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To the Editor: In examining the relationship of dietary sodium intake and health outcome, Dr He and colleagues1 have refined and extended our earlier analysis2 of the long-term mortality experience of the National Health and Nutrition Examination Survey (NHANES) participants. Their findings support our prediction that the nature of this relationship would be affected by other patient characteristics. Indeed, He et al now report that, in the obese minority of a subset of the entire NHANES population, increased sodium intake was associated with increased mortality. This was not true in the majority (72%) who were not obese.
There were meaningful differences in the methods of the 2 studies. In seeking to understand universal recommendations for sodium intake, we included all respondents with data on sodium and mortality in this national sample. By contrast, He et al arbitrarily excluded the 1470 (13%) participants reporting a low-salt diet or a history cardiovascular disease (CVD), limiting the generalizability of their results. We adhered to a standard definition of mortality due to CVD.3 Among the 1970 cardiovascular deaths we observed, there were 28 deaths (1%) ascribed to diseases of the pulmonary circulation and rheumatic heart disease. The arbitrary and unexplained definition applied by He et al would have excluded 374 (19%) of the available CVD deaths. The authors should explain why deaths from cardiac arrest, atherosclerosis, and unspecified CVD were excluded from their classification of CVD deaths.
Their multivariate models also differed in interaction terms and other covariates. Yet despite differences in methods, the important point is the similarity between the results of the 2 analyses. If one compares the whole NHANES cohort we examined with the 72% of the subset who were not obese examined by He et al, the confidence intervals (CIs) for the hazard ratio estimates overlap substantially. We reported a hazard ratio of sodium intake for mortality due to CVD of 0.89 (95% CI, 0.77-1.02) and for sodium-to-energy ratio of 1.13 (95% CI, 1.04-1.24). The corresponding values of He et al were 1.00 (95% CI, 0.84-1.19) and 1.02 (95% CI, 0.85-1.22). The data for all-cause mortality were similar.
Finally, He et al present a striking dissociation between results and conclusions. They focus on a smaller (28%) stratum of a subset and dismiss very different results in the larger (72%) stratum of the study among whom no association of dietary sodium and mortality was found. The authors conclude that a "reduced sodium intake may be especially efficacious in overweight persons." 1 In fact, a positive association of adverse sodium to outcome was observed only (not "especially") in overweight persons. He et al correctly claim to be the first to document a positive relationship between dietary sodium intake and CVD risk. However, an association in a minority stratum of a subset of 1 observational study hardly justifies universal sodium restriction.
We believe that the heterogeneity within the available data suggests that, in terms of dietary sodium, one size probably does not fit all. In short, there is no empirical basis for a single universal target for sodium intake.
Country-Specific Mortality and Growth Failure in Infancy and Yound Children and Association With Material Stature
Use interactive graphics and maps to view and sort country-specific infant and early dhildhood mortality and growth failure data and their association with maternal
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