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Background: Vitamin D deficiency (VDD) is associated with coronary heart disease (CHD) and poor outcomes, but supplementation does not improve prognosis. VDD has been implicated in and may promote greater risk through inflammation and impaired progenitor cell function. Objectives: The authors examined VDD, high-sensitivity C-reactive protein (hsCRP), circulating progenitor cell (CPC) counts, and outcomes in patients with CHD. They hypothesized that the higher risk with VDD is mediated by inflammation and impaired regenerative capacity. Methods: A total of 5,452 individuals with CHD in the Emory Cardiovascular Biobank had measurement of 25-hydroxyvitamin D, subsets of whom had hsCRP measurements and CPCs estimated as CD34-expressing mononuclear cell counts. Findings were validated in an independent cohort. 25-hydroxyvitamin D <20 ng/mL was considered VDD. Cox and Fine-Gray models determined associations between marker levels and: 1) all-cause mortality; 2) cardiovascular mortality; and 3) major adverse cardiovascular events, a composite of adverse CHD outcomes. Results: VDD (43.6% of individuals) was associated with higher adjusted cardiovascular mortality (HR: 1.57, 95% CI: 1.09-2.28). There were significant interactions between VDD and hsCRP and CPC counts in predicting cardiovascular mortality. Individuals with both VDD and elevated hsCRP had the greatest risk (HR: 2.82, 95% CI: 2.16-3.67). Only individuals with both VDD and low CPC counts were at high risk (HR: 2.25, 95% CI: 1.46-3.46). These findings were reproduced in the validation cohort. Conclusions: VDD predicts adverse outcomes in CHD. Those with VDD, inflammation and/or diminished regenerative capacity are at a significantly greater risk of cardiovascular mortality. Whether targeted supplementation in these high-risk groups improves risk warrants further study.
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Drawing on social identity theory and research on digital media and polarization, this study uses a quasi-experimental design with a random sample (n = 3304) to provide causal evidence on perceptions of who is to blame for the initial spread of COVID-19 in India. According blame to three different social and political entities-Tablighi Jamaat (a Muslim group), the Modi government, and migrant workers (a heterogeneous group)-are the dependent variables in three OLS regression models testing the effect of the no-blame treatment, controlling for Facebook use, social identity (religion), vote in the 2019 national election, and other demographics. Results show respondents in the treatment group were more likely to allay blame, affective polarization (dislike for outgroup members) was social identity based, not partisan based, and Facebook/Instagram use was not significant. Congress and United Progressive Alliance voters in 2019 were less likely to blame the Modi government for the initial spread. Unlike extant research in western contexts, affective and political polarization appear to be distinct concepts in India where social identity complexity is important. This study of the first wave informs perceptions of blame in future waves, which are discussed in conclusion along with questions for future research.
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[Figure: see text].