Cost effectiveness of a government supported policy strategy to decrease sodium intake: global analysis across 183 nationsBMJ 2017; 356 doi: https://doi.org/10.1136/bmj.i6699 (Published 10 January 2017) Cite this as: BMJ 2017;356:i6699
All rapid responses
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
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. http://my.americanheart.org/idc/groups/ahamah-public/@wcm/@sop/@scon/documents/downloadable/ucm_458223.pdf (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.
12) Harbord RM, Higgins JPT. Meta-regression in Stata. The Stata Journal 2008; 8:493-519.
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. http://www.fda.gov/Food/IngredientsPackagingLabeling/FoodAdditivesIngred.... Posted June 1, 2016.
Competing interests: No competing interests
Re: Cost effectiveness of a government supported policy strategy to decrease sodium intake: global analysis across 183 nations
Webb et al have added a further dimension to their existing 2-step model linking sodium intake to health outcome. (1) Their basic hypothesis joins two independent associations – sodium to blood pressure, and blood pressure to health outcome, to predict morbidity and mortality benefits. To this, they have added a cost benefit analysis to predict what might result from worldwide sodium reduction They now further postulate that a “soft” government sponsored program involving mandatory reduction of the sodium content of processed food would yield enormous economic benefit. The mathematics seem convincing. However, advancing science has exposed the fragility of their longstanding assumptions.
The basic model assumes a linearity of sodium intake to blood pressure, and of blood pressure to cardiovascular mortality. In reality, a 1 gram reduction in sodium does not significantly reduce blood pressure in neither the 75% of the population that does not have hypertension, nor among those consuming less than 3 grams of sodium. (2) Moreover, new science has also established that there are multiple effects, beyond blood pressure, with deficient sodium associated with adverse physiological consequences. (3) Disappointingly, the impact of these scientific advances was not addressed in the manuscript.
The relation of sodium in 6 individual studies (as well as a meta-analysis of 21 studies involving nearly 70,000 participants) have found a “J” shaped association of sodium to all-cause and CVD mortality. Mortality is greater both when sodium intake is below 3.0g/d and/or above 5000 mg/d (4,5) The lowest mortality is experienced by those whose intake is between (2.8 and 5.0g/d). Mortality does not vary within that broad range. Ironically, the range associated with optimal health outcomes is virtually identical to the intakes of 90% of the world’s population. (6).
Sodium, is like all other essential nutrients, since deficient intake is incompatible with life, and excesses often carry their own risks. (4.5) Neither here, nor in previous reports, have the authors presented evidence that reduction of intake to <2.0g/d would be either safe or beneficial.
The current report further assumes that a particular government sponsored program can, over 10 years, produce a sustained reduction of 10% and a cost benefit ratio of 1.7. The 400mg fall achieved over 10 years would cost very little, and generate a net economic gain. Beyond the fact that there is no scientific evidence to establish a health effect of lowering sodium intake, there is also no evidence that this particular program would actually lower human sodium consumption. The available experience is hardly encouraging. Some 35 years of vigorous exhortation has failed to budge average US consumption. (7) More directly, a UK experiment designed to reduce sodium, similar to that proposed here, has failed to significantly decrease intake over 8 years. (8)
The authors have neither provided empiric support for their hypotheses, nor addressed their possible limitations.
Public health advances depend upon bold hypotheses that are validated. Absent rigorous experimentation, no matter the passion and persistence of its advocates, invalidated hypotheses should not guide public policy – particularly when it effects 90% of the population. Unlike horse racing, whose currency is the dollar, the value of Public Health is denominated in trust. The damage of a misguided program may therefore exceed any immediate harm, to threaten the entire Public Health endeavor.
1. BMJ 2017;356:i6699
2. Mente, A, O’Donnell M, et al. Association of Urinary Sodium and Potassium Excretion with Blood Pressure. NEJM 2014 :371;601.
3. Graudal N, Hubeck-Graudal T, Jürgens G. Effects of sodium restriction on blood pressure, renin, aldosterone, catecholamines, cholesterols, and triglyceride. Cochrane Database Syst Rev 2011; 11: CD004022
4. 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.
5. 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
6. McCarron DA, Kazaks AG, Geerling JC, Stern JS,Graudal NA. Normal range of human dietary sodium intake: a perspective based on 24-hour urinary sodium excretion worldwide. Am J Hypertens 2013; 26: 1218–23.
7. U Bernstein A M , Willett W C. Trends in 24-h urinary sodium excretion in the United States, 1957-2003 a systematic review Am J Clin Nutr 2010;92:1172-1180
8.www.gov.uk/government/uploads/system/uploads/attachment_data/file/213420.... Accessed June 20, 2016.
Competing interests: No competing interests
In recent years the increasing production of more and more processed food, rapid urbanization, and changing lifestyles are transforming dietary patterns in the world's population. Highly processed foods are increasing in availability and becoming more affordable. People around the world are consuming more energy-dense foods that are high in saturated fats, trans fats, sugars, and salt even in under developed and in developing countries. Salt is the primary source of sodium, and increased consumption of sodium is associated with hypertension and increased risk of heart disease and stroke and other non-communicable diseases.
In India, people consume more than 10.98 grams of salt per day, which is 120% more than the recommended limit of five grams per day of salt by the World Health Organization.
In Tamil Nadu, the average intake of salt per day is around 6.7 to 8.1 grams.
A higher in take of salt is associated with stroke, heart attack, migraine, cancer and renal disease.
So awareness is important about salt and health.
In India, to increase awareness and to control salt intake the Government should consider implementing a "national salt control program" at primary health care level.
At the international level, the World Health Organisation should adopt "World Salt Awareness Day" or "World Non-Communicable Diseases Day" every year on May 22. On that date only in 2004 the Fifty-seventh World Health Assembly recalled and recognised the importance of a "Global strategy for diet, physical activity and health".
Competing interests: No competing interests