Internet interventions provide an option for those who either cannot or choose not to engage with traditional treatments. Most research on internet interventions involves guided or supported interventions. However, unsupported interventions offer considerably more scalability and cost-effectiveness, which makes them attractive for large-scale implementation. In this study, 309 participants recruited via Google AdWords entered an unsupported cognitive-behavioral internet intervention for depressive symptoms. To maximize the ecological validity of the study, participants received no incentives or live contact with study personnel. Furthermore, the study was open to individuals at any level of depressive symptoms, and all participants received the active intervention. The main outcome measures were depressive symptom level and self-efficacy in managing depressive symptoms. At follow-up, depression scores were significantly lower than baseline scores at each follow-up point (1, 2, 4, and 7 months), with pre-post effect sizes ranging from medium to large. Follow-up depression self-efficacy scores were significantly higher than baseline scores at each follow-up point, with pre-post effect sizes in the medium range. The results remained significant when analyzing only participants with depression scores indicative of a presence of a major depressive episode; results likewise remained significant when employing the conservative last observation carried forward convention, even in the presence of high attrition observed in this study. The results illustrate the potential of unsupported internet intervention to address the health needs of the global community.

Background

Socioeconomic adversity in early life is related to cardiovascular risk in adulthood; however, no studies have examined whether such adversity may be related to endogenous sex hormones, which are themselves associated with cardiovascular outcomes, or whether the timing of adversity exposures (childhood vs. puberty) matters.

Objective

The goal of the current study was to separately examine neighborhood socioeconomic status (SES) during periods of childhood and puberty in relation to adulthood levels of endogenous sex hormones (estradiol [E2], testosterone), sex hormone binding globulin (SHBG), and a derived index of bioavailable testosterone (free androgen index).

Methods

In a sample of 143 premenopausal women (mean age = 36.8 [SD = 5.5]; 51.7% White, 32.2% African American, 5.6% Latina, 7.0% Chinese, and 3.5% Filipina), retrospective reports of residential address information in designated periods of childhood and puberty were used to derive U.S. census-based neighborhood SES composite scores characterizing the socioeconomic environments of women during these periods.

Results

In covariate-adjusted analyses, higher neighborhood SES in puberty predicted higher levels of SHBG in adulthood, but neighborhood SES during childhood did not (standardized regression coefficient = .24, p = .01 vs. standardized regression coefficient = .04, p = .75, respectively). Neighborhood SES was not predictive of other hormones (E2, testosterone, and free androgen index).

Discussion

The current findings suggest that puberty may be a time of particular vulnerability to the effects of neighborhood SES on SHBG levels, which have been linked to cardiovascular risk factor profiles and atherosclerotic disease progression.

Objective

The aim of this study was to evaluate the extent to which mild disruptions in ovarian function, indexed by changes in menstrual cycle length, may relate to cardiometabolic and psychological health in premenopausal women.

Methods

Among 804 healthy, regularly cycling women (aged 25-45 y; mean [SD] age, 35.5 [5.5] y), patterns of any change (shortening, lengthening, or increased variability) versus no change in menstrual cycle length were examined in relation to a composite of cardiometabolic risk and individual risk factors (high-density lipoprotein, triglycerides, waist circumference, glucose, and hypertensive status), as well as in relation to depression indicators (Center for Epidemiological Studies Depression Scale score ≥16 [yes/no], lifetime depression diagnosis [yes/no], and lifetime antidepressant medication use [yes/no]). Models were also explored to test whether changes in menstrual cycle length mediated relations between depression history and cardiometabolic risk.

Results

In covariate-adjusted models compared with no change, any change in menstrual cycle length was associated with higher cardiometabolic risk composite scores and lower high-density lipoprotein (P < 0.05). In addition, compared with no change, any change in menstrual cycle length was associated with a Center for Epidemiological Studies Depression Scale score of 16 or higher, having received a depression diagnosis, and having used antidepressant medications (P < 0.05). In exploratory analyses, any change in menstrual cycle length partially mediated the relation between depression history and cardiometabolic risk (b = 0.152, P = 0.040), which attenuated (b = 0.129, P = 0.083) when any change in menstrual cycle length was covaried.

Conclusions

Findings suggest that disruptions in ovarian function, marked by subtle changes in menstrual cycle length, may relate to aspects of cardiometabolic and psychological health among healthy, premenopausal women.