The comorbidity of substance use disorders and eating disorders in women: Prevalence, etiology, and treatment

Addictive Behaviors 35 (2010) 392–398

Contents lists available at ScienceDirect

Addictive Behaviors

The comorbidity of substance use disorders and eating disorders in women: Prevalence, etiology, and treatment Erin N. Harrop a,⁎,1, G. Alan Marlatt b a b

University of Washington, Seattle, WA 98195-1629, USA Department of Psychology, Box 351629, University of Washington, Seattle, WA 98195-1629, USA

a r t i c l e Keywords: Eating disorders Anorexia nervosa Bulimia nervosa Substance abuse Drug use disorder Alcohol use disorder

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a b s t r a c t Substance use disorders often co-occur with eating disorders in female populations. This review addresses the prevalence and etiology of this comorbidity in women. Thirteen peer-reviewed journal articles are reviewed. Conclusions are drawn concerning prevalence rates, theory, and implications for treatment. Current research supports distinct etiologies and growth trajectories for both disorders. Thus, comorbidity presents with unique challenges, and often, worse outcomes. Though comorbidity rates are high, little research has been done concerning treatment. Given the high prevalence rates of these comorbid disorders, a specific treatment needs to be developed that targets both disorders simultaneously. © 2009 Elsevier Ltd. All rights reserved.

Contents 1. 2. 3.

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Method . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Results . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.1. Prevalence . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.1.1. Themes concerning prevalence . . . . . . . . . . . . . 3.1.2. Prevalence of AUDs and EDs in clinical populations . . . . 3.1.3. Prevalence of SUDs and EDs in clinical populations . . . . 3.1.4. Prevalence of SUDs and EDs in community populations . . 3.1.5. Conclusions about prevalence . . . . . . . . . . . . . . 3.2. Theories of etiology . . . . . . . . . . . . . . . . . . . . . . . 3.2.1. Addictions model . . . . . . . . . . . . . . . . . . . . 3.2.2. Genetic and familial heritability model . . . . . . . . . . 3.2.3. Biological model . . . . . . . . . . . . . . . . . . . . 3.2.4. Personality traits and temperamental vulnerabilities model 3.2.5. Developmental trajectories . . . . . . . . . . . . . . . 3.2.6. Conclusions concerning etiology . . . . . . . . . . . . . 3.3. Implications for treatment . . . . . . . . . . . . . . . . . . . . 3.3.1. Practitioner instructions for treatment of comorbidity . . . 3.3.2. Professional education, screening, and diagnosis . . . . . 3.3.3. Additions to current treatment . . . . . . . . . . . . . 3.3.4. Prevention . . . . . . . . . . . . . . . . . . . . . . . 4. Discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.1. Conclusions concerning prevalence, etiology and treatment . . . . 4.2. Implications for research and theory . . . . . . . . . . . . . . . 4.3. Implications for society . . . . . . . . . . . . . . . . . . . . . Role of Funding source . . . . . . . . . . . . . . . . . . . . . . . . . . . Contributors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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⁎ Corresponding author. Tel.: + 1 206 685 1395; fax: + 1 206 685 1310. E-mail addresses: [email protected] (E.N. Harrop), [email protected] (G.A. Marlatt). 1 Permanent address: 19805 Sunnyside Dr. N. #K205, Shoreline, WA 98133-2766, USA. 0306-4603/$ – see front matter © 2009 Elsevier Ltd. All rights reserved. doi:10.1016/j.addbeh.2009.12.016

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Conflict of Interest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 398 . Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 398 . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 398 .

1. Introduction Many women with substance use disorders also struggle with eating disorders. Of considerable concern is that both disorders are associated with the highest mortality risks of all psychological disorders (Franko et al., 2005; Harris & Barraclough, 1998). Individually, both disorders present with complex physical, emotional, and social challenges; together, they are a particularly dangerous combination (Franko et al.). Further, when both disorders are present, diseases have worse courses and outcomes (Keel, Mitchell, Miller, Davis, & Crow, 1999; Pearlstein, 2002). In the past 20 years, significant research has been done in both the eating disorder (ED) and addiction fields to determine the prevalence of comorbidity. Several theories have been posited to explain the etiology of these co-occurring disorders. However, few investigators have explored treatment options when these disorders present concurrently. The research poses three main questions: (a) how prevalent is the comorbidity of substance use disorders (SUDs) and EDs? (b) what theories exist to explain this comorbidity? and, (c) what are the implications for treatment? This paper reviews current literature concerning the comorbidity of eating and substance use disorders. After reviewing the major themes in prevalence and etiological research, it is argued that treatment efficacy research should be given the highest priority in this field. Given the high prevalence rates of these comorbid disorders, a specific treatment needs to be developed that targets both disorders simultaneously. 2. Method To identify pertinent research, searches were performed on Psych Info and Medline. The key words used were: anorexia nervosa (AN), bulimia nervosa (BN), eating disorders, substance use, substance abuse, chemical use, chemical abuse, chemical dependency, alcohol use disorder (AUD) and drug use disorder (DUD). Articles were eliminated if they addressed only: BN populations, male populations, binge eating disorder (BED), and highly specific populations. Ultimately, 13 articles were selected for review. This research is the basis for the findings reported in the following sections addressing prevalence, etiology, and treatment. 3. Results 3.1. Prevalence Substance use disorders are reported to occur in women with a lifetime prevalence rate of 18% (Pearlstein, 2002). Exploration of SUD prevalence rates raises several key classification issues. The research covers many degrees of substance abuse, ranging from one-time use to physiological dependence. In addition, researchers often choose to focus on specific substances, such as alcohol or opiates. This review addresses both alcohol use disorders and drug use disorders as they occur in association with EDs. Some studies address AUDs and DUDs separately. When referred to collectively, AUDs and DUDs will be called SUDs. Classification of eating disorders is similarly difficult. Currently, the American Psychiatric Association (APA) recognizes three types of eating disorders in the Diagnostic and Statistical Manual of Mental Disorders Fourth Edition (DSM-IV): anorexia nervosa, eating disorder not otherwise specified, and bulimia nervosa (APA, 1994). This review

focuses on BN and AN, and addresses both subtypes of AN, anorexia restricting type (ANr) and anorexia binge/purge type (ANbp). Because of the stringent criteria set forth in the DSM-IV, research sometimes examines disordered eating, a term applied to behaviors indicative of problematic eating and body image. This research is analogous to substance use research that examines sub-threshold SUDs and onetime usage. Research on these sub-threshold disorders offers insight into the developmental trajectories of both disorders and will be included in this review for that reason. Anorexia nervosa has a lifetime prevalence rate in women of 0.5–1.0%, with some studies suggesting that it is as high as 3.7% (APA, 1994, 2000; Pearlstein, 2002). Bulimia nervosa has a slightly higher prevalence rate in women, ranging from 1 to 3%, with others reporting it as high as 4.2% (APA, 1994, 2000; Pearlstein). Interestingly, these prevalence rates are elevated in addicted populations (Bulik et al., 1992; Gilchrist, Gruer, & Atkinson, 2007; Peveler & Fairburn, 1990; Wiederman & Pryor, 1996). 3.1.1. Themes concerning prevalence When exploring comorbidity prevalence rates, three key themes are discussed: the issue of clinical versus community samples, the type of ED diagnosis, and the connection between ED symptomatology to SUDs. First, most prevalence research has been conducted on clinical populations, leading to inflated estimates of diagnoses (Gadalla & Piran, 2007b). Alternatively, community research studies sample much larger pools of participants, resulting in more accurate data. However, such large studies are complicated, costly, and involve greater ambiguity of diagnosis (Gadalla & Piran). While clinical studies tend to rely consistently on DSM-IV classification of EDs and subtypes, community research studies often rely solely on self-report and various questionnaires (Gadalla & Piran). Thus, a combination of clinical and community samples is required to obtain the most accurate picture of comorbidity. Second, the type of ED diagnosis is gaining increasing attention in the literature of comorbidity. ED subtypes were not classified by the DSM until the fourth edition. For that reason many studies either failed to specify ED subtype, or did so without consistent criteria. Of particular interest to researchers is the suggestion that BN and ANbp result in significantly higher rates of SUD comorbidity. Generally, ANr is associated with increased levels of avoidance and obsessional behaviors. Researchers have suggested that ANr patients would be likely to restrict chemicals in addition to food (Bulik et al., 1992). Yet, BN and ANbp are associated with increased behavioral and emotional dysregulation as well as poorer impulse control. These behaviors are also characteristic of SUD. Given these similar characteristics, several theories have been posited regarding the correlation between binge/ purge behavior and SUD. Third, current researchers have focused on the similarity of ED and SUD symptomatology. Both disorders often involve disruption in appetite and satiation, obsessive and compulsive behaviors, selfdestructive behavior, denial, and severe medical consequences (APA, 1994; Cooper, 1989). These factors suggest similarities in etiology and have important implications for treatment. The topics of etiology and treatment are discussed, in turn, in later sections. 3.1.2. Prevalence of AUDs and EDs in clinical populations Peveler and Fairburn (1990) conducted an early study on the incidence of EDs in women with AUDs, using sample of women attending an impatient alcohol treatment center. Questionnaires were

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used to determine both severity of alcohol dependence and probable diagnosis of an eating disorder. Twenty-six percent of participants had clinical EDs. EDNOS diagnoses were twice as common as BN and AN diagnoses, 7% currently reported full symptoms of AN, and 19% reported a history of AN. The prevalence of a history of AN was particularly noteworthy. These prevalence rates of ED's are significantly higher than rates found in the general population. This research replicated earlier studies suggesting increased prevalence rates of EDs in AUD populations. The high comorbidity rates found in this study led researchers to question whether one condition was secondary to the other or if both conditions were expressions of the same underlying problem. Following early prevalence studies such as Peveler and Fairburn's (1990), research studies addressing the comorbidity of AUDs and EDs increased. Gadalla and Piran (2007a) reviewed this literature in a meta-analysis of over 40 studies. Overall, significant associations were reported between AUD and EDs. Associations between AUDs with BN and EDNOS were particularly strong. However, contrary to Peveler and Fairburn's study, associations between AN and AUD were not found. This discrepancy may be explained by the fact that some ANbp populations were categorized by researchers as BN populations, despite DSM-IV procedure (Bulik et al., 1992). There was significant heterogeneity in diagnostic criteria and multiple versions of the DSM were used. In order to determine the influence of EDs and AUDs on each other, Franko et al. (2005) examined the development of AUDs in ED patients over the course of 9 years. Over a quarter of participants reported lifetime occurrence of AUD; 17% had a history of AUD at intake, and 10% developed AUD over the course of the study. Significant differences between AN and BN in lifetime AUD prevalence rates were not found. However, women with ANbp had significantly higher rates of comorbidity than women with ANr. Interestingly, alcohol use disorders did not lengthen recovery time from ED episodes. The influence of EDs on AUDs appears greater than the influence of AUDs on EDs. This should not be ignored, because nearly 10% of patients diagnosed with comorbid ED and AUD died in the course of the study. This is a particularly high rate of mortality for a study lasting only eight years. Across ED types, mortality rates vary significantly. AN has the highest mortality rates of any psychiatric illness, with crude estimates ranging from 4 to 13% (Neumarker, 2000). Alternatively, BN mortality rates are estimated at 0.3% (Neumarker). AUD also results in elevated mortality rates. One longitudinal study found that women alcoholics who received treatment had mortality rates 3–5 times higher than women in the general population (Haver, Gjestad, Lindberg, & Franck, 2009). Similar research found that an increase of consumption of 1 L of pure alcohol was associated with an increase in mortality rates of 1.3% (Her & Rehm, 1998). Both EDs and AUDs are dangerous illness often resulting in death. The research suggests that these two disorders produce a frightening mortality rate when combined. These staggering mortality rates merit aggressive treatment for those with both disorders. 3.1.3. Prevalence of SUDs and EDs in clinical populations While examining the prevalence of neurotic symptomatology in female drug users, Gilchrist et al. (2007) also examined the presence of comorbid EDs. Of these addicted women, 14% reported having AN, and 14% reported having BN. A history of ED was associated with severity of neurotic symptoms in SUD patients and indicative of increased need for treatment. It is important to note that the rates of sexual and physical abuse were unusually high in this population, ranging from 50 to 65% respectively. Connors and Morse (1993) reviewed sexual abuse prevalence research in the general population and conservatively estimated that prevalence ranges from 10 to 30%. Eating disordered populations typically report prevalence rates of sexual abuse nearly double that of the general population (Calam &

Slade, 1989; Deep, Lelenfeld, Plotnicov, Pollice, & Kaye, 1999). Similarly, rates of physical abuse against women in the general population, estimated at 25%, are also lower than rates of physical abuse reported by ED patients (Bostock, Plimpton & Pratt, 2009; Gilchrist, et al.; Vize & Cooper, 1995). Furthermore, ED patients with comorbid SUD tend to have abuse rates nearly double that of their non-addicted counterparts (Deep, et al.). This suggests an association between SUDs, EDs and history of abuse that may explain aspects of comorbidity. Further research should examine abuse history as a mediator of comorbidity. When examining clinical ED populations, Bulik et al. (1992) found similar rates of comorbidity. Usage rates among ED patients were elevated for a variety of substances. Also, use rates may have been even higher if alcohol history had been measured in addition to current alcohol consumption. Though BN patients reported higher rates of poly drug use, these differences in ED subtype may be explained by the authors' classification of ANbp as BN. Though ED subtype may not be accurately reflected in this report, this research augments current findings concerning EDs and SUDs. Bulik et al.'s (1992) study highlights an important issue in comorbidity research: the similarity and ambiguity of ED and SUD symptomatology. Often, withdrawal and addiction symptoms mirror those of food deprivation. For example, Bulik et al. measured withdrawal based on these symptoms: craving, nervousness, irritability, headaches, restlessness, difficulty concentrating, shaking, drowsiness, sadness, increased/decreased appetite, constipation, edema, diarrhea, cramping, bloating, nausea, and dehydration. Of these, only craving is unique to substance withdrawal. Without additional measures it would be impossible to tell if these were symptoms of withdrawal or of the ED. In addition to prevalence research, Wiederman and Pryor (1996) examined specific associations of ED symptomatology and substance use. Substance use was elevated in ED populations with BN patients reporting higher rates than AN patients. Severity of caloric restriction predicted amphetamine use, binging predicted tranquilizer use, and purging predicted alcohol, cocaine, cigarette and poly drug use. It seems the type and severity of ED symptomatology is more indicative of substance use than ED subtype diagnosis. This suggestion may clarify future prevalence and etiological research. 3.1.4. Prevalence of SUDs and EDs in community populations In order to accurately gauge comorbidity prevalence, it is important to review both clinical studies and community studies. Gadalla and Piran (2007b) presented a community study exploring the association between DE attitudes and behaviors and substance use. In a national study of over 20,000 women, they determined that in the last year, 2.8% were at risk for EDs, 2% had alcohol dependence or interference, and 1% had dependence or interference of illicit drugs. Co-occurrence of ED and alcohol interference was 4.4 times more likely than would occur by chance. Eating disorder risk was strongly associated with both alcohol use and illicit drug use. The rates found in this community sample study support comorbidity rates found in clinical prevalence studies. 3.1.5. Conclusions about prevalence Both clinical and community sample studies report high levels of comorbid SUDs and EDs. Comorbidity prevalence rates range from 17 to 46% depending on the type of ED and subtype. Though some studies report comorbidity differences within ED subtypes, others do not. Rather, symptom type and severity appear to be more closely correlated with prevalence rates. Exploration of etiological factors, including family and genetic links, personality factors, and common underlying abnormalities may explain these high prevalence rates. 3.2. Theories of etiology In the fields of addiction and EDs, several theories attempt to explain this striking comorbidity. Pearlstein (2002) reviewed recent

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research and suggested several models of etiology: addictions model, genetic/familial heritability model, biological model and a personality/temperament model. The addictions model focuses on the similar symptoms underlying both disorders, including craving, lack of control and denial. The genetic and familial heritability model examines the genetic links between both disorders as well as familial risk factors. The biological model addresses the similarities in neurological systems affected by both disorders. Finally, the personality model suggests personality traits and temperaments that make an individual vulnerable to both disorders. In addition, growth trajectories research suggests two mediating factors in comorbidity. Each model contributes to the understanding of this etiology. 3.2.1. Addictions model One of the earliest models that attempted to explain the comorbidity of SUDs and EDs was the biopsychosocial addictions model proposed by Cooper (1989). This model highlighted the similarities between the symptoms of both disorders. Cooper argued that EDs and SUDs serve similar purposes, though they differ in disease manifestation. Additionally, ED and SUD patients share similar interplays of genetics, family histories, personality traits, and societal and cultural influences. Given these similarities, Cooper proposed that a biopsychosocial addictions model could explain the comorbidity of EDs and SUDs. He suggested both inpatient and outpatient treatments and emphasized the need for relapse prevention treatment, given high relapse rates in both disorders. Though these observations accurately reflect the occurrence of similarities in these disorders, this model is overly simplistic. Evidence for this approach is rooted more in addiction literature than ED literature. EDs present with physical complications that need to be addressed specifically in treatment. Given the complexities of EDs, eating disorder research should be included to buttress this model. Also, this model fails to explain differences between the disorders, such as high rates of antisocial personality disorder in SUDs and high compliance rates in EDs (Thompson-Brenner et al., 2008). A more integrated model is needed to address the complex needs of this patient group. 3.2.2. Genetic and familial heritability model Several researchers have suggested the possibility of heritable factors leading to the comorbidity of SUDs and EDs (Pearlstein, 2002; Peveler & Fairburn, 1990). Ranson, McGue, and Iacono (2003) investigated the association of EDs and SUDs in families by examining the correlation between parents' SUD and ED symptoms and daughters' SUD and ED symptoms. Though mothers' EDs were associated with daughters developing disordered eating, mothers' EDs were not associated with daughters' SUD symptoms. Similarly, parental SUD was associated with daughter development of SUD symptoms, but not with development of ED symptoms. It seems there are genetic links for both ED and SUD symptoms, but they are not cross-transmitted. Separate, non-interacting genetic factors appear to be active in each disorder. This suggests that SUDs and EDs are not different manifestations of the same disorder. Rather, they are two distinct disorders which share similar symptoms. 3.2.3. Biological model A biological model of comorbidity raises important considerations about the physical aspects of both disorders. First, disturbance in the dopaminergic system is a salient aspect of SUDs and EDs (Pearlstein, 2002; Rothman, Blough, & Baumann, 2008). Additional disturbances in serotonin, gamma-aminobutyric acid, and endogenous opiate systems are also thought to contribute to both disorders (Rothman; Pearlstein). The biological model suggests that development of each disorder can be traced back to these physical abnormalities; the root causes of comorbidity are the shared biological factors (Pearlstein).

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This model also emphasizes the importance of physical symptoms. Prolonged substance use and ED behaviors produce similar physical symptoms. Both disorders often involve the following: weight loss, appetite increase/decrease, decreased/increased heart rate, amenorrhea, fatigue, muscle weakness, insomnia, vomiting, diarrhea, anxiety, sexual dysfunction, constipation, nausea, restlessness, and difficulty concentrating (APA, 1994). SUDs and EDs are intricately connected to the body. Both disorders manipulate the state and function of the body— whether by malnutrition or substances. It is important to realize the effects these physiological changes have on mood and cognition. Of particular interest is the impact of starvation on substance use. Bulik et al. (1992) cited previous animal research that found that rats deprived of food consumed larger quantities of alcohol than a control group. These results were replicated with the administration of other drugs, exercise and intracranial self-stimulation in place of alcohol. Food deprivation may increase the biologically reinforcing effects of substances, and exercise. Given the extensive physical compensatory behaviors of starved bodies, it is not unreasonable to suspect that starved bodies react differently to substances (Woodside & Staab, 2006). However, more research is required to understand the efficacy of substances under starved conditions. 3.2.4. Personality traits and temperamental vulnerabilities model Eating disorder subtypes differ significantly in regard to behaviors and personality traits. AN is characterized by significant malnutrition and weight loss and fear of fat and weight gain, and is accompanied by body image disturbances (APA, 1994). Both AN subtypes involve foodrestriction behaviors, and patients exhibit symptoms of starvation such as decreased mental functioning and depression (APA, 1994). However, ANr patients are characterized only by food restriction and excessive exercise, whereas ANbp patients also engage in purging behaviors such as vomiting and laxative abuse. These differences in behavior are also reflected in patients' personality traits. All AN patients tend to possess traits of obsessionality, compliance, perfectionism and sensitivity (Vitovsek & Manke, 1994). However, ANr patients are more likely to be described as shy, anxious and dysphoric while ANbp patients are more likely to be described sociable and outgoing, and experience a less stable affect (Vitovsek & Manke). BN is characterized by distinctly different behaviors and personality traits. BN patients experience fewer symptoms of starvation and may not necessarily experience significant decreases in weight (APA, 1994). BN patients engage in binging behavior, often accompanied by unhealthy compensatory behaviors such as vomiting and laxative abuse. Similar to AN patients, BN patients also inappropriately evaluate themselves based on body shape and weight (APA, 1994). These distinct behaviors tend to be accompanied by more erratic behavior patterns that oscillate between the extremes of restraint and disinhibition (Vitovsek & Manke, 1994). BN patients are considered more compulsive, impulsive, and outgoing than their AN counterparts; patients also demonstrate less stability in affect (Vitovsek & Manke). While some of these characteristics may develop in response to behaviors, others predate ED onset. Pearlstein (2002) reported several personality traits that increase risk for development of AN and BN. For AN these traits include: perfectionism, obsessionality, harm avoidance, neuroticism and social isolation. For BN these traits include: impulsivity, stress reactivity, novelty seeking, affective dysregulation, interpersonal sensitivity, and low self-esteem (Pearlstein). Many of these traits are also risk factors in SUDs, including novelty seeking, high negative emotionality, low constraint, neuroticism, disinhibition, and negative affectivity (Grekin, Sher, & Wood, 2006). Personality models of comorbidity suggest that similar personality traits and temperaments create vulnerabilities in individuals that lead to the development of both disorders simultaneously. Thompson-Brenner et al. (2008) investigated the personality traits associated with comorbid substance abuse, and found that different personality traits appear to support the development of EDs and SUDs.

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While behavioral dysregulation traits predicted SUDs, avoidantinsecure and obsessional sensitive traits predicted EDs. Though SUDs and EDs appear to have many personality traits in common, other factors, such as drug use history, were better predictors of future symptoms. Thus, though personality research augments etiology theories, it is not sufficient to explain comorbidity. 3.2.5. Developmental trajectories Measelle, Stice, and Hogansen (2006) studied the developmental trajectories of these disorders. They hoped that an examination of the temporal associations with other disorders would shed light on the etiology of comorbidity. Eating disorder onset peaks between the ages of 14 and 18 years (APA, 1994). Substance use rates also increase during adolescence (Brown, Catalano, Fleming, Haggerty, & Abbott, 2005). Trajectories of depression, disordered eating behaviors, antisocial behaviors and substance abuse were determined. Depression and disordered eating behavior both increased linearly, while substance use followed an increasing non-linear “unspecified model” (Measelle et al.). All four conditions were significantly associated with one another, though degrees of association differed. Of particular interest was the unidirectional relationship of disordered eating and substance use. Though disordered eating predicted substance use, substance use did not predict increased disordered eating. This unidirectional relationship between disordered eating and substance use supports the idea that separate higher order factors mediate SUDs and EDs. Latent growth curve models determined that a two-factor higher order model fit the four trajectories best. One higher order factor was associated with antisocial and substance use behavior, and a second higher order factor was associated with depressive and disordered eating behavior. 3.2.6. Conclusions concerning etiology Though similarities are observed between the symptoms and development of EDs and SUDs, the differences are equally salient. Both disorders appear to have genetic components. However, data from heritability studies suggest separate genetic transmission of EDs and SUDs (Ranson et al., 2003). There is a striking absence of crosstransmission. Personality studies report surface similarities in ED and SUD personality types. However, deeper investigation of temperaments reveals unique ED and SUD personality traits (ThompsonBrenner et al., 2008). Finally, examination of developmental trajectories suggests two higher order factors mediate the relationship between SUDs and EDs, as opposed to one underling factor (Measelle et al., 2006). Though sharing many facets, these disorders appear to be distinct. Perhaps that makes comorbidity particularly dangerous. Individuals presenting with both disorders may be receiving, in effect, a double-dose of risk factors and vulnerabilities. 3.3. Implications for treatment The dangerous nature and high mortality rates of both disorders necessitate aggressive treatment. Most researchers recommended early intervention and dual care for those presenting with both disorders. However, no empirical studies addressed treatment efficacy. One article reported brief instructions for practitioners treating EDs (Woodside & Staab, 2006). Other researchers made brief suggestions as to the treatment applications of their study. It is imperative that these suggestions gain empirical support with treatment efficacy studies. 3.3.1. Practitioner instructions for treatment of comorbidity Woodside and Staab (2006) suggested several practical applications for comorbid treatment of SUDs and EDs. They repeatedly emphasized the importance of recognizing the physical, psychological and cognitive effects of starvation. Starvation and unstable eating profoundly alter mood and cognition. As is the case with most disorders co-occurring with EDs, little improvement can occur when

the body is starved. Interventions aimed at stabilizing body weight are necessary for additional treatment to be effective. Because both disorders are difficult to treat, patients with comorbid disorders should receive priority in care. According to Woodside and Staab (2006), it is preferable to have inpatient care for both EDs and SUDs. This is particularly necessary with AN patients. If inpatient facilities specializing in both disorders are not available, another option involves a 30 day “dry out” period for the patient in a SUD treatment center, followed by inpatient care for the ED (Woodside & Staab). It is important that both centers are aware of the patient's comorbid diagnosis. Unfortunately, Woodside and Staab did not specify how SUD treatment centers should treat diagnosed ED patients; they only stated that facilities should be “aware” of the eating disorder. Further instruction for treatment of comorbid individuals should be offered to SUD facilities. Pharmacological treatments are also discouraged (Woodside & Staab, 2006). This is in part due to the starved body's unpredictability in processing substances and in part due to risk of exacerbating SUD symptoms. Thus, ED professionals should be particularly careful when prescribing psychotropic medications to patients. Before prescribing such medications, patients should be screened for a history of drug use and possible SUD diagnosis. Just as ED professionals should use discretion when prescribing medications, SUD professionals should use discretion when prescribing diet and exercise. Chemical dependency professionals often discuss issues of self-care, such as eating and exercise, with clients. Typically, diet changes and regular exercise enhance recovery in addicted individuals (Weinstock, Barry, & Petry, 2008). However, women presenting with SUD and an ED may experience exacerbated symptoms and compulsive behavior with added exercise or dietary restrictions. 3.3.2. Professional education, screening, and diagnosis The issue of co-occurrence of EDs and SUDs impacts professionals from both fields. Often practitioners are not trained in the detection and treatment of the comorbid disorder. Professionals in both fields should receive education about the comorbidity of these disorders, and terminology should be clarified across the disciplines to ensure that diagnosis is consistent and specific. Since comorbidity rates are high, professionals need to screen for both EDs and SUDs when doing patient intakes (Gadalla & Piran, 2007b; Gilchrist et al., 2007; Peveler & Fairburn, 1990). Thus, simple, reliable screening instruments should be developed which are understood by both fields (Gadalla & Piran). Also, given the possible mediating role of physical and sexual abuse, professionals should also screen for histories of abuse in patients (Gilchrist et al.). These suggestions require both chemical dependency professionals and ED professionals to communicate and work together. Continuing to treat comorbid patients for only one disorder may trigger the other disorder or exacerbate current symptoms (Woodside & Staab, 2006). Diagnostic criteria for comorbid disorders should also be clarified (Gadalla & Piran, 2007b). This is especially important in the area of EDs. Patients should be evaluated carefully by an educated professional; diagnostic methods should not rely solely on self-report. Medical professionals may need to be involved at this step. Because diagnostic criteria are stringent and specific, some SUD women with disordered eating will fall below the threshold of an AN or BN diagnosis (APA, 1994). However, given their increased risk for developing these disorders, they should be monitored regularly and treated for sub-threshold eating issues and DE behaviors. 3.3.3. Additions to current treatment The research is unanimous in its suggestion to develop treatment approaches that address SUDs and EDs simultaneously (Bulik et al., 1992; Cooper, 1989; Franko et al., 2005; Gadalla & Piran, 2007a,b). This is particularly important with inpatient treatment centers. Acutely sick ED patients have complex physiological problems

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requiring medical supervision and care (Woodside & Staab, 2006). Many treatments with high efficacy in a normal population are less effective in nutritionally deprived individuals (Woodside & Staab). Similarly, the addicted ED patient faces increasingly complex problems with withdrawal and dependency (Bulik et al.). Ideally acute patients should be treated by a medical team, with knowledge of both SUDs and EDs. Though some centers attempt to treat both disorders, there has yet to be a treatment specifically developed for comorbid patients (Woodside & Staab). In addition to comorbid treatment centers, Cooper (1989) suggested the addition of RP to traditional treatment plans for each disorder. Given the chronic nature of both SUDs and EDs, patients need be educated about potential lapses into harmful behaviors. Also, Bulik et al. (1992) suggested a connection between relapses in substance use and disordered eating behaviors. It is possible that alcohol risk factors and BN risk factors magnify each other. There may be a particularly strong correlation between purging behaviors and alcoholic lapses (Bulik et al.; Wiederman & Pryor, 1996). With skills training and RP programs, harm caused by relapses can be reduced. Given the general agreement in the literature about the chronic, recurrent nature of these disorders, RP should be an integral part of treatment. 3.3.4. Prevention In addition to improving treatment options for comorbid individuals, prevention interventions should target SUDs and EDs simultaneously (Gadalla & Piran, 2007a). Given the adolescent ages of onset for both disorders, interventions should begin in elementary and middle school students (Measelle et al., 2006). Prevention programs should focus on building resiliency in at-risk youth, particularly those with family histories of these disorders. In adult female populations, prevention interventions should target disordered eating patterns as well as alcohol consumption (Gadalla & Piran, 2007a,b). Finally, professionals should also strive for identification of early symptomatology (Woodside & Staab, 2006). It is hoped that early intervention for comorbid individuals may decrease the severity of symptoms experienced. Given the high prevalence and mortality rates associated with these two disorders, treatment should be vigorous, and detection early. 4. Discussion 4.1. Conclusions concerning prevalence, etiology and treatment Concerning prevalence, individuals with one disorder have increased risk for the other disorder (Bulik et al., 1992; Gilchrist et al., 2007; Peveler & Fairburn, 1990; Wiederman & Pryor, 1996). In fact, women with SUD or an ED were over four times more likely to develop the other disorder than women in the general population not presenting with such disorders (Gadalla & Piran, 2007b). Eating disorder symptomatology appears to be more indicative of SUD than ED type (Wiederman & Pryor). Severity of caloric restriction and purging are two key factors in predicting comorbidity (Wiederman & Pryor). Type of ED is also argued to influence the rate of SUD comorbidity (Franko et al., 2005). However, here the literature is divided. Some researchers argued that BN and AUD share core risk factors and symptomatology (Bulik et al.). Others failed to find significant differences between AN and BN diagnosis and rate of comorbidity (Franko et al.). By standardizing diagnostic criteria of ED subtype and synchronizing methodology, these issues may become clearer. Research has established that this area of comorbidity is a prominent issue in women's health and merits aggressive treatment (Pearlstein, 2002). Concerning etiology, several theories were discussed. The biopsychosocial model of addiction was offered as a model for both disorders (Cooper, 1989). However, though EDs and SUDs share similar

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symptomatology and development, there are critical differences unexplained by this model (Measelle et al., 2006). The genetic/ familial heritability model suggests that transmission of both disorders is largely due to the same genetic and biological factors. Examination of growth trajectories revealed that different higher order factors are involved in the development of SUD and ED pathology (Measelle et al.). Disordered eating behaviors cause neurological changes that mimic the effects of substance use (Pearlstein, 2002). It is hypothesized that these biological factors could explain the increased rates of comorbidity. When coupled with a model addressing personality and temperamental risk factors, this model may be a good fit for the data (Thompson-Brenner et al., 2008). A more complex and integrative model is needed in order to explain the intriguing similarities and differences between SUDs and EDs. Concerning treatment, the literature is disappointingly quiet. Though many suggestions have been made, there is an urgent need for empirical research about the treatment of SUD and ED simultaneously. It is suggested that practitioners use screening methods to identify additional disorders, and that comorbid individuals receive early, aggressive care (Gadalla & Piran, 2007a). Women presenting with both disorders may require additional medical services, particularly when severely malnourished (Woodside & Staab, 2006). Because of the chronic nature of both disorders, relapse prevention programs are recommended for treatment (Cooper, 1989). Further research on treatment efficacy is necessary before treatment programs specializing in comorbid SUDs and EDs can be developed.

4.2. Implications for research and theory The implications of comorbidity reach across fields of study and research domains. Though there is a growing body of work investigating the comorbidity of these disorders, further research is needed. Research should focus on treatment, and include treatment efficacy and outcome studies (Franko et al., 2005; Pearlstein, 2002). The dearth of empirical evidence of dual programs leaves practitioners little information when deciding courses of treatment. Relapse and RP studies may also prove useful in this population which is particularly prone to lapses. When researching prevalence, studies should expand the number of substances studied to include prescription medication abuse, ecstasy and hallucinogens. Also, the connection between methamphetamine use and EDs may be a particularly useful field of study (Gadalla & Piran, 2007b). Finally, when conducting comorbidity research, participant compensation should not be food-related, as sometimes occurs in addictions research. Such compensation may trigger disordered eating behaviors in patients and decrease study participation rates. As the etiology of comorbidity is considered, two areas of study are suggested: mediating factors and physiological factors. There is a growing body of literature suggesting separate mediating factors for SUDs and EDs (Measelle et al., 2006; Ranson et al., 2003). Exploration of specific mediating factors may lead to a more appropriate model. Several factors have been suggested as core mediating factors in comorbidity. Some researchers focused on abuse, trauma, and PTSD issues (Gadalla & Piran, 2007b; Gilchrist et al., 2007; Ranson et al., 2003). Others hypothesized impulsivity and emotional instability were the more likely mediators (Bulik et al., 1992; Wiederman & Pryor, 1996). Still others suspected depression, negative affect and temperamental differences to be the important mediators (Gadalla & Piran; von Ronson et al.). Because several studies point to two main mediating factors, it would be interesting to see a two-part latent growth model used to analyze the development of these comorbid behaviors (Measelle et al.; Ranson et al.). Finally, physiological studies involving food deprivation, drug efficacy and neurotransmitter systems may augment this etiological research (Pearlstein, 2002).

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4.3. Implications for society Research on ED and SUD comorbidity has important social implications. The themes of abuse and adolescence recur throughout the literature. Many women with EDs report histories of sexual and physical abuse; similarly, many women with SUDs report histories of sexual and physical abuse (Gilchrist et al., 2007). Those women with both disorders report staggering abuse rates. Prevention and intervention programs should address abuse as well as SUD and ED treatment. During adolescence substance use behaviors and disordered eating behaviors increase significantly (Measelle et al., 2006). This is a critical time for young women. Prevention and early interventions should address the risk factors associated with SUDs and EDs in adolescence, such as depression and negative affect (Measelle et al.). Early interventions should be geared specifically to this vulnerable population and emphasize skills training and resiliency. This literature offers a unique view into the complex pathology of women with these comorbid disorders. Because comorbidity rates are high, it is imperative that effective, empirically-supported treatments be developed to treat SUDs and EDs simultaneously. Early intervention could improve the course of these chronic diseases. With further research in the field, prevention and intervention techniques can be developed to combat this dangerous combination of disorders. Role of Funding source This review was not funded financially by any sources. Contributors Harrop conducted literature searches, provided summaries of previous research, and composed the first draft of the manuscript. Marlatt provided background information of previous research and assisted in revision of the document. Both authors contributed to and have approved the final manuscript. Conflict of Interest There are no conflicts of interest declared by either author. Acknowledgements The authors wish to thank Mike Beck and Jared Harrop who assisted in editing the manuscript.

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