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1 6
THE PSYCHOLOGY
OF OBESITY
ashley moskovich , jeffrey
hunger , and traci mann
The fi eld of psychology traditionally focuses on the study of individuals, their
internal mental processes, and their behavior; as such, it has adopted this approach
in the study of obesity. Rather than examining larger groups, such as communities,
or distal factors, such as laws, policies, or environmental barriers, psychologists
have explored people’s emotions, beliefs, goals, and behaviors as causes and conse-
quences of obesity. In recent years, however, and paralleling the direction of the
fi eld as a whole, psychologists have broadened their focus to include the infl uence
of relationships and social networks on obesity, as well as the role of genetic
and neurological factors in the development of obesity. With regard to treatment,
psychologists have focused primarily on behavioral rather than medical interven-
tions, and recently have begun to explore whether weight loss is a reasonable or
even necessary goal in treatments for obesity.
Causes of Obesity
A substantial body of work in psychology has been dedicated to exploring the causes
of obesity. Psychology originally viewed obesity as a result of psychopathology or as
a response to a signifi cant trauma in a person’s past (Kolata 2007 ). However, sup-
port for these assumptions has been mixed, and these explanations are not thought
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1to account for most cases of obesity (Stunkard and Wadden 1992 ). Rather, the focus
has been on individual factors such as thoughts, behaviors, and biology, as well as
aspects of the individual’s social environment such as familial and peer infl uences.
Many early theories of obesity continue to be refi ned and incorporated into current
etiological models.
The Individual
In 1957 it was proposed that obesity was the result of overeating — a behavioral fac-
tor — and was not exclusively due to impaired metabolic functioning (Kaplan and
Kaplan 1957 ). Much of the work within the fi eld has since focused on behavioral,
rather than biological, causes of obesity, and on overeating in particular. Early
research focused on differences in eating between obese and non-obese individuals,
but over time it became clear that many of the factors that promote overeating in
obese individuals also promote overeating in some non-obese individuals. Interest
has not only focused on determining who o v e r e a t s , b u t a l s o when a n d why overeating
occurs. Four major individual factors have been explored as causes of overeating:
interoceptive awareness (i.e., sensitivity to internal bodily states), response to
emotional experience, cognition, and biology.
Schacter’s internal-external theory of eating holds that different factors guide
eating for obese individuals from those that guide eating for non-obese individuals
(Schacter 1968 ; Schacter, Goldman, and Gordon 1968 ). According to this theory,
non-obese individuals use the internal sensations of hunger and satiety to guide
their eating, whereas obese individuals are less interoceptively aware and instead
rely on external cues such as the time of day or the presence of appetizing foods to
regulate eating. Although this theory is intuitive and parsimonious, original sup-
port for it was mixed and its basic premises have since been questioned (Rodin
1981 ). In particular, some have challenged the assertion that an overreliance on
external cues by obese individuals necessarily indicates that they are less interocep-
tively aware than non-obese individuals (Rodin 1981 ; Herman and Polivy 2008 ).
Furthermore, it has also been argued that non-obese individuals are not better than
obese people at using internal cues to regulate their eating, and that they are also
infl uenced by external cues (Rodin 1981 ; Herman and Polivy 2008 ).
Although it has been challenged, the internal-external hypothesis has not been
abandoned; rather, recent work has instead been expanding upon it. For example,
Herman and Polivy ( 2008 ) posit that the confl icting fi ndings from past research
actually demonstrate a clear pattern of eating behavior. They argue that some types
of external cues (e.g., portion size), which the authors refer to as normative cues,
infl uence everyone, whereas other cues (e.g., palatability), called sensory cues , only
impact the eating of obese and dieting individuals. Thus the internal-external
hypothesis is still present in the way in which we view the causes of obesity.
Differences in the way individuals respond to emotional experience is another
factor that is thought to play a role in the development of obesity. According to the
psychosomatic hypothesis (Kaplan and Kaplan 1957 ), obese people overeat as a way
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1of coping with emotional distress. Obese individuals are thought to have learned
that eating reduces feelings of anxiety and therefore overeat as a way to self-soothe.
This results in a continuous cycle in which overeating aimed at reducing distress
actually promotes further distress and subsequent overeating (Kaplan and Kaplan
1957 ). Similarly, and foreshadowing the internal-external hypothesis, Bruch theo-
rized that obese individuals have diffi culties with interoceptive awareness and
therefore misinterpret emotional states as hunger (Bruch 1961 ).
Although these early theories have received only mixed support (Greeno and
Wing 1994 ), eating in response to emotional experience is still viewed as an impor-
tant contributor to overeating and obesity (Canetti, Bachar, and Berry 2002 ).
Research shows that some individuals, not exclusively obese individuals, exhibit a
tendency to overeat when in the presence of strong emotion, particularly negative
affect (e.g., Van Strien and Ouwens 2003 ; Polivy, Herman, and McFarlane 1994 ).
While emotional eating is well documented, it is still unclear why such behavior
occurs. Many studies have been unable to demonstrate that emotional eating atten-
uates negative affect (i.e., negative emotion states such as anxiety) (e.g., Herman
and Polivy 1975 ). Recent work, however, found that eating palatable food improved
mood among individuals classifi ed as emotional eaters (Macht and Mueller 2007 ).
Replication of this effect and clarifi cation of moderators and mechanisms will be
essential to this growing body of work.
The third individual factor thought to contribute to overeating, cognitive con-
trol, was introduced in a study by Herman and Mack ( 1975 ). This study highlighted
what has been termed the disinhibition effect — the phenomenon that restrained
eaters, or dieters, engage in overeating after a perceived diet violation. This phe-
nomenon is considered a cognitive one (as opposed to a physiological one, for
example) because what matters is not whether restrained eaters actually violated
their diets, but whether they think that they did. Research supporting the role of
cognition shows that restrained eaters will overeat if they believe they have violated
their diet when in fact they did not, but they will not overeat after an actual diet
violation if they are led to believe that the food they consumed did not actually
violate their diet (Polivy and Herman 1985 ).
An individual’s self-imposed restraint essentially functions as a form of self-
control and is therefore susceptible to a broad range of factors known to contribute
to regulatory failures. These factors, such as ego threats (Heatherton, Herman, and
Polivy 1991 ), stress (Greeno and Wing 1994), and distraction (Mann and Ward
2000 ), have been shown to lead to overeating among restrained eaters, but not
among non-restrained individuals. Although restraint status has proven to be a
reliable indicator of overeating and has generated a considerable amount of research,
there is controversy over how it is best conceptualized and measured (Ruderman
1986 ); many believe that restraint only leads to self-regulation failure among
individuals who are also disinhibited eaters.
The fourth factor that has been explored as a source of overeating is individual
differences in biology. In an effort to explain discrepant results of externally based
eating behavior among obese individuals, Nisbett proposed a biological explanation
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1known as set-point theory (Nisbett 1972 ). According to Nisbett, everyone has
a biologically determined and physiologically defended weight set-point that ulti-
mately guides eating behavior. Regardless of current weight status, obese and non-
obese individuals may at times be below their actual set-point, causing them to be
in a state of deprivation that promotes externally guided eating. When individuals
are at their set-point, deprivation ceases and externally guided eating diminishes.
Set-point theories suggest that biology is a key predictor of obesity, but they
are impossible to prove or disprove and cannot account for a variety of eating phe-
nomenon, ultimately limiting their utility (Pinel, Assanand, and Lehman 2000 ).
Current research is examining how underlying differences in neurobiology
guide eating behavior. For example, there are promising results in neuroimaging
research on impulsivity, craving, binge eating, and restraint (Lowe et al. 2009 ). Such
work may help explain confl icting results found in behavioral research and may
provide necessary insight into the transactional relationship between internal and
external variables.
The Environment
In addition to individual variables that contribute to overeating and the development
of obesity, psychologists also focus on environmental causes, including familial and
social infl uences.
Because obese children are likely to become obese adults (Epstein, Wing, and
Valoski 1985 ), factors associated with the development of pediatric obesity, includ-
ing the family environment, are the focus of much research. Parents affect the eating
of their children both directly and indirectly. Parental infl uence, whether by model-
ing eating behavior, directly controlling their children’s eating behavior, or provid-
ing feedback regarding the child’s weight and shape, has been shown to foster
restrained and disinhibited eating in children (e.g., Cutting et al. 1999 ; Pike and
Rodin 1991 ; Carper, Fisher, and Birch 2000 ; Francis and Birch 2005 ). A restrained
eating style, as mentioned above, promotes vulnerability to disinhibition and over-
eating, increasing the likelihood that obesity will result.
Preliminary evidence suggests that chronic levels of psychological stress in the
family are related to obesity in children (Koch, Sepa, and Ludvigsson 2008 ).
Psychological stress encountered in childhood may lead to the development of an
emotional eating style. A recent study conducted by Greenfi eld and Marks ( 2009 )
found that individuals who reported experiencing physical and psychological vio-
lence from their parents when they were children had a greater risk for adult obesity
than those who had not experienced such violence. Moreover, the association
between a past history of physical and psychological violence and obesity was par-
tially mediated by the use of food as a coping response to stress. Family stress levels,
like parental infl uences over eating, appear to contribute to obesity by fostering
individual behaviors that are associated with overeating.
In addition to familial infl uences on overeating and obesity, researchers have
also looked at other social infl uences. A recent study by Christakis and Fowler ( 2007 )
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1investigated the “social spread” of obesity; that is, they examined whether weight
gain in one individual was correlated with weight gain in members of their social
networks. Their results suggest that obesity can spread through social ties. While
the fi ndings are not able to speak to mechanisms through which this may occur, the
authors suggest that social infl uences may promote obesity by changing norms for
acceptability of being overweight and also by directly infl uencing individual behav-
iors such as eating. A study exploring social infl uences of obesity in adolescents
found similar results as overweight adolescents were more likely to have overweight
friends than their normal weight peers (Valente et al. 2009 ). Recent work, however,
has critiqued the methodology used to investigate social network effects and has
argued that the studies should be interpreted with caution (Cohen-Cole and
Fletcher 2008 ).
The past 50 years of research on the psychological causes of obesity have helped
to isolate many important predictive factors and to clarify that obesity results from
a variety of intra- and inter-individual factors. We hope that these factors (and
other newly isolated factors) can ultimately be combined into an integrated model
that can predict who will become obese and why.
Correlates or Consequences of Obesity
Because research on the causes and consequences of obesity is correlational by
nature, any variable that is found to be associated with obesity can technically only
be considered a correlate, as opposed to a predictor or a consequence. However, the
literature does divide the correlates of obesity into those that have been shown to
precede obesity in time and are thought to be causes, and those that follow obesity
and are thus considered to be consequences. In this section, we focus on factors that
may be consequences of obesity, or perhaps only correlates, but that we are reason-
ably certain are not causes.
Stigma and Discrimination
Overweight and obese individuals face stigmatization and unfair treatment simply
because of their weight. It is often assumed that denigration and derision of over-
weight individuals can only serve to help motivate weight loss, justifying prejudice
and discrimination as “for their own good” (Brownell 2005 ). In actuality, perceived
weight discrimination and stigmatization likely have negative effects on an indi-
viduals’ psychological well-being (Hatzenbuehler, Keyes, and Hasin 2009 ) and may
contribute to the physical health problems (Maclean et al. 2009 ) that are usually
directly attributed to obesity.
Implicit bias against overweight is particularly strong (Teachman et al. 2003 ),
equivalent — if not greater than — bias due to age, race, and gender (Nosek, Banaji,
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1and Greenwald 2002 ). Moreover, Puhl, Andreyeva, and Brownell ( 2008 ) demon-
strated that approximately 5 percent of overweight (BMI between 25 and 30) men
and 10 percent of overweight women experienced weight discrimination on a
daily basis. For individuals with a BMI greater than 35, these numbers jumped to
28 percent and 45 percent for men and women, respectively. Among this segment
of society, daily interpersonal discrimination — through decreased civility and
increased harassment and rejection — is the agonizing norm.
Physicians and other health care professionals routinely endorse negative ste-
reotypes about their overweight and obese patients. In a recent survey involving
primary care physicians, more than half of the physicians in the sample believed
that their obese patients were awkward, unattractive, and non-compliant, and a
third believed that they were weak-willed, lazy, and sloppy (Foster et al. 2003 ).
Given the sensitive nature of explicitly admitting such beliefs, this number is
undoubtedly an underestimation. Similar stigmatizing attitudes are also expressed
by the next generation of doctors, medical students (Wear et al. 2006 ). Particularly
concerning is how this biased perception translates into diminished care for
overweight patients. Nearly 70 percent of overweight and obese women reported
weight stigmatization from their physician (e.g., inappropriate comments about
their weight), and 46 percent reported similar experiences from nurses (Puhl
and Brownell 2006 ). Given how likely it is for obese patients to view the medical
setting as stigmatizing or threatening, it is not surprising that many patients avoid
or delay treatment (Drury and Louis 2002 ). This under-utilization of health care
services may lead to some of the physical health problems that are attributed
to obesity.
Overweight individuals also face noticeable discrimination in employment set-
tings, where they tend to be stereotyped as less conscientious and agreeable than
non-overweight employees (Polinko and Popovich 2001 ). A meta-analytic review
of weight discrimination in employment concluded that overweight applicants
were at a particular disadvantage when applying for jobs with considerable contact
with the public, and that they were rated less favorably when being evaluated as a
potential coworker (Roehling et al. 2008 ). In a survey of over 2,000 overweight
employees, 54 percent reported experiences of weight stigma by their fellow employ-
ees, and 43 percent reported such experiences by their employer (Puhl and Brownell
2006 ). This type of workplace discrimination ranges from inappropriate comments
and abusive joking to denied promotions and termination (Puhl and Heuer 2009 ).
Weight bias can also have a negative effect on romantic relationships (Chen
and Brown 2005 ), customer service interactions (King et al. 2006 ), and the educa-
tional environment (e.g., Puhl and Latner 2007 ). Given the unmistakably harmful
impact that weight bias has on the lives of millions of overweight and obese indi-
viduals, and the lack of success in reducing obesity itself, social and behavioral
scientists should consider it a priority to develop and test effective strategies
for eliminating this pervasive bias. Attempts to reduce weight bias have involved
providing information about the etiology of obesity or trying to create empathy
for the daily struggles of obese people, but these efforts have had mixed results
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1(e.g., Teachman et al. 2003 ) . I t m a y b e t h e c a s e t h a t u s i n g m u l t i p l e s t i g m a - r e d u c t i o n
approaches in concert will be necessary to combat such a strong bias.
Mental Health Consequences
Given the myriad ways in which obese people are discriminated against and stigma-
tized in our society, it would not be surprising if mental health problems resulted.
And because it was thought that obesity was caused by psychopathology, many
studies explored whether obesity and a variety of mental disorders co-occurred.
Thus resulted several decades of cross-sectional studies that were similar in that
they included a measure of obesity and a measure of at least one emotional prob-
lem, but that varied according to how they defi ned obesity, and how they defi ned
and measured emotional problems (Friedman and Brownell 1995 ). In that genera-
tion of studies, individuals usually self-reported their weights, and trained clini-
cians almost never used diagnostic criteria to assess mental disorders, which were
often measured with a single self-reported item. Findings from these studies rarely
found evidence for the relationship between obesity and psychopathology, but
because of the overall inconsistency of the results, it was possible to use them to
support whatever conclusion one desired. The majority of reports concluded that
obesity was not related to mental illness (see Stunkard and Wadden 1992 for a
review), but some suggested that obesity was associated with increases in the preva-
lence of mental illness, while still others argued, in what became known (rather
condescendingly, in our view) as the “jolly fat hypothesis,” that obesity was actually
related to improvements in emotional health (Crisp and McGuinness 1976 ).
In more recent years, a number of studies (Hasler et al. 2004 ; Mather et al.
2009 ; Onyike et al. 2003 ; Pickering et al. 2007 ; Scott et al. 2007 ; Simon et al. 2006 )
have addressed this question with carefully attained nationally representative sam-
ples and clinical measurement of mental illness. Like the prior generation of
research, the results of these studies were inconsistent, with some fi nding evidence
for associations between obesity and increased risk for depression or anxiety,
and others fi nding no signifi cant relationships (or in one case, the opposite: that
obesity was associated with a lower risk of anxiety; Hasler et al. 2004 ). Even when
signifi cant associations are found, they tend to be small effects, with odds ratios
around 1.3.
The most rigorous tests of the link between obesity and mental illness come
from prospective longitudinal studies, and these have focused primarily on depres-
sion (Bjerkeset et al. 2008 ; Herva et al. 2006 ; Roberts et al. 2000 , 2003 ). These stud-
ies measured BMI at baseline and then depression from one to 17 years later. All
three found a signifi cant relationship between baseline obesity and increased
depression at follow-up, although in the study with the 17-year follow-up, the rela-
tionship was found for men, but not women. Importantly, the one prospective
study that controlled for baseline depression still found a signifi cant relationship
between obesity and later depression (Roberts et al. 2003 ). In addition, that study
also tested the reverse path, and found that baseline depression did not predict later
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1obesity (controlling for baseline obesity), suggesting, in what appears to be the most
rigorous test to date, that the causal direction of the relationship may be obesity
preceding depression rather than the reverse.
Considering the fi ndings from the nationally representative cross-sectional
studies and the prospective longitudinal studies, it seems that a reasonable conclu-
sion is that obesity does seem associated with later depression, but that this rela-
tionship is not particularly strong. Only one prospective study looked at anxiety,
and it did not fi nd evidence for a link between obesity and anxiety (Bjerkeset et al.
2008 ). In general, the evidence for a link between obesity and anxiety seems weaker
and more tenuous than that between obesity and depression.
What does seem clear, however, is that regardless of whether obesity causes
diagnosable mental disorders, it does have psychological consequences. Research
with children and adolescents generally fi nds that obesity is related to body dissat-
isfaction (Ricciardelli and McCabe 2001 ; Wardle and Cooke 2005 ) and low self-es-
teem (French, Story, and Perry 1995 ; Wardle and Cooke 2005 ). When individuals of
all ages and genders are studied, it appears that the relationship between obesity
and low self-esteem is stronger in women than in men, gets stronger from child-
hood through college age, and then starts to weaken (but remains signifi cant)
among adults (Miller and Downey 1999 ).
The relationship between obesity and self-esteem may be mediated by the stig-
matizing behaviors of others, such as, among children, weight-related teasing
(Davison and Birch 2002 ; Thompson et al. 1995 ). It may also be mediated by indi-
viduals’ own internalization of stigma, such as believing their obesity is entirely
under their control (Pierce and Wardle 1997 ), or by the emotional toll of chronic
and repeated diet failures (Miller and Downey 1999 ).
Physical Health Consequences
It has long been thought that obesity leads to physical health consequences, and the
particular ailments attributed to obesity have included cardiovascular disease,
strokes, hypertension, many cancers, diabetes, gallstones, chronic renal failure, fatty
liver disease, gout, osteoarthritis, migraines, dementia, carpal tunnel syndrome,
asthma, infertility, pregnancy complications, polycystic ovaries, erectile dysfunc-
tion, hirsutism, sleep apnea, and incontinence (NHLBI Expert Panel 1998 ). It has
not been shown, however, that obesity per se actually causes these ailments, because
the primary type of study that can show such causal links cannot be conducted for
obesity. That type of study, the randomized controlled trial, is not possible because
it requires randomly assigning individuals to either be obese or not obese, and then
watching those individuals over the next several decades to see which diseases they
contract.
Researchers must settle for the next best form of evidence, prospective longitu-
dinal studies, in which individuals who happen to be obese (or not obese) are
observed over many decades. Health differences found between obese and non-
obese people in these studies may appear to have been caused by obesity, but in fact
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1may have actually been caused by some additional factor that also varies between
obese and non-obese people. It is all too easy for people not versed in research
methods to mistakenly assume that such studies are convincing evidence of obesity’s
causal role in many diseases.
In the last 20 years, scientists (as well as activists and journalists) have begun to
explore a variety of confounding factors that may account for the relationship
between obesity and physical health problems (Campos et al. 2005 ). This has led to
a contentious and politicized debate (described in Kolata 2007 ) that is unlikely to be
easily resolved. The confounding factors that may play an important role in this
relationship are obese people’s greater likelihood (than non-obese people) of lead-
ing sedentary lifestyles, repeatedly gaining and losing weight (known as “weight
cycling”), avoiding health care, and being in lower socioeconomic groups (Campos
2004 ; Ernsberger and Koletsky 1999 ). These factors have been shown to be associ-
ated with poor health and, to the extent that they are more likely to occur among
obese people than non-obese people, may account for the relationship between
obesity and disease.
Another factor that muddies the evidence for obesity as a cause of health prob-
lems is data suggesting that obesity does not shorten an individual’s lifespan, or at
least not until extremely high levels of obesity are reached (Flegal et al. 2005 ). It is
diffi cult (although not impossible) to convincingly argue that obesity causes such a
long list of ailments but somehow does not shorten one’s life. The evidence is also
called into question because studies supporting the relationship between obesity
and health outcomes tend to be conducted by researchers with signifi cant confl icts
of interest (Fraser 1998 ).
As researchers with no vested interests on either side of this debate (as we study
psychological outcomes of diets and obesity rather than physical ones), we have
observed this debate from the outside. It is our conclusion that the links between
obesity and some diseases are quite convincing, such as that between obesity and
type 2 diabetes (Colditz et al. 1995 ; Ford, Williamson, and Liu 1997 ) and osteoarthri-
tis (Hochberg et al. 1995). However, it is equally clear to us that the strength of the
links between obesity and many other ailments has been overstated (Olshansky
et al. 2005 ). Even if these relationships cannot be entirely explained away by con-
founding variables, they do not seem strong enough to warrant the amount of alarm
they receive from the media, scientists, and the government.
Treatment of Obesity
Despite imperfect models regarding its etiology, strong beliefs in the physical health
consequences of obesity have led researchers to develop treatment interventions.
Most of these interventions have been diets designed to promote weight loss.
More recent efforts, however, have included interventions aimed at treating the
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1self-esteem and body dissatisfaction that result from obesity, without necessarily
focusing on weight loss.
Treating the Physical Health Consequences of Obesity
Given the fi eld of psychology’s long history of research on behavior change, it is not
surprising that its approach to the treatment of obesity is to try to alter people’s
eating habits by teaching them diet strategies. Over the past 60 years, psychologists
have studied dozens of behavioral weight loss techniques to see which are effective
(Leon 1976 ; Ayyad and Andersen 2000 ). They have taught dieters how to select
appropriate foods to eat, count calories, resist temptation, monitor how much food
they eat, and to reward (or punish) themselves for eating the right (or wrong)
amount of food (see Leon 1976 for a review). In some treatments they gave the diet-
ers all the food that they were allowed to eat, and in some cases the dieters were
required to do all their eating in a researcher’s laboratory or clinic (e.g., Wing and
Jeffrey 2001 ; Musante 1976 ). Psychologists have also explored the effectiveness of
having dieters give some of their own money to researchers and then trying to earn
it back by losing certain amounts of weight (e.g., Harris and Bruner 1971 ). They also
tested whether using social pressure could get obese people to reduce their con-
sumption (e.g., Wollersheim 1970 ). Finally, in efforts to create negative associations
with desired foods, researchers have paired dieters’ favorite foods with horrible
odors, and in other cases have actually jolted obese patients with electric shock
whenever they tried to eat a food they craved (e.g., Foreyt and Kennedy 1971 ; Meyer
and Crisp 1964 ).
As silly (or cruel) as some of these treatments may sound, by and large, what-
ever psychologists attempted generally led to at least some weight loss during the
early months of the diet (Jeffery et al. 2000 ; Perri and Fuller 1995 ). Across over 200
diet studies conducted from 1966 up until 2000, participants lost from 8 to 22
pounds in as many weeks — about a pound a week (Wing 2002 ). For a diet to truly
be considered successful, however, individuals must not just lose weight in the short
term, but they also must keep it off. The majority of diet studies do not follow par-
ticipants long enough to see if that happened. In fact, only 6 percent of over 800 diet
studies found by researchers in the year 2000 had follow-ups of three years or more,
and two-thirds of those had such serious fl aws that they offered little useful infor-
mation (Ayyad and Andersen 2000 ).
Across 14 studies with long-term follow-ups, participants initially lost an aver-
age of 30 pounds, but by four or fi ve years later, they had gained back all but 7 of
those pounds (Mann et al. 2007 ). These results likely infl ate the success of these
diets because the studies have multiple sources of systematic bias — all of which
make the diets look more successful than they were. For example, most of the people
who start these diet studies do not fi nish them, and the people who do fi nish are the
ones who do the best on the diets. In addition, many of the people in these studies
are not actually weighed by the researchers, but rather just tell the researchers their
weight over the phone or by mail. Since most people lie about their weight — and
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1say they weigh less than they actually do — this fl aw causes the diets to look like they
led to more weight loss than they really did. Another source of systematic bias in
these studies is that many of the participants went on additional diets during the
long follow-up period. This makes it appear as if the original diet had led to sus-
tained weight loss, when, in fact, these dieters likely gained back a lot — if not all — of
the weight before they started a new diet.
If the goal of obesity treatment is to have obese people lose enough weight to
make them non-obese, and to maintain that weight loss in the long term, then it
seems clear to us that behavioral treatments for obesity are unsuccessful. However,
it is the association between obesity and physical health problems that makes effec-
tive obesity treatment a high priority in our country’s research agenda. Given that,
we suggest that it doesn’t make sense to use weight loss — an indirect and imperfect
measure of health — as a marker of successful obesity treatment when we could
be measuring improvements in physical health more directly (Ernsberger and
Koletsky 1999 ). The next generation of obesity treatment research should focus on
physical health outcomes such as heart rate, blood pressure, and cholesterol levels,
rather than weight change. Indeed, research on exercise interventions show positive
health benefi ts on all of these outcomes, even in the absence of weight loss (Caudwell
et al. 2009 ).
Treating the Mental Health Consequences of Obesity
Early psychological interventions focused on altering eating behavior to the neglect
of mental health sequelae. It has even been argued that some mental health conse-
quences of obesity, especially body distress, are important motivators for behavior
change and that addressing them would be detrimental to weight-loss efforts.
While there has been some support for this, the negative social and psychological
effects of body distress and obesity are important areas of concern (Heinberg,
Thompson, and Matzon 2001 ; Schwartz and Brownell 2004 ; Wilson 1996 ). Body
image and self-acceptance themselves became primary aims of treatment due to the
combination of these negative consequences and ineffective long-term weight loss
treatments (Wilson 1996 ; Schwartz and Brownell 2004 ; Rosen et al. 1995 ).
It has been assumed that weight loss is a necessary prerequisite for improve-
ment in body image. However, research fi ndings have produced mixed results (see
Schwartz and Brownell 2004 ). A randomized control trial comparing a cognitive
behavioral body image therapy (CBT) or a no-treatment condition found that
although weight status remained unchanged, individuals who received CBT showed
signifi cant improvement in body image as well as improvement in psychological
symptoms, self-esteem, overeating, and eating guilt (Rosen et al. 1995 ). Another
study found that the promotion of body and self-acceptance in a non-diet wellness
intervention improved not only body image, but also physical health parameters,
without changes in weight (Bacon et al. 2002 ). These positive psychological and health
outcomes were sustained at a two-year follow-up, whereas initial improvements in
the diet group were generally not maintained (Bacon et al. 2005 ). In contrast,
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1a study comparing a combined body image treatment and weight control program
to a weight control program alone did not fi nd any additional improvement in
body image (Ramirez and Rosen 2001 ).
In addition to being targets of treatment, body image and weight acceptance
may also promote successful weight maintenance after weight loss occurs. A cogni-
tive behavioral therapy intervention for obesity created by Cooper and Fairburn
( 2001 ) encourages a shift from weight loss to acceptance of weight stability follow-
ing a pre-set period of time. Such promotion of weight- and self-acceptance is
thought to prevent psychological barriers, including focusing on unattainable
weight loss, from interfering with weight maintenance. In support of this, satisfac-
tion with body weight has been associated with improved maintenance of weight
loss, but fi ndings have been inconsistent and more research is needed (Foster et al.
2004 ; Byrne, Cooper, and Fairburn 2004 ; Ames et al. 2005 ; Gorin et al. 2007 ).
Targeting body image dissatisfaction and self-acceptance either in isolation or
in conjunction with behavior change therapy aimed at weight loss appears to be a
promising component of treatment. While continued research is needed to explore
the effects of these treatments, it is clear that the mental health consequences of
obesity should not take a back seat to treatments aimed solely at the physical health
consequences.
Conclusion
In 1999, psychologists, nutritionists, and other experts proposed a paradigm shift in
research and policy on dieting and obesity (Cogan and Ernsberger. 1999 ). They sug-
gested a health-centered, rather than a weight-centered approach to obesity. This
approach would encourage obesity researchers to design their interventions with
the goal of promoting fi tness rather than weight loss, and to use health markers as
their outcome variables, rather than relying on weight as the primary and critical
measure of success. Work consistent with this approach is accumulating, and
although the proposed shift has not occurred, we believe that it would be a positive
direction for the fi eld. It seems to us that even though interventions based on this
new paradigm may not reduce the prevalence of obesity, they are likely to improve
the nation’s health, and by helping to unlink the association between obesity and
illness, may even reduce the stigma of obesity.
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