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BEHAVIORAL
THIRTY
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@ 1993 Pergamon Press Ltd
TREATMENT
OF OBESITY:
YEARS AND COUNTING
G. Terence Wilson
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
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G. T. Wilson
2 Although the authors used the term self-control, they were describing situational
control by the arrangement of relevant environmental contingencies.
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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
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
Initial
Treatment Trials
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G. T. Wilson
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
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G. T. Wilson
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
39
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
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
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G. T. Wilson
41
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
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.
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G. T. Wilson
Behavioral
Treatment
of Obesity
43
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G. T. Wilson
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
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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
Treatment Be Improved?
48
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.
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G. T. Wilson
51
Than Treatment?
52
G. T. Wilson
4 A recent study by Wadden, Foster, Letizia, and Wilk (1992) failed to replicate these
findings, however.
BehavioralTreatment of Obesity
53
Treatments?
Health risks
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.
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G. T. Wilson
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
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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
57
FD
Etiology
Assumptions
Emphasis
Focus on behavioral
techniques
Source of
support
Family; friends
Peers
Nutritional
component
Self-monitored
caloric intake
restricted intake
quantified
58
G. T. Wilson
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).
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fat
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.
61
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.
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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
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G. T. Wilson
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
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G. T. Wilson
67
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