Structural racism, which is embedded in past and present operations of the U.S. housing market, is a fundamental cause of racial health inequities. We conducted an ecologic study to 1) examine historic redlining in relation to current neighborhood lending discrimination and three key indicators of societal health (mental health, physical health, and infant mortality rate (IMR)) and 2) investigate sustained lending disinvestment as a determinant of current neighborhood health in one of the most hypersegregated metropolitan areas in the United States, Milwaukee, Wisconsin. We calculated weighted historic redlining scores from the proportion of 1930s Home Owners' Loan Corporation residential security grades contained within 2010 census tract boundaries. We combined two lending indicators from 2018 Home Mortgage Disclosure Act data to capture current neighborhood lending discrimination: low lending occurrence and high cost loans (measured via loan rate spread). Using historic redlining score and current lending discrimination, we created a 4-level hierarchical measure of lending trajectory. In Milwaukee neighborhoods, greater historic redlining was associated with current lending discrimination (OR = 1.73, 95%CI: 1.16, 2.58) and increased prevalence of poor physical health (β = 1.34, 95%CI: 0.40, 2.28) and poor mental health (β = 1.26, 95%CI: 0.51, 2.01). Historic redlining was not associated with neighborhood IMR (β = −0.48, 95%CI: −2.12, 1.15). A graded association was observed between lending trajectory and health: neighborhoods with high sustained disinvestment had worse physical and mental health than neighborhoods with high investment (poor physical health: β = 5.33, 95%CI: 3.05, 7.61; poor mental health: β = 4.32, 95%CI: 2.44, 6.20). IMR was highest in ‘disinvested’ neighborhoods (β = 5.87, 95%CI: 0.52, 11.22). Our findings illustrate ongoing legacies of government sponsored historic redlining. Structural racism, as manifested in historic and current forms of lending disinvestment, predicts poor health in Milwaukee's hypersegregated neighborhoods. We endorse equity focused policies that dismantle and repair the ways racism is entrenched in America's social fabric.

Human herpesviruses (HHV) cause a variety of clinically relevant conditions upon primary infection of typically young and immunocompetent hosts. Both primary infection and reactivation after latency can lead to more severe disease, such as encephalitis, congenital defects and cancer. Infections with HHV are also associated with cardiovascular and neurodegenerative disease. However, most of the associations are based on retrospective case-control analyses and well-powered prospective cohort studies are needed for assessing temporality and causality. To enable comprehensive investigations of HHV-related disease etiology in large prospective population-based cohort studies, we developed HHV Multiplex Serology. This methodology represents a low-cost, high-throughput technology that allows simultaneous measurement of specific antibodies against five HHV species: Herpes simplex viruses 1 and 2, Varicella zoster virus, Epstein-Barr virus, and Cytomegalovirus. The newly developed HHV species-specific (‘Monoplex’) assays were validated against established gold-standard reference assays. The specificity and sensitivity of the HHV species-specific Monoplex Serology assays ranged from 92.3% to 100.0% (median 97.4%) and 91.8% to 98.7% (median 96.6%), respectively. Concordance with reference assays was very high with kappa values ranging from 0.86 to 0.96 (median kappa 0.93). Multiplexing the Monoplex Serology assays resulted in no loss of performance and allows simultaneous detection of antibodies against the 5 HHV species in a high-throughput manner.

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Scattered evidence indicates that a lower basal body temperature may be associated with prolonged health span, yet few studies have directly evaluated this relationship. We examined cross-sectional and longitudinal associations between early morning oral temperature (95.0-98.6°F) and usual gait speed, endurance walk performance, fatigability, and grip strength in 762 non-frail men (52 %) and women aged 65-89 years participating in the Baltimore Longitudinal Study of Aging. Since excessive adiposity (body mass index ≥35 kg/m 2 or waist-to-height ratio ≥0.62) may alter temperature set point, associations were also examined within adiposity strata. Overall, controlling for age, race, sex, height, exercise, and adiposity, lower temperature was associated with faster gait speed, less time to walk 400 m quickly, and lower perceived exertion following 5-min of walking at 0.67 m/s (all p ≤ 0.02). In the nonadipose (N = 662), these associations were more robust (all p ≤ 0.006). Direction of association was reversed in the adipose (N = 100), but none attained significance (all p > 0.22). Over 2.2 years, basal temperature was not associated with functional change in the overall population or non-adipose. Among the adipose, lower baseline temperature was associated with greater decline in endurance walking performance (p = 0.006). In longitudinal analyses predicting future functional performance, low temperature in the non-adipose was associated with faster gait speed (p = 0.021) and less time to walk 400 m quickly (p = 0.003), whereas in the adipose, lower temperature was associated with slower gait speed (p = 0.05) and more time to walk 400 m (p = 0.008). In older adults, lower basal body temperature appears to be associated with healthy aging in the absence of excessive adiposity.

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