Sodium balance is achieved within a matter of days and everything that enters should come out;
sodium stores are of questionable relevance and
sodium accumulation is accompanied by
weight gain. Careful balance studies oftentimes conflicted with this view, and long-term studies suggested that total body
sodium (TBNa) fluctuates independent of intake or
body weight. We recently performed the opposite experiment in that we fixed
sodium intake for weeks at three levels of
sodium intake and collected all urine made. We found weekly (circaseptan) patterns in
sodium excretion that were inversely related to
aldosterone and directly related to
cortisol. TBNa was not dependent on
sodium intake, but instead exhibited far longer (greater than or equal to monthly) infradian rhythms independent of extracellular water, body weight or blood pressure. To discern the mechanisms further, we delved into
sodium magnetic resonance imaging (Na-MRI) to identify
sodium storage clinically. We found that
sodium stores are greater in men than in women, increase with age and are higher in hypertensive than normotensive persons. We have suggestive evidence that these
sodium stores can be mobilized, also in dialysis patients. The observations are in accordance with our findings that immune cells regulate a hypertonic interface in the skin interstitium that could serve as a protective barrier. Returning to our balance studies, we found that due to biological variability in 24-h
sodium excretion, collecting urine for a day could not separate 12, 9 or 6 g/day
sodium intakes with the precision of tossing a coin. Every other daily urine sampling correctly classified a 3-g difference in
salt intake less than half the time, making the gold standard 24-h urine collection of little value in predicting
salt intake. We suggest that wobbles in expected outcomes can lead to novel clinical insights even with respect to banal
salt questions.