The genetic and environmental etiology of the five-factor model of personality as measured by the revised NEO Personality Inventory (NEO-PI-R) was assessed using 123 pairs of identical twins and 127 pairs of fraternal twins. Broad genetic influence on the five dimensions of Neuroticism, Extraversion, Openness, Agreeableness, and Conscientiousness was estimated at 41%, 53%, 61%, 41%, and 44%, respectively. The facet scales also showed substantial heritability, although for several facets the genetic influence was largely nonadditive. The influence of the environment was consistent across all dimensions and facets. Shared environmental influences accounted for a negligible proportion of the variance in most scales, whereas nonshared environmental influences accounted for the majority of the environmental variance in all scales.

Genetic factors can influence the risk of exposure to some forms of trauma, perhaps through individual differences in personality that influence environmental choices. Consistent with symptoms in combat veterans, PTSD symptoms after noncombat trauma are also moderately heritable. Moreover, many of the same genes that influence exposure to assaultive trauma appear to influence susceptibility to PTSD symptoms in their wake.

The results support the following conclusions. First, the stable structure of traits across clinical and nonclinical samples is consistent with dimensional representations of personality disorders. Second, the higher-order traits of personality disorder strongly resemble dimensions of normal personality. This implies that a dimensional classification should be compatible with normative personality. Third, the residual heritability of the lower-order traits suggests that the personality phenotypes are based on a large number of specific genetic components.

The common variance among personality traits can be summarized in the factors of the five-factor model, which are known to be heritable. This study examined heritability of the residual specific variance in facet-level traits from the Revised NEO Personality Inventory. Analyses of raw and residual facet scales across Canadian (183 monozygotic [MZ] and 175 dizogotic [DZ] pairs) and German (435 MZ and 205 DZ pairs) twin samples showed genetic and environmental influences of the same type and magnitude across the 2 samples for most facets. Additive genetic effects accounted for 25% to 65% of the reliable specific variance. Results provide strong support for hierarchical models of personality that posit a large number of narrow traits in addition to a few broader trait factors or domains. Facet-level traits are not simply exemplars of the broad factors they define; they are discrete constructs with their own heritable and thus biological basis.

Schizophrenia is thought to be a multifactorial disease with complex mode of inheritance. Using a two-stage strategy for another complex disorder, a number of putative IDDM-susceptibility genes have recently been mapped. We now report the results of a two-stage genome-wide search for genes conferring susceptibility to schizophrenia. In stage I, model-free linkage analyses of large pedigrees from Iceland, a geographical isolate, revealed 26 loci suggestive of linkage. In stage II, ten of these were followed-up in a second international collaborative study comprising families from Austria, Canada, Germany, Italy, Scotland, Sweden, Taiwan and the United States. Potential linkage findings of stage I on chromosomes 6p, 9 and 20 were observed again in the second sample. Furthermore, in a third sample from China, fine mapping of the 6p region by association studies also showed evidence for linkage or linkage disequilibrium. Combining our results with other recent findings revealed significant evidence for linkage to an area distal of the HLA region on chromosome 6p. However, in a fourth sample from Europe, the 6p fine mapping finding observed in the Chinese sample could not be replicated. Finally, evidence suggestive of locus heterogeneity and oligogenic transmission in schizophrenia was obtained.