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Letters |

Public Policy and Dietary Sodium Restriction

Nancy R. Cook, ScD; Frank Sacks, MD; Graham MacGregor, FRCP
JAMA. 2010;303(19):1916-1918. doi:10.1001/jama.2010.588.
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To the Editor: In his Commentary describing the effects of sodium on CVD, Dr Alderman1 suggested that the evidence is balanced, pro and con. However, we believe that this conclusion is based on poor-quality studies and errors in interpretation.

We believe that the studies by Alderman providing evidence of a protective effect of sodium on CVD (references 13, 15, and 16 in a review by Alderman,2 and reference 5 in the Commentary) contain serious methodological flaws. The workplace study (reference 13 of Alderman2) involved an unusual cohort of hypertensive patients temporarily taken off antihypertensive therapy. The patients were instructed to avoid high-salt foods prior to sodium excretion measurement, leading to distorted levels. The National Health and Nutrition Examination Survey (NHANES) studies showing a protective effect (references 15 and 16 of Alderman,2 and reference 5 in the Commentary) used a single 24-hour recall to assess sodium, an imprecise measure that biases to the null. They also failed to adjust for total energy intake; adjusted for blood pressure, which is in the causal pathway to CVD; and/or adjusted for table salt, part of total sodium intake.

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References

May 19, 2010
David A. McCarron, MD; Judith S. Stern, ScD; Niels Graudal, MD, DrMedSci
JAMA. 2010;303(19):1916-1918. doi:10.1001/jama.2010.587.
May 19, 2010
Michael H. Alderman, MD
JAMA. 2010;303(19):1916-1918. doi:10.1001/jama.2010.589.
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