Jim Stevenson¹

It has been suggested that there is a genetic mechanism whereby males may be disadvantaged in social cognition (D.H.Skuse et al.,1997, Nature, 387, 705-708). That study found that girls with Turner's syndrome receiving their single X-chromosome from their fathers had higher scores on a measure of social cognition than those having a maternal X-chromosome. It was suggested that there is an imprinted gene on the X chromosome influencing this ability which is not expressed if transmitted on the maternal X chromosome. If this is correct, it would be expected that the MZ correlation for females on this social cognition measure would be lower than that for MZ males pairs. Using a sample of 147 MZ, 133 DZ same sex and 102 opposite sex twin pairs this proposed X-linked genetic mechanism was examined. Although replicating the male deficit in this aspect of social cognition, there was no difference in the similarities within MZ male (r = 0.823) and female (r = 0.833) pairs. Sex-limitation models were fitted to these data to test whether the genetic correlation between males and females had been lowered by this imprinted X-linked locus. The best model was the common effects sex limitation model (² = 31.73, df = 11, p< .001). This model had common additive genetic and nonshared environmental influences with h² = 0.78 and e² = .22 for both males and females. The significant improvement over an AE model that constrained all terms to be equal for males and females (² = 40.66, df = 13, p< .001) was a consequence of accounting for variance differences between the sexes. There is no evidence from this twin study to support different genetic contributions to social cognition in normal males and females.

Address:   Dept. of Psychology, University of Southampton, Highfield, Southampton SO17 1BJ., Tel: +44 1703 592583 Fax: +44 1703 594719 email : jsteven@psy.soton.ac.uk.

¹Department of Psychology, University of Southampton, Southampton, UK.

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