In their commentary (1) on our article (2), de Boer and Kestenbaum briefly summarized recent research on the relationship between salt intake (estimated from urinary sodium excretion) and cardiovascular disease (CVD). They cite a recent article by O'Donnell et al. (3) in which casual urine samples were used to characterize individual sodium intakes and an apparent J-shaped association was observed between sodium intake and CVD risk, de Boer and Kestenbaum state that "a very low intake of dietary sodium may truly increase the risk of CVD" (1, p. 1193); in contrast, an editorial (4) accompanying the article by O'Donnell et al. and subsequent publications (5-7) have highlighted methodological concerns about interpretation of the study findings. These include the use of a clinical trial population with established CVD or diabetes; high rates of medication usage among trial participants; use of a single casual urine sample to estimate individual sodium intake; inclusion of participants with sodium intakes at the bottom end of the distribution who appeared to be sicker than the rest of the study population (reverse causality); and use of data sets not specifically designed to address the sodium-CVD relationship.
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