Association between childhood maltreatment and cortical folding in women with eating disorders.

Childhood maltreatment (CM) is associated with distinct clinical and biological characteristics in people with eating disorders (EDs). The measurement of local gyrification index (lGI) may help to better characterize the impact of CM on cortical structure. Thus, the present study investigated the association of CM with lGI in women with EDs. Twenty-six women with anorexia nervosa (AN) and 24 with bulimia nervosa (BN) underwent a 3T MRI scan. All participants filled in the Childhood Trauma Questionnaire. All neuroimaging data were processed by FreeSurfer. LGI maps underwent a general linear model to evaluate differences between groups with or without CM. People with AN and BN were merged together. Based on the Childhood Trauma Questionnaire cutoff scores, 24 participants were identified as maltreated and 26 as non-maltreated. Maltreated people with EDs showed a significantly lower lGI in the left middle temporal gyrus compared with non-maltreated people, whereas no differences emerged in the right hemisphere between groups. The present study showed that in people with EDs, CM is associated with reduced cortical folding in the left middle temporal gyrus, an area that could be involved in ED psychopathology. This finding corroborates the hypothesis of a 'maltreated ecophenotype', which argues that CM may allow to biologically, other than clinically, distinguish individuals with the same psychiatric disorder.

Bi-allelic Variants in RALGAPA1 Cause Profound Neurodevelopmental Disability, Muscular Hypotonia, Infantile Spasms, and Feeding Abnormalities.

Ral (Ras-like) GTPases play an important role in the control of cell migration and have been implicated in Ras-mediated tumorigenicity. Recently, variants in RALA were also described as a cause of intellectual disability and developmental delay, indicating the relevance of this pathway to neuropediatric diseases. Here, we report the identification of bi-allelic variants in RALGAPA1 (encoding Ral GTPase activating protein catalytic alpha subunit 1) in four unrelated individuals with profound neurodevelopmental disability, muscular hypotonia, feeding abnormalities, recurrent fever episodes, and infantile spasms . Dysplasia of corpus callosum with focal thinning of the posterior part and characteristic facial features appeared to be unifying findings. RalGAPA1 was absent in the fibroblasts derived from two affected individuals suggesting a loss-of-function effect of the RALGAPA1 variants. Consequently, RalA activity was increased in these cell lines, which is in keeping with the idea that RalGAPA1 deficiency causes a constitutive activation of RalA. Additionally, levels of RalGAPB, a scaffolding subunit of the RalGAP complex, were dramatically reduced, indicating a dysfunctional RalGAP complex. Moreover, RalGAPA1 deficiency clearly increased cell-surface levels of lipid raft components in detached fibroblasts, which might indicate that anchorage-dependence of cell growth signaling is disturbed. Our findings indicate that the dysregulation of the RalA pathway has an important impact on neuronal function and brain development. In light of the partially overlapping phenotype between RALA- and RALGAPA1-associated diseases, it appears likely that dysregulation of the RalA signaling pathway leads to a distinct group of genetic syndromes that we suggest could be named RALopathies.

Childhood maltreatment is associated with cortical thinning in people with eating disorders.

Childhood maltreatment (CM) is a non-specific risk factor for eating disorders (ED) and is associated with a greater severity in their clinical presentation and poorer treatment outcome. These data suggest that maltreated people with ED may be biologically other than clinically different from non-maltreated people. The aim of the present study was to investigate cortical thickness (CT), a possible biomarker of neurodevelopment, in people with ED with or without history of CM and in healthy women. Twenty-four healthy women, 26 with anorexia nervosa and 24 with bulimia nervosa underwent a 3T MRI scan. All participants filled in the childhood trauma questionnaire. All neuroimaging data were processed by FreeSurfer. Twenty-four participants with ED were identified as maltreated and 26 participants with ED as non-maltreated. All healthy women were non-maltreated. Compared to healthy women, maltreated people with ED showed lower CT in the left rostral anterior cingulate gyrus, while compared to people with ED without history of CM showed lower CT values in the left superior frontal and in right caudal middle frontal and superior parietal gyri. No significant differences emerged in CT measures between healthy women and people with ED without history of CM. The present findings show for the first time that in adult people with ED childhood maltreatment is associated with cortical thinning in areas implicated in the modulation of brain processes that are acknowledged to play a role in the psychopathology of ED.

Relationship between Orexigenic Peptide Ghrelin Signal, Gender Difference and Disease.

Growth hormone secretagogue receptor 1a (GHS-R1a), which is one of the G protein-coupled receptors (GPCRs), is involved in various physiological actions such as energy consumption, growth hormone secretion promoting action, and cardiovascular protective action. The ligand was searched for as an orphan receptor for a while, but the ligand was found to be acylated ghrelin (ghrelin) discovered by Kangawa and Kojima et al. in 1999. Recently, it has also been reported that dysregulation of GHS-R1a mediates reduced feeding in various diseases. On the other hand, since the physiological effects of ghrelin have been studied exclusively in male mice, few studies have been conducted on gender differences in ghrelin reactivity. In this review, we describe (1) the characteristics of GHS-R1a, (2) the role of ghrelin in hypophagia due to stress or anticancer drugs, and (3) the gender differences in the physiological effects of GHS-R1a and the influence of stress on it.

Novel NGLY1 gene variants in Chinese children with global developmental delay, microcephaly, hypotonia, hypertransaminasemia, alacrimia, and feeding difficulty.

NGLY1 deficiency is the first and only autosomal recessive congenital disorder of N-linked deglycosylation (NGLY1-CDDG). To date, no patients with NGLY1 deficiency has been reported from mainland China or East Asia in English literature. Here, we present six patients with a diagnosis of NGLY1-CDDG on the basis of clinical phenotype, genetic testing, and functional studies. We retrospectively analyzed clinical phenotypes and NGLY1 genotypes of six cases from four families. Informed consent was obtained for diagnosis and treatment. In-silico tools and in vitro enzyme activity assays were used to determine pathogenicity of NGLY1 varaints. All patients had typical features of NGLY1-CDDG, including global developmental delay, microcephaly, hypotonia, hypertransaminasemia, alacrimia, and feeding difficulty. Dysmorphic features found in our patients include flat nasal bridge, loose and hollow cheeks, short stature, malnutrition, and ptosis. Pachylosis could be a novel cutaneous feature that may be explained by lack of sweat. We found three novel variants, including one missense (c.982C > G/p.Arg328Gly), one splice site (c.1003+3A > G), and one frame-shift (c.1637-1652delCATCTTTTGCTTATAT/p.Ser546PhefsTer) variant. All mutations were predicted to be disease causing with in-silico prediction tools, and affected at least one feature of gene splicing. Protein modeling showed missense variants may affect covalent bonding within the protein structure, or interrupt active/binding amino-acid residues. In vitro studies indicated that proteins carrying missense variants (p.Arg328Gly and p.Tyr342Cys) lost the enzyme activity. We expanded clinical phenotype and genetic mutation spectrum of NGLY1-CDDG by reporting six cases, three novel variants, and novel clinical features from mainland China.

The orbitofrontal cortex, food intake and obesity

Obesity is a major health challenge facing many people throughout the world. Increased consumption of palatable, high-caloric foods is one of the major drivers of obesity. Both orexigenic and anorexic states have been thoroughly reviewed elsewhere; here, we focus on the cognitive control of feeding in the context of obesity, and how the orbitofrontal cortex (OFC) is implicated, based on data from preclinical and clinical research. The OFC is important in decision-making and has been heavily researched in neuropsychiatric illnesses such as addiction and obsessive­compulsive disorder. However, activity in the OFC has only recently been described in research into food intake, obesity and eating disorders. The OFC integrates sensory modalities such as taste, smell and vision, and it has dense reciprocal projections into thalamic, midbrain and striatal regions to fine-tune decision-making. Thus, the OFC may be anatomically and functionally situated to play a critical role in the etiology and maintenance of excess feeding behaviour. We propose that the OFC serves as an integrative hub for orchestrating motivated feeding behaviour and suggest how its neurobiology and functional output might be altered in the obese state.

Dysregulated Sexuality in Women with Eating Disorders: The Role of Childhood Traumatic Experiences.

The present study explored the psychopathological, behavioral, and putative biological underpinnings of dysregulated sexuality in eating disorders (EDs), focusing on the role of childhood trauma - evaluated with the Childhood Trauma Questionnaire (CTQ). The comparison between Binge-Purging and Restricting patients outlined the predominance of markers of dysregulated sexuality in the first subgroup. In the clinical sample, hypersexuality - measured through the Hypersexual Behavior Inventory (HBI) - was associated with severe psychopathology, emotion dysregulation, childhood trauma, adverse consequences, and higher ghrelin levels. Moderation analyses showed that hypersexuality was associated with emotion dysregulation and psychopathology only in those patients reporting childhood traumatic experiences.

Identifying duration criteria for eating-disorder remission and recovery through intensive modeling of longitudinal data.

OBJECTIVE: Outcome states, such as remission and recovery, include specific duration criteria for which individuals must be asymptomatic. Ideally, duration criteria provide predictive validity to outcome states by reducing symptom-return risk. However, available research is insufficient for deriving specific recommendations for remission or recovery duration criteria for eating disorders. METHOD: We intensively modeled the relation between duration criteria length and rates of remission, recovery, and subsequent symptom return in longitudinal data from a treatment-seeking sample of women with anorexia nervosa (AN) and bulimia nervosa (BN). We hypothesized that the length of the duration criterion would be inversely associated with both rates of remission and recovery and with subsequent rates of symptom return. RESULTS: Generalized estimating equations supported our hypotheses for all investigated eating-disorder features except for symptom return when using the Psychiatric Status Rating for AN. DISCUSSION: We recommend that 6 months be used for remission definitions applied to binge eating, purging, and BN symptom composite measures, whereas no duration criteria be used for low weight and AN symptom composites. We further recommend that 6 months be used for recovery definitions applied to BN symptom composites and AN symptom composites, whereas 18 months be used for individual symptoms of binge eating, purging, and low weight. The adoption of these duration criteria into comprehensive definitions of remission and recovery will increase their predictive validity, which in turn, maximizes their utility.

Fractures in women with eating disorders-Incidence, predictive factors, and the impact of disease remission: Cohort study with background population controls.

OBJECTIVE: Malnutrition and low weight in eating disorders (EDs) are associated with increased fracture risk compared to the general population. In a cohort study, we aimed to determine fracture rates compared to age and gender matched controls (ratio 5:1), assess the impact of disease remission on fracture risk, and establish predictive factors for fractures. METHOD: Of note, 803 ED patients referred to specialized ED treatment between 1994 and 2004 were included. In 2016, data on fractures were obtained through the Danish National Registry of Patients. RESULTS: Fracture risk was increased in anorexia nervosa (AN; IRR 2.2 [CI 99%: 1.6-3.0]) but not in bulimia nervosa (BN; IRR 1.3, ns) or other specified feeding or eating disorders (OSFED; IRR 1.8, ns). IRR in the AN group were increased for vertebral fractures (IRR 3.8 [CI 99%: 1.4-10.3]), upper arm (IRR 3.0 (CI 99% 1.6-5.5) and hip (IRR 6.6 [CI 99%: 2.6-18.0]). Disease remission in AN is associated to lower fracture risk compared to active disease, but higher fracture risk compared to controls (IRR 1.7 [CI 99%: 1.1-2.7]). In regression analysis, age at debut of disease, nadir BMI and duration of disease before referral to treatment, independently predicted fracture. DISCUSSION: We confirm increased fracture risk in AN, and show significant differences in fracture risk between patients in disease remission and patients with active disease. Furthermore, we show that age at debut of disease and duration of disease before referral to treatment is positively correlated to fracture risk, whereas nadir BMI is negatively correlated to fracture risk.

Increased rates of eating disorders and their symptoms in women with major depressive disorder and anxiety disorders.

BACKGROUND: Individuals with eating disorders (EDs) have increased rates of major depressive disorder (MDD) and anxiety disorders. Yet, few studies have investigated rates of EDs and their symptoms in individuals presenting with MDD/anxiety disorders. Identifying potential disordered eating in people with MDD/anxiety disorders is important because even subclinical disordered eating is associated with reduced quality of life, and undiagnosed eating pathology may hinder treatment progress for both MDD/anxiety disorders and comorbid EDs. METHOD: We compared rates of EDs (anorexia nervosa, bulimia nervosa, binge-eating disorder, and other specified feeding and eating disorders) and their symptoms in 130 women with, and 405 women without, lifetime MDD or an anxiety disorder (generalized anxiety disorder, obsessive-compulsive disorder, social phobia, specific phobia, panic disorder, agoraphobia, or post-traumatic stress disorder) recruited from the population-based Michigan State University Twin Registry. Lifetime ED and MDD/anxiety diagnoses, and lifetime clinically significant disordered eating behaviors (e.g., binge eating, excessive exercise) were assessed using the Structured Clinical Interview for DSM-IV (SCID). RESULTS: Among participants with lifetime MDD or any anxiety disorder, 13% met criteria for a lifetime ED and 39% reported engaging in at least one lifetime clinically significant disordered eating behavior (e.g., binge eating) on the SCID. In contrast, only 3% of participants without a history of MDD/an anxiety disorder met criteria for a lifetime ED, and only 11% reported lifetime clinically significant disordered eating behavior. DISCUSSION: Our findings suggest that women with MDD and anxiety disorders have elevated rates of EDs, and it is therefore imperative to screen for disordered eating in these populations.

Beneficial effects of leptin substitution on impaired eating behavior in lipodystrophy are sustained beyond 150 weeks of treatment.

AIM: Metreleptin treatment in lipodystrophy patients improves eating behavior with increased satiety and reduced hunger. However, no data are available whether effects are maintained beyond 52 weeks of treatment. METHODS: A prospective study with measurements at baseline and at >150 weeks of metreleptin treatment was performed. Five female lipodystrophy patients with indication for metreleptin were included. Behavioral aspects of hunger- and satiety regulation were assessed by validated eating behavior questionnaires and visual analog scales assessing hunger and satiety feelings before and after a standardized meal. RESULTS: Hunger rated on visual analog scales at 120 min after the meal significantly decreased from 46 ±â€¯10 mm at baseline to 17 ±â€¯6 mm at long-term assessment. Furthermore, satiety at 5 and 120 min after the meal significantly increased from baseline to long-term assessment (5 min: 70 ±â€¯7 mm to 87 ±â€¯3 mm; 120 min: 43 ±â€¯10 mm to 79 ±â€¯8 mm). On the Three Factor Eating Questionnaire, the mean value of factor 3 (hunger) significantly decreased from 9.2 ±â€¯0.2 at baseline to 2.6 ±â€¯1.5 at long-term assessment. In the Inventory of Eating Behavior and Weight Problems Questionnaire, mean values for scale 2 (strength and triggering of desire to eat) and scale 7 (cognitive restraint of eating) significantly decreased from baseline (31.6 ±â€¯4.8 and 11.4 ±â€¯2.2, respectively) to long-term assessment (14.0 ±â€¯2.1 and 10.0 ±â€¯1.9). CONCLUSION: First evidence is presented that long-term metreleptin treatment of >150 weeks has sustained effects on eating behavior with increased satiety, as well as reduced hunger and hunger-related measures.

Neurobiology of food intake in health and disease.

Under normal conditions, food intake and energy expenditure are balanced by a homeostatic system that maintains stability of body fat content over time. However, this homeostatic system can be overridden by the activation of 'emergency response circuits' that mediate feeding responses to emergent or stressful stimuli. Inhibition of these circuits is therefore permissive for normal energy homeostasis to occur, and their chronic activation can cause profound, even life-threatening, changes in body fat mass. This Review highlights how the interplay between homeostatic and emergency feeding circuits influences the biologically defended level of body weight under physiological and pathophysiological conditions.

Role of eating disorders-related polymorphisms in obesity pathophysiology.

Human biological system provides innumerable neuroendocrine inputs for food intake control, with effects on appetite's modulation and the satiety signs. Its regulation is very complex, engaging several molecular interactions with many tissues, hormones, and neural circuits. Thus, signaling molecules that control food intake are critical for normal energy homeostasis and a deregulation of these pathways can lead to eating disorders and obesity. In line of this, genetic factors have a significantly influence of the regulation of neural circuits controlling the appetite and satiety pathways, as well as the regulation of brain reward systems. Single Nucleotide Polymorphisms (SNPs) in genes related to hypothalamic appetite and satiety mechanisms, further in multiple neurotransmitter systems may contribute to the development of major Eating Disorders (EDs) related to obesity, among them Binge Eating Disorder (BED) and Bulimia Nervosa (BN), which are discussed in this review.

Navigating the university transition among women who self-report an eating disorder: A qualitative study.

OBJECTIVE: Although developmental milestones have been observed to alter eating disorder (ED) symptom burden, it remains unknown how the transition to university affects symptomatology. To address this gap, we designed a qualitative study to elucidate how students with an ED perceive their general university experience and to describe how the university environment shapes their ED. METHOD: Undergraduate students who self-reported an ED were recruited through fliers, an undergraduate advocacy organization, and local treatment centers. We conducted audio-recorded semi-structured individual interviews. Two investigators separately coded verbatim transcripts using an editing approach, and final themes emerged from the pattern of descriptors. RESULTS: Fifteen undergraduate students participated. Participants endorsed a variety of ED symptoms and sought various levels of treatment. Most participants transitioned to university with an already-established diagnosis. Participants described that ED symptoms tended to worsen in university for a variety of reasons including (a) minimization of ED severity, (b) loss of external accountability, (c) use of ED symptoms as a coping mechanism, and (d) glorification of ED behaviors in campus diet culture. Subsequently, the ED disrupted the university experience by (e) hindering participants' ability to focus on academic responsibilities and (f) leading to social isolation on campus. DISCUSSION: We identified challenges unique to the university experience that can be addressed by ED treatment teams in order to provide anticipatory guidance and patient-centered care. Study limitations include lack of formal diagnostic ED assessment by research team and sampling of students from one university.

Etiological influences on continuity and co-occurrence of eating disorders symptoms across adolescence and emerging adulthood.

OBJECTIVE: The role of common and symptom-specific genetic and environmental influences in maintaining eating disorder symptoms across development remains unclear. This study investigates the continuity and change of etiological influences on drive for thinness, bulimia, and body dissatisfaction symptoms and their co-occurrence, across adolescence and emerging adulthood. METHOD: In total, 2,629 adolescent twins (mean age = 15.20, SD = 1.95) reported eating disorders symptoms across three waves of data collection. Biometric common pathways model was fitted to estimate genetic and environmental contributions to the continuity of each symptom over time, as well as time- and symptom-specific influences. RESULTS: Drive for thinness and body dissatisfaction symptoms showed a pattern of high continuity across development and high correlations with each other, whereas bulimia symptoms were moderately stable and less associated with the other two symptoms. Latent factors reflecting continuity of each symptom were largely under genetic influence (Al = 0.60-0.82). New genetic influences contributing to change in the developmental course of symptoms were observed in emerging adulthood. Genetic influences correlated considerably between the three symptoms. Non-shared environmental influences were largely time-and symptom-specific, but some contributed moderately to the continuity across development (El = 0.18-0.40). The etiological overlap was larger between drive for thinness and body dissatisfaction symptoms than with bulimia symptoms. DISCUSSION: The results provide preliminary evidence that stable as well as newly emerging genetic influences contribute to the co-occurrence of drive for thinness, bulimia, and body dissatisfaction symptoms across adolescence and emerging adulthood. Conversely, environmental influences were less stable and contributed to change in symptoms over time.

Transactions among thinness expectancies, depression, and binge eating in the prediction of adolescent weight control behaviors.

OBJECTIVE: Binge eating, the transdiagnostic risk associated with depression, and the eating disorder-specific risk associated with expectancies for reinforcement from thinness have been identified as risk factors for the development of weight control behaviors. The purpose of this study was to examine if these risk factors transact to further predict risk in youth. METHOD: Binge eating, depressive symptoms, thinness expectancies, and weight control behaviors were assessed in 1,758 adolescents three times during the transitional period between middle school and high school. We tested six different possible transactional processes. RESULTS: Mediation tests demonstrated that both 8th grade binge eating and 8th grade depressive symptoms predicted 10th grade weight control behaviors through their predictive influence on thinness expectancies in 9th grade. However, our results were not consistent with a mediational process in which 8th grade thinness expectancies predicted 9th grade depression to further predict 10th grade weight control behaviors. No interactions among binge eating, depressive symptoms, or thinness expectancies predicted weight control. Results did not differ between girls and boys. DISCUSSION: Thinness expectancies appear to mediate the predictive influence of binge eating and depressive symptoms on risk for engaging in weight control behaviors. These results add to theoretical understanding of risk and suggests potential intervention pathways for clinicians.

Why is premorbid BMI consistently elevated in clinical samples, but not in risk factor samples, of individuals with eating disorders?

Body image disturbance is widely viewed as contributing to the development and maintenance of disordered eating. Yet this perspective is not inconsistent with the possibility that elevated premorbid BMIs also increase the risk of developing eating disorders. Research examining whether actual body size may play a role in eating disorder development reveals a curious pattern of findings. Few prospective risk factor studies conducted with community-based samples found a relationship between premorbid BMI and subsequent eating disorder pathology whereas retrospective research conducted with clinical samples indicates a consistent pattern of elevated premorbid BMIs relative to population norms or control groups. This study documents these disparate findings, considers potential explanations for them and proposes further study of premorbid BMI as a factor contributing to the psychopathology of eating disorders, particularly among those who come to the attention of treatment providers.

Depressive symptoms, alcohol and other drug use, and suicide risk: Prevention and treatment effects from a two-country online eating disorder risk reduction trial.

OBJECTIVE: Eating disorders are known to have high comorbidity, and the current report outlines the impact of an online eating disorder risk reduction program on brief, self-report measures of depressive symptoms, alcohol and other drug use, and suicidality. METHOD: An online pragmatic, randomized-controlled trial was conducted with N = 316 young-women (M age = 20.80 years) across Australia and New Zealand. Media Smart-Targeted (MS-T) was a 9-module program released weekly while control participants received positive body image tips. Prevention effects (asymptomatic at baseline) and treatment effects (symptomatic at baseline) were investigated. RESULTS: MS-T participants were 94% and 91% less likely than controls to develop Moderate or higher depressive symptoms at 6-month (MS-T = 3.3%; controls = 35.4%) and 12-month follow-up (MS-T = 3.4%; controls = 29.4%), respectively. MS-T participants did not commence using recreational drugs at any assessment point, compared to 18.2% of controls at a least one assessment point. Regarding treatment effects, MS-T participants were 84% more likely to no longer be using recreational drugs at 12-month follow-up (MS-T = 60%; controls = 21.1%). Mutitvariate logistic regressions revealed group, depressive symptoms and alcohol use to be significant predictors of elevated suicide risk, where being an MS-T participant, without depressive symptoms and not drinking alcohol, significantly lowered likelihood of developing elevated suicide risk. Disordered eating at post-program mediated the relationship between group and depressive symptoms across post-program to 12-mnoth follow-up. DISCUSSION: MS-T shows promise as a program with important mental health benefits in addition to previous reports of lowered eating disorder diagnosis, risk and impairment.

Psychiatric and medical correlates of DSM-5 eating disorders in a nationally representative sample of adults in the United States.

OBJECTIVE: To examine psychiatric and somatic correlates of DSM-5 eating disorders (EDs)-anorexia nervosa (AN), bulimia nervosa (BN), and binge-eating disorder (BED)-in a nationally representative sample of adults in the United States. METHOD: A national sample of 36,309 adult participants in the national epidemiologic survey on alcohol and related conditions III (NESARC-III) completed structured diagnostic interviews (AUDADIS-5) to determine psychiatric disorders, including EDs, and reported 12-month diagnosis of chronic somatic conditions. Prevalence of lifetime psychiatric disorders and somatic conditions were calculated across the AN, BN, and BED groups and a fourth group without specific ED; multiple logistic regression models compared the likelihood of psychiatric/somatic conditions with each specific ED relative to the no-specific ED group. RESULTS: All three EDs were associated significantly with lifetime mood disorders, anxiety disorders, alcohol and drug use disorders, and personality disorders. In all three EDs, major depressive disorder was the most prevalent, followed by alcohol use disorder. AN was associated significantly with fibromyalgia, cancer, anemia, and osteoporosis, and BED with diabetes, hypertension, high cholesterol, and triglycerides. BN was not associated significantly with any somatic conditions. CONCLUSIONS: This study examined lifetime psychiatric and somatic correlates of DSM-5 AN, BN, and BED in a large representative sample of U.S. adults. Our findings on significant associations with other psychiatric disorders and with current chronic somatic conditions indicate the serious burdens of EDs. Our findings suggest important differences across specific EDs and indicate some similarities and differences to previous smaller studies based on earlier diagnostic criteria.

Eating disorders and substance use in adolescents: How substance users differ from nonsubstance users in an outpatient eating disorders treatment clinic.

OBJECTIVE: The relationship between eating disorders (EDs) and substance use (SU) has only been briefly described in literature using mainly adult populations. This study examined the prevalence and characteristics of SU among patients of an adolescent ED outpatient treatment program. METHOD: A retrospective chart analysis was conducted to determine and subsequently compare medical status, psychosocial factors, treatment course and outcome between patients with and without SU. RESULTS: Over 60% of patients with SU status (n = 203) reported regularly consuming substances. 33.4% of substance users received a diagnosis involving purging behaviors compared to 5.9% of nonusers. Females composed 96.4% and 81.7% of users and nonusers, respectively. Users reported significantly more self-harm (57.7% of users vs. 38.6% of nonusers) but did not differ significantly in terms of trauma (abuse or victimization; 48.3% of users vs. 44.9% of nonusers). The percentage of ideal body weight significantly improved throughout treatment and did not differ by SU with a mean increase of 5.29% (SD = 13.6) among nonusers compared to 5.45% (SD = 7.5) of users. While users and nonusers did not differ before and after treatment in ED severity, users were more likely than nonusers to drop-out of treatment (41.5% of users vs. 25.2% of nonusers). DISCUSSION: Adolescents with SU benefit from ED outpatient treatment as much as those without SU, however, users are more likely to drop-out. Therefore, treatment should target these adolescents' emotional dysregulation to improve treatment compliance. Further research is necessary to determine the efficacy of such an approach.