Postulating that the predisposition to illness in Claridge's disease model of schizophrenia can be equated with the personality dimensions S or Insensitivity, (low) E or Extraversion, and N or Neuroticism, as measured by Van Kampen's 3DPT, and assuming that the mode of transmission of schizophrenia is basically polygenic, the genetic and environmental etiology of S, E, and N was assessed in a sample of 52 MZ and 76 DZ twin pairs and their parents by means of LISREL. Besides, in a sample of 2118 subjects MAXCOV–HITMAX analyses were conducted for these factors as well as for the personality dimension G or Orderliness, but now assessed by the 4DPT, in order to find out whether a discrete or quasi-discrete variable might also underlie these dimensions, giving support to the possibility of dominance or epistasis. The results obtained in these investigations favoured a model for all three dimensions, allowing for both additive and non-additive genetic effects in combination with non-shared environmental influences. It was not possible to choose between a model involving dominance and a model involving epistatic genetic effects. With the use of scores corrected for sex and age, which were converted to normal scores, the proportion of variance explained by additive genetic factors was 20% for S, 40–41% for E, and 26–29% for N. Dominance or multiple-gene epistasis accounted for 37–38% (S), 19–20% (E), and 30–31% (N), and unshared environmental influences for 42–43% (S), 41% (E), and 42–43% (N) respectively.
|Number of pages||8|
|Journal||European Journal of Personality|
|Publication status||Published - 1999|