Melinda Wenner Moyer, a journalist at Scientific American, recently published a new article titled: It’s Time to End the War on Salt. I was anxious to read an article with such a dramatic headline (do I need to adjust my perspective?) as Melinda strikes me as progressive and current with articles such as this one that covers recent research suggesting we switch the hard focus off saturated fat and onto refined carbohydrates. After reading the article and digging deeper, however, I found that most of the article’s references didn’t support the conclusions, and in fact there are some glaring errors that sometimes completely misrepresent scientists and their research. As with most nutritional issues, there are many ambiguities and disagreements in the literature and you can find evidence to support whatever side you want. The salt research is especially difficult to navigate, as the debate has been intensively ongoing for decades. In my opinion, Moyer missed an opportunity to show the public what is still contentious, instead only looking to develop a one-sided piece to downplay the advice we have been told for years she thinks is wrong: to watch how much salt we eat. This post is not meant to get into extreme detail of the debate but to show what is incorrect about the article.
“This week a meta-analysis of seven studies involving a total of 6,250 subjects in the American Journal of Hypertension found no strong evidence that cutting salt intake reduces the risk for heart attacks, strokes or death in people with normal or high blood pressure.”
The paper (a Cochrane review) (1) however did not find that there is “no strong evidence,” but instead that there is insufficient data to draw conclusions based on the long-term (at least 6 months follow-up) human randomized controlled trials that salt directly effects cardiovascular endpoints, because there is not enough data on cardiovascular events to have sufficient statistical power. It did find small reductions in blood pressure: systolic and diastolic decreased by about 1 mmHg in normotensive subjects and by about 2-4 mmHg in hypertensives and those with heart failure. This may be significant at the population level, as discussed below.
Scott Gavura on Science Based Medicine wrote about the poor reporting on this research in SciAm as well as many other places.
Here is a direct quote from the paper:
“Our findings are consistent with the belief that salt reduction is beneficial in normotensive and hypertensive people. However, the methods of achieving salt reduction in the trials included in our review, and other systematic reviews, were relatively modest in their impact on sodium excretion and on blood pressure levels, generally required considerable efforts to implement and would not be expected to have major impacts on the burden of CVD.”
This brings up the inherent problems with evidence-based nutrition in that RCTs (in which Cochrane reviews generally only cover) are sometimes viewed as the only evidence in which decisions should be based on. Certainly they should have weight when applicable, but as much larger trials and a larger separation between salt intakes in subjects for years to decades (which we already know from current trials is difficult- motivation to reduce salt tapers with time), it would come at a considerable expense, and may be unethical considering the whole evidence-base. All evidence must be considered, and as Gavura points out, it tends to support salt reduction.
As he also found, even the lead author spoke out on the interpretations:
“Professor Rod Taylor, the lead researcher of the review, is ‘completely dismayed’ at the headlines that distort the message of his research published today. Having spoken to BBC Scotland, and to CASH, he clarified that the review looked at studies where people were advised to reduce salt intake compared to those who were not and found no differences, this is not because reduced salt doesn’t have an effect but because it’s hard to reduce salt intake for a long time. He stated that people should continue to strive to reduce their salt intake to reduce their blood pressure, but that dietary advice alone is not enough, calling for further government and industry action.”
Since this review is so new, there hasn’t been much time for scientists to respond yet, but this week He & MacGregor (well known in this area) published a comment in the Lancet (2). They criticized the wording of the Cochrane’s plain language summary and press release as well that led to so much misinterpretation. In a reanalysis of the data, they dropped 1 of the 7 trials (disagree on its inclusion) and combined the normotensive and hypertensive data together to gain more statistical power. They conclude:
“Our results show that there is now a significant reduction in cardiovascular events by 20% (p<0.05) and a non-significant reduction in all-cause mortality (5-7%), despite the small reduction in salt intake of 2.0-2.3 g per day.”
Moyer does not seem to recognize that this is a Cochrane review that updates a previous one, as she doesn’t identify it as such and later in her article writes about the older one:
“In 2004 the Cochrane Collaboration, an international, independent, not-for-profit health care research organization funded in part by the U.S. Department of Health and Human Services, published a review of 11 salt-reduction trials. Over the long-term, low-salt diets, compared to normal diets, decreased systolic blood pressure (the top number in the blood pressure ratio) in healthy people by 1.1 millimeters of mercury (mmHg) and diastolic blood pressure (the bottom number) by 0.6 mmHg. That is like going from 120/80 to 119/79. The review concluded that “intensive interventions, unsuited to primary care or population prevention programs, provide only minimal reductions in blood pressure during long-term trials.”
2 of the authors from the new review were involved in this one (in fact 5 of the trials included here were included in the newest review). It analyzed 11 (3) (again randomized, controlled) trials (followup of each at least 26 weeks), of 3,514 subjects; the earlier attempt to determine if dietary salt interventions reduced cardiovascular endpoints. There was insufficient data to conclude anything about the effect on mortality (only 17 deaths occurred), cardiovascular events, or quality of life. Systolic blood pressure, as Moyer reports was reduced by 1.1 mmHg, diastolic pressure by 0.6 mmHg, and urinary sodium excretion by 35.5 mmol/24 hours. However, some subgroups may benefit more than others:
“The data suggest that a low salt diet may help people on anti-hypertensives to stop their medication without losing blood pressure control. The data from TONE suggest that for every 7 patients assigned a goal of achieving a sodium intake of less than 80 mmol/day, one would remain off antihypertensive medication witha BP less than 150/90 mmHg and with no adverse cardiovascular events.”
Not that a 1.1 mmHg reduction is insignificant, either:
“The resulting falls of 1.1 mmHg systolic and 0.6 mmHg in diastolic blood pressure may be useful at a population level; however the intensify of intervention applied to individuals required to achieve this is not realistic for community control of high blood pressure, which would need to be through changes in food production and catering practices.”
To quote the newest review:
“Sustained long-term reductions of BP of 1 and 4 mm Hg would be predicted to reduce CVD mortality by 5% and 20%, respectively.”
The true issue isn’t that salt reduction doesn’t decrease blood pressure, it is that the degree of salt reduction in trials tends to decrease as subjects lose motivation. The 2004 review lists 6 previous systematic reviews that include shorter-term trials that collectively lead to reductions in systolic blood pressure of about 4 mmHg (which might reduce CVD mortality by 20%) and diastolic of about 2 mmHg. So it cannot be dismissed on the basis of this research that salt reduction could be beneficial. Considering that about 75% of the salt we consume is that added from food manufacturers, I completely agree with the authors’ conclusions that “changes in food production and catering practices” should be the priority, more so than the individual. But that means the “war on salt” should not be over.
Moyer then writes:
“A 2003 Cochrane review of 57 shorter-term trials similarly concluded that “there is little evidence for long-term benefit from reducing salt intake.”"
She draws this quote from the ‘Plain Language Summary’ section of the review (4). The full passage is: “However, a pair of Cochrane reviews has found that there is little evidence for long-term benefit from reducing salt intake. This review looked at mostly short-term strategies to reduce salt intake. The other review (Hooper 2003) looked at long-term strategies to reduce the amount of salt in foods and drinks.” As in the 2011 Cochrane plain language summary, this one is worded oddly. This (“57 trial”) review was not on long-term trials, thus the quote Moyer used seems to summarize the Cochrane review she already wrote about, not this one! And clearly the “little evidence” doesn’t mean the evidence suggests that it doesn’t help, it is that there is insufficient evidence from RCTs in humans on endpoints other than blood pressure. So that is an inappropriate summary of this review, but she also got the description wrong that it is a review of “57 shorter-term trials.” The review had 57 shorter-term trials in normotensive subjects (average intervention time of 8 days), and 58 from subjects with elevated blood pressure (average intervention of 28 days).
She conveniently leaves out this passage which was also in the Plain Language Summary: “for people with high blood pressure low salt diet caused a larger reduction in blood pressure, and would be useful as part of a program to reduce blood pressure.” Considering about 30% of Americans have hypertension, I would consider this relevant. In these trials, the average blood pressure reduction was 4.18 for systolic and 1.89 for diastolic. From the normotensive trials, the average reduction of systolic pressure was 1.27 mmHg and diastolic 0.54 mmHg. These are still relevant at the population level (and likely at the individual level for those of us with elevated blood pressure).
Of course this review also concluded that there isn’t sufficient RCT data to determine if salt reduction reduces deaths and cardiovascular events.
Moyer should put emphasis on the fact that Cochrane reviews often only cover human RCTs and this is not the full evidence-base.
Now to rewind a bit to the second reference she made:
“In May European researchers publishing in the Journal of the American Medical Association reported that the less sodium that study subjects excreted in their urine—an excellent measure of prior consumption—the greater their risk was of dying from heart disease.”
This one received (5) considerable media attention when it was published as well, but the response was one of skepticism as Harvard simultaneously published a report calling it flawed based on a number of limitations in the methodology, in which Willett is quoted. If there are reasons why Moyer thinks these limitations are not necessary to discuss, I would have liked to see them brought up.
After this, she gives a short historical perspective:
“Fears over salt first surfaced more than a century ago. In 1904 French doctors reported that six of their subjects who had high blood pressure—a known risk factor for heart disease—were salt fiends. Worries escalated in the 1970s when Brookhaven National Laboratory’s Lewis Dahl claimed that he had “unequivocal” evidence that salt causes hypertension: he induced high blood pressure in rats by feeding them the human equivalent of 500 grams of sodium a day. (Today the average American consumes 3.4 grams of sodium, or 8.5 grams of salt, a day.)”
“Furthermore, the evidence is unequivocal that, as the amount of salt ingested daily is increased, both incidence and severity of the hypertension will be increased.”
This passage is clearly under the heading “Experimental hypertension,” (animal) and the “Human hypertension” heading is directly below. He is NOT claiming that the relationship between salt and hypertension in humans is unequivocal.
In the second paper:
“The evidence that salt induces permanent and fatal hypertension is direct, quantitative, and unequivocal in the rat. Because the extensive evidence is circumstantial in man, it is therefore dismissed almost casually by some.”
And his conclusions are based on much more than inducing “high blood pressure in rats by feeding them the human equivalent of 500 grams of sodium a day,” as Moyer writes, but by over 20 years of research on over 32,000 rats (with varying doses of sodium) up to his 1972 paper. Animal studies are important to show consistent replication of nutrient-disease relationships. And he drew upon other evidence than just this.
“Dahl also discovered population trends that continue to be cited as strong evidence of a link between salt intake and high blood pressure. People living in countries with a high salt consumption—such as Japan—also tend to have high blood pressure and more strokes. But as a paper pointed out several years later in the American Journal of Hypertension, scientists had little luck finding such associations when they compared sodium intakes within populations, which suggested that genetics or other cultural factors might be the culprit.”
It doesn’t take long to find a paper from 1979 that suggested this is because of a high degree of intra-individual variability of sodium intake and proposed a statistical method around it. Why wasn’t this noted?
Moyer then uses the Intersalt study (6) to support her argument:
“Intersalt, a large study published in 1988, compared sodium intake with blood pressure in subjects from 52 international research centers and found no relationship between sodium intake and the prevalence of hypertension. In fact, the population that ate the most salt, about 14 grams a day, had a lower median blood pressure than the population that ate the least, about 7.2 grams a day.”
I am unsure how she came to the idea that it found no relationship between sodium intake and hypertension, because it is exactly the opposite of what it found. And those numbers (14 grams and 7.2 grams) are not in the original Intersalt paper.
It must be that Moyer came to her conclusion based on something from another paper- perhaps by Michael Alderman, who she quotes later in her article. In a point-counterpoint series in the International Journal of Epidemiology between Alderman and Jeremiah Stamler (a principal investigator of Intersalt) and Paul Elliott (a coordinator of Intersalt), Alderman writes about Intersalt:
“Analysis limited to those 48 cosmopolitan centres [where salt was freely accessible] revealed no association between sodium intake and blood pressure.”
Stamler and Elliott reply with the following:
“Correspondingly, Alderman’s discussion of INTERSALT findings is critically flawed, repeating his previously published incorrect assertions despite our written communications setting the record straight. Thus, he continues to claim that INTERSALT found no association between sodium and blood pressure when analyses were restricted to 48 population samples (excluding four low sodium population samples). In fact, the highly significant within-population association between urinary sodium excretion and SBP across all 52 population samples was virtually unchanged when the four low-sodium populations were excluded (N = 9343 instead of 10074), and the association between sodium excretion and upward slope of blood pressure with age found across 52 population samples persisted across 48 samples.”
Since this is one of the major studies in which the advice to reduce salt intake was first based on, Moyer should have devoted more time to dissecting it.
Moyer subsequently uses one of Alderman’s NHANES analyses (7) as support:
“Studies that have explored the direct relationship between salt and heart disease have not fared much better. Among them, a 2006 American Journal of Medicine study compared the reported daily sodium intakes of 78 million Americans to their risk of dying from heart disease over the course of 14 years. It found that the more sodium people ate, the less likely they were to die from heart disease.”
“Studies that have explored the direct relationship between salt and heart disease have not fared much better.” I have to wonder what this means; what were the previous studies supposedly exploring? Given the critical letters about using NHANES data (especially the fact that salt intake is estimated with a 24-hour dietary recall) in response to their first analysis (here, here, & here), these limitations should have been brought up.
Moyer follows with:
“And a 2007 study published in the European Journal of Epidemiology followed 1,500 older people for five years and found no association between urinary sodium levels and the risk of coronary vascular disease or death. “
Indeed, in this one they concluded (8) that
“Salt intake was not consistently related to CVD or mortality in our study. An explanation for the absence of a positive relationship, apart from regression dilution bias, may be the relatively narrow range of salt intake in the Netherlands and the lack of contrast in exposure within a single population.”
They did find a difference in the overweight subgroup:
“In overweight subjects, we did find a positive relationship between urinary sodium/potassium ratio and overall mortality (19% increase in risk per unit change in sodium/potassium ratio).”
Moyer takes an easy escape from diving deep into the salty waters by writing:
“For every study that suggests that salt is unhealthy, another does not.”
It isn’t about the quantity of studies on each side, it is about the quality and methodologies of each. But at least she finally acknowledges the research that does in fact suggest salt has a negative relationship with relevant cardiovascular surrogates, as up to then she cherry picked pieces of research that did not in fact support her summaries.
Moyer’s next 2 paragraphs emphasize the individual variability to salt consumption and highlighting a recent estimate in the NEJM (9) that 44,000 American lives could be saved per year with a 35% reduction in salt (even though blood pressure reduction is small), though she dismisses this as “conjecture” as “such estimates are not evidence.” And she writes more to support Alderman et al.’s contentions:
“And low-salt diets could have side effects: when salt intake is cut, the body responds by releasing renin and aldosterone, an enzyme and a hormone, respectively, that increase blood pressure.”
Though the view that this is significant in terms of disease (though I would suggest “maintains blood pressure” instead of “increases) is not shared by all scientists, as MacGregor and HE de Wardener take him to task on this in the aforementioned point-counterpoint series. It doesn’t change the fact that higher sodium intake on average increases blood pressure (which even Alderman concedes).
Giving more attention to Alderman, Moyer concludes with the following:
“Rather than create drastic salt policies based on conflicting data, Alderman and his colleague Hillel Cohen propose that the government sponsor a large, controlled clinical trial to see what happens to people who follow low-salt diets over time. Appel responds that such a trial “cannot and will not be done,” in part because it would be so expensive. But unless we have clear data, evangelical antisalt campaigns are not just based on shaky science; they are ultimately unfair. “A great number of promises are being made to the public with regard to this enormous benefit and lives saved,” Cohen says. But it is “based on wild extrapolations.”"
An RCT large enough to detect significant differences long-term would be enormously expensive and comes with huge risks- existing research shows how difficult it is to keep people on a low salt diet long-term. It would not answer the question of the significance of salt on morbidity and mortality if the differences between diets is too small. Evidence-based nutrition must come to terms with the fact that sometimes extrapolations must be made based on evidence other than huge RCTs.
It seems to me that the majority of salt researchers support reduction, with a few opponents suggesting otherwise. The opponents received nearly all of the support in this poorly researched article.
1. Rod S Taylor, Kate E Ashton, Tiffany Moxham, Lee Hooper, & Shah Ebrahim (2011). Reduced dietary salt for the prevention of cardiovascular disease
The Cochrane Library : 10.1002/14651858.CD009217
2. He, F., & MacGregor, G. (2011). Salt reduction lowers cardiovascular risk: meta-analysis of outcome trials The Lancet, 378 (9789), 380-382 DOI: 10.1016/S0140-6736(11)61174-4
3. Lee Hooper, Christopher Bartlett, George Davey Smith, & Shah Ebrahim (2004). Advice to reduce dietary salt for prevention of cardiovascular disease
Cochrane Database of Systematic Reviews DOI: 10.1002/14651858.CD003656.pub2
4. Gesche Jürgens, & Niels Albert Graudal (2004). Effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterols, and triglyceride Cochrane Database of Systematic Reviews DOI: 10.1002/14651858.CD004022.pub2
5. Stolarz-Skrzypek, K., Kuznetsova, T., Thijs, L., Tikhonoff, V., Seidlerova, J., Richart, T., Jin, Y., Olszanecka, A., Malyutina, S., Casiglia, E., Filipovsky, J., Kawecka-Jaszcz, K., Nikitin, Y., Staessen, J., & , . (2011). Fatal and Nonfatal Outcomes, Incidence of Hypertension, and Blood Pressure Changes in Relation to Urinary Sodium Excretion JAMA: The Journal of the American Medical Association, 305 (17), 1777-1785 DOI: 10.1001/jama.2011.574
6. Intersalt Cooperative Research Group (1988). Intersalt: an international study of electrolyte excretion and blood pressure. Results for 24 hour urinary sodium and potassium excretion. Intersalt Cooperative Research Group. BMJ, 297 (6644), 319-328 DOI: 10.1136/bmj.297.6644.319
7. COHEN, H., HAILPERN, S., FANG, J., & ALDERMAN, M. (2006). Sodium Intake and Mortality in the NHANES II Follow-up Study The American Journal of Medicine, 119 (3), 2147483647-2147483647 DOI: 10.1016/j.amjmed.2005.10.042
8. Geleijnse, J., Witteman, J., Stijnen, T., Kloos, M., Hofman, A., & Grobbee, D. (2007). Sodium and potassium intake and risk of cardiovascular events and all-cause mortality: the Rotterdam Study European Journal of Epidemiology, 22 (11), 763-770 DOI: 10.1007/s10654-007-9186-2
9. Bibbins-Domingo K, Chertow GM, Coxson PG, Moran A, Lightwood JM, Pletcher MJ, & Goldman L (2010). Projected effect of dietary salt reductions on future cardiovascular disease. The New England journal of medicine, 362 (7), 590-9 PMID: 20089957