Development Of Anorexia Nervosa Research Articles

Genetic and epigenetic findings in anorexia nervosa

Abstract Polygenic factors are relevant for the genetic predispositions to the eating disorder anorexia nervosa (AN). The most recent genome-wide association study (GWAS) for AN comprised almost 17,000 patients with AN and controls. A total of eight genome-wide significant polygenic loci associated with AN have been identified. Each single polygenic locus makes only a small contribution to the development of AN. Analyses across different traits successfully identified regions/genes for AN that had not been detected by analyses of the single traits. Functional studies of the genes derived by GWAS studies aim to improve the understanding of the biological mechanisms involved in eating disorders. Epigenetic studies have not yet successfully contributed to the understanding of AN.

Heightened self-reported punishment sensitivity, but no differential attention to cues signaling punishment or reward in anorexianervosa.

This study examined whether adolescents with anorexia nervosa (AN) are more sensitive to punishment and less sensitive to reward than a non-eating disorder comparison group. Both self-report and performance measures were used to index reward and punishment sensitivity. Participants were adolescents with AN (n = 69) and an individually matched comparison group with healthy weight (n = 69). They completed the Behavioral Inhibition Scale/Behavioral Activation Scale and the Sensitivity to Punishment and Sensitivity to Reward Questionnaire to index self-reported reward and punishment sensitivity, and performed the Spatial Orientation Task to index attention to cues signaling reward and punishment. There was extremely strong evidence (BF10 > 100), that adolescents with AN reported higher sensitivity to punishment than adolescents without an eating disorder. However, adolescents with AN did not differ from the comparison group on self-reported reward sensitivity, and attention to cues signaling reward or punishment. Adolescents with AN clearly show heightened punishment sensitivity, yet this was not paralleled by a heightened proneness to detect signals of punishment. An important next step would be to examine whether punishment sensitivity is a reliable risk factor for the development or maintenance of AN.

The Ghrelin-AgRP Neuron Nexus in Anorexia Nervosa: Implications for Metabolic and Behavioral Adaptations.

Anorexia Nervosa (AN) is viewed as primarily a psychiatric disorder owing to the considerable behavioral and genetic overlap with mood disorders and other psychiatric traits. However, the recent reconceptualization of AN as one of both psychiatric and metabolic etiology suggests that metabolic circuits conveying hunger, or sensitive to signals of hunger, may be a critical nexus linking metabolic dysfunction to mood disturbances. Within the brain, hunger is primarily percieved by Agouti-related (AgRP) neurons and hunger increases plasma concentrations of the hormone ghrelin, which targets ghrelin receptors on AgRP neurons to facilitate metabolic adaptations to low energy availability. However, beyond the fundamental role in maintaining hunger signaling, AgRP neurons regulate a diverse range of behaviors such as motivation, locomotor activity, negative reinforcement, anxiety, and obsession and a key factor involved in the manifestation of these behavioral changes in response to activation is the presence or absence of food availability. These changes can be considered adaptive in that they promote affective food-seeking strategies in environments with limited food availability. However, it also suggests that these neurons, so well-studied for their metabolic control, shape mood-related behaviors in a context-dependent manner and dysfunctional control leads not only to metabolic problems but also potentially mood-related problems. The purpose of this review is to underline the potential role of AgRP neurons and ghrelin signaling in both the metabolic and behavioral changes observed in anorexia nervosa. We aim to highlight the most recent studies on AgRP neurons and ghrelin signaling and integrate their metabolic and behavioral roles in normal function and highlight how dysfunction may contribute to the development of AN.

Altered brain levels of arachidonic acid-derived inflammatory eicosanoids in a rodent model of anorexia nervosa

Increasing evidence underline the role of inflammation in the behavioral, emotional and cognitive dysregulations displayed in anorexia nervosa (AN). Among the inflammatory mediators acting at both peripheral and central levels, growing attention receives a class of lipids derived from arachidonic acid (AA), called eicosanoids (eiCs), which exert a complex, multifaceted role in a wide range of neuroinflammatory processes, peripheral inflammation, and generally in immune system function. To date, little is known about their possible involvement in the neurobiological underpinnings of AN. The present study evaluated whether the activity-based model of AN (ABA) may alter AA-metabolic pathways by changing the levels of AA-derived eiCs in specific brain areas implicated in the development of the typical anorexic-like phenotype, i.e. in prefrontal cortex, cerebral cortex, nucleus accumbens, caudate putamen, amygdala, hippocampus, hypothalamus and cerebellum. Our results point to brain region-specific alterations of the cyclooxygenase (COX), lipoxygenase (LOX) and cytochrome P450 epoxygenase (CYP) metabolic pathways rendering altered levels of AA-derived eiCs (i.e. prostaglandins, thromboxanes and hydroxyeicosatetraenoic acids) in response to induction of and recovery from the ABA condition. These changes, supported by altered messenger RNA (mRNA) levels of genes coding for enzymes involved in eiCs-related methabolic pathways (i.e., PLA2, COX-2, 5-LOX and 15-LOX), underlie a widespread brain dysregulation of pro- and anti-inflammatory eiC-mediated processes in the ABA model of AN. These data suggest the importance of eiCs signaling within corticolimbic areas in regulating key neurobehavioral functions and highlight eiCs as biomarker candidates for monitoring the onset and development of AN, and/or as possible targets for pharmacological management.

Emotion regulation, emotion recognition, and empathy in adolescents with anorexia nervosa.

Emotional functions may play an important role in anorexia nervosa (AN). The onset of the disorder generally occurs during adolescence, which is a critical period of emotional development. However, most studies that evaluated emotional functions in AN were conducted in adult patients. The aim of this study was to evaluate emotion regulation, emotion recognition, and empathy skills in adolescent girls with AN by controlling for the effects of depression and anxiety symptoms, childhood traumatic experiences, and attachment security on emotional functions. Thirty-two adolescent girls with AN and 32 healthy counterparts completed the Difficulties in Emotion Regulation Scale, the Reading the Mind in the Eyes Test, Toronto Alexithymia Scale-20, and the Child and Adolescent KA-SI Empathic Tendency Scale-Adolescent Form. The results revealed that adolescents with AN were found to have more difficulties in emotion regulation, higher alexithymic tendencies, and lower empathy skills compared with the control group. However, emotion recognition was not found to be significantly different between the two groups. These results were the same when controlling for the effects of depression and anxiety symptoms, childhood traumatic experiences, and attachment security except for empathy skills. Alexithymia and depressive symptoms were significantly related to emotion regulation difficulties in adolescents with AN. Considering the results, it seems that emotion regulation and alexithymia may play a crucial role in the development and maintenance of AN. Accordingly, it is necessary to focus on the improvement of these skills during the treatment of AN. Furthermore, interventions promoting these skills during adolescence may be preventive. Level III,case-control study.

EXPANDING THE EMPATHIC GRASP IN THE TREATMENT OF ANOREXIA NERVOSA: ADDING A NEUROSCIENCE PERSPECTIVE

This paper uses data from neuroscience to describe a phenotype of the person prone to developing Anorexia Nervosa, the brain changes that contribute to perpetuating the disorder and the challenges facing the Anorectic patient as s/he works to break the destructive patterns. We suggest that neuroscience data integrated into a psychodynamic clinical process expand the way the clinician conveys empathy and understanding to the patient. This approach facilitates weight gain and creates a platform for deeper psychodynamic work once weight is stabilized. A lengthy clinical example illustrates this approach.

Clinical and socio-demographic features in childhood vs adolescent-onset anorexia nervosa in an Asian population.

Childhood-onset anorexia nervosa (AN) may be under-recognised and under-treated due to atypical presentations. The aims of this study are: (1) describe features of AN in patients ≤ 18years in an Asian population; and (2) compare childhood-onset and adolescent-onset AN. This study involved a retrospective chart review of patients ≤ 18years in a Asian population who were treated for anorexia nervosa at the Eating Disorders Service at Singapore General Hospital between Jan 2003 and Dec 2014 (n = 435). Childhood-onset AN was defined as onset < 13years, while adolescent-onset AN was defined as onset between 13 and 18years. Patients were predominantly female (95.4%) and Chinese (83%). The childhood-onset group (8.3%) had mean age of onset 11.5 ± 1.0years, compared to 15.2 ± 1.6years for the adolescent-onset group. The childhood and adolescent-onset groups were similar in socio-demographic variables, as well as gender distribution, AN subtype, number of psychiatric comorbidities, family history of psychiatric illness, body image issues and excessive exercise. The childhood-onset group had significantly longer duration of illness prior to presentation (4.75 vs 2.62years), greater frequency of comorbid obsessive-compulsive disorder (19.4% vs 5.3%) and were more likely to report teasing as a trigger for AN (58.3% vs 31.6%). The childhood-onset group had significantly longer duration of inpatient stay (5.97 vs 3.22weeks), as well as a greater number of total admissions (2.78 vs 1.37). Our results suggest that cultural factors may impact the development or identification of AN in an Asian context. Possible delay in diagnosis of childhood-onset AN may lead to a more unfavorable clinical course. Level V, descriptive study.

Prenatal and perinatal risk factors for eating disorders in women: A population cohort study.

The fetal programming model hypothesizes that developmental programming in utero and in early life induces adaptations that predetermine the adult phenotype. This study investigated whether prenatal/perinatal complications are associated with lifetime eating disorders in women. Participants included 46,373 adult women enrolled in the Norwegian Mother and Child Cohort Study (den norske Mor & barn-undersøkelsen [MoBa]). MoBa mothers and their mothers (MoBa grandmothers) were the focus of the current study. MoBa mothers with lifetime eating disorders were compared to a referent group. MoBa mothers who weighed more at birth (birth weight, adjusted odds ratio [OR] = 1.14; 95% confidence interval [CI]: 1.10-1.19) or were born large-for-gestational-age (adjusted OR = 1.39; 95% CI: 1.27-1.52) were more likely to develop binge-eating disorder in later life. MoBa mothers who weighed less at birth were more likely to develop anorexia nervosa (birth weight, adjusted OR = 0.88; 95% CI: 0.81-0.95). Bulimia nervosa and purging disorder (PD) were not significantly predicted by the prenatal and perinatal factors examined. Results of this study, which include the first known investigation of prenatal and perinatal factors in binge-eating disorder and PD, suggest that fetal programming may be relevant to the development of anorexia nervosa and binge-eating disorder. Future genetically informative research is needed to help disentangle whether these associations are a function of genetic influences or a true environmental fetal programming effect.

Anorexia Nervosa and a Lost Emotional Self: A Psychological Formulation of the Development, Maintenance, and Treatment of Anorexia Nervosa.

In this paper, we argue that Anorexia Nervosa (AN) can be explained as arising from a ‘lost sense of emotional self.’ We begin by briefly reviewing evidence accumulated to date supporting the consensus that a complex range of genetic, biological, psychological, and socio-environmental risk and maintenance factors contribute to the development and maintenance of AN. We consider how current interventions seek to tackle these factors in psychotherapy and potential limitations. We then propose our theory that many risk and maintenance factors may be unified by an underpinning explanation of emotional processing difficulties leading to a lost sense of ‘emotional self.’ Further, we discuss how, once established, AN becomes ‘self-perpetuating’ and the ‘lost sense of emotional self’ relentlessly deepens. We outline these arguments in detail, drawing on empirical and neuroscientific data, before discussing the implications of this model for understanding AN and informing clinical intervention. We argue that experiential models of therapy (e.g., emotion-focused therapy; schema therapy) be employed to achieve emergence and integration of an ‘emotional self’ which can be flexibly and adaptively used to direct an individual’s needs and relationships. Furthermore, we assert that this should be a primary goal of therapy for adults with established AN.

M42 - WHOLE GENOME SEQUENCE ANALYSIS OF A COUSIN PAIR WITH RESTRICTING ANOREXIA NERVOSA

Background Anorexia Nervosa (AN) is a serious mental illness that often has an onset during adolescence. AN is characterized by emaciation, fear of gaining weight despite being underweight, and the highest mortality rate of all psychiatric illnesses. AN is highly heritable and recent meta-analyses in 3,495 anorexia nervosa cases and 10,982 controls has identified a region on chromosome 12 at genome-wide significance, significant common genetic heritability, and genetic correlations with both psychiatric and metabolic traits. AN symptoms and personality traits tend to be present in unaffected family members of the patients, suggesting that certain shared genetic factors within each family may contribute to the unique risk underlying an affected individual's phenotype. Methods To gain insight into the role that unique, family-specific variants may play in the development of AN, we performed whole genome sequencing analysis (Complete Genomics) and extensive annotation of high quality variants (Cypher Genomics, SG-Advisor, ANNOVAR) to search for genetic variants that may influence AN risk in six individuals, consisting of two maternally-linked cousins with severe AN and their parents. We focused on maternally-inherited shared segments; the preferred transmission model for variant filtering was the dominant model. We reviewed results from the Psychiatric Genomic Consortium AN GWAS and other -omic databases at identified genes. Results Of the approximately 5.3 million variants per individual that were analyzed, 494,712 were shared Identical-By-Descent (IBD) by the cousin pair based on maternally derived haplotypes. Based on extensive genetic variant annotations within maternally inherited shared segments, we identified variants in TTC22, MRPS9, DNAJC30, HEPACAM2, USP20, ESF1, and CDK5RAP1. Multiple prediction methods suggest that six of these variants are likely to affect protein function. The region proximal to MRPS9 exhibits an excess of nominally significant findings in the PGC AN GWAS, and eQTLs to MRPS9 and to an uncharacterized antisense gene in many tissues. MRPS9 SNPs are associated in blood with 4-androsten-3beta,17beta-diol disulfate 2 and dehydroisoandrosterone sulfate (a metabolite and a precursor of steroid sex hormones, respectively). Discussion By capitalizing on the homogeneity of the disease presentation and the genomic makeup among two cousins with a diagnosis of restricting-type AN, we exploited whole genome sequence analysis and variant annotation approaches to identify a set of novel variants and genes that may influence AN. Our results suggest that there may be utility in whole genome sequencing of families with affected individuals to detect variants that contribute to a complex disease such as AN.

Developmental Premorbid Body Mass Index Trajectories of Adolescents With Eating Disorders in a Longitudinal Population Cohort.

To examine whether childhood body mass index (BMI) trajectories are prospectively associated with later eating disorder (ED) diagnoses. Using a subsample from the Avon Longitudinal Study of Parents and Children (N= 1,502), random-coefficient growth models were used to compare premorbid BMI trajectories of individuals who later developed anorexia nervosa (n= 243), bulimia nervosa (n= 69), binge-eating disorder (n= 114), and purging disorder (n= 133) and a control group without EDs or ED symptoms (n= 966). BMI was tracked longitudinally from birth to 12.5 years of age and EDs were assessed at 14, 16, and 18 years of age. Distinct developmental trajectories emerged for EDs at a young age. The average growth trajectory for individuals with later anorexia nervosa veered significantly below that of the control group before 4 years of age for girls and 2 years for boys. BMI trajectories were higher than the control trajectory for all other ED groups. Specifically, the mean bulimia nervosa trajectory veered significantly above that of controls at 2 years for girls, but boys with later bulimia nervosa did not exhibit higher BMIs. The mean binge-eating disorder and purging disorder trajectories significantly diverged from the control trajectory at no older than 6 years for girls and boys. Premorbid metabolic factors and weight could be relevant to the etiology of ED. In anorexia nervosa, premorbid low weight could represent a key biological risk factor or early manifestation of an emerging disease process. Observing children whose BMI trajectories persistently and significantly deviate from age norms for signs and symptoms of ED could assist the identification of high-risk individuals.

Not the Function of Eating, but Spontaneous Activity and Energy Expenditure, Reflected in "Restlessness" and a "Drive for Activity" Appear to Be Dysregulated in Anorexia Nervosa: Treatment Implications.

Anorexia nervosa (AN) is uncommon as a syndrome, despite widespread dieting or voluntary food restriction, especially among female adolescents. This suggests that restriction of caloric intake might not be the only component driving weight loss in AN. Historical observations and experimental evidence from energy expenditure studies and recordings from movement sensors reviewed in this paper reveal that AN is associated with motor activity levels and with an energy output not significantly different from that in normal-weight healthy age-matched controls. By contrast, other conditions of prolonged caloric under-nutrition are typically associated with loss of energy, slowing of movements and a decrease in self-initiated activity and well-being. Several hypotheses can be inferred from the findings: (a) that long term severe caloric restriction fails in downregulating movements and energy expenditure in AN. (b) Clinically and subjectively observable as mental and physical restlessness and continued motor activity, this restless energy, differing in intensity, seems to serve as the permissive factor for and possibly to drive exercise and hyperactivity in AN. (c) Such restless energy and increased arousal, generated sometime in the course of the weight loss process, appear to enhance the person’s self-perception and wellbeing, to heighten proprioception, to intensify body awareness and to improve self-esteem. (d) Restlessness and continued motor activity may constitute a phenotype of AN. The therapeutic value of the concept of an abnormality in the energy regulatory system, likely the result of a host of genetic and epigenetic changes in AN, lies primarily in its heuristic and explanatory power and its potential for disease prevention. Restless energy as a permissive and important component for the development and in the maintenance of AN, does not fundamentally alter treatment, since prolonged food deprivation is the principal causal factor for the development of AN. Re-nutrition within a structured treatment plan, to include individual and family therapy and, if indicated, heat application, remains the most effective symptomatic treatment for AN. Corroboration of the concept of restless activation will require the patient’s cooperation and input to identify and capture more precisely the experiences, sensations, and changes that allow the emaciated patient to remain mobile and active.

Anxiety and the development and maintenance of anorexia nervosa: protocol for a systematic review

BackgroundSeveral aetiological models of anorexia nervosa (AN) hold non-eating/weight-gain-related anxiety as a factor relevant to the onset and maintenance of the disorder. Longitudinal studies that allow assessment of this hypothesis have been conducted; however, the evidence has not yet been aggregated in a systematic manner. The proposed study will systematically review articles describing prospective investigations of the relationship between anxiety and AN development or maintenance, with the aim of providing a balanced summary of current understanding and identifying areas for further research.Methods/designElectronic databases will be searched for articles investigating the longitudinal influence of non-eating/weight-gain-related anxiety (anxiety disorders and trait anxiety) on the development/maintenance of AN. References of eligible articles will be searched to ensure the identification of all relevant studies. Two independent reviewers will complete the title and abstract, and full-text, screening, with a third independent reviewer resolving any conflicts at each stage. A systematic review will be completed, and the quality of the included studies, as well as the strength of the body of evidence generated, will be assessed and reported.DiscussionAlthough there are limitations to the present review, understanding the current evidence for the role of non-eating/weight-gain-related anxiety in AN can direct future research that may ensure accurate aetiological models of AN and effective treatments.Systematic review registrationThe study is registered on PROSPERO under the reference number CRD42017069644

Anorexie mentale chez une fille de migrants chinois : apports de la psychiatrie transculturelle

BackgroundAnorexia nervosa has for a long time been considered to be an occidental culture bound syndrome, but it also exists in other cultural areas such as China. It has been diagnosed at migrant females of Asian origins as well. It should rather be considered as a syndrome linked with rapid social changes or appearing during migration. We question the way cultural factors and transcultural factors, culture clash or acculturation are entangled in this pathology. MethodWe analyzed the clinical situation of an anorexic teenager, Laure, the daughter of Chinese immigrants in France, with the qualitative method of thematic analysis and with the tools provided by a transcultural clinic: a psychiatric and anthropological reading. ResultsFour themes were identified that seemed linked to Laure's anorexia development: acculturation, culture clash, identity construction, and family difficulties. This clinical situation is quite unique because of its history, her strong resistance to being cared for, and also because transcultural and cultural factors are entangled. DiscussionLaure's acculturation could be responsible for two atypical symptoms of anorexia nervosa, as compared with those occurring among Chinese anorexic girls: fat phobia and denial about thinness. Laure's difficulties encountered with her first name, the fact that she refused to learn the Chinese language and her atypical food restriction on Chinese food show intense internal conflicts. Laure meets difficulties with her self-esteem and identity construction which could be linked to the vulnerability induced by migration and also by the effects of racism from which she suffered. The construction of the parents-child relationship and in-between siblings could be more complex in a migration context because of cultural and family breaks it leads to. For instance, migration could result in different acculturation features inside the family or in a culture clash. Consequently, it could be suggested in such a clinical case to provide specific care: transcultural care associated with other forms of care such as individual and familial care. ConclusionTranscultural factors, acculturation and cultural identity conflicts could weaken identity construction and family ties and therefore be risk factors for developing anorexia nervosa among migrants’ children. Transcultural approach is then essential for a better understanding of these disorders, for improving therapeutic alliance, for a better care and for aiding with cultural mixing.

How extreme dieting becomes compulsive: A novel hypothesis for the role of anxiety in the development and maintenance of anorexia nervosa

The US National Institute of Mental Health’s Research Domain Criteria (NIMH RDoC) advocates the study of features common to psychiatric conditions. This transdiagnostic approach has recently been adopted into the study of anorexia nervosa (AN), an illness that can be considered compulsive in nature. This has led to the development of an account of AN that identifies key roles for the heightened reinforcement of starvation, leading to its excessive repetition, and goal-directed system dysfunction. Considering models of illness in other compulsive disorders, we extend the existing account to explain the emergence of reinforcement and goal-directed system abnormalities in AN, proposing that anxiety is central to both processes. As such we emphasise the particular importance of the anxiolytic effects of starvation, over other reinforcing outcomes, in encouraging the continuation of starvation within a model that proposes a number of mechanisms by which anxiety operates in the development and maintenance of AN. We suggest the psychopathology of AN mediates the relationship between the anxiolytic effects of starvation and excessive repetition of starvation, and that compulsive starvation has reciprocal effects on its determinants. We thus account for the emergence of symptoms of AN other than compulsive starvation, and for the relationship between different features of the disorder. By extending and adapting an existing explanation of AN, we provide a richer aetiological model that invites new research questions and could inform novel approaches to prevention and treatment.

Regional decrease in gray matter volume is related to body dissatisfaction in anorexia nervosa

Anorexia nervosa (AN) is a psychiatric disorder, in which the prognosis for some patients is poor. The etiology and effective treatments for AN have not been established. We examined morphometric changes in the brain of AN and clarified how the changes were associated with symptoms and pathophysiology. We enrolled 52 participants: 7 with the restrictive type of AN, 13 with the binge-eating/purging type, 3 with eating disorder not otherwise specified, and 29 healthy controls. Participants underwent T1-weighted MRI. Group differences between patients and controls in gray matter volume (GMV) were analyzed using voxel-based morphometry. Age and body mass index (BMI) were considered covariates. Correlations between regional GMVs and drive for thinness and body dissatisfaction were examined. Patients had decreased GMV in the superior/middle temporal gyrus (STG/MTG), pulvinar, and superior frontal gyrus after correction for age and BMI, and in the STG/MTG, middle frontal gyrus, and cingulate after correction for age. A correlational group difference was detected for body dissatisfaction and GMV in the STG. Our findings suggest that decreased GMV in the STG is related to body dissatisfaction that could come from impaired visuospatial perception, together with GMV decreases in several regions, which may be involved in development of AN.

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.

“Holy anorexia”—relevant or relic? Religiosity and anorexia nervosa among Finnish women

Since medieval times, an association between religiosity and anorexia nervosa has been suggested, but few systematic studies exist. This study examines in a nationwide setting whether personal or family religiosity is associated with lifetime anorexia nervosa among women in adolescence and early adulthood. Women (N = 2,825) from the 1975 to 1979 birth cohorts of Finnish twins were screened for lifetime DSM-5 anorexia nervosa (N = 92). Parental religiosity was assessed by self-report when the women were aged 16 years. The women self-reported their religiosity at ages 16 and 22 to 27 years. Parental religiosity did not increase the risk of lifetime anorexia nervosa, and neither did religiosity of the women themselves in adolescence. In early adulthood, a J-shaped curve was compatible with the data, indicating increased risk both at low and high levels of religiosity, but this result was statistically non-significant. Religiosity was weakly negatively correlated with body dissatisfaction. There was some suggestive evidence for socioregional variation in the association of religiosity with lifetime anorexia nervosa. In this first population study to directly address religiosity and anorexia nervosa, no evidence was found for a significant association of religiosity with anorexia nervosa either at the personal or family level. Some regional differences are possible. A modest protective association of religiosity with body dissatisfaction is also possible. Despite compelling case descriptions of "holy anorexia," religiosity does not appear to be a central factor in the development of anorexia nervosa in Finland, a highly secularized Christian country.

Immune disorders in anorexia.

Anorexia nervosa is a disease involving eating disorders. It mainly affects young people, especially teenage women. The disease is often latent and occurs in many sub-clinical and partial forms. Approximately from 0.3% to 1% of the population suffers from anorexia. It has been shown that patients with anorexia develop neurotransmitter-related disorders, leading to uncontrolled changes in the immune and endocrine systems. Interactions between cytokines, neuropeptides, and neurotransmitters play an important role in disease development. Significant malnutrition induces disorders and alterations in T-cell populations. The cellular response in patients with anorexia nervosa has been shown to be normal, although opinions on this issue are controversial. Laboratory studies on neutrophils in anorexia patients showed decreased adhesion and reduced bactericidal and cell activities. Despite such unfavourable results, patients with anorexia are resistant to infections, which are very rare in this group. Glutamine improves the performance of the human immune system. The administration of glutamine to anorexia patients, as a supplement to parenteral nutrition, has resulted in significant improvements in immune system parameters. The results of previous studies on the causes and risk factors in the development of anorexia nervosa are still ambiguous. One can hope that the differences and similarities between patients with anorexia nervosa and those with other forms of protein-calorie malnutrition may be helpful in determining the relationship between nutritional status and body defences and susceptibility to infection, and can help to broaden the knowledge about the aetiopathogenesis of anorexia nervosa.

Temporal discounting across three psychiatric disorders: Anorexia nervosa, obsessive compulsive disorder, and social anxiety disorder.

Temporal discounting refers to the tendency for rewards to lose value as the expected delay to receipt increases. Individuals with anorexia nervosa (AN) have been found to show reduced temporal discounting rates, indicating a greater preference for delayed rewards compared to healthy peers. Obsessive-compulsive disorder (OCD) and social anxiety disorder (SAD) commonly co-occur with AN, and anxiety has been related to development and prognosis of AN. We examined whether reduced temporal discounting is present across these potentially related disorders, and explored the relationship between temporal discounting and anxiety transdiagnostically. One hundred ninety six individuals (75 healthy controls (HC); 50 OCD; 27 AN; 44 SAD) completed two temporal discounting tasks in which they chose between smaller-sooner and larger-later monetary rewards. Two measures of discounting-discount rate and discount factor-were compared between diagnostic groups, and associations with anxious traits were examined. Individuals with AN showed decreased temporal discounting compared to HC. OCD and SAD groups did not differ significantly from HC. Across the sample, anxiety was associated with decreased discounting; more anxious individuals showed a greater preference for delayed reward. We replicated the findings that individuals with AN show an increased preference for delayed reward relative to HC and that individuals with OCD do not differ from HC. We also showed that individuals with SAD do not differ from HC in discounting. Across this large sample, two measures of anxious temperament were associated with temporal discounting. These data raise new questions about the relationship between this dimensional trait and psychopathology.