Publication: BPD's Interpersonal Hypersensitivity Phenotype: A Gene-Environment-Developmental Model
Open/View Files
Date
2008
Published Version
Journal Title
Journal ISSN
Volume Title
Publisher
Guilford Publications
The Harvard community has made this article openly available. Please share how this access benefits you.
Citation
Gunderson, John G., and Karlen Lyons-Ruth. 2008. “BPD’s Interpersonal Hypersensitivity Phenotype: A Gene-Environment-Developmental Model.” Journal of Personality Disorders 22 (1) (February): 22–41. doi:10.1521/pedi.2008.22.1.22.
Research Data
Abstract
This paper explores the development of BPD as it might emerge in the child's early interpersonal reactions and how such reactions might evolve into the interpersonal pattern that typifies BPD. It begins to bridge the relevant bodies of clinical literature on the borderline's prototypic interpersonal problems with the concurrently expanding relevant literature on early child development. We will start by considering how a psychobiological disposition to BPD is likely to include a constitutional diathesis for relational reactivity, that is, for hypersensitivity to interpersonal stressors. Data relevant to this disposition's manifestations in adult clinical samples and to its heritability and neurobiology will be reviewed. We then consider how such a psychobiological disposition for interpersonal reactivity might contribute to the development of a disorganized-ambivalent form of attachment, noting especially the likely contributions of both the predisposed child and of parents who are themselves predisposed to maladaptive responses, leading to an escalation of problematic transactions. Evidence concerning both the genetics and the developmental pathways associated with disorganized attachments will be considered. Emerging links between such developmental pathways and adult BPD will be described, in particular the potential appearance by early- to middle-childhood of controlling-caregiving or controlling-punitive interpersonal strategies. Some implications from this gene-environment interactional theory for a better developmental understanding of BPD's etiology are discussed.
Description
Other Available Sources
Keywords
Terms of Use
This article is made available under the terms and conditions applicable to Other Posted Material (LAA), as set forth at Terms of Service