Among 296 community-dwelling Japanese adults (mean age 68.7), those in the highest quartile of 24-hour urinary sodium-to-potassium (Na/K) ratio faced 2.48-fold greater odds of deep white matter lesions (DWMLs) compared to the lowest quartile (OR 2.48; 95% CI 1.16–5.29). Crucially, the association was driven primarily by low potassium excretion rather than elevated sodium alone — urinary potassium was inversely associated with DWMLs while sodium excretion independently showed no significant effect.
DWMLs, detectable via MRI Fazekas scoring, represent cerebral small vessel disease and are established precursors to cognitive decline, dementia, and stroke. This finding aligns with a growing body of evidence implicating dietary potassium deficiency — not merely sodium excess — as a key vascular risk driver. Potassium's role in endothelial function, arterial stiffness, and blood pressure regulation offers a plausible mechanistic pathway to microangiopathy. Practically, the urinary Na/K ratio is a more actionable dietary target than sodium alone, attainable through increased fruit and vegetable consumption alongside reduced processed food intake.
Limitations are significant: this cross-sectional design cannot establish causality, the cohort is small and ethnically homogeneous, and confounding from unmeasured lifestyle variables remains possible. Single 24-hour urine collections also carry day-to-day variability. As an unreviewed preprint posted on medRxiv, these results await peer scrutiny and should be interpreted cautiously. Still, the potassium-specific signal is a meaningful, incremental contribution to brain aging research.
