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date: 14 November 2019

Overview of the Contents of This Volume and an Introduction to a Developmental Perspective on Genetic Research in Eating Disorders

Abstract and Keywords

This chapter provides an introduction and overview to this book. Because eating disorders develop predominantly during childhood and adolescence, there is a need to take a developmental focus on these disorders. The book provides a comprehensive discussion of epidemiology, risk, diagnosis, and treatment through a developmental lens. The second part of this chapter reviews the data about genetics and eating disorders. Recent data suggest that genetic risks appear to be expressed during adolescence. These findings may result from biological and social changes during this period interacting with these genetic risks.

Keywords: Eating disorders, adolescents, children, development, genetics, anorexia nervosa, bulimia nervosa, diagnosis, treatment

Overview of the Contents of This Volume

This book is inspired by the increasing need to consider developmental factors in our understanding of the etiology and treatment of mental diseases and, in particular, eating disorders. Data on differences in children and adults in terms of risks for developing eating disorders (C. M. Bulik et al., 2006; Essex et al., 2006), clinical presentations of eating disorders (Nicholls, Chater, & Lask, 2000; Peebles, Wilson, & Lock, 2006), diagnosis of eating disorders (Workgroup & Adolescents, 2007), and treatment response in eating disorders (Steinhausen, 2009) provide compelling evidence that considering developmental factors is key to moving forward in the field. This book draws together experts in these various areas who illustrate how developmental theory and observations specifically inform eating disorders.

The first part of the volume, Development Considerations in Epidemiology and Risk for Eating in Children and Youth, contains five chapters on themes related to this topic. Leora Pinhas and Susan J. Bondy (Pinhas & Bondy, 2011, Chapter 2, this volume) take a developmental focus on the epidemiology of eating disorders as they pertain to children and adolescents. Their thorough review identifies problems and limitations in the current epidemiological database related to children and adolescents with eating disorders (Hoek & Hoeken, 2003; Keski-Rahkonen et al., 2007). It appears that incidence rates of adolescent anorexia nervosa (AN) increased throughout the 1980s, but have stabilized in the last two decades (Lucas, Beard, & O’Fallon, 1991; van Son et al., 2006). For adolescent bulimia nervosa (BN), even less is known; in fact, existing studies appear to provide conflicting results about changing incidence patterns (Hoek & Hoeken, 2003). For both AN and BN, incidence rates on boys are almost completely lacking. By far the largest group of eating disordered adolescents—about 60% of cases—is categorized as eating disorder not otherwise specified (EDNOS) (Turner & Bryant-Waugh, 2004). Again, little information about this group is available aside from clinical surveys. Pinhas and Bondy provide a lucid description of the problems in the database and suggest ways of constructively moving forward to increase our epidemiological database for children and youth. (p. 2) Progress of this type should lead to a better understanding of onset, progression, management, outcomes, and the evolution of these disorders.

Hans Steiner and his coauthors (Huener, Hall, & Steiner, 2011, Chapter 3 this volume) describe a developmentally based model for risk of onset and symptom development in the context of the growing child (Steiner et al., 2003; Steiner & Lock, 1998). Steiner views eating disorders as psychosomatic in character (Lock, Reisel, & Steiner, 2001). Rather than a phenomenologically descriptive approach, Steiner conceptualizes etiology along multiple layers of accumulating risk and protective factors until, in some cases, risk overcomes protective factors to result in full-blown syndromal disorders. This approach bridges continuity and discontinuity between pathology and normality, complexity of mental states and clinical presentation, and social and temporal context as determinants of psychopathology (Steiner, Lock, Chang, & Wilson, 2004).

A sociocultural risk factor often implicated in the onset of eating disorders is exposure to media messages about the importance of weight, shape, and appearance (Groesz, Levine, & Murnen, 2002; Levine & Harrison, 2004; McCabe, Ricciardelli, & Finemore, 2001). Rebecka Peebles and Rebecca Carr (2011, Chapter 4, this volume) describe the special effects that media, especially developing media in terms of the Internet, are having on youth in the context of eating disorders. They summarize the current understanding of media influence on the development of eating disorders in adolescents, particularly BN, AN, EDNOS, and obesity. Adolescents, with their propensity to use technology and their developmentally informed interest in appearance, are at particular risk for turning to the Internet for information (and misinformation) while also likely being less able to judge the quality and accuracy of that information.

Cognitive processes and emotion regulation are under rapid development in the context of the adolescent brain and behavior (Luna & Sweeney, 2004). Nancy Zucker and Christopher Harshaw (2011, Chapter 5, this volume) describe a model of how these processes interrelate in adolescent AN. Specifically, they describe how individuals with AN suppress emotional experience (C. M. Bulik et al., 2006; Wade et al., 2008) to achieve performance standards, making them overly adept at emotion regulation (Dahl, 2001), although the manner in which they attempt such regulation likely has negative implications not only on the course of their illness, but also on the development of self-awareness and interpersonal proficiency during adolescence.

As noted above, not much is known about boys who develop eating disorders (Lock, 2008), but Alison Darcy (2011, Chapter 6, this volume) provides a comprehensive overview of eating problems in boys from childhood through young adulthood. Although data suggest that eating disorders occur at the same rate in boys and girls before puberty, after this time, a marked gender difference in prevalence is seen (Braun, Sunday, Huang, & Halmi, 1999). However, EDNOS and partial syndromes show less difference in diagnostic rates (Andersen & Holman, 1997; Carlat, Camargo, & Herzog, 1997). Eating disorder symptoms are prevalent among adolescent males. Darcy concludes that it is critical to develop a better understanding of how males experience eating disorders because the differences between boys and girls likely relates to subtle differences in symptom expression between the genders based on differing psychosexual, sociocultural, and biogenetic factors.

In the second part of this volume, Developmental Consideration in Assessment, we turn to the application of the developmental considerations described in the first part of the book in terms of clinical manifestations of eating disorders and how they differ in younger populations.

In Chapter 7, the problems of diagnosing and assessing children and adolescents with eating disorders are described by Jennifer Couturier and Sherry Van Blyderveen (2011, Chapter 7, this volume). They review problems inherent in the Diagnostic and Statistical Manual of Mental Disorders (DSM) and International Classification of Mental and Behavioural Disorders (ICD) classification systems and in the current assessment instruments available (Workgroup & Adolescents, 2007). Both the diagnostic systems and the assessment instruments are designed for adult populations, and thus are often developmentally inappropriate for youth. These authors support the development of diagnostic criteria and assessment instruments designed at inception for youth, taking their developmental stages into account. This likely will require multimethod assessments and include reports from collaterals—particularly parents—if we are to be able to make accurate clinical diagnoses of eating problems in younger patients (Couturier & Lock, 2006; Couturier, Lock, Forsberg, Vanderheyden, & Lee, 2007).

As Hans Steiner suggested in his description of eating disorders as psychosomatic disorders composed of an interplay of physical and psychiatric (p. 3) symptoms, there are important physical health impacts on young people who develop eating disorders (Peebles, Hardy, Wilson, & Lock, in press; Peebles et al., 2006). Rebecca Peebles and colleagues (Sadler & Peebles, 2011, Chapter 8, this volume) describe the current state of the literature on the specific nature of these effects (Rome et al., 2003). They highlight complications that have been explicitly studied in a pediatric population, with a specific emphasis on those that may have long-term and potentially irreversible health impacts, such as growth retardation, bone loss, and death.

For the most part, eating disorders in youth develop in the context of family life. Elizabeth Dodge (2011, Chapter 9, this volume) explores the impact of this on the individual physical and psychological processes and how these change and evolve in the family context. Although families are no longer seen as playing a central role in the etiology of eating disorders, problematic interactions in the family may play an important role in disrupting or maintaining the disorders (Eisler, 2005). Dodge describes how family therapy theoretic constructs can be used to better understand these possibilities. Although the main focus of the chapter is on family process in AN, because most of the literature relates to this, specific issues in relation to BN are also discussed (Dodge, Hodes, Eisler, & Dare, 1995).

Corrina Jacobi and colleagues (2011, Chapter 10, this volume) provide an important view for framing the risks for eating disorders in the context of development from early childhood through adulthood. This important chapter provides a segue between the focus of the second part of this volume on clinical phenomenology to the topic of the third part on interventions with younger patients with eating disorders.

The third part of the volume, Intervention, focuses on how treatments can be developed and implemented for eating disorders in younger patients. As a starting point, the choice of treatment setting is discussed by Simon Gowers and Claire Bullock (2011, Chapter 11, this volume). These authors argue that choosing a developmentally sensitive setting is an important starting point for treating children and adolescents with eating disorders. They note that eating disorders generally arise in young people who seem to be struggling with the demands of adolescence (Crisp, 1997). Thus, close-to-home treatment needs to be considered, since keeping adolescents in their communities is likely to make working on these dilemmas more relevant. Further, balancing the need to stop dangerous eating disordered behaviors with the burgeoning autonomy of adolescents requires recognition of both parental authority and adolescent developmental needs. Although research literature is scant, existing evidence suggests that lengthy psychiatric inpatient care is not needed for the majority of patients and that outpatient is more cost-effective and yields higher levels of patient and parent satisfaction (Byford et al., 2007; Crisp et al., 1991; Gowers et al., 2007).

Eating disorders in younger patients are poorly researched. Irene Chatoor (2011, Chapter 12, this volume) provides an important chapter describing the clinical presentation of feeding and eating problems in young children (Bryant-Waugh, Markham, Kreipe, & Walsh, 2010, published online ahead of print). She focuses on problems of diagnosis and assessment using current classification systems that echo complaints registered by Couturier and Van Blyderveen. She argues that the current definition of feeding disorder is so narrow that it does not address feeding disorders broadly enough and excludes those that are not accompanied by growth failure or that have associated medical conditions (Workgroup for Adolescents, 2007). Chatoor presents a refined classification of Feeding Disorders that identifies six feeding disorders: feeding disorder of state regulation, feeding disorder of caregiver–infant reciprocity, infantile anorexia, sensory food aversions, post-traumatic feeding disorder, and feeding disorder associated with a medical condition. Chatoor next describes interventions designed to assist children with these feeding and eating problems of young childhood. Importantly, she notes that each feeding disorder responds differently to different interventions based on symptoms, age, and parental roles.

Dasha Nichols and Hilary Davies (2011, Chapter 13, this volume) describe how children in the middle years of childhood present with both classical eating disorders (AN and BN) as well as more atypical presentations of eating problems that are consistent with how psychopathological problems can be expressed in this age group. They also describe the main developmental challenges and dilemmas of middle childhood and how AN and BN and variants of these typical eating disorders manifest and are treated in a developmentally informed manner (Nicholls & Bryant-Waugh, 2003; Nicholls, Randall, & Lask, 2001). In addition, the presentation and treatment of atypical eating problems—such as selective eating, food avoidance disorders, and food and swallowing phobias—are discussed.

(p. 4) Kara Fitzpatrick (2011, Chapter 14, this volume) next describes how adolescent AN is best treated from an adolescent developmental perspective (Lock, 2002). Because AN typically onsets during adolescence, Fitzpatrick reviews significant changes in physiology, cognition, and social/independence behaviors during adolescence that form important considerations when conceptualizing treatment (Ackard & Peterson, 2001; Luna & Sweeney, 2004; McCabe et al., 2001). Based on these developmental perspectives, she argues that there are reasons to consider both family and individual treatments for AN, and she describes developmentally sensitive treatment based on these considerations (Fitzpatrick, Moye, Hostee, Le Grange, & Lock, 2010; Lock, Le Grange, Agras, & Dare, 2001).

Denise Wilfley and colleagues (2011, Chapter 15, this volume) focus on psychological, behavioral, physical, and emotional problems associated with child and adolescent obesity (Fairburn & Brownell, 2002). Eating disorders in the context of obesity include binge eating disorder (BED) and BN. They discuss the empirical support for and common practices of treating children, adolescents, and young adults with these conditions. Most treatments focus on involving parents, but cognitive-behavioral therapy and interpersonal therapy adjusted for use with younger populations are also described (Le Grange & Lock, 2007; Tanofsky-Kraff et al., 2010; Wilfley et al., 2002; Wilfley et al., 1993).

Medications can be effective treatment for many psychiatric disorders. Compared to other types of disorders, however, medications appear to have a more limited use for eating disorders, especially for younger patients. In their chapter on this subject, Jennifer Hagman and Guido Frank (2011, Chapter 16, this volume) review the limited studies relevant to psychopharmacology in children and adolescents with eating disorders and discuss approaches to treating comorbid diagnoses (Couturier & Lock, 2007). They note, however, that nascent research in the neurosciences may lead to more effective and targeted psychopharmacologic interventions in the future (Bailer et al., 2007; Bergen et al., 2005; Kaye, Frank, & McConaha, 1999). At the same time, no randomized controlled trials demonstrate efficacy for any psychotropic medication for children or adolescents with eating disorders. Thus, all medications used in children and adolescents for treatment of an eating disorder are currently prescribed “off-label.” They also note that, although some preliminary studies are promising, there is insufficient evidence at this time to support prescription of selective serotonin reuptake inhibitors (SSRIs) or atypical neuroleptics for the treatment of AN or BN in children and adolescents (Hagman et al., 2009; Kotler, Devlin, Davies, & Walsh, 2003; Walsh et al., 2006).

Some eating problems develop in the context of medical problems and are first assessed and treated as part of a psychiatric consultation service. Shaw and colleagues (Froehlich, Ularntinon, & Shaw, 2011, Chapter 17, this volume) offer a comprehensive review of the kinds of eating and weight problems that can present in the pediatric medical setting. This review encompasses the most common medical and psychosomatic syndromes associated with changes in appetite and weight, as well as those that present with vomiting, which in turn may contribute to changes in appetite.

I close the volume with a discussion of possible future directions in developmental research for eating disorders (Lock, 2011, Chapter 18, this volume). I focus on the need for developmental translational research integrating insights from genetics (see below), neuroscience, and biology to better inform our understanding of how eating disorders develop and how better to treat them.

Genetic Studies in Eating Disorders: Developmental Starting Points

The earliest developmental influences are genes. Genomic medicine is advancing our knowledge of how DNA variants influence a wide variety of complex medical disorders (cardiovascular, respiratory, immunologic, oncogenic, and reproductive; Human Genome Project Information, Nutritional and Metabolic Diseases, Genes and Diseases). Advances in how genes effect behavior and are involved psychiatric disorders has been slower, although progress is being made (Berrettini, 2000; Hudziak & Faracone, 2010). In this context, the progress in understanding genetic contributions to the development of eating disorders is similarly circumscribed (Gorwood, Ades, & Foulon, 2003; Kaye et al., 2008; Klump & Gobrogge, 2005). Current information is limited by the types of data available and the scale and scope of those data. Family studies, twin studies, molecular genetics (Genomewide Linkage and Candidate Gene Association Studies), and Genome Wide Association Studies (GWAS) are all approaches in which preliminary data are being found to link genes to eating disorders. A somewhat newer focus is on phenotypic and endophenotypic studies that allow for broader behavioral constructs than do diagnostic groups to assess the genetic (p. 5) contribution to eating disorder disease processes. Contributions from each of these domains of genetic research will be discussed in this chapter.

Family studies show that AN and BN cluster in families and that this is the result—to a substantial degree—of genetic factors (Lilenfeld et al., 1998; Strober, Freeman, Lampert, Diamond, & Kaye, 2000). These studies suggest that the rates of these disorders are about five times the expected rates in unaffected families, although this increased risk is not specific for AN or BN (Tozzi et al., 2005). Reports suggest that genetic factors likely account for more than 50% of the heritable risk for developing an eating disorder (C. M. Bulik, 2004; Lilenfeld et al., 1998). However, although family aggregation studies cannot separate genetic and environmental contributions on familial transmission of risk, twin studies can. Monozygotic (MZ) twins are assumed to be genetically identical, thus differences in trait expression likely result from environmental influences. At the same time, dizygotic (DZ) twins share 50% of the same genes, and differences in trait expression could be due to either genes or environment. By comparing differences between trait expression in DZ twins to MZ twins, the relative contribution of genetic and environmental factors can be approximated (C. Bulik, Sullivan, Wade, & Kendler, 2000). Twin studies find heritability estimates ranging from approximately 30% to 75% in AN and from 28% to 85% in BN (C. Bulik, Slof-Op’t Land, van Furth, & Sullivan, 2007; C. Bulik et al., 2006; C. Bulik, Sullivan, Wade, & Kendler, 2000; C. M. Bulik, Sullivan, & Kendler, 1998).

The specific clinical and diagnostic features of eating disorders have also been explored in twin studies. For example, in one report by Mazzeo and colleagues, heritability for amenorrhea was about 16%, severe weight loss was 34%, and lowest lifetime body mass index (BMI) was 33% (Mazzeo et al., 2009). In addition, eating disordered attitudes and behaviors (e.g., weight and shape concerns, binge eating, purging) were found to have heritability estimates in similar ranges (34%–65%). Because these types of thoughts and behaviors commonly precede the onset of a full-spectrum eating disorder, risks of these types also appear to be heritable.

A few twin studies are available to shed light specifically on the influence of genes and eating disorders in terms of general child and adolescent development. Klump et al. (2000) found that genetic and environmental influences on eating disordered thoughts and behavior differed by age (K. L. Klump, McGue, & Iacona, 2000). For 11-year-old twins, genetic influences were marginal, but in 17-year-old twins, heritability was high. In following-up this study, Klump et al. (2007) used longitudinal data to examine changes in genetic and environmental influences on eating disordered thinking and behavior in female twins aged 11, 14, and 18 years (Klump, Burt, McGue, & Iacona, 2007). Their findings supported the original cross-sectional study because genetic influences increased with age (age 11 = 6%; age 14 = 46%, age 18 = 46%). These data suggested that the genetic risk was expressed between the ages of 11 and 14 years, an age group known to be at highest risk for developing eating disorders (Hoek & Hoeken, 2003).

In addition to these studies, other twin studies examined how eating and internalizing symptoms (anxiety and depression) were longitudinally expressed (Silberg & Bulik, 2005). Children and early adolescents (aged 8–13 years) were compared to middle/late adolescents (aged 14–17 years). A unique genetic factor was found for the younger adolescent group for eating disorders. A more recent study (Klump et al. 2010) examined the relationship between age and genetic vulnerability for eating disorders in a twin study incorporating twins (aged 10–41 years) using three large twin registries and assessing shape and weight concerns employing the Eating Disorder Examination Questionnaire (EDE-Q; Klump et al., 2010). Again, the authors found that for preadolescents, genetic effects on shape and weight concerns as assessed by the EDE-Q were nominal, but that these effects increased from early adolescence through middle adulthood. Interestingly, environmental effects were greatest in the youngest patients and diminished during adolescence and adulthood, whereas nonshared environmental influences were constant over age groups.

Although these studies found that genes influenced liability in a younger group of adolescents in one group (Silberg & Bulik, 2005) and a slightly older group of adolescents in the other (Klump, Burt et al., 2007; K. L. Klump et al., 2000), the two studies taken together support the idea that expression of heritability of liability for eating disorders may be tied to age or development, specifically stage of adolescence. One possible explanation for this finding is that hormonal changes during adolescence could effect gene expression during puberty. Several studies support this hypothesis. Klump et al. (2003) found that pubertal status moderated genetic effects (K. L. Klump, McGue, & Iacona, 2003). These authors found that 11-year-olds who had begun puberty had similar genetic (p. 6) effects (i.e., greater) to adults, whereas adolescents had higher genetic effects. In a follow-up study using pubertal status as a continuous variable, Klump et al. (2007) found that genetic influences on eating disordered thoughts and behaviors increased in a linear fashion with pubertal development (K. L. Klump, Perkins, Burt, McGue, & Iacona, 2007).

The finding that pubertal status affects the expression of genetic risk in eating disorders has been partially replicated by Colbert and colleagues using a different twin sample (Culbert, Burt, McGue, Iacona, & Klump, 2009). In addition, Colbert and colleagues identified the type of key pubertal marker needed to best capture the interaction between genes and puberty in adolescents. The authors found that menarche itself, rather than mid-puberty, demonstrated the clearest genetic effects. Studies of the effects of pubertal hormones on genetic expression in eating disorders have also been reported. In a twin study of 10- to 15-year-old female twins, Klump and colleagues found that estradiol levels moderated genetic influence on disordered eating—higher estradiol levels increased genetic effects (K. L. Klump, Keel, Sisk, & Burt, in press).

Turning now to molecular genetic data, we examine what genomewide linkage and candidate gene approaches have found to contribute to our understanding of eating disorders. It should be noted that large samples of multiplex pedigrees are required for linkage analysis studies, and these are difficult to find in the context of eating disorders. To conduct these studies, anonymous genetic markers are genotyped to identify chromosomal regions that contain genes that influence the trait of interest. Candidate genes located in such linkage peaks are explored using case–control association to see if they are associated with the phenotype of interest. Thus, in case–control association studies, cases who display the phenotypic trait are compared to controls who do not. Genetic marker (single nucleotide polymorphisms, SNPs) frequencies that are hypothesized to relate to the trait of interest are contrasted in cases versus controls. Thus, linkage studies are used when sufficient knowledge is available to implicate specific genetic variants.

Linkage studies in eating disorders are relatively few. For AN, several studies have been conducted. One study, using a sample of pure restricting-type AN found evidence for a susceptibility locus on chromosome 1 (Grice et al., 2002). Incorporating a trait variable for drive for thinness and obsessionality in the linkage analyses found additional loci on chromosome 2 and 13 (Devlin et al., 2002). Interestingly, the serotonin ID receptor (HTR1D) and the delta opioid receptor (OPRD1) located on chromosome 1 correspond to a linkage peak identified by Grice and colleagues and previously suggested to be related to the development of AN (Bergen, van den Bree, Yeager, & al., 2003). Other linkage reports have found statistically significant findings on chromosome 1 related to eating behavior and satiety (e.g., cannabinoid receptor CNR2). Nonetheless, these findings are all from the same sample, and results should be interpreted with caution as they may be nonspecific or false signals.

Case–control association studies have explored genes encoding for proteins related to feeding, weight, and neurotransmitters that regulate eating behaviors (Kaye, 2008). Of published exploratory studies, most are underpowered. One area of promise is examining genes related to the serotonin (5-hydroxytryptamine or 5-HT) pathway. Dysregulation of serotonin pathways may contribute to the pathogenesis of eating disorders (Ferguson, La Via, Crossan, & Kaye, 1999) because disturbances in serotonin pathways are associated with impulsivity, obsessive-compulsivity, anxiety, depression, fear, rumination, and disturbed appetite regulation (Frank et al., 2002; Kaye, Gwirtsman, George, & Ebert, 1991). Three case–control association studies have tested this possibility. Two studies focused on the 1D gene, finding several polymorphisms associated with AN (Bergen et al., 2003; Brown et al., 2007). Patients with BN also show abnormalities in the orbital-frontal serotonergic circuits, which are known to contribute to behavioral dyscontrol.

The dopaminergic system is also of interest in eating disorders (McConaha et al., 2004) because food aversion, weight loss, hyperactivity, distorted body image, and obsessive-compulsive behaviors are associated with disturbances in this neurotransmitter system. Dopamine D2 and D4 receptor genes have been examined using case–control association studies in AN (Bachner-Melman et al., 2007; Bergen et al., 2005), finding preliminary data supporting this linkage.

In addition to these neurotransmitter studies, the role of brain-derived neurotrophic factor (BDNF), which plays a role in synaptic plasticity and neuronal growth and development (Kuipers & Bramham, 2006;), appears to also affect feeding and weight regulation (Kernie, Liebl, & Parada, 2000; Pellymounter, Cullen, & Wellman, 1995). (p. 7) Case–control association genetic linkage studies have found mixed results (de Krom et al., 2005; Ribases et al., 2004, 2005). Nonetheless, as BDNF may play a particularly important role in adolescent brain development and reorganization during puberty—and possibly eating disorders onset during this period—further studies are important.

In addition to the neurotransmitter studies, examination of genetic contributions to cognitive processes related to thinking styles in eating disorders are being undertaken. Some have suggested that a more successful approach may be to perform genetic studies using cognitive and neurophysiological endophenotypes (Fossella, Bishop, & Casey, 2003). Because cognitive function is highly genetic, some recent research has focused on cognitive features in AN as a possible endophenotype (Buyske et al., 2006; Fossella et al., 2003; Friedman et al., 2008; Goldberg & Weinberger, 2004; Gosso et al., 2006; Koten et al., 2009). Inefficiencies in the area of cognitive flexibility (set-shifting) and central coherence have been identified in adults with AN that meet criteria for an endophenotype (e.g., found in acute and recovered states, found in unaffected family members) (Holliday, Tchanturia, Landau, & Collier, 2005; Tchanturia, Morris, Surguladze, & Treasure, 2002). Weak central coherence, an overfocus on detail to the neglect of the whole, has been found in adults with AN as well (Sherman et al., 2006; Southgate, Tchanturia, & Treasure, 2009). Because executive functioning is under development during adolescence (Luna & Sweeney, 2004) and eating disorders often begin in this age group, these traits—which may well be partially genetically based—might be an additional risk factor specific to eating disorder development. Thus, future studies might examine the genetic basis of these features.

Taken together, the existing genetic studies provide an incomplete but suggestive picture. A variety of temperamental (C. Bulik et al., 2006; Kaye et al., 2004; K. Klump et al., 2000; Woodside et al., 2002), cognitive, and pubertal factors may be set in motion by a genetic propensity for traits that ultimately support the development or maintenance of eating disordered behaviors and thoughts. The notion that earlier genetic vulnerability is expressed in childhood temperament and anxiety, whereas cognitive factors and eating disorder related–specific genetic risks appear to operate more significantly during early adolescence. The development of these variables likely interacts with a dynamic neurotransmitter system also influenced by genetic factors. Fitting the pieces of this puzzle together to identify areas to target for prevention and intervention is a goal of future genetic translational research.


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