Sir—Hugh de Wardener and Graham MacGregor ignore the significant inverse association of sodium to all-cause mortality (p=0·0069) reported from NHANES 1 and note the borderline significance (p=0·086) of sodium to cardiovascular (CVD) mortality. The values we reported were for the full Cox model. In the best-fit model, in which variables with a p value greater than 0·10 were eliminated, sodium showed a highly significant inverse association with CVD mortality: the hazard ratio was 0·86 (95% CI 0·81—0·93); p<0·0001. Although common practice is to report the best-fit model, we conservatively chose to present the full model.
The independent associations, in opposite directions, of sodium and sodium/calorie to mortality, probably reflect different physiological events. On the basis of additional analyses, we can now report that the inverse sodium to mortality associations persisted within each sodium/calorie quartile.
de Wardener and MacGregor also note the imprecision with which table salt is estimated in NHANES 1. In multivariate analysis, the responses (always, sometimes, never) were not significantly associated with mortality, which probably reflects the small contribution of table salt compared with salt consumed within food. For discretionary salt to change the results of our study, it would be necessary for those reporting low table salt to have eaten a high sodium diet, which contradicts reports that individuals who have low-sodium diets also tend to use less table salt and vice versa.1
de Wardener and MacGregor repeat a previous, inaccurate, statement2
about baseline sodium in our study of hypertensives,3
which we have already answered at length.4
Briefly, patients were uniformly advised to maintain usual diet while avoiding high-sodium foods. Their sodium intake matched that seen in US Intersalt sites. Inaccurate assessments were likely to have been distributed throughout the population, resulting in an underestimation of the true magnitude of the observed inverse relation of sodium to events.
Karl Engelman comments on the unreliable estimation of sodium intake by dietary recall. We agree that NHANES 1 probably underestimated sodium. The real concern, however, is not that across-the-board under reporting occurred, but whether errors in reporting of sodium biased the observed relation. We used stratified and multivariate analyses to account for the possibility that sicker patients might have consumed less sodium and died sooner. The inverse relation of sodium to mortality held. We are now able to report two further analyses. Exclusion of 2161 participants who reported recent change in appetite or dietary alteration produced sodium to mortality results for the restricted group consistent with the whole. When we excluded 1926 participants who reported less than a 1000 kcal intake daily, the results were similar.
Heikki Karppanen and Eero Mervaala refer to ecological reports of communities with aggregate changes in several behaviours that have enjoyed a coincidental decline in mortality. Sodium intake was not measured in the studies cited, but referenced from different, serial cross-sectional studies. There were concurrent changes in dietary fat and other nutrients. Without direct linkage of various changes in the characteristics of individuals to their outcomes, it is mere speculation to attribute a decline in mortality to one of the many factors (sodium) that changed.