Epilepsy is associated with a high rate of premature mortality from direct and indirect effects of seizures, epilepsy, and antiseizure therapies. Sudden unexpected death in epilepsy (SUDEP) is the second leading neurologic cause of total lost potential life-years after stroke, yet SUDEP may account for less than half of all epilepsy-related deaths. Some epilepsy groups are especially vulnerable: individuals from low socioeconomic status groups and those with comorbid psychiatric illness die more often than controls. Despite clear evidence of an important public health problem, efforts to assess and prevent epilepsy-related deaths remain inadequate. We discuss factors contributing to the underestimation of SUDEP and other epilepsy-related causes of death. We suggest the need for a systematic classification of deaths directly due to epilepsy (e.g., SUDEP, drowning), due to acute symptomatic seizures, and indirectly due to epilepsy (e.g., suicide, chronic effects of antiseizure medications). Accurately estimating the frequency of epilepsy-related mortality is essential to support the development and assessment of preventive interventions. We propose that educational interventions and public health campaigns targeting medication adherence, psychiatric comorbidity, and other modifiable risk factors may reduce epilepsy-related mortality. Educational campaigns regarding sudden infant death syndrome and fires, which kill far fewer Americans than epilepsy, have been widely implemented. We have done too little to prevent epilepsy-related deaths. Everyone with epilepsy and everyone who treats people with epilepsy need to know that controlling seizures will save lives.

Genetic and behavioral factors do not fully explain the development of hypertension, and there is increasing evidence suggesting that psychosocial factors may also play an important role. Exposure to chronic stress has been hypothesized as a risk factor for hypertension, and occupational stress, stressful aspects of the social environment, and low socioeconomic status have each been studied extensively. The study of discrimination is a more recent and rapidly growing area of investigation and may also help to explain the well-known racial disparities in hypertension. Research regarding mechanisms underlying stress effects on hypertension has largely focused on cardiovascular reactivity, but delayed recovery to the pre-stress level is increasingly being evaluated as another possible pathway. Recent findings in each of these areas are reviewed, and directions for future research are discussed.

Background Observational studies of patients with rheumatoid arthritis have suggested that racial and ethnic disparities exist for minority populations. We compared disease activity and clinical outcomes across racial and ethnic groups using data from a large, contemporary United States registry. Methods We analyzed data from two time periods (2005-2007 and 2010-2012). The Clinical Disease Activity Index was examined as both a continuous measure and as dichotomous measures of disease activity states. Outcomes were compared in unadjusted and a series of cross-sectional and longitudinal multivariable regression models. Results For 2005-2007, significant differences of mean disease activity level (p<0.001) were observed across racial and ethnic groups. Over the five-year period, modest improvements in disease activity were observed across all groups, including whites [3.7 (95% CI 3.2 - 4.1) compared with African Americans [4.3 (95% CI 2.7 – 5.8)] and Hispanics [2.7 (95% CI 1.2 – 4.3)]. For 2010-2012, significant differences of mean disease activity level persisted (p<0.046) across racial and ethnic groups, ranging from 11.6 (95% CI 10.4-12.8) in Hispanics to 10.7 (95% CI 9.6-11.7) in whites. Remission rates remained significantly different across racial/ethnic groups across all models for 2010-2012, ranging from 22.7 (95% CI 19.5-25.8) in African Americans to 27.4 (95% CI 24.9-29.8) in whites. Conclusions Despite improvements in disease activity across racial and ethnic groups over a 5-year period, disparities persist in disease activity and clinical outcomes for minority groups versus white patients.

BACKGROUND Reduced nocturnal blood pressure (BP) dipping is more prevalent among blacks living in the United States than whites and is associated with increased target organ damage and cardiovascular risk. The primary aim of this study was to determine whether socioeconomic and psychosocial factors help to explain racial differences in dipping. In order to address the limited reproducibility of dipping measures, we investigated this question in a sample of participants who underwent multiple ambulatory BP monitoring (ABPM) sessions. METHODS The study sample included 171 black and white normotensive and mildly hypertensive participants who underwent three ABPM sessions, each 1 month apart, and completed a battery of questionnaires to assess socioeconomic and psychosocial factors. RESULTS As expected, blacks showed less dipping than whites, after adjusting for age, sex, body mass index (BMI), and mean 24 h BP level (mean difference = 3.3%, P= 0.002). Dipping was related to several of the socioeconomic and psychosocial factors examined, with higher education and income, being married, and higher perceived social support, each associated with a larger dipping percentage. Of these, marital status and education were independently associated with dipping and together accounted for 36% of the effect of race on dipping. CONCLUSIONS We identified a number of socioeconomic and psychosocial correlates of BP dipping and found that reduced dipping among blacks vs. whites is partially explained by marital status (being unmarried) and lower education among blacks. We also present results suggesting that repeated ABPM may facilitate the detection of associations between dipping and other variables.