BACKGROUND: Individual differences in fear and fearlessness have been investigated at their extremes in relation to markedly different forms of psychopathology--anxiety disorders and psychopathy, respectively. A documented neural substrate of fear-related traits and disorders is defensive reactivity as reflected in aversive startle potentiation (ASP). METHOD: The current study extended prior work by characterizing, in a sample of adult twins from the community (n = 2511), the phenotypic and etiologic structure of self-report measures of fear and fearlessness known to be associated with ASP. RESULTS: Analyses revealed a hierarchical structure to the trait fear domain, with an overarching, bipolar fear/fearlessness dimension saturating each measure in this domain, and subfactors labeled 'distress,' 'stimulation seeking' and 'sociability' accounting for additional variance in particular measures. The structure of genetic and non-shared environmental associations among the measures closely mirrored the phenotypic structure of the domain. CONCLUSIONS: The findings have implications for proposals to reconceptualize psychopathology in neurobiological terms.
BACKGROUND: Individual differences in fear and fearlessness have been investigated at their extremes in relation to markedly different forms of psychopathology--anxiety disorders and psychopathy, respectively. A documented neural substrate of fear-related traits and disorders is defensive reactivity as reflected in aversive startle potentiation (ASP). METHOD: The current study extended prior work by characterizing, in a sample of adult twins from the community (n = 2511), the phenotypic and etiologic structure of self-report measures of fear and fearlessness known to be associated with ASP. RESULTS: Analyses revealed a hierarchical structure to the trait fear domain, with an overarching, bipolar fear/fearlessness dimension saturating each measure in this domain, and subfactors labeled 'distress,' 'stimulation seeking' and 'sociability' accounting for additional variance in particular measures. The structure of genetic and non-shared environmental associations among the measures closely mirrored the phenotypic structure of the domain. CONCLUSIONS: The findings have implications for proposals to reconceptualize psychopathology in neurobiological terms.
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