Methylation of BDNF in women with bulimic eating syndromes: Associations with childhood abuse and borderline personality disorder

Thaler, Lea; Gauvin, Lise; Joober, Ridha; Groleau, Patricia; Guzman, Rosherrie de; Ambalavanan, Amirthagowri; Israël, Mimi; Wilson, Samantha; Steiger, Howard

doi:10.1016/j.pnpbp.2014.04.010

Cited by 96 publications

(94 citation statements)

References 36 publications

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“…Similarly, BDNF DNA methylation changes have been found in the peripheral blood of patients suffering from depression (13), bipolar disorder (12), schizophrenia (14), and eating disorders (51), and a change in BDNF DNA methylation status correlated with a positive response to psychotherapy in borderline personality disorder (52). In addition, within a psychiatric population, high BDNF DNA methylation was strongly associated with the history of child maltreatment (51,52). It seems likely that BDNF DNA methylation status may represent a more stable and reliable marker of psychiatric vulnerability compared with the levels of BDNF protein.…”

Section: Discussionmentioning

confidence: 94%

“…Recent studies suggested that concentrations of BDNF protein in the blood (serum or plasma) may represent peripheral manifestation of depression (48) and schizophrenia (49) and could be used as a biomarker for therapeutic efficacy (50). Similarly, BDNF DNA methylation changes have been found in the peripheral blood of patients suffering from depression (13), bipolar disorder (12), schizophrenia (14), and eating disorders (51), and a change in BDNF DNA methylation status correlated with a positive response to psychotherapy in borderline personality disorder (52). In addition, within a psychiatric population, high BDNF DNA methylation was strongly associated with the history of child maltreatment (51,52).…”

Section: Discussionmentioning

confidence: 99%

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DNA methylation of BDNF as a biomarker of early-life adversity

Kundaković

Gudsnuk

Herbstman

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

368

244

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Early-life adversity increases the risk for psychopathology in later life. The underlying mechanism(s) is unknown, but epigenetic variation represents a plausible candidate. Early-life exposures can disrupt epigenetic programming in the brain, with lasting consequences for gene expression and behavior. This evidence is primarily derived from animal studies, with limited study in humans due to inaccessibility of the target brain tissue. In humans, although there is evidence for DNA methylation changes in the peripheral blood of psychiatric patients, a fundamental question remains as to whether epigenetic markers in the blood can predict epigenetic changes occurring in the brain. We used in utero bisphenol A (BPA) exposure as a model environmental exposure shown to disrupt neurodevelopment and exert long-term effects on behavior in animals and humans. We show that prenatal BPA induces lasting DNA methylation changes in the transcriptionally relevant region of the Bdnf gene in the hippocampus and blood of BALB/c mice and that these changes are consistent with BDNF changes in the cord blood of humans exposed to high maternal BPA levels in utero. Our data suggest that BDNF DNA methylation in the blood may be used as a predictor of brain BDNF DNA methylation and gene expression as well as behavioral vulnerability induced by early-life environmental exposure. Because BDNF expression and DNA methylation are altered in several psychiatric disorders that are associated with early-life adversity, including depression, schizophrenia, bipolar disorder, and autism, BDNF DNA methylation in the blood may represent a novel biomarker for the early detection of psychopathology.epigenetics | biomarker | BDNF | bisphenol A | early life

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

DNA methylation of BDNF as a biomarker of early-life adversity

Kundaković

Gudsnuk

Herbstman

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

368

244

View full text Add to dashboard Cite

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“…In a comprehensive assessment of the GR-chaperone FKBP5, childhood maltreatment was associated with allele-specific demethylation in intron 7 of saliva-obtained FKBP5 in a cross-sectional study of 76 participants [50]. Finally, a study examining lymphocyte methylation patterns in women diagnosed with bulimia nervosa (n = 64) and controls (n = 32), examining the BDNF promoter region [51]. The study showed significant hypermethylation in bulimia related to childhood abuse in five (sexual abuse) or seven (physical abuse) out of 30 CpGs.…”

Section: Other Candidate Genesmentioning

confidence: 99%

Traumatic Stress and Human DNA Methylation: A Critical Review

et al. 2015

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Animal studies have identified persistent and functional effects of traumatic stress on the epigenome. This review discusses the clinical evidence for trauma-induced changes in DNA methylation across the life span in humans. Studies are reviewed based on reports of trauma exposure during the prenatal period (13 studies), early life (20 studies), and adulthood (ten studies). Even though it is apparent that traumatic stress influences the human epigenome, there are significant drawbacks in the existing human literature. These include a lack of longitudinal studies, methodological heterogeneity, selection of tissue type, and the influence of developmental stage and trauma type on methylation outcomes. These issues are discussed in order to present a way in which future studies can gain more insight into the functional relevance of trauma-related DNA methylation changes. Epigenetic studies investigating the detrimental effects of traumatic stress have great potential for an improved detection and treatment of trauma-related psychiatric disorders.

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“…Epigenetic responses to sustained childhood threats are likely mechanisms for the development of binge-type EDs. Indeed, preliminary data implicate altered DNA methylation in specific GR and BDNF promoter regions in BN (Steiger et al 2013, Thaler et al 2014), which may program early vulnerability to stressors that manifest as persistent anxiety, depression, and LOC-eating later in development.…”

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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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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Methylation of BDNF in women with bulimic eating syndromes: Associations with childhood abuse and borderline personality disorder

Cited by 96 publications

References 36 publications

DNA methylation of BDNF as a biomarker of early-life adversity

DNA methylation of BDNF as a biomarker of early-life adversity

Traumatic Stress and Human DNA Methylation: A Critical Review

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

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