviors to perpetuate the weight loss. On the other hand, patients with a poor prognosis (e.g., child-onset obesity with a long previous history of dieting failures) should be treated more realistically. These patients need to learn that their genetic, biological, and/or developmental makeup contribute to a state of obesity that is highly resistant to change. It should be pointed out, though these patients may already realize, that repeated dieting failures may produce negative psychological consequences, such as feelings of depression, anxiety, and a preoccupation with food (Halmi, Stunkard, & Mason, 1980). In addition, the strain of numerous dieting attempts, rather than the obesity itself, may contribute to the development or exacerbation of medical problems. After providing this information however, a patient who still wishes to attempt weight loss should not be denied treatment. The emphasis in treatment, though, should be somewhat different than for patients with a favorable prognosis. Individuals with a lengthy history of obesity have undoubtedly endured the prejudice and discrimination so common in our present culture. Clinicians need to provide supportive therapy for these individuals, while helping them develop a healthier attitude regarding their body-image

462

M. E. Smith and W J. Fremouw

and self-worth. This may be accomplished by encouraging the patient to maintain hobbies, activities outside of the a healthy lifestyle that includes friendships, home, consistent exercise, and a healthy diet, while de-emphasizing weight loss as the primary goal. As more people learn to accept their obese state, their changing self-image will help reshape the attitudes of society, and our obsession with weight control and the stigma of obesity may eventually be eliminated. REFERENCES Abraham, S., & Nordsieck, M. (1960). Relationship of excess weight in children and adults. Public Health Reports, 75, 263-273. Abramson, E. E. (1982). Behavioral approaches to the treatment of obesity. In B. B. Wolman (Ed.), Psychologiml aspects ofobesity: A handbook (pp. 207-224). New York: Van Nostrand Reinhold. Allon, N. (1982). The stigma of overweight in everyday life. In B. B. Wolman (Ed.), Psychological aspects of obesity: A handbook (pp. 130-174). N ew York: Van Nostrand Reinhold. Apfelbaum, M., Bostsarron, J., & Lacatis, D. (1971). Effect of caloric restriction and excessive caloric intake on energy expenditure. Am&m Journal ofClinical Nutrition, 24, 1405-1409. Arch, J. R. S., DPhil, M. A., & Ainsworth, A. T. (1983). Th ermogenic and antiobesity activity of a novel B-adrenoceptor agonist (BRL 26830A) in mice and rats. AmericanJournal of Clinical Nutrition, 38, 549-558. Ashby, W. A., & Wilson, G. T. (1977). Behavior therapy for obesity: Booster sessions and long-term maintenance of weight loss. Behaviour Research and Therapy, 15, 45 l-463. Ashwell, M., Priest, P., Bondoux, M., & Garrow, J. S. (1975). Resistance to slimming: Adipose tissue cellularity studies. Proceedingsofthe Nutrition Society, 34, 85A-86A. Beneke, W. N., & Paulsen, B. K. (1979). Long-term efficacy of a behavior modification weight loss program: A comparison of two follow-up maintenance weight loss strategies. Behavior Therapy, 10, 8-13. Bernstein, R. S., Thornton, J. C., Yang, M. U., Wang, J., Redmond, A. M., Pierson, R. N., PiSunyer, F. X., & Van Itallie, T. B. (1983). Prediction of the resting metabolic rate in obese patients. AmericanJournal ofclintial Nutrition, 37, 595-602. Bjiirntorp, P., Carlgren, G., Isaksson, B., Krotkiewski, M., Larsson, B., & Sjostrom, L. (1975). Effect of an energy-reduced dietary regimen in relation to adipose tissue cellularity in obese women. AmericanJournal ojClinical Nutrition, 28, 445-452. Bjorntorp, P., & Sjijstriim, L. (1971). Number and size of adipose tissue fat cells in relation to metabolism in human obesity. Metabolism, 20, 703-713. Boyle, P. C., Storlien, L. H., Harper, A. E., & Keesey, R. E. (1981). Oxygen consumption and locomotor activity during restricted feeding and realimentation. Amxr&znJacrwl oj PbGlogy, 241, R392-R397. Boyle, P. C., Storlien, L. H., & Keesey, R. E. (1978).1 ncreased efficiency of food utilization following weight loss. PhystiloQ and Behavtor, 21, 261-264. Bradfield, R. B., Curtis, D. E., & Margen, S. (1968).Effect of activity on caloric response of obese women. AmericanJournal ofClinicalNutrition, 21, 1208-1210. Bullen, B. A., Reed, R. B., & Mayer, J. (1964). Physical activity of obese and non-obese adolescent girls appraised by motion picture sampling. AmericanJournal ofClinicalNutrition, 4, 21 l-233. Chirico, A. M., & Stunkard, A. J. (1960). Physical activity and human obesity. New EnglandJournal ofMedicine, 263, 935-940. Colvin, R. H., & Olson, S. B. (1983). A descriptive analysis of men and women who have lost significant weight and are highly successful at maintaining the loss. Addictive Behaviors, 8, 287-295. Division of Chronic Diseases, Heart Disease Control Program. (1966). Obesity and health (PHS Publication No. 1485). Washington, DC: U.S. Government Printing Office. Duncan, K. H., Bacon, J. A., & Weinsier, R. L. (1983). The effects of high and low energy density diets on satiety, energy intake, and eating time of obese and nonobese subjects. AmericanJournal of Clinical Nutrition, 37, 763-767. Durrant, M. L., Royston, J. P., & Wloch, R. T. (1982). Effect of exercise on energy intake and eating patterns in lean and obese humans. PhysioloQ and Behavior, 29, 449-454. Faust, I. M., Johnson, P. R., Stern, J. S., & Hirsch, J. (1978). Diet-induced adipocyte number increase in adult rats: A new model of obesity. AmericanJournal of Physiology, 235, E279-E286.

Obesity

463

Foch, T. T., & McClearn, G. E. (1980). G enetics, body weight, and obesity. In A. J. Stunkard (Ed.), Obesity (pp. 48-71). Philadelphia: W. B. Saunders. Garren, L., Garren, M., Garren, R., & Giordano, F. (1985). Gastric balloon implantation for weight loss in the morbidly obese. American Journal of Gastroenterolo~, 80, 860. Garrow, J. (1974). Eneru balarue andobesity in man. New York: American Elsevier. Garrow, J. S., Durrant, M. L., Mann, S., Stalley, S. F., & Warwick. P. M. (1978). Factors determining weight loss in obese patients in a metabolic ward. InternationalJournal of Obesi~, 2, 441-447. Gotto, A. M., Foreyt,aJ. P., & Scott, L. W. (1976). Cardiovascular risk parameters. In B. J. Williams, S. Martin, &J. P. Foreyt (Eds.), Obesity: Behavioral approaches lo dietary management (pp. 109-120). New York: Brunner/Mazel. Griffiths, M., & Payne, P. R. (1976). Energy expenditure in small children of obese and non-obese parents. Nature, 260, 698-700. Gwinup, G. (1975). Effects of exercise alone on the weight of obese women. Archives of Internal Medicine, 135, 676-680. Hall, S. M., Bass, A., & Monroe, J. (1978). Continued contact and monitoring as follow-up strategies: A long-term study of obesity. Addictive Behaviors, 3, 139-147. Halmi, K. A., Stunkard, A. J., & Mason, E. E. (1980). Emotional responses to weight reduction by three methods: gastric bypass, jejunoileal bypass, diet. American journal of Clinical Nutrition, 33, 446-451. Hawkins, R. C., & Clement, P. E (1980). D evelopment and construct validation of a self-report measure of binge eating tendencies. Addtitive Behaviors, 5, 219-226. Hirsch, J., & Knittle, J. L. (1970). Cellularity of obese and nonobese human adipose tissue. Federation Proceedings, 29, 15 16- 152 1, Howard, B. V., Klimes, I., Vasquez, B., Brady, D., Nagulesparan, M., & Unger, R. H. (1984). The antilypolytic action of insulin in obese subjects with resistance to its glucoregulatory action. Journal of Clinical Endocrinology and Metabolism, 58, 544-548. Jahr, H., Ratzmann, K. P., Beckert, R., Besch, W., & Hahn, H. J. (1983). Enhanced synthesis, storage, and secretion of insulin in pancreatic islets derived from obese individuals. Metabolism, 32, 1101-l 106. Johnson, W. G., & Wildman, H. E. (1983). Influence on external and covert food stimuli on insulin secretion in obese and normal persons. Behavioral Neuroscience, 97, 1025-1028. Jung, R. T., Shetty, P. S., &James, W. P. T. (1980). Nutritional effects on thyroid and catecholamine metabolism. ClinicalScience, 58, 183-191. Keys, A. (1980). Overweight, obesity, coronary heart disease, and mortality. Nutrition Review, 38, 297-307. Kingsley, R. G., & Wilson, G. T. (1977). A comparative investigation of long-term efficacy. Journal of Consulting and Clinical Psychology, 45, 288-298. Knittk J. L. (1975). Basic concepts in the control of childhood obesity. In M. Winick (Ed.), Childhood obesity (pp. 135-140). New York: John Wiley. Leon, A. S., Conrad, J., Hunninghake, D. B., & Serfan, R. (1979). Effects of a vigorous walking program on body composition and carbohydrate and lipid metabolism of obese young men. AmericanJournal ofClinical Nutritti, 32, 1776-1787. Lowe, M. R., & Fisher, E. B. (1983). Emotional reactivity, emotional eating, and obesity: A naturalistic study.Journalof Behavioral Medicine, 6, 135-149. Miller, D. S., & Parsonage, S. (1975). Resistance to slimming: Adaptation or illusion? Lancet,1, 773-775. Nisbett, R. E. (1972). Hunger, obesity, and the ventromedial hypothalamus. PsychaIog~aIReview, 79, 433-453. Palmblad, J., Levi, L, Burger, A., Melander, A., Westgren, U., von Schenck, H., & Skude, G. (1977). Effects of total energy withdrawal (fasting) on the levels of growth hormone, thyrotropin, cortisol, adrenaline, noradrenaline, T4, T3, and rT3 in healthy males. Anti Medtia Scandi&ica, 201, 15-22. Pyle, R. L., Mitchell, J. E., & Eckert, E. D. (1981). B u 1‘lmia: A report of 34 cases.Journal of Clinical Psychiatry, 42, 60-64. Rodin, J. (1981). Current status of the internal-external hypothesis for obesity: What went wrong? American Psychologist, 36, 361-372. Rodin, J. (1982). Obesity: Why the losing battle? In B. B. Wolman (Ed.), Psychological aspects of obesity: A handbook (pp. 30-87). N ew York: Van Nostrand Reinhold.

464

M.

E. Smith

and W J. Frernouw

Ruderman, A. J., & Wilson, G. T. (1979). Weight, restraint, cognitions, and counterregulation. Behauiour Research and Therapy, 17, 581-590. Salans, L. B., Knittle, J. L., & Hirsch, J. (1968). The role of adipose cell size and adipose tissue insulin sensitivity in the carbohydrate intolerance of human obesity. Journal ofClinical Znoestigation, 47, 153-165. Schacter, S. (1982). Recidivism and self-cure of smoking and obesity. American Psychologist, 37, 436-444. Schultz, C. K., Bernauer, E., Mole, P. A., Superko, H. R., & Stern, J. S. (1980). Effects of severe caloric restriction and moderate exercise on basal metabolic rate and hormonal status in adult humans. Federation Proceedings, 39, 783. Sclafani, A., & Springer, D. (1976). Dietary obesity in adult rats: Similarities to hypothalamic and human obesity syndromes. Physiology and Behaoior, 17, 461-471. Sims, E. A., Goldman, R. F., Gluck, C. M., Horton, E. S., Kelleher, P. C., & Rowe, D. W. (1968). Experimental obesity in man. ?iansactions oj the Association ofAmericanPhysicians, 81, 153- 170. Slochower, J. (1976). Emotional labeling and overeating in obese and normal-weight individuals. Psychosomatic Medicine, 38, 131-139. Slochower, J., & Kaplan, S. P. (1980). Anxiety, perceived control, and eating in obese and normalweight persons. Appetite, 1, 75-83. Slochower, J., Kaplan, S. P., & Mann, L. (1981). The effects of life stress and weight on mood and eating. Appetite, 2, 115-125. Sorlie, P., Gordon, T., & Kannel, W. B. (1980). Body build and mortality. Journal of the American Medical Association, 243, 1828-1831. Sours, H. E., Frattali, V. P., Brand, C. D., Feldman, R. A., Forbes, A. L., Swanson, R. C., & Paris, A. L. (1981). Sudden death associated with very low calorie weight reduction regimens. American Journal ofClinicalNutrition, 34, 453-461. Stern, J. S. (1984). Is obesity a disease of inactivity? In A. J. Stunkard & E. Stellar (Eds.), Eatinland its disorders (pp. 131-139). New York: Raven Press. Stout, C., Morrow, J., Brandt, E. N., & Wolf, S. (1964). U nusually low incidence of death from myocardial infarction: Study of an Italian American community in Pennsylvania. Journal of the American MedicalAssociation, 188, 845-849, or 121-125. Strain, G. W., Strain, J. J., Zumoff, B., & Knittle, J. (1984). Do fat cell morphometrics predict weight loss maintenance? International Journal of Obesity,8, 53-59. Stuart, R. B., & Davis, B. (1972). Slim chance in afat world: Behavioral control ojobesip. Champaign, IL: Research Press. Stunkard, A. J. (1975). From explanation to action in psychosomatic medicine: The case of obesity. Psychosomatic Medicine, 37, 195-236. Stunkard, A. J. (1984). The current status of treatment for obesity in adults. In A. J. Stunkard & E. Stellar (Eds.), Eating and its disorders (pp. 157-173). New York: Raven Press. Stunkard, A., & Burt, V. (1967). Obesity and the body image: II. Age at onset of disturbances in the body image. American Journal of Psychiatry, 123, 1443-1447. Stunkard, A. J., & Penick, S. B. (1979). Behavior modification in the treatment of obesity: The problem of maintaining weight loss. Archives ojGeneral Psychiatry, 36, 801-806. Stunkard, A. J., & Rush, J. (1974). Dieting and depression reexamined: A critical review of reports of untoward responses during weight reduction for obesity. Annals ofInternal Medicine, 81, 526-533. Stunkard, A. J,, Serensen, T. I. A., Hanis, C., Teasdale, T. W., Chakraborty, R., Schull, W. J., & Schulsinger, F. (1986). An adoption study of human obesity. New England Journal OfMedicine, 314, 193-198. Symposium. (1980). Surgical treatment of morbid obesity. American Journal of Clinical Nutrition, 33, 353-530. Van Itallie, T. B. (February, 1977). Diet related to killer diseases. II. Hearings before the Select Committee on Nutrition and Human Needs of the United States Senate, Ninety-Fifth Congress (First Session), Part 2, Obesity, p. 44. Van Itallie, T. B. (1979). Obesity: Adverse effects on health and longevity. American Journal of Clinical Nutrition, 32, 2723-2733. Van Itallie, T. B., & Campbell, R. B. (1972). Multidisciplinary approach to the problem of obesity. Journal ojthe Arm&an Dietetic Association, 61, 385-390. Wadden, T. A., Stunkard, A. J., & Brownell, K. D. (1983). Very 1ow calorie diets: Their efficacy, safety, and future. Annals ofInternal Medicine, 99, 675-684.

Obesig

465

Wardle, J, (1980). Dietary restraint and binge eating. BehaoiouralAnalysir andModifzk&n, 4, 201-209. Webb, P., & Abrams, T. (1983). Loss of fat stores and reduction in sedentary energy expenditure from undereating. Humnn Nutrition: Clinical Nutrition, 37C, 271-282. Wood, J. D., & Reid, J. T. (1975). The influence of dietary fat on fat metabolism and body fat deposition in meal-feeding and nibbling rats. British Journal ofNutrition, 34, 15-24. Wooley, S. C., & Wooley, 0. W. (1984). Should obesity be treated at all? In A. J. Stunkard & E. Stellar (Eds.), Eating and its disor&rs (pp. 185-192). New York: Raven Press. Wurtman, J. J., & Wurtman, R. J. (1982183). Studies on the appetite for carbohydrates in rats and humans. Journal ofPsychiatric Research, 17, 213-221. Yang, M. U., Barbosa-Saldivar, J. L., Pi-Sunyer, F. X., & Van Itallie, T. B. (1981). Metabolic effects of substituting carbohydrate for protein in a low-calorie diet: A prolonged study in obese patients. IntenmtimalJournal ofobesity, 5, 231-236. Yen, T. T. (1984). The antiobesity and metabolic activities of LY79771 in obese and normal mice. Intem&mal Journal ofObesity,8, 69-78. Zuti, W. B., & Golding, L. A. (1976). Comparing diet and exercise as weight reduction tools. Physician and Sportsmedicine,4, 49-53.