This analysis, in part because of the large number of normotensive trials now published, does not support one of the goals of the Nutrition Labeling and Education Act (1990), that of lowering blood pressure in the normotensive population at large, and questions the wisdom of universal dietary sodium restriction without better evidence of the long-term benefits and safety of such an intervention.
"These results do not support a general recommendation to reduce sodium intake. Reduced sodium intake may be used as a supplementary treatment in hypertension. Further long-term studies of the effects of high reduction of sodium intake on blood pressure and metabolic variables may clarify the disagreements as to the role of reduced sodium intake, but ideally trials with hard end points such as morbidity and survival should end the controversy."
- Most people consume far more sodium than is necessary for survival.
- All studies of sodium consumption and reduction thereof are subject to severe methodological and logistical limitations.
- There are associations between sodium intake and blood pressure, and between blood pressure and clinical outcomes of interest.
- Reduction of sodium intake in patients with hypertension lowers blood pressure.
- None of this establishes a causal link between sodium intake or reduction thereof and clinical outcomes of interest other than hypertension in hypertensive persons.
Added 6/7/2013: See this NYT article about the recent IOM report on reducing sodium intake.
Added 2/10/15: The PURE study was published in the NEJM in August, 2014. I wrote this letter to the editor, which I thought had a high likelihood of publication, but alas it did not. Suffice it to say that the PURE study suffers from some of the same limitations described above:
Two important limitations could have profound implications for the interpretation of the PURE Investigators' results [1, 2]. Firstly, the use of a single urinary sodium measurement assumes that sodium balance is in a steady state at the time of measurement. This assumption may be false if a sodium retaining state such as heart failure is developing. This would lead to misclassification of a person with incident cardiovascular disease as having lower than actual sodium intake. Secondly, the urinary sodium surrogate ignores the substantial sodium lost in sweat (on the order of 1 gram sodium per liter sweat). This will lead to misclassification of lower sodium intake in those who exercise vigorously. If they also have low blood pressure and low mortality, it will be attributed to the spuriously low sodium excretion rather than vigorous exercise. The analysis included self-reported physical activity but perceptions of physical activity are known to be inaccurate and the temperature and humidity in which the activity takes place affect the amount of sweat and its sodium content [3, 4].Reference List1. Mente A, O'Donnell MJ, Rangarajan S, McQueen MJ, Poirier P, Wielgosz A, et al. Association of Urinary Sodium and Potassium Excretion with Blood Pressure. New England Journal of Medicine 2014; 371(7):601-611.2. O'Donnell M, Mente A, Rangarajan S, McQueen MJ, Wang X, Liu L, et al. Urinary Sodium and Potassium Excretion, Mortality, and Cardiovascular Events. New England Journal of Medicine 2014; 371(7):612-623.3. Bates G, Miller V. Sweat rate and sodium loss during work in the heat. Journal of Occupational Medicine and Toxicology 2008; 3(1):4.4. Canning KL, Brown RE, Jamnik VK, Salmon A, Ardern CI, Kuk JL. Individuals Underestimate Moderate and Vigorous Intensity Physical Activity. PLoS ONE 2014; 9(5):e97927.