The efforts of the authors to examine the various methodologies to monitor salt intakes are appreciated. Two matters stand out. The first involves the dietary recall surveys. While these are acknowledged to have limitations for several well-known reasons (memory, perception issues, etc.), one of the most significant contributors to their lack of accuracy is seldom dealt with. This is the amount of waste - what people leave over in the plate. This has been estimated to be in the range of 25% of the food served, but is not uniformly treated in food surveys. Ignoring this naturally leads to an over-estimation of consumption.

The second, more important question is why so much time, resources and emphasis is placed on a nutrient (sodium) whose relationship to morbidity and mortality has been demonstrated to be benign?

The authors’ reference to a “salt advocacy community” is instructive. The 100+ year history of the salt/hypertension hypotheses has been characterized by an advocacy-driven approach. Major personalities driving the issue in the past include Allen (Allen FM. Arterial Hypertension. JAMA. 1920;74:653-653.), who avowed that if anyone with hypertension was not found experimentally to have elevated chloride levels (thought to be the crucial pressor at the time), then the laboratory analysis was wrong; Kempner of the fruit/rice diet fame, who admitted to whipping those patients who did not strictly follow his diet and attributed the drop in blood pressure to exclusively to low sodium while ignoring the high potassium intakes and accompanying weight loss; and Dahl, who observed elevated blood pressure in rats that were fed levels of salt approaching the LD50 of sodium chloride. In 1949, Chapman and Gibbons described much work on the salt/hypertension hypothesis to have “had influence out of all proportion to their intrinsic worth and are responsible for vast amounts of wasted research endeavor on the part of later investigators (Chapmann CP, Gibbons TB. The diet and hypertension. A review. Medicine. 1949;29:29-69.). Advocacy played a more significant role in advancing the saly/hypertension hypothesis than evidence did.

This historical tradition of actively advocating salt reduction as a means of population-wide control of hypertension continues until today. However, advocacy cannot take the place of actual evidence. In justifying the work of this publication, the authors refer only to those publications that support population-wide salt production, while totally ignoring every peer-reviewed publication that cautions against it. A few examples of these publications from the last two years include:

DiNicolantonio JJ, Di Pasquale P, Taylor RS, Hackam DG. Low sodium versus normal sodium diets in systolic heart failure: systematic review and meta-analysis. Heart (2012). doi:10.1136/heartjnl-2012-302337

Todd AS, MacGinley RJ, Schollum JBW, Williams SM, Sutherland WHJ, Mann JI, Walker RJ. Dietary sodium loading in normotensive healthy volunteers does not increase arterial vascular reactivity or blood pressure. Nephrology. (2012);17;249–256.

Alderman MH, Cohen HW. Dietary Sodium Intake and Cardiovascular Mortality: Controversy Resolved? American Journal of Hypertension. (2012); 25(7): 727-734.

Alexy U, Cheng G, Libuda L, Hilbig A, Kersting M. 24h-Sodium excretion and hydration status in children and adolescents – Results of the DONALD Study. Clinical Nutrition. (2012);31:78-84.

Maillot M. Drewnowski A. A Conflict Between Nutritionally Adequate Diets and Meeting the 2010 Dietary Guidelines for Sodium. Am J Prev Med. (2012);42(2):174 –179.

O'Donnell MJ, Yusuf S, Mente A, Gao P, Mann JF, Teo K, McQueen M, Sleight P, Sharma AM, Dans A, Probstfield J, Schmieder RE. Urinary sodium and potassium excretion and risk of cardiovascular events. JAMA. (2011);306(20):2229-38.

Graudal NA, Hubeck-Graudal T, Jurgens J. Effects of Low-Sodium Diet Vs High-Sodium Diet on Blood Pressure, Renin, Aldosterone, Catecholamines, Cholesterol and Triglyceride [Cochrane Review]. Am J Hypertension. (2012);25(1):1–15.

Stolarz-Skrzypek K, Kuznetsova T, Thijs L, et al. Fatal and Nonfatal Outcomes, Incidence of Hypertension, and Blood Pressure Changes in Relation to Urinary Sodium Excretion. JAMA. (2011);305(17):1777-85.

Taylor RS, Ashton KE, Moxham T, Hooper L, Ebrahim S. Reduced dietary salt for the prevention of cardiovascular disease. Cochrane Database of Systematic Reviews. May 2011. Issue 7.

Ekinci EI, Clarke S, Thomas MC, et al., Dietary Salt Intake and Mortality in Patients With Type 2 Diabetes. Diabetes Care. (2011);34:703-09 .

Thomas MC, Moran J, Forsblom C, et al; for the FinnDiane Study Group. The Association between Dietary Sodium Intake, ESRD, and All-Cause Mortality in Patients With Type 1 Diabetes. Diabetes Care. (2011);34(4):861-866. Epub 2011 Feb 9.

Although it may be consistent with activist advocacy, the selective picking of evidence is not consistent with good science. As we enter the second century of the salt/hypertension hypothesis, it may be far more beneficial to consumers if we adhere to the science and consign “advocacy” to the dustbin.