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Background: This study explored state-related tendencies in DNA methylation in people with anorexia nervosa. Methods: We measured genome-wide DNA methylation in 75 women with active anorexia nervosa (active), 31 women showing stable remission of anorexia nervosa (remitted) and 41 women with no eating disorder (NED). We also obtained postintervention methylation data from 52 of the women from the active group. Results: Comparisons between members of the active and NED groups showed 58 differentially methylated sites (Q < 0.01) that corresponded to genes relevant to metabolic and nutritional status (lipid and glucose metabolism), psychiatric status (serotonin receptor activity) and immune function. Methylation levels in members of the remitted group differed from those in the active group on 265 probes that also involved sites associated with genes for serotonin and insulin activity, glucose metabolism and immunity. Intriguingly, the direction of methylation effects in remitted participants tended to be opposite to those seen in active participants. The chronicity of Illness correlated (usually inversely, at Q < 0.01) with methylation levels at 64 sites that mapped onto genes regulating glutamate and serotonin activity, insulin function and epigenetic age. In contrast, body mass index increases coincided (at Q < 0.05) with generally increased methylation-level changes at 73 probes associated with lipid and glucose metabolism, immune and inflammatory processes, and olfaction. Limitations: Sample sizes were modest for this type of inquiry, and findings may have been subject to uncontrolled effects of medication and substance use. Conclusion: Findings point to the possibility of reversible epigenetic alterations in anorexia nervosa, and suggest that an adequate pathophysiological model would likely need to include psychiatric, metabolic and immune components. [ABSTRACT FROM AUTHOR]

Epigenetic mechanisms are believed to link environmental exposures to alterations in gene expression, and in so doing, to provide a physical substrate for the activation of hereditary potentials by life experiences. In keeping with this idea, accumulating data suggest that epigenetic processes are implicated in eating-disorder (ED) etiology. This paper reviews literature on putative links between epigenetic factors and EDs, and examines ways in which epigenetic programming of gene expression could account for gene-environment interactions acting in the EDs. The paper also presents evidence suggesting that epigenetic processes link malnutrition and life stresses (gestational, perinatal, childhood, and adult) to risk of ED development. Drawing from empirical evidence and clinical experience, we propose that an epigenetically informed understanding of ED etiology can benefit patients, caregivers, and clinicians alike, in the sense that the perspective can reduce judgmental or blameful attitudes on the part of clinicians and caregivers, and increase self-acceptance and optimism about recovery on the part of those affected. [ABSTRACT FROM AUTHOR]

Background: Adolescence and young adulthood is a high-risk period for the development of eating disorders. In recent years, there has been an increase in use of technology-based interventions (TBIs) for the treatment of eating disorders. The objective of this study was to determine the types of technology used for eating disorder treatment in youth and their effectiveness. Methods: A scoping review was conducted according to PRISMA-ScR guidelines. Four databases were searched. Eligible articles included: (1) a TBI (2) participants with a mean age between 10- and 25-years and meeting DSM-IV or DSM-5 criteria for any eating disorder and (3) qualitative or quantitative designs. Quantitative and qualitative studies were assessed for quality. Results: The search identified 1621 articles. After screening of titles and abstracts, 130 articles were read in full and assessed for eligibility by two raters. Forty-nine (29 quantitative and 20 qualitative, observational, or mixed methods studies) met inclusion criteria. Quality ratings indicated that 78% of quantitative studies had a low risk of bias and 22% had a moderate risk. Technologies reviewed in our study included videoconference therapy, mobile applications, and online self-help. We considered interventions used both within sessions with clinicians as well as those used in between sessions by patients alone. Fifteen of 18 (83%) quantitative studies found that TBIs reduce eating disorder symptomatology, with nine of those reporting medium-to-large effect sizes. Qualitative data was of high quality and suggested that virtual interventions are acceptable in this population. Conclusions: Although identified studies are of high quality, they are limited in number. More research is needed, particularly regarding videoconferencing and mobile applications. Nonetheless, TBIs show promise for the treatment of eating disorders in youth. Trial registration: Not applicable. Plain English summary: The use of virtual care to treat adolescents and young adults with eating disorders has increased in recent years. To better understand what types of technologies are being used in virtual care and these technologies' effectiveness, we systematically reviewed research studies that discussed the use of any technology to treat youth (which was defined as young people aged 25 years or under) with an eating disorder. We found 49 relevant studies. They revealed that videoconference therapy, mobile applications, and online self-help are most frequently used for virtual treatment. Of the 18 studies evaluating the effectiveness of these technologies, 15 found virtual care to be effective for reducing eating disorder symptoms. Studies describing patient experiences with these technologies, of which there were nine, suggested that patients overall were satisfied with receiving virtual care. Although these results are promising, research on virtual treatment is still lacking, especially on videoconferencing therapy and mobile applications. [ABSTRACT FROM AUTHOR]