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Background: Eating Disorders are highly prevalent and widespread mental health problems, with marked risk of chronicity and refractoriness to treatment. Affected individuals are hesitant to change their behaviours and therefore struggle to maintain motivation for therapy. This review aims to produce the first high-quality meta-analysis of the literature on the impact of level of motivation for change on post-treatment outcomes in anorexia nervosa, bulimia nervosa, binge-eating disorder, and other specified feeding or eating disorder (OSFED). Methods: A systematic review will be conducted using Cochrane library, Embase, MEDLINE, and PsychINFO. Research registrars and bibliographies of included articles will be screened, and experts will be contacted. The search strategy consists of terms related to eating disorders, motivation, and outcome. Randomized controlled trials, clinical controlled trials, time series, and before-after studies will be included. Participants will be adolescents and adults who are diagnosed with anorexia nervosa, bulimia nervosa, binge-eating disorder or OSFED and who are entering psychotherapy treatment. The predictor studied is defined as motivation for change at the beginning of treatment. The primary outcome will be an overall change in eating-disorder symptomatology at the end of treatment and at less than, and over 6-month follow-up. Other outcomes of interest include change in restricting, binging, and compensatory behaviours, change in shape, weight and eating concerns, change in psychiatric comorbidities, weight restoration, and dropout rates. Articles will be selected, data will be extracted, and the risk of bias will be assessed by independent reviewers using forms pre-created on Eppi-Reviewer 4 software. Results will be combined using a random-effects model. Studies of all sizes and qualities will be included in the analyses. Heterogeneity will be examined by funnel plot, Cochran's Q, and I2 statistic. Sensitivity analyses will be performed to account for clinical and methodological differences across studies. Discussion: This systematic review will help determine the predictive value of motivation for change on treatment outcomes in eating disorders. [ABSTRACT FROM AUTHOR]

This review identified and synthesized published training programs on eating disorders (ED) (anorexia nervosa or bulimia nervosa) for professionals, natural supporters of people with ED, or the public. A scoping review using the Arksey and O'Malley (2005) framework was conducted. Four data bases were searched, for all years, and manual searches from three additional sources were also conducted. Experts on ED were consulted for validation of the identified studies. A narrative synthesis was performed. A total of 20 evaluation studies from five countries were identified, and reviewed in relation to 14 ED training programs. Characteristics of the training programs, and study characteristics, were highly diverse, as shown on Table 1 which compiles results from the charted data. Evaluations were equally divided between training for healthcare and education professionals (9), and training for families or other carers of people with ED (10). One study evaluated ED training for the general public. We found that training orientation varies with the interests and needs of different trainee groups. While most studies assessed trainee outcomes, future research needs to give greater consideration to patient perspectives, and to the relationship between training and evaluation approaches, improved knowledge, and better care. [ABSTRACT FROM AUTHOR]

Background: Low-function alleles of the serotonin transporter promoter polymorphism (5HTTLPR) have been linked to various psychopathological entities, especially in individuals exposed to prior stressors. In women with bulimic syndromes, we explored associations with personality pathology of 5HTTLPR and prior sexual or physical maltreatment. Methods: Ninety-two women with bulimic syndromes were genotyped for 5HTTLPR short (S) and long (LG and LA) alleles and were then assessed for eating symptoms, dimensional personality disturbances, history of sexual or physical abuse and borderline personality disorder (BPD). Results: With a classification based on a biallelic model of 5HTTLPR (i.e., presence or absence of at least 1 S-allele copy), multiple regression analyses indicated significant proportions of variance in stimulus seeking and insecure attachment to be explained by abuse × genotype interaction effects, with greater psychopathology always occurring in S-allele carriers who had been abused. Likewise, a logistic regression analysis linked BPD to significant main effects of genotype and abuse. Analyses that aggregated carriers according to a triallelic model of 5HTTLPR (i.e., presence or absence of at least 1 copy of a presumably low-function S or LG allele) produced similar patterns but no statistically significant effects. Conclusions: Traits such as sensation seeking and insecure attachment are, on average, elevated in 5HTTLPR S-allele carriers with bulimic syndromes who report prior physical or sexual maltreatment. These results add to the literature associating pronounced psyohopathological manifestations, with conjoint effects of stress and the 5HTTLPR polymorphism. [ABSTRACT FROM AUTHOR]

Reduced brain serotonin (5-hydroxytryptamine: 5-HT) transporter activity has been associated with susceptibility to various forms of psychopathology, including bulimia nervosa (BN) and related syndromes characterized by appetitive or behavioural dysregulation. We applied density (Bmax) of platelet [3H-]paroxetine binding as a proxy for central 5-HT reuptake activity in two groups of women (33 with BN-spectrum disorders and 19 with no apparent eating or psychiatric disorders), most of these individuals' mothers (31 and 18, respectively), and a small sampling of their sisters (seven and eight, respectively). Hierarchical linear modeling techniques were used to account for nesting of individuals within families and diagnostic groupings. Bulimic probands, their mothers, and their sisters all displayed significantly lower density (Bmax) of platelet-paroxetine binding than did ‘control’ probands, mothers, or sisters—even when relatives showing apparent eating or psychiatric disturbances were excluded. In addition, in bulimic probands and mothers, significant within-family correlations were obtained on Bmax. These findings imply a heritable trait (or endophenotype), linked to 5-HT activity, and carried by BN sufferers and their first-degree relatives (even when asymptomatic). We propose that, under conducive circumstances, such a trait may increase risk of binge-eating behavior, or associated symptoms of affective or behavioral dysregulation.Neuropsychopharmacology (2006) 31, 1785–1792. doi:10.1038/sj.npp.1301011; published online 11 January 2006 [ABSTRACT FROM AUTHOR]

Findings show brain serotonin (5-hydroxytryptamine (5-HT)) activity to be altered in individuals who have had bulimia nervosa (BN), even after substantial remission of symptoms. Such findings could reflect persistent sequelae due to BN, or a vulnerability 'trait' that exists independently of active eating-disorder manifestations. We compared women with full-blown BN (BN; n = 22), BN in remission (BN-R; n = 11), and no eating or psychiatric disturbances (n = 22) on measures of platelet [³H]paroxetine binding, eating symptoms and psychopathology. The BN-R group showed normal-range scores on eating and psychopathological symptoms, but reductions in density (Bmax) of binding sites for paroxetine similar to those obtained in the actively ill women. Both BN groups had substantially lower Bmax than did healthy controls. Our results corroborate other findings indicating recovered BN patients to have anomalous 5-HT functioning. While such effects could represent a lasting 'injury' to the system, reported covariations between personality traits and 5-HT indices in BN encourage us to favor the argument that some alterations of 5-HT activity (in this case, consistent with reduced transporter activity) represent a 'trait' associated with the risk of developing BN and/or associated psychopathology. [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]