A Multivariate Twin Study of Female Sexual Dysfunction
Version of Record online: 2 AUG 2012
© 2012 International Society for Sexual Medicine
The Journal of Sexual Medicine
Volume 9, Issue 10, pages 2671–2681, October 2012
How to Cite
Burri, A., Greven, C., Leupin, M., Spector, T. and Rahman, Q. (2012), A Multivariate Twin Study of Female Sexual Dysfunction. Journal of Sexual Medicine, 9: 2671–2681. doi: 10.1111/j.1743-6109.2012.02861.x
- Issue online: 9 OCT 2012
- Version of Record online: 2 AUG 2012
- Female Sexual Dysfunction;
Introduction. There is little work on the etiology of female sexual dysfunction (FSD), a highly contentious and heterogeneous disorder from classification and clinical perspectives. Clarifying causative mechanisms may enhance current psychiatric nosology.
Aim. To elucidate the structure of genetic and environmental risk factors underlying the major subtypes of FSD.
Methods. Self-report questionnaires and multivariate twin model fitting on a population-based adult twin register (TwinsUK, London) including 1,489 female twins aged 18 to 85, comprising 244 MZ pairs, 189 DZ pairs, and 623 women whose co-twins did not participate.
Main Outcome Measures. Scores on the Female Sexual Function Index–Lifelong and its six dimensions (desire, arousal, lubrication, orgasm, satisfaction, and pain) were subject to univariate and multivariate variance component analysis.
Results. The best-fitting multivariate model was an ACE Cholesky model, in which both additive genetic effects and non-shared environmental effects loaded on four FSD dimensions. There was significant genetic sharing between desire, arousal, lubrication and orgasm, but there was also significant genetic sharing between arousal, lubrication and orgasm independent of desire. These genetic loadings were small to modest effects (7% to 33%). Bivariate heritabilities suggested that a third of the covariance between these dimensions was genetic. Desire shared the least amount of genetic association with lubrication and orgasm. Non-shared environmental effects (which were stronger than genetic effects) were somewhat more dimension-specific.
Conclusions. FSD is not etiologically homogeneous. There are at least two genetic factors to FSD symptomatology, and a tendency for more dimension-specific non-shared environmental factors as a more important indicative of unique factors involved in specific types of sexual problems reported by women. These results emphasize genetic factors as possible organizing principles for an etiologically based classification approach of FSD. Burri A, Greven C, Leupin M, Spector T, and Rahman Q. A multivariate twin study of female sexual dysfunction. J Sex Med **;**:**–**.