Contributions of the glucocorticoid receptor polymorphism (Bcl1) and childhood abuse to risk of bulimia nervosa

Steiger, Howard; Bruce, Kenneth R.; Gauvin, Lise; Groleau, Patricia; Joober, Ridha; Israël, Mimi; Richardson, Jodie; Kin, Francois Ng Yin

doi:10.1016/j.psychres.2010.10.021

Cited by 29 publications

(17 citation statements)

References 19 publications

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“…As such, these genetic predispositions may confer heightened emotional response to NVS stressors that exacerbate LOC-eating tendencies, but may not necessarily determine their initial onset. Adults with binge-eating, BN, or BED are more likely to carry low-function variants of glucocorticoid receptor (GR) polymorphisms (Cellini et al 2010, Steiger et al 2011, Steiger et al 2012). Thus, GR gene variants that promote inhibitory feedback insensitivity of the hypothalamic-pituitary-adrenal (HPA)-axis may predispose individuals to LOC-eating via secondary neurophysiological effects promoting non-homeostatic (e.g., eating due to negative states) feeding.…”

Section: Geneticsmentioning

confidence: 99%

“…Among carriers of the 5-HTTLPR s -allele, repeated childhood exposure to maltreatment escalates risk for greater binge-eating severity in adolescent girls (Akkermann et al 2012). Similarly, carriers of at least one C allele of the Bc l I GR polymorphism with exposure to child maltreatment are at greatest risk for BN (Steiger et al 2011). Consistent with a diathesis-stress model, acute threat exposure may promote the expression of latent genetic risk-factors for LOC-eating via expressed NVS dysfunction in serotonergic and glucorticoid signaling (Trace et al 2013).…”

Section: Geneticsmentioning

confidence: 99%

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Behavioral and neurodevelopmental precursors to binge-type eating disorders: support for the role of negative valence systems

et al. 2015

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Background Pediatric loss-of-control eating is a robust behavioral precursor to binge-type eating disorders. Elucidating precursors to loss-of-control eating and binge-type eating disorders may refine developmental risk models of eating disorders and inform interventions. Method We review evidence within constructs of the Negative Valence Systems (NVS)-domain, as specified by the Research Domain Criteria framework. Based on published studies, we propose an integrated NVS model of binge-type eating disorder risk. Results Data implicate altered corticolimbic functioning, neuroendocrine dysregulation, and self-reported negative affect as possible risk-factors. However, neuroimaging and physiological data in children and adolescents are sparse, and most prospective studies are limited to self-report measures. Conclusions We discuss a broad NVS framework for conceptualizing early risk for binge-type eating disorders. Future neural and behavioral research on the developmental trajectory of loss-of-control and binge-type eating disorders is required.

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Section: Geneticsmentioning

confidence: 99%

Section: Geneticsmentioning

confidence: 99%

Behavioral and neurodevelopmental precursors to binge-type eating disorders: support for the role of negative valence systems

et al. 2015

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“…This study was concerned with the latter association. Based on findings indicating generally altered glucocorticoid functioning in BN, 8,9 and a role of a main GR gene polymorphism in bulimic and associated phenomenology, 6,7 we explored the possibility that women with BN, when compared to noneating-disordered (NED) women, might display propensities toward hypermethylation of the GR gene promoter. We also explored two alternative hypotheses: The first, based on evidence linking developmental stress to altered GR methylation in animals and humans, [15][16][17][18] was that GR gene methylation might be more characteristic of individuals with BN who reported exposure to childhood abuse than of people with BN alone; the second, based on studies associating suicidality 18 and BPD 20,21 with increased GR gene methylation, was that GR methylation might be more pronounced in individuals with BN who also displayed comorbid ''borderline'' or ''suicidal'' manifestations, than of people with BN alone.…”

Section: Epigenetic Processesmentioning

confidence: 99%

“…2,4 Forming a direct rationale for the current study, we have observed the combination of low-function variants of the glucocorticoid receptor (GR) polymorphism, Bcll, and exposure to childhood sexual or physical abuse to be significantly more common in women with BN than in women who eat normally and, furthermore, to predict more-pronounced affective symptoms in women with BN. 6,7 The GR plays a critical role in modulating individual stress reactiv-ity. Based on the preceding, we infer that traumatic stress may contribute particularly strongly to risk of BN (and related symptoms) in individuals who are genetically disposed towards lower GR modulation of stress responses.…”

Section: Introductionmentioning

confidence: 99%

Methylation of the glucocorticoid receptor gene promoter in bulimic women: Associations with borderline personality disorder, suicidality, and exposure to childhood abuse

Steiger

Labonté

Groleau

et al. 2013

Intl J Eating Disorders

Self Cite

113

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Objective: To compare levels of methylation of the glucocorticoid receptor (GR) gene (NR3C1) promoter between women with bulimia nervosa (BN) and women with no eating disorder (ED), and also to explore, in women with BN, the extent to which methylation of the GR gene promoter corresponds to childhood abuse, suicidality, or borderline personality disorder (BPD). Method:We measured methylation levels in selected NR3C1 promoter regions using DNA obtained from lymphocytes in 64 women with BN (32 selected as having a history of severe childhood abuse and 32 selected as having no such history) and 32 comparison women with no ED or history of childhood abuse.Results: Compared to noneating disordered women, women with BN and comorbid BPD (or BN with a history of suicidality) showed significantly more methylation of specific exon 1C sites. There was also a (nonsignificant) result indicative of greater methylation in some 1C sites among women with BN, when compared (as a group) to women with no ED. No parallel effects owing to childhood abuse were observed. Discussion: Our findings associate BN (when accompanied by BPD or suicidality) with hypermethylation of certain GR exon 1C promoter sites. We discuss theoretical and clinical implications of our findings. V V C 2013 by Wiley Periodicals, Inc.

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“…Specific genetic and/or epigenetic factors1213 and induced emotional dysregulation14 may directly promote the emergence of EDs. But the hypothesis of a nonspecific effect cannot be ruled out.…”

mentioning

confidence: 99%

Associations between adverse childhood experiences and clinical characteristics of eating disorders

Guillaume

Jaussent

Maı̈moun

et al. 2016

Sci Rep

102

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Patients with eating disorders (EDs) frequently report a history of childhood trauma (CT). We investigated whether certain subtypes of CT are associated with more severe features of EDs, independently of psychiatric comorbidity, and whether they act additively. One hundred and ninety-two patients with DSM-V-defined EDs were consecutively recruited. Five clinical characteristics were assessed: restraint, eating, shape and weight concerns on the EDE-Q, and daily functioning. CT was assessed by the childhood traumatism questionnaire. The clinical features were associated with at least one CT subtype (emotional, sexual or physical abuse, emotional neglect). Multivariate analyses adjusted for lifetime comorbid psychiatric disorders revealed that emotional abuse independently predicted higher eating, shape and weight concerns and lower daily functioning, whereas sexual and physical abuse independently predicted higher eating concern. A dose-effect relationship characterised the number of CT subtypes and the severity of the clinical features, suggesting a consistent and partly independent association between CT and more severe clinical and functional characteristics in EDs. Emotional abuse seems to have the most specific impact on ED symptoms. Last, not all CT subtypes have the same impact but they do act additively.

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Contributions of the glucocorticoid receptor polymorphism (Bcl1) and childhood abuse to risk of bulimia nervosa

Cited by 29 publications

References 19 publications

Behavioral and neurodevelopmental precursors to binge-type eating disorders: support for the role of negative valence systems

Behavioral and neurodevelopmental precursors to binge-type eating disorders: support for the role of negative valence systems

Methylation of the glucocorticoid receptor gene promoter in bulimic women: Associations with borderline personality disorder, suicidality, and exposure to childhood abuse

Associations between adverse childhood experiences and clinical characteristics of eating disorders

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