The role of salt in the pathogenesis of hypertension has been fired in the crucible of fierce debate amidst claims of industrial collusion and statistical manipulation. However, careful consideration of the evidence does provide us with some facts. In a cross-sectional observational study across 48 centers around the world, sodium excretion was significantly related to the upward slope of blood pressure with age but not to median or prevalence of blood pressure. This association was weakened somewhat when body mass index and alcohol intake were considered, but a possible role for dietary sodium intake and the rise in blood pressure with age was reported. The authors also estimated that a 100 mmol/day lower sodium intake would reduce on average blood pressure by 2.2 mm Hg systolic and 0.1 mm Hg diastolic, and suggested important public health benefits might result. Indeed, trials of treatment for hypertension would lend support to this contention with substantial reductions in stroke and cardiac events to be anticipated.

However, the results of a recent Cochrane review which collated more event data than previous reports suggested there is still insufficient evidence to exclude clinically important effects of reduced dietary salt on mortality or cardiovascular mortality in normotensive or hypertensive populations. This view has been challenged because of the inclusion of a study in heart failure: when excluded, the findings are positive. But there are reports of a harmful effect of sodium reduction on patients with heart failure and diabetes. So is there merit in advocating a community-based reduction in salt intake?

Graudal and colleagues have now performed a study in collaboration with the Nordic Cochrane Centre to estimate the effects of low vs. high sodium intake on blood pressure, renin, aldosterone, catecholamines, and lipids. One hundred and sixty seven studies were included. The effects on blood pressure were heterogeneous: in normotensive Caucasians blood pressure fell 1.3/0.05 mm Hg, in blacks 4/2 mm Hg, and Asians 1.3/1.7 mm Hg. The fall in systolic pressure in blacks was significant. In hypertensives the falls were more impressive: Caucasians 5.5/2.8, Blacks 6.4/2.4 and Asians 10.2/2.6. There were predictable rises in plasma, renin, aldosterone, catecholamines, and lipids.

Given that every community is going to comprise a mixture of ethnic backgrounds, hypertensive individuals, and some with premorbid conditions such as diabetes and heart failure, what should we do? Certainly dietary sodium reduction will have a beneficial effect by lowering blood pressure in those with the established disease, but there will be a need for this reduction to be quite substantial. Then it is probable that the achieved falls would be sufficient to reduce hypertension-associated risk regardless of the effects on the serum levels of renin, aldosterone, and catecholamines—which will be seen with thiazide diuretic use anyway. The issue then is whether whole communities will benefit. For the 70% who are normotensive, an intensive and sustained dietary change must be undertaken with a modest predicted lowering of blood pressure dependent upon ethnicity, and the possibility of some being harmed. It could be argued that the age-associated rise in pressure will be ameliorated but this is unproved. And were it to be so, over-the-counter sales of very low-dose thiazide diuretics might be preferred for pharmacist-screened individuals. A concerted campaign to reduce obesity and alcohol intake may be more rewarding and less risky.

Source:AJH