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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., Introduction Anorexia nervosa can devastate medical, psychological and social adjustments, and despite treatment advances, only about half of people with the condition achieve full remission after 10 or more years. [...]

Background: Previous research has shown that many people experience a temporary worsening of mood following acute tryptophan depletion (ATD) and that concurrent use of serotonergic medications may influence such mood responses. We investigated mood and other consequences of ATD in women with bulimia nervosa who were or were not using concurrent serotonergic medications compared with women without bulimia. Methods: Women self-referred for treatment of bulimia who were either not currently using psychoactive medications (n= 26) or who were using serotonin reuptake inhibitor medications exclusively (n= 13), as well as medication-free normaleater control women (n= 25) completed interviews and questionnaires assessing eating and comorbid psychopathology and then participated in an ATD procedure involving balanced and tryptophan-depleted conditions. Results: In the tryptophan-depleted condition, the groups displayed similar and significant decrements in plasma tryptophan levels and mood. Women with bulimia who were using serotonin reuptake inhibitors, but not the other groups, also reported an increased urge to binge eat in the tryptophan-depleted condition. Limitations: Application of medication in participants with bulimia was not random. Conclusion: Acute reductions in serotonin availability produced similar mood-reducing effects in bulimic and nonbulimic women. To the extent that ATD affected subjective experiences pertinent to eating (i.e., urge to binge eat), such effects appeared to depend upon ATD-induced competition with the therapeutic effects of serotonergic medications., Introduction Bulimia nervosa has been associated with alterations in central serotonin (5-HT) function, (1) thought to implicate constitutional (e.g., hereditary) influences (2-5) and state-related (e.g., dietary) factors. (2,6) Whereas pertinent [...]

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 [...]

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]

Background: Thought-Shape Fusion (TSF) and Thought-Action Fusion (TAF) are cognitive distortions that are associated with eating and obsessional pathology respectively. Both involve the underlying belief that mere thoughts and mental images can lead to negative outcomes. TSF involves the belief that food-related thoughts lead to weight gain, body dissatisfaction, and perceptions of moral wrong-doing. TAF is more general, and involves the belief that merely thinking about a negative event (e.g., a loved one getting into a car accident) can make this event more likely to happen, and leads to perceptions of moral wrong-doing. However, the shared susceptibility across related cognitive distortions-TAF and TSF-has not yet been studied. Method: The effects of TSF and TAF inductions in women with an eating disorder (n = 21) and a group of healthy control women with no history of an eating disorder (n = 23) were measured. A repeated-measures design was employed, with all participants exposed to a TSF, TAF and neutral induction during three separate experimental sessions. Participants' cognitive and behavioral responses were assessed. Results: Individuals with eating disorders were more susceptible to TSF and TAF than were control participants, demonstrating more neutralization behavior after TSF and TAF inductions (i.e., actions to try to reduce the negative effects of the induction), and reporting higher levels of trait TAF and TSF than did controls. Conclusions: Individuals with eating disorders are particularly susceptible to both TAF and TSF. Clinical implications of these findings will be discussed. [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]

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]

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.