A Multivariate Twin Study of Female Sexual Dysfunction

Authors

  • Andrea Burri PhD,

    Corresponding author
    1. Department of Twin Research and Genetic Epidemiology, King's College London, London, UK
    2. Department of Psychology, University of Zürich, Zürich, Switzerland
      Andrea Burri, PhD, Department of Twin Research and Genetic Epidemiology, King's College London, St. Thomas' Hospital, Westminster Bridge Road, London SE1 EH7, UK. Tel: 00447943802987; Fax: 00442071886718; E-mail: andrea.burri@kcl.ac.uk
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  • Corina Greven PhD,

    1. Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Centre Nijmegen, Nijmegen, the Netherlands
    2. MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, King's College London, London, UK
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  • Myriam Leupin MSc,

    1. Department of Psychology, University of Zürich, Zürich, Switzerland
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  • Timothy Spector Prof,

    1. Department of Twin Research and Genetic Epidemiology, King's College London, London, UK
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  • Qazi Rahman PhD

    1. Biological and Experimental Psychology Group, School of Biological and Chemical Sciences, Queen Mary University of London, London, UK
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Andrea Burri, PhD, Department of Twin Research and Genetic Epidemiology, King's College London, St. Thomas' Hospital, Westminster Bridge Road, London SE1 EH7, UK. Tel: 00447943802987; Fax: 00442071886718; E-mail: andrea.burri@kcl.ac.uk

ABSTRACT

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 **;**:**–**.

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