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Does the level of family dysfunction moderate the impact of genetic factors on the personality trait of neuroticism?

Published online by Cambridge University Press:  26 June 2003

K. S. KENDLER
Affiliation:
Department of Psychiatry and Department of Human Genetics, Medical College of Virginia/Virginia Commonwealth University and Virginia Institute for Psychiatric and Behavioral Genetics, Richmond, VA, USA
S. H. AGGEN
Affiliation:
Department of Psychiatry and Department of Human Genetics, Medical College of Virginia/Virginia Commonwealth University and Virginia Institute for Psychiatric and Behavioral Genetics, Richmond, VA, USA
K. C. JACOBSON
Affiliation:
Department of Psychiatry and Department of Human Genetics, Medical College of Virginia/Virginia Commonwealth University and Virginia Institute for Psychiatric and Behavioral Genetics, Richmond, VA, USA
M. C. NEALE
Affiliation:
Department of Psychiatry and Department of Human Genetics, Medical College of Virginia/Virginia Commonwealth University and Virginia Institute for Psychiatric and Behavioral Genetics, Richmond, VA, USA

Abstract

Background. While the family environment can directly influence later risk for psychopathology, dysfunction in the family of origin may also moderate the impact of genetic factors on liability for psychiatric disorders. Can a similar pattern be seen for the personality trait of Neuroticism (N) – which is a risk factor for many psychiatric conditions?

Method. Our sample of 957 complete female–female twin pairs from a population-based register had measures of self-reported N and multiple reporters (twin, co-twin, mother, father) for family dysfunction (FD). Statistical analysis was conducted by traditional regression analysis and a moderator structural equation twin model operationalized in the computer program Mx.

Results. Dividing the sample into quartiles based on increasing levels of FD, the mean of N increased substantially while correlations of N in monozygotic (MZ) and dizygotic (DZ) twins were relatively constant. Regression analyses did not suggest greater twin resemblance for N with increasing levels of FD. The best-fit structural equation model was the standard un-moderated model in which the proportion of variance in N due to genetic (39%) and unique environmental effects (61%) remained constant across values of FD.

Conclusions. Although a false-negative result due to limited power cannot be excluded, these analyses do not support the hypothesis that FD moderates the impact of genetic factors on levels of N.

Type
Research Article
Copyright
© 2003 Cambridge University Press

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