Salt and BP have been linked for more than a century. Recent data indicate that, given free access to sodium, in most populations, intake is between 100 and 200 mmol/d, although individual variation is wide. There is good evidence that individual differences are influenced by genetics, environment, and behavior. There is also solid clinical trial data suggesting that substantial reduction in sodium intake (75 to 100 mmol/d) will, on average, lower diastolic pressure by approximately 1 mmHg and systolic by approximately 3 to 5 mmHg. In addition, there is good evidence that sodium restriction is accompanied by other hemodynamic and nonhemodynamic effects. The health effect of sodium restriction can be assessed only by outcome study in humans. The best available evidence in this regard derives from observational study. The several available studies in the general population are inconsistent and demonstrate heterogeneity across subgroups in the relation of sodium intake to cardiovascular morbidity and mortality. Only a single study has been reported in hypertensive patients that links baseline sodium, measured by 24-h urinary excretion, and subsequent cardiovascular outcomes. In that study, controlling for other risk factors, there was a significant, independent, inverse association of urinary sodium excretion and coronary morbidity and mortality. Indeed, an increase of 66 mmol/24 h was associated with a 36% reduction in events. Taken together, these data provide no support for the notion that either normotensive or hypertensive individuals should routinely decrease (or increase) dietary sodium intake.