Overlap and specificity of genetic and environmental influences on excessive acquisition and difficulties discarding possessions: Implications for hoarding disorder

Ashley E. Nordsletten, Benedetta Monzani, Lorena Fernández de la Cruz, Alessandra C. Iervolino, Miquel A. Fullana, Juliette Harris, Fruhling Rijsdijk, David Mataix-Cols

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Resum

A reluctance to discard items, leading to severely cluttered living spaces, is the landmark feature of hoarding disorder (HD). Many, but not all, individuals with HD also excessively acquire, buy or even steal items that they do not need and for which no space is available. In DSM-5, "excessive acquisition" can be coded as a specifier of HD. Despite their consistent co-occurrence, the question of whether excessive acquisition and difficulties discarding possessions share a common etiology remains unanswered. The current study sought to flesh out this relationship by examining the extent of shared genetic and environmental influences on the association between excessive acquisition and difficulties discarding in a community sample of adult, female twins. A total of 5,022 female twins (2,529 pairs; mean age=55.5 years) completed a self-report measure of hoarding symptoms, including items assessing excessive acquisition and difficulties discarding. The data were analyzed using bivariate twin modeling methods in the statistical program Mx. As expected, we found a strong phenotypic correlation (0.63) between excessive acquisition and difficulty discarding items. Both traits were moderately heritable. The genetic correlation between the traits was estimated to be 0.77 (95% CI: 0.69-0.85), indicating a substantial but imperfect genetic overlap. The non-shared environmental correlation (0.50 [95% CI: 0.42-0.57]), though lower, was also significant. The findings demonstrate a substantial genetic, and more modest environmental, etiological overlap between the excessive acquisition of possessions and difficulties discarding them, providing a possible explanation for their frequent co-occurrence in HD. However, given that the etiological overlap is not perfect, unique etiological influences, particularly environmental, on each phenotype seem plausible. © 2013 Wiley Periodicals, Inc.
Idioma originalAnglès
Pàgines (de-a)380-387
RevistaAmerican Journal of Medical Genetics, Part B: Neuropsychiatric Genetics
Volum162
Número4
DOIs
Estat de la publicacióPublicada - 1 de juny 2013

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