Anorexia nervosa: 30-year outcome.
Ontology highlight
ABSTRACT:
SUBMITTER: Dobrescu SR
PROVIDER: S-EPMC7557598 | biostudies-literature | 2020 Feb
REPOSITORIES: biostudies-literature
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Project description:BackgroundLong-term consequences of comorbid autism spectrum disorder (ASD) in individuals with anorexia nervosa (AN) are inadequately investigated.MethodsIn the 1980s, 51 adolescent-onset AN cases (AN group) and 51 matched controls (COMP group) were recruited from the community. They have been examined on five occasions. The four last assessments included the Morgan-Russell Outcome Assessment Schedule (MROAS) to assess eating disorder outcomes (weight, dieting, menstruation), and related problems including psychiatric, psychosexual and socioeconomic state. In the present study, at age 44, when 30 years had elapsed, MROAS data were compared with previous results. At age 16, 21, 24 and 32 years, all individuals had been assessed regarding ASD. At the 30-year follow-up, the impact of the ASD on the MROAS data was analysed.ResultsIn the AN group, all core anorectic symptoms (weight, dieting, menstruation) were on a par with the COMP group at the 30-year follow-up, but the positive outcomes were limited to those who had never had an ASD diagnosis. Psychiatric state was significantly worse in the AN group, particularly in the subgroup who had an ASD diagnosis assigned. The AN group-again particularly those with ASD-had a more negative attitude to sexual matters than the COMP group. The AN group had worse outcomes than the COMP group for 'personal contacts', 'social contacts,' and 'employment record' at the 30-year follow-up and the outcomes were worse the more often an ASD diagnosis had been assigned.LimitationsRare data collection points throughout 30 years (only 5 assessments). ASD was assessed in the first four studies but was not assessed again at the 30-year follow-up.ConclusionsMental health, psychosexual, and socioeconomic status were compromised up to 30 years after AN onset. Coexisting ASD contributed to the poor outcome. Core anorectic symptoms had "normalised" three decades after AN onset. Some individuals with anorexia nervosa (AN) also suffer from autism. In this study we have investigated outcome of AN 30 years after the onset of AN and whether the presence of autism affects the outcome. Since the 1980s we have followed 51 individuals with teenage-onset AN and 51 healthy controls. They have been examined on five occasions, and an instrument that measures symptoms of AN (weight, dieting, body image), psychiatric symptoms, ability to work, and relationships with partner, family, and friends has been used to assess outcome. Autism was assessed in the first four studies. Symptoms of AN had normalised at 30-year follow-up, but only among those without autism. Psychiatric symptoms, ability to work, and relationships were issues that persisted after 30 years in the AN group, and those who had both autism and a history of AN had even more pronounced problems in these areas. The AN group had a more negative attitude to sexual matters than the control group, the outcome was worse the more often an autism diagnosis had been assigned.ConclusionsMental health, psychosexual, and socioeconomic status are affected up to 30 years after AN onset, particularly among those with autism.
| S-EPMC8744255 | biostudies-literature
Project description:Anorexia nervosa (AN) is a psychiatric disorder with an estimated heritability of around 70%. Although the largest genome-wide association study meta-analysis on AN identified independent loci-conferring risk to the disorder, the molecular mechanisms underlying the genetic basis of AN remains to be elucidated. To explore AN, we ran a transcriptome profiling in peripheral blood mononuclear cells of 15 AN subjects and 15 healthy controls. We validated our mean results in a mouse model of chronic food restriction mimicking several aspects of AN. Through this exploratory study we identified 673 significantly differentially expressed genes in AN. Among these genes, we identified the Vanin-1 (Vnn1) gene that appears to play a major role in the regulation of multiple metabolic pathways. We confirmed an underexpression of Vnn1, especially in the liver, in a mouse model of chronic food restriction. These results indicate that quantitative food restriction affects Vnn1 expression, suggesting that this gene may contribute to the anorexic phenotype in the chronic food restriction mouse model as well as in patients affected by AN. We believe that this report highlights promising candidate genes and gene pathways for AN and reveals Vnn1 as a biomarker that may be used as molecular targets to predict and/or to understand AN.
2023-10-31 | GSE245978 | GEO
Project description:Gyrification brain abnormalities are considered a marker of early deviations from normal developmental trajectories and a putative predictor of poor outcome in psychiatric disorders. The aim of this study was to explore cortical folding morphology in patients with anorexia nervosa (AN). A MRI brain study was conducted on 38 patients with AN, 20 fully recovered patients, and 38 healthy women. Local gyrification was measured with procedures implemented in FreeSurfer. Vertex-wise comparisons were carried out to compare: (1) AN patients and healthy women; (2) patients with a full remission at a 3-year longitudinal follow-up assessment and patients who did not recover. AN patients exhibited significantly lower gyrification when compared with healthy controls. Patients with a poor 3-year outcome had significantly lower baseline gyrification when compared to both healthy women and patients with full recovery at follow-up, even after controlling for the effects of duration of illness and gray matter volume. No significant correlation has been found between gyrification, body mass index, amount of weight loss, onset age, and duration of illness. Brain gyrification significantly predicted outcome at follow-up even after controlling for the effects of duration of illness and other clinical prognostic factors. Although the role of starvation in determining our findings cannot be excluded, our study showed that brain gyrification might be a predictor of outcome in AN. Further studies are needed to understand if brain gyrification abnormalities are indices of early neurodevelopmental alterations, the consequence of starvation, or the interaction between both factors.
| S-EPMC6869411 | biostudies-literature
Project description:ObjectiveRelapse after weight restoration in anorexia nervosa (AN) is a critical problem. Higher body fat percentage after weight gain has been shown to predict better weight maintenance outcome. Leptin, a fat-derived hormone, has been associated with progress during weight gain, but its association with weight maintenance is unknown. This study aims to determine whether leptin levels after weight restoration in AN are associated with weight maintenance.MethodParticipants were 41 women with AN hospitalized for inpatient treatment. Participants were evaluated 2-4 weeks after weight restoration to body mass index (BMI) ≥ 19.5 kg/m2 for plasma leptin and body composition. Weight maintenance outcome was defined by whether a participant maintained a BMI of at least 18.5 kg/m2 at the end of 1 year following hospital discharge.ResultsTwenty (48.8%) out of 41 patients maintained their weight at 1 year. Percent body fat and leptin were significantly higher in the group who maintained weight (body fat, p = .004, Hedges' g = 0.944; log-leptin, p = .010, Hedges' g = 0.821), but there were no differences in predischarge BMI, duration of illness, and duration of amenorrhea. Using regression modeling, only higher log-leptin (pWald = .021) and percent body fat (pWald = .010), as well as fat-adjusted leptin (pWald = .029), independently predicted weight maintenance at 1 year.DiscussionsOur findings suggest that for acutely-weight restored women with AN, higher predischarge leptin measurements are associated with better outcome in the year following treatment. Prospective studies examining leptin as well as other parameters of metabolic health could offer insights into biomarkers that may improve clinical outcomes.
| S-EPMC9851598 | biostudies-literature
Project description:Expressed emotion (EE) has been associated with poor outcomes in anorexia nervosa (AN); however, whether changes in EE predict superior treatment outcomes is unknown. The current study examined whether decreases in EE during an open trial of a novel family-based treatment for AN predicted symptoms at end of treatment. Forty-seven adolescents (12-18 years of age) with AN or sub-threshold AN and their parents (mothers: n = 47, fathers: n = 39) participated in 6 months of family treatment. Measures of AN symptomatology (Eating Disorder Examination completed by adolescent and end of treatment recovery status) and parental EE (Family Questionnaire completed by parents which measures two facets of EE: critical communication [CC] and emotional over-involvement [EOI]) were collected at baseline and end of treatment. Parental EOI, but not CC, significantly decreased during the course of treatment. Change in mothers', but not fathers', EE accounted for additional variance in AN symptomatology at end of treatment above baseline EE and baseline AN symptom levels. Findings suggest a greater emphasis on parent support during treatment may improve outcomes.
| S-EPMC6361377 | biostudies-literature
Project description:As part of the Genetic Consortium for Anorexia Nervosa (GCAN) and Wellcome Trust Case
Control Consortium 3 (WTCCC3), we have amassed the largest anorexia nervosa (AN)
sample in the world (~4,000). Following the WTCCC3 GWAS, we secured funding from the
Klarman Family Foundation to extend the genetic analyses to variants on the exome chip
(CoreExome array). This pre-lim relates to carrying out genotyping on the CoreExome array
on up to a maximum of 580 new samples.
| EGAS00001000913 | EGA
Project description:Anorexia nervosa (AN) is a complex debilitating disease characterized by intense fear of weight gain and excessive exercise. It is the deadliest of any psychiatric disorder with a high rate of recidivism, yet its pathophysiology is unclear. The Activity-Based Anorexia (ABA) paradigm is a widely accepted mouse model of AN that recapitulates hypophagia and hyperactivity despite reduced body weight, however, not the chronicity. Here, we modified the prototypical ABA paradigm to increase the time to lose 25% of baseline body weight from less than 7 days to more than 2 weeks. We used this paradigm to identify persistently altered genes after weight restoration that represent a metabolic memory of under-nutrition and may contribute to AN relapse. We focused on adipose tissue as it was identified as a major location of metabolic memory of over-nutririon. We identified 300 persistently dysregulated genes, including Calm2 and Vps13d, which could be potential global regulators of metabolic memory in both chronic over- and under-nutrition. However, despite being on the opposite spectrum of weight perturbations, the majority of metabolic memory genes of under- and over-nutrition do not overlap, suggestive of the different mechanisms involved in these extreme nutritional statuses.
2023-08-23 | GSE229316 | GEO
Project description:ObjectiveAntidiuretic hormone (ADH) is involved in the response to stress and in depression and anxiety. However, studies on ADH in anorexia nervosa (AN) show conflicting results. A major reason for this may be methodological challenges due to short half-life of ADH in circulation and rapid degradation in vitro. To overcome these obstacles, copeptin, the C-terminal fragment stemming from the ADH precursor, has been increasingly used as a stable clinical measure for ADH. Furthermore, copeptin has been recognized as a biomarker of insulin resistance in obesity.MethodsWe measured fasting copeptin in plasma from 25 normohydrated, stable women with AN (BMI 13.0 ± 2.0) and 25 age-matched women.ResultsNo difference in copeptin levels was found (6.8 ± 1.8 vs. 5.5 ± 0.5 pmol/L). Confirmatory, copeptin concentrations were correlated to insulin resistance assessed by the homeostasis model assessment of insulin resistance.DiscussionWe report for the first time that copeptin level as a marker of ADH activity is not altered in fluid- and electrolyte-stabilized patients with severe AN patients, indicating that ADH may not be crucial in the pathophysiological involvement of psychologic stress in AN.
| S-EPMC7177552 | biostudies-literature
Project description:Purpose of reviewGenetic factors contribute to the etiology of anorexia nervosa (AN). This review synthesizes the current state of knowledge about the genetic etiology of AN, provides directions for future research, and discusses clinical implications for this research.Recent findingsCandidate gene meta-analyses indicate serotonin genes may be involved in the genetic etiology of AN. Three genome-wide association studies have been conducted and one genome-wide significant locus was identified. Cross-disorder analyses suggest shared genetic risk between AN and several psychiatric, educational, and medical phenotypes. Much has been learned about the genetic etiology of AN over the past 3 decades. However, to fully understand the genetic architecture, we must consider all aspects including common variation, cross-disorder analysis, rare variation, copy number variation, and gene-environment interplay. Findings have important implications for the development of treatment and prevention approaches and for how AN, and psychiatric and medical diseases in general, are conceptualized.
| S-EPMC6139670 | biostudies-literature
Project description:Alexithymia is of great interest as an outcome predictor of recovery from anorexia nervosa, since it may interfere with both treatment compliance and patients' ability to benefit from the adopted interventions. For this reason, in the last years new treatment approaches targeting emotion identification, expression, and regulation have been applied and tested. Using the PRISMA methodology, we performed a scoping review of the literature about treatment outcome in anorexia nervosa, in terms of changes in alexithymia as assessed by its most commonly used self-report measure, the Toronto Alexithymia Scale (TAS). The Medline and Scopus databases were searched, and articles were included if matching the following criteria: dealing with patients affected by anorexia nervosa, without limits of age; involving the application of any kind of targeted therapy or treatment; assessing alexithymia and the effect of a treatment intervention on alexithymia, using the TAS. Ten studies were eventually included; overall, according to the selected studies, alexithymia levels often remain high even after specific treatment. Further research aimed at a deeper understanding of the actual impact of alexithymia on the outcome of anorexia, as well as exploring alternative treatment strategies for alexithymia in eating disorders (EDs), are warranted.
| S-EPMC7033613 | biostudies-literature