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Chapter 67 Toward an Integrated Biopsychosocial Model of Eating Disorders
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67
Toward an Integrated Biopsychosocial
Model of Eating Disorders
Linda Smolak and Michael P. Levine
Copyright © 2015. John Wiley & Sons, Incorporated. All rights reserved.
Department of Psychology, Kenyon College, USA
For at least 40 years theorists have argued that etiological models of eating disorders (EDs)
should be multidimensional (Garfinkel & Garner, 1982). Indeed, there are many such models
available, including recent variants presented by Kaye, Bailer, and Klabunde (2012) and
Wertheim, Paxton, and Blaney (2009). Most theorists, researchers, and clinicians in the field
endorse a multidimensional approach.
It is, then, a bit surprising that the two dominant paradigms in current ED theory emphasize
almost opposite approaches to etiology. One, the biopsychiatric or biologically based mental
illness (BBMI) approach, emphasizes genetic factors and brain functioning (Kaye et al., 2012;
Klump, Bulik, Kaye, Treasure, & Tyson, 2009; Nunn, Lask, & Frampton, 2011; Strober &
Johnson, 2012; see also Chapters 17, 28, & 30). In contrast, the sociocultural model focuses
on cultural themes and practices that are transmitted through convergent social messages about
body shape, weight, and the controllability or malleability of weight and shape (Stice, 1994;
Thompson, Heinberg, Altabe, & Tantleff‐Dunn, 1999; see also Chapters 21, 26, 29, & 31).
Certainly both types of theory routinely include other variables, most commonly personality
or temperament characteristics (e.g., perfectionism, harm avoidance; see Chapter 32) and
environmental stressors (e.g., poor parenting, sexual abuse, subcultures that enforce a drive for
thinness and a fear of fat; see Chapters 34 & 35). Furthermore, while both have made contributions to our understanding of EDs, they also each have important weaknesses (Levine &
Smolak, 2014). Yet each largely ignores or even disparages the major features and claims of the
other model. How, then, can we reasonably hope to integrate the approaches into a truly multidimensional model? Indeed, is it even reasonable to try? Or are the two models actually
opposing and irreconcilable scientific paradigms, like behaviorism and psychoanalysis?
The overarching goal of this chapter is to provide guideposts for a more inclusive multidimensional model of the development and maintenance of EDs. We do not intend to offer
a model, even as an example. This is partly because we are trying to avoid diagrams or a sequence
of paragraphs that will necessarily grant primacy to one variable or set of variables. In other
words, we are attempting to begin to defuse at least some of the disagreements between the
BBMI and sociocultural camps. We do, however, want to analyze the various components of
The Wiley Handbook of Eating Disorders, First Edition. Edited by Linda Smolak and Michael P. Levine.
© 2015 John Wiley & Sons, Ltd. Published 2015 by John Wiley & Sons, Ltd.
Smolak, L., & Levine, M. P. (2015). The wiley handbook of eating disorders. John Wiley & Sons, Incorporated.
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an inclusive, integrative model. To that end we suggest that a model of ED needs to consider
at least the following:
1
2
3
4
5
6
EDs have stages of development that need to be explained.
There are similarities across EDs as well as differences between ED and non‐ED populations,
particularly in terms of body image and eating behaviors.
Certain types of data are required to establish causal relationships.
Specific influences need to be distinguished from nonspecific influences.
We must account for gender, ethnicity, age, and cultural differences.
How separable are biological, environmental, sociocultural, and psychological influences?
Copyright © 2015. John Wiley & Sons, Incorporated. All rights reserved.
Stages of a Disorder
The behaviors associated with anorexia nervosa (AN) and bulimia nervosa (BN) are extreme
and unusual (Strober & Johnson, 2012; see also Chapters 8 & 9). It is unlikely that they suddenly appear overnight. Furthermore, there is a developmental path to all behaviors, whether
they are normative, idiosyncratic, or pathological. Thus, there is a pathway to ED. Models
should describe this development, establishing both causal and correlative factors. Research of
various sorts (Connors, 1996; Garfinkel & Garner, 1982; Steiger & Bruce, 2007), including
clinical experience, indicates that it is a virtual certainty that there will be multiple pathways,
demonstrating the developmental psychopathology principle of equifinality (Cicchetti &
Rogosch, 1996). In its current form, the BBMI model has little to say about these developmental pathways. Although there is a small amount of genetic developmental data (Klump,
Burt, McGue, & Iacono, 2007; Klump et al., 2012; see also Chapter 28), there are no prospective neuroscience data. Without prospective data, the premorbid brain functioning and
the pathway that brought the person to the brain associated with an ED (see Chapters 17 &
30) cannot be identified. On the other hand, although more data are needed, the sociocultural
model does have data predicting the onset of disordered eating and EDs (The McKnight
Investigators, 2003) as well as data from fairly young children (Dohnt & Tiggemann, 2006)
elucidating the development of risk factors for EDs. However, no model has defined an entire
developmental pathway.
At some point, a person decides to purge or to ingest only starvation levels of food. Some
developmental process creates a vulnerability. Then there may need to be a “trigger” that moves
the individual into a full‐blown ED. For example, the pioneering writings of Bruch (1973) and
Crisp (1983) suggested triggers related to indicators of maturation into adulthood. It may also
be, as is the case for other severe forms of psychopathology (Ingram & Price, 2010), that there
is some threshold level of cumulative risk factors or vulnerabilities. Once the risk factors or
vulnerabilities have accumulated to that level, the pathological behaviors emerge, perhaps as a
coping mechanism. A frequent critique of the sociocultural approach by BBMI theorists is that
many women demonstrate body dissatisfaction and use weight control techniques, but only a
small group develop ED (Levine & Smolak, 2014). Although a sociocultural model is theoretically capable of using multiplicative probabilities to explain how a high prevalence of risk
factors leads to a low incidence and prevalence of ED (Levine & Smolak, 2014), neither the
sociocultural nor the BBMI model has clearly identified how an ED is activated. That trigger,
or shift in levels of vulnerabilities, or emerging convergence of vulnerabilities and risks needs to
be explained.
Smolak, L., & Levine, M. P. (2015). The wiley handbook of eating disorders. John Wiley & Sons, Incorporated.
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Toward an Integrated Biopsychosocial Model of Eating Disorders
931
EDs are treatable, but it is often difficult to achieve complete remission, and relapse is fairly
common (see Chapters 12 & 55–62). Thus, it is important to distinguish factors that maintain
or worsen the disorder from factors that cause the disorder. Whereas some maintenance variables may be similar to those that cause the disorder, others may be different. BBMI models
suggest that neurochemistry is responsible for maintenance or exacerbation of eating disorders
(see Chapters 17 & 30), while cognitive theorists implicate the social and self‐generated
rewards associated with the pathological attitudes and behaviors (see Chapters 18 & 56).
There may be relationships between these maintaining factors and those that make a person
more resistant to treatment or more likely to relapse. Or, again, the resistance/relapse influences may be different factors, including, perhaps, elements of the treatment protocol.
It may be that no single model can identify developmental factors, activating forces, maintenance influences, and treatment success variables. However, it is important that model
designers identify which phase of the disorder they are seeking to explain in ways that can
guide research. Recognizing the different phases may be an important way of integrating
various models.
Copyright © 2015. John Wiley & Sons, Incorporated. All rights reserved.
What Needs to be Explained
It is important to outline what an etiological model of EDs must explain (Nunn et al., 2011).
We believe that one should begin by asking: what are the similarities across EDs that distinguish an ED from other phenomena, ranging from dieting to mood disorders? This question
acknowledges the fundamental importance of explaining (a) characteristics that are unique to
EDs, such as the self‐starvation that marks AN or the binge‐purge cycle that defines BN; and
(b) the “transdiagnostic” similarities within the family of currently recognized EDs (Fairburn,
2008). Then there are those attributes, such as a rigid and ruminative thinking, high levels of
harm avoidance, and dysregulation of the hypothalamic‐pituitary‐adrenal axis, which are associated with EDs but also with a number of other psychiatric disorders, such as depression and
anxiety disorders (Jokinen & Nordström, 2009; Nyman et al., 2011; Olatunji, Naragon‐
Gainey, & Wolitzky‐Taylor, 2013). We argue that specifying and explaining the hallmark ED
characteristics must be the central focus of any etiological theory. We also want to emphasize
that at this point we are not trying to identify causes; this section addresses only ED signs,
symptoms, and correlates.
Body Image Disturbances
In both AN and BN—and their clinically significant variants that were previously part of
“eating disorder not otherwise specified” (ED‐NOS) and are now recognized as “other specified feeding and eating disorders” (OSFED)—but not Binge Eating Disorder (BED), body
image disturbances are part of the current core diagnostic criteria (American Psychiatric
Association, 2013; see also Chapter 1). In AN, this takes the form of (a) a distorted perception
of the body as being fat when, in fact, it is emaciated; and (b) an extreme and unrealistic fear
of becoming fat. In BN, the body image‐related criteria are (a) body shape and weight unduly
influence self‐esteem and self‐definition; and (b) compensatory behaviors (e.g., vomiting) are
used to avoid becoming fat. These are defining features of the disorders. And the disorders are
not as distinct as a classification system makes them appear: the disorders are concurrent in
some people, and in others AN later gives way to BN (see Chapter 55).
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In addition, body image disturbances, particularly in the form of body dissatisfaction or
overconcern with weight and shape, are excellent predictors of the development of eating disturbances and disorders (Stice, 2002; The McKnight Investigators, 2003; see also Chapter 22).
In fact, Stice (2002) argued that body dissatisfaction was the single best predictor of eating
disturbances and disorders. This is consistent with the finding that levels of weight and shape
concerns are arguably the single best predictor of treatment failures, ranging from dropout to
relapse (see Chapters 55 & 64). Clearly, then, body dissatisfaction and weight/shape concerns
are more than simply markers of EDs. They are a crucial part of the core pathology of EDs and
hence must be a central element of any model of AN or BN.
BED symptoms are less focused on body weight and shape (see Chapter 10). Instead, the
criteria are eating‐related. This important distinction between BED and AN or BN raises the
likelihood that separate models will be needed for the disorders. Given this, the remainder of
this chapter emphasizes AN and BN. The link between AN and BN is further underscored by
the shifting between the disorders that is frequently noted, whereas crossover from AN or BN
to BED is substantially less common (Strober & Johnson, 2012; see also Chapter 55).
Copyright © 2015. John Wiley & Sons, Incorporated. All rights reserved.
Eating Disturbances
Again, eating disturbances are at the core of both AN and BN (American Psychiatric
Association, 2013). In AN the eating disturbance is severe, relentless, and all‐consuming dietary restriction, with caloric intake significantly below healthy levels long enough to produce
dangerously low body weight. Indeed, this self‐starvation can be sufficient to cause organ
damage or organ failure, leading to death (see Chapters 8, 12, 14, & 52). Such levels of dieting may result in neurochemical changes that maintain the problematic eating. The restriction
may also actually be negatively reinforcing in terms of arousal or anxiety management and
avoidance of postprandial distress (Kaye, Wierenga, Bailer, Simmons, & Bischoff‐Grethe,
2013), and/or positively reinforcing because restriction creates and sustains a sense of control
and achievement, particularly for a person obsessed with weight and shape (see Chapter 18).
Regardless of the cause, it does appear that severe caloric restriction is self‐maintaining.
Interference with this extreme dieting—or even the threat of refeeding—can result in withdrawal from treatment.
In BN the eating disturbance is binge eating followed by purging. Again, this is a potentially
life‐threatening set of behaviors, particularly self‐induced vomiting as a form of purging.
Physical damage to the cardiovascular or gastrointestinal systems presents a long‐term threat,
while aspirating vomit or hemorrhaging from the esophagus or stomach poses immediate
danger (see Chapter 14). There are also various long‐term and serious risks (e.g., to intestinal
functioning) created by abuse of laxatives and diuretics. Clients do not typically show the high
levels of resistance to ending binge eating and purging that those with AN demonstrate in
relation to restriction. However, about one third of those with BN relapse after treatment
(see Chapter 55), indicating that in a significant number of instances binge eating and purging
likely fulfill several psychological functions and are difficult to give up permanently (Johnson
& Connors, 1987).
Interestingly, calorie restriction, in the form of dieting and fasting, may play a role in the
onset of BN. Several prospective studies (Neumark‐Sztainer et al., 2006; Stice, Davis, Miller, &
Marti, 2008; see also Chapter 24) have indicated that self‐imposed dieting or fasting increases
the risk of bulimic behaviors and symptoms. For some people, avoiding certain foods, especially
foods of high caloric density, increases the reward value of those foods (Stice, Burger, & Yokum,
Smolak, L., & Levine, M. P. (2015). The wiley handbook of eating disorders. John Wiley & Sons, Incorporated.
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Toward an Integrated Biopsychosocial Model of Eating Disorders
933
2013). Thus, explaining the decision to restrict calories may be a particularly important component of any model attempting to explain the developmental pathways to AN and BN.
Other Characteristics
Most models of EDs focus on factors other than the body image and eating disturbances. For
example, genetic models often emphasize genetically mediated variables such as temperament,
including harm avoidance, while neuroscience perspectives describe neurochemical and
­hormonal differences between those diagnosed with ED and other women (Kaye et al., 2012,
2013; Striegel‐Moore & Bulik, 2007; Strober & Johnson, 2012). Sociocultural models may
highlight individual difference variables, including high levels of negative affect or a tendency
to engage in social comparison (Stice, 2001; Thompson et al., 1999). Table 67.1 lists and
briefly describes some of the more commonly cited differences between clinical EDs and
Table 67.1 Characteristics of eating disorders (EDs), beyond body image and eating patterns,
that theories should consider.
Variable
Comment
Cognition
Weight and shape schema may determine how people interpret messages and
experiences. Information processing biases re food and weight. Rigid,
absolute thinking concerning body
Most people with ED diagnoses also have other diagnoses. Depression and
anxiety disorders are particularly common
The nature, type, and frequency of ED appears to vary across cultures.
Cultural research also indicates that the introduction of American media
or body image values may increase ED
In the United States Blacks may experience fewer restricting EDs but not be
“protected” against other forms. Other U.S. ethnic differences have not
been consistently documented
Women experience EDs, particularly AN and BN, at higher rates than men.
These gaps may be narrowing
Women with first‐degree relatives suffering from an ED are more likely to
develop ED than those without ED in their families. Twin research
indicates a moderate to strong heritability
Women in the acute phase of ED have different levels of several
neurotransmitters in the serotonin, dopamine, and GABA systems
compared to those not suffering from ED. Some of these differences
continue even after recovery
Biopsychiatric proponents tend to emphasize “temperament” characteristics
that they argue are genetically based. These include harm avoidance and
negative affect. Theorists from a variety of perspectives have focused on
perfectionism. Sociocultural theorists often discuss individual
characteristics including self‐esteem, and a tendency to engage in social
comparison
Sexual abuse is generally accepted as a nonspecific influence on the
development of BN. Other forms of sexual violence, ranging from
harassment to rape, have been shown to be at least correlates. Other forms
of abuse have received less attention but may also be relevant
Comorbidity
Culture
Ethnicity
Copyright © 2015. John Wiley & Sons, Incorporated. All rights reserved.
Gender
Genetics
Neurochemistry
Personality
Trauma
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control samples. Note that these factors represent differences, which are essentially correlations, and not necessarily causal relationships.
It is also noteworthy that some reviews focus very heavily on personality or cognitive factors
that appear to be part of the clinical presentation of EDs (Nunn et al., 2011; Strober & Johnson,
2012). Such factors are often important in treatment, and rigorous research may eventually
establish their relevance to the etiology of EDs (Levine & Smolak, 2014; Smolak, 2012). But the
core components of EDs, those with important predictive abilities for the onset of EDs as well
as treatment success, are the body image and eating problems. While a model should include
other constructs, there must be a clear emphasis on the body image and eating dysfunctions.
Copyright © 2015. John Wiley & Sons, Incorporated. All rights reserved.
Data and Establishing Causality
In order to establish causality, especially in a relatively young scientific field such as EDs, caution
and good science require a network of data interpreted within theory. It is entirely possible that
every element of the biopsychiatric and sociocultural theories is correct; modern physics makes
it clear that the same set of phenomena looks and appears to act very differently, depending on
the scientist’s perspective (Greene, 2003). It is probable that many of the elements of each are
indeed factual. But we need data in order to establish which ones are correct. As indicated by
the logical positivism, empiricism, and emphasis on falsification that have long defined the
Western scientific model (Popper, 1959), these data need to be of a particular type.
Experimental data continue to be the gold standard of scientific research. Certainly, ethics
render some types of experimental studies impossible. However, imaginative use of convergent
data from treatment and prevention interventions, as well as case‐controlled retrospective
studies that incorporate psychiatric controls (Jacobi & Fittig, 2010), may provide at least a
partial solution. Furthermore, research must, at the very least, convincingly demonstrate that
a putative cause predates the onset of a symptom or disorder (Kraemer et al., 1997). Prospective
data are essential. Furthermore, it is critical that data collection begin in early childhood in
order to fully track the developmental precursors of ED. While there are both experimental
and prospective data for the sociocultural model (Smolak, 2012; Stice, 2002; Wertheim et al.,
2009; see also Chapters 26, 29, & 31), there are virtually none for neurobiological theories
and scant prospective data for genetic approaches (Klump et al., 2012). To be explicit, there
are no experimental data for the BBMI approach, unless one counts Stice et al.’s (2013) data
showing that fasting affects brain functioning. However, since BBMI theorists often minimize
the role of body image or dieting (because of their “normative” nature), these data do not
appear to be part of this model per se.
Neuropsychiatric researchers and theorists sometimes argue that evaluating brain functioning during and after an ED provides information about causality (Kaye et al., 2013). The
idea is that a neurochemical difference between ED and control women that exists only during
the acute phase of the illness (i.e., that disappears after recovery) is an outcome of the illness
per se. On the other hand, if the difference continues postrecovery (i.e., when the person is
restored to a normal state and normal functioning), it likely predated the illness and may be a
causal contributor. Thus, the acute phase of the illness is viewed as analogous to a “natural
experiment.” However, by definition, a “natural experiment” is not substantially better controlled and informative than any correlational study.
Furthermore, developmental neuroscientists have long established that any experience can
and does alter neurological structure and functioning (Cichetti & Curtis, 2006). Given the
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Toward an Integrated Biopsychosocial Model of Eating Disorders
935
duration, severity, and physiological effects of both AN and BN, there is little doubt that the
illnesses can result in long‐term and, perhaps, permanent alterations in the brain. Again, only
prospective research can identify precursors to EDs. Without either, or preferably both, experimental or prospective evidence, it is inappropriate to claim a “causal” factor has been identified. At best, one can claim to have uncovered a correlate. Of course, correlations are subject
to the possibility of confounding variables influencing or even determining the correlation.
The possible or even likely impact of a third variable raises two other points regarding methodology. First, studies attempting to identify contributing or causal factors in the development
and maintenance of EDs need to control for at least the most likely third variables. Studies that
measure only one predictor variable cannot do this. Second, replication is crucial. When findings are difficult to replicate, it raises the possibility that some third variable created the relationship. For example, it is possible that some of the brain‐ED correlation is actually attributable
to a comorbid disorder, a factor that is only sometimes considered through inclusion of either
psychiatric controls or covariance analysis.
Copyright © 2015. John Wiley & Sons, Incorporated. All rights reserved.
Specific versus Nonspecific Influences
We need to distinguish specific influences on EDs from nonspecific influences on various forms
of psychopathology (Connors, 1996). Nonspecific risk factors may certainly be important;
indeed, they may be crucial and, particularly in interaction with specific factors, even causal.
However, by definition, and as established through research across multiple outcomes (Ingram
& Price, 2010), nonspecific factors are not likely to result in the unique behaviors and attitudes
that are the hallmark of EDs. Thus, when identifying risk factors, it is important to delineate
what their roles are likely to be in EDs and what types of behaviors they may or may not explain.
The roles should include direct, indirect, interactional, and transactional pathways.
There are several factors that contribute to numerous forms of psychopathology, including
EDs. For example, sexual abuse has been related to ED, depression, anxiety disorders, and
personality disorders (Smolak, 2012; Thompson & Wonderlich, 2004; see also Chapter 34). In
almost all instances it is important to address the abuse experiences in therapy, independently
of the diagnosis. Yet, that will not typically relieve the ED symptoms. And some treatments
that are effective with other diagnoses, such as cognitive‐behavioral therapy (CBT), are most
successful with EDs if they are adapted specifically to EDs (see Chapter 56). In fact, Fairburn,
Cooper, and Shafran (2008) emphasize that the comparatively effective clinical intervention
known as enhanced cognitive behavior therapy (CBT‐E) “is a treatment for eating disorder
psychopathology, rather than an eating disorder diagnosis” (p. 23). And pharmacological
treatments that help reduce anxiety or depression symptoms have proven to be of limited value
with EDs (see Chapter 59). Addressing the risk factors and maladaptive psychological processes
that are specific to body image and eating dysfunction is most likely to reduce ED symptomology. It is noteworthy that arguably the most effective treatment and prevention techniques are
rooted in cognitive theory and target specific beliefs about weight and shape (Fairburn et al.,
2008; see also Chapters 18 & 56).
Much of the research based on the sociocultural model focuses on factors that influence
body image and weight control techniques. Internalization of the thin ideal has been a particular
emphasis. As noted earlier, body image is a particularly powerful predictor of the onset of EDs
as well as of treatment success. From the BBMI perspective, there certainly has been discussion
of specific genetic factors related to body image or disordered eating (Klump et al., 2012).
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However, no loci have been identified despite large‐scale genome‐wide studies (Verweij et al.,
2010). Furthermore, the BBMI model has frequently emphasized personality factors that are
not specific to ED over ED‐specific behaviors (Levine & Smolak, 2014).
Comorbid conditions are also important here. Somewhere between 60% and 80% of women
diagnosed with EDs have one or more comorbid conditions (Hudson, Hiripi, Pope, & Kessler,
2007; see also Chapters 15 & 54). Any research, then, needs to consider how the depression,
anxiety, personality disorders, or other psychiatric conditions might mediate or moderate
the relationship between the variable under investigation and EDs. While this is especially
important with nonspecific risk factors, it holds with specific risk factors too. For example,
body dissatisfaction is probably related to both depression and EDs, at least among women
(Stice, Hayward, Cameron, Killen, & Taylor, 2000).
Gender, Ethnicity, and Cultural Differences
Copyright © 2015. John Wiley & Sons, Incorporated. All rights reserved.
We must account for the gender, ethnicity, and cultural differences (see Chapters 23, 25, &
27). This principle reminds us, regardless of paradigmatic or theoretical orientation, that it is
inadequate to begin a model with a claim that all a model need do is explain why females
(or Whites or people living in Western cultures) develop EDs. Gender is not a fixed risk factor.
Researchers and theorists need to explain how and why females are more susceptible. The
same is true for ethnic, cultural, and sexuality differences.
Feminist theory likely represents the most intensive and complete interrogation of gender
and sexuality differences in EDs (Bartky, 1990; Bordo, 1993; Smolak & Murnen, 2004; see
also Chapters 19 & 27). Sociocultural perspectives also give some consideration to these issues,
though most of the specific theories (Stice, 1994, 2001; Thompson et al., 1999) give little
precise attention to them. Nonetheless, these theories do imply that anything that influences
the cultural messages involved in thin‐ideal internalization will be important. On the other
hand, BBMI models only rarely consider gender explicitly, instead assuming that women are
more likely to develop EDs (Kaye et al., 2013). These theorists have given little or no attention
to ethnicity or cultural differences, either in their theorizing or their research samples.
Biological versus Environmental versus Sociocultural versus
Psychological: How Separable Are They?
Some theorists seem inclined to argue that a particular set of variables has primacy over the
others. For example, Strober and Johnson (2012) suggest that genetic, neurochemical, and
genetically mediated personality variables are more important than sociocultural variables in
determining ED. Certainly we all want to generate the most parsimonious model possible.
However, the data are clear that sociocultural variables play a role in focusing women on body
shape, body management, and management of appetites, including eating. Similarly, it is evident that women whose EDs are active show neurochemical differences from those whose
EDs are remitted or controls. Furthermore, women are undoubtedly more affected than men.
All of these, and other, facts should be included in any model.
As we have emphasized throughout this chapter, this means that a variety of potentially
explanatory factors will need to be considered. It is the nature of the way that we do science,
and perhaps of human cognition, that we like to categorize risk factors as, for example,
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Toward an Integrated Biopsychosocial Model of Eating Disorders
937
biological or social. The current preference for flow‐chart type of models (e.g., as in Nunn
et al., 2011, or Wertheim et al., 2009), charting a path for our understanding, and perhaps for
a path analysis, encourages us to select a starting point. Yet, we should keep in mind that these
truly are heuristic conveniences, rather than accurate reflections of reality.
Let’s assume for a moment that we begin a model with the infant brain. We prefer this over
the construct of a “genetic predisposition” as a starting point because it is more measurable.
Even the brain of a newborn reflects the effects of genetic endowment, prenatal environment,
and perinatal complications or difficulties. If we were able to measure harm avoidance in a
newborn, which we cannot, we already would be unable to specify whether a high level was
attributable to genetics or perinatal complications. Similarly, by the time we look at a young
infant, we would be unable to tell whether negative affect, which can be effectively measured
during the first 6 months, is primarily rooted in genetics, exposure to prenatal stress or drugs,
or postnatal parenting, or some reciprocal interaction of factors. Developmental psychologists
have long argued that it is futile and misleading to try to separate such influences (Reese &
Overton, 1970).
The development of an ED, as with all development, occurs within a context. As
Bronfenbrenner (1979) first argued over 30 years ago, characteristics of the individual (understood at multiple levels of analysis, including the neurophysiological), the immediate environment, the environment influencing other people who in turn influence the individual, and
cultural values are all in constant reciprocal interaction in producing behavior and development
(see also Markus & Kitayama, 2010). As these relationships vary over time, it is important to
consider the timing of an influence. Among the possibilities included in timing effects are a
synchrony of events, periods of particularly high neuroplasticity, and transitions where there
are limited social supports available (Smolak & Levine, 1996). All of these examples may be
times when someone is more vulnerable to social messages or environmental trauma.
Copyright © 2015. John Wiley & Sons, Incorporated. All rights reserved.
Conclusions and Future Directions
There are several different models of EDs—psychodynamic, cognitive‐behavioral, feminist,
sociocultural, and biopsychiatric (see Chapters 17–21). Given its evidence base, the cognitive‐
behavioral model remains very influential in therapeutic interventions for BN and BED, while
the sociocultural and biopsychiatric approaches currently dominate risk factor research. In
many ways, the latter two models would appear to be incompatible. Few sociocultural theorists give attention to neurobiology or genetics, and some biopsychiatric theorists actually
dismiss sociocultural influences as central to ED (Levine & Smolak, 2014). Yet, there are some
attempts to integrate the perspectives, both theoretically (Striegel‐Moore & Bulik, 2007) and
in research (Suisman et al., 2012), suggesting that both make important and complementary
contributions. The goal of this chapter was to offer some suggestions as to what an integration
of these two, or any other theories, into a multidimensional, biopsychosocial theory, should
take into account.
Our focus has been on AN and BN, substantially because of their shared symptoms.
Specifically, both feature negative or distorted body image and eating dysfunction in their
symptomology. It is important to reiterate that these are not only symptoms but also predictors of the onset and recovery from EDs. On both a theoretical and applications level, it is
crucial that theories emphasize disordered body image and eating. Of course, these are not the
only characteristics of people with clinical EDs; differences between ED and control samples
Smolak, L., & Levine, M. P. (2015). The wiley handbook of eating disorders. John Wiley & Sons, Incorporated.
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938
Linda Smolak and Michael P. Levine
in terms of cognitive, personality, neurochemical, and genetic factors, as well as psychosocial
and environmental stressors, may be important to explain also. With this fundamental principle in mind, we offer the following as critical principles and directions for further EDs
research:
1
2
3
Copyright © 2015. John Wiley & Sons, Incorporated. All rights reserved.
4
5
If there are no experimental and no prospective data for a variable, it should not be discussed as causal. Gathering prospective data, particularly if data collection begins prior to
the onset of any symptoms, is difficult on many levels. But such data are absolutely crucial.
Because EDs, especially AN, are rare, procuring a large enough sample may well require
collaboration. Nevertheless, this may be a good starting point for integration of sociocultural and biopsychiatric models. Identifying high‐risk samples through genetic studies
(in terms of familial vulnerability) and high‐risk cultural groups (such as gymnasts or
dancers) might make it easier to end up with enough symptomatic participants to actually
draw conclusions.
Researchers should quit considering gender as a “fixed” variable. Feminist theorists argue
that most gender differences are rooted in culturally defined experiential differences. Even
physiological sex differences, such as hormonal levels, are affected by experiences. These
experiences, ranging from toys that encourage investment in appearance (Dittmar,
Halliwell, & Ive, 2006), to clothing that emphasizes girls’ sexiness (Goodin, Van Denberg,
Murnen, & Smolak, 2011), to sexual violence (Piran & Teall, 2012), need to be defined
and examined as causal factors in the development of EDs and as possible mediators and
moderators of other variables. Similar arguments can be made about ethnicity and culture.
Gender, ethnic, cultural, and age group differences may help to elucidate universal and
group‐specific contributors to ED.
The interactive and cumulative roles of cognitive, psychological, neurochemical, genetic,
social, and cultural factors need to be given more attention. Too many studies look only at
media or only genetics, for example. Certainly, it is not realistic to think that all things can
be examined in a single study. But we need to expend more energy combining levels of
influence and analysis, thereby testing new relationships.
Factors such as body image (particularly weight and shape concerns) that appear to
influence all stages of EDs (onset, maintenance, recovery) deserve particular attention. In
the case of body image, understanding what moves someone from “normative discontent”
to pathology or what distinguishes the two continues to be a particularly pressing issue.
We should always remember that the principal goal of our research is to find ways to prevent and treat EDs. Certainly, there is some value to just understanding the disorders,
including precise descriptions of symptom development and transformation over time. For
example, recognizing the role of trauma has led to changes in therapy protocols. But if a
causal factor truly is “fixed” and not amenable to intervention it is less deserving of research
attention than “variable” factors that can be more readily addressed in prevention and
treatment. It is noteworthy that genetic and neurochemical influences should probably not
be thought of as fixed, as they are consistently affected by environmental factors.
We believe that attention to these principles will enable researchers, who inevitably hold one
or more of a variety of perspectives, to clarify the model(s) from which they are working while
abandoning as futile the tendency to presume, and then seek validation for, the proposition
that one category of factors (e.g., “biological”) is primary. Borrowing a principle that has been
central in developmental psychology for well over 40 years (Reese & Overton, 1970), we need
Smolak, L., & Levine, M. P. (2015). The wiley handbook of eating disorders. John Wiley & Sons, Incorporated.
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Toward an Integrated Biopsychosocial Model of Eating Disorders
939
to insist that the adjective “biopsychosocial” be indicative of a nonreductive, integrative
approach that captures the complexity of the development, maintenance, and treatment of
eating disorders.
Copyright © 2015. John Wiley & Sons, Incorporated. All rights reserved.
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