Genetic and Environmental Contributions to the Co-Occurrence of Depressive Personality Disorder and DSM-IV Personality Disorders

Abstract

One of the main controversies with regard to depressive personality disorder (DPD) concerns the co-occurrence with the established DSM-IV personality disorders (PDs). The main aim of this study was to examine to what extent DPD and the DSM-IV PDs share genetic and environmental risk factors, using multivariate twin modeling. The DSM-IV Structured Interview for Personality was applied to 2,794 young adult twins. Paranoid PD from Cluster A, borderline PD from Cluster B, and all three PDs from Cluster C were independently and significantly associated with DPD in multiple regression analysis. The genetic correlations between DPD and the other PDs were strong (.53-.83), while the environmental correlations were moderate (.36-.40). Close to 50% of the total variance in DPD was disorder specific. However, only 5% was due to disorder-specific genetic factors, indicating that a substantial part of the genetic vulnerability to DPD also increases the vulnerability to other PDs.Depressive personality disorder (DPD) was first formally introduced in the fourth version of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV; American Psychiatric Association, 1994), where it was placed in Appendix B among other diagnostic categories in need of further studies. In the ongoing work on DSM-5, the Personality and Personality Disorders Work Group suggests that DPD is not included as a specific type, but is represented by a combination of core impairment in personality functioning and a set of prominent personality traits (www.dsm5.org).One of the key questions originally posed by the DSM-IV personality disorder (PD) work group was to what extent DPD can be distinguished from Axis I mood disorders and from the 10 established DSM-IV PDs (Phillips, Hirschfeld, Shea, & Gunderson, 1995). Several studies addressing diagnostic overlap have been published, both with regard to mood disorders (Klein & Miller, 1993;Klein & Shih, 1998;McDermut, Zimmerman, & Chelminski, 2003;Ryder, Bagby, & Dion, 2001;Ryder, Bagby, & Schuller, 2002) and PDs (Huprich, 2004;Huprich, Zimmerman, & Chelminski, 2006;Klein & Shih, 1998; © 2012 The Guilford Press Address correspondence to Dr. Ragnhild E. Ørstavik, Norwegian Institute of Public Health, Box 4404, Nydalen N-0403, Oslo, Norway; ragnhild.orstavik@fhi.no. This article was accepted under the editorship of Paul S. Links. Markowitz et al., 2005;McDermut et al., 2003), where there is evidence for substantial cooccurrence between DPD and borderline PD in Cluster B and the three Cluster C PDs (for review, see Huprich, 2009). NIH Public AccessAn important criterion for diagnostic validity is familial aggregation (Robins & Guze, 1970). Familial aggregation can be the result of both common genetic or environmental factors, and twin studies can be used to distinguish these causes (Plomin, DeFries, McClearn, & McGuffin, 2001). If twin studies are extended to include multiple disorders, it is possible to examine the causes of familial co-aggregation of several disorders, that is, whether their c...

The beauty, logic and limitations of twin studies

“…Norwegian studies have examined genetic and environmental influences on anxiety and depression (Ask et al, 2016;Czajkowski et al, 2011;Nes et al, 2007;Reichborn-Kjennerud et al, 2002;, personality disorders (Gjerde et al, 2011;Ørstavik et al, 2012;Torgersen et al, 2008), wellbeing and happiness (Nes & Røysamb, 2015;Nes et al, 2006;Røysamb et al, 2002Røysamb et al, , 2003Røysamb et al, , 2014, educational attainment Ørstavik et al, 2014;Tambs et al, 2012), intelligence (Sundet et al, 1994(Sundet et al, , 2005, pain (Nielsen et al, 2008;Reichborn-Kjennerud et al, 2002;Vassend et al, 2011), personality traits (Vassend et al, 2013), sleep problems (Nes et al, 2005) body mass index , smoking, alcohol and drug use (Seglem et al, 2015;Ystrom et al, 2014aYstrom et al, , 2014b, sick leave and disability pension Torvik et al, 2013), resilience and self-efficacy (Waaktaar & Torgersen, 2012, 2013 and asthma and allergies (Harris et al, 1997;Nystad et al, 2005).…”

New directions for an old construct: Depressive personality research in the DSM‐5 era

“…He noted that centuries of observation in clinical and nonclinical literature suggests that a group of individuals exist who are chronically melancholic and pessimistic. And in more modern times, genetic and family history data now exist that support an underlying biological predisposition to DP (Klein, 1990(Klein, , 1999Klein & Miller, 1993;rstavik, Kendler, Czajkowski, Tambs, & Reichborn-Kjennerud, 2007;rstavik et al, 2012). Even the DSM-5 chairs have proposed that neural circuitry become a line of investigation by which psychiatric disorders are classified (Regier et al, 2009).…”