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The recovered possess the key to overcoming anorexia. Although individual sufferers do not know how the affliction takes hold, piecing their stories together reveals two accidental afflictions. One is that activity disorders—dieting, exercising, healthy eating—start as virtuous practices, but become addictive obsessions. The other affliction is a developmental disorder, which also starts with the virtuous—those eager for challenge and change. But these overachievers who seek self-improvement get a distorted life instead. Knowing anorexia from inside, the recovered offer two watchwords on helping those who suffer. One is \"negotiate,\" to encourage compromise, which can aid recovery where coercion fails. The other is \"balance,\" for the ill to pursue mind-with-body activities to defuse mind-over-body battles.

Characterized primarily by a low body-mass index, anorexia nervosa is a complex and serious illness 1 , affecting 0.9–4% of women and 0.3% of men 2 – 4 , with twin-based heritability estimates of 50–60% 5 . Mortality rates are higher than those in other psychiatric disorders 6 , and outcomes are unacceptably poor 7 . Here we combine data from the Anorexia Nervosa Genetics Initiative (ANGI) 8 , 9 and the Eating Disorders Working Group of the Psychiatric Genomics Consortium (PGC-ED) and conduct a genome-wide association study of 16,992 cases of anorexia nervosa and 55,525 controls, identifying eight significant loci. The genetic architecture of anorexia nervosa mirrors its clinical presentation, showing significant genetic correlations with psychiatric disorders, physical activity, and metabolic (including glycemic), lipid and anthropometric traits, independent of the effects of common variants associated with body-mass index. These results further encourage a reconceptualization of anorexia nervosa as a metabo-psychiatric disorder. Elucidating the metabolic component is a critical direction for future research, and paying attention to both psychiatric and metabolic components may be key to improving outcomes. Genome-wide analyses identify eight independent loci associated with anorexia nervosa. Genetic correlations implicate both psychiatric and metabolic components in the etiology of this disorder, even after adjusting for the effects of common variants associated with body mass index.

Eating disorders are life-threatening conditions that are challenging to address; however, the primary care setting provides an important opportunity for critical medical and psychosocial intervention. The recently published Diagnostic and Statistical Manual of Mental Disorders, 5th ed., includes updated diagnostic criteria for anorexia nervosa (e.g., elimination of amenorrhea as a diagnostic criterion) and for bulimia nervosa (e.g., criterion for frequency of binge episodes decreased to an average of once per week). In addition to the role of environmental triggers and societal expectations of body size and shape, research has suggested that genes and discrete biochemical signals contribute to the development of eating disorders. Anorexia nervosa and bulimia nervosa occur most often in adolescent females and are often accompanied by depression and other comorbid psychiatric disorders. For low-weight patients with anorexia nervosa, virtually all physiologic systems are affected, ranging from hypotension and osteopenia to life-threatening arrhythmias, often requiring emergent assessment and hospitalization for metabolic stabilization. In patients with frequent purging or laxative abuse, the presence of electrolyte abnormalities requires prompt intervention. Family-based treatment is helpful for adolescents with anorexia nervosa, whereas short-term psychotherapy, such as cognitive behavior therapy, is effective for most patients with bulimia nervosa. The use of psychotropic medications is limited for anorexia nervosa, whereas treatment studies have shown a benefit of antidepressant medications for patients with bulimia nervosa. Treatment is most effective when it includes a multidisciplinary, team-based approach.

There is a growing recognition that both the gut microbiome and the immune system are involved in a number of psychiatric illnesses, including eating disorders. This should come as no surprise, given the important roles of diet composition, eating patterns, and daily caloric intake in modulating both biological systems. Here, we review the evidence that alterations in the gut microbiome and immune system may serve not only to maintain and exacerbate dysregulated eating behavior, characterized by caloric restriction in anorexia nervosa and binge eating in bulimia nervosa and binge eating disorder, but may also serve as biomarkers of increased risk for developing an eating disorder. We focus on studies examining gut dysbiosis, peripheral inflammation, and neuroinflammation in each of these eating disorders, and explore the available data from preclinical rodent models of anorexia and binge-like eating that may be useful in providing a better understanding of the biological mechanisms underlying eating disorders. Such knowledge is critical to developing novel, highly effective treatments for these often intractable and unremitting eating disorders.

Purpose This study examines the connection between infections and the abrupt onset or exacerbation of anorexia nervosa (AN) in the context of PANS (Pediatric Acute–Onset Neuropsychiatric Syndrome) and PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections). Methods The authors conducted a literature review and present a case study of a 17-year-old girl treated at the University of Turin Eating Disorder Unit, whose AN presented with an abrupt onset following an infection and was characterized by a rapid and favorable course. Results The review includes 30 cases derived from six studies, suggesting that AN can manifest as PANS/PANDAS, with subjects, mainly adolescents, experiencing sudden or exacerbated eating restrictions alongside obsessive–compulsive behaviors. Some cases improved with antibiotics or standard psychiatric treatments, although age, symptom severity, and diagnostic markers like D8/17 varied across studies. Data on treatment follow-up also varied. The report refers to the case of V., a 17-year-old girl who developed AN following an intestinal infection. After significant weight loss and amenorrhea, she was hospitalized for 29 days, receiving psychiatric care, nutritional rehabilitation, and pharmacological treatment. Over 2 months of residential care and ongoing outpatient therapy, she improved notably, though mild body dysmorphophobia persisted. Conclusions While evidence suggests a possible link between infections and AN, research is still limited and inconsistent. Infections may trigger AN through autoimmune mechanisms or by initiating weight loss, particularly in younger patients. Although further studies are needed to clarify this relationship, infections should be considered in AN diagnosis, especially in pediatric cases. Level of Evidence: Level V, a narrative review and a case report.

Perceived parental influence on diet in early adolescence in the context of the parental relationship had previously not been studied in a clinical sample. The aim of this study was to investigate a possible association between eating disorders and characteristics of the relationship with parents and the parental feeding practices in early adolescence. 21 female adolescents and young adults with an eating disorder (ED)-bulimia nervosa or anorexia nervosa-and 22 females without eating disorder (healthy control; HC), aged between 16 and 26, were assessed via self-report questionnaires for problematic eating behaviour, relationship with parents, perceptions of parent's feeding practices at the age of 10-13 years and personality. Statistical evaluation was performed by means of group comparisons, effect sizes, regression analyses and mediator analyses. Adolescent and young adult females with ED reported more fears/overprotection and rejection/neglect by their mothers and less self-responsibility in terms of eating behaviour during adolescence than did the HC. The relationship with the fathers did not differ significantly. Females who perceived more cohesion, rejection/neglect and fears/overprotection by the mother were more likely to suffer from an ED. Rejection/neglect by both parents were associated with less self-acceptance of the young females with even stronger effect sizes for the fathers than the mothers. Harm prevention in the young females was a partial mediator between fears/overprotection and the drive for thinness. The parental relationship is partly reflected in the self-acceptance and self-responsibility in eating of the adolescent and young females, both of them are particularly affected in EDs. Stressors in the parent-child relationship should be targeted in treatment of eating disorders. Nutritional counselling for parents might be useful in early adolescence.

Psychiatric conditions in which symptoms arise involuntarily ('diseases') might be assumed to be more heritable than those in which choices are essential (behavioral disorders). We sought to determine whether psychiatric 'diseases' (Alzheimer's disease, schizophrenia, and mood and anxiety disorders) are more heritable than behavioral disorders (substance use disorders and anorexia nervosa). We reviewed the literature for recent quantitative summaries of heritabilities. When these were unavailable, we calculated weighted mean heritabilities from twin studies meeting modern methological standards. Heritability summary estimates were as follows: bipolar disorder (85%), schizophrenia (81%), Alzheimer's disease (75%), cocaine use disorder (72%), anorexia nervosa (60%), alcohol dependence (56%), sedative use disorder (51%), cannabis use disorder (48%), panic disorder (43%), stimulant use disorder (40%), major depressive disorder (37%), and generalized anxiety disorder (28%). No systematic relationship exists between the disease-like character of a psychiatric disorder and its heritability; many behavioral disorders seem to be more heritable than conditions commonly construed as diseases. These results suggest an error in 'common-sense' assumptions about the etiology of psychiatric disorders. That is, among psychiatric disorders, there is no close relationship between the strength of genetic influences and the etiologic importance of volitional processes.

The Diagnostic and Statistical Manual of Mental Disorders (i.e., DSM-5) currently recognizes three primary eating disorders: anorexia nervosa, bulimia nervosa, and binge eating disorder. The origins of eating disorders are complex and remain poorly understood. However, emerging research highlights a dimensional approach to understanding the multifactorial etiology of eating disorders as a means to inform assessment, prevention, and treatment efforts. Guided by research published since 2011, this review summarizes recent findings elucidating risk factors for the development of eating disorders across the lifespan in three primary domains: (1) genetic/biological, (2) psychological, and (3) socio-environmental. Prospective empirical research in clinical samples with full-syndrome eating disorders is emphasized with added support from cross-sectional studies, where relevant. The developmental stages of puberty and the transition from adolescence to young adulthood are discussed as crucial periods for the identification and prevention of eating disorders. The importance of continuing to elucidate the mechanisms underlying gene by environmental interactions in eating disorder risk is also discussed. Finally, controversial topics in the field of eating disorder research and the clinical implications of this research are summarized.

Anorexia nervosa (AN) is an often chronic, difficult to treat illness that leads to brain volume reductions in gray and white matter. The underlying pathophysiology is poorly understood, despite its potential importance in explaining the neuropsychological deficits and clinical symptoms associated with the illness. We used the activity-based anorexia model (ABA), which includes food reduction and running wheel access in female rats to study brain changes after starvation and refeeding. Longitudinal animal MRI and post-mortem brain sections confirmed a reduction in the mean brain volumes of ABA animals compared to controls. In addition, the mean number of astrocytes was reduced by over 50% in the cerebral cortex and corpus callosum, while the mean number of neurons was unchanged. Furthermore, mean astrocytic GFAP mRNA expression was similarly reduced in the ABA animals, as was the mean cell proliferation rate, whereas the mean apoptosis rate did not increase. After refeeding, the starvation-induced effects were almost completely reversed. The observation of the astrocyte reduction in our AN animal model is an important new finding that could help explain starvation-induced neuropsychological changes in patients with AN. Astrocyte-targeted research and interventions could become a new focus for both AN research and therapy.

Background: Anorexia nervosa is a serious eating disorder that mainly affects children and adolescents. Most patients present with extreme body dissatisfaction and an obsessive focus on body weight and food. Anorexia nervosa is a complex and multifactorial condition characterised by biological, psychological, and social factors. However, studies that have explored the cumulative risk that predisposes to anorexia nervosa are limited. This study aims to explore the potential risk factors for a severe form of the disease in patients affected by anorexia nervosa and to identify whether they may interact and reinforce each other, contributing to the severity of the disorder. Methods: For this study, we enrolled children and adolescents under 18 years of age hospitalised at IRCCS Bambino Gesù Pediatric Hospital, Rome, Italy, for anorexia nervosa from 1 December 2022 to 31 August 2024, identifying and analysing potential risk factors. Elevated shape and weight concerns were found in all patients. Psychiatric and neurodevelopment comorbidities were identified in 76 patients (51.35%), life stress events in 69 (46.62%), and a family history of eating and weight control behaviours in 39 (26.35%). Out of the sample size, 20.27% of patients did not live in a traditionally structured family. This study used the Kiddie-SADS-Present and Lifetime Version interview, the Coddington Life Events Scales, and the Trauma Symptom Checklist for Children questionnaires. Results: Patients with an extreme or severe index of anorexia nervosa are more likely to have multiple predisposing factors. In detail, four predisposing factors were found in 18.6% of patients with an extreme severity index, in 15.5% of those with a severe score, and in 10.3 and 10.6% of those with a moderate and mild score, respectively. Conclusions: Cumulative potential risk factors are more likely to be found in cases of severe course disease and patients hospitalised for anorexia. Prompt identification of predisposing factors and an effective plan of action are required to avoid a severe course disorder.