Sodium intake and mortality

Abstract

Sir—Michael Alderman and colleagues (March 14, p 781) claim that sodium intake significantly and inversely relates to cardiovascular mortality. This claim is incorrect because the relation is not significant (table 3 p<0·086, 95% CI 0·77–1·02). Their second claim, that salt density (sodium/calories) is directly related to cardiovascular mortality, is correct (p<0·006). The contradictory nature of these findings accords with the unreliability of the method used by the National Health and Nutrition Examination Survey (NHANES I). It consisted of one 24 h recall of the food consumed, with no assessment or measurement of salt added during the cooking and at the table. In the 1970s when NHANES I was carried out, added salt accounted for around 50% of intake, so dietary calculation of sodium intake based only on the sodium content of food gave misleading results. It is about 25 years since those critical of the relation of salt to blood pressure were dismissive of conclusions based on such an inaccurate and haphazard way of assessing salt intake. Alderman and co-workers try to prop up their claim by stating that it agrees with previous findings of theirs in treated hypertensive patients, and that in “both studies baseline sodium intake was assessed”. This statement is not true. It suggests that the assessment of sodium intake in the two studies was the same. In Alderman’s previous study, however, the usual (baseline) sodium intake of the hypertensive individual was not measured. Instead, the investigators used the sodium content of a 24 h urine collected after 5 days of temporary salt restriction to stimulate renin to construct a reninsodium profile. Not to point this fact out, and to then claim that the hypertensive patients who consumed “the lowest salt diet had a fourfold greater likelihood of myocardial infarction than did those with a higher salt intake” was misleading. The term salt diet suggested that this was the hypertensives’ usual (baseline) intake of salt, when it was the salt intake on the fifth day of a temporary reduction. There is no evidence that urinary excretion of sodium after a temporary reduction in salt intake for 5 days bears any relation to the patients’ (usual) baseline intake. It will depend on the patient’s ability to follow instructions. This study in hypertensives is therefore irrelevant and does not contribute in any way to the relation between usual (baseline) salt intake and outcome. Alderman and colleagues also state that there is “convincing evidence of adverse effects of a low sodium diet on important physiological characteristics” Detailed reading of the papers does not support this assertion, indeed, one report they cite is outstandingly irrelevant. The results were based on a questionnaire answered by 11 150 people. Daily salt intake from salt in the food was calculated to be 8 g daily and another 8·6 g was calculated to be added either during cooking or at the table. Therefore, average daily salt intake was 16·6 g—a much higher salt intake than the average for the USA. A dietary assessment showed that a substantial number of participants consumed less than two-thirds of the recommended dietary intake of vitamin B6, calcium, magnesium, and iron. For some bizarre reason, the authors then proposed that, theoretically, these potential dietary deficiencies could have been produced by a low salt intake. It does not embellish Alderman and co-workers’ crusade against the worldwide recognition that the present consumption of salt should be reduced, to misrepresent previous work, make misleading statistical claims, and introduce other irrelevant material.