INTRODUCTION
Female sexual dysfunction (FSD) is a considerably underestimated condition, affects 41% of sexually active women aged 45-64 in the dimensions of sexual desire, arousal, lubrication, orgasm, satisfaction, and pain.1 Prevalence for FSD is reported in up to 50% of women, at least in one dimension, regardless of age.2 Oksuz et al. stated that FSD prevalence was 48.3% in Turkish women, and smoking, older age, menopause and marital status were contributing risk factors.3
Distal vagina, urethra and clitoris create the clitoral complex. Clitoris receive (a) somatic fibres (a branch of the pudendal nerve) that supply the skin as the dorsal nerve of the clitoris, and (b) visceral fibres (cavernous nerves) that supply arteries to the erectile tissue. Vascular engorgement and clitoral tumescence are controlled by visceral nerves in the reflex arc and motor fibres that may be augmented or suppressed voluntarily. Sexual desire and arousal are thought to be under the control of parasympathetic and sympathetic arousal with the support of sex hormones and psychological factors. Cortex, limbic hippocampal structures, midbrain central gray, hypothalamic nuclei (the medial preoptic area, ventromedial nucleus, paraventricular nucleus, and anterior hypothalamic region) are the highest centers where the control of sexual arousal is regulated. Dopamine, norepinephrine, melanocortin, oxytocin, testosterone, estradiol and progesterone were central sexual stimulating mediators; serotonin, prolactin and opioids are sexually inhibiting neuromediators4 and serotonergic stimulation increases blood flow in the clitoris, bulbs, periurethral erotic tissue and vagina. Testosterone and estradiol also contribute to vasocongestion.5 Serotonin reduces genital sensation; sympathetic stimulation decreases genital blood flow. While vasoactive intestinal polypeptide (VIP) and NO are the primary neurotransmitters that provide tumescence by relaxing the clitoral smooth muscles during sexual stimulation; VIP, NO, calcitonin gene-related peptide (CGRP), neuropeptide-Y (NPY) and noradrenaline (NA) are peripheral neurotransmitters involved in vasomotion that provide vaginal transudation.6 As a consequence, engorgement of the clitoral complex with sexual stimulus, vulvar swelling occurs, and secretory response is initiated in the distal vagina and urethra. Depending on the increase in blood flow with sexual stimulation, a 2-3 fold increase in size occurs in the labia minora. The labial evertion caused by the increase in size makes vaginal introitus suitable for penile penetration. Non-erectile vascular tissues in the urethral orifice and vaginal wall are also sensitive to sexual stimuli. Sufficient sexual arousal stimulates the Skene (female prostate) and Bartholin’s glands, causing an increase in secretion. Sexual function in women is achieved not only by psychological but also by the harmonious interaction of neurochemical and organic factors.7Somatic diseases such as diabetes mellitus, spinal cord injury or pelvic surgeries can complicate FSD by causing damage to the blood vessels and nervous system.8 Chronic ischemia in female genital tissues causes structural and functional changes leading to decreased arousal and lubrication.9
According to the Basson’s sexual response cycle, enhancing intimacy or bonding to feel attractive or desired may be motivated to engage in sexual activity, and a state of “sexual neutrality” may result in a sexual experience.10 Disruption of at least one of these stages can cause a decrease in desire and lubrication. Except for sexual activity, surfaces of the vagina are covered by a thin film of fluid, preventing friction. However, the amount of fluid is insufficient for painless penile penetration. One of the subdomains of FSD is pain that can be explained by hypersensitivity to pain sensation or a decreased vestibular nociceptor threshold.10
Many factors may contribute to FSD, including diabetes mellitus, smoking, hyperlipidemia, heart diseases, liver failure, alcoholism, depression, drug abuse or medications. Diabetes mellitus may provoke an atherosclerotic process that could be a reason for decreased vaginal lubrication.8 The FSD associated with obesity is one of the commonly reported etiological factors.
To date, obesity and its impact on various diseases have been studied in many studies using the body mass index (BMI) or waist circumference (WC).12 The fact that WC mainly measures subcutaneous tissue and BMI cannot predict body fat homogeneously has led to an increase in scientific studies investigating more reliable markers.13 The visceral adiposity index (VAI) measures visceral adiposity.14 The VAI was used in many studies as a useful tool.15
Conflicting data have been published regarding the impact of metabolic syndrome or obesity without metabolic syndrome on female sexual function. Based on this, we aimed whether the VAI was a good predictor of female sexual dysfunction. To our knowledge, this study is the first to evaluate the impact of visceral adiposity index on different domains of female sexual function compared to body mass index and waist circumference.