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Summary: People with disrupted circadian rhythms, such as shift workers, have shown a higher risk of hypertension. However, it is unclear whether more subtle differences in diurnal rest–activity rhythms in the population are associated with hypertension. Clarifying the association between the rest–activity rhythm, a modifiable behavioural factor, and hypertension could provide insight into preventing hypertension and possibly cardiovascular diseases. In this study, we investigated the association between rest–activity rhythm characteristics and hypertension in a large representative sample of United States adults. Cross‐sectional data were obtained from the National Health and Nutrition Examination Survey 2011–2014 (N = 6726; mean [range] age 49 [20–79] years; 52% women). Five rest–activity rhythm parameters (i.e., pseudo F statistic, amplitude, mesor, amplitude:mesor ratio, and acrophase) were derived from 24‐h actigraphy data using the extended cosine model. We performed multiple logistic regression to assess the associations between the rest–activity rhythm parameters and hypertension. Subgroup analysis stratified by age, gender, race/ethnicity, body mass index and diabetes status was also conducted. A weakened overall rest–activity rhythm, characterised by a lower F statistic, was associated with higher odds of hypertension (odds ratio quintile 1 versus quintile 5 [OR Q1vs.Q5 ] 1.61, 95% confidence interval [CI] 1.26–2.05; p trend < 0.001). Similar results were found for lower amplitude (OR Q1vs.Q5 1.51, 95% CI 1.13–2.03; p trend = 0.01) and amplitude:mesor ratio (OR Q1vs.Q5 1.34, 95% CI 1.01–1.78; p trend = 0.03). The results were robust to the adjustment of confounders, individual behaviours including physical activity levels and sleep duration and appeared consistent across subgroups. Possible interaction between the rest–activity rhythm and body mass index was found. Our results support an association between weakened rest–activity rhythms and higher odds of hypertension. [ABSTRACT FROM AUTHOR]

Background: Systemic inflammation has been suggested to be associated with Alzheimer's-disease progression, although whether it is a cause or a downstream effect is still controversial. This study aims to assess the effect of systemic inflammatory regulators on Alzheimer's disease within a bidirectional Mendelian-randomization design.Methods: Genetic associations with Alzheimer's disease were obtained from the largest and most up-to-date genome-wide association study (GWAS) (cases and proxy cases: 71 880; controls: 383 378) and with inflammatory regulators from two recent GWASs on the human proteome and cytokines. Estimates were obtained by inverse-variance weighting with sensitivity analyses using MR-Egger, weighted median and MR-PRESSO. Possible bias due to selective survival and competing risk was also considered.Results: None of 41 systemic inflammatory regulators was associated with risk of Alzheimer's disease with consistent results in validation analysis. Conversely, Alzheimer's disease was suggestively associated with five systemic inflammatory regulators, i.e. basic fibroblast growth factor, granulocyte-colony-stimulating factor, interferon gamma, interleukin-13 and interleukin-7.Conclusion: The systemic inflammatory regulators considered did not appear to be associated with the risk of Alzheimer's disease. Conversely, specific systemic inflammatory regulators may be downstream effects of Alzheimer's disease or consequences of common factors causing both inflammation and Alzheimer's disease. [ABSTRACT FROM AUTHOR]