One of the difficulties of drawing conclusions about the importance of dietary or other lifestyle changes in cardiovascular disease is the gap in the evidence that relates to mortality. One has to accept that outcome studies in the population are extremely difficult and there is unlikely to ever be outcome evidence on mortality for any dietary variable, e.g. saturated fat, fruit and vegetables or other lifestyle changes e.g. losing weight, or taking exercise. For instance, a study on salt would need to randomise subjects at the time of conception to a lower and higher salt intake and then follow up the two groups of offspring on a high and low salt intake for the rest of their lives. Such studies are impractical and would be unethical in the light of current knowledge.
Alderman has attempted to look at the effect of salt on outcome of cardiovascular disease. The first study was in hypertensives who had renin profiling performed prior to entering a study of long term follow up on blood pressure lowering drugs (1). In order to perform the renin profiling, all subjects had their salt intake restricted for five days to stimulate the release of the kidney hormone called renin. This enabled the subjects to be sub-grouped into low, normal or high renin groups. Alderman found that the 24 hour urinary sodium excretion on the fifth day of a reduced salt intake was related to subsequent myocardial infarction and made the extraordinary claim that a lower salt intake led to more heart attacks. However, no measurement of salt intake had been carried out on the subjects' normal diet. Furthermore, no attempt was made to monitor salt intake during the subsequent follow-up period. Analysis of the 24 hour urinary sodium data also revealed severe methodological problems as the lowest salt quartile had a much lower 24 hour urinary creatinine excretion. This demonstrated that many of those who had been attributed to the lowest salt quartile on the fifth day of a reduced salt intake were in this group not because they had been more successful in reducing their salt intake, but had collected incomplete 24 hour urine collections (2).
Alderman's second study involved the NHANES 1 - a dietary survey of US adults from the mid 1970s (3). However, any analysis of salt intake from this study is difficult to judge as 24 hour urinary sodium excretion was not measured and dietary salt was assessed by dietary history with no account taken of discretionary salt (i.e. salt added at the table or in cooking), which at this time would have accounted for more than half of the salt intake. Alderman claimed that salt intake was inversely related to cardiovascular disease. However, examination of the data showed major discrepancies, e.g. subjects in the lower salt intake were on a calorie intake that was near starvation levels compared to the higher salt group and yet the lower calorie group weighed 4 kgs more than those in the higher salt and calorie group.
A well conducted study from Finland using a random sample of the Finnish adult population showed that salt intake is related to increased cardiovascular mortality and total mortality. For a 6 gram increase in salt intake there were large increases in both coronary heart disease, cardiovascular disease and total mortality (4) (Fig 1).
Outcome trials of reducing salt intake or increasing fruit and vegetable consumption etc will never be carried out because of the number of individuals needed, the difficulty of maintaining differences in diet over a long period of time, and most importantly the ethics of feeding for instance one group of people a high salt intake compared to a group on a low salt intake. Public health decisions about changing our lifestyle or the food we eat have to be taken in the light of current knowledge.
Figure 1. The hazards ratios for coronary heart disease (CHD), cardiovascular disease (CVD), and all-cause mortality associated with a 6 g/day increase in salt intake as judged by 24 hour urinary sodium excretion. (Adapted from Ref. 4).
(1) Alderman M H, Madhavan S, Cohen H, Sealey J E, Laragh J H. Low urinary sodium is associated with greater risk of myocardial infarction among treated hypertensive men. Hypertension. 1995;25:1144-52.
(4) Tuomilehto J, Jousilahti P, Rastenyte D, Moltchanov V, Tanskanen A, Pietinen P, Nissinen A. Urinary sodium excretion and cardiovascular mortality in Finland: a prospective study. Lancet. 2001;357:848-51.