The PMDD is occurring at times of hormonal fluctuations, and the most effective treatment for PMDD is by suppression of ovulation and suppression of the cyclical hormonal changes by hormone therapy [1, 17]. These evidences supported that the direct activating effect of hormones plays an essential role in the pathogenesis of PMDD, and at least reproductive hormones may precipitate the presentation of PMDD. Moreover, recently, the possible role of organizational effects of prenatal sex hormones during PMDD has got attentions. The researches made by Kaneoke et al. who used the 2D:4D ratios as a marker of prenatal sex hormones exposure, indicated that the prenatal sex hormones exposure may influence individual differences in the severity of premenstrual symptoms [9], and could be a factor in the development of PMDD. A recent preclinical animal study clearly showed that prenatal androgenization induced anxiety-like behavior in adult female rats, implying that prenatal exposure to high concentrations of testosterone may influence the development of neural networks and impose the risk of anxiety-like behavior later in life [18]. We used the 2D:4D ratios, AGD-AC, AGD-AF, and CUMD, as the indicators of prenatal androgen hormone exposure in order to study the association of PMDD with these measures. The left/right 2D:4D ratios, AGD-AC and AGD-AF between PMDD and controls did not show any difference, but a significant longer CUMD was seen in the patients with PMDD. As the CUMD is supposed to be positive association with prenatal androgen levels, therefore, atypical high prenatal androgen exposure might predispose individuals to be susceptible to PMDD.
Recently, several studies demonstrated that AGD in adult patients with the polycystic ovarian syndrome (PCOS) was longer than control, implying that extreme prenatal androgen exposure contributes to PCOS [15, 19, 20]. The PCOS is a hyperandrogenic, oligomenorrhea/amenorrhea, fertility problems and metabolic disorder found in 6–7% of reproductive-aged women [21]. Therefore, the clinical features and pathophysiological processes of PMDD are totally different from ones of PCOS. So it is not unusual that PMDD patients did not show abnormal AGD. But both of PMDD and PCOS were probably related to the higher prenatal androgen exposures, why did PMDD patients have a longer CUMD and PCOS patents have a longer AGD? It is awaited future studies. At present, it can be inferred that there are other factors led to discrepant perineum appearances.
Several reports demonstrated the presence of premenstrual symptoms correlated negatively with sexual satisfaction [22–24]. Sexual pleasure and orgasm during copulation in women depends on many factors, such as past experience, stimulation of one or all of these triggering zones, autonomic arousal, and partner- and contextual-related cues, etc.[25] The clitoral complex in relation to the urethra, vulva, and vagina is the essential sensory triggering zone[25]. A longer CUMD in a woman decreased her likelihood of experiencing orgasm in sexual intercourse, as the longer CUMD may decrease penile-clitoral contact during sexual intercourse or decrease penile stimulation of internal aspects of the clitoris [12]. Therefore, the longer CUMD might contribute the sexual difficulties of women with premenstrual symptoms, according to our results.
This is a preliminary study with limited samples. There are some major defects, for instance, we did not study the association of individual differences in the severity of premenstrual symptoms with the left/right 2D:4D ratios, AGD-AC, AGD-AF and CUMD. Moreover, we did not collect data about the sexual function/satisfaction of subjects, at same time.