American journal of epidemiology
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The coronavirus disease 2019 (COVID-19) pandemic presents a unique set of risk exposures for populations, which might lead to an increase in suicide. While large-scale traumatic events are known to increase psychological disorders, thus far the science has not shown a clear link between these events and suicide. In this issue of the Journal, Elbogen et al. (Am J Epidemiol. 2020;189(11):1266-1274) used representative data from the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) to show that 4 dimensions of financial strain-financial debt/crisis, unemployment, past homelessness, and lower income-are associated with subsequent suicide attempts. ⋯ Second, these data show the centrality of financial stressors, marking the current moment as distinct from other disasters or large-scale trauma. Third, the data teach us that financial stressors are linked and cumulative. In this way, Elbogen et al. provide a sobering harbinger of the potential effects on suicide of the collective stressors borne by the COVID-19 pandemic and other mass traumatic events that are accompanied by substantial financial stressors.
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More than 1.6 million Americans have been infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and more than 10 times that number carry antibodies to it. High-risk patients with progressing symptomatic disease currently have only hospitalization treatment, with its high mortality, available to them. An outpatient treatment that prevents hospitalization is desperately needed. ⋯ Five studies, including 2 controlled clinical trials, have demonstrated significant major outpatient treatment efficacy. HCQ + AZ has been used as the standard of care in more than 300,000 older adults with multiple comorbid conditions; the estimated proportion of such patients diagnosed with cardiac arrhythmia attributable to the medications is 47 per 100,000 users, among whom estimated mortality is less than 20% (9/100,000 users), as compared with the 10,000 Americans now dying each week. These medications need to be made widely available and promoted immediately for physicians to prescribe.
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In the 1930s, maps created by the federal Home Owners' Loan Corporation (HOLC) nationalized residential racial segregation via "redlining," whereby HOLC designated and colored in red areas they deemed to be unsuitable for mortgage lending on account of their Black, foreign-born, or low-income residents. We used the recently digitized HOLC redlining maps for 28 municipalities in Massachusetts to analyze Massachusetts Cancer Registry data for late stage at diagnosis for cervical, breast, lung, and colorectal cancer (2001-2015). ⋯ For example, a substantially elevated risk of late stage at diagnosis occurred among men with lung cancer residing in currently privileged areas that had been redlined (risk ratio = 1.17, 95% confidence interval: 1.06, 1.29), whereas such risk was attenuated among men residing in census tracts lacking such current privilege (risk ratio = 1.01, 95% confidence interval: 0.94, 1.08). Research on historical redlining as a structural driver of health inequities is warranted.
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Whether persons without prevalent cardiovascular disease (CVD) but elevated levels of high-sensitivity cardiac troponin T (hs-cTnT) or N-terminal pro-B-type natriuretic peptide (NT-proBNP) are at high risk of infection is unknown. Using 1996-2013 data from the Atherosclerosis Risk in Communities Study, we estimated hazard ratios for incident hospitalization with infection in relation to plasma hs-cTnT and NT-proBNP concentrations among participants without prevalent CVD and contrasted them with hazard ratios for persons with prevalent CVD (coronary heart disease, heart failure, or stroke). In a multivariable Cox model, prevalent CVD was significantly associated with risk of hospitalization with infection (hazard ratio (HR) = 1.31, 95% confidence interval (CI): 1.19, 1.45). ⋯ The 15-year cumulative incidences of hospitalization with infection were similar for participants with prevalent CVD and participants who did not have prevalent CVD but had hs-cTnT ≥14 ng/L or NT-proBNP ≥248.1 pg/mL. Thus, hs-cTnT and NT-proBNP were independently associated with infection risk. Persons without CVD but with elevated hs-cTnT or NT-proBNP levels should be recognized to have similar infection risks as persons with prevalent CVD.