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Nighttime blood pressure (BP) and BP dipping (daytime–nighttime BP) are prognostic for cardiovascular disease. When compared with other racial/ethnic groups, Black Americans exhibit elevated nighttime BP and attenuated BP dipping. Neighborhood deprivation may contribute to disparities in cardiovascular health, but its effects on resting and ambulatory BP patterns in young adults are unclear. Therefore, we examined associations between neighborhood deprivation with resting and nighttime BP and BP dipping in young Black and White adults. We recruited 19 Black and 28 White participants (23 males/24 females, 21 ± 1 yr, body mass index: 26 ± 4 kg/m2) for 24-h ambulatory BP monitoring. We assessed resting BP, nighttime BP, and BP dipping (absolute dip and nighttime:daytime BP ratio). We used the area deprivation index (ADI) to assess average neighborhood deprivation during early and mid-childhood and adolescence. When compared with White participants, Black participants exhibited higher resting systolic and diastolic BP (Ps ≤ 0.029), nighttime systolic BP (114 ± 9 vs. 108 ± 9 mmHg, P = 0.049), diastolic BP (63 ± 8 vs. 57 ± 7 mmHg, P = 0.010), and attenuated absolute systolic BP dipping (12 ± 5 vs. 9 ± 7 mmHg, P = 0.050). Black participants experienced greater average ADI scores compared with White participants [110 (10) vs. 97 (22), P = 0.002], and select ADI scores correlated with resting BP and some ambulatory BP measures. Within each race, select ADI scores correlated with some BP measures for Black participants, but there were no ADI and BP correlations for White participants. In conclusion, our findings suggest that neighborhood deprivation may contribute to higher resting BP and impaired ambulatory BP patterns in young adults warranting further investigation in larger cohorts. NEW & NOTEWORTHY: We demonstrate that young Black adults exhibit higher resting blood pressure, nighttime blood pressure, and attenuated systolic blood pressure dipping compared with young White adults. Black adults were exposed to greater neighborhood deprivation, which demonstrated some associations with resting and ambulatory blood pressure. Our findings add to a growing body of literature indicating that neighborhood deprivation may contribute to increased blood pressure. [ABSTRACT FROM AUTHOR]

Several human studies have used the mitochondrial antioxidant MitoQ. Recent in vitro data indicating that MitoQ may induce nephrotoxicity caused concern regarding the safety of MitoQ on the kidneys, but the doses were supraphysiological. Therefore, we sought to determine whether acute MitoQ elicits changes in urinary biomarkers associated with tubular injury in healthy adults with our hypothesis being there would be no changes. Using a randomized crossover design, 32 healthy adults (16 females and 16 males, 29 ±11 yr old) consumed MitoQ (100-160 mg based on body mass) or placebo capsules. We obtained serum samples and a 4- to 6-h postcapsule consumption urine sample. We assessed creatinine clearance and urine kidney injury biomarkers including the chitinase 3-like-1 gene product YKL-40, kidney-injury marker-1, monocyte chemoattractant protein-1, epidermal growth factor, neutrophil gelatinase-associated lipocalin, interleukin-18, and uromodulin using multiplex assays. We used t tests, Wilcoxon tests, and Hotelling's T² to assess global differences in urinary kidney injury markers between conditions. Acute MitoQ supplementation did not influence urine flow rate (P = 0.086, rrb = 0.39), creatinine clearance (P = 0.085, rrb = 0.42), or urinary kidney injury markers (T²2,8 = 30.6, P = 0.121, univariate ps > 0.064). Using exploratory univariate analysis, MitoQ did not alter individual injury markers compared with placebo (e.g., placebo vs. MitoQ: YKL-40, 507 ±241 vs. 442 ±236 pg/min, P = 0.241; kidney injury molecule-1, 84.1 ±43.2 vs. 76.2 ±51.2 pg/min, P = 0.890; and neutrophil gelatinase-associated lipocalin, 10.8 ±10.1 vs. 9.83 ±8.06 ng/min, P = 0.609). In conclusion, although longer-term surveillance and data are needed in clinical populations, our findings suggest that acute high-dose MitoQ had no effect on urinary kidney injury markers in healthy adults. [ABSTRACT FROM AUTHOR]

Vitamin D is associated with sleep quality and duration, but it is unclear whether vitamin D status influences sleep variability. Therefore, we sought to determine whether vitamin D status was associated with sleep variability in healthy adults. We assessed objective sleep, including timing and duration standard deviation (SD) using the Philips Actiwatch Spectrum and subjective sleep quality using the Pittsburgh Sleep Quality Index (PSQI) in 130 adults. We measured plasma 25(OH)D concentration to assess vitamin D. We used one-way ANOVAs and Kruskal-Wallis tests to compare sleep in participants characterized as vitamin D deficient (<20 ng/mL), insufficient (21-29 ng/mL), and sufficient (>30ng/mL). We used covariate-adjusted linear regression to assess associations between vitamin D status and sleep metrics. We compared differences in "low" and "high" sleep variability based on vitamin D status using the Chi-squared test. There was an effect of vitamin D status on sleep timing SD (Kruskal-Wallis, P = 0.021) and sleep duration SD (Kruskal-Wallis, P < 0.001). There was an inverse association between vitamin D status with sleep duration SD (after covariate adjustment R 2  = 0.267, P < 0.001, deficient vs. sufficient P = 0.050, insufficient vs. sufficient P = 0.022). There was no effect of vitamin D status on objective sleep duration, efficiency, or PSQI scores ( P > 0.05). We did not observe differences in "low" and "high" sleep timing SD based on vitamin D status (χ 2 = 5.43, P = 0.066), but we did for sleep duration SD (χ 2 = 22.4, P < 0.001). Our data indicate that individuals with poor vitamin D status exhibit greater objective sleep variability. Clinical Trial Registry: https://www.clinicaltrials.gov/; Unique identifiers NCT04334135, NCT04244604, and NCT04576338. NEW & NOTEWORTHY Our findings reveal that individuals with lower circulating vitamin D concentrations experience greater sleep variability compared with those with higher circulating concentrations. This supports the growing body of evidence suggesting an important link between vitamin D status and sleep health.

Background: Ambulatory blood pressure ( BP ) monitoring measures nighttime BP and BP dipping, which are superior to in-clinic BP for predicting cardiovascular disease ( CVD ), the leading cause of death in America. Compared with other racial/ethnic groups, Black Americans exhibit elevated nighttime BP and attenuated BP dipping, including in young adulthood. Social determinants of health contribute to disparities in CVD risk, but the contribution of neighborhood deprivation on nighttime BP is unclear. Therefore, we examined associations between neighborhood deprivation with nighttime BP and BP dipping in young Black and White adults., Methods: We recruited 21 Black and 26 White participants (20 M/27 F, mean age: 21 years, body mass index: 25±4 kg/m 2 ) for 24-hour ambulatory BP monitoring. We assessed nighttime BP and BP dipping (nighttime:daytime BP ratio). The area deprivation index ( ADI ) was used to measure neighborhood deprivation. Associations between ADI and ambulatory BP were examined., Results: Black participants exhibited higher nighttime diastolic BP compared with White participants (63±8 mmHg vs 58±7 mmHg, p =0.003), and attenuated BP dipping ratios for both systolic (0.92±0.06 vs 0.86±0.05, p =0.001) and diastolic BP (0.86±0.09 vs 0.78±0.08, p =0.007). Black participants experienced greater neighborhood deprivation compared with White participants (ADI scores: 110±8 vs 97±21, p <0.001), and ADI was associated with attenuated systolic BP dipping (ρ=0.342, p =0.019)., Conclusions: Our findings suggest neighborhood deprivation may contribute to higher nighttime BP and attenuated BP dipping, which are prognostic of CVD, and more prevalent in Black adults. Targeted interventions to mitigate the effects of neighborhood deprivation may help to improve nighttime BP., Clinical Trial Registry: URL: https://www.clinicaltrials.gov; Unique identifier: NCT04576338., Competing Interests: Conflict of Interest: None