The association between urinary sodium and the risk of dementia: Evidence from a population-based cohort study

Abstract

BackgroundSodium intake reduction is crucial for cardiovascular health, however, its lasting impact on dementia remains unclear. MethodsWe included 458,577 UK Biobank participants without dementia at baseline. We estimated 24-h urinary sodium (E24hUNa) using spot urinary parameters and obtained the incidence of all-cause dementia, Alzheimer's disease, and vascular dementia from multiple sources. ResultsThe mean E24hUNa was 3.0 g (1st-99th percentile: 1.5 g–5.1 g). Over a mean follow-up of 13.6 years, 7886 (1.7 %) participants developed all-cause dementia, including 3763 (0.8 %) Alzheimer's disease and 1851 (0.4 %) vascular dementia. In the restricted cubic spline model, we identify a potential cutoff of 3.13 g for E24hUNa, below which each 1 g decrease in E24hUNa was associated with 21 % (95 % confidence interval [CI] 1.11–1.34) higher all-cause dementia risk and 35 % (95 % CI 1.11–1.63) higher vascular dementia risk (P-value <0.001 for non-linearity). The hazard ratios were 1.15 (95 % CI, 1.07–1.24) for all-cause dementia and 1.21 (95 % CI 1.04–1.40) for vascular dementia among individuals with E24hUNa below 3.13 g compared to those with E24hUNa higher than 3.13 g. LimitationsOne of the major limitations is the estimation of 24-h urinary sodium with spot urine samples. ConclusionsAn E24hUNa level below 3.13 g, equivalent to 3.37 g daily sodium intake, is associated with increased risks of all-cause and vascular dementia. This exploratory study suggests a potential lower limit below which the risk of dementia increases with a lower sodium level. Future studies are necessary to validate our findings.