Salt and osteoporosis
Renal stones/osteoporosis
A high salt intake is a major cause of renal stones in humans. This is due to the effect salt has on urinary calcium excretion. Salt intake is the main determinant of urinary calcium excretion. The higher the urinary sodium excretion, the higher the urinary calcium excretion. Until recently, it was assumed that when salt intake was increased, the increase in calcium excretion was compensated for by an exact increase in intestinal calcium absorption. There is now evidence to suggest that this is incorrect and that there is a negative calcium balance which stimulates mechanisms not only to increase intestinal absorption of calcium, but to mobilise calcium from bone. A study in post-menopausal women showed that the loss of hip bone density over two years was related to the 24 hour urinary sodium excretion at entry to the study and was as strong as that relating to calcium intake at entry to the study (1) .
It was calculated that a modest reduction in salt intake from 10g to 5g would have the same effect on hip bone density as an increase in calcium intake of 1000mg, a difficult amount to achieve without resorting to supplements.
Diuretics, through a reduction in extra cellular volume, reduce calcium excretion leading to a positive calcium balance, increase bone density and reduce bone fractures. Salt reduction is likely to do the same but there are as yet no trials of salt reduction looking at a reduction in fractures.
References
(1)Devine A, Criddle R A, Dick I M, Kerr D A, Prince R L. A longitudinal study of the effect of sodium and calcium intakes on regional bone density in postmenopausal women. Am J Clin Nutr. 1995;62:740-5.