Differences in health outcomes across racial groups are among the most commonly reported findings in health disparities research. Often, these studies do not explicitly connect observed disparities to mechanisms of systemic racism that drive adverse health outcomes among racialized and other marginalized groups in the United States. Without this connection, investigators inadvertently support harmful narratives of biologic essentialism or cultural inferiority that pathologize racial identities and inhibit health equity. This paper outlines pitfalls in the conceptualization, contextualization, and operationalization of race in quantitative population health research and provides recommendations on how to appropriately engage in scientific inquiry aimed at understanding racial health inequities. Race should not be used as a measure of biologic difference, but rather as a proxy for exposure to systemic racism. Future studies should go beyond this proxy use and directly measure racism and its health impacts.

Background Food insecurity (FIS) is an important public health issue associated with cardiovascular risk. Given the association of FIS with diets of poorer nutritional quality and higher salt intake as well as chronic stress, numerous studies have explored the link between FIS and hypertension. However, no systematic review or meta-analysis has yet to integrate or analyze the existing literature. Methods We performed a wide and inclusive search of peer-reviewed quantitative data exploring FIS and hypertension. A broad-terms, systematic search of the literature was conducted in PubMed, Embase, Scopus, and Web of Science for all English-language, human studies containing primary data on the relationship between FIS and hypertension. Patient population characteristics, study size, and method to explore hypertension were extracted from each study. Effect sizes including odds ratios and standardized mean differences were extracted or calculated based on studies’ primary data. Comparable studies were combined by the random effects model for meta-analyses along with assessment of heterogeneity and publication bias. Results A total of 36 studies were included in the final analyses. The studies were combined into different subgroups for meta-analyses as there were important differences in patient population characteristics, methodology to assess hypertension, and choice of effect size reporting (or calculability from primary data). For adults, there were no significantly increased odds of elevated blood pressures for food insecure individuals in studies where researchers measured the blood pressures: OR = 0.91 [95%CI: 0.79, 1.04; n = 29,781; Q(df = 6) = 7.6; I2 = 21%]. This remained true upon analysis of studies which adjusted for subject BMI. Similarly, in studies for which the standardized mean difference was calculable, there was no significant difference in measured blood pressures between food secure and FIS individuals: g = 0.00 [95%CI: -0.04, 0.05; n = 12,122; Q(df = 4) = 3.6; I2 = 0%]. As for retrospective studies that inspected medical records for diagnosis of hypertension, there were no significantly increased odds of hypertension in food insecure adults: OR = 1.11 [95%CI: 0.86, 1.42; n = 2,887; Q(df = 2) = 0.7; I2 = 0%]. In contrast, there was a significant association between food insecurity and self-reports of previous diagnoses of hypertension: 1.46 [95%CI: 1.13, 1.88; n = 127,467; Q(df = 7) = 235; I2 = 97%]. Only five pediatric studies were identified which together showed a significant association between FIS and hypertension: OR = 1.44 [95%CI: 1.16, 1.79; n = 19,038; Q(df = 4) = 5.7; I2 = 30%]. However, the small number of pediatric studies were not sufficient for subgroup meta-analyses based on individual study methodologies. Discussion In this systematic review and meta-analysis, an association was found between adult FIS and self-reported hypertension, but not with hypertension determined by blood pressure measurement or chart review. Further, while there is evidence of an association between FIS and hypertension among pediatric subjects, the limited number of studies precluded a deeper analysis of this association. These data highlight the need for more rigorous and longitudinal investigations of the relationship between FIS and hypertension in adult and pediatric populations.

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Although the cardiotoxic effects of cocaine are universally recognized, the association between cocaine and cardiomyopathy and/or heart failure is poorly understood. To conduct a comprehensive review and meta-analysis on the association between cocaine, heart failure, and cardiomyopathy, we first conducted a broad-term search in PubMed, Embase, Web of Science, and Scopus for human studies containing primary data on the relationship between cocaine and heart failure or cardiomyopathy. We were interested in studies with data beyond acute coronary syndromes. Retrieved studies were grouped into different categories based on possible hypotheses to test by meta-analysis. A second search with specific terms was then conducted. For grouped studies with sufficient clinical and methodological homogeneity, effect sizes were calculated and combined for meta-analysis by the Random Effects model. There is in general a need for more primary data studies that investigate heart failure and/or cardiomyopathy in cocaine users for mechanisms independent of ischemia. There were, however, enough studies to combine by meta-analyses that showed that chronic cocaine use is associated with anatomical and functional changes more consistent with diastolic heart failure instead of the commonly taught dilated cardiomyopathy pathway. In patients without a history of ACS, chronic cocaine use was not associated with significantly reduced EF. The few studies on acute cocaine had conflicting results on whether single-dose intravascular cocaine results in acute heart failure. Studies identified that included beta-blockade therapy in cocaine users with cardiac disease suggest that beta-blockers are not unsafe and that may be effective in the treatment of cocaine-associated heart failure. Chronic cocaine use is associated with anatomical and physiological changes of the heart muscle that are potentially reversible with beta-blockade therapy.

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