Too much salt could mean to too little calcium, say researchers

High dietary intake of sodium could lead to depletion of calcium in the body, according to new research.

The study – published in the American Journal of Physiology – Renal Physiology – reveals that sodium and calcium extraction are regulated by the same cellular systems, meaning that when the body tries to excrete excess sodium from a high-salt-diet it also flushes calcium out.

"We asked a simple question with our research – could sodium and calcium absorption be linked?" explains Dr Todd Alexander, from the University of Alberta, Canada, who led the research. "And we discovered that they are." He says the findings provide ‘very real’ biological evidence that a relationship between sodium and calcium balance “is real and linked."

"When the body tries to get rid of sodium via the urine, our findings suggest the body also gets rid of calcium at the same time," he says. “This is significant because we are eating more and more sodium in our diets, which means our bodies are getting rid of more and more calcium. Our findings reinforce why it is important to have a low-sodium diet and why it is important to have lower sodium levels in processed foods."

The researchers warn that as calcium is excreted in urine it raises the risk of developing kidney stones while inadequate levels of calcium in the body can lead to an increased risk of osteoporosis.

Study details

The authors note that while it has been long known that the sodium–hydrogen exchanger 3 (NHE3) molecule was responsible for sodium absorption in the body, the discovery that it also plays a role in regulating calcium levels is new. "We found a molecule that seems to have two jobs – regulating the levels of both calcium and sodium in the body,” says Alexander.

In their research, the team worked with lab models that lacked the gene to code for the NHE3 receptor molecule. They found those animals with no NHE3 receptor had urine that contained high levels of calcium.

Alexander and his team add that because calcium was not absorbed and retained by the body, the bones of the lab animals became thin.

Source: American Journal of Physiology – Renal Physiology

Volume 302, Number 8, Pages F943-F956, doi: 10.​1152/​ajprenal.​00504.​2010

“The epithelial sodium/proton exchanger, NHE3, is necessary for renal and intestinal calcium (re)absorption”

Authors: Wanling Pan, Jelena Borovac, Zachary Spicer, Joost G. Hoenderop, René J. Bindels, et al