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Salt intake, cardiovascular disease and public health

We need to do more than take the salt shaker off the table

MJA 1997; 166: 396


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The contribution of dietary salt intake to cardiovascular morbidity and mortality is a subject of ongoing discussion and controversy.1,2 What is unquestionable is that the average salt intake of most people in most nations exceeds physiological requirements (10-20 mmol/day) by a factor of between five and 30, and this relatively high intake contributes significantly to the average blood pressure of a population, and hence to the prevalence of hypertension.3

The relationship between blood pressure levels and morbidity and mortality from heart attack and stroke suggests that any reduction in levels of salt intake in a population would result in a corresponding reduction in cardiovascular morbidity and mortality. For example, it has been argued that a mean reduction in sodium intake of 50 mmol per day across the whole population in the United Kingdom would reduce coronary death rates there by 16% and stroke death rates by 22%, and create substantial monetary savings from the reduced prevalence of these and related diseases.4

there is unlikely
to be much further progress in reducing Australians' salt intake unless more low-salt foods which are easily identifiable and affordable become available
Such epidemiological observations have led national and international health authorities to set targets for reductions in population salt consumption.5,6 The Australian Government has set a target sodium intake of 100 mmol per day to be achieved by the year 2000. It is reasonable to ask whether this target (or any other for salt intake) is justified on public health grounds and whether it is achievable. For such a target to be appropriate requires that it be both safe and cost effective in reducing cardiovascular morbidity and mortality .

Despite the consistent epidemiological data and experimental evidence, clinical trial data are limited. There are no randomised controlled trials of effects of varying sodium intake on cardiovascular outcome other than on blood pressure levels per se. However, there is experimental and limited clinical trial data suggesting that salt intake influences left ventricular mass independently of blood pressure,7 which is relevant in that left ventricular hypertrophy is itself a powerful predictor of cardiovascular morbidity and mortality.

Is a target of 100 mmol/day realistic in countries like Australia? In this issue of the Journal Beard et al. have attempted to measure salt intake in an Australian population sample in the light of our national target for the year 2000. Using 24-hour urine collections to estimate sodium excretion, they found that only 6% of men and 36% of women had reached the year 2000 target. As only 52% of the eligible population were studied and as there was underepresentation of younger people and lower socioeconomic groups, these figures are likely to underestimate the true levels of sodium intake and to overestimate the extent to which the target was reached.

Interestingly, among both men and women, and among both those who did and those who did not comply with the sodium intake target, most stated that they never or rarely added salt to food. This apparent anomaly may raise doubts about the reliability of the participants' reports, but is probably more readily explained by the poor reliability of a single 24-hour urine specimen for estimating usual sodium intake, and the high proportion of dietary salt hidden in food.8 The actual values for the percentage of the population complying with targets should perhaps be taken with "a pinch of salt", while the estimates of population average salt intake are in accord with other Australian data and those from countries (such as the United States) with similar dietary habits and are probably realistic.

If the target of less than 100 mmol/day is desirable for most of the population why are we so far from achieving it, and is it realistic? As Beard et al. point out, at least 75% of salt in the British diet and those of other affluent societies comes from processed foods.8 Given the proportion of participants in the study by Beard et al. who claim not to add salt to food or in cooking, the figure may be higher in Australia. Bread is a major source of dietary salt, along with canned foods and preserves. Take-away foods are more likely to be salted, and the growing habit of eating out leaves the consumer with less control over salt intake. The smaller body mass, and hence lower total food consumption, of women compared with men may at least partly explain their lower salt intake -- perhaps the target for sodium intake for women should be lower than that for men.

Beard et al. point out that there has been relatively little publicity about the national dietary target for salt and that, although some food manufacturers have taken initiatives to reduce salt use, shoppers receive relatively little advice or encouragement. The picture is perhaps not quite as bleak as it seems. The National Heart Foundation and State health departments have long been publicising the benefits of reducing salt intake as part of a more general healthy diet that includes eating more fresh fruit and vegetables and reducing saturated fat intake. These measures may have much greater value in cardiovascular health if adopted in combination with other lifestyle changes.9-11

However, there is unlikely to be much further progress in reducing Australians' salt intake unless more low-salt foods which are easily identifiable and affordable, as well as being economically viable for the food industry, become available. This will require more concerted efforts and cooperation between the food industry, government, consumers and food scientists. Novel approaches should be explored, such as the use of salt substitutes, which has resulted in long term blood pressure reduction in older patients with hypertension in Holland.12

Perhaps it is timely that the National Health and Medical Research Council consider a fresh approach to the problem that includes working with the food industry and food scientists to make it easier for consumers to reduce unnecessarily high and harmful levels of salt intake. A randomised controlled trial that showed that reducing salt intake decreased morbidity and mortality would undoubtedly dispel any lingering doubts on this issue and accelerate efforts. While purists might argue that such evidence should be as rigorously demanded of lifestyle changes as of new drugs or surgery, in the case of dietary salt we are in something of a "Catch-22" situation -- it is unlikely that an adequate trial could be mounted unless low salt foods were much more widely available than they are at present. However, a precedent for major public health initiatives in the absence of definitive clinical trial data has been set with the multitude of campaigns against cigarette smoking. The cumulative evidence for the benefits of moderating dietary salt intake is sufficient to justify more active public health initiatives now.

Lawrie J Beilin
Professor, Department of Medicine, University of Western Australia, Perth, WA

  1. Dyer AR, Stamler R, Elliot P, Stamler J. Dietary salt and blood pressure. Nature Med 1995; 1: 994-996.
  2. Wardener HL, Kaplan NM. On the assertion that a moderate restriction of sodium intake may have adverse health effects. Am J Hypertension 1993; 6: 810-814.
  3. Intersalt Cooperative Research Group. Intersalt: an international study of electrolyte excretion and blood pressure. Results of 24 hour urine sodium and potassium excretion. BMJ 1988; 297: 319-328.
  4. Law MR, Frost CD, Wald MJ. By how much does dietary salt lower blood pressure? III. Analysis of data from trials of salt reduction. BMJ 1991; 302: 819-823.
  5. National High Blood Pressure Education Program. National High Blood Pressure Education Program Working Group report on primary prevention of hypertension. Arch Intern Med 1993; 153: 186-208.
  6. Health Targets and Implementation (Health for All) Committee. Health for all Australians. Canberra: AGPS, 1988: 38.
  7. Langenfeld MRW, Schmeider RE. Salt and left ventricular hypertrophy: what are the links? J Hum Hypertens 1995; 9: 909-916.
  8. James WPT, Ralph A, Sanchez-Castillo CP. The dominance of salt in manufactured food in the sodium intake of affluent societies. Lancet 1987; 1: 426-429.
  9. Ascherio A, Rimm EB, Giovanucci EL, et al. A prospective study of nutritional factors and hypertension among US men. Circulation 1992; 86: 1475-1484.
  10. Beilin LJ. Non-pharmacological management of hypertension: optimal strategies for reducing cardiovascular risk. J Hypertens 1994; 12 Suppl 10: S71-S81.
  11. Jennings GL, Sudhir K. Initial therapy of primary hypertension. Med J Aust 1990; 152: 198-203.
  12. Geleeijnse JM, Witteman JCM, Bak AAA, et al. Reduction in blood pressure with a low sodium, high potassium, high magnesium salt in older subjects with mild to moderate hypertension. BMJ 1994; 309: 436-440.

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