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Cost effectiveness of a government supported policy strategy to decrease sodium intake: global analysis across 183 nations

BMJ 2017; 356 doi: https://doi.org/10.1136/bmj.i6699 (Published 10 January 2017) Cite this as: BMJ 2017;356:i6699

Rapid Response:

Response to Alderman and Graudal

We thank Alderman and Graudal for their engagement with our study. The present response replies point by point to Graudal. Alderman was a reviewer of the original manuscript; we would direct interested readers to the peer review documents available in the ‘Peer review’ section above for point by point replies to his questions, which he also made during the review process. That said, his points are very similar to those of Graudal, so this reply also addresses the issues that he raises now.

Graudal makes three points, which we address in turn.

First, Graudal writes that “population based sodium reduction intervention programmes do not work.” To support this, he cites a meta-analysis (1) that, in fact, concluded, “Population-level interventions in government jurisdictions for dietary sodium reduction have the potential to result in population-wide reductions in salt intake from pre-intervention to post-intervention, particularly if they are multi-component (more than one intervention activity) and incorporate intervention activities of a structural nature (e.g. food product reformulation).” The programme we model in our paper (2) is multi-component and includes food product reformulation.

Other high-quality evidence exists to support the efficacy of these programmes. For example, an analysis (3) of the UK salt reduction programme just published (January 2017) by respected independent economists found that it resulted in a significant population-wide decrease in salt consumption.

Second, Graudal writes that “the reported dose-response relationship between sodium reduction and blood pressure… is overestimated” due to “a skewed distribution of hypertensive (65%) and normotensive study populations (35%) in the model, further amplified by using a no-constant function.”

Graudal’s assumptions about our statistical analyses for evaluating the effects of sodium reduction on blood pressure are incorrect. These analyses, which have been previously published, are detailed in (4). We evaluated multiple representative sets of RCTs of sodium reduction and blood pressure, accounted for differences in effects by hypertensive status as well as by age and race, and did include a constant in our meta-regression equation. We refer Gradual and other interested readers to that publication for the detailed methods: in particular, page 6 of the Supplementary Appendix, available online at (5).

Graudal also writes that “results from a study of non-representative overweight prehypertensive and hypertensive individuals does not justify exclusion from the model of representative observational data from healthy populations.” We would draw Graudal’s attention to the reasons we cite for distrusting the correlations in this observational data. The most important sources of bias include reverse causation (at-risk subjects, such as those with hypertension, actively lowering sodium); confounding by physical activity (given the very strong correlation between sodium and total energy intake, with r>0.8); confounding by frailty and other reasons for low total energy intake (given the very strong correlation between sodium and total energy intake); and incomplete 24-hour urine collections (sicker individuals proving less urine, artificially lowering their estimated sodium intake). Accordingly, in many studies and especially those in Western populations, participants with very low estimated sodium intakes (e.g., <2300 mg/d) represent a very small and relatively unique subset of the population. These limitations together could entirely explain the apparent “J-shape” seen in certain observational studies.

Third, Graudal writes that “documented adverse effects of sodium reduction… were also excluded from the model.” As summarised in our prior publications (4) as well as in the supplementary materials for the present paper, many national and international organizations have reviewed the evidence for the health effects of dietary sodium and, like us, concluded that there is no convincing evidence for any meaningful harms of modest sodium reduction. Consistent with this, the present investigation modelled a modest 10% population reduction over 10 years.

(1) McLaren L, Sumar N, Barberio AM et al. Population-level interventions in government jurisdictions for dietary sodium reduction. Cochrane Database Syst Rev 2016;9:CD010166.
(2) Webb M, Fahimi S, Singh GM, et al. Cost effectiveness of a government supported policy strategy to decrease sodium intake: global analysis across 183 nations. BMJ 2017; 356:i6699.
(3) Griffith, Rachel, Martin O'Connell, and Kate Smith. "The importance of product reformulation versus consumer choice in improving diet quality." Economica 84.333 (2017): 34-53.
(4) Mozaffarian D, Fahimi S, Singh GM, et al. Global sodium consumption and death from cardiovascular causes. N Engl J Med 2014;37:624-634.
(5) http://www.nejm.org/doi/suppl/10.1056/NEJMoa1304127/suppl_file/nejmoa130... Accessed February 10, 2017.

Competing interests: No competing interests

10 February 2017
Michael Webb
Doctoral candidate
Dariush Mozaffarian
Stanford University
Stanford University