Diet is a major contributor to variation in the occurrence of hypertension and cardiovascular disease, including stroke, worldwide. Dietary salt intake plays a critical role in blood pressure regulation. However the question of whether high dietary salt intake increases risk of stroke, either indirectly via effects on blood pressure or directly via alternative mechanisms has received limited attention. Narrative review of evidence linking dietary salt intake with left ventricular hypertrophy and cardiovascular disease end-points. There is accumulating evidence that high salt intake predicts left ventricular hypertrophy, independent of other variables including body mass index and blood pressure. Data are now available from nine different studies worldwide consistent with a significant independent effect of salt intake on left ventricular hypertrophy. There is also evidence from animal experiments and ecological studies of an independent association between salt intake and risk of stroke. However, data from prospective observational studies on the relation between sodium intake and cardiovascular endpoints (including stroke) are sparse and inconsistent. Data from Alderman et al suggesting that there may be a significant inverse association between urinary sodium excretion and risk of cardiovascular disease has attracted controversy. In a number of prospective studies no association between salt intake and cardiovascular disease end-points (including stroke) has been observed. In a recent analysis from the US NHANES follow-up study, there was evidence that high salt intake is strongly and significantly associated with risk of stroke, other cardiovascular disease and all cause mortality in overweight persons, but not in those of normal weight. These findings need to be replicated. However, current data on the association between salt intake, blood pressure and left ventricular hypertrophy support public policy recommendations on the need for a moderate reduction in dietary salt intake at the population level.
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