A Burri1, Q Rahman, T Spector. 1. Department of Twin Research and Genetic Epidemiology, King's College London, UK. a.burri@qmul.ac.uk
Abstract
BACKGROUND: 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. METHOD: 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. RESULTS: 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). CONCLUSIONS: 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.
BACKGROUND: 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. METHOD: 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. RESULTS: 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). CONCLUSIONS: 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.