Psychological Medicine



Original Article

A dopamine transporter polymorphism is a risk factor for borderline personality disorder in depressed patients


PETER R. JOYCE a1c1, PATRICK C. McHUGH a2, JANICE M. McKENZIE a1, PATRICK F. SULLIVAN a3, ROGER T. MULDER a1, SUZANNE E. LUTY a1, JANET D. CARTER a1, CHRISTOPHER M. A. FRAMPTON a1, C. ROBERT CLONINGER a4, ALLISON M. MILLER a2 and MARTIN A. KENNEDY a2
a1 Department of Psychological Medicine, Christchurch School of Medicine & Health Sciences, Christchurch, New Zealand
a2 Department of Pathology, Christchurch School of Medicine & Health Sciences, Christchurch, New Zealand
a3 Departments of Genetics, Psychiatry and Epidemiology, University of North Carolina, Chapel Hill, NC, USA
a4 Department of Psychiatry, Washington University Medical School, St. Louis, MO, USA

Article author query
joyce pr   [PubMed][Google Scholar] 
mchugh pc   [PubMed][Google Scholar] 
mckenzie jm   [PubMed][Google Scholar] 
sullivan pf   [PubMed][Google Scholar] 
mulder rt   [PubMed][Google Scholar] 
luty se   [PubMed][Google Scholar] 
carter jd   [PubMed][Google Scholar] 
frampton cm   [PubMed][Google Scholar] 
robert cloninger c   [PubMed][Google Scholar] 
miller am   [PubMed][Google Scholar] 
kennedy ma   [PubMed][Google Scholar] 

Abstract

Background. Borderline personality disorder (BPD) is often co-morbid with major depression and may complicate its treatment. We were interested in differences in genetic and developmental risk factors between depressed patients with or without a co-morbid BPD.

Method. Out-patients with major depressive disorder were recruited for two treatment trials. Assessment of depressed patients included the assessment of personality disorders, developmental risk factors and DNA samples for genetic analyses.

Results. In each study there was a significant association between the 9-repeat allele of the dopamine transporter (DAT1) and BPD, with odds ratios (OR) >3 and p[less-than-or-eq, slant]0·02. This association remained significant when developmental risk factors for BPD (childhood abuse and neglect and borderline temperament) were also included in the analyses. The OR was even larger in the depressed patients aged [gt-or-equal, slanted]35 years (OR 9·31, p=0·005).

Conclusion. This replicated association in depressed patients between the 9-repeat allele of DAT1 and BPD may provide clues to understanding the neurobiology of BPD. The finding that the association is larger in the older depressed patients, suggests that the 9-repeat allele may be associated with a poorer prognosis BPD, rather than a young adult limited variant of BPD.


Correspondence:
c1 Department of Psychological Medicine, Christchurch School of Medicine & Health Sciences, PO Box 4345, Christchurch, New Zealand. (Email: peter.joyce@chmeds.ac.nz)


Metrics