Abstract
The controversial issue of the relationship between dietary NaCl (referred to as “salt” in this article) intake and health was framed nicely in the superb review by Prof Eberhard Ritz.1 When salt was not readily available, it was a relatively essential commodity, but in the modern world salt has become plentiful, and it is actually difficult to achieve a low salt intake without exerting a significant amount of effort.2 One of the effects of higher salt intake is increased blood pressure, which was clearly illustrated in chimpanzees fed with a diet containing 35 versus 120 mmol of sodium per day. In contrast, after providing a diet containing ≈248 mmol of sodium per day for 2 years, subsequent reduction in daily dietary salt intake to ≈126 mmol reduced blood pressure compared with animals that were continued on the increased salt diet.3 Other than affecting blood pressure, excess salt in the modern diet is increasingly recognized as an additional health risk, particularly for those individuals who demonstrate salt sensitivity, defined basically as an abnormal increase in blood pressure in response to increased salt intake. Japanese patients initially found to have salt-sensitive hypertension subsequently had a greater incidence of left ventricular hypertrophy and rate of nonfatal and fatal cardiovascular events compared with hypertensive patients who were not salt sensitive.4 Weinberger et al5 observed a similar trend in a cohort of patients in the United States, but another striking finding of this study was that salt-sensitive patients who were initially normotensive at the time of study had an impressive increase in mortality rate on follow-up evaluation compared with normotensive salt-resistant patients. These studies provide the impetus to understand the underlying mechanisms of salt sensitivity and to identify and perhaps quantify this cardiovascular risk factor in the population. Salt sensitivity …
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