Risk Factors For Anorexia Nervosa Research Articles

Interplay of polygenic liability with birth-related, somatic, and psychosocial factors in anorexia nervosa risk: a nationwide study.

Although several types of risk factors for anorexia nervosa (AN) have been identified, including birth-related factors, somatic, and psychosocial risk factors, their interplay with genetic susceptibility remains unclear. Genetic and epidemiological interplay in AN risk were examined using data from Danish nationwide registers. AN polygenic risk score (PRS) and risk factor associations, confounding from AN PRS and/or parental psychiatric history on the association between the risk factors and AN risk, and interactions between AN PRS and each level of target risk factor on AN risk were estimated. Participants were individuals born in Denmark between 1981 and 2008 including nationwide-representative data from the iPSYCH2015, and Danish AN cases from the Anorexia Nervosa Genetics Initiative and Eating Disorder Genetics Initiative cohorts. A total of 7003 individuals with AN and 45 229 individuals without a registered AN diagnosis were included. We included 22 AN risk factors from Danish registers. Risk factors showing association with PRS for AN included urbanicity, parental ages, genitourinary tract infection, and parental socioeconomic factors. Risk factors showed the expected association to AN risk, and this association was only slightly attenuated when adjusted for parental history of psychiatric disorders or/and for the AN PRS. The interaction analyses revealed a differential effect of AN PRS according to the level of the following risk factors: sex, maternal age, genitourinary tract infection, C-section, parental socioeconomic factors and psychiatric history. Our findings provide evidence for interactions between AN PRS and certain risk-factors, illustrating potential diverse risk pathways to AN diagnosis.

Do risk factors differentiate DSM-5 and drive for thinness severity groups for anorexia nervosa?

BackgroundThe current study examined whether risk factors for anorexia nervosa (AN) were related to different levels of severity based on (a) the DSM-5/body mass index (BMI) and (b) drive for thinness (DT) severity ratings.MethodsThe sample comprised 153 pairs of individuals with a lifetime diagnosis AN per DSM-IV criteria and their non-ED sisters (N = 306, mean age = 26.53; mean current BMI = 20.42 kg/m2). The Oxford risk factor interview was used to establish AN-related risk factors. Individuals were categorised into the DSM-5 severity groups based on their lowest BMI, while the DT subscale from the eating disorder inventory-2 was used to classify individuals with AN into low and high DT groups.ResultsMultinominal regression models showed similar risk factors (e.g., perfectionism, having a history of being teased about weight and shape) contributed to the development of AN using the DSM-5 and DT severity ratings. Follow-up analyses across the severity groups for both indices revealed that only childhood perfectionism was found to be more common in the extreme severe DSM-5 BMI severity group compared to the severe DSM-5 group.ConclusionOverall, this study found little evidence for AN risk factors being related to the DSM-5 and DT severity ratings. However, given the novelty of this study, replication of the current results is warranted.

An updated report on trauma in Anorexia Nervosa: Confirmation and novel data

ObjectiveLiterature reported a great occurrence of Traumatic Events (TEs) and post-traumatic symptoms in anorexia nervosa (AN). The present study aims to: a) describe the prevalence and the characteristics of TEs in AN, also comparing TEs related to Post-traumatic Stress Disorder (PTSD) to those without this link; b) compare patients with and without TEs and with and without PTSD in terms of clinical picture; c) compare patients who suffered the TE before AN onset to those with TE after AN onset. MethodsThe sample consisted of 126 patients with AN who were interviewed with the Structured and Clinical Interview for DSM 5 (SCID-5), and completed self-reported questionnaires to investigate the general and eating-related psychopathology. ResultsThe results showed that the majority of the patients with AN reported a TE, and TEs related to PTSD were more relational and sexual-related compared to TEs not leading to PTSD. Moreover, after Bonferroni correction was applied to the results, no significant differences emerged between patients with and without TEs, and between individuals with TEs before and after AN onset; differently, patients with PTSD presented a more severe global clinical picture than those without PTSD, partially independent of diagnostic AN subtype. ConclusionThe study highlights that, despite TEs are risk factors for AN, the diagnosis of PTSD makes the difference in terms of clinical presentation and severity, impacting not only eating-related symptoms but also general psychopathology. A careful screening for PTSD in patients with AN is suggestable, especially when relational trauma and sexual violence are reported.

Risk Factors That Predict Future Onset of Anorexia Nervosa, Bulimia Nervosa, Binge Eating Disorder, and Purging Disorder in Adolescent Girls

Because very few prospective studies have identified risk factors that predicted future onset of threshold/subthreshold anorexia nervosa (AN), bulimia nervosa (BN), binge eating disorder (BED), and purging disorder (PD), we analyzed prospective data collected from a large cohort of adolescent girls followed over an 8-year period to advance knowledge about risk factor specificity. Adolescent girls recruited from middle schools in Texas (N = 492; M age = 13.02 [SD = 0.73], age range = 11–15) completed questionnaires assessing risk factors at baseline and diagnostic interviews assessing eating disorders annually over 8 years. Only low BMI predicted future AN onset. Pressure to be thin, thin-ideal internalization, body dissatisfaction, negative emotionality, low parent support, and modeling of eating pathology predicted future BN onset. Pressure to be thin, thin-ideal internalization, negative emotionality, low parent support, and modeling of eating pathology predicted future BED onset. Pressure to be thin, body dissatisfaction, dietary restraint, low parent support, modeling of eating pathology, and high BMI predicted future PD onset. Predictive effects were medium-to-large. Results support etiological theories of eating disorders that postulate the pursuit of the thin ideal, body dissatisfaction, negative affect, dietary restraint, and interpersonal issues increase risk for most eating disorders. The evidence that girls with low body weight are at risk for AN, whereas girls with high body weight are at risk for PD are novel. Although several risk factors predicted future onset of BN, BED, and PD, results suggest that risk factors for AN are qualitatively distinct and should be investigated further.

The causality between gut microbiome and anorexia nervosa: a Mendelian randomization analysis

Background and aimNutrient production by intestinal microbiota corresponds to regulate appetite while gut microbial composition was influenced by diet ingestion. However, the causal relationship between gut microbial taxa and anorexia nervosa (AN) remains unclear. Mendelian Randomization (MR) is a novel research method that effectively eliminates the interference of confounding factors and allows for the exploration of the direct causal effects between exposure and outcome. This study employs MR to explore the causal effect between AN and specific gut microbiome.MethodsLarge-scale Genome Wide Association Study (GWAS) data of AN and 211 gut microbes were obtained from the IEU open GWAS project and Mibiogen Consortium. Two-sample MR was performed to determine the causal relationship between gut microbiota and AN. Furthermore, a bi-directional MR analysis was to examine the direction of the causal relations. The Bonferroni correction test was used to adjust potential correlations among microbial taxa.ResultIn forward MR analysis, 10specific gut microbial taxa have an impact on the occurrence of AN (the p value of IVW <0.05). The high abundance of Genus Eubacteriumnodatumgroup ID: 11297 (OR:0.78, 95% CI:0.62–0.98, p = 0.035) and Class Melainabacteria ID: 1589 (OR:0.72, 95% CI:0.51–0.99, p = 0.045) may be considered protective factors for AN. But after Bonferroni correction, only Class Actinobacteria ID:419 (OR:1.53, 95% CI:1.19–1.96, p = 0.00089) remained significantly associated and high abundance of Class Actinobacteria ID:419 considered as a risk factor for AN. In the reverse MR analysis, AN influences 8 gut microbial taxa with none-statistically significant associations after adjustment.ConclusionWe identified a significant correlation between AN and 18 microbial taxa which have not been previously reported. Among them, 10 kinds of gut bacteria may affect the occurrence of AN, and the status of AN would affect 8 kinds of gut bacteria. After correction, the Class Actinobacteria ID:419 continued to exert an influence on AN.

Risk factors for anorexia nervosa: A population-based investigation of sex differences in polygenic risk and early life exposures.

To examine sex differences in risk factors for anorexia nervosa (AN). This population-based study involved 44,743 individuals (6,239 AN cases including 5,818 females and 421 males, and 38,504 controls including 18,818 females and 19,686 males) born in Denmark between May 1981 and December 2009. Follow-up began on the individual's sixth birthday and ended at AN diagnosis, emigration, death, or December 31, 2016, whichever occurred first. Exposures included socioeconomic status (SES), pregnancy, birth, and early childhood factors based on data from Danish registers, and psychiatric and metabolic polygenic risk scores (PRS) based on genetic data. Hazard ratios were estimated using weighted Cox proportional hazards models stratified by sex (assigned at birth), with AN diagnosis as the outcome. The effects of early life exposures and PRS on AN risk were comparable between females and males. Although we observed some differences in the magnitude and direction of effects, there were no significant interactions between sex and SES, pregnancy, birth, or early childhood exposures. The effects of most PRS on AN risk were highly similar between the sexes. We observed significant sex-specific effects of parental psychiatric history and body mass index PRS, though these effects did not survive corrections for multiple comparisons. Risk factors for AN are comparable between females and males. Collaboration across countries with large registers is needed to further investigate sex-specific effects of genetic, biological, and environmental exposures on AN risk, including exposures in later childhood and adolescence as well as the additive effects of exposures. Sex differences in the prevalence and clinical presentation of AN warrant examination of sex-specific risk factors. This population-based study indicates that the effects of polygenic risk and early life exposures on AN risk are comparable between females and males. Collaboration between countries with large registers is needed to further investigate sex-specific AN risk factors and improve early identification of AN.

Genetic investigation of the contribution of body composition to anorexia nervosa in an electronic health record setting

Anorexia nervosa (AN) is a psychiatric disorder defined by anthropometric symptoms, such as low body weight, and cognitive-behavioral symptoms, such as restricted eating, fear of weight gain, and distorted body image. Recent studies have identified a genetic association between AN and metabolic/anthropometric factors, including body mass index (BMI). Although the reported associations may be under pleiotropic genetic influences, they may represent independent risk factors for AN. Here we examined the independent contributions of genetic predisposition to low body weight and polygenic risk (PRS) for AN in a clinical population (Vanderbilt University Medical Center biobank, BioVU). We fitted logistic and linear regression models in a retrospective case-control design (123 AN patients, 615 age-matched controls). We replicated the genetic correlations between PRSBMI and AN (p = 1.12 × 10−3, OR = 0.96), but this correlation disappeared when controlling for lowest BMI (p = 0.84, OR = 1.00). Additionally, we performed a phenome-wide association analysis of the PRSAN and found that the associations with metabolic phenotypes were attenuated when controlling for PRSBMI. These findings suggest that the genetic association between BMI and AN may be a consequence of the weight-related diagnostic criteria for AN and that genetically regulated anthropometric traits (like BMI) may be independent of AN psychopathology. If so, individuals with cognitive-behavioral symptomatology suggestive of AN, but with a higher PRSBMI, may be under-diagnosed given current diagnostic criteria. Furthermore, PRSBMI may serve as an independent risk factor for weight loss and weight gain during recovery.

Anorexia nervosa and familial risk factors: a systematic review of the literature

Anorexia Nervosa (AN) is a psychological disorder involving body manipulation, self-inflicted hunger, and fear of gaining weight.We performed an overview of the existing literature in the field of AN, highlighting the main intrafamilial risk factors for anorexia. We searched the PubMed database by using keywords such as “anorexia” and “risk factors” and “family”. After appropriate selection, 16 scientific articles were identified. The main intrafamilial risk factors for AN identified include: increased family food intake, higher parental demands, emotional reactivity, sexual family taboos, low familial involvement, family discord, negative family history for Eating Disorders (ED), family history of psychiatric disorders, alcohol and drug abuse, having a sibling with AN, relational trauma. Some other risk factors identified relate to the mother: lack of maternal caresses, dysfunctional interaction during feeding (for IA), attachment insecurity, dependence. Further studies are needed, to identify better personalized intervention strategies for patients suffering from AN.

Is set-shifting a risk factor for anorexia nervosa or a broader range of disordered eating?

Steegers et al. using data from the Generation R cohort study examined whether set-shifting difficulties at age 4 predict body dissatisfaction, weight status, and restrictive eating at age 9 as a way to examine whether cognitive rigidity was a risk factor for an eating disorder. The authors concluded that set-shifting difficulties problems were predictive of features of anorexia nervosa. An alternative interpretation is that set shifting is predictive of large weight changes and eating behaviors more generally. It is not clear that set-shifting predicts becoming underweight. Set shifting appears protective against larger weight gains. It is possible that set shifting is related to degree to which the children resist the myriad of cues to eat for reasons other than hunger. Whether this is due to a higher degree of awareness, genetics, or other reasons should be investigated. The results demonstrate that the cognitive process that relate to restrictive behaviors are complex. To better understand those relationships, it will be essential for the field to adopt a conceptualization of eating disorders that includes the earliest stages (disordered eating) of the full range of eating disorders.

Acute Stress Exposure Alters Food-Related Brain Monoaminergic Profiles in a Rat Model of Anorexia

BackgroundAdverse life experiences are a major risk factor for anorexia nervosa (AN). Eating-provoked anxiousness associated with AN is postulated to be due to food-related exaggerated serotonin activity in the brain and imbalances of monoamine neurotransmitters. ObjectivesUsing a rodent model of stress-induced hypophagia, we investigated if stress exposure augments food-related serotonin turnover and imbalances in measures of brain serotonin and dopamine activity in manners consistent with anxiousness toward food and restricted eating. MethodsAdult male F344 rats were conditioned to associate an audio cue with daily food over 2 weeks, after which half of the rats were exposed to a single episode of tail shocks (stress) or left undisturbed (nonstressed). All rats were killed 48 h later, during a control period, the food-associated cue, or a period of food access. Serotonin, dopamine, and norepinephrine, as well as metabolite concentrations, were assessed across brain regions comprising reward, emotion, and feeding circuits relevant to AN in acutely stressed and nonstressed rats using HPLC. Statistical significance level was 5%. ResultsStress-induced rat hypophagia paralleled an augmented serotonin turnover in response to the food-associated cue in the hypothalamus and hippocampus, as well as food access in the hypothalamus and cortical areas (all P < 0.05). Stress exposure increased the ratio of serotonin to dopamine metabolites across several brain areas, but the magnitude of this imbalance was further augmented during the food-associated cue and food access in the brainstem, hippocampus, and cortical areas (all P < 0.05). Finally, stress lowered norepinephrine concentrations by 18% in the hypothalamus (P < 0.05). ConclusionsThe observed stress-induced changes to monoamine profiles in rats could have key implications for physiological states that contribute to restricted eating and may hold relevance for the development of AN precipitated by adverse life experiences.

Common Genetic Variation and Age of Onset of Anorexia Nervosa

BackgroundGenetics and biology may influence the age of onset of anorexia nervosa (AN). The aims of this study were to determine whether common genetic variation contributes to age of onset of AN and to investigate the genetic associations between age of onset of AN and age at menarche. MethodsA secondary analysis of the Psychiatric Genomics Consortium genome-wide association study (GWAS) of AN was performed, which included 9335 cases and 31,981 screened controls, all from European ancestries. We conducted GWASs of age of onset, early-onset AN (<13 years), and typical-onset AN, and genetic correlation, genetic risk score, and Mendelian randomization analyses. ResultsTwo loci were genome-wide significant in the typical-onset AN GWAS. Heritability estimates (single nucleotide polymorphism–h2) were 0.01–0.04 for age of onset, 0.16–0.25 for early-onset AN, and 0.17–0.25 for typical-onset AN. Early- and typical-onset AN showed distinct genetic correlation patterns with putative risk factors for AN. Specifically, early-onset AN was significantly genetically correlated with younger age at menarche, and typical-onset AN was significantly negatively genetically correlated with anthropometric traits. Genetic risk scores for age of onset and early-onset AN estimated from independent GWASs significantly predicted age of onset. Mendelian randomization analysis suggested a causal link between younger age at menarche and early-onset AN. ConclusionsOur results provide evidence consistent with a common variant genetic basis for age of onset and implicate biological pathways regulating menarche and reproduction.

Mendelian randomization studies of brain MRI yield insights into the pathogenesis of neuropsychiatric disorders

BackgroundObservational studies have identified various associations between neuroimaging alterations and neuropsychiatric disorders. However, whether such associations could truly reflect causal relations remains still unknown.ResultsHere, we leveraged genome-wide association studies (GWAS) summary statistics for (1) 11 psychiatric disorders (sample sizes varied from n = 9,725 to 1,331,010); (2) 110 diffusion tensor imaging (DTI) measurement (sample size n = 17,706); (3) 101 region-of-interest (ROI) volumes, and investigate the causal relationship between brain structures and neuropsychiatric disorders by two-sample Mendelian randomization. Among all DTI-Disorder combinations, we observed a significant causal association between the superior longitudinal fasciculus (SLF) and the risk of Anorexia nervosa (AN) (Odds Ratio [OR] = 0.62, 95 % confidence interval: 0.50 ~ 0.76, P = 6.4 × 10− 6). Similar significant associations were also observed between the body of the corpus callosum (fractional anisotropy) and Alzheimer’s disease (OR = 1.07, 95 % CI: 1.03 ~ 1.11, P = 4.1 × 10− 5). By combining all observations, we found that the overall p-value for DTI − Disorder associations was significantly elevated compared to the null distribution (Kolmogorov-Smirnov P = 0.009, inflation factor λ = 1.37), especially for DTI − Bipolar disorder (BP) (λ = 2.64) and DTI − AN (λ = 1.82). In contrast, for ROI-Disorder combinations, we only found a significant association between the brain region of pars triangularis and Schizophrenia (OR = 0.48, 95 % CI: 0.34 ~ 0.69, P = 5.9 × 10− 5) and no overall p-value elevation for ROI-Disorder analysis compared to the null expectation.ConclusionsAs a whole, we show that SLF degeneration may be a risk factor for AN, while DTI variations could be causally related to some neuropsychiatric disorders, such as BP and AN. Also, the white matter structure might have a larger impact on neuropsychiatric disorders than subregion volumes.

Genetics of eating disorders in the genome-wide era.

Enabled by advances in high throughput genomic sequencing and an unprecedented level of global data sharing, molecular genetic research is beginning to unlock the biological basis of eating disorders. This invited review provides an overview of genetic discoveries in eating disorders in the genome-wide era. To date, five genome-wide association studies on eating disorders have been conducted - all on anorexia nervosa (AN). For AN, several risk loci have been detected, and ~11-17% of the heritability has been accounted for by common genetic variants. There is extensive genetic overlap between AN and psychological traits, especially obsessive-compulsive disorder, and intriguingly, with metabolic phenotypes even after adjusting for body mass index (BMI) risk variants. Furthermore, genetic risk variants predisposing to lower BMI may be causal risk factors for AN. Causal genes and biological pathways of eating disorders have yet to be elucidated and will require greater sample sizes and statistical power, and functional follow-up studies. Several studies are underway to recruit individuals with bulimia nervosa and binge-eating disorder to enable further genome-wide studies. Data collections and research labs focused on the genetics of eating disorders have joined together in a global effort with the Psychiatric Genomics Consortium. Molecular genetics research in the genome-wide era is improving knowledge about the biology behind the established heritability of eating disorders. This has the potential to offer new hope for understanding eating disorder etiology and for overcoming the therapeutic challenges that confront the eating disorder field.

Childhood Maltreatment and Eating Disorders: A Prospective Investigation

To determine whether childhood maltreatment is a risk factor for two eating disorders (anorexia nervosa and bulimia nervosa) using objective and subjective case definitions. Using a prospective cohorts design, children with documented cases of physical abuse, sexual abuse, and neglect (ages 0-11) from 1967 to 1971 in a Midwestern metropolitan county area were matched on age, race, sex, and approximate family socioeconomic status with non-maltreated children. Both groups were followed up. Retrospective self-reports about childhood maltreatment were collected at age 29. DSM-IV anorexia nervosa (AN) and bulimia nervosa (BN) disorders were assessed at age 41 (N = 807). Logistic and linear regression results are reported. Using documented cases, childhood maltreatment was not a significant risk factor for AN or BN diagnoses or symptoms in adulthood. However, adults who retrospectively reported any maltreatment and physical and sexual abuse reported significantly more symptoms of AN than those who did not. The prediction that childhood maltreatment is a risk factor for anorexia nervosa and bulimia nervosa was partially supported in this longitudinal study. While misattribution of cases might have occurred, these results suggest that researchers and clinicians should use caution in drawing inferences about these relationships and designing interventions.

Risk factors for anorexia nervosa and bulimia nervosa in Japan and compared to a U.S. sample.

This study provides the first systematic investigation of environmental exposure to putative psychosocial risk factors for eating disorders in individuals with AN and BN in Japan. It also provides a comparison of risk factors for the development of AN and BN in Japan versus the United States. Participants in Japan were 96 women with a current DSM-IV AN or BN primary diagnosis (AN, n = 60; BN, n = 36) and 57 women with no current psychiatric diagnosis (NC group). Participants in the United States were 137 women with a current DSM-IV AN or BN primary diagnosis (AN-U.S., n = 71; BN-U.S., n = 66). A standardized semi-structured interview retrospectively assessed exposure to risk factors prior to first symptom onset, which were analyzed using General Linear Model analyses. Perfectionism and negative affectivity, family relationship issues, and, to a lesser degree, parental psychopathology predicted the emergence of AN and BN in Japan. Physical and sexual abuse and family eating and weight concerns were not significant risk factors in Japan. Compared to their respective diagnostic U.S. groups, the Japanese AN group reported higher levels of individual mental health factors and lower levels of family dieting and family overweight, and the Japanese BN group reported higher levels on individual mental health factors, lower exposure to problems with their parents, and lower exposure to family weight and eating concerns. These country-specific data from Japan contribute to an increasingly nuanced and global understanding of risk factors for eating disorders.

M43 - A CROSS-DISORDER GENOME-WIDE ASSOCIATION STUDY OF ANOREXIA NERVOSA AND OBSESSIVE-COMPULSIVE DISORDER

Background This work is presented on behalf of the Eating Disorders and Tourette's/Obsessive-Compulsive Disorder Working Groups of the Psychiatric Genomics Consortium. Anorexia Nervosa (AN) is a serious psychiatric disorder with high mortality and morbidity, and Obsessive-Compulsive Disorder (OCD) is an idiopathic psychiatric condition that often follows a chronic course. Overlap of hallmark symptoms (e.g., compulsivity, cognitive rigidity), notable comorbidity, shared family history, and a high genetic correlation provide converging lines of evidence for shared etiology of AN and OCD, but the biological mechanisms behind this shared risk have yet to be uncovered. The aim of the present study was to examine the shared genetic risk factors for AN and OCD. Methods Under the umbrella of the Psychiatric Genomics Consortium, we conducted a meta-analysis of the most recent and largest AN and OCD Genome-Wide Association Studies (GWASes) to investigate risk variants common to both disorders. A total of 6,183 cases (3,495 AN and 2,688 OCD) and 18,013 controls were included in the meta-analysis of 8,062,640 variants conducted using METAL through the Ricopili pipeline. Results Although no variant reached genome-wide significance, the closest nearby genes for the variants with p Discussion In this first cross-disorder GWAS for AN and OCD, our preliminary results provide encouraging evidence for the shared genetic architecture of these two psychiatric disorders. Additional approaches such as gene- and gene-set based analyses, partitioned heritability analyses, and those making use of gene-expression data are underway and will supplement current results.

Prenatal stress exposure as a risk factor for anorexia nervosa: A controlled study

IntroductionPrenatal risk factors, such as gestational complications and exposure to stress during pregnancy, may have a role in the development of many psychiatric disorders including eating disorders.AimTo investigate the impact of prenatal stress exposure on the development and clinical features of anorexia nervosa.MethodsOne hundred and nine patients with a lifetime diagnosis of anorexia nervosa and 118 healthy controls underwent a clinical assessment, which included interviews, questionnaires and a neuropsychological battery. The mothers of the patients and controls underwent a specific interview focused on stressful life events, which occurred during pregnancy. Obstetric and neonatal records were consulted.ResultsThe mothers of patients experienced more severe stressful episodes during pregnancy than the mothers of controls and the perceived distress showed significant positive correlation with both total number of obstetrical complications and placental weight. In patients, the severity of stressful events was strongly associated to cognitive rigidity and perseverance.ConclusionsPrenatal stress exposure might be a risk factor for the development of anorexia nervosa and it is associated with cognitive traits of rigidity and perseverance.Disclosure of interestThe authors have not supplied their declaration of competing interest.

The Association of Anorexia Nervosa and Climate Revisited: A Bibliometric Perspective

Objective: A decade ago a first bibliometric study considered the worldwide distribution of scientific publications of anorexia nervosa to be an indirect indicator of its prevalence at different latitudes. This bibliometric approach was grounded on the hypothesis that the prevalence for a particular disorder in a geographical area could be associated to an increase in the allocation of funds and health care resources supporting clinical and research programs, which in turn would be associated with an increase in the production of related scientific literature. Method: References to anorexia nervosa, anxiety disorders and seasonal affective disorders were retrieved from PubMed and PsycINFO databases and collected for the period 2000-2014. The distributions of the bibliographic references were mapped according to the institutional affiliation of their first author. Furthermore, according to their geographical coordinates each reference was catalogued in accordance with the Koppen classification system. Results: A remarkable similarity in the distribution of references to anorexia nervosa for the two periods was observed as well as a differential association of anorexia nervosa to mid-latitudes climates in comparison to references to anxiety disorders and seasonal affective disorders. Discussion: The distribution of references for anorexia nervosa have remained considerably stable over the last 25 years associated to higher but not extreme latitudes and to climates with regular seasons with no severe temperature variations across seasons. The replication of the data for these two time periods implies that ambient temperature should be included in the list of environmental risk factors for anorexia nervosa.

Psychological and behavioural characteristics of females with anorexia nervosa in Singapore.

This study aimed to compare a sample of females with anorexia nervosa in Singapore with international clinical and population samples from published data in terms of endorsement of risk factors related to anorexia nervosa, severity of eating pathology and levels of psychosocial impairment and to explore the nature of the relationships between the anorexia nervosa risk factors and adherence to Asian cultural values. Data from the Eating Disorder Inventory-3 (EDI-3), the Eating Attitudes Test (EAT-26), the Perceived Sociocultural Pressure Scale (PSPS), the Ideal Body Stereotype Scale (IBSS), the Eating Disorder Examination Questionnaire (EDE-Q), the Clinical Impairment Assessment Questionnaire, and the Asian American Values Scale-Multidimensional (AAVS-M) were collected from 41 female patients (13-31years old) who presented for treatment of anorexia nervosa at the Singapore General Hospital. The profile and presentation of anorexia nervosa in Singapore was comparable to that observed in the Western clinical samples in terms of levels of endorsement of the risk factors for anorexia nervosa. No protective benefit of orientation to Asian culture was found. The observed pattern of general similarity of presentation between Western data and Singaporean data, together with the finding that no protective benefit of orientation to Asian culture was observed, suggests that it may be appropriate to directly apply evidence-based Western models of intervention to the treatment of anorexia nervosa in Singapore.

Childhood body mass index in adolescent-onset anorexia nervosa.

Although weight history is relevant in predicting eating disorder symptom severity, little is known about its role in the etiology of anorexia nervosa (AN). This study aimed to determine whether BMI or BMI trajectory differed between individuals who later developed adolescent-onset AN and a comparison group of HCs between school grades 1 through 6. This study was based on longitudinal data that identified 51 adolescents with AN and 51 matched HCs. Cases were identified through community screening in Sweden and included individuals born in 1969 through 1977. Measured weights and heights were retrieved and BMIs and weight trajectories of the AN and HC groups were compared using growth curve analysis. Main outcome measures included measured BMI and BMI trajectories from grades 1-6. Secondary outcomes examined included ponderal index at birth and maternal body weight. Individuals who later developed AN had higher BMIs than HCs between grades 1 and 6, by an average of 1.42 BMI-units. There was no difference in rate of weight gain between groups. Ponderal index at birth was higher for the AN as compared with HC group. Maternal weight did not differ significantly between groups. These findings, combined with those previously reported on the premorbid BMIs of those with bulimia nervosa, suggest that a predisposition toward elevated premorbid BMIs during childhood characterizes those who later develop anorexia or bulimia nervosa. These findings are consistent with a transdiagnostic perspective and suggest shared risk factors for AN and obesity. © 2016 Wiley Periodicals, Inc. (Int J Eat Disord 2016; 49:1002-1009).