Psychosocial Stress, Cortisol Levels, and Maintenance of Vaginal Health

Abstract

Stress stimuli are ubiquitous and women do not enjoy any exemptions. The physiologic “fight-or-flight” response may be deleterious to the female lower genital tract microbiome if the stress stimuli persist for longer than necessary. Persistent exposure to psychosocial stress and stimulation of the hypothalamic-pituitary-adrenal (HPA) and sympathetic-adrenal-medullary (SAM) axes, and associated hormones are risk factors for several infections including genitourinary tract infections. Though this could be due to a dysregulated immune response, a cortisol-induced inhibition of vaginal glycogen deposition may be involved especially in the instance of vaginal infection. The estrogen-related increased vaginal glycogen and epithelial maturation are required for the maintenance of a healthy vaginal ecosystem (eubiosis). The ability of cortisol to disrupt this process as indicated in animal models is important in the pathogenesis of vaginal dysbiosis and the subsequent development of infection and inflammation. This phenomenon may be more crucial in pregnancy where a healthy Lactobacillus-dominated vaginal microbiota is sacrosanct, and there is local production of more corticotropin-releasing hormone (CRH) from the decidua, fetal membranes and placenta. To highlight the relationship between the stress hormone cortisol and the vaginal microbiomial architecture and function, the potential role of cortisol in the maintenance of vaginal health is examined.

Reviewing the Composition of Vaginal Microbiota: Inclusion of Nutrition and Probiotic Factors in the Maintenance of Eubiosis

“…These challenges can be lifetime events, emotions, and relations that unfavorably affect the individual's comfort or generate perceived detrimental responses. Very recently, the role of stress over the female lower genital tract has been reviewed [90]. For instance, working with animal models, it has been reported that the persistent exposure to psychosocial stress can lead to an encouragement of the hypothalamic-pituitary-adrenal and sympathetic-adrenal-medullary axes.…”

“…This, in turn, drives a cortisol-induced inhibition of glycogen deposition in vagina, which is translated into an interruption in epithelial maturation that is crucial to keep vaginal homeostasis (included as negative modifiable factor in Figure 1). This phenomenon is especially relevant during pregnancy, where local production of high levels of corticotropin-releasing hormone occurs in the decidua, fetal membranes and placenta [90].…”

“…Given the heterogeneity of the type of intravaginal practices, the variety of products for this purpose and their wide dissemination among cultures/races, additional research is desirable to clarify the effects on resident microbial communities of vaginal flora [79,81,83]. In addition, it has also been reported that the alkalinity of menstruation or semen neutralizes vaginal pH temporarily and could impact the vaginal microbiota [36,76,90]. Relative to systemic practices, the improper or prolonged use of antibiotics can permeate vaginal exudate, causing alteration in the ecosystem of the vagina.…”

Determinants of Vaginal Microbiota Composition

“…Antibiotic use is known to disrupt eubiosis in multiple body niches, but a number of studies in the vagina specifically found that these disruptions do not appear to last (Ding and Schloss, 2014 ; Dunlop et al, 2019 ). A number of studies have identified chronic psychosocial stress as an important mediator of vaginal health (Holtgrave and Crosby, 2003 ; Nansel et al, 2006 ), as mediated by the effect of cortisol on glycogen deposition and mucosal immune function (Amabebe and Anumba, 2018 ). Chronically elevated cortisol levels are known to be immunosuppressive and deplete glycogen stores, potentially impacting the VMB because glycogen-rich epithelium encourages Lactobacillus growth.…”

Effect of a Nonoptimal Cervicovaginal Microbiota and Psychosocial Stress on Recurrent Spontaneous Preterm Birth

“…[16][17][18][19][20][21][22][23][24][25][26] While precise mechanisms remain unknown, it has been postulated that stress influences hormonal pathways leading to changes in host immune response, thereby affecting the cervicovaginal ecosystem. [27][28][29][30] These findings raise questions as to whether stress may promote colonization of the cervicovaginal space with a nonoptimal microbiota in pregnancy.…”