Disruptions in ovarian function are related to depression and cardiometabolic risk during premenopause.

摘要: Although risk for cardiovascular disease (CVD) increases during the menopausal transition,1–12 processes underlying emergence of CVD this period may begin pre-menopausally as is suggested by studies documenting fatty streaks well clinically significant atherosclerotic lesions in young, pre-menopausal women and adolescent girls.13–16 To date, however, factors contributing to development that explain variability post-menopausally are poorly understood. In context, Kaplan Manuck have proposed “precocious acceleration” hypothesis, suggesting disruptions ovarian function (even when mild) can promote atherosclerosis, leading an accelerated course increased post-menopausal CVD.17–18 This hypothesis supported which with apparent impairments function, marked anovulation, lower estrogen, menstrual cycle irregularity, exhibited or more problematic factor profiles.19–25 Poorer psychological health has been associated indexed characteristics. Findings drawn from three, largely separate literatures show i) psychiatric disorders frequently experience abnormalities including irregularity patterns both shorter longer length26–29; ii) stress, especially extreme, play etiological role cessation menses30–33; iii) depressive symptoms peri-menopause, a time cycles become less regular due reproductive aging.34 Poorer also CVD. particular, depression, major minor disorder symptomatology, shown predict incident myocardial infarction, cardiac-specific, all-cause mortality.35–40 With respect examination factors, among women, confers metabolic syndrome41–43 negative broadly correlated (although not always41–42) individual components syndrome (i.e., high-density lipoprotein [HDL], triglycerides, waist circumference, glucose, blood pressure).43–45 To integrate extend existing literature, primary goal current study was evaluate whether mild healthy, regularly-cycling related markers cardio-metabolic depression. Given inter-relations between secondarily, we explored model were mediating (at least partially) linking depression risk. The objectives pursued multi-ethnic sample 804 whom examined having experienced any change shortening, lengthening, becoming variable) compared no length relation standard symptomatology history.