Objective In this conceptual review, we propose a novel mechanistic candidate in the etiology of depression with onset in the menopause transition (a.k.a. perimenopausal depression) involving alterations in stress-responsive pathways, induced by ovarian hormone fluctuation. Methods The relevant literature in perimenopausal depression was reviewed, including its prevalence, predictors, and treatment with estrogen therapy. Subsequently, the growing evidence from animal models and clinical research in other reproductive mood disorders was synthesized to describe a heuristic model of perimenopausal depression development. Results The rate of major depressive disorder and of clinically meaningful elevations in depressive symptoms increases two- to threefold during the menopause transition. While the mechanisms by which ovarian hormone fluctuation might impact mood are poorly understood, growing evidence from basic and clinical research suggests that fluctuations in ovarian hormones and their derived neurosteroids result in altered GABAergic regulation of the hypothalamic-pituitary-adrenal (HPA) axis. Our heuristic model suggests that for some women, failure of the GABAA receptor to regulate overall GABAergic tone in the face of shifting levels of these neurosteroids may induce HPA axis dysfunction, thereby increasing sensitivity to stress, and generating a period of greater vulnerability to depression. Conclusions The proposed model provides a basis for understanding the mechanisms by which the changing hormonal environment of the menopause transition may interact with the psychosocial environment of mid-life to contribute to perimenopausal depression risk. Future research investigating this model may inform the development of novel pharmacological treatments for perimenopausal depression and related disorders such as postpartum depression and premenstrual dysphoric disorder.

With the loss of estrogen that occurs with menopause, physiologic and structural changes occur within the vulvovaginal mucosa that lead to a condition commonly called atrophic vaginitis. Although mild genital changes occur in most women, 10-47% of postmenopausal women will develop one or more debilitating symptoms that include vulvovaginal dryness, dyspareunia, vulvar itching or pain, recurrent urinary tract infections, as well as abnormal vaginal discharge. Topical estrogen replacement therapies reverse these mucosal changes and are effective treatments for the symptoms of atrophic vaginitis. Vaginal moisturizers and lubricants also provide symptomatic relief for vaginal dryness and dyspareunia, respectively.

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