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Background and purposeDepression is associated with stroke, but the effects of changes in depressive symptoms on stroke risk are not well understood. This study examined whether depressive symptom changes across 2 successive annual assessments were associated with incident stroke the following year.MethodsWe used visit data from 4319 participants of the Cardiovascular Health Study who were stroke free at baseline to examine whether changes in depressive symptoms classified across 2 consecutive annual assessments predicted incident first stroke during the subsequent year. Depressive symptoms were assessed using the 10-item Center for Epidemiologic Studies Depression scale (high versus low at ≥10). Survival models were inverse probability weighted to adjust for demographics, health behaviors, medical conditions, past depressive symptoms, censoring, and survival.ResultsDuring follow-up, 334 strokes occurred. Relative to stable low scores of depressive symptoms, improved depression symptoms were associated with almost no excess risk of stroke (adjusted hazards ratio, 1.02; 95% confidence interval, 0.66-1.58). New-onset symptoms were nonsignificantly associated with elevated stroke risk (adjusted hazards ratio, 1.44; 95% confidence interval, 0.97-2.14), whereas persistently high depressive symptoms were associated with elevated adjusted hazard of all-cause stroke (adjusted hazards ratio, 1.65; 95% confidence interval, 1.06-2.56). No evidence for effect modification by race, age, or sex was found.ConclusionsPersistently high symptoms of depression predicted elevated hazard of stroke. Participants with improved depressive symptoms had no elevation in stroke risk. Such findings suggest that strategies to reduce depressive symptoms may ameliorate stroke risk.

BackgroundFew longitudinal studies compare changes in instrumental activities of daily living (IADLs) among stroke-free adults to prospectively document IADL changes among adults who experience stroke. We contrast annual declines in IADL independence for older individuals who remain stroke free to those for individuals who experienced stroke. We also assess whether these patterns differ by sex, race, or Southern birthplace.MethodsHealth and Retirement Study participants who were stroke free in 1998 (n = 17,741) were followed through 2010 (average follow-up = 8.9 years) for self- or proxy-reported stroke. We used logistic regressions to compare annual changes in odds of self-reported independence in six IADLs among those who remained stroke free throughout follow-up (n = 15,888), those who survived a stroke (n = 1,412), and those who had a stroke and did not survive to participate in another interview (n = 442). We present models adjusted for demographic and socioeconomic covariates and also stratified on sex, race, and Southern birthplace.ResultsCompared with similar cohort members who remained stroke free, participants who developed stroke had faster declines in IADL independence and lower probability of IADL independence prior to stroke. After stroke, independence declined at an annual rate similar to those who did not have stroke. The black-white disparity in IADL independence narrowed poststroke.ConclusionRacial differences in IADL independence are apparent long before stroke onset. Poststroke differences in IADL independence largely reflect prestroke disparities.

Objectives: To comprehensively evaluate the association of ERCC1 C8092A and ERCC2 Lys751Gln polymorphisms with the risk of glioma. Methods: Potential studies were searched and selected through the Pubmed/MEDLINE, EMBASE, the China National Knowledge Infrastructure (CNKI) platforms, WanFang and VIP database up to June 2013. Two investigators independently reviewed full text and included studies met inclusion criteria. Combined odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated in a fixed-effects model or a random-effects model according to results of heterogeneity test. All analyses were performed by Revman 5.2 and Stata 10.0 software. Results: A total of 10 studies were included in our meta-analysis, including 3,580 glioma patients and 4,728 controls. Overall, ERCC1 C8092A polymorphism was associated with the risk of glioma (AA vs. CC: OR = 1.29, 95%CI: 1.07–1.55, P = 0.01; recessive model: OR = 1.29; 95% CI: 1.07–1.55, P = 0.01). When stratified by ethnicity, significant association was only observed in the Chinese population (AA vs. CC: OR = 1.37, 95%CI: 1.03–1.81, P = 0.03; recessive model: OR = 1.34; 95% CI: 1.02–1.75, P = 0.04). For ERCC2 Lys751Gln polymorphism, no significant association was found between ERCC2 Lys751Gln polymorphism and the risk of glioma in different genetic models. A significant association of ERCC2 Lys751Gln polymorphism with the risk of glioma was identified in the Caucasian population under recessive model (OR = 0.87; 95% CI: 0.78–0.98, P = 0.02), but not in the Chinese population. Conclusion: This meta-analysis suggested that the AA genotype of ERCC1 C8092A polymorphism might increase the susceptibility of glioma in the Chinese population. And the TT genotype of ERCC2 Lys751Gln polymorphism may decrease the risk of glioma in the Caucasian population. But the small number of studies and moderate methodological quality require cautious interpretation of the study results. [ABSTRACT FROM AUTHOR]

Objectives To compare typical age-related changes in activities of daily living ( ADLs) independence in stroke-free adults with long-term ADL trajectories before and after stroke. Design Prospective, observational study. Setting Community-dwelling Health and Retirement Study ( HRS) cohort. Participants HRS participants who were stroke free in 1998 and were followed through 2008 (average follow-up 7.9 years) (N = 18,441). Measurements Strokes were assessed using self- or proxy-report of a doctor's diagnosis and month and year of event. Logistic regression was used to compare within-person changes in odds of self-reported independence in five ADLs in those who remained stroke free throughout follow-up (n = 16,816), those who survived a stroke (n = 1,208), and those who had a stroke and did not survive to participate in another interview (n = 417). Models were adjusted for demographic and socioeconomic covariates. Results Even before stroke, those who later developed stroke had significantly lower ADL independence and were experiencing faster independence losses than similar-aged individuals who remained stroke free. Of those who developed a stroke, survivors experienced slower pre-stroke loss of ADL independence than those who died. ADL independence declined at the time of stroke and decline continued afterwards. Conclusion In adults at risk of stroke, disproportionate ADL limitations emerge well before stroke onset. Excess disability in stroke survivors should not be entirely attributed to effects of acute stroke or quality of acute stroke care. Although there are many possible causal pathways between ADL and stroke, the association may be noncausal. For example, ADL limitations may be a consequence of stroke risk factors (e.g., diabetes mellitus) or early cerebrovascular ischemia. [ABSTRACT FROM AUTHOR]

Background: While self‐reported trans–fatty acid (TFA) consumption is linked to coronary heart disease (CHD), relationships between objective biomarkers of TFA subtypes (t‐16:1n9, total t‐18:1, and cis/trans‐(c/t‐), t/c‐ and t/t‐18:2) and cardiovascular disease (CVD) or total mortality are not well established. Methods and Results: We evaluated 2742 adults in the Cardiovascular Health Study, aged 74±5 years and free of prevalent CVD, with plasma phospholipid TFA measures in 1992. Incident fatal and nonfatal CHD events, CVD and non‐CVD mortality, and total mortality were centrally adjudicated through 2010. Risks were assessed using Cox proportional hazards. During 31 494 person‐years, 1735 total deaths and 639 total CHD events occurred. In the multivariate model including mutual adjustment for the 5 TFA subtypes, circulating t/t‐18:2 was associated with higher total mortality (extreme quintile hazard ratio (HR)=1.23, 95% CI=1.04 to 1.44, P‐trend=0.01), CVD mortality (HR=1.40, 95% CI=1.05 to 1.86, P‐trend=0.02), and total CHD (HR=1.39, 95% CI=1.06 to 1.83, P‐trend=0.01). t/c‐18:2 was positively related to total mortality (HR=1.19, P‐trend=0.05), total CHD (HR=1.67, P‐trend=0.002), and nonfatal CHD (HR=2.06, P‐trend=0.002) after mutual adjustment; these associations were insignificant without mutual adjustment. Neither t‐16:1n9 nor t‐18:1 was significantly associated with total mortality or CVD, nor was c/t‐18:2 if we excluded early cases. Conclusions: Among circulating TFAs, t/t‐18:2 was most adversely associated with total mortality, mainly due to the increased risk of CVD. t/c‐18:2 was also positively associated with total mortality and CHD, but only after adjustment for other TFAs. These results highlight the need for further investigation of dietary sources, nondietary determinants, and health effects of specific TFA subtypes, especially t‐18:2 isomers.