ABSTRACT

Since the earliest descriptions of OCD, it has been observed that there appears to be a familial pattern to this disorder. However, finding a genetic “cause” for OCD remains elusive. In contrast to simple Mendelian disorders (e.g., Huntington’s disease, cystic fibrosis), in which a single genetic variant is necessary and sufficient to cause the disorder, neuropsychiatric disorders such as OCD are classified as “complex” genetic disorders or traits in which segregation at more than one genetic locus is likely involved (Elston, 2000). Such phenomena as pleiotropy (the same gene produces more than one possible phenotype), genetic heterogeneity (more than one gene may produce a given trait), epistasis (genes interact in a non-additive fashion to produce a trait), and gene-environment interaction may all be involved in causation of a complex trait. For such multifactorial conditions, genetic causes are best conceptualized as “probabilistic” (the cause increased the probability of a condition occurring) or “counterfactual” (the cause makes a difference in the outcome when it is present compared with when it is absent; Page, George, Go, Page, & Allison, 2003; Parascandola & Weed, 2001). This definition of causation provides a necessary antidote to claims of genetic determinism, in an era when a gene “for” a disorder is reported in the media on a regular basis.