A gene that is linked to both an individual’s craving for salt and blood pressure control has been identified by a team led by experts at the University of Southern Denmark.
Dr Thorbjorn Christensen and colleagues investigated the basis of appetite for salt by examining the activity of the Hsd11b2 gene in the brain.
They tested mice that had reduced Hsd11b2 function, and found no effects on basal blood pressure, electrolytes and circulating corticosteroids. However, when offered salt water to drink, these mice drank three times more than normal mice, and developed hypertension. Normal mice did not develop hypertension when fed the same amount of salt water.
The appetite for salt water among reduced Hsd11b2 mice could be inhibited by giving the drug spironolactone, used to treat fluid build-up.
Further tests showed that the salt sensitivity of reduced Hsd11b2 mice was not caused by impaired renal sodium excretion, the team explain in yesterday’s (29 March) issue of Circulation.
They conclude: "Reduced Hsd11b2 activity in the brain does not intrinsically cause hypertension but promotes a hunger for salt and a transition from salt-resistance to salt-sensitivity."
Co-author Dr Matthew Bailey, of Edinburgh University, UK, added: "We routinely eat much more salt than our bodies need. For most people this is bad for our heart, blood vessels and kidneys. Our study shows that we have a genetic drive to consume salty food. Understanding how this process works may help us reduce the amount of salt we eat and make it easier for people to follow low-salt diets."
The experts will now investigate whether the established drug dexamethasone, currently used to treat heart disease in some countries, could reduce salt cravings in heart failure patients.
Evans, L. C. et al. Conditional Deletion of Hsd11b2 in the Brain Causes Salt Appetite and Hypertension. Circulation 29 March 2016 doi: 10.1161/CIRCULATIONAHA.115.019341
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