(PDF) Confronting the Failure of Behavioral and Dietary Treatments for Obesity

Clinical Psychology Rmew, Vol. 11, pp. 729-780, 1991

Copyright 0 1991 Pergamon Press plc

CONFRONTING THE FAILURE OF

BEHAVIORAL AND DIETARY

TREATMENTS FOR OBESITY

David M. Garner

Michigan State University

Susan C. Wooley

University of Cincinnati

ABSTRACT. This review questions the appropriateness of behavioral and dietar)r treat-

ments of obesity in light of overwhelming evidence that they are ineffective in producing

lasting weight loss. The stigmatization of obesity, the overstatement of health risks, and the

pervasive influence of the lucrative diet industry have maintained public demand for di-

etary treatment. However, decades of research on the biology of weight regulation make

clear the unlikelihood of success with dietary treatment, information which the health

professions have been slow to integrate. Recommendations are made for improving life-

style, health risk factors, body image, and the self-esteem of the obese without requim’ng

weight loss.

It has been over a decade since two major reviews questioned the effectiveness

and social appropriateness of behavioral treatments for obesity (Stunkard & Pen-

ick, 1979; Wooley, Wooley, & Dyrenforth, 1979b). Other papers and books have

since appeared challenging the basic precepts which underlie dietary treatments

for obesity (Bennett, 1984, 1987; Bennett 8c Gurin, 1982; Ernsberger 8c Haskew,

1987; Fitzgerald, 198 1; Foreyt, Goodrick, & Gotto, 1981; Krieshok & Karpowitz,

1988; Wooley & Wooley, 1982, 1984; Wooley, Wooley, & Dyrenforth, 1979a).

Their arguments, however, have not been embraced, accepted, or in many cases,

even addressed by the mainstream of behavioral scientists and health care pro-

Correspondence should be addressed to David M. Garner, Ph.D., Department of Psychia-

try, Michigan State University, B107 West Fee Hall, East Lansing, MI 48824.

729

730 D. M. Garner and S. C. Wooley

fessionals who treat obesity. It is still widely held within the health care profes-

sions that obesity confers significant health risks warranting weight reduction.

Weight loss as a means for achieving health and happiness is vigorously pro-

moted by the commercial weight loss industry, now a major economic force in

North America.

Behavioral or dietary treatments for mild and moderate obesity’ continue to

be advocated despite weak and often conflicting epidemiological data suggesting

that these levels of obesity are linked to significant health risks (cf. Ernsberger &

Haskew, 1987; Mann, 1974a, 1974b), and despite overwhelming evidence from

controlled studies that weight loss programs are ineffective in producing lasting

weight change (cf. Bennett, 1987; Stunkard & Penick, 1979). One can point to

behavioral programs for weight control recommended in the same publications

which document physiological resistances to weight change, seemingly without

recognition of the contradictions or problems involved in trying to override the

body’s biological regulatory mechanisms. Our failure to fully confront these is-

sues has meant that, despite new knowledge, there has been no fundamental

change in our practices. Old diets with new names, such as the “set point diet,”

seem almost to parody the efforts of scientists to understand the causes of obe-

sity and provide treatments consistent with this understanding.

Another expository review of obesity treatment studies is unnecessary since the

topic has been comprehensively reviewed elsewhere (Bennett, 1986; Brownell,

1982; Brownell & Wadden, 1986; Foreyt, 1977; Foreyt et al., 1981; Jeffery,

1987; Stunkard & Mahoney, 1976; Wilson & Bronwell, 1980). Instead, the pri-

mary aim of this paper is to provide an evaluative and integrative appraisal of

weight loss treatments within the context of what is known about (a) long-term

treatment efficacy, (b) the biology of weight regulation, (c) eating patterns of the

obese, (d) the genetic determinants of obesity, and (e) the health risks associated

with obesity. In view of this evidence, it will be argued that mental health pro-

fessionals should, under most circumstances, be advised uguinst the delivery of

dietary or behavioral treatments for mild or moderate obesity rather than pro-

posing more aggressive dietary approaches (Brownell & Jeffery, 1987). When

weight reduction is offered, consumers should be given complete information

about risks and probable outcome. Rather than expending further resources on

traditional treatments of obesity, health professionals should be encouraged to

further develop alternative approaches that more adequately address the physi-

‘There have been many attempts to define and classify obesity using either weight rela-

tive to norms, height to weight ratios, measures of body fat, or regional distribution of fat

(cf. Bjorntorp, 1987; Bray, 1978; NRC, 1989). Stunkard (1984) has proposed a simple

scheme of defining obesity relative to norms as mild (20%-40% overweight), moderate

(41%-100% overweight), or severe (more than 100% overweight). According to this deli-

nition, about 35% of women in this country are obese and of this group, 90.5% are

mildly, QLTO are moderately, and 0.5% severely obese (Stunkard, 1984). These definitions

of obesity are all arbitrary in the sense that they define the condition using cutoff points

along a normal distribution of body weight or fat, without reference to etiology or dis-

ease. Most of the behavioral and dietary research that will be summarized in this review

has been directed toward the mild and moderate groups. In the interest of avoiding te-

dium, the current review will not define the way that the term was used in each study

cited unless it has specific relevance to the interpretation of the results.

Failure of Obesity Treatment 731

cal, psychological, and social hazards associated with obesity without requiring

dieting or weight loss.

THE SOCIAL CONTEXT OF OBESITY TREATMENT

The enormity of the efforts directed toward eradicating obesity is perhaps best

illustrated in economic terms. According to a recent market analysis summarized

by Obesity and Health (“What’s Ahead?,” 1989), the 1988 cost of weight loss prod-

ucts and services in the United States alone was estimated at over $29 billion. To

put this figure in perspective, the Federal Government of the United States

spent a total of $31.9 billion in 1988 on education, training, employment, and

social services (Office of Management and Budget [OMB], 1990). According to

the weight loss industry report in 1988, $4.5 billion were spent in 1988 in hospi-

tal based clinics and weight loss programs, another $1.5 billion in the almost

13,000 nonhospital programs, and about the same amount on residential spas

offering weight loss programs. Americans additionally spent $8 billion on health

spas and exercise clubs, $382 million on 54 million diet books, $10 billion on

diet soft drinks, and billions more on low calorie foods and artificial sweeteners.

Surgery is not included in this analysis, but there are an estimated 30,000 stom-

ach redution and jaw wiring operations per year. Additionally, about 100,000

liposuction procedures were performed at a cost of $3,500 apiece. The weight

loss industry is a major economic force in this country, projected to reach over

$50 billion by 1995.

For several decades the fashion, entertainment, and publishing industries have

bombarded women with role models for physical attractiveness so gaunt as to

represent virtually no women in the actual population (Garner & Garfinkel,

1980; Garner, Rockert, Olmsted, Johnson, & Coscina, 1985). These representa-

tions imply that not only beauty but also success, personal happiness, and self-

worth can be achieved through slenderness. There seems little doubt that

cultural pressures for slimness have intensified in the past 30 years (Garner,

Garfinkel, Schwartz, & Thompson, 1980; Silverstein, Perdue, Peterson, Vogel, &

Fantini, 1986). Although the reasons for this are unclear, one argument holds

that as women have moved into previously male-dominated activities, the “tradi-

tional” female body shape has developed negative connotations while the mascu-

line shape has come to symbolize self-discipline and competency (Bennett &

Gurin, 1982; Wooley & Wooley, 1985). Indeed, Silverstein et al. (1986) found

that curvaceousness went out of style both in the 1920s and in the 1970s and

198Os, both periods of peak activity on the part of women to gain male preroga-

tives. Marketing geniuses, if not responsible for these trends, have certainly capi-

talized on them by promoting self-consciousness and personal discontent so that

consumers will believe that they require the remedies the advertisers offer

(Ewen, 1976; Wachtel, 1989).

The power of these influences is evidenced in studies showing that the major-

ity of adolescent and young adult women feel fat even when their weight falls

within the normal range (e.g., Dwyer, Feldman, & Mayer, 1967; Huenemann,

Shapiro, Hampton, 8c Mitchell, 1966; Klesges, 1983; Moses, Banilivy, & Lifshitz,

1989; Nylander, 1971; Wardle & Beales, 1986). This has led Rodin, Silberstein,

and Striegel-Moore (1985) to characterize the shape dissatisfaction endemic to

young women as “normative discontent.” Given these attitudes, it is not surpris-

73.2 D. M. Garner and S. C. Wooley

ing that about two out of every three high school girls report that they are try-

ing to lose weight (Rosen & Gross, 1987). Increasingly, there are reports

indicating that substantial numbers of young women use harmful weight control

behaviors, such as self-induced vomiting, with a subgroup of these manifesting

serious eating disorders (Crowther, Post, SC Zaynor, 1985; Killen et al., 1987;

Pyle, Halvorson, Neuman, & Mitchell, 1986). Recent studies indicate that feeling

fat and restricting food intake are not uncommon in schoolchildren 8-13 years

of age (Davies & Furnham, 1986; Maloney, McGuire, Daniels, & Specker, 1989;

Wardle 8c Beales, 1986). One of the more alarming manifestations of the fear of

obesity is a subgroup of children with short-stature syndrome and delayed pu-

berty caused by rigorous dieting due to fear of fatness (Puglifse, Lifshitz, Grad,

Fort, & Marks-Katz, 1983). The desperation connoted by these behaviors is eas-

ily overlooked in a cultural climate which champions thinness as an indisputable

virtue. Many of the behaviors used for diagnoses of anorexia nervosa and bu-

limia nervosa are culturally syntonic, considered neither uncommon nor abnor-

mal by the lay public (Huon, Brown, 8c Morris, 1988). Even anorexia nervosa

itself has developed a not altogether unfavorable connotation in our culture

(Branch & Eurman, 1980; Bruch, 1985; Garner et al., 1985; Wooley & Wooley,

1982).

The intensity of the prevailing cultural pressures for thinness and the psycho-

logical risks that they impart have particularly serious implications for those who

suffer from moderate to extreme obesity (Wooley et al., 1979a). Shape dissatis-

faction and attempts to restrict food intake are evident in all but a small minor-

ity of women who are statistically overweight (Davies & Furnham, 1986; Wardle

& Beales, 1986), and extreme body image disparagement has been recognized

for years as a grim consequence of obesity (Stunkard & Burt, 1967; Stunkard &

Mendelson, 1967; Wadden & Stunkard, 1985).

The social stigma against obesity is extraordinary in its magnitude and perva-

siveness. As Fitzgerald (1981) notes: “Public derision and condemnation of fat

people is one of the few remaining social prejudices . . . allowed against any

group based solely on appearance” (p. 223). It is well documented that obese

people are denied educational opportunities, jobs, promotions, and housing be-

cause of their weight (Bray, 1976; Canning & Mayer, 1966; Karris, 1977). The

affront to those who are obese goes beyond the almost uniform judgment that

they are unattractive (Furnham & Radley, 1989) and includes negative stereo-

types that begin early in childhood. The aversion to obesity is evident by kinder-

garten (Lerner, 1969; Lerner & Gelbert, 1969), and grade-school children

consistently associate larger body shapes with adjectives such as “stupid,” “dirty,”

“lazy, ” “sloppy,” “mean,” “ugly,” and “sad” (Maddox, Black, & Liederman, 1968;

Staffieri, 1967, 1972; see Wooley et al., 1979a for a review).

Harsh attitudes toward the obese depend on the assumption that they bring

their condition on themselves through lack of willpower and self-control (cf.

Harris & Smith, 1982; Maddox et al., 1968). In the face of the o~~erwhelming

social rejection, obese individuals may seek professional support; however, re-

search has shown that health professionals share in the culture’s perjorative view

of obesity and that this prejudice may influence their clinical judgement (Brot-

man, Stern, & Herzog, 1984; Maiman, Wang, Becker, Finlay, & Simonson, 1979;

Richardson, Goodman, Hastorf, & Dornbusch, 1961; Young & Powell, 1985). A

negative attitude toward obesity is suf~ciently ingrained in our social fabric that,

Failure of Obesity Treatment 733

in addition to social rewards for success, obesity treatment programs have at

times included social shaming procedures as a treatment principle. Many au-

thors have advocated a critical attitude toward obese patients (cf. Wooley &

Wooley, 1980). Confronted with evidence of consistent failure of behavioral

treatment programs - a failure seemingly understandable only as a conse-

quence of widespread patient noncompliance - several respected researchers

concluded that social pressure on obesity needed to be increased:

The ultimate social pressure treatment would be to increase the social sanctions

against obesity, so that being overweight would be a tremendously shameful thing.

In this manner, obesity would be under external control, as are other social behav-

iors for which society has learned that internal control is not enough for some, as in

the case of sexual or criminal acts. Obesity control would then be inculcated into

the normal socialization process for children. (Foreyt et al., 1981, p. 170)

This statement no doubt expressed for a generation of researchers the frustra-

tion of reported failure and needs to be understood not as the position of an

individual but as an illustration of the way in which ineffective treatment strate-

gies lead, as an almost inevitable consequence, to blaming the victim.

BEHAVIORAL AND DIETARY TREATMENT OF OBESITY

The Paradox of Dietary Treatment of Obesity

There are two indisputable facts regarding dietary treatment of obesity. The first

is that virtually all programs appear to be able to demonstrate moderate success

in promoting at least some short-term weight loss. The second is that there is

virtually no evidence that clinically significant weight loss can be maintained over

the long-term by the vast majority of people. Since health professionals and pro-

fessional societies recommend weight loss as the treatment of choice for the 23

million or so Americans judged to be overweight, the apparent inconsistency be-

tween the short- and long-term treatment findings needs to be illuminated.

Short-Term Follow-Up Studies

Behavioral weight control programs for obesity are often described as demon-

strating promising treatment effects that are well maintained during the first

year of follow-up (cf. Bennett, 1986; Brownell & Jeffery, 1987; Wadden 8~

Stunkard, 1989). In an analysis of the results from 105 behavioral studies, Ben-

nett (1986) reported a mean weight loss for the 6,121 participants of 5.38 kg

after an average of 13.37 weeks of treatment. The modest treatment effects were

maintained in the short-term with a mean weight loss of 5.11 kg recorded for

5,453 participants followed for an average of 35.5 weeks.

Although most of the behavioral treatment studies have involved oniy short-

term evaluation of effectiveness, follow-up duration has increased in recent

years. Brownell and Jeffery (1987) have reported that the average length of fol-

low-up for a sample of studies appearing in several major psychology journals

was 15.5 weeks in 1974, 30.3 weeks in 1978, 58.4 weeks in 1984, and 44 weeks

in 1986. The duration of treatments provided and the amount of weight loss

achieved has increased over the same period, although the number of pounds

lost per week has not changed dramatically (Brownell & Jeffery, 1987).

734 D. M. Garner and S. C. Wooley

There has been a move away from short-term, strictly “behavioral” programs

to greater emphasis on multicomponent interventions that incorporate exercise,

social influence, longer treatment duration, and continued therapeutic contact

after the end of formal treatment. These strategies have been found to promote

greater weight losses and improved maintenance during the first 18 months af-

ter treatment (Perri, McAdoo, McAllister, Lauer, & Yancey, 1986; Perri et al.,

1988; Perri, Nezu, Patti, & McCann, 1989), leading some authors to the conclu-

sion that obesity might be reconceptualized as a chronic condition “requiring

some form of continuous-care program long after completing an initial period

of treatment” (Perri et al., 1988, p. 533). However, over and over again the ini-

tial encouraging findings are eroded with time. Following up their initially im-

pressive treatment results, Perri et al. (1989), for example, state “After clients

conclude their active involvement in obesity treatment, they typically abandon

weight loss strategies and begin to regain weight” (p. 452).

The problem is a subtle one that occurs repeatedly; results are presented as

positive when, in fact, all indications are that the long-term projections are quite

poor. This matter of interpretation is an especially questionable convention since

there are consistent data on the pattern of weight gain that follows weight loss

achieved through a wide range of treatment strategies. To give a fairly typical

example, the findings of Craighead, Stunkard, and O’Brien (1981) are often

cited as one of the more successful behavioral programs in maintaining weight

loss (Figure 1). It is evident from Figure 1 that the active treatments led to statis-

tically significant weight loss and that there was a trend for the drug and com-

bined treatments to produce weight loss superior to the behavioral therapy

alone. At one year follow-up, however, the behavior therapy group showed the

least regain. In discussing these results, Stunkard (1984) states:

This most recent study provides grounds for optimism as to the future of behav-

ioral treatment of obesity . over the long run, behavior therapy clearly outper-

formed the most potent alternative treatment with which it has yet been compared.

(p. 1’35)

This interpretation does not reflect an appreciation of the apparent trajectory

of the posttreatment weight rebound for all treatment groups. The most parsi-

monious interpretation of these findings is that the participants are returning to

their pretreatment weight, and the graph is simply a snapshot of this process

one year after the end of treatment. It also fails to acknowledge that the trend

toward weight gain, together with similar findings from other studies, probably

represents a basic underlying mechanism unlikely to show a reversal or levelling

off if data were to be collected at subsequent follow-up points.

Brownell and Jeffery (1987) have similarly avoided the most obvious implica-

tion of these and comparable results, arguing that the negative findings may ac-

tually be positive since those who have regained most or all of their weight at

follow-up might have weighed even more had they not received treatment. To

give this speculation more credence than the alternative possibilities that obese

individuals would be at the same or lower weights if they had not received any

treatment goes beyond data on long-term weight fluctuations in the obese

(Williamson & Levy, 1988). Findings from another study by Brownell and col-

leagues (Brownell, Greenwood, Stellar, & Shrager, 1986), as well as others to be

Failure of Obesity Treatment 735

COMBINED

TREAWENT

PHARMAco-

THERAPY

BEHAVIOR

THERAPY

0 2 4 6 8 IO I2 14 16 18

L \ I

Treatment Follow-up

MONTHS

FIGURE 1. Weight Changes During 6-mo Treatment and 12-mo Follow-

Up. (Vertical lines represent 1 SEM. From “Behavior Therapy and Phar-

macotherapy for Obesity” by L. W. Craighead, A. J. Stunkard, and R. M.

O’Brien, 1981, Archives of General Psychiatry, 38, pp. 763-768. Copyright

1981 by the American Medical Association. Reprinted by permission.)

discussed later, support the hypothesis that dieting itself may lead to enhanced

metabolic efficiency (i.e., greater energy storage at a fixed energy inake) and a

possible tendency to maintain a higher body weight.

Brownell and Jeffery (1987) also assert that the failure to demonstrate success

in clinical samples does not obviate the possibility that weight loss may be a real-

istic goal for those who do not seek treatment. It is reasoned that treatment stud-

ies draw participants from clinical settings; these may be the most recalcitrant

individuals from the potential pool of candidates for weight loss. While this is

obviously a theoretical possibility and is supported by one study on a highly se-

lected sample (Schachter, 1982), it seems to stretch the weight loss litany to its

limits and leads to the curious interpretation that treatment is most appropriate

for those who do not seek professional help.

Against a tradition in science which assumes that there are no treatment ef-

fects until they are demonstrated, there is an unchallenged convention by which

weight loss interventions are presumed effective until there is explicit evidence

736 D. M. Garner and S. C. Wooley

to the contrary. The reality is that we do not have effective treatment to offer,

and we should be candid about this until there is reliable evidence to the con-

trary. To avoid confronting the failures of obesity treatment is to mislead a pub-

lic desperately waiting with cash in hand for an effective remedy.

Another criticism of behavioral and certain other treatments for obesity is that

the amount of weight loss achieved, while statistically significant, is generally too

small to be of practical consequence (Wing & Jeffery, 1979). According to

Brownell and Jeffery (1987), the mean weight loss for controlled behavioral tri-

als reported in 1984 was 15.4 lb, with an average of just over 13 weeks of treat-

ment; however, the initial mean weight of participants was 197 lb.

In answer to the rather modest weight losses achieved by most dietary ap-

proaches, it has been recommended that more aggressive methods be imple-

mented in order to achieve greater initial losses (Brownell & Jeffery, 1987).

These have included very low calorie diets (VLCD); longer treatments; and the

addition of exercise, financial contracts, relapse prevention, and social support

to behavioral regimens (Brownell & Jeffery, 1987; Brownell, Marlatt, Lichten-

stein, & Wilson, 1986). These proposals all appear to presume that main-

tenance of weight loss is a realistic expectation and/or that failure to maintain

weight loss does no harm. As will be more evident later, both of these assump-

tions are inconsistent with much of what we know.

Long- Term Folio w- Up Studies

In contrast to the body of literature indicating that both traditional and behav-

ioral treatments for obesity produce weight loss that is reasonably well main-

tained after one year, it is evident that weight is gradually regained over time,

with many individuals eventually weighing more than they did at the start of

treatment (Adams, Grady, Lund, Mukaida, & Wolk, 1983; Dubbert & Wilson,

1984; Kirschenbaum, Stalonas, Zastowny, & Tomarken, 1985; Murphy, Bruce, &

Williamson, 1985; Rosenthal, Allen, & Winter, 1980). This effect becomes more

conspicuous the longer that the follow-up is extended, and it is apparent that

most individuals will regain most or all of their weight after four or five years

(Bjorvell 8c Rossner, 1985; Graham, Taylor, Hovell, & Siegel, 1983; Jordan,

Canavan, & Steer, 1985; Kramer, Jeffery, Forster, & Snell, 1989; Murphy et al.,

1985; Stalonas, Perri, & Kerzner, 1984; Stunkard & Penick, 1979). For example,

in a 5-year follow-up, Stalonas et al. reported that the average participant had

gained 11.9 lb since the end of a behavioral program, making him or her 1.49 lb

heavier than when treatment began. Murphy et al. found that the average self

reported weight loss after four years for several different treatment conditions was

7.12 lb, but the average measured weight loss was actually about one pound. Jor-

dan et al. (1985) studied selected patients who had achieved at least a 15-lb

weight loss during treatment. They found that patients showed distinct patterns

of weight fluctuation, with only 12.2% remaining consistently below their post-

treatment weights for 5 years. The odds against maintaining long-term weight

loss are dramatically illustrated by Kramer et al. in a recent study of 114 men

and 38 women who had successfully completed a 15-week behavioral weight loss

program. They reported that less than 3% of the patients maintained their post-

treatment weight throughout the four yearly follow-up assessments. Monotonic

weight regain was the predominant pattern for the men, whereas the women

tended to lose and regain weight more often during the follow-up period.

Failure of Obesity Treatment 737

In a study that is interesting because it did not rely on a sample of patients

seeking weight loss treatment, Binnie (1977) identified and treated 43 individu-

als in a rural general practice who were above “ideal” weight.’ After 10 years,

only one patient had achieved ideal weight, and only two had achieved 80% of

their goal. These results are similar to other long-term studies indicating that

only a small minority of patients are able to achieve and maintain ideal weight

goals. Stunkard and Penick (1979) found that after 5 years, the majority of pa-

tients receiving both behavioral and traditional treatment regained most of the

weight originally lost.

The very few long-term studies reporting somewhat less dismal findings are

problematic because of possible bias in the sample of subjects studied at fol-

low-up (Graham et al., 1983; Grinker, Most, Hirsch, Borsdorf, & Wayler, 1985).

The most impressive results were those of Grinker et al., who reported that 55%

of subjects followed after a residential treatment program had maintained at

least a 5-kg weight loss; however, there was only a 38% response rate. Similarly,

Graham et al. targeted 62 of 138 initial participants in a weight loss program on

the basis of having telephone numbers and addresses available; it is unclear from

the report why such a high percentage was lost to follow-up

The effects of treatment do not stop with an initial weight loss or maintenance

period. Weight rebound seems to be almost as reliable a consequence of treat-

ment as initial loss. The pattern of weight gain recorded in extended follow-up

indicates that short-term results are frankly misleading indicators of long-term

outcome. Our tradition of reporting and interpreting data provides a model,

used in the promotion of virtually all weight loss programs and products, in

‘The terms “ideal” or “desirable” weight are typically derived from insurance company

actuarial tables to indicate weights at which insurance policy holders can expect greatest

longevity. They are widely used by health professionals and the lay public to characterize

the goal weight that one should try to achieve for greatest health. They have been criti-

cized on a number of technical grounds such as sampling, variability of methodologies

used to gather weight and mortality data, and the fact that they do not take into consid-

eration individual differences in lean body mass, skeletal size, and regional fat distribu-

tion (Harrison, 1985; Knapp, 1983). “Frame sizes” reported in the 1983 Metropolitan Life

Insurance height-weight tables were not derived from anthropometric measurements but

were based on arbitrary groupings of the data (Weigley, 1984). Perhaps the greatest con-

cern regarding “ideal” and “desirable” weights relates to the interpretation of the weight

table figures. They fail to take into consideration that body weight, like other physical

attributes, could be expected to vary naturally in the population (measures of dispersion

are not included in the weight tables used to recommend desirable weights). Diverse ge-

netic propensities within the population may mean that what is a healthy weight for a

population may not have any relevance to the individual. Moreover, there is little attempt

to actually inform individuals of the magnitude of risk associated with particular deviations

from specified weights. Results from Sorlie et al. (1980) indicate that for both men and

women within the middle three quintiles of the weight distribution, there is no relation-

ship between weight and mortality. For women of average height (5 ft 3 in. to 5 ft 6 in.)

the risk of death was virtually identical for those between 115 lb and 194 lb. While women

in the highest and lowest 20% of the weight distribution had a higher risk of death, this

was considerably lower than the mortality rate for thin and average weight men. Finally,

even though certain weights may be related to longevity in the insurance company sam-

ples, as will be discussed more fully later, it is mere speculation that changing one’s weight

category will actually alter longevity.

738 D. M. Garner and S. C. Wooley

which it is implied that treatments can be adequately evaluated by their immedi-

ate effects. However, if treatment studies are to be relevant, the maintenance of

clinically meaningful weight loss must be the agreed-upon standard.

One would expect that existing data would lead to unanimity in the research

community about the need for long-term evaluations in order to draw conclu-

sions about treatment efficacy. It is not that failures of dietary treatment are un-

known to researchers. Indeed, a number of well respected researchers have

based their repeated calls for long-term follow-up upon these observations

(Brownell et al., 1986; Foreyt et al., 1981; Stunkard, 1975; Wilson, 1978). Nev-

ertheless, many others have remained undaunted by the failure to demonstrate

long-term success and have argued not for the abandonment of dietary treat-

ment but instead have called for more “agressive approaches” to treatment such

as the very low calorie diet (VLCD; e.g., Brownell & Jeffery, 1987).

Very Low Calorie Diets

The very low calorie diet of 300-500 calories per day was enthusiastically re-

ceived because of its ability to produce large and rapid weight loss. In a compre-

hensive review, Wadden, Stunkard, and Brownell (1983) described the VLCD as

“the most important recent development in the medical treatment of obesity” (p.

675). More recently, Brownell and Jeffery (1987) suggested that the VLCD “may

be the treatment of choice for persons who are severely obese and who have had

difficulty losing sufficient weight on more moderate dietary regimens” (p. 363).

Initial trials of VLCDs combined with behavior therapy seemed to support the

initial fervor by achieving significant weight loss, reasonably well maintained at

one year follow-up (Wadden & Stunkard, 1986; Wadden et al., 1983). However,

as with most approaches, the initial optimism has been dampened by a sobering

series of long-term follow-up studies indicating that the pattern with the VLCD

is the same as with other dietary treatments.

In their initial report, Wadden and Stunkard (1986) found that the VLCD

combined with behavior therapy produced significant weight loss (mean = 19.2

kg) and was more effective than either the behavioral or VLCD therapy alone.

At the end of one year, the weight loss for the combined treatment was reason-

ably well maintained (12.9 kg), but after three years virtually all of the treatment

effects were reversed, particularly when results were corrected for the effects of

intervening weight loss efforts (Wadden, Stunkard, 8c Liebschutz, 1988). Failure

of this approach is even more evident in a follow-up of 497 patients receiving a

combination of a VLCD (Optifast) and behavior modification through a large

health maintenance organization (Hovel1 et al., 1988). Hovel1 and colleagues

found that 55% of the patients who started treatment dropped out before com-

pletion. While the remaining 45% lost a mean of 83.9% of their “excess weight,”

the four follow-up groups, illustrated in Figure 2, regained between 59% and

82% of their initial excess weight by 30 months from the start of treatment. Pa-

tients began treatment, on average, about 50% over “ideal weight” defined by

weight norms.

Although there is an upward trajectory for all groups in Figure 2, it is inter-

esting to note that the group least consistently available for follow-up assess-

ments had the steepest slope. This may have implications for results of studies

that have selected subsamples for follow-up based upon availability. These re-

sults are consistent with those of another recent study that compared VLCD with

Failure of Obesity Treatment 739

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* group 4

End TX

2 mo 18 mo 30 mo

Follow-up Measures

FIGURE 2. Mean Percent of Excess Weight and 95% Confidence Inter-

vals of Patient Groups Followed After Supplemented Fasting Regimen.

(Groups were defined by consistent membership across follow-up peri-

ods: Group 1 is an average of all patients available at a given follow-up,

Group 2 patients were available for two, Group 3 for three, and Group 4

for all follow-up periods. From “Long-Term Weight Loss Maintenance:

Assessment of a Behavioral and Supplemented Fasting Regimen” by M.

F. Hovell, A. Koch, C. R. Hofstetter, C. Sipan, P. Faucher, A. Dellinger,

G. Barok, A. Forsythe, and V. J. Felitti, 1988, American Journal of Public

Association. Reprinted by permission.)

gastroplasty and found that after five years only 3% of the VLCD group could

be considered successful compared to 16% of the surgery group (Andersen,

Stokholm, Backer, & Quaade, 1988). Moreover, there was no apparent leveling

off of the weight regain even after 5 years.

The failure of the VLCD to lead to sustained weight loss should not have been

a suprise since 15 years earlier Sohar and Sneh (1973) reported that most of the

small proportion of patients who were actually able to complete a low calorie

diet returned to within 10% of their pretreatment weight at a 14-year follow-up.

Even those who were below their pretreatment weight at follow-up remained

obese by most standards.

740 D. hf. Gamer and S. C. Wooley

Perhaps of even greater concern than the negative findings is the unjustified

optimism found in the initial reports of some of the more recent VLCD studies.

A year prior to publication of the findings in the Optifast VLCD study men-

tioned earlier, a news release from the manufacturer of the protein supplement

attributed the following summary of the results to one of the researchers:

Weight loss can now be easily, safely and routinely accomplished with good proba-

bility of maintaining the loss . . .[F]ive years ago this just wasn’t the case. The fron-

tier of dieting has moved from simply accomplishing a weight loss to maintaining

the loss long-term. (San Diego VLCD Study, 1989)

Although the rate and magnitude of weight loss have been the basis for rec-

ommending the VLCD, its most remarkable feature is the speed of weight re-

gain following treatment. The association between large weight losses during

treatment and rapid regain was observed by Stunkard and Penick (1979) in ref-

erence to behavioral and traditional treatments. They noted that this pattern was

similar to that found following fasting treatments. In recalculating the weight

losses reported by Swanson and Dine110 (1970), Stunkard and Penick (1979)

found that the more weight lost during treatment, the higher the follow-up

weight. Accordingly, Swanson and Dine110 (1970) reported that 78% of their 18

super obese patients had returned to their original weight within 3 years of end-

ing a fasting treatment.

These findings are consistent with those of Johnson and Drenick (1977), who

followed 121 moderately obese patients for an average of 7.3 years after losing

an average of 28.2 kg through a supervised fast. After 2-3 years, 50% of the

group had reverted to their original admission weight and 90% had done so af-

ter nine years. As Figure 3 illustrates, only 7 of the patients (5.7%) remained at

reduced weights during the follow-up period. According to the authors, this out-

come “required continuous conscious dieting [and] the rate of regain was quite

uniform, regardless of baseline weight, degree of weight loss, length of the fast,

or the duration of obesity” (p. 1382). In another report of these findings, it was

stated that L‘a sizable number of patients who had maintained a stable obese

weight for several years prior to treatment eventually ended up considerably

more obese than before weight reduction” (Drenick SC Johnson, 1980, p. 33). Al-

though fasting is now regarded as carrying an unacceptable mortality risk (Wad-

den et al., 1983), it is important to note that the poor maintenance found with

this approach is consistent with the more recent results with VLCDs.

Irrespective of the relative merits of the VLCDs and the behavioral or dietary

approaches to obesity, there is remarkable consistency in the pattern of weight

regain. It would seem that the correct interpretation of long-term findings is

quite straightforward. Most approaches lead to weight loss during active treat-

ment, and many individuals continue to lose in the interval directly following

treatment; however, most participants ultimately regain to levels that approxi-

mate their pretreatment weight. It is only the rate of weight regain, not the fact

of weight regain, that appears open to debate. While this may be discouraging to

the individual intent on weight loss, it should also provide some solace to the

many individuals who have failed at dieting and have attributed the failure to a

personal lack of will power.

Failure of Obesity Treatment 741

90-

so-

70-

60-

so-

Months Post Weight Loss

(mean loss from 143 kg to 106 kg)

FIGURE 3. Percent of Patients Remaining at Reduced Weights at Vari-

ous Time Intervals After Achieving Weight Loss. (Solid line represents

mean for all patients. From “Therapeutic Fasting in Morbid Obesity:

Long-Term Follow-Up” by D. Johnson and E. J. Drenick, 1977, Archives

can Medical Association. Adapted by permission.)

What Really Accounts for the Failure to Maintain Weight loss?

There is remarkable resemblance between the pattern of weight regain seen in

humans following treatment, illustrated in Figures l-3, and the results from ex-

periments in which laboratory animals are exposed to caloric deprivation, made

to lose weight, then returned to unrestricted eating. Figure 4 presents the results

from one study in which laboratory rats lost weight in response to caloric restric-

tion (Mitchel & Keesey, 1977). When ad lib eating was restored, the animals re-

gained to body weight levels that were very close to their nondeprived littermates

- all of this without the benefit of bathroom scales or (presumably) social pres-

sure. As further illustrated in Figure 4, the same pattern of body weight defense

was evident in a group of animals with lesions to the lateral hypothalamus, ex-

cept that the absolute weight levels were lower.

The concept of “set point” has been proposed to account for these and other

data from human and animal studies showing that there is remarkable stability

in body weight over time. According to the set point concept, body weight is

regulated by physiological mechanisms that oppose the displacement of body

weight caused by either over or underfeeding (Nisbett, 1972; Powley & Keesey,

1970). There is some debate about the precise physiological mediators and the

factors that influence the absolute levels at which weight regulation occurs, lead-

ing some to question the utility of the set point concept (Mrosovsky & Powley,

1977). Nevertheless, there are impressive data indicating that:

742 D. M. Garner and S. C. Wooley

sso-

I

300- A

I

c; I

5 I

2 am-

E

&

(3 400-

iii

3

z 350 - 0 CONTROL-CONTROL W-3)

is

l CONTFtOL-DEPRIVED w5)

A Ul-CONTROL (N=S)

l U-DEPRIVED (N=O)

300. I I

0 IO 20 30 40 SO 60 70

DAYS

FIGURE 4. Recovery of Body Weight by Control and L-H-Lesioned Rats

Following Food Restriction and return to Ad Libitum Feeding Schedule.

(From “Defense of a Lowered Weight Maintenance Level by Lateral Hy-

pothalamically Lesioned Rats: Evidence From a Restriction-Refeeding

Regimen” by J. S. Mitchel and R. E. Keesey, 1977, Physiology and Behav-

permission.)

1.

2.

3.

4.

Displacement of body weight usually results in “homeostatic” metabolic ad-

justments designed to return the organism to the body weight normally

maintained.

This body weight “defense” occurs in obese as well as nonobese animals.

Genetic factors influence both regulated weight and the propensity toward

upward and downward regulation of body weight under certain circum-

stances in response to environmental challenges.

Certain environmental factors, such as diet palatability, exercise, smoking,

climate, and certain drugs, appear to influence the absolute levels (within

certain limits) at which body weight is regulated (Keesey, 1986), and thus

the term “set point” is probably less satisfactory than “regulated weight.”

Metabolic Adaptation to Changes in Body Weight

It is so commonly assumed that obesity reflects a failure of body weight regula-

tion that the idea it may represent an adaptive or “normal” state seems almost

inconceivable. However, there is consistent evidence from both human and ani-

mal studies that weight loss in the obese as well as nonobese leads to reductions

of 15-30s in energy requirements (Barrows & Snook, 198’7; Boyle, Storlien,

Failure of Obesity Treatment 743

Harper, & Keesey, 1981; Bray, 1969; Donahoe, Lin, Kirschenbaum, & Keesey,

1984; Dull00 & Girardier, 1990; Elliot, Goldberg, Kuehl 8c Bennett, 1989; Finer,

Swan, 8~ Mitchell, 1986; Geissler, Miller, & Shah, 1987; Keesey, 1988: Leibel &

Hirsch, 1984; Ravussin, Burnand, Schutz, & Jequier, 1982). Corbett, Stern, and

Keesey (1986) reported that reducing the body weight of rats by 14.9% through

caloric restriction led to a 24.6% decline in resting metabolic rate. Comparable

declines in metabolic rate have been demonstrated in humans exposed to semi-

starvation conditions (Keys, Brozek, Henschel, Mickelson, & Taylor, 1950).

Obese patients have been shown to make the same or greater metabolic adjust-

ments as their lean controls during reduced caloric intake and weight loss (Bar-

rows & Snook, 1987; Elliot et al., 1989; Finer et al., 1986; Leibel & Hirsch,

1984). Leibel and Hirsch reported that obese humans who had lost a significant

amount of weight (52 kg) and were still judged to be 60% overweight had ca-

loric requirements 28% below pre-weight-loss levels, which were themselves 25%

lower than would be predicted from body size alone. Even short-term restric-

tions involving small decrements in weight are accompanied by rather dramatic

metabolic adjustments. For example, Bray (1969) has reported a 17% decline in

resting metabolic rate in obese patients with only a 3% weight reduction! This

observation parallels Keesey’s (1988) finding that, while the resting metabolism

of genetically obese rats was initially 26% higher than that of lean littermates,

following only a 4.4% diet-induced weight loss, energy requirements were re-

duced to that of the lean controls weighing less than half as much. Studies of

metabolic changes during weight loss indicate that there is tremendous individ-

ual variability in the degree of resistance to displacement resulting from caloric

restriction. Absolute weight alone provides little information about caloric needs

and the speed of weight loss given a set caloric intake (Miller & Parsonage,

1975).

Importantly, when food intake is normalized after a period of food restriction,

there is a tendency for energy to be redeposited preferentially as body fat (Dul-

loo & Girardier, 1990; Ozelci, Romsos, & Leveille, 1978). In animal studies, Dul-

loo and Girardier (1990) have shown that this is true even if the fat content of

the diet is negligible during regain (i.e., 3%). Their research has also shown that

when the extra energy cost of fat synthesis during refeeding is considered it ac-

counts for even further metabolic efficiency.

Wadden, Foster, Letizia, and Mullen (1990) have recently challenged the in-

terpretation that Resting Metabolic Rate (RMR) is adversely affected by severe

caloric restriction by showing that the dramatic initial decline in RMR following

a VLCD is largely reversed when the diet is stopped. In this study, 18 obese

women were assigned to either a Balanced Deficit Diet (BDD), in which 1200

calories were prescribed for the 48 weeks of the study, or a VLCD in which 420

calories were consumed for 16 of the first 17 weeks and a conventional reducing

diet was followed for the remainder of 48 weeks of treatment. Resting Metabolic

Rate and body weight were assessed nine times over the course of the 48 weeks

(see Table 1). Although Table 1 illustrates that the dramatic short-term decline

in RMR following the VLCD is partially reversed when participants increased

their intake, several findings are particularly noteworthy. First, although the au-

thors concluded that “neither dietary regimen, combined with modest physical

activity, was associated with long-term reductions in metabolic rate that exceeded

decreases anticipated with the achievement of a lower body weight” (p. 707), the

caloric intake for both groups indicates that they were still actively restricting

744 R. M. Gamer md S. C. Wooley

TABLE 1. Changes in Weight and Resting Metabolic Rate Over 48 Weeks in

Patients in the BDD and VLCD Conditions

Week

5

9

13

17

19

21

25

48

Changes in Weight, kg”

BDD VLCD

-4.1 i 0.7

-7.0 5 1.0

-8.7 & 1.8

-11.0 -+ 2.0

-12.9 * 2.1

- 12.6 t 2.5

- 14.3 t 3.0

- 18.2 * 3.5

-7.5 i_ 0.6”

- 14.2 -+ 0.7%

- 18.7 % 1.0”

-23.1 rfr 1.1”

-25.2 r 1.6”

-26.0 2 1.6*

-24.7 I 2.5”

-21.6 z!z 2.9

Changes in Resting

Metabolic Rate, kJ/d”

BDD

-808 rt 396

-895 rt 267

-1114 It 295

- 1053 rf: 356

-1035 ~fr 234

-936 -t- 264

-786 1?7 341

-851 i: 358

VLCD

- 1622 -e 397**

-1629 t 3%3**

- 1677 2 33a***

- 1865 * 552*“”

- 1237 f 321

- 1095 ?? 397

- 948 t 330

- 697 t 200

Note. BDD indicates balanced-deficit diet; VLCD, very-low-calorie diet. Values are mean

* SEM. Through Week 21, n = 9 for both conditions; n = 8 and n = 7 in both condi-

tions at weeks 25 and 48, respectively. From “Long-Term Effects of Dieting on Resting

Metabolic Rate in Obese Outpatients” by T. A. Wadden, G. D. Foster, K. A. Letizia, and

J. L. Mullen, 1990, Journal qf the A~e~c~n clerical Associatiorl, 244, pp. 707-71 I. Copyright

1990 by the American MedicaI Association. Reprinted by permission.

“Changes in weight and resting metabolic rate were significantly different from baseline

for both conditions at all assessment periods (p<.OOl).

*Difference between conditions was significant at p<.OOl. **Difference between

conditions was significant at pc.01. ***Difference between conditions was significant at

pc.05.

their food intake. The VLCD and the BDD subjects reported a mean caloric in-

take at Week 25 of 1118 calories and 1198 calories, respectively, and at Week 48

of 1392 and 1285 calories, respectively. Although RMR for both conditions was

less than 10% below baseline (adjusted for changes in weight), it should be

pointed out that levels of caloric intake at the end of treatment were approxi-

mately 500 calories a day below the average caloric requirements for the average

woman of the same age (National Research Council [NRC], 1968). Secondly, by

Week 25 it is evident that the weight of the women in the VLCD was beginning

to rebound, indicating that metabolic homeostasis had not vet been achieved de-

spite continued caloric restriction. Finally, the obese condition was not cured in

these women. The women began treatment at an average of more than 235

pounds (at 5 ft 5 in. tall), and at the end of the 48

Confronting the Failure of Behavioral and Dietary Treatments for Obesity

Abstract and Figures