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Abstract
Female sexual dysfunction (FSD) is multidimensional with a complex interplay of biopsychosocial factors modulating the clinical expression of sexual symptoms and associated distress. During the entire reproductive lifespan, intra- and interpersonal experiences shape human neuroendocrine and neurovascular sexual pathways. These are dependent on genetic and epigenetic mechanisms, including acquired medical conditions. Understanding the genetic basis of FSD can help to determine clinical phenotypes of women and therefore postulate the most effective intervention according to biological, psychological or environmental determinants. However, there is a paucity of studies demonstrating a genetic contribution to FSD and a diverse modulation of innate and acquired factors on discrete domains of sexual response and distress. This is evident from menarche to menopause. Pharmacogenomics is still in its infancy in the field of sexual medicine and most data regarding genetic polymorphisms of drug targets associated with susceptibility to sexual dysfunction have been obtained in males. Pharmacogenomics may be the future of medical practice in women with FSD and may guide an individualized approach by predicting both therapeutic effects at varying dosages of hormonal and non-hormonal agents, and disadvantageous side-effects and drug interactions.
Conflict of interest During the past 2 years, Dr Nappi had financial relationships (lecturer, member of advisory boards and/or consultant) with Bayer-Schering Pharma, Ely Lilly, HRA Pharma, Merck Sharpe & Dohme, Novo Nordisk, Pfizer Inc, TEVA/Theramex. Ms Domoney has been supported for lecturing and conference attendance by Astellas, Pfizer, Novo Nordisk and Bayer-Schering.
Source of funding Nil.