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.