Objective Women’s risk of obstructive sleep apnea (OSA) increases substantially during and after the menopause transition, when depression risk is also elevated, raising the possibility that estrogen withdrawal contributes to OSA vulnerability, in turn contributing to mood disturbance. We examined the association between estradiol levels and OSA in depressed peri- and postmenopausal women. Methods Thirty depressed peri/postmenopausal women (mean BMI 30.82 kg/m2) without known OSA completed routine polysomnography concurrent with serum estradiol levels. Estradiol in women with apnea-hypopnea indices (AHI)≥15 indicating moderate-to-severe OSA was compared against those with AHI <15 using logistic regression adjusting for age and body mass index (BMI). Results Thirteen women (43%) had AHI≥15 (median AHI 21.6). Estradiol levels were lower (p=0.02) in those with OSA (median 19, interquartile range [IQR] 9–25, pg/ml) than without OSA (median 29, IQR 19–66, pg/ml). On univariate analysis, higher estradiol was associated with reduced odds of OSA (odds ratio [OR] 0.95, 95% confidence interval [CI] 0.90–0.99, p=0.04). After adjusting for age and BMI, E2 levels remained associated with lower odds of OSA (OR 0.90), but the association was no longer statistically significant (95% CI 0.76–1.05, p=0.18). Montgomery Åsberg Depression Rating Scale scores did not differ between those with and without OSA. Conclusions These preliminary results suggest that, in addition to higher BMI and age, lower estradiol may be associated with increased OSA risk in depressed women during the peri- and postmenopause, raising the possibility that estradiol withdrawal associated with menopause influences upper-airway patency in women.

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Objective: We applied the experimental therapeutics approach to test whether acute treatment outcomes for winter seasonal affective disorder (SAD) are mediated by a cognitive mechanism in cognitive–behavioral therapy (CBT-SAD) versus a chronobiologic mechanism in light therapy (LT). Method: Currently depressed adults with major depression, recurrent with seasonal pattern (N = 177; 83.6% female, 92.1% non-Hispanic White, M age = 45.6) were randomized to 6 weeks of LT or group CBT-SAD. SAD symptoms were assessed weekly on the Structured Clinical Interview for the Hamilton Rating Scale for Depression–SAD Version. At pre-, mid-, and posttreatment, participants completed measures of general depressogenic cognitions (Dysfunctional Attitudes Scale; DAS); SAD-specific negative cognitions (Seasonal Beliefs Questionnaire; SBQ); chronotype (Morningness–Eveningness Questionnaire; MEQ); and depressive symptoms (Beck Depression Inventory–Second Edition). Results: Parallel-process growth models showed evidence for hypothesized mechanisms. For SAD-specific negative cognitions (SBQ), both symptom measures showed (1) an effect of treatment group on the slope of the mediator, with CBT-SAD demonstrating greater decreases, and (2) an effect of the slope of the mediator on the slope of the outcome. These effects held for the SBQ but not the broader measure of depressogenic cognitions (DAS). For the chronotype measure (MEQ), treatment assignment affected change, whereby LT was associated with reduced “eveningness,” but this was unrelated to change in symptoms. Conclusions: CBT-SAD promoted decreases in SAD-specific negative cognitions, and these changes were related to decreases in symptoms. Consistent with the theory that LT corrects misaligned circadian rhythms, LT reduced eveningness, but this did not correspond to symptom improvement.

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