a1 Department of Psychiatry, University of California San Francisco, San Francisco, CA, USA
a2 Department of Clinical and Health Psychology, Utrecht University and Altrecht Academic Anxiety Disorders Center, Utrecht, the Netherlands
a3 Department of Biological Psychology, VU University, Amsterdam, Amsterdam, the Netherlands
Background Until recently, hoarding was considered an obsessive–compulsive symptom (OCS). However, current evidence suggests that these two phenotypes may be clinically, and perhaps etiologically, distinct. Both hoarding and OCS have a genetic etiology, but the degree of unique and shared genetic contributions to these phenotypes has not been well studied.
Method Prevalence rates were assessed for hoarding and OCS in a sample of adult twin pairs (n = 7906 twins) and their family members from the Netherlands Twin Register (total sample = 15 914). Using Mplus, genetic analyses using liability threshold models were conducted for both phenotypes, for their co-morbidity, and for specific hoarding symptoms (cluttering, discarding and acquiring).
Results Of the total sample, 6.7% met criteria for clinically significant hoarding; endorsement of all three hoarding symptoms was ≥79%. Men had slightly higher rates than women. Also, 5.7% met criteria for clinically significant OCS; rates were similar in males and females. Genetic factors accounted for 36% of the variance for hoarding and 40% of the variance for OCS. The genetic correlation between hoarding and OCS was 0.10. There was no evidence of sex-specific genetic contributions for hoarding or OCS. There was evidence for a genetic contribution to all hoarding symptom subtypes. Only cluttering showed evidence of a contribution from the shared environment.
Conclusions OCS and hoarding are common in this population-based sample, have prevalence rates similar to those previously reported, and show significant heritability. Genetic factors contributed to the co-morbidity of both traits, although the genetic correlation between them was low.
(Received August 15 2013)
(Revised January 17 2014)
(Accepted January 17 2014)
(Online publication February 20 2014)
c1 Address for correspondence: C. A. Mathews, M.D., Department of Psychiatry, University of California, San Francisco, 401 Parnassus Avenue, San Francisco, CA 94143-0984, USA. (Email: firstname.lastname@example.org)
† These authors contributed equally to this work.