Another what bites the dust? Another one of the shibboleths of “healthy living” that the nutritional establishment has been pounding us over our heads with for decades: the idea that salt is bad for us.
Now, in the wake of the three Woman’s Health Initiative studies showing that fat doesn’t seem to cause heart disease nor cancers or the breast or colon, comes a study from the venerable NHANES II data showing that not only does salt intake (or to be more precise, sodium intake) not cause premature death from heart disease it actually seems to protect against it. And consuming more sodium appears to protect against premature deaths from not just heart disease but from all other causes as well. It’s been a bad couple of weeks for the holier-than-thou crowd.
In the current issue of The American Journal of Medicine is a study filled with much interesting information that gives a peephole into the way the pinheads in the government issue edicts that affect the health of all those ignorant enough to abide by them. This study shows that the subjects who consumed the least sodium in the late 1970s had greater rates of death from cardiovascular disease and from all other causes than those who consumed more sodium. Before we delve into all that, however, let’s look at what the paper shows about how government works.
The US Department of Health and Human Services and the US Department of Agriculture 2005 nutritional guidelines (click here to read in full in a large pdf download) recommend that Americans consume less than 2300 mg of sodium per day (which is less than the 2400 mg recommended in the 2000 guidelines) in order to “prevent or delay the onset of high blood pressure..” and “to lower elevated blood pressure” Seems rationale enough until one considers that there is really no good evidence that sodium intake causes blood pressure to increase other than that shown in short-term clinical trials, a number of which are inconclusive or contradictory. It’s just like with the idea of low-fat: somewhere, sometime, someone got it into his or her head that dietary sodium is bad, the word spread, and researchers start doing studies to prove it. As long as a study here or there confirms this bias, then the idea is held in the minds of many people not simply as an hypothesis, but as a truth. In the case of the nutritional guidelines, the scientific committee making recommendations did so
largely based on the blood pressure reduction associated with lower sodium in short-term clinical trials. However, these trials could not assess the long-term cardiovascular morbidity and mortality consequences of lower sodium. Of concern is that lower sodium intake can generate increased activity of the renin-angiotensin and sympathetic nervous systems, and possibly increased insulin resistance, and each of these could have adverse cardiovascular effects. Morbidity and mortality outcomes will be influenced by unfavorable and favorable effects, as well as the unknown consequences of a diet altered to achieve lower sodium intake. In the absence of clinical trial data, several observational studies, with contradictory results, are available.
So, it’s not even really a case of unintended consequences. The scientific committee chose to overlook evidence clearly showing that there could easily be a downside to sodium restriction in favor of their built-in bias against salt. In fact, based on no good evidence they lowered the recommendation from that of the time before. Gives one a lot of faith in the nutritional guidelines, doesn’t it?
Basically here is how the study was done. Researchers used the data from NHANES II study (a large pdf of the NHANES II study can be downloaded by clicking here) to determine if sodium intake correlated with premature death. The NHANES II researchers interviewed and examined participants and collected data in 1976-1980. The nutrient intake data came from one 24 hour recall done by trained interviewers, which isn’t as good as a 3 or 4 day food diary, but is better that a food frequency questionnaire. The study was followed up by evaluating the mortality statistics as of December 31, 1992 to determine the numbers of deaths in the study subjects and their causes. As the researchers put it in reference to these study subjects without a hint of tongue in cheek:
Those not found to be deceased were assumed alive at that date.
Indeed. I wonder if there were another choice.
The researchers set the breakpoint of their data analysis at the 2300 mg of sodium recommended in the nutritional guidelines. After analyzing the nutritional and mortality data on this basis it turned out that those subjects who consumed less than 2300 mg of sodium per day had a 1.37 times increased risk (95% CI 1.03-1.81, P=.033) of dying from heart disease and a 1.28 times increased risk (95% CI 1.1-1.5, P=.003) of dying from all causes as compared to those who consumed more than 2300 mg of sodium per day.
As the authors of the study put it:
The principal finding in this representative sample of US adults is that sodium intake, measured as a continuous variable and adjusted for calories by each of three distinct methods, had a statistically significant and inverse association with CVD mortality, independent of known cardiovascular risk factors. Results were consistent for all-cause, CHD, and cerebrovascular-specific mortality, although these latter associations were not statistically significant. In addition, individuals reporting consumption of sodium consistent with the most recent US dietary guidelines of
Makes you glad you spent all that time watching your salt doesn’t it?
I have a little different take on the results of this study from a statistical standpoint. Harkening back to the long and complex post about confidence intervals a while back you might remember that the parenthetical expression after the risk ratio shows what the range is statistically with 95% confidence that it will actually fall in that range. In the case above for the cardiovascular mortality risk of 1.37 what those figures actually mean is that there is a 95% probability (not 100%) that the actual risk will fall into the range of 1.03 to 1.81. In other words we can say that with 95% confidence if you consume less than 2300 mg of sodium per day you have somewhere in the range of 1.03 to 1.81 times greater risk of dying prematurely from heart disease than if you consume more than 2300 mg of sodium per day.
Because of the 5% uncertainty (100% minus 95%) and the fact that it could just as easily be the 1.03 figure as the 1.81 figure for risk I don’t like to take these things as gospel unless the risk ratio is at least 2.0. But that’s just me. Others who are less statistically nit picky are more than happy to go with the lower risk ratios.
Based on my more statistically rigid interpretation of the data, I can conclude that at the very least it doesn’t make any difference how much sodium you consume. To me, that’s the take home message.
Oh, one other take home message: don’t believe scientific committees. In the discussion part of this paper the authors laid out a sampling of studies looking at sodium intake verses disease:
Eight previous observational studies examined clinical outcomes associated with sodium levels. Sodium intake was inversely and significantly associated with higher CVD mortality for the entire sample of NHANES I, with myocardial infarction among male participants in a prospective cohort study of treated hypertensives and with all-cause mortality in men in the Scottish Heart Study. By contrast, a statistically significant direct association of sodium with CVD and all-cause mortality was observed in a Finnish community sample, among the overweight subset of NHANES I, with CHD incidence among women in the Scottish study, and with stroke in a community sample in Japan. No statistically significant associations were reported either among Japanese-American men of the Honolulu Heart Study or in the MRFIT cohort.
All these studies were done and published long before the scientific committee made their recommendations for the nutritional guidelines and were inconsistent and inconclusive at best, so how could the recommendation to lower sodium even further be even contemplated much less done? Bias. Or its synonym prejudice.
Ambrose Bierce (one of my favorite writers) defined prejudice as:
A vagrant opinion without visible means of support.
Please pass the salt.
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Conventional Wisdom on Salt Questioned
ReplyDeleteA JAMA study calls into question the current dogma on limiting the population's salt intake and on salt's health effects. Initial reaction to the study, as reported in the New York Times, is skeptical.
Researchers followed a European cohort comprising roughly 3700 subjects without cardiovascular disease at baseline. All had 24-hour urine sodium excretion measured at enrollment.
After a median follow-up of almost 8 years, cardiovascular mortality was highest among participants in the lowest tertile of sodium excretion, and the inverse-association trend retained statistical significance after multivariable adjustment. Sodium excretion was not associated with all-cause mortality.
The incidence of hypertension did not rise with increasing tertiles of sodium excretion. Each 100-mmol increase in excretion was associated with a 1.7-mm Hg increase in systolic pressure, but diastolic pressure did not correlate with excretion.
The authors note that their findings "do not negate the blood pressure-lowering effects of a dietary salt reduction in hypertensive patients." Critics echo the authors' own list of their study's limitations, including the relative youthfulness of the cohort (averaging about age 40), and the inclusion of only white Europeans.
NHANES 2 -The American Journal of Medicine
ReplyDeleteVolume 119, Issue 3 , Pages 275.e7-275.e14, March 2006
Conclusion
The inverse association of sodium to CVD mortality seen here raises questions regarding the likelihood of a survival advantage accompanying a lower sodium diet. These findings highlight the need for further study of the relation of dietary sodium to mortality outcomes.
NOW
http://www.nytimes.com/2011/05/04/health/research/04salt.html
JAMA. 2011;305(17):1777-1785. doi: 10.1001/jama.2011.574
Conclusions In this population-based cohort, systolic blood pressure, but not diastolic pressure, changes over time aligned with change in sodium excretion, but this association did not translate into a higher risk of hypertension or CVD complications. Lower sodium excretion was associated with higher CVD mortality.
Medical evidence relating to salt is reviewed in this study of 462 research papers
DeleteJay Walker, Alastair David MacKenzie, Joel Dunning, Autumn 2007
This study addressed the question of whether restricting dietary salt intake would provide protection from adverse cardiovascular events or mortality. Using the 462 papers, of which 14 were identified as representing the best evidence on the subject, the review concluded that there was no conclusive proof of a link between salt and heart attacks and strokes due to the lack of adequately powered randomised trials or observational studies conducted with sufficient rigour.
i, I'm Dr. Henry Black. I'm a Clinical Professor of Internal Medicine at the New York University School of Medicine and Immediate Past President of the American Society of Hypertension. Some things simply never go away. After decades of research on the importance of sodium (ie, salt) and hypertension in public health, this issue doesn't ever seem to get buried the way I think it should be. If we take it back to the 1950s, there's a very interesting study that Lewis Dahl at Brookhaven conducted in a large audience. He asked a group of people, "How many of you put salt on your food before you even taste it?" The majority of people raised their hands. He then asked how many of them put salt on their food if it doesn't taste salty enough, and a large number of people did. Very few people never put salt on their food regardless of how it tasted. This was in the 1950s.
ReplyDeleteHe then helped develop rats that were salt-sensitive and salt-resistant. He repeated this experiment about 20 years later, maybe even a little bit later, and things shifted around. More people didn't put salt on food regardless of how it tasted, and very few people put it on no matter how it tasted before they tasted it. Yet, over the past decades, there have been numerous studies -- epidemiological in particular, but also clinical trials -- that have shown that populations that eat a lot of salt or segments of a population that eat a large amount of salt tended to have higher blood pressures. Epidemiologically, at least, they seemed to have more events -- stroke in particular, although rates of coronary disease were higher as well.
These data were considered so compelling that 32 countries in the world right now have started programs to reduce the amount of salt in food. If you're going to do that, you have to concentrate on processed food because approximately 75% of the sodium that we eat is put into the food during processing. Some people used to say that salt is what you put in food to make it taste good, just the way they used to say that about cholesterol -- you put cholesterol in food to make it taste good. There clearly is a problem in the amount of salt we take in and the ultimate outcomes.
This was challenged, this idea of the relationship between salt and blood pressure and outcomes, by Alderman and his colleagues in the 1980s. They measured the 24-hour urinary sodium excretion, which is the most accurate way to do it, one time. Of almost 2700 people, they found that those who had the lowest sodium intake, who reduced their salt down to 65 mmol of sodium per day, had the worst blood pressure and more unfavorable outcomes. They had a physiological explanation for this, because if you do an epidemiological study and you can't explain it pathobiologically, it may not matter. Their idea was that by lowering sodium intake, you raise plasma renin activity and activate the renin-angiotensin system, which could be harmful
That study was appropriately criticized because the people were instructed to reduce their salt intake for 4 or 5 days before they measured it, so it may not have been an accurate reflection. Furthermore, that same laboratory had shown years earlier that reducing your sodium to 65 mmol per day didn't really change what happened in the renin-angiotensin system axis; you had to go much lower than that before you really activated it. People didn't pay much attention to that study until this year, when a paper in JAMA [1] that came from Europe suggested very much the same thing. This was important enough to actually make the front page of the New York Times. They took 2 separate populations: one that was studied for genes and one that was studied for blood pressure. They started out with about 6000 or 8000 people, and by the time they got through excluding hypertensive patients, excluding people with pre-existing cardiovascular disease, and excluding people who didn't have complete 24-hour urines, they calculated that people who had the lowest tertile of sodium intake actually had worse outcomes. Not so with blood pressure, but the outcomes that they measured, which were few, seemed to suggest that the low-sodium intake was associated with bad outcomes. Remember that this is epidemiological, not a trial.
ReplyDeleteIf you look at that paper carefully and see how much it applies to the United States population or to the population in the rest of the world, there are a lot of things that turn out. First of all, these people began at about age 40 and were followed for 7 years, maybe a little longer for the first cohort, and they were all from Northern Belgium. The findings may not apply to people who we think are salt-sensitive, who are older people, and particularly the black population in the United States, who are the ones whose blood pressure rises the most when you feed them a high salt load.
Also, they did a lot of very elegant statistical manipulations, which one might call data dredging, to try to find an association that fit. They didn't find it on their initial hypothesis, only later on. They found it for this top tertile, but within these data are a lot of inconsistencies. There is not a clear finding. They did show that over time (they followed some people for as long as 13 years), the systolic blood pressure rose almost 2 mm Hg. Diastolic pressure didn't change much, but these people were coming from their 40s into their 50s, which is when we start seeing that diastolic pressure is not as important as systolic pressure. Biology actually tends to reduce it.
It's a very credible study, done the way it was. The principal investigator is a highly respected individual. However, we have to be very careful, not about what their findings are, but about how the public has been attracted to it and how the New York Times article could have been detrimental. The article itself is quite fair and it's quite balanced. It has quotes from Dr. Alderman as well as from Dr. Lawrence Appel, who has helped write some of the US guidelines and recommendations. However, the headline writers tell us that maybe we shouldn't reduce our salt. I would agree that if you were a young white individual who is healthy, that's probably okay. But if you're an older individual (and most older people are salt sensitive), or certainly an African American individual, that's not necessarily good advice.
The other problem with this is that we have to look at clinical trials. This was recently analyzed by a group in Germany that intended to do something I had never seen before. They took systematic reviews done by others (ie, large database analyses or large trial analyses). They pooled 4 of them that began in the 1980s and went through about 2003. They didn't actually repeat the work. They then looked at clinical trials from 2005-2010, found a few more to add, and then concluded, as I would have expected, that the more sodium intake you have, whether it's within as little as 4 weeks or up to a year, the higher your blood pressure.
ReplyDeleteThey said very clearly that with such a short follow-up, you're not going to be able to assess outcome differences. But it's clear that as blood pressure goes up, common sense would tell us that that's not necessarily a good thing. What about the harm? What's the harm in reducing your salt to the current recommendations in these 32 countries that now include the United States? In certain individuals, such as people in a hot climate who might lose a lot of salt through sweating, you have to be careful not to get dehydrated. People with salt-losing nephropathy, who are unusual, might have to be very careful about that. For the general population, this kind of advice is good advice. The calculations about how much money we would save, that's a little bit of a reach. But certainly, if we reduce the stroke rate, left ventricular hypertrophy, and proteinuria, all of which have been shown in these studies, we're likely to improve the public health and the harm is very little.
The campaigns to have food processing companies reduce the amount of salt, in my opinion, is a healthy thing to do. If your patients should ask you what they should do, I think you can tell them now. Thank you very much-References
Stolarz-Skrzypek K, Kuznwtsova T, Thijs L, et al. Fatal and nonfatal outcomes, incidence of hypertension, and BP changes in relation to urinary sodium excretion. JAMA. 2011;305:1777-1785.
Reductions in dietary salt are not followed by reductions in all-cause mortality or cardiovascular events, according to an updated Cochrane meta-analysis in the American Journal of Hypertension.
ReplyDeleteResearchers examined seven randomized, controlled trials encompassing some 6300 participants who either restricted salt intake or acted as controls. Studies included normotensives, hypertensives, mixed populations, and patients with heart failure.
Salt reduction was associated with a mean decrease in systolic blood pressure between 1 and 4 mm Hg. Rates of mortality and cardiovascular events were not significantly lowered among normotensives or hypertensives. Patients with heart failure showed an increased risk for all-cause mortality after salt restriction.
Although the authors say their findings are not inconsistent with "the belief that salt reduction is beneficial in normotensive and hypertensive people," they admit that their conclusions are hampered by the small amount of evidence. They call for rigorous research "capable of definitively demonstrating the [cardiovascular] benefit of dietary salt reduction."
[Editor's note: The American Journal of Hypertension has not yet posted this article online, although the embargo has passed. We've linked to the journal's advance online publication page, where the article should appear shortly.]
American Journal of Hypertension advance online publication page (Free)