SY 09-2 SALT INTAKE: HOW MUCH SHOULD WE REDUCE?

Salt (sodium chloride) is the primary source of sodium in the diet. Sodium is an essential nutrient, required for normal human physiology. Excess sodium intake is a risk factor for hypertension and cardiovascular disease. Observational studies have reported a curvilinear increase in blood pressure with increasing sodium intake, more marked in people with high sodium intakes and hypertension. Interventional clinical trials have demonstrated the efficacy of reduced sodium intake on reducing blood pressure, although the interventions employed in these trials are not generalizable to most settings (intensive dietary counselling or feeding trials). Evidence from these blood pressure clinical trials forms the basis for recommending low sodium intake in the entire adult population (e.g., <2.0 g/day recommended by the WHO). Mean intake of sodium in a global population is estimated at 3.95 g/day (with regional variations), meaning that achieving current guideline recommended targets will require a dramatic reduction in mean sodium intake. The recommendation for low sodium intake in the entire population is based on the assumption that all reductions in sodium intake will translate into reductions in CVD, irrespective of baseline sodium intake and blood pressure levels. However, a number of recent prospective cohort studies have reported a J-shaped association between sodium intake and CVD/mortality, with an increased risk at sodium intakes below 2.6 g/day and above 5.0 g/day, and lowest risk associated with moderate sodium intake. Inconsistent findings from research studies has resulted in controversy regarding the optimal sodium intake range for cardiovascular health. While there is consensus on the cardiovascular benefits of reducing dietary sodium in populations with high sodium intake (>4-5 g/day of sodium), there is uncertainty about the health benefits (and feasibility) of targeting low sodium intake levels for CV prevention in the entire population. A major knowledge gap is the absence of large definitive randomised controlled trials, comparing the effect of low sodium intake to moderate intake on CVD and mortality.