Early life stressors and genetic influences on the development of bipolar disorder: The roles of childhood abuse and brain-derived neurotrophic factor

  • Liu R
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Objectives: Although there is increasing research exploring the psychosocial influences and biological underpinnings of bipolar disorder, relatively few studies have specifically examined the interplay between these factors in the development of this illness. Social-biological models within a developmental psychopathology perspective are necessary to advance our understanding of the processes involved in the onset and course of bipolar disorder. This article presents a review of the empirical literature linking childhood abuse to bipolar disorder, the research to date on the possible role of brain-derived neurotrophic factor (BDNF) in the development of this disorder, followed by a discussion of how childhood abuse may interact with BDNF. Methods: A literature search was conducted using Psycinfo to identify relevant articles on childhood abuse, BDNF, and bipolar disorder. Results: The extant research implicates both childhood abuse and BDNF in the etiology of bipolar disorder. Specifically, there is growing evidence associating early abuse to the development of bipolar disorder. Similarly, the BDNF Val66 allele has been linked with increased susceptibility to bipolar disorder. Based on existing research, a genetic diathesis-transactional stress model is proposed incorporating childhood abuse and the BDNF gene in the pathogenesis of bipolar disorder. Conclusions: Although there is some support for this model, the relatively modest amount of relevant literature highlights the need for further research. An integrative theoretical framework including both social and biological processes in bipolar disorder is important for the development of effective prevention and treatment strategies for this disorder. © 2010 Elsevier Ltd.

Author-supplied keywords

  • Bipolar disorder
  • Brain-derived neurotrophic factor
  • Child abuse
  • Gene-environment interaction
  • Polymorphism

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