The DSM-V Working Group is currently re-evaluating distress as a primary diagnostic criterion for female sexual dysfunction (FSD). Here, for the first time, we explored the epidemiology of sexual distress and its putative aetiological relationship to FSD by estimating the influence of genetic and environmental risk factors.

Questionnaire data on a representative sample of 930 British female twins using validated scales of FSD and sexual distress were subject to variance components analyses to quantify latent genetic and environmental factors influencing phenotypic variation and covariation. Multiple regression analyses were used to identify other potential risk factors of sexual distress.

Of 319 women with any sexual problems, only 36.5% reported distress. Of women classified as functional, 16.5% felt sexual distress. Sexual distress had a heritability of 44% [95% confidence interval (CI) 0.33–0.54]. Bivariate analysis suggested that the majority (91% CI 86–99%) of the covariance between sexual distress and FSD was due to unique environmental effects common to both traits. Associations were found between sexual distress and other risk variables, including relationship dissatisfaction [odds ratio (OR) 1.6, p<0.001], anxiety sensitivity and obsessive–compulsive symptomatology (OR 1.2, p<0.01, for both).

There seems to be a weak phenotypic and genetic basis for including sexual distress as a diagnostic indicator of FSD. Instead, the data indicate that unrelated psychological factors play an important role in sexual distress and tentatively suggest that sexual distress is less a consequence of FSD and more related to general anxiety among women.

Previous studies have shown moderate heritability for female orgasm. So far, however, no study has addressed the pattern of genetic and environmental influences on diverse sexual dysfunctions in women, nor how genetic and environmental factors contribute to the associations between them.

The sample was drawn from the Genetics of Sex and Aggression (GSA) sample and consisted of 6446 female twins (aged 18–43 years) and 1994 female siblings (aged 18–49 years). The participants responded to the Female Sexual Function Index (FSFI), either by post or online.

Model fitting analyses indicated that individual differences on all six subdomains of the FSFI (desire, arousal, lubrication, orgasm, satisfaction, and pain) were primarily due to non-shared (individual-specific) environmental influences. Genetic influences were modest but significant, whereas shared environmental influences were not significant. A correlated factors model including additive and non-additive genetic and non-shared environmental effects proved to have the best fit and suggested that both correlated additive and non-additive genetic factors and unique environmental factors underlie the co-occurrence of the sexual function problems.

The findings suggest that female sexual dysfunctions are separate entities with some shared aetiology. They also indicate that there is a genetic susceptibility for sexual dysfunctions. The unique experiences of each individual are, however, the main factors determining if, and which, dysfunction develops.