a1 Department of Psychiatry, University of Chicago, Chicago, Illinois, United States of America. email@example.com
a2 Genetic Epidemiology Laboratory, Queensland Institute of Medical Research, Brisbane, Australia.
a3 Department of Psychology, Northwestern University, Evanston, Illinois, United States of America.
a4 Virginia Institute of Psychiatric and Behavioral Genetics, Richmond, Virginia, United States of America.
a5 Genetic Epidemiology Laboratory, Queensland Institute of Medical Research, Brisbane, Australia.
This study reports on genetic and environmental influences on the frequency of orgasm in women during sexual intercourse, during other sexual contact with a partner, and during masturbation. Participants were drawn from the Australian Twin Registry, and recruited from a large, partly longitudinal twin-family study. Three thousand and eighty women responded to the anonymous self-report questionnaire, including 667 complete monozygotic (MZ) pairs and 377 complete dizygotic (DZ) same-sex pairs, 366 women from complete DZ opposite-sex pairs, and 626 women whose co-twins did not participate. Significant twin correlations were found for both MZ and DZ twin pairs for all three items of interest. Age effects were statistically significant for some items. Models incorporating additive genetic, shared and nonshared environmental influences provided the best fit for Items 1 and 3, while a model with additive and nonadditive genetic influences along with nonshared envir-onment fitted the data from Item 2. While an independent pathway model fits the data most par-simoniously, a common pathway model incorporating additive genetic (A), shared environment (C), and unique environment (E) effects cannot be ruled out. Overall, genetic influences account for approximately 31% of the variance of frequency of orgasm during sexual intercourse, 37% of the variance of frequency of orgasm during sexual contact other than during intercourse, and 51% of the variance of frequency of orgasm during masturbation. Following Baker (1996), we speculate that this additive genetic variance might arise from frequency-dependent selection for a variety of female sexual strategies.
(Received November 03 2004)
(Accepted December 01 2004)
c1 Address for correspondence: Khytam Dawood, PhD, Department of Psychiatry, University of Chicago, 5841 S. Maryland Ave, MC 3077, Chicago, IL 60637, USA.