Person:

Glymour, Maria

Objective: Previous studies suggest that unemployment predicts increased cardiovascular disease (CVD) risk, but whether unemployment insurance programs mitigate this risk has not been assessed. Exploiting US state variations in unemployment insurance benefit programs, we tested the hypothesis that more generous benefits reduce CVD risk. Methods: Cohort data came from 16,108 participants in the Health and Retirement Study (HRS) aged 50–65 at baseline interviewed from 1992 to 2010. Data on first and recurrent CVD diagnosis assessed through biennial interviews were linked to the generosity of unemployment benefit programmes in each state and year. Using state fixed-effect models, we assessed whether state changes in the generosity of unemployment benefits predicted CVD risk. Results: States with higher unemployment benefits had lower incidence of CVD, so that a 1% increase in benefits was associated with 18% lower odds of CVD (OR:0.82, 95%-CI:0.71–0.94). This association remained after introducing US census regional division fixed effects, but disappeared after introducing state fixed effects (OR:1.02, 95%-CI:0.79–1.31).This was consistent with the fact that unemployment was not associated with CVD risk in state-fixed effect models. Conclusion: Although states with more generous unemployment benefits had lower CVD incidence, this appeared to be due to confounding by state-level characteristics. Possible explanations are the lack of short-term effects of unemployment on CVD risk. Future studies should assess whether benefits at earlier stages of the life-course influence long-term risk of CVD.

RATIONALE:

Higher social integration is associated with lower cardiovascular mortality; however, whether it is associated with incident coronary heart disease (CHD), especially in women, and whether associations differ by case fatality are unclear. OBJECTIVES:

This study sought to examine the associations between social integration and risk of incident CHD in a large female prospective cohort. METHODS AND RESULTS:

Seventy-six thousand three hundred and sixty-two women in the Nurses' Health Study, free of CHD and stroke at baseline (1992), were followed until 2014. Social integration was assessed by a simplified Berkman-Syme Social Network Index every 4 years. End points included nonfatal myocardial infarction and fatal CHD. Two thousand three hundred and seventy-two incident CHD events occurred throughout follow-up. Adjusting for demographic, health/medical risk factors, and depressive symptoms, being socially integrated was significantly associated with lower CHD risk, particularly fatal CHD. The most socially integrated women had a hazard ratio of 0.55 (95% confidence interval, 0.41-0.73) of developing fatal CHD compared with those least socially integrated (P for trend <0.0001). When additionally adjusting for lifestyle behaviors, findings for fatal CHD were maintained but attenuated (P for trend =0.02), whereas the significant associations no longer remained for nonfatal myocardial infarction. The inverse associations between social integration and nonfatal myocardial infarction risk were largely explained by health-promoting behaviors, particularly through differences in cigarette smoking; however, the association with fatal CHD risk remained after accounting for these behaviors and, thus, may involve more direct biological mechanisms. CONCLUSIONS:

Social integration is inversely associated with CHD incidence in women, but is largely explained by lifestyle/behavioral pathways.

BACKGROUND: Although research has demonstrated that depressive symptoms predict stroke incidence, depressive symptoms are dynamic. It is unclear whether stroke risk persists if depressive symptoms remit. METHODS AND RESULTS: Health and Retirement Study participants (n=16 178, stroke free and noninstitutionalized at baseline) were interviewed biennially from 1998 to 2010. Stroke and depressive symptoms were assessed through self-report of doctors' diagnoses and a modified Center for Epidemiologic Studies - Depression scale (high was ≥3 symptoms), respectively. We examined whether depressive symptom patterns, characterized across 2 successive interviews (stable low/no, onset, remitted, or stable high depressive symptoms) predicted incident stroke (1192 events) during the subsequent 2 years. We used marginal structural Cox proportional hazards models adjusted for demographics, health behaviors, chronic conditions, and attrition. We also estimated effects stratified by age (≥65 years), race or ethnicity (non-Hispanic white, non-Hispanic black, Hispanic), and sex. Stroke hazard was elevated among participants with stable high (adjusted hazard ratio 2.14, 95% CI 1.69 to 2.71) or remitted (adjusted hazard ratio 1.66, 95% CI 1.22 to 2.26) depressive symptoms compared with participants with stable low/no depressive symptoms. Stable high depressive symptom predicted stroke among all subgroups. Remitted depressive symptoms predicted increased stroke hazard among women (adjusted hazard ratio 1.86, 95% CI 1.30 to 2.66) and non-Hispanic white participants (adjusted hazard ratio 1.66, 95% CI 1.18 to 2.33) and was marginally associated among Hispanics (adjusted hazard ratio 2.36, 95% CI 0.98 to 5.67). CONCLUSIONS:In this cohort, persistently high depressive symptoms were associated with increased stroke risk. Risk remained elevated even if depressive symptoms remitted over a 2-year period, suggesting cumulative etiologic mechanisms linking depression and stroke.