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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: (Published 10 January 2017) Cite this as: BMJ 2017;356:i6699

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Surrealistic fantasies on cost-effectiveness of decreased sodium intake

A computer generated model concluding that government regulated sodium reduction is projected to be highly cost-effective (1) is a variation of a previously published simulated model by the NutriCoDE group (2). Such studies based on statistical linking of uncoupled data can be considered as substitutes, which have been produced, because direct evidence of beneficial effects of sodium reduction does not exist (3, 4). Factually unsupported premises explain why the fabricated health benefit of the models (1, 2) are at odds with the genuine neutral or harmful outcomes of sodium reduction found in randomized controlled trials (RCTs) (5) and population studies (6, 7).

In a 3-year sodium reduction RCT the sodium intake regressed towards the baseline level during the course of the study (8). A recent meta-analysis revealed that very few intervention studies intending to reduce sodium intake in the general population were associated with a decrease in population consumption of salt, and on the average 25 such studies showed no effect (9). This meta-analysis did not include the only known population based RCT, which showed that exchange of sodium chloride with potassium rich salt was associated with a 5% lower sodium intake and no effect on BP (10). Despite attempts to bias the conclusions in favour of sodium reduction (8-10), these studies actually document that population based sodium reduction intervention programmes do not work.

A second premise in the computer model (1) is “the effect of sodium reduction on systolic blood pressure, including variation in this effect by age, race, and hypertensive status”. This premise was defined in the previous NutriCoDE group study (2), in which the literature search from a Cochrane review (11) to identify the studies to be included in a dose-response analysis of the association between the amount of sodium reduction and the blood pressure response was appropriately cited (2); however the selective use of a significant fraction of the Cochrane data (11) to advance the model was not justified or cited. This omission is emphasized in the present analysis (1), where the previous analysis (2) falsely is cited as the source of the data. The reported dose-response relationship between sodium reduction and blood pressure (3.8 mmHg/100 mmol sodium) (2) is overestimated because of a skewed distribution of hypertensive (65%) and normotensive study populations (35%) in the model, further amplified by using a no-constant function, i.e. by forcing the dose-response regression line through zero, a procedure which assumes no confounding and therefore is discouraged by the manual of the statistical software used to perform the analyses (12). The actual dose-response relationship when not forced through zero is 2.2 mmHg/100 mmol (13). Furthermore the separate effect on blood pressure in the normotensive fraction of the studies was 0 mmHg/100 mmol sodium, and therefore the premise of proportionality between sodium reduction and blood pressure does not exist in the vast majority of a population.

Documented adverse effects of sodium reduction (11, 14), which potentially could explain the increased mortality associated with low sodium intake observed in population studies (6, 7) were also excluded from the model. The authors acknowledge that “some prior observational studies suggest a J-shaped relation between sodium intake and cardiovascular disease” but state “this could be explained by potential biases of sodium assessment in observational studies”. To support this view the authors refer to a study, which after many statistical dodges claim a linear relationship between sodium intake and mortality below 2300 mg (15), although a few additional events in the group below 2300 mg due to wide confidence intervals would change the socalled linear relationship to a U-shaped relationship. However, results from a study of non-representative overweight prehypertensive and hypertensive individuals (15), does not justify exclusion from the model of representative observational data from healthy populations, which instead should have been included with appropriate reservations. Such reservations should also have been made for the population studies linking blood pressure with mortality that constitute a key component in the simulation model: ”In our model, we assumed a log-linear dose-response between blood pressure and cardiovascular disease until a systolic blood pressure level of 115 mm Hg”. Doing this the authors ignore that there is no dose-response relationship between sodium reduction and systolic blood pressure in the interval 115-140 mmHg, and that RCTs have documented that there is no effect of blood pressure reduction on health outcomes in normotensive individuals (16, 17).

Thus the facts ignored in this cost-effectiveness analysis are
1) No sodium reduction study in healthy individuals has been able to document a beneficial effect of sodium reduction on health outcomes.
2) Population based sodium reduction initiatives have been shown not to work.
3) Within the complete normal blood pressure range of the population there is no dose-response relationship between sodium reduction and blood pressure.
4) Sodium reduction has potentially harmful side-effects.
5) Population studies consistently show an association between health authority recommended sodium intake below 2300 mg and increased mortality.
6) In spite of the association between blood pressure and mortality in the population, blood pressure reduction in individuals with normal blood pressure has no beneficial health effects.

The potential salt intake range is 1-40g/day. Sodium conserving hormones and stress hormones increase exponentially below 6 g/ day. 95% of the worlds populations has a salt intake in the interval 6-12 g/day , i.e. a neurohormonally regulated salt intake in the low end of the possible range, just above the limit for side-effects. Therefore the idea that the majority of populations have a high salt intake is not rational. Consequently, questioning the present sodium reduction policy is relevant (18). Unfortunately health authorities use surrealistic results from simulated salt projections to forward the sodium reduction policy (19, 20). The potential cost-effectiveness of this procedure is waste of billions of dollars and loss of an undefined number of human lives.

1) 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.
2) Mozaffarian D, Fahimi S, Singh GM, et al. Global sodium consumption and death from cardiovascular causes. N Engl J Med 2014;37:624-634.
3) Graudal N. A Radical Sodium Reduction Policy Is Not Supported by Randomized Controlled Trials or Observational Studies: Grading the Evidence. Am J Hypertens 2016; 29:543-8.
4) Graudal N. Con: Reducing salt intake at the population level: is it really a public health priority? Nephrol Dial Transplant 2016; 31:1398-403.
5) Adler AJ, Taylor F, Martin N, Gottlieb S, Taylor RS, Ebrahim S. Reduced dietary salt for the prevention of cardiovasculardisease. Cochrane Database Syst Rev 2014 Dec 18;12: 2014;CD009217.
6) Graudal N, Jürgens G, Baslund B, Alderman MH. Compared with usual sodium intake, low- and excessive-sodium diets are associated with increased mortality: a meta-analysis. Am J Hypertens 2014;27:1129-1137.
7) Mente A, O'Donnell M, Rangarajan S et al. Associations of urinary sodium excretion with cardiovascular events in individuals with and without hypertension: a pooled analysis of data from four studies. Lancet 2016;388:465-75.
8) The Hypertension Prevention Trial: three-year effects of dietary changes on blood pressure. Hypertension Prevention Trial Research Group. Arch Intern Med. 1990;150:153-62.
9) 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.
10) Li N, Yan LL, Niu W et al. China Rural Health Initiative Sodium Reduction Study: the effects of community-based sodium reduction program on 24hr urinary sodium and blood pressure in rural China. AHA Scientific Sessions, Dallas, November 18, 2013. (28. okt 2016).
11) Graudal N, Hubeck-Graudal T, Jürgens G. Effects of Sodium Restriction on Blood Pressure, Renin, Aldosterone, Catecholamines, Cholesterols, and Triglyceride Cochrane Database of Systematic Reviews 2011, Issue CD004022.
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13) Graudal N. Dietary Sodium and Cardiovascular Disease Risk. N Engl J Med. 2016;375:2405-6.
14) Graudal NA, Hubeck-Graudal T, Jürgens G. Reduced Dietary Sodium Intake increases Heart Rate. A Meta-Analysis of 63 Randomized Controlled Trials Including 72 Study Populations. Front Physiol; 7:111.
15) Cook NR, Appel LJ, Whelton PK. Lower levels of sodium intake and reduced cardiovascular risk. Circulation. 2014;129:981-9
16) Brunström M, Carlberg B. Effect of antihypertensive treatment at different blood pressure levels in patients with diabetes mellitus: systematic review and meta-analyses. BMJ. 2016; 352: i717 mkjk
17) Lonn EM, Bosch J, López-Jaramillo P for the HOPE-3 Investigators. Blood-pressure lowering in intermediate-risk persons without cardiovascular disease. N Engl J Med 2016; 374: 2009–2020
18) Editorial: Evidence-based policy for salt reduction is needed. Lancet. 2016 30; 388 (10043):438.
19) Frieden TR. Sodium Reduction--Saving Lives by Putting Choice Into Consumers' Hands. JAMA 2016;316:579-80.
20) Sodium reduction. FDA website. Posted June 1, 2016.

Competing interests: No competing interests

22 January 2017
Niels Graudal
Senior consultant
Copenhagen University Hospital, Rigshospitalet
Blegdamsvej 9, DK 2100, Copenhagen, Denmark