Treatment for Addictive and Compulsive Behavior Disorders - Essay Example

Running Head: EATING DISORDER Eating Disorder of the of the Eating Disorder Introduction Eating disorders rank among the 10 leading causes of disability among young women (Mathers, Vos, Stevenson, & Begg, 2000), and anorexia nervosa has the highest mortality rate of all mental disorders (Millar et al., 2005; Sullivan, 1995; Zipfel, Lowe, Reas, Deter, & Herzog, 2000). Fueled by these ominous indicators of their clinical significance, efforts to identify risk or causal factors for eating disorders are indicated for at least four critical reasons. First, identification of causal mechanisms satisfies the need to understand why certain people develop the problem in question and others do not. Indeed, some experts believe that such an understanding helps decrease the stigma associated with a mental disorder: If the cause is seen as out of the individuals control, less blame is assigned than if the disorder is seen as “volitional” (Crisp, Gelder, Rix, Meltzer, & Rowlands, 2000). A Newsweek magazine story titled “Fighting Anorexia: No One to Blame” stressed recent findings on genetic vulnerability to explain risk for the development of anorexia nervosa (Tyre, 2005). Second, ideally, nosology is based on etiology, yet the current classification schema for eating disorders, as articulated in the Diagnostic and Statistical Manual of Mental Disorders (4th ed. [DSM–IV]; American Psychiatric Association, 1994), is based solely on the observed clustering of signs and symptoms. The eating disorder criteria remain the subject of considerable debate, in large part because they fail to result in clearly defined subgroups or to account for changing symptomatology over the course of the illness. Most individuals who experience a clinically significant eating disorder do not meet diagnostic criteria for anorexia nervosa or bulimia nervosa but, rather, meet criteria for eating disorder not otherwise specified (EDNOS), a diagnosis intended to capture a residual group (Hoek & van Hoeken, 2003; Hudson, Hiripi, Harrison, & Kessler, 2005; Striegel-Moore et al., 2005). Binge-eating disorder (BED) is the most widely studied specific example of an EDNOS (for review, see M. J. Devlin, Goldfein, & Dobrow, 2003). Third, treatment is best accomplished when we know the causes of a disorder. The current evidence base for treatment of anorexia nervosa, in particular, is weak (Berkman, Bulik, Brownley, & Lohr, in press). A classic example from the history of psychiatry is the treatment of neurosyphilis. As recently as the mid-19th century, advanced neurosyphilis with psychiatric manifestations was a ticket to treatment in an asylum. With the discovery of the Spirochaeta pallida (Treponema pallidum; Schaudinn & Hoffman, 1905), the search for biological cures ultimately led to the discovery of the efficacy of penicillin in the treatment of this sexually transmitted disease, leading to a rapid decline in incidence and changing treatment forever. Fourth, identification of risk factors is important for determining high-risk groups for targeted interventions, designing prevention program content, and informing public policy. The single best predictor of risk for developing an eating disorder is being female, prompting the question why women? And indeed, most studies have been restricted to girls or women; yet, clearly, female sex is not a sufficient condition for explaining risk, prompting a second question: Which women in particular? (Striegel-Moore, Silberstein & Rodin, 1996). In the present review, we describe the state of knowledge of risk and causal factors for eating disorders as gleaned from studies on human populations. Changing Perspectives on Risk Factors for Eating Disorders Eating disorders (compared with many other psychiatric disorders) are newcomers to the official psychiatric nomenclature. Since their earliest appearances in the literature, the field has been bifurcated in the search for etiological explanations. In this section, we review briefly the history of our understanding of anorexia nervosa and bulimia nervosa. Anorexia Nervosa Anorexia nervosa was introduced as a new illness in the late 19th century in separate yet almost simultaneous accounts by British psychiatrist William Gull (1874, 1888) and French physician Charles Lasègue (1873). Although both Gull and Lasègue characterized anorexia nervosa as a “nervous” disease, each man emphasized different aspects of his patients clinical presentation. Gulls clinical description elaborated on the physiological correlates that resulted from a “perversion of the will” and attributed them to “simple starvation” without detailed discussion of what might have caused this “perversion.” Lasègue described anorexia nervosa as a “hysteria of the gastric center” and paid considerable attention to the psychological or social factors that he believed were involved in the development of this disorder (cited in Brumberg, 2000, pp. 118–119). At the risk of oversimplification, Gull focused more on biological processes and disruptions, whereas Lasègue focused more on psychosocial and psychological roots. In both cases, however, the treatment was somatic, involving nutritional restoration. Bulimia Nervosa Russell (1999) described bulimia nervosa as “an ominous variant of anorexia nervosa,” and although he widely has been credited with introducing this disorder into the nomenclature, a few years prior, Boskind-Lodahl (1996) offered a feminist formulation of the binge–purge syndrome as a culture-bound syndrome that arose from Western cultures obsession with female thinness in particular and the restrictions of female gender role stereotypes in general. As with anorexia nervosa, numerous theoretical models proliferated, yet most risk-factor studies have tested variables representing various risk domains rather than testing a particular theoretical model (Jacobi et al., 2004; Stice, 2002; Striegel-Moore et al., 1996; for review, see Striegel-Moore & Cachelin, 2001). Nevertheless, too often, discussion of the etiology of eating disorders becomes polarized into “cultural” versus “biological” explanations that ignore the fact that biological and environmental variables are inextricably linked. Advances in Conceptualizing Risk Fundamentally, risk-factor research seeks to understand the factors that cause an outcome of interest (a full discussion of the epistemological and methodological challenges of such research is beyond the scope of this article; see, e.g., Haynes, 2002). A risk factor is a characteristic (e.g., allele), event (e.g., teasing), or experience (e.g., growing up in a culture that values extreme thinness) that precedes the onset of the outcome of interest (e.g., an eating disorder) and that, “if present, is associated with an increase in the probability (risk) of a particular outcome over the base rate of the outcome in the general (unexposed) population” (Kazdin, Kraemer, Kessler, Kupfer, & Offord, 1997, p. 377). For causality to be inferred, it further needs to be shown that the association between the risk factor and the outcome is not due to confounding influences, that the results are replicable, and that there are plausible explanations for the processes mediating the relation between the hypothesized factor and the outcome (Kazdin et al., 1997). No one study can meet all of these requirements; rather, risk-factor research involves piecing together the puzzle by drawing on multiple studies using a range of designs and methods. As discussed in previous comprehensive reviews (Jacobi et al., 2004; Stice & Shaw, 2002; Striegel-Moore & Cachelin, 2001), the state of knowledge concerning the risk and causal factors of eating disorders is frustratingly incomplete. Notwithstanding the fact that they are central to advancing etiological models, most epidemiological studies have not included eating disorders among the psychiatric disorders to be assessed in the population (Wittchen & Jacobi, 2005). In the United States, the first epidemiological study of a nationally representative sample was conducted only in 2001–2003 (Hudson, Hiripi, Pope, & Kessler, 2007). Few studies have moved beyond the first (important, yet preliminary) step of demonstrating statistical association between the factor and the outcome to the second step of establishing the factors precedence, and fewer studies yet have used an experimental manipulation as the ultimate test of causal hypotheses (Jacobi et al., 2004). For example, anorexia nervosa has been shown to be associated with abnormalities in the serotonergic system during the acute illness stage as well as after recovery (Kaye, Bailer, Frank, Wagner, & Henry, 2005). This research suggests that the serotonin system is a potentially fruitful area of further study, yet before they can be considered to be of etiological significance, it needs to be established whether these abnormalities simply represent concurrent symptoms or consequences (biological scars) of the eating disorder. Research Approaches to Uncovering Risk Factors for Eating Disorders The core features of eating disorders include disturbance in body image (e.g., overvaluation of thinness, weight or shape concerns), over- or undercontrol of eating (e.g., severe dietary restriction, binge eating), and extreme behaviors to control weight or shape (e.g., compulsive exercise, purging). This suggests a research focus on biological structures and processes involved in appetite, satiety, and weight regulation and on cultural factors that shape attitudes and behaviors related to body image and eating. For decades, the primary focus of risk-factor research has been sociocultural and family influences on etiology of eating disorders, yet very few specific, replicated candidate environmental risk factors have emerged (Jacobi et al., 2004). Culture and Risk for Eating Disorders Sociocultural models of eating disorders have emphasized “Western” cultures female beauty ideal of extreme thinness and objectification of the female body as specific risk factors for the development of an eating disorder. The cultural models describe these steps: exposure to the thin ideal; internalization of the ideal; and experience of a discrepancy between self and ideal, which in turn leads to body dissatisfaction, dietary restraint, and restriction. In some individuals, restraint and/or restriction leads to overeating, in turn amplifying body image concerns and, thus, precipitating further restraint and/or purging (Polivy & Herman, 1995; Striegel-Moore et al., 1996). Objectification of the female body contributes to risk by teaching girls and women that they are valued primarily for their looks, reinforcing the need to pursue attractiveness (Moradi, Dirks, & Matteson, 2005). To explain why some but not all girls or women develop an eating disorder in this cultural climate, additional variables have been proposed that serve to amplify or mitigate against risk arising from the thin beauty ideal (Striegel-Moore et al., 1996). These include social pressure to be thin (this may take the form of being exposed to media images, peer teasing, or admonishments to lose weight, to name a few), high social class (with, presumably, more attention being paid to and more resources being available for working toward the beauty ideal), personality traits such as perfectionism (making one more eager to comply with the social norms), high social anxiety (increasing ones susceptibility to social feedback), elevated weight or obesity (moving ones body further away from the ideal), high impulsivity (making maintenance of restrictive eating more challenging and amplifying risk for binge eating), individual differences in biological response to starvation, and individual differences in the reward value of starvation or eating. These models cannot explain why some individuals go on to develop binge eating whereas others engage only in extreme dietary restriction and other forms of inappropriate weight-control behaviors (e.g., excessive exercise). Four lines of evidence have been considered as supporting the cultural models: (a) the preponderance of female cases of anorexia nervosa and bulimia nervosa; (b) the rising incidence of anorexia nervosa and bulimia nervosa in girls or women coinciding with the decreasing body-size ideal for women; (c) cross-cultural differences in the incidence or prevalence of eating disorders, with higher incidence–prevalence in cultures that value extreme female thinness; and (d) the significant prospective relationship between internalization of the thin ideal and disordered eating. Eating Disorders: Primarily a Female Psychopathology Worldwide, females with an eating disorder outnumber males by a sizeable margin in every study (Hoek, 2006; Wittchen & Jacobi, 2005). For example, the National Comorbidity Survey Replication (Kessler et al., 2004; Kessler, Chiu, Dernier, & Walters, 2005), which examined eating disorders in a subset of this representative sample of household residents in the United States ages 18 years and older, found lifetime prevalence rates of 0.3% in men and 0.9% in women for anorexia nervosa and 0.5% in men and 1.5% in women for lifetime bulimia nervosa. In a representative sample of Oregon high school students (ages 14–18 years), none of the boys and 0.74% of the girls met criteria (current or past) for anorexia nervosa, and 0.14% of boys and 1.6% of girls met criteria for bulimia nervosa (Lewinsohn, Hops, Roberts, Seeley, & Andrews, 1993). Sex differences are far less pronounced in BED or when eating disorders are defined more broadly to include partial syndromes (Hudson et al., 2007; John, Meyer, Rumpf, & Hapke, 2006; Woodside et al., 2001). Indeed, recurrent binge eating has been shown to be as common in men as in women (Hay, 1998; Lewinsohn, Seeley, Moerk, & Striegel-Moore, 2002; Reagan & Hersch, 2005; Woodside et al., 2001). Men who binge eat are significantly less likely than women to report extreme weight-control behaviors such as purging (Hay, 1998), and they often use different compensatory methods with different goals (e.g., reducing body fat and increasing muscularity; Anderson & Bulik, 2004). This may account in part for the lower prevalence of bulimia nervosa in males compared with females and also suggests that the diagnostic criteria themselves may be sex-biased. Hence, the eating disorders for which weight concerns are defining features are considerably more common among females than among males. In contrast, sex appears to be a less potent marker of risk for eating disturbances that are not marked by weight and shape concerns (as currently defined) and extreme compensatory behaviors. Adolescence: The period of greatest vulnerability With remarkable consistency, research has shown that anorexia nervosa and bulimia nervosa typically occur during adolescence and that onset thereafter is uncommon (Garfinkel et al., 1995; Hudson et al., 2005; Kendler et al., 1991; Striegel-Moore et al., 2005; Woodside et al., 2001). It is of note that onset of BED does not seem to follow this pattern: Onset has been reported to occur well into adulthood (Hudson et al., 2005, 2007; Kinzl, Traweger, Trefalt, Mangweth, & Biebl, 1999). Socioeconomic status Worldwide, studies have shown that in affluent countries, higher status individuals on average are thinner than lower status individuals (Sobal & Stunkard, 1999). On the basis of these observations, anorexia nervosa has long been described as a disease of affluence (Bruch, 1993), and a few studies have found anorexia nervosa to be more common among individuals of high socioeconomic status (Lindberg & Hjern, 2003; McClelland & Crisp, 2001. In contrast, no relationship was found between parental education and bulimia nervosa in the only epidemiological study examining this association (Kendler et al., 1991). Studies that combined anorexia nervosa and bulimia nervosa (Favaro, Ferrara, & Santonastaso, 2003; Lewinsohn, Striegel-Moore, & Seeley, 2000; Moya, Fleitlich-Bilyk, & Goodman, 2005; Wittchen, Nelson, & Lachner, 1998) found no association between socioeconomic status and eating disorders; yet in combining all eating disorders, the possible differences between anorexia nervosa and bulimia nervosa concerning socioeconomic status were obscured. Males with an eating disorder The cultural models emphasize the female beauty ideal and gender role socialization in explaining the sex imbalance in the risk for eating disorders; accordingly, homosexual males may be at elevated risk because of gay cultures increased emphasis on physical appearance relative to that of heterosexual male culture (Boroughs & Thompson, 2002; Silberstein, Mishkind, Striegel-Moore, Timko, & Rodin, 1999). We were able to locate only one risk-factor study that addressed this issue (omitting several studies with inadequate comparison groups). Specifically, a survey of 4,374 adolescent boys (mean age = 14.3 years) found that boys who described themselves as gay or bisexual reported making more efforts to look like boys or men in magazines than did boys who described themselves as heterosexual. There were no differences in the frequency of dieting efforts reported across sexual orientation, but the gay–bisexual boys were more likely to binge eat than the heterosexual boys (Austin et al., 2004). Given that trying to look like boys or men in magazines does not necessarily represent a causal continuity with eating disorders, and given the young age of this sample, little can be concluded regarding the nature of homosexuality as a risk factor for the development of eating disorders in males. Race/ethnicity It long has been assumed that eating disorders are rare among ethnic minority populations, in part because in clinical practice or in treatment trials, few ethnic minority individuals have been found (Smolak & Striegel-Moore, 2001). Regardless of types of psychiatric disorders, patient samples are biased toward an overrepresentation of White women (Kessler et al., 2005). Studies in the United States have found that ethnic minority women compared with White women are disproportionately less likely not only to seek care but, when they do seek care, to receive treatment for the eating disorder (Becker, Franko, Speck, & Herzog, 2003; Cachelin & Striegel-Moore, 2006; Striegel-Moore et al., 2003; Wilfley, Pike, Dohm, Striegel-Moore, & Fairburn, 2001). We were able to locate only one study in the United States that examined race/ethnicity as a marker of eating disorders in a community sample that used a rigorous diagnostic screening and assessment procedure. In a cohort of 2,054 young adult African American (Black) and White American women (mean age = 21 years), all eating disorders were less common among the Black women, and there were no Black women with anorexia nervosa (compared with 1.5% of the White women; Striegel-Moore et al., 2003). However, the two groups differed in parental socioeconomic status, making it difficult to determine whether the results reflected the fact that few of the Black girls came from affluent households and accounted for the differences in prevalence of anorexia nervosa. In the same sample, an empirically based classification of eating disorders found that the clustering of eating disorder symptoms varied by ethnicity: Purging behaviors in the absence of binge eating were significantly more common among the White women, whereas binge eating in the absence of purging was more common among the Black women (Striegel-Moore et al., 2005). In conclusion, female sex is a potent and well-replicated fixed marker for anorexia nervosa and bulimia nervosa (Jacobi et al., 2004), but it appears to be less strongly a predictor of BED. Adolescence marks the period of greatest risk for onset. Few studies offer clues about the importance of other demographic characteristics, yet there are hints that variables such as socioeconomic status or race/ethnicity may differentially signify risk for anorexia nervosa, bulimia nervosa, and BED. If confirmed, this would support a nosological distinction of syndromes involving severe dietary restriction or purging from syndromes involving binge eating without compensatory behaviors. Secular Trends in the Incidence of Eating Disorders Ideal female body size significantly decreased during the 20th century, with marked decreases in media images having been documented for the period between 1958 and 1988 (e.g., Wiseman, Gray, Mosimann, & Ahrens, 1992). To examine whether there has been a corresponding increase in eating disorder incidence (absent epidemiological data), experts have examined changes in the number of new patients being treated. Hoek and van Hoeken (2003) found that the incidence of anorexia nervosa increased markedly from 1930 through 1970 and has remained unchanged since then. Similarly, the prevalence of anorexia nervosa in Sweden, studied in 31,406 twins, was significantly higher in individuals born between 1945 and 1958 than in individuals born between 1935 and 1944 (Bulik et al., 2006). Likely, this increased incidence is not simply the result of greater public awareness or availability of specialized treatment resources for anorexia nervosa in recent years: Anorexia nervosa did not receive much public attention, nor were there many eating disorder treatment facilities or experts, until the latter quarter of the 20th century (Brumberg, 1998). Bulimia nervosa was not officially recognized until 1979, precluding an exploration of changes in incidence across the period of time when the female body ideal drastically shrank in size (1950–1980). Epidemiological studies suggest a secular increase in the incidence of bulimia nervosa during the latter half of the past century: Lifetime prevalence was significantly lower among age cohorts born before 1944 (Hudson et al., 2007), 1950 (Bushnell, Wells, Hornblow, Oakley-Browne, & Joyce, 1990), or 1960 (Kendler et al., 1991) than among more recent age cohorts. Moreover, studies identifying new patients receiving medical care in the Netherlands (Hoek et al., 1995), the United Kingdom (Treasure et al., 1996), and the United States (Soundy, Lucas, Suman, & Melton, 1995) reported significant increases in the incidence of bulimia nervosa between 1985 and 1995. The evidence of increased incidence of eating disorders points to the importance of cultural factors in their etiology, but it does not preclude the important role of biological factors. A parallel example in a related field is the rapid escalation of the prevalence of obesity. Although the genetic underpinnings for obesity are undisputable (Maes, Neale, & Eaves, 1997; Perusse et al., 2005), the rapid increase in prevalence can only be attributable to environmental shifts, because the gene pool cannot change that quickly. Intriguingly, this argues for careful consideration of other mechanisms of gene–environment interplay rather than genetic main effects—such as genetic sensitivity to changes in the environment—which, as yet, remain unstudied in eating disorders. Cross-Cultural Studies Some have described eating disorders as “culture-bound syndromes,” either in the sense that they occur uniquely in a limited number of cultures (Prince, 1995) or in the sense that they represent the culturally shaped (i.e., culture-specific) expression of an underlying (culturally universal) disease (Swartz, 1995). Within this framework, anorexia nervosa and bulimia nervosa, as defined in the DSM–IV, should not be found in cultures that do not subscribe to the social norms about female thinness and the importance that women pursue beauty to affirm their sense of femininity and secure interpersonal or vocational success (Rodin, Silberstein, & Striegel-Moore, 1995). We have already noted the dearth of epidemiological studies; consequently, the data needed to answer the question of whether risk for eating disorders varies across cultures are incomplete at best. Eating disorders have been shown to occur across the globe (Becker & Fay, 2006; Keel & Klump, 2003; Makino, Tsuboi, & Dennerstein, 2004), yet few studies have used designs suitable for testing the hypothesis that eating disorders are less common in nonthin-ideal cultures than in thin-ideal cultures. We caution that with one notable exception (Hoek et al., 2005; Hoek, van Harten, van Hoeken, & Susser, 1998), these studies have relied on samples of convenience, used diagnostic assessments that were not validated for use in the population under investigation, and failed to take socioeconomic status into account. Given these limitations, it is not surprising that prevalence estimates vary considerably across studies (Keel & Klump, 2003; Makino et al., 2004). Consistent with the cultural models, Hoek et al. (1998, 2005) found that the overall incidence of anorexia nervosa was much lower on Curaçao, an island on which the majority population is Black and values large female bodies, than in the Netherlands or the United States, but the incidence among White or mixed-race women was on par with that in the comparison countries. Specifically, all of the Curaçao cases were of mixed race (and, as such, were navigating two cultures) or were White. The authors noted that all mixed-race cases had been abroad, were more affluent than the population average, and described (in in-depth qualitative interviews) how they were aspiring to lead a “Western” lifestyle (Katzman, Hermans, van Hoeken, & Hoek, 2004). In conclusion, the literature on cross-cultural differences has accumulated clear evidence that eating disorders do occur across the globe, yet it has been less successful in providing unambiguous evidence for the role of culture in risk, because of methodological limitations. Accelerating globalization offers the perfect opportunity to study the impact of changing body ideals on eating disorders risk as well as the potential to elucidate mechanisms whereby such an effect would occur. Conclusion Evidence has accumulated in support of both biological (genetic and early developmental trauma) and cultural factors contributing to the increased risk for the development of eating disorders or associated behaviors and attitudes. Research on biological factors and cultural factors has progressed largely along parallel tracks. Future studies must explore these two classes of risk factors in tandem while remaining cognizant of the broader cultural context in which the disorders emerge. Entire classes of risk factors (e.g., personality, familial environment factors) have not yet been studied prospectively. Multi-method research approaches are needed to advance our understanding of the etiology of eating disorders. Comprehensive epidemiological studies are needed that capture more fully the clinical presentation of eating disorders in demographically diverse populations. Empirically based classification systems should be validated using hypothesized risk factors. Researchers need to exploit more fully the availability of longitudinal data that have been collected in samples that have been followed from birth or early childhood to generate hypotheses about the contribution of risk variables like personality feature or early family environment to the development of eating pathology. In addition, new longitudinal studies need to be initiated that are designed to test etiological hypotheses. Clearly, samples sizes numbering in the tens of thousands will be required to ensure adequate power for examining risk for the onset of full-syndrome disorders. The existing literature also points to the promise of experimental studies with high-risk populations (e.g., offspring of mothers with eating disorders) for testing the contribution of certain risk factors. Our review points to several conclusions about stigma, nosology, treatment, and prevention of eating disorders. The evidence shows that we live in a culture that values thinness and that exposure or social pressure to conform to this norm contributes to body image concerns. The cultural context of thin idealization provides an all-too-easy explanation of eating disorders as the consequence of pursuit of beauty, contributing to a perception that these problems are self-inflicted and undeserving of serious consideration. The evidence is fairly strong that biological factors contribute to risk factors for anorexia nervosa. The dissemination of such findings may finally dispel the damaging and disrespectful myth that anorexia nervosa is vanity run amok. Moreover, the almost wholesale exclusion from research of individuals from racial or ethnic minority groups and the marginalization of males cannot be justified with (unsubstantiated) arguments that eating disorders affect only White girls or women and contribute to stigmatization of members of these underresearched groups when they present with an eating disorder. The findings also point to population groups at high risk (e.g., offspring of mothers with anorexia nervosa, children with certain neonatal complications) and suggest the need to test targeted preventive interventions for these groups. The genetic branch of eating disorders research is in its infancy. Extensions of genetic research exploring not only the genetics of risk but also the genetics of course of illness and treatment response (both biological and psychological interventions), as well as more sophisticated models of Gene × Environment interplay, will launch the next generation of genetic investigations. Moreover, although not reviewed here, greater cross-talk between animal and human researchers will help us unveil new biological mechanisms that influence eating disorders, and greater cross-talk between obesity and eating disorders researchers could only serve to enrich and inform both fields. Perhaps most critical, as a field, we have also been a victim of marginalization. The U.S. Centers for Disease Control has failed to collect rigorous epidemiologic data regarding eating disorders and disordered eating behavior. The World Health Organization has not published facts on disability-adjusted life years (DALYs) for anorexia nervosa or bulimia nervosa, whereas DALYs for similarly prevalent conditions (e.g., obsessive–compulsive disorder) have been reported. 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