Wilson (1994) Behavioral Treatment of Obesity. Thirty Years and Counting

Adv. Behav. Res. Thu. Vol. 16, pp. 31-75, 1594.
Printed in Great Britain. All rights reserved.
BEHAVIORAL
THIRTY
0146.64W94 $24.00
@ 1993 Pergamon Press Ltd
TREATMENT
OF OBESITY:
YEARS AND COUNTING
G. Terence Wilson
Graduate School of Applied and Professional Psychology, Rutgers University, Busch

Campus, P.O. Box 819, Piscataway, NJ 08855, U.S.A.
Abstract - Beginning with the purely theoretical extrapolation of Skinnerian
principles to changing eating behavior in 1962, behavioral treatment has since
become the principal means of managing mild to moderate obesity. Over the years
treatments have become longer and more intensive, often being combined with
aggressive Very Low Calorie Diets. Weight loss has been correspondingly greater.
Yet a fundamental problem noted from the outset has remained: the inexorable
pattern of relapse irrespective of diverse attempts to improve long-term maintenance.
Although most patients maintain weight loss for at least a year, five year follow-ups
have shown that virtually everyone returns to their baseline weight. The health effects
of this pattern of loss and regain are unknown, but should not necessarily be judged
to be harmful. Reactions to the long-term ineffectiveness of weight control treatment
have varied. Whereas some critics have called for an end to treatment, proponents
have suggested that innovative maintenance strategies can be devised, and that
subtypes of obesity more amenable to behavioral treatment can be identified. It
is argued here that an understanding of the mechanisms that cause or at least
maintain obesity should determine treatment. This premise makes it unlikely that
behavioral treatments can be improved, but rather points to the direct modification
of the biological processes that regulate body weight. Cognitive-behavioral
treatment
is effective in reducing binge eating and other maladaptive behavior associated with
obesity. It can potentially improve nutrition and increase physical activity, resulting
in significant health benefits if not weight loss.
INTRODUCTION
The first formal behavioral analysis of obesity and its treatment was
published 30 years ago (Ferster, Nurnberger, & Levitt, 1962). The title
of the journal in which this paper was published - Journal of Muthetic.sl
- has long since receded into the realm of being a favorite trivia question,
but not so the behavioral approach to the treatment of obesity which this
pioneering paper spawned. No one would have anticipated the remarkably
* From the Greek mathein meaning to learn (see Kazdin, 1978). The founder of
this journal defined mathetics as the systematic application of reinforcement theory to
the analysis and reconstruction of those complex behavior repertoires usually known as
subject-matter mastery, knowledge, and skill (Gilbert, 1962, p. 8). Publication of
the journal was discontinued after only two issues. One wonders how many behaviorists
- unfamiliar with such an arcane term and assuming a typological error - went searching
for the Journal of Mathematics. More than one review of the Ferster et al. (1962) paper
understandably referenced it in the Journal of Marhematics (e.g., Stunkard, 1976).
JABRT 16:1-C
31
32
G. T. Wilson
rapid professional embrace of behavioral treatment of obesity, even in

those heady and naively optimistic days of the beginning of behavior
therapy. It is now accepted as a matter of course that behavioral treatment
is a necessary component of any adequate obesity treatment program
(Wadden & VanItallie, 1992). Significantly, behavioral treatment has also
become a basic feature of commercial weight control programs such as
Weight Watchers (Stuart & Guire, 1978) and Optifast (Sandoz Nutrition
Co., 1987; Wadden, Foster, Letizia, & Stunkard, 1992).
The paper by Ferster and his colleagues (1962) which started all of this
was a speculative extension of the principles of operant conditioning to
modifying eating behavior, or what the authors in their behavioristic zeal
repeatedly referred to as the act of putting food into ones mouth.
The well-known principles of stimulus control, chaining, shaping, and
reinforcement were brought to bear on developing self-control*
over
what the authors saw as the self-evident problem in obesity, namely eating
too much. As they put it, the act of putting food into ones mouth is
reinforced and strongly maintained by its immediate consequences: the
local effects in the gastro-intestinal system. But excessive eating results
in increased body-fat and this is aversive to the individual (p. 87). The
strategy, therefore, was to manipulate reinforcement contingencies so that
the ultimate aversive consequences of becoming fat came to control
current eating behavior and hence limit the amount of weight that was
gained. For example, Ferster et al. (1962) proposed that patients recite
the adverse effects of being fat and look at unattractive pictures of
themselves in a bathing suit. Among the other learning-based strategies
these psychologists recommended were: gradual weight loss to ensure
that deprivation
did not undermine self-control (food restriction); a
balanced diet to avoid increasing the reinforcing value of a particular
foodstuff; discriminative control, namely, narrowing the conditions under
which food was eaten; and seeking alternative, prepotent reinforcers with
which to supplant eating.
It is noteworthy that Ferster et al. (1962) reported no data in what was
to be so influential a paper. However, citing personal communication from
Ferster, a subsequent publication by Penick, Filion, Fox, and Stunkard
(1971) reported that the results of the Ferster et al. (1962) approach were
disappointing.
The modal weight loss of the 10 patients in (Fersters)
program was only 10 pounds, with a range from 5 to 20 (p. 49).
The early application of behavioral (reinforcement) principles to the
treatment of obesity also took place via a different route. Impressed by
2 Although the authors used the term self-control, they were describing situational
control by the arrangement of relevant environmental contingencies.
Behavioral Treatment of Obesity
33
the success of operant conditioning principles in the treatment of anorexia

nervosa, (Blinder, Freeman, & Stunkard, 1970), Stunkard experimented
with the use of reinforcement principles with a small number of carefully
selected obese patients (see Stunkard, 1976). This was a significant
development because Stunkard was a leading authority on obesity, and
the author of what were already on their way to becoming the two classic
summary verdicts on the relative ineffectiveness of the treatment of obesity.
The first was that Most obese persons will not stay in treatment for obesity.
Of those who stay in treatment most will not lose weight and of those who
do lose weight, most will regain it (Stunkard, 1958, p. 79). The second
was that regardless of what treatment was used, only 25% of obese patients
lose as much as 20 pounds, and only 5% as much as forty pounds (Stunkard
& McLaren-Hume,
1959). Stunkard summarized his initial experience with
the behavioral treatment of obesity as follows: After an initial weight loss
of 10 or 15 pounds, the patient had stopped losing weight . . . the program
did seem to have some influence, but it was disappointingly weak and
short-lived (reported in Stunkard, 1976, p. 216). This outcome did not
improve on his earlier gloomy evaluation of treatment effectiveness. He
decided to abandon behavior therapy for obesity. Then, in 1967, there
occurred the event which not only reversed Stunkards decision at the
time, but also fundamentally changed the way obesity would be treated
in the future.
Drawing upon Ferster et al.3 (1962) behavioral analysis of obesity, Stuart
(1967) implemented a multicomponent behavioral treatment program with
10 patients. Two of the 10 patients were excluded, one because she became
pregnant, the other (a probable psychotic) because she wanted some
other form of therapy. Of the remaining eight patients, all lost more
than 20 pounds, and half lost more than 40 pounds, following a mean
of only 26 half-hour treatment sessions over a one year period. Strikingly,
all showed a continuing trend for weight loss over the course of the
entire year. Stunkard (1976) described his excitement on learning of
these results as follows: I could hardly believe my eyes when I read
it. For in this report on Behavioral Control of Overeating,3 Richard
Stuart . . . reported the best results that had ever been obtained in the
outpatient treatment of obesity (Stunkard, 1976, p. 217). The impact
on the field was dramatic. Clinical practice was transformed. Based on
on this report and a subsequent elaboration of the treatment program
(Stuart, 1971), and a best-selling book describing the program (Stuart &
Davis, 1972), this behavioral approach was virtually institutionalized as the
3 Note in the title the then standard assumption that overeating

treatment of obesity.
is the target in the
34
G. T. Wilson
treatment for obesity. Clinical research was galvanized, and there followed
a remarkable increase in research activity on the treatment of obesity.
BEHAVIORAL
Assumptions
TREATMENT
IN THE 1970s
About the Nature of Obesity
Nowhere in the Ferster et al. (1962) analysis of obesity was there any
mention of genetic predisposition to obesity, individual differences, or the
biology of fat metabolism and weight regulation. Consistent with their
philosophy of radical behaviorism, the authors concentrated simply on
eating behavior - the act of putting food into ones mouth. This analysis
must be put in historical context. Those were the days of the beginning of
behavioral treatment, when the young Turks surged into the analysis and
modification of a wide range of clinical problems armed with the apparent
power and precision of learning principles and procedures.
In a revealing observation, Stunkard (1976) noted that at the time of
his landmark 1967 publication, Stuart had chosen obesity as a subject
of study for two simple reasons: it provided a convenient and objective
measure of the effectiveness of the treatment (i.e., pounds lost); and
a detailed description of a behavioral program for obesity was already
available (p. 217). The basic assumption behind behavioral treatment
was that obesity was due to excess food intake, which was the product
of maladaptive eating habits. Logically, therefore, treatment focused on
directly modifying eating behavior. The relevance of exercise began to
be noted in the 197Os, and increasing the behavior of physical activity
became a complementary treatment target (Mahoney & Mahoney, 1976;
Stuart & Davis, 1972). The biological basis of obesity was ignored or at
least de-emphasized, as it was in other clinical disorders targeted by the
early applications of behavior modification.
Somewhat lost in all the optimistic focus on modifying eating behavior
was the expression of a broader and more cautionary view. For example, in
an early warning, Stunkard and Mahoney (1976) concluded that given the
complex nature of the various factors involved in regulating body weight, a
behavior modification program which is successful in reducing body weight
and body fat may not be simply a matter of unlearning maladaptive eating
habits and learning more appropriate ones. Such a program may instead
have helped a person who biologically should be obese to maintain a
statistically normal, but biologically abnormally low, body weight (p. 54).
Stunkard and Mahoneys warning accurately predicted what was later to
become an overriding issue in the field.
The decade ended with a prescient critique of behavioral treatments
of obesity by Wooley, Wooley, and Dyrenforth (1979) in the Journal
35
of Applied Behavior Analysis, the bastion of applied behaviorism. They

argued that the application of behavioral techniques would result in
failure - failure having less to do with the ingenuity and technical
adequacy of techniques than with limitations in the explanatory power
of the (behavioral) model itself (p. 4). Wooley et al. (1979) underscored
two major problems with the behavioral model. The first was that neither
maladaptive eating behavior nor the conditions responsible for faulty
learning of eating habits had ever been identified. The evidence even
suggested that obesity was not characterized by a distinctive eating pattern.
The second major problem was that, contrary to a core assumption of the
behavioral model, the evidence at the time indicated that obese people, in
general, did not eat more than their lean counterparts. (As discussed below,
subsequent studies employing improved methodology have disputed this
claim, at least for some obese patients.)
Beyond calling attention to the limitations of the behavioral model of
obesity, Wooley and her colleagues (1979) underscored the importance
of understanding the biology of weight regulation, and introduced into
the behavior modification literature a feminist perspective painting the
obese as misunderstood and maltreated victims of societal prejudice. They
ended their critical analysis by offering a different agenda for behavioral
researchers. Instead of applying themselves to conventional weight loss
programs, Wooley et al. called upon behavior therapists to
acquaint patients with the facts about obesity, including the lack of evidence that
the obese eat more than others, the effects of dieting on metabolism, and the modest
outcomes of most treatment, and to engage them in a process of goal-setting based
on these facts. Although therapists tend to be reluctant to discourage patients, the
facts of their own experience will have discouraged them or given them hope. If the
experience of dieting has been one of constant failure, despite enormous effort, they
will be relieved to have their experience confirmed and understood, and some may
be better able to withstand the difficulties knowing that they are not exclusively
attributable to their own failings. Some may choose to give up dieting and work
on minimizing the negative consequences of being obese. Others will recognize
that weight loss is, in fact, relatively easy for them and worth the effort. It
has been our experience that few patients embrace these pieces of information
as rationalizations; the concept of rationalization, of course, implies a self-serving
denial of the truth, which in the case of obesity is not known. Put otherwise,
patients typically become interested in discovering what holds true for them. What
is their weight maintenance calorie level? How rapidly and for how long will they
lose at a given level? How unpleasant is it? What, exactly, are the benefits to be
expected from weight loss? (Wooley et al., 1979, p. 20).
Initial
Treatment Trials
Behavioral researchers attacked the problem of obesity as they had

other clinical disorders, with an emphasis on well-controlled studies of
short-term effects. One set of studies compared the effects of behavioral
treatments with those of comparison conditions designed to control for
36
G. T. Wilson
nonspecific therapeutic effects (e.g., Wollersheim, 1970) or alternative

interventions (e.g., Levitz & Stunkard, 1974). Behavioral methods proved
to be consistently superior to the methods with which they were compared.
Another set of studies adopted the dismantling strategy which had
been pioneered with such success in the development and evaluation
of systematic desensitization for phobic reactions (Lang, 1969). These
studies were designed to identify which of the many techniques used
in broad-spectrum treatment programs were responsible for weight loss
(e.g., Mahoney, 1974; Romanczyk, Tracey, Wilson, & Thorpe, 1973).
In an assessment of the state-of-the-art in the field, Jeffery, Wing, and
Stunkard (1978) concluded that research on the behavioral treatment of
obesity has achieved a popularity verging on faddism (p. 189).
Even at this early stage, however, caveats about the effectiveness of
behavioral interventions were beginning to be issued. In the introduction
of one of the first anthologies of behavioral treatments of obesity,
Foreyt and Frowirth (1977) cautioned that more recent findings . . . are
beginning to cast doubt on the efficacy of some of these newer techniques
in the maintenance of long-term weight loss (p. 1). Among others,
OLeary and Wilson (1975) noted that treatment studies produced only
modest weight losses. More substantial weight loss was precluded, they
argued, by the relatively brief duration of behavioral treatments. Since
the goal of these programs was gradual weight loss of no more than one
or two pounds a week, clinically significant weight loss would require
longer interventions. These authors also called for the development of
specific maintenance strategies which would promote continued weight
loss. Among the maintenance strategies which were suggested were:
booster sessions or continued, periodic contact with the treatment program
to sustain self-regulation of weight control; the active involvement of
significant others in providing social support; and individual tailoring
of treatment interventions to patients particular needs.
In still another state-of-the-art review of the behavioral treatment of
obesity, Wilson (1979) conceded that It may be that the effects of
biological factors in maintaining obesity cannot (or, possibly, should not)
be overcome through the use of behavioral methods aimed at altering
eating and exercise habits (p. 203). Nevertheless, he put forward the
alternative interpretation that the poor follow-up findings were due to
inadequate or incomplete applications of behavior therapy (p. 203). In
addition to the maintenance strategies noted above, Wilson (1979) joined
others in advocating the incorporation of the new cognitive principles
and procedures which were changing the nature of behavior therapy. In
particular, the implications of Banduras (1977) newly minted self-efficacy
theory, and Marlatt and Gordons (1979) relapse prevention model,
seemed to promise ever more powerful ways of promoting maintenance of
37
behavior change. This analysis foreshadowed what was to become the main
response of behavioral researchers to persistent evidence of the long-term
ineffectiveness of treatment, namely, that the solution could be found in
the further elaboration and refinement of behavioral strategies (Brownell
& Jeffery, 1987; Perri, 1992; Wadden & Foster, 1992). These optimistic
prescriptions are predicated on the assumption that long-term maintenance
of weight loss is a realistic objective.
The exception to this fundamentally optimistic view of the modification
of obesity was Yatess (1975) blunt conclusion that the treatment of obesity
was an example of when behavior therapy fails. This antipodean verdict
was ignored. One of the rare responses to Yatess pronouncement deemed
it premature (Franks & Wilson, 1975). With the benefit of hindsight it
can be seen that Yates (1975) anticipated the current critical reaction to
the apparent ineffectiveness of behavioral treatment. Especially relevant
was his consideration of different theories of obesity, particularly Nisbetts
(1972) then radical thesis that some individuals have no choice but to be
fat . . . and they are biologically programmed to be fat . . . (p. 433). As
Yates (1975) observed, If Nisbetts arguments are valid, then it may well
be futile, if not positively dangerous to attempt to induce weight reduction
in some obese persons (p. 148). (Stunkard and Mahoney (1976) were
to voice the same concern, as noted above.) Garner and Wooley (1991)
recently reached the same judgment, now much-publicized.
BEHAVIORAL
Assumptions
TREATMENT
IN THE 1980s
About the Nature of Obesity
This period marked the publication of several influential studies that

established the importance of genetic influences on obesity (Stunkard et
al., 1986, 1990) as well as the nature of some of the biological mechanisms
in the development and maintenance of obesity. Although the notion of a
set point around which body weight was biologically regulated remained
controversial, it became widely accepted that once obesity developed it
was defended by the body (Stallone & Stunkard, 1991). It became clear
that among the obstacles to permanent weight loss were the irreversible
increase in fat cell number caused by sufficient weight gain (Bjorntorp,
1986), increased metabolic efficiency following weight loss (Leibel &
Hirsch, 1984), and increased LPL activity following weight loss in obese
individuals (Kern et al., 1990).
Despite these findings on the genetic and biological bases of obesity,
behavioral treatment increasingly became the norm in attempts to modify
obesity. The point was made that genetic predisposition did not mean
that behavioral treatment would necessarily be ineffective. The rationale
38
G. T. Wilson
for behavioral treatment was pragmatic: the promotion of a negative

energy balance even though it was recognized that biological mechanisms
might make this unusually difficult for many obese individuals. There was,
however, little direct investigation of the specific mechanism(s) whereby
behavioral treatment produced a negative energy balance.
In their analysis of behavioral interventions, Craighead and Agras (1991)
pointed out that
treatment works primarily through enhancing restraint during the weight loss stage.
Although we cannot yet document them, there are quite likely many specific
ways through which that occurs. For subjects who were not initially practicing
high restraint, we hypothesize that the procedures teach them how to become
moderately high restrainers. Subjects learn to reduce intake by carefully structuring
eating behavior. The structured eating minimizes the occurrence of strong hunger
cues and provides cues to stop eating early, before the usual satiety cues. Subjects also
learn coping skills to handle eating that occursin responseto social,environmental,
and emotional cues, so fewer regulatory failures occur (Craighead & Agras, 1991,
p. 116).
The foregoing analysis summarized the thinking behind most comprehensive weight loss programs. However, Craighead and Agras (1991) went on
to state that Because most subjects do not continue to lose weight once
treatment is terminated, we hypothesize that the motivation to continue
the moderate levels of restraint suggested in behavioral programs comes
largely from social factors associated with being in treatment. It appears that
the benefits of weight loss are usually not intrinsically sujj5ciently reinforcing
to maintain restraint adequate to continue a negative energy balance (i.e.,
losing weight) (emphasis added) (p. 116). This conclusion not only
repudiates the rationale of Ferster et al.% (1962) original behavioral
analysis, it also attributes successful weight loss to ongoing contextual
influence of treatment. The implication is clear: continued weight loss or
even maintenance of treatment-induced weight loss depends on continual
treatment.
Despite the growing evidence on the biological regulation of weight,
most behavioral investigators still favored psychological explanations of
the failure to achieve lasting weight loss. In a well-known study, Craighead,
Stunkard, and OBrien (1981) compared behavioral with pharmacological
(fenfluramine) treatment. The result that attracted a great deal of attention
was the more rapid relapse of the combined behavioral and fenfluramine
treatment as opposed to the relative stability of the behavioral treatment

alone. The commonly proposed explanation was couched in terms of
attribution theory, i.e., patients in the combined treatment ostensibly
attributed their initial success to the drug, which when withdrawn, left
them without a sense of control or self-efficacy about regulating their weight
(Rodin, 1986; Wilson, 1986). Craighead et al. (1981) had not obtained
any data on their patients attributions, but this seemingly plausible
39
explanation derived directly from laboratory research on attribution theory

and maintenance of behavior change (Davison & Valins, 1969). Weintraub
et al. (1992d) have subsequently shown that administering and then discontinuing DL-fenfluramine did not produce what they called negative
learning effects; these patients later did as well on a behavioral program
as patients who had received only placebo.
Stunkard (1989) offered a more compelling explanation. Drawing on
findings from animal research, he suggested that fenfluramine lowers the
level at which body weight is regulated. The effect is lost once the drug
is discontinued. Subsequent research on obese patients provides strong
support for the view that fenfluramine acts directly via specific biological
mechanisms to alter the level at which body weight is regulated (GuyGrand et al., 1992; Weintraub et al., 1992~). That fenfluramines actions
are biologically mediated does not negate the importance of a patients
attributions in weight loss programs. On the contrary, they need to be
addressed directly as indicated below.
Treatment Outcome Studies
Table 1. Summary Analysis of Selected Studies from 1974 to 1990 Providing Treatment
by Behavior Therapy and Conventional Reducing Diet
Number of studies
Sample size
Initial weight (kg)
Initial % overweight
Length of treatment (wk)
Weight loss (kg)
Loss per week (kg)
Attrition (%)
Length of follow-up (wk)
Loss at follow-up
1974
1978
1984
15
53.1
73.4
49.4
8.4
3.8
0.5
11.4
15.5
4.0
17
54.0
87.3
48.6
10.5
4.2
0.4
12.9
30.3
4.1
15
71.3
88.7
48.1
13.2
6.9
0.5
10.6
58.4
4.4
Source: Wadden, & Bartlett, (1992) (Copyright

sion.)
Guilford
1985-1987 19881990
13
71.6
87.2
56.2
15.6
8.4
0.5
13.8
48.3
5.3
5
21.2
91.9
59.8
21.3
8.5
0.4
21.8
53.0
5.6
Press. Reprinted with permis-
Table 1 summarizes the changing pattern of results in studies of the

behavioral treatment of obesity from 1974 to 1988-90 (Wadden & Bartlett,
1992). On average, weight loss in studies in the 1980s was almost double
that obtained in 1974. This improvement is attributable to the significantly
longer treatments. Not only had treatments become longer, they had
also become more intensive, multifaceted, and sophisticated. Behavioral
self-control methods aimed at altering eating habits and restricting caloric
intake were increasingly complemented by a focus on better nutrition, and
40
G. T. Wilson
strategies designed to increase physical exercise, improve interpersonal

relationships, and develop less dysfunctional attitudes about eating and
weight control (e.g., Brownell, 1989). The principles and procedures of
relapse prevention burst upon the scene of behavior change in the 1980s
(Marlatt & Gordon, 1985), and were quickly incorporated into behavioral
treatment programs for obesity (Brownell, 1992; Perri et al., 1988). In a
significant development, signalling the use of a more aggressive approach
to weight loss than the principle of gradualism that had characterized
earlier treatment, behavior modification was combined with Very Low
Calorie Diets (VLCDs) of 800 calories or less to produce substantially
greater amounts of weight loss (Craighead et al., 1981; Wadden & Bartlett,
1992; Wadden, Sternberg, Letizia, Stunkard, & Foster, 1989).
Despite these advances, two major problems remained. The first was that
although longer treatments produced greater weight loss, the effect was
limited. Per-r-i, Nezu, Patti, and McCann (1989) extended their treatment
program to 40 weeks. Subjects lost 9.9 kg during the first 20 weeks, but
only an extra 3.6 kg from week 21 to 40 even though they remained clearly
obese. The second problem was the continuing failure to achieve long-term
maintenance of weight loss regardless of length or breadth of the initial
treatment.
The long-term ineffectiveness of behavioral treatments
Table 1 not only shows greater weight losses in more recent studies,
but also longer follow-ups. Weight loss produced by combined behavioral
and VLCD treatment was maintained reasonably well at one year followup; roughly two-thirds of weight loss is kept off (Wadden, Stunkard, &
Liebschutz, 1988). Combined behavioral and VLCD treatment resulted in
significantly better maintenance than VLCD treatment alone (Wadden &
Bartlett, 1992). In possibly the most impressive demonstration of long-term
weight loss, Ohno and his colleagues (1991) in Japan showed that the
majority of their obese patients maintained their weight loss at two and
even three year follow-ups. Nevertheless, although progress was made
during the 198Os, with longer and more intensive treatment programs
producing greater weight loss and forestalling relapse for longer periods,
the fundamental problem remained. All follow-up studies showed the
same inexorable pattern, namely, gradual regain of weight over time.
The pace at which this weight regain occurs may vary across studies, but
the trend towards a return to baseline values is clear. This is even the case
in studies in which specific maintenance strategies have been implemented
during the follow-up period, as illustrated in the research of Perri and his
colleagues (1988). Even though the different maintenance strategies were
effective during the first six months following treatment, all conditions
41
began to show unmistakable signs of consistent weight regain by the 12

month mark.
Given the trend towards weight regain in one and two year follow-ups,
it is not surprising that a five year follow-up showed that, on average,
virtually all patients had regained their weight, there being not even a
hint of the effectiveness of behavioral treatment (Wadden et al., 1989,
p. 45) (see Table 2). The investigators attributed the relapse to patients
failure to adhere to the behavioral strategies they had learned and that had
proved effective. It should also be noted that fully 55% of the patients in
this study sought other treatment for weight control treatment during the
five year follow-up period. (The corrected data in Table 2 are patients
self-reported weights at the time they received additional treatment.)
Table 2. Mean Weight Changes in Kilograms (from Baseline) at Post-treatment and One
and Five Year Follow-ups
Follow-Up
Condition
End of
Therapy
1 Year
5 Year
(uncorrected)
5 Year
(corrected)
Diet alone
Behavior therapy
Combined therapy
23
22
31
-13.1 k1.0
-13.0 f1.4
-16.8 f1.2
-4.7 51.5
-6.6 k1.9
-10.6 f1.6
-5.1 22.6
+2.9 f1.7
+0.8 k2.4
+l.O f1.6
-12.7 +I.8
+2.9 f2.4
Source: Wadden et al. (1989). Copyright Buildford
Press. Reprinted with permission.
This additional treatment did little to alter the final results. The longterm failure of this comprehensive, state-of-the-art program combining
behavioral treatment with a VLCD, implemented by highly respected
experts in the treatment of obese patients, is discouraging. The data,
however, are consistent with previous five year evaluations of the outcome
of behavioral interventions (Stalonas, Perri, & Kerzner, 1984; Stunkard
& Penick, 1979). These findings from Wadden and his colleagues (1992)
reaffirm once more the validity of Stunkards (1958) edict that among
those patients who lose weight, most will regain it.
BEHAVIORAL
TREATMENT
IN THE 1990s
Behavioral and dietary treatment of obesity is at the crossroads. Increasingly it is the focus of critical attention, as exemplified in the recent
NIH Technology Assessment Conference (NIH, 1992). Reactions to
the evidence showing the disappointing long-term outcome of behavioral
treatment, and to the criticism this has engendered, have taken very
different forms.
42
G. T. Wilson
Do Existing Data Underestimate the Effectiveness of Behavioral

Treatment?
Measuring the effectiveness of treatment
The long-term effectiveness of treatment of obesity is typically framed in
terms of the extent to whichpatientsarebelow the pretreatmentor baseline
level. As Brownell and Jeffery (1987) have pointed out, this assumes that
these individuals would have maintained a stable weight in the absence of
any treatment. Yet there is evidence that people gain weight over time,
and that this tendency is marked in the obese (Shah, Hannan, & Jeffery,
1991). Accordingly, Brownell and Jeffery (1987) suggested that long-term
effects of treatment must be interpreted with a probable weight gain as
the comparative yardstick.
Garner and Wooley (1991) have challenged this suggestion. They charge
that alternative outcomes, such as obese individuals maintaining a stable
weight or even losing weight had they not received treatment, are as
plausible as weight gain over time. Although Gamer and Wooley are
technically correct in noting that different reference points are possible for
evaluating long-term effects of treatment of obesity, the available evidence
would appear to lend credence to Brownell and Jefferys (1987) suggestion.
Nonetheless, even if it is conceded that the results of behavioral treatment
should be compared against a presumed increase in baseline weight over
time, the five year outcome data would arguably still be modest at best.
Formal treatment versus self-initiated change
Another interpretation of dismal long-term effects of dietary and behavioral treatment of obesity is that they are based on a biased sample
of obese people. According to this view, patients who seek treatment
in controlled clinical trials are those who have the most difficulty losing
weight (Brownell, 1992). For example, binge eaters are over-represented in
obese patients seeking clinical treatment. It is estimated that 30% or more
of obese patients report regular binge eating, compared with only 2% in
the general population (Bruce & Agras, 1992; Spitzer et al., 1992).
Studies have consistently shown significantly greater levels of psychopathology in obese binge-eaters compared with obese non-bingers. Marcus
et al. (1990) found that 60% of obese binge eaters had a history of at least
one psychiatric disorder, as opposed to 28% of non-bingers. Schwalberg,
Barlow, Alger, and Howard (1992) found a 60% lifetime prevalence of
affective disorder and a 70% lifetime rate of anxiety disorders in their
sample of obese binge eaters (see also Hudson et al., 1988; Yanovski,
1993). The presence of this comorbid psychopathology is very likely to
complicate treatment of obesity. It has commonly been assumed that binge
Behavioral
Treatment
of Obesity
43
eating in obese patients is associated with greater attrition from treatment

and poorer weight loss (Keefe et al., 1984; Spitzer et al., 1993; Wilson,
1976). Recent data indicate otherwise, however. For example, a study by
Wadden et al. (in press) found that behavioral treatment combined with a
VLCD showed no differences between obese binge eaters and non-bingers
in drop-out rate or post-treatment weight loss. Other studies have similarly
failed to show that binge eating is a negative prognostic factor (Brody,
Walsh, & Devlin, 1993; Marcus et al., 1990; Telch & Agras, 1993; Yanovski
& Sebring, in press).
Whether on account of the presence of binge eating or other complications, it would be well to avoid Berksons bias (Helzer & Pryzbeck,
1988) and not generalize from the results of randomized clinical trials to
all obese individuals. Brownell (1992) underscores this point in raising the
possibility that the results from informal, self-initiated attempts to lose
weight might be superior to those from formal clinical trials which are
cited to document the long-term ineffectiveness of dietary and behavioral
treatment. Brownell (1992) buttresses this argument with reference to
Schachters (1982) much-cited but largely anecdotal observations about
people who quit smoking and lost weight by themselves without any
involvement in formal treatment. According to Schachter (1982), the
success rates of these self-quitters were substantially better than those
in the clinical literature. Rzewnicki and Forgays (1987) published a similar
report.
In contrast to Schachters (1982) conclusion, a searching and systematic
analysis of the scientific literature by Cohen et al. (1989) showed that
cessation rates were no better for unselected individuals who tried to
quit smoking cigarettes on their own, than for those obtained in formal
treatment trials. If this is true for cigarette smoking, there is little reason
to believe that self-initiated attempts at weight control would prove more
successful than professional treatment. If anything, it could be argued that
obesity is a more intractable problem than cigarette smoking on both
theoretical and empirical grounds, as argued below.
There are still other reasons to question whether unselected obese
individuals in the general population do better in maintaining weight loss
than the patients represented in published clinical trials. Several studies
have investigated the effects of behavioral interventions in community
settings and worksite programs. It can be argued that the participants
in these studies are similar to the general population. Yet the results
of these studies have been as disappointing as those from clinic-based
studies (Jeffery, 1992; Stunkard, Cohen, & Felix, 1989). People who attend
commercial weight loss programs might have a less severe weight problem
with fewer complications than those who enter university-based treatment
programs. Stunkard (1989) made this assumption in recommending that
44
G. T. Wilson
commercial programs may be the intervention of choice for people with

only mild obesity. Unfortunately,
there are no data to substantiate this
reasonable recommendation.
Skeptics will be quick to suggest that the
failure of these programs to publish any systematic evaluation of long-term
weight loss in these programs is not a coincidence. Research that would
provide this information is a priority.
In sum, it certainly is plausible to assume that the patients in predominantly university-based treatment programs that have yielded such
disappointing long-term results are not representative of the full spectrum
of obese people trying to control their weight. It may be that unselected
obese individuals in the population are more successful in their weight
control efforts. Nevertheless, the reality of the long-term ineffectiveness
of behavioral treatment for those patients who seek formal treatment
programs remains a problem, and it is this population that is the focus
of the present paper.
Can Specific Treatments Be Matched to Particular Subgroups of Patients?
It is now widely acknowledged that most clinical disorders are heterogeneous in nature, with no single treatment appropriate for all patients.
This is likely to be true of obesity, and it has been proposed that the
better treatment outcome will result from matching specific treatments
to particular subgroups of homogeneous patients (Brownell & Wadden,
1992). Treatments might be matched to subgroups of patients identified
either according to biological or behavioral characteristics. As an example
of the former, Stallone and Stunkard (1991) speculate that behavioral
treatment might be appropriate for patients whose metabolic rate does
not decline in response to weight loss (non-regulated
obesity) but
inappropriate for those in whom this occurs (regulated obesity).
A problem with matching treatments to subgroups, however, is that
reliable predictors of treatment outcome have yet to be established
(Wadden & Letizia, 1992). The identification of treatment-specific predictors of outcome is even more elusive. The rationale for the search
for predictors of outcome is predicated on the assumption that there is
considerable variation in response to weight loss treatments (Brownell &
Wadden, 1992). This conclusion, however, is accurate only with respect
to short-term outcome. All of the available evidence indicates that there
seems to be remarkably little variation in outcome in long-term treatment
follow-ups. Most patients return to their baseline weights (Wadden et
al., 1989).
Whether or not matching individual patient characteristics to particular
treatments will improve long-term weight loss remains to be seen. It
warrants continued research attention. In the meantime the identification
45
of subgroups of obese patient with different needs can be useful in other

ways, as Brownell and Wadden (1992) have indicated. Consider obese
binge eaters who, as discussed above, appear to be a distinctive subgroup
of patients. Initial studies indicate that both pharmacological (McCann &
Agras, 1990) and psychological (Smith, Marcus & Kaye, 1992; Telch et al.,
1990; Wilfley et al., 1993) therapies show promise in reducing binge eating
in obese patients. The available evidence shows that successful reduction
of binge eating in these patients does not result in significant weight loss.
Nevertheless, several benefits can be anticipated from the elimination of
binge eating in obese patients.
First, it might make it easier for them to participate and remain in more
conventional weight control treatments, the putative benefits of which are
discussed below. Second, it might prevent future weight gain. If binge
eating is a risk factor for obesity in some individuals, then successful
treatment of binge eating before the person becomes overweight might
prevent obesity (Agras et al., 1992). (The potential importance of early
intervention in the development of obesity is emphasized later in this
paper.) Third, it should increase patients sense of personal control,
which has a variety of positive psychological sequelae, including improved
adherence to behavior change strategies. Fourth, it should improve mood
and reduce associated psychopathology, important goals in their own
right.
Binge eating is a distinctive pattern of behavior (Fairburn & Wilson,
1993), whereas obesity is more akin to a chronic biological disorder. It is
not surprising, therefore, that behavioral treatment appears to be effective
in overcoming the former but not the latter. The current interest in binge
eating in a subgroup of obese patients should not prematurely narrow
the focus on differences in eating patterns among obese people. The
inclusion in DSM-IV of binge eating disorder (BED) as an example of
EDNOS could well have this undesirable effect (Fairburn, Welch, & Hay,
1993). Rather, the study of eating behavior of obese individuals should
be broadened to include all forms of dietary restriction and overeating.
Wadden et al. (in press) provide an illustration of the importance of taking
an inclusive view of different patterns of overeating. These investigators
failed to confirm previous reports that binge eating is associated with
greater drop-out rates and less weight loss in obese patients. Overeating
in the absence of loss of control, however, was associated with a poorer
response to behavioral treatment.
Another example of the value of a broad behavioral analysis of eating
behavior in obese patients is provided by Schlundt et al. (1991). A
hierarchical cluster analysis of two weeks of detailed self-monitoring
of eating habits produced the following five different eating patterns:
moderately healthy eating habits; chronic food restriction; alternating
46
G. T. Wilson
patterns of restriction and binge eating; emotional overeating; and unrestricted overeating. Significantly, the chronically restricting cluster had less
lean body mass, lower resting metabolic rate, and higher waist-to-hip
ratios than the unrestricted overeaters. Over the course of behavioral
treatment the different groups did not differ in drop-out rates, amount
of weight loss, or exercise compliance. Consistent with other research,
the alternating dieting-binge eating cluster reported greater emotional
maladjustment than the other four clusters.
There is good reason to continue the behavioral analysis of eating
behavior of obese individuals. Following a series of studies in the 197Os, it
was commonly assumed that obese individuals ate no more than their lean
counterparts (Wooley et al., 1979). The so-called myth of overeating
was attributed to selective attention by biased observers whose availability
heuristic primed them to see fat people eat a large amount of food
(Garner & Wooley, 1991). If obese patients do not overeat relative to nonobese people, it would undermine the rationale of behavioral treatment
aimed at reducing energy intake. That many obese individuals who have
lost weight show reduced energy requirements and do not overeat has
been shown (Leibel & Hirsch, 1984). Nonetheless, recent research using
doubly labeled water to objectively measure total energy expenditure has
shown that some obese patients eat significantly more and exercise less
than they report (Lichtman et al., 1992). The subjects in this important
study attributed their inability to lose weight to genetic and metabolic
factors rather than their eating behavior. This discrepancy between actual
and perceived energy intake and expenditure has obvious implications
for treatment. The reasons for the discrepancy remain to be explored,
although there is reason to discount deliberate falsification (Danforth
& Sims, 1992). It does, however, focus attention on patterns of eating
and exercise, and underscores the potential value of behavioral analysis
of consumption.
Should Treatment Goals be Reassessed?
Brownell and Wadden (1992) have proposed that we abandon traditional
weight loss goals based on weight tables in favor of what they describe as
reasonable weight. The notion of determining a reasonable weight for
individual patients is not without problems, and Brownell and Wadden
(1992) provide only general guidelines that will leave most practitioners
in doubt. Nevertheless, this proposal recognizes that significant health
benefits are associated with relatively modest weight losses that fall far
short of the healthy ideal and patients own aesthetic ideals. The rationale
is that these goals are unrealistic and hence will only discourage efforts at
lasting weight loss. The hope is that a more modest goal will result in
47
improved maintenance. (In his discussion of the limitations of his landmark,

3 l/2 year long study of drug and behavioral treatment which is discussed
below, Weintraub (1992, p. 644) speculated that a less demanding and
individually-tailored
goal weight might have improved outcome for some
of the patients.)
Emphasizing the primary importance of the health benefits of weight
loss in the obese, Blackburn and Rosofsky (1992) have similarly proposed
a 10% solution for weight goals, namely, losing just 10% of body weight.
This relatively modest amount of weight loss can be shown to have positive
effects on health.
Brownell and Waddens (1992) proposal is both sensible and humane.
Nevertheless, whether the adoption of the more modest and flexible
concept of a reasonable weight will lead to improved maintenance is
debatable. The available data give no particular reason to expect patients
to maintain a weight loss of 10 lbs as opposed to 30 lbs.
Can Behavioral
Treatment Be Improved?
Another response is to emphasize the improvement in clinical outcome

from the 1970s to the 1980s as summarized in Table 1, and to argue that
continued technical advances in intervention programs will produce still
greater improvements (Brownell, 1992; Kirschenbaum et al., 1992; Perri,
1992; Wolfe & Marlatt, 1992). As described earlier above, this faith in our
ability to develop still more powerful forms of behavioral treatment has
been a consistent theme in the behavior therapy literature on obesity. In
support of this view is the evidence of successive refinement of cognitivebehavioral treatments for other clinical disorders with increasingly favorable clinical outcomes (Barlow, 1993). Nor can it be denied that as they
have become more comprehensive and longer in duration, behavioral
treatments for obesity have produced better results. Nonetheless, the
long-term outcome has not changed, and the possibility that this is no
longer a realistic expectation in the treatment of obesity must be given
serious consideration.
If behavioral treatment for obesity is to become more effective, what
are the new concepts from psychological science which will inform this
therapeutic retooling? The modern advocates of improving the effectiveness of behavioral treatment identify little, if anything, which is conceptually new (Brownell & Wadden, 1992; Gremouw & Darner, 1992;
Perri, 1992; Wolfe & Marlatt, 1992). For example, consistent appeal
is made to the presumed utility of the philosophy and procedures of
relapse prevention. Yet relapse prevention, the creative formulation of
Marlatt and Gordon (1979) within the field of alcohol abuse, was quickly
introduced into the behavioral literature on obesity (Wilson, 1979), and
JAW 16:1-O
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G. T. Wilson
has been a feature of many behavioral treatment programs over the past
decade (Brownell, 1989; Brownell, Marlatt, Lichtenstein, & Wilson, 1986;
Sternberg, 1985).
In a recent elaboration of relapse prevention philosophy applied to the
treatment of obesity, Wolfe and Marlatt (1992) reject the dichotomous
framework in which one is either on or off a diet, in favor of a broader
focus on healthy lifestyle changes. A rejection of traditional diet thinking
was an integral feature of the original Stuart and Davis (1972) prototype of
behavioral treatment. An explicit cognitive perspective on the maladaptive
nature of dichotomous thinking and related dysfunctional cognitions goes
back at least to Mahoney and Mahoneys (1976) analysis (cognitive
ecology: cleaning up what you say to yourself) in their straightforward
extension of cognitive restructuring to the treatment of obesity.
Arguing that the futility lies not in pursuing effective weight management approaches, but rather in evaluating them against inappropriate
standards (p. lSS>, Wolfe and Marlatt (1992) suggest reframing weight
management success. Instead of setting specific goal weights, the emphasis
shifts to approaching
their weight as a symptom of an undesirable lifestyle and focused on living a more
desirable life, knowing it would improve their bodies. They counted their successesin
small but exceedingly varied steps, such as learning the difference between complex
and simple carbohydrates, resisting an offered treat, losing a dress size, and gaining
the confidence to undertake new challenges. Each step enriched their lives and moved
them further from where they began. They were not on a diet, therefore, they never
had to begin maintenance or worry about relapsing. They actively chose to pursue
an improved quality of life. In the process, they lost the symptoms of the excessive
lifestyle they had left behind (Wolfe & Marlatt, 1992, p. 188).
Again, there is little here that will strike veterans in this field as new,
influenced as virtually all behavior therapists have been for some time
by Marlatt and Gordons (1985) pathbreaking analysis of the relapse
prevention model with its emphasis on lifestyle balance.
The contribution of relapse prevention training to the behavioral treatment of obesity has been systematically evaluated (Fremouw & Darner,
1992; Per-r-i, 1992). In one study, adding relapse prevention to a basic
behavioral treatment program was helpful only when combined with
continuing professional contact via telephone or mail (see Perri, 1992,
Table 19.1). In another, both relapse prevention and continuing post-treatment contact respectively facilitated maintenance of weight loss but did not
differ from one another (see Perri, 1992, Table 19.5). Most importantly,
the longest follow-up in these studies was only 18 months. Although the
data are admittedly still preliminary (Brownell, 1992; Fremouw & Darner,
1992) the relatively modest effects obtained with relapse prevention
training to date do not suggest that it will improve much upon the
disappointing outcome at five years.
49
The limits of behavioral treatment

Behavioral treatment of obesity assumes that excess body weight is a
function, at least in part, of environmental influences (Ferster et al., 1962).
There is little question that this is the case. Although it is well-established
that body-mass index is strongly influenced by genetic factors (Sorensen,
Holst, Stunkard, & Skovgaard, 1992; Stunkard et al., 1990), this genetic
predisposition is expressed in interaction with specific environmental
conditions. A behavior genetic analysis by Grilo and Pogue-Geile (1991)
confirmed the importance of environmental
influences on weight and
obesity, although they accounted for less variance than genetic factors.
This analysis also demonstrated that it is non-shared environmental
influence that is important. Shared influence seemed irrelevant. Grilo
and Pogue-Geile comment that it is remarkable that individuals within
families who apparently share similar diets resemble each other so little
in weight (1991, p. 535).
Several other lines of evidence point to the importance of environmental
influences on obesity. The evidence for a trend of increasing weight gain
in the U.S.A. in recent decades is one (Gortmaker, Dietz, Sobol, &
Wehler, 1987; Jeffery, Folsom, Luepker, & Jacobs, 1984). Another is the
robust finding of an inverse correlation between socioeconomic status
(SES) and obesity (Sobal & Stunkard, 1989). This correlation can be
seen as showing that obesity leads to lower SES. It can also be argued,
however, that social class affects obesity. Women in higher social classes
seem more committed to societal ideals of thinness and have greater
resources to control their weight through dietary restriction and exercise.
There is evidence that eating disorders are more common among women
in higher social classes and that this is due in part to their higher rates of
dieting and pursuit of thinness (Hsu, 1990). Garn and Clark (1976) found
that adolescent females in higher income families started out fatter but
ended up leaner than those in lower income families.
The evidence for environmental influence on obesity seems clear. In
principle this environmental influence could be used to produce weight
loss or gain. Yet we have been unable to harness the power of these
environmental influences in formal treatment programs. Our environment
currently serves to encourage weight gain and undermine organized efforts
to lose weight. The hope that some new behavioral concept or procedure
will at last succeed in promoting long-term maintenance of weight loss
has worn thin. The prospect that no amount of fine-tuning of behavioral
principles will improve upon the current state of affairs must be faced.
Behavioral treatment, no matter how sophisticated, has had little long-term
success in lowering weight. With the wisdom of hindsight we should not be
surprised.
50
G. T. Wilson
Obesity is influenced strongly by genetic factors and once established, is

maintained by several potent biological mechanisms, including irreversible
fat cell formation (Bjorntorp,
1986) and increased metabolic efficiency
(Shah & Jeffery, 1991). Genetic influence is only predisposition and
not predestination, but it would be folly to ignore the power of this
predisposition as it plays out in an environment which exacerbates the
risk to the vulnerable person. Whether it is biological pressure that must
be resisted, or vulnerability that must be protected against, obese people
have to impose endless control (be it cognitive, behavioral, or more broadly
environmental)
on energy intake/expenditure.
Good, multicomponent
behavioral interventions provide training and support in shoring-up this
control. In principle it could be maintained for a lifetime, and a small
number of patients seem to be able to do just that, especially with
the help of social support and physical exercise. But these efforts are
up against an environment that (a) features abundant food, especially
fast food and other tempting sources of high calorie intake, and (b)
an increasingly sedentary lifestyle. We may have been asking too much
of obese people to exercise control continuously in the face of these
unremitting environmental influences. With respect to long-term weight
loss, the title of Stuart and Daviss (1972) influential book - Slim Chance
in a Fat World - was more telling than we appreciated at the time.
The plight of the obese person can be compared with that of someone
with psychoactive substance abuse disorder or an eating disorder. Alcoholics, for example, can stop drinking completely (and for the ones who
are physically dependent on alcohol this is the recommended course).
Despite environmental cues to drink, they can avoid the biggest threat
to self-control, namely, consumption of alcohol. The same applies to
cigarette smoking. In contrast, obese people have to eat each day of their
lives. They are necessarily in daily contact with internal and external cues
which regulate eating. Behaviorally speaking, the threat to control must
be greater under these conditions. It has been repeatedly documented
that obese patients on a VLCD not only lose a large amount of weight
quickly, but seem to do so with relative ease. Even obese binge eaters
cease to binge while on a VLCD (Telch & Agras, 1993). There is no
mystery here, no special property of the VLCD. As patients themselves
are quick to point out, a VLCD provides a structured form of energy
intake that artificially removes patients from the real world temptations
and frustration of coping with the demands of conventional eating. They
neither have to choose one food over another, nor expose themselves to
food-related cues in purchasing and preparing meals. It is the refeeding
period, the transition to normal eating with its inevitable demands on
self-control, that results in overeating and weight gain.
With problems such as alcohol abuse and eating disorders, putting aside
51
the highly questionable disease theory view of addiction (Fingarette,

1987), the focus is on behavioral disorders. They are not chronic illnesses
of the sort obesity is now said to be. With alcohol abuse we can completely
eliminate maladaptive behavior (become totally abstinent) rather than seek
to regulate an underlying condition that will not change. Alcoholics may
have their own genetic/biological vulnerabilities,
but the evidence for
genetic predisposition is not as strong (many would argue it is quite weak,
e.g., McGue et al., 1992) as it is for obesity. In contrast to the biological
condition of obesity, the binge eating is a behavioral disorder that should,
in theory, be modifiable via behavioral treatment. The evidence indicates
that this is the case (Telch et al., 1990; Wilfley et al., 1993). As for
obesity, this analysis suggests that for the majority of patients, longterm weight reduction is feasible only to the extent that some form of
restructuring of their environment is made in which external controls are
imposed indefinitely. The closest approximation of such an intervention is
continual treatment. The available evidence indicates that the continued
contact of one form or another with a treatment program is the best
means of maintaining weight loss (Perri, 1992). But how feasible is such a
strategy? Would patients continue to attend formal maintenance sessions?
Clinical experience strongly suggests that attendance and adherence would
taper off.
Is Prevention More Important
Than Treatment?
The development of obesity is associated with biological changes, such

as an increase in number of fat ceHs, that make it difficult to lose weight
(DiGerolamo, 1991). The body comes to defend an obese state. It follows
from this that the focus should be on preventing excess weight gain in the
first place. For example, there is animal evidence showing that duration
and severity of weight gain influences the reversibility of dietary obesity
(Hill, Dorton, Sykes, & DiGirolamo,
1989). After 17 days of a high fat
diet, rats switched to ad lib feeding of low fat chow returned to control
levels of body weight and composition. After 30 days of the high fat diet,
however, rats did not return to control weight level, showing increased
energy expenditure and reduced energy requirements. The data underscore
previous findings that obesity is not simply maintained by overeating, and
that once established, dietary obesity is resistant to modification.
Dietz (1992) has pointed out that early onset obesity (in childhood and
adolescence) predicts more severe adult obesity and greater cardiovascular
morbidity in adult obesity. Moreover, the effect of adolescent obesity on
adult morbidity and mortality occurred independent of its impact on adult
weight status. These results point once more to the importance of early
prevention of weight gain.
52
G. T. Wilson
There is reason to believe that prevention might be more effective than

the treatment of established obesity. Epstein and his colleagues evaluated
the effects of two different forms of an eight month, family-based weight
loss program for obese children (ages 6-12 years) (Epstein, Valoski, Wing,
& McCurley, 1990). In the treatment that emphasized lifestyle change
and weight control in both the children and their parents, children lost a
significant amount of weight, most of which was maintained at a 10 year
follow-up. At that point, the children were maintaining a loss of seven
percent of their initial percent overweight. The treatment that focused
solely on changes in the childrens behavior resulted in relapse by the
five year follow-up. Parents in both treatments fared less well, returning
to their baseline weight at five years and showing increases in percent
overweight at the 10 year follow-up. Epstein (personal communication)
has reported that the long-term success of his family-based program has
been replicated in a subsequent study.
Given the well-documented failure to maintain weight loss in adults,
the long-term success of Epstein et al.% (1990) program may come as a
surprise. Uncovering the reasons for the discrepancy in outcomes would
seem to have significant theoretical as well as practical implications. One
prosaic hypothesis is that it is easier to establish healthy eating and activity
habits in children than adults. Another, drawing from the Hill et al. (1989)
data, is that early intervention is less likely to encounter the biological
obstacles posed by established obesity in adults.
It would be well to issue a caveat about interventions aimed at preventing
obesity in children. Care would have to be taken to ensure that they receive
adequate nutrition and do not develop the type of dietary restraint that
has been linked to the development of eating disorders and other forms of
psychological distress. More than anything else it would seem important to
encourage sensible eating habits, healthy nutritional choices, and increased
physical activity.
Prevention of excessive weight gain might also be attempted using a
different strategy. Binge eating appears to become more prevalent as
degree of overweight increases (Spitzer et al., 1992; Telch, Agras, &
Rossiter, 1988).4 Moreover, a large number of obese adults who binge
report that their binge eating preceded the development of obesity
(Wilson, Nonas, & Rosenblum, 1993). Accordingly, Agras et al. (1992)
have speculated that binge eating might be a risk factor for obesity in
some individuals. The elimination of binge eating in adults with established
obesity does not result in weight loss (Marcus, 1993). Agras et al. (1992),
4 A recent study by Wadden, Foster, Letizia, and Wilk (1992) failed to replicate these
findings, however.
BehavioralTreatment of Obesity
53
however, suggest that successful treatment of binge eating (for which

methods exist) in non-obese individuals might forestall the development
of obesity. If binge eating is viewed as a form of dietary-induced obesity,
the parallel to Hill et al.s (1989) data is obvious.
Do The Risks Outweigh the Benefits of Behavioral
Treatments?
Health risks
In their broadside against behavioral treatment of obesity, Gamer and

Wooley (1991) not only underscore its long-term ineffectiveness, but also
charge that it may often be harmful. The reason is that diet-induced
weight loss will be followed by weight regain, a pattern that has come
to be known as weight cycling (Brownell et al., 1986). Drawing largely
from animal studies, the generalizability of which to humans they admit is
unclear, Garner and Wooley (1991) caution that weight cycling can have
the following untoward effects: reduction in lean body mass relative to
body fat; enhanced metabolic efficiency, making future weight loss even
more difficult or even leading to still greater obesity; and increased risk
of cardiovascular disease. It may be weight cycling and not obesity per se,
they suggest, which is linked to morbidity and mortality in obese people.
The data on weight cycling are conflicting and controversial. Wing
(1992a) concluded that the bulk of the available evidence shows that weight
cycling has no effect on body composition, metabolic rate, or distribution
of body fat. In contrast, Rodin (1992) has shown that weight cycling is
associated with increased fat cellsize and LPL activity in abdominal fat.
According to Wing (1992a), the evidence on health outcomes in people,
despite inconsistencies, does suggest that weight variability has a negative
impact on all-cause mortality, and particularly cardiovascular mortality
(see also Lee & Paffenberger, 1992).5 Drawing causal inferences from
existing studies linking variability in weight to health outcomes is fraught
with difficulties, however.
One of the problems in interpreting these epidemiological findings is
determining whether the cycles of weight loss were voluntary or not.
The possibility that weight loss reflected an existing illness is difficult
to discount. Nevertheless, in their analysis of change in body weight
and longevity in Harvard alumni, Lee and Paffenberger (1992) carefully
excluded individuals with existing cardiovascular disease and cancer.
5 Note that these data come from epidemiological studies of weight variability, and not
the outcomes of behavioral treatment. There has been no direct evaluation of the long-term
health effects of dietary and behavioral treatment.
54
G. T. Wilson
Another argument in favor of rejecting an interpretation of their findings

as due to involuntary weight loss is that weight variability was associated
with cardiovascular disease but not cancer. The latter, more than the
former, would likely be associated with weight loss. Finally, it should be
noted that contrary to Garner and Wooleys (1991) suggestion that it is
weight cycling rather than obesity that constitutes the health hazard, Lee
and Paffenberger (1993) caution that their data in no way imply that those
obese persons should remain obese, since alumni in the top quintile of body
mass index were at significantly higher risk of mortality from all causes and
from coronary heart disease when compared with their counterparts in the
lowest quintile. However, weight loss or gain - which may be associated
with weight cycling - also may adversely affect longevity (p. 2049).
The scientific rationale for weight loss treatment is that it reduces
the health risks associated with obesity (National Institutes of Health
Consensus Development and Conference Statement, 1985). Garner and
Wooley (1991), however, question the health risks of obesity. Nevertheless,
the National Institutes of Health Technology Assessment Conference on
Methods for Voluntary Weight Control (1992) arrived at the following
conclusion: Being overweight can seriously affect health and longevity. It
is associated with elevated serum cholesterol, elevated blood pressure, and
non-insulin-dependent
diabetes mellitus. Excessive weight also increases
the risk for gallbladder disease, gout, coronary heart disease, and some
types of cancer and has been implicated in the development of osteoarthritis
of the weight-bearing joints (NIH, 1992, p. 1). Moreover, there is
impressive evidence that even modest weight loss can significantly reduce
health risks in obese people (Wadden & VanItallie, 1992). Willett (1992)
points out that even in the absence of abnormalities in blood pressure or
lipids, obesity cannot be regarded as a benign condition, because it is
predictive of such complications.
Binge eating
Garner and Wooley (1991) suggest that the dietary treatment of obesity
may also contribute to the development of binge eating. Two studies have
tested this hypothesis directly. In the first, Telch and Agras (1993)
assessed the frequency of binge eating episodes during a combined Very
Low Calorie Diet and behavioral weight loss program. Once the low
calorie formula diet ended and patients were reintroduced to food, 30%
of those who had been identified as non-binge eaters prior to treatment
reported binge eating episodes. Treatment did not increase binge eating
in those patients identified as binge eaters, however. In fact, 39% of these
patients ceased binge eating as a result of treatment. These preliminary
data indicate that strict dieting may trigger binge eating in some obese
55
patients. In the second study, Yanovski and Sebring (in press) showed
that a standard VLCD program reduced the frequency and size of binge
eating episodes in obese binge eaters. There was no iatrogenic effect on
non-binge eaters.
A third study is also relevant in this context. Treating obese Type II
diabetic patients, Wing (1992b) compared the rates of dietary lapses
during behavioral treatment combined with either a VLCD (400 kcal)
or a balanced diet (100&1500 kcal). The two dietary programs did not
differ on either objective (intake of food 20% or more above daily calorie
goal) or subjective (patients perceptions that they had transgressed calorie
limits) lapses. A concern with the possible occurrence of binge eating
in obese patients in treatment should be part of a more general focus
on eating behavior. The issue is of theoretical and clinical significance.
Treatment programs need to monitor patients progress carefully to assess
this iatrogenic effect.
Adverse psychological
sequelae
The most extensively studied psychological consequence of diet-induced

weight loss has been depression. When all treatments of obesity are
considered, both increases and decreases in depression have been found. In
a comprehensive review of this literature, Smoller, Wadden, and Stunkard
(1987) argued that changes in depression following weight loss have been
primarily a function of the method used to assess psychological effects.
Related adverse reactions may have been the result of interpretive bias in
that they were ascertained through retrospective and subjective assessment
methods. Reported beneficial effects of weight loss have been shown
by more objective measures of outcome. Behavioral treatments have
produced reliable and significant decreases in depression and anxiety from
pre- to post-treatment.
Behavioral weight control treatments also result in other beneficial
short-term psychological effects. Body image dissatisfaction is decreased
and body size estimation is reduced (Dubbert & Wilson, 1984; ONeill &
Jarrell, 1992). Enhanced self-esteem, improved interpersonal functioning,
and increased marital satisfaction have also been reported. Although
the long-term psychological effects have received relatively little study,
Wadden, Stunkard, and Liebschutzs (1988) data indicate that treatmentinduced reduction in depression returns to baseline level at a three year
follow-up. Their patients reported that regaining weight had adverse effects
on their self-esteem and general happiness. In the absence of comparable
data from untreated obese individuals, it is difficult to interpret these
reports. Whereas the biological consequences of weight cycling have been
56
Ci. T. Wilson
studied in some detail (Brownell & Rodin, 1993; Wing, 1992a), the putative
psychological impact has been neglected.
Wooley and Garner (1991) argue that obesity treatment has several
adverse psychological consequences. These include: repeated failure experiences which patients attribute to their personal inadequacies rather
than the ineffectiveness of the program; contact with professionals who
hold biased and demeaning views about obesity; and the neglect of relevant
emotional problems in favor of a narrow-minded focus on weight loss.
There seems little doubt that this has been the unhappy lot of too many
obese patients. But it need not be the case. Behavioral treatment can be
framed so as to minimize or obviate the very real concerns voiced by
Garner and Wooley (1991). The conceptual framework for doing this was
spelled out by Marlatt and Gordon (1985) in their analysis of different
models of attribution of responsibility for therapeutic change. They liken
the premises of behavioral treatment to the philosophy of what Brickman
et al. (1982) called the compensatory model of behavior change. This model
allows people to direct their energies outward, working on trying to solve
problems or transform their environment without berating themselves for
their role in creating these problems, or permitting others to create them, in
the first place. The compensatory model also allows recipients to command
the maximum possible respect from their social environment. They are
not blamed for their problems, but are given credit for coming up with
solutions (Brickman et al., 1982, p. 372).
In applying this framework to obesity treatment, it must be made dear
to patients that they are not to blame for being obese. They are responsible
for taking action that might improve their condition. The primary focus
would be on improved nutrition (i.e., reduction in saturated fat intake)
and increased physical activity, and this might include weight loss for
some individuals. Those who try but cannot sustain weight loss can be
helped to accept their condition, find other sources of self-esteem, and
cope constructively with societal prejudice. In general, these guidelines
repeat the advice prescribed by Wooley and her colleagues in their 1979
paper, which is quoted earlier in this article.
ALTERNATIVE
TREATMENT
MODELS
OF OBESITY
In their review of the state-of-the-art of behavioral treatment of obesity,

Brownell and Wadden (1992) emphasized the importance of theory in
improving long-term weight loss. Their point is well taken. As noted above,
behavioral treatment of obesity has consisted of a largely atheoretical,
pragmatic approach to weight loss. It is argued here, however, that it will
be an improved understanding of the mechanisms involved in the etiology
57
Table 3. Comparison of Behavioral Self-Management (BSM) with Food Dependence (FD)

Models for Treatment of Obesity
BSM
FD
Etiology
Due to lack of skill in

controlling stimuli
and rewards that
control eating
Uncontrolled eating caused by

by dieting and distorted
cognitions related to social
pressure and body image
Assumptions
Rational mode1 of humans;

amenable to selfmanagement techniques
Irrational model; control

not possible without strong
support
Emphasis
Focus on behavioral
techniques
Focus on cognitions, emotions

related to obesity, and
social support
Source of
support
Family; friends
Peers
Nutritional
component
Self-monitored
caloric intake
restricted intake
quantified
Healthful eating; eat only

when hungry; quality
emphasized
From Goodrich and Foreyt (1991).
and maintenance of obesity, rather than theories of behavior change, that

will provide therapeutic advances.
The following models have all been put forward as superior options to
traditional behavioral weight control treatment.
The Food Dependency Model

Accepting that traditional behavioral treatments of obesity fail in the long
term, Goodrick and Foreyt (1991) have proposed an alternative approach
based on what they call a food dependency model of obesity. Table
3 summarizes the principal features of this model and how Goodrick
and Foreyt (1991) view it as different from a traditional behavioral
approach. The seminal assumption of this model is that obesity is a
form of addiction.
Obesity is viewed as a product of the inability
to control eating and exercise behaviors to control body fat, the result
of an addictive process driven by a vicious cycle of distorted thinking
and physiological imbalances (p. 294). Eating, or more precisely binge
eating, had superficial similarities to psychoactive substance abuse. But
this reasoning by analogy has been criticized (VanderEycken, 1990). Binge
58
G. T. Wilson
eating is not a form of psychoactive substance abuse (Wilson, 1993). There

is even less justification for viewing obesity as an addiction. The addictive
process is not explained. Nor are the physiological imbalances specified.
Other related claims, such as the assertion that two thirds of all obese
persons may be carbohydrate cravers6 are lacking in support.
Many of Foreyt and Goodricks (1991, pp. 295-96) treatment recommendations overlap with those of the more standard behavioral program,
namely, gradual reduction in fat intake, reasonable caloric restriction
if necessary, physical exercise, strategies for improving self-regulation
of eating and exercise, and social support. These are the elements of
the state-of-the-art LEARN obesity treatment manual (Brownell, 1989).
In other recommendations,
such as the emphasis on flexibility of food
choice, Foreyt and Goodrick (1991) are advocating some of the principles
of cognitive-behavioral
treatment for binge eating (Fairbum, Marcus, &
Wilson, 1993).7 What is important in the Foreyt and Goodrick (1991)
recommendations is the explicit recognition that external control of eating
and exercise behaviors would be required for a lifetime (p. 295). The
validity of this statement stems not from the pseudo-biological constructs
of an addiction model, but from what is known about the biology of obesity
and the environment in which this condition must be managed.
The evidence clearly indicates that weight regain following behavioral
treatment is associated with poor compliance with weight loss strategies
(Perri, 1992). Patients stop self-monitoring,
become less vigilant about
what and when they eat, and discontinue exercise. The longer the formal
treatment program, or at least contact with the program, is continued,
the better the maintenance of weight control (Bjorvell & Rossner, 1985).
The goal of Foreyt and Goodricks (1991) treatment model is to provide
continuing external support for weight control behavior by fostering peer
group pressure. Whether this treatment strategy will succeed is an open
question. Nonetheless, there is good reason to question the long-term
effectiveness of any form of social support or external control that does
not fundamentally change the environmental conditions which have been
responsible for the growing incidence of obesity in the United States this
century. These conditions are the increased availability of foods high in
calories and fat, and an increasingly sedentary lifestyle.
6 Both clinical and laboratory studies have discredited the notion that binge eating, in
either normal weight patients with bulimia nervosa or obese binge eaters, is a product of
carbohydrate craving (Yanovski et al., 1992; Walsh, 1993).
7 The use of CBT in the treatment of binge eating is conceptually at odds with the
philosophy of an addiction model of food dependence (Wilson, 1993).
59
LifestyZe Change verse Weight Loss
As an alternative to weight loss treatment, Garner and Wooley (1991)

proposed that it may be more prudent to focus directly on lifestyle
rather than obesity (p. 761). Lifestyle change would include: a reduction
in alcohol consumption, dietary fat, and sugar; increased exercise; and
modification of negative body image. The goals of this focus would be to
promote health and happiness in people who would be likely to remain
fat.
This proposal carries the implication that current behavioral treatment
programs ignore lifestyle modification. Yet the direct attempt to improve
nutrition (most notably the reduction in saturated fat) and increase exercise
have been integral components of behavioral treatment of obesity for some
time (e.g., Brownell, 1989). Garner and Wooley (1991) assume that there
is a big difference between lifestyle modification with and without a direct
focus on weight loss (i.e., caloric restriction). This remains to be seen.
Reducing dietary
fat
Among their recommendations for improving the results of behavioral

treatment, Brownell and Wadden (1992) list the importance of a low
fat diet. The focus on reducing fat intake and increasing carbohydrate
consumption has been a staple of comprehensive behavioral treatments
for some time. Fat is not only more calorically dense than complex
carbohydrates, but it is also stored more easily. Dietary fat is more
fattening than carbohydrates. Compared with complex carbohydrates,
high fat foods have a weak effect on satiation (i.e., termination of eating
within a meal) and satiety (i.e., postprandial inhibition of future eating)
(Blundell & Hill, 1993). Reducing the fat content of a diet can produce
weight loss. At least in the short term, people do not compensate for
reduced fat content by increasing total caloric consumption even when
no limits are placed on the amount of food consumed (Kendall, Levitsky,
Strupp, & Lissner, 1991). Rolls (1992), however, notes that the subjects in
this study were allowed to eat only low fat foods. Other research, in which
the fat content of just some foods were reduced and subjects had access
to other high fat foods, has shown overall caloric compensation (Foltin et
al., 1992).
The trouble is that high fat foods taste good! It may prove to be
difficult to alter peoples dietary intake of fat in the long term. There
is little evidence of significant success in modifying unhealthy diets even
in individuals most in need of this behavioral change, such as patients
with hypertension (Jeffery, 1991) or heart disease (Wrisley & Rubenfire,
1988). Southard et al. (1992) asserted that we cannot point to a singular
exemplar of effective dietary intervention in the primary care setting for
G. T. Wilson
60
hypercholesterolemia
(p. 23). On a more positive note, however, an
analysis of one year follow-data from the Womens Health Trial showed
that subjects had maintained most of the low fat dietary habits they had
developed during the dietary intervention (Kristal et al., 1992). Moreover,
the investigators were able to identify which low fat habits were adopted
and maintained with greater ease or difficulty. Information of this sort
could help behavioral researchers to develop more refined interventions.
Increasing exercise
Exercise facilitates weight loss and its maintenance over a one year
period (Wood et al., 1991). The benefits of exercise are clear, but so
are the difficulties in promoting long-term adherence. Obese individuals
who increase their level of physical activity show significant improvement
in health even if they do not lose weight (Blair et al., 1989). The problem
is the sustaining of increased physical activity. The failure of patients to
continue to adhere to dietary and exercise strategies is responsible for
relapse in behavioral weight loss treatment (Perri, 1992). Garner and
Wooley (1991) assert that obese individuals will persist in exercising if
it is not coupled with the discouraging enterprise of dieting (p. 762).
There is no evidence to support this speculation. In her review of the
exercise literature, Dubbert (1992) has pointed out that In contrast to
impressive advances in delineating the health effects of exercise during the
past decade, progress toward understanding and modifying physical activity
and exercise behavior has been disappointing (p. 615). As is the case in
dietary change, exercise adherence is poor even in non-obese people for
whom it is important for health reasons.
Obesity as a Chronic Biological Disorder
Obesity is primarily a biological disorder rather than a behavioral

problem. It is more accurate to view obesity as a form of genetic
or adaptive malregulation of biology, similar to hypertension (Bray,
1992; Weintraub, 1992), than as a specific behavioral disorder such
as binge eating. Acceptance of this model of obesity has profound
implications for its treatment. Obesity could still be modified by behavioral
interventions, but as Goodrick and Foreyt (1991) among others have noted,
these would necessitate a lifelong approach. In principle, this could be
done. As discussed earlier in this paper, however, continued psychosocial
intervention of this sort would encounter serious obstacles. The practical
problems of sustaining the needed social or environmental control are
daunting.
61
Given the model of obesity as a chronic biological disorder, a more

direct and potentially powerful treatment would be aimed at correcting
or modifying the maladaptive biological mechanisms responsible for the
cause or at least the maintenance of obesity. From this perspective, the
choice would be some form of pharmacological intervention, or, in cases
of extreme obesity, surgery. s The model dictates that an appropriate
anti-obesity
drug would have to be administered on a chronic basis,
analogous to the long-term pharmacological treatment of hyptertension
(Bray, 1992; Stunkard, 1989; Weintraub, 1992). Discontinuance of the
drug would restore the underlying pathophysiological
process(es) that
were maintaining obesity. Such is the case with the most intensively
studied and promising anti-obesity drug to date, namely, fenfluramine.
The evidence on the short-and long-term efficacy of this drug is reviewed
by Bray (1992) and Guy-Grand (1992). The most impressive data are
those from Weintraubs (1992) study. A combination of DL-fenfluramine
and phentermineg produced significantly superior weight loss than a pill
placebo in obese patients, all of whom received comprehensive diet and
behavioral treatment, both in the short- and long-term. Patients receiving
the drug treatment showed successful maintenance of significant weight
loss over a 31/2 year period. In addition, they reported greater control of
hunger, increased satiety, and better adherence to the nutritional guidelines
of the program. When patients were weaned from the drug after 190 weeks
of participation in the study, they regained virtually all of the weight
they had lost, despite the continuing behavioral program emphasizing
improved nutrition and exercise (Weintraub et al., 1992~). These findings
are consistent with previous results on the long-term ineffectiveness of
behavioral treatment.
Both animal research (Levitsky & Troiano, 1992) and the human
studies referred to above (Guy-Grand et al., 1992; Weintraub et al.,
1992a) indicate that fenfluramine decreases weight by altering biological
regulatory processes. Tolerance does not develop, and the therapeutic
s The evidence indicates that surgical approaches are far more effective in the treatment
of extreme obesity than dietary and behavioral treatments of mild to moderate obesity. Kral
(1992) estimates that about 50% of severely obese patients undergoing surgical treatment
maintain a reduction of greater than 50% of excess body weight 5 years after surgery
(p. 504). Of special theoretical significance is the conclusion that the weight loss and
associated emotional and behavioral changes, which are unusually positive, seem due to
a fundamental change in the biological regulation of weight rather than simple restriction
of food intake. Stunkard (1989) has argued that successful surgery results in lowering of
the set point.
9 Phentermine is a centrally acting adrenergic agent. It is chemically related to
amphetamines, but is nonaddictive. Fenfluramine is a centrally acting serotonin agonist.
62
G. T. Wilson
effect is lost when the drug is stopped even after lengthy periods of
sustained drug-induced weight loss.
The evidence would seem to show that fenfluramine (perhaps in combination with phentermine) is a promising treatment for obesity. It is far
from being a magic bullet, however. Although significantly greater than
that of the placebo and behavioral program, and in excess of what would
be required for substantial health benefits (Blackburn & Rosofsky, 1992),
the amount of weight loss produced by the active drug treatment in the
Weintraub et al. (1992a) study was limited (14.3 kg or 15.6% of weight
at baseline). Weight loss reached its nadir at six months and remained
stable at this level in the drug treatment. In the placebo (and behavior
modification) treatment, patients similarly ceased losing weight at the six
month point and then began to regain. Perri et al. (1989) reported the
same pattern in behavioral treatment of weight loss reaching a nadir
at six months, followed by gradual regain despite continuing treatment
sessions.
Acceptance of fenfluramine or any other future anti-obesity drug that
must be taken continually will depend on its being proven to be safe, with no
long-term harmful physical or phychological effects. There is good reason to
be cautious in this regard. The recent evidence indicating that drug-induced
reductions in cholesterol may increase all-purpose mortality rates, is a case
in point. Even if a safe and effective drug is developed, it raises the question
of whether patients will adhere to such a treatment regimen. It is the gradual
erosion of compliance with previously effective self-control strategies that
results in relapse following dietary and behavioral treatments. Might
adherence to taking medication for life not similarly decrease over time?
An important determinant of adherence will be the nature and extent
of the drugs side-effects. Although investigators have emphasized that
DL-fenfluramine is well-tolerated
by patients, it does have side-effects
that will pose problems for some patients (Weintraub et al., 1992~). During
the study, 15.7% of patients dropped out because of negative side-effects,
especially the drugs interference with sleep. In some cases these adverse
side-effects lasted for the entire 31/2 years of treatment.
A crucial question is whether lifelong administration of an anti-obesity
drug will prove to be more feasible and effective than attempts to
maintain some type of continual psychosocial intervention. The difficulties
in maintaining adherence to drug treatment of chronic conditions such as
hypertension are well known. It makes good behavioral sense, however, to
expect greater adherence to an anti-obesity agent such as fenfluramine than
anti-hypertensive medication. Hypertension is an asymptomatic condition,
whereas obesity produces tangible and observable effects. Anti-hypertensive drugs have delayed, long-term effects, whereas an anti-obesity drug
will have immediate reinforcing effects in terms of weight loss. Although
63
the potential complications with lifelong drug treatment should not be

underestimated, and will be a priority for research, it does seem clear that
it would be more convenient and less exacting than behavioral interventions
that necessarily demand continual vigilance and self-regulatory effort.
As in the treatment of other medical conditions such as hypertension,
cognitive-behavioral strategies can be used to facilitate adherence to drug
treatment (Meichenbaum & Turk, 1989).
Not all patients respond to fenfluramine (or fenfluramine plus phentermine). This is not surprising. Presumably, the biological mechanisms
that maintain obesity in different individuals will vary, and will arguably
require different interventions. A variety of other drugs, affecting different
biological processes that seem related to weight regulation, are under
development (Bray, 1992). The challenge for pharmacological researchers
is to develop a drug that not only controls weight satisfactorily in the long
term, but is proven to be safe and acceptable to patients.
Is there a role for behavioral treatment?
The development of effective pharmacological treatments would require

an analysis of how behavioral methods can be useful as part of an integrative
treatment program. In neither the Craighead et al. (1981) nor Weintraub
(1992) studies did the combination of behavioral treatment with the active
drug have any beneficial effect on weight loss or its maintenance. In
the second phase of the Weintraub study the progress of patients who
were taken off the active drug treatment for brief, intermittent periods
was compared with that of patients who took the drug continuously
(Weintraub et al., 1992~). In what amounted to a reversal design, patients
who stopped taking the drug started regaining weight that they then lost
when the drug was readministered. If behavioral treatment were to have
a positive complementary effect one would expect it would be to facilitate
weight loss during these brief time-outs from the drug. Yet the ongoing
behavioral program failed to attenuate the fluctuations in weight caused by
the use or non-use of the fenfluramine-phentermine
treatment (Weintraub
et al., 1992~).
The Weintraub (1992) study, unlike the Craighead et al. (1981) investigation, did not compare the combination of the two approaches with
drug alone. Even if drug treatment alone is as effective as a combined
drug and behavioral treatment, as in the Craighead et al. (1981) study, it
is possible that patients will be less accepting of any drug-only condition.
Clinical experience from the treatment of eating disorders suggests that it
is more difficult to recruit subjects and then to keep them in controlled
clinical trials in drug-only treatments compared with combined drug and
behavioral treatments.
JABRT 16:1-E
64
G. T. Wilson
Despite the absence of any evidence of a positive effect on weight

loss, behavioral treatment did add significantly to the broader, healthrelated effects of the Weintraub study. Treatment succeeded in increasing
high-density lipoprotein cholesterol (HDL-C), and decreasing total cholesterol/HDL-C
ratios and triglycerides even though weight was largely
regained at the end of the four year study. Weintraub, Sundaresan, and
Schuster (1992d) concluded that The beneficial lipid changes seen in this
study seem more likely to be related to the total intervention, primarily
caloric restriction and exercise, than to the medications. Persistence of
higher HDL-C levels and desirable ratios for 210 weeks, despite regain
of weight, support the overall value of the program (p. 640). Combining
behavioral treatment with bariatric surgery shows a similar outcome.
Patients who underwent surgery received either six months of behavioral
weight control treatment or minimal intervention (Tucker, Samo, Rand, &
Woodward, 1991). The results of a two year follow-up indicated that the
two groups had maintained their weight loss, but did not differ significantly.
Patients who had received behavioral treatment, however, reported better
postoperative psychosocial functioning, greater daily physical activity, and
reduced consumption of dietary fat than the controls. Although the data
are sketchy, it appears that combining behavioral interventions with
particular pharmacological surgical treatments may produce significant
lifestyle changes but not additional weight loss. Such a pattern is consistent
with the revamped model of obesity put forward by Weintraub (1992) and
others.
Finally, fenfluramine may not be effective in treating the binge eating
that may afflict over 30% of patients. A well-controlled study by Fahy,
Eisler, and Russell (1993) showed that D-fenfluramine added nothing to
the therapeutic effects of cognitive-behavioral
treatment for binge eating
in normal weight patients with bulimia nervosa. To the extent that binge
eating in bulimia nervosa patients is comparable to that in obese patients,10
treatment with fenfluramine would not address a significant source of
personal distress. In contrast, as noted above, cognitive-behavioral
treatment appears to be a promising form of treatment for binge eating in the
obese (Marcus, 1993).
10 Dieting is believed to be a critical proximal antecedent of binge eating in patients with

bulimia nervosa (Hsu, 1990). The link between dieting and binge eating in obese binge
eaters appears to be different. In contrast to bulimia nervosa, the onset of binge eating in
obese binge eaters seems to precede dieting (Agras et al., 1992; Berkowitz & Stunkard,
in press; Spitxer et al., 1992; Wilson, Nonas, & Rosenblum, 1993). Moreover, obese binge
eaters exhibit significantly less dietary restraint than patients with bulimia nervosa (Marcus
et al., 1992; Rossiter et al., 1992).
65
CONCLUSIONS
Behavioral treatment is a safe and effective means of producing weight
loss. Many patients maintain most of their weight loss for a period of a
year or more. In the long run, however, they regain the weight. Behavioral
treatment is ineffective as a means of sustaining weight loss in the long
term, i.e., beyond three to five years. The evidence from a wide range of
different studies points inexorably in this direction.
It is one matter to conclude that treatment is ineffective in the long
run. It is quite another to charge, as some critics have done, that weight
control treatment is harmful. The available evidence does not suggest that
appropriately administered, comprehensive behavioral treatment harms
obese patients. The negative biological effects of weight cycling on body
composition and fat redistribution may have been exaggerated. In any
event, the gradual weight loss produced by state-of-the-art behavioral
treatment programs, followed by gradual regain often extending over a
period of a year or more, is arguably not an instance of yo-yo weight
loss/regain as it is usually studied. The negative metabolic and health
effects of weight cycling that have been observed in animal studies seem
to be associated with rapid loss of a relatively large amount of weight.
The evidence on the putative effects of weight cycling on the behavioral
treatment of obese patients is sparse. With regard to metabolic effects,
Wadden (1991) has reported some preliminary data from a small sample
of patients who had lost approximately 12 kg and then regained the weight
over a period of four to five years. There was no evidence that this pattern
was associated with an increased percentage of body fat. Nor does the
bulk of the evidence indicate that previous weight cycling predicts an
unfavorable response to weight loss treatment (Wing, 1992a; Wadden
et al., 1992). The key question, as Wadden (1992) put it, is whether it
is better to have lost (weight) and regained than to have never lost at all
(p. 67). The answer is unknown.
Looking Forward to the Past
The failure of behavioral treatment to produce long-term maintenance
of weight loss should cause no surprise given what is now known about the
causes and maintenance of obesity. It is a complex metabolic disorder with a
strong genetic predisposition. These genetic determinants are expressed in
an environment that increasingly favors weight gain because of the ready
availability of highly palatable, high fat foods and a sedentary lifestyle.
Long-term maintenance of caloric restriction and modification of eating
under such circumstances will exceed the self-regulatory capacities of most
obese individuals, Behavior change is most effective when the target is a
66
G. T. Wilson
specific behavior that can be influenced by rearranging the environmental

contingencies of which it is a function. In obesity, by contrast, the target
is a metabolic disorder only loosely linked to specific behavior (eating and
exercise) under environmental contingencies that are difficult to alter.
The history of behavioral treatment of obesity is dotted with observations
about long-term ineffectiveness, as the present paper illustrates. There
should now be a consensus on recognizing this reality.
Back to the Future
The treatment of obesity must be informed by the understanding of the
factors that cause and maintain the disorder. Treatment can be aimed at the
biological mechanisms that cause or maintain obesity, and/or at radically
restructuring environments to promote healthier eating habits and greater
physical activity. The inability to achieve the latter largely explains the
long-term failure of past and present behavioral treatments. The former
offers a theoretically more compelling alternative for which there is some
preliminary empirical support. Surgery for extreme obesity is an effective
technique, and pharmacological treatment for moderate obesity has shown
some promise.
Behavioral treatment can complement drug therapy for obesity but for
reasons other than those that are commonly accepted. In the past the
rationale for combined treatment of this sort was that the behavioral
treatment would promote improved maintenance of weight loss once the
drug was withdrawn after a limited time of administration. (This is the
thinking behind combined behavioral and pharmacological treatments of
psychiatric disorders such as depression (e.g., Hollon, Shelton, & Loosen,
1991) and eating disorders (e.g., Craighead & Agras, 1991)) It now
appears that drug treatment would have to be continued indefinitely. The
main focus of behavioral treatment should shift from modifying obesity to
treating obese patients, as critics of the field have long advocated.
Behavioral treatment will be most beneficial in treating specific behavioral abnormalities and psychological problems. In this regard, behavioral
treatment promises to be of value in modifying behaviors that are linked
to adverse health effects and psychological distress without necessarily
causing weight loss. These include: improved (reduced fat) nutrition;
increased exercise; elimination of binge eating (which might also result in
reduction of associated psychopathology); greater assertiveness in coping
with the social sequelae of obesity (ridicule, rudeness, and discrimination);
enhanced self-esteem; and less dissatisfaction with body image. Last, and by
no means least, behavioral interventions have shown promise in preventing
the development of obesity. It is a truism in virtually all disorders to note
that prevention would be more cost-effective than cure (assuming that the
67
latter is available). In the case of obesity this is especially true. In view of

the refractory nature of obesity once it is established, prevention efforts
should be a priority for future research efforts.
Acknowledgements
- I am grateful to W. Stewart Agras, Christopher C. Fairbum,
Michael Lowe, Albert J. Stunkard, B. Timothy Walsh, and members of the MacArthur
Foundation Health and Behavior Research Network for their helpful comments in the
preparation of this manuscript.
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Adv. Behav. Res. Thu. Vol. 16, pp. 31-75, 1594.

Printed in Great Britain. All rights reserved.

Graduate School of Applied and Professional Psychology, Rutgers University, Busch

rapid professional embrace of behavioral treatment of obesity, even in

Behavioral Treatment of Obesity

the success of operant conditioning principles in the treatment of anorexia

3 Note in the title the then standard assumption that overeating

is the target in the

About the Nature of Obesity

Behavioral Treatment of Obesity

of Applied Behavior Analysis, the bastion of applied behaviorism. They

Behavioral researchers attacked the problem of obesity as they had

nonspecific therapeutic effects (e.g., Wollersheim, 1970) or alternative

Behavioral Treatment of Obesity

About the Nature of Obesity

This period marked the publication of several influential studies that

for behavioral treatment was pragmatic: the promotion of a negative

treatment as opposed to the relative stability of the behavioral treatment

Behavioral Treatment of Obesity

explanation derived directly from laboratory research on attribution theory

Source: Wadden, & Bartlett, (1992) (Copyright

Press. Reprinted with permis-

Table 1 summarizes the changing pattern of results in studies of the

strategies designed to increase physical exercise, improve interpersonal

Behavioral Treatment of Obesity

began to show unmistakable signs of consistent weight regain by the 12

Source: Wadden et al. (1989). Copyright Buildford

Press. Reprinted with permission.

Do Existing Data Underestimate the Effectiveness of Behavioral

eating in obese patients is associated with greater attrition from treatment

commercial programs may be the intervention of choice for people with

Behavioral Treatment of Obesity

of subgroups of obese patient with different needs can be useful in other

Behavioral Treatment of Obesity

improved maintenance. (In his discussion of the limitations of his landmark,

Another response is to emphasize the improvement in clinical outcome

Behavioral Treatment of Obesity

The limits of behavioral treatment

Obesity is influenced strongly by genetic factors and once established, is

Behavioral Treatment of Obesity

the highly questionable disease theory view of addiction (Fingarette,

The development of obesity is associated with biological changes, such

There is reason to believe that prevention might be more effective than

however, suggest that successful treatment of binge eating (for which

In their broadside against behavioral treatment of obesity, Gamer and

Another argument in favor of rejecting an interpretation of their findings

Behavioral Treatment of Obesity

The most extensively studied psychological consequence of diet-induced

In their review of the state-of-the-art of behavioral treatment of obesity,

Behavioral Treatment of Obesity

Table 3. Comparison of Behavioral Self-Management (BSM) with Food Dependence (FD)

Due to lack of skill in

Uncontrolled eating caused by

Rational mode1 of humans;

Irrational model; control

Focus on cognitions, emotions

Healthful eating; eat only

From Goodrich and Foreyt (1991).

and maintenance of obesity, rather than theories of behavior change, that

The Food Dependency Model

eating is not a form of psychoactive substance abuse (Wilson, 1993). There

Behavioral Treatment of Obesity

LifestyZe Change verse Weight Loss

As an alternative to weight loss treatment, Garner and Wooley (1991)