Salt
NACL PROTECTS AGAINST PREMATURE DEATH NHANES 2
"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."
Michael Eades MD
Conventional Wisdom on Salt Questioned
A 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
Volume 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
"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."
Michael Eades MD
Conventional Wisdom on Salt Questioned
A 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
Volume 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
posted by vanwash at 6:21 PM
2 Comments:
Am J Med. 2006 Mar;119(3):275.e7-14.
Sodium intake and mortality in the NHANES II follow-up study.
Cohen HW1, Hailpern SM, Fang J, Alderman MH.
Author information
Abstract
PURPOSE:
US Dietary Guidelines recommend a daily sodium intake <2300 mg, but evidence linking sodium intake to mortality outcomes is scant and inconsistent. To assess the association of sodium intake with cardiovascular disease (CVD) and all-cause mortality and the potential impact of dietary sodium intake <2300 mg, we examined data from the Second National Health and Nutrition Examination Survey (NHANES II).
METHODS:
Observational cohort study linking sodium, estimated by single 24-hour dietary recall and adjusted for calorie intake, in a community sample (n = 7154) representing 78.9 million non-institutionalized US adults (ages 30-74). Hazard ratios (HR) for CVD and all-cause mortality were calculated from multivariable adjusted Cox models accounting for the sampling design.
RESULTS:
Over mean 13.7 (range: 0.5-16.8) years follow-up, there were 1343 deaths (541 CVD). Sodium (adjusted for calories) and sodium/calorie ratio as continuous variables had independent inverse associations with CVD mortality (P = .03 and P = .008, respectively). Adjusted HR of CVD mortality for sodium <2300 mg was 1.37 (95% confidence interval [CI]: 1.03-1.81, P = .033), and 1.28 (95% CI: 1.10-1.50, P = .003) for all-cause mortality. Alternate sodium thresholds from 1900-2700 mg gave similar results. Results were consistent in the majority of subgroups examined, but no such associations were observed for those <55 years old, non-whites, or the obese.
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.
Compared With Usual Sodium Intake, Low- and Excessive-Sodium Diets Are Associated With Increased Mortality: A Meta-Analysis
Niels Graudal1, Gesche Jürgens2, Bo Baslund1 and Michael H. Alderman3
+ Author Affiliations
1 Department of Rheumatology IR4242, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
2 Department of Clinical Pharmacology, Bispebjerg University Hospital, Copenhagen Denmark.
3 Albert Einstein College of Medicine, New York.
Correspondence: Niels Graudal (graudal@dadlnet.dk).
Received August 26, 2013.
Accepted January 24, 2014.
Abstract
BACKGROUND The effect of sodium intake on population health remains controversial. The objective was to investigate the incidence of all-cause mortality (ACM) and cardiovascular disease events (CVDEs) in populations exposed to dietary intakes of low sodium (<115 mmol), usual sodium (low usual sodium: 115–165 mmol; high usual sodium: 166–215 mmol), and high sodium (>215 mmol).
METHODS The relationship between individual measures of dietary sodium intake vs. outcome in cohort studies and randomized controlled trials (RCTs) measured as hazard ratios (HRs) were integrated in meta-analyses.
RESULTS No RCTs in healthy population samples were identified. Data from 23 cohort studies and 2 follow-up studies of RCTs (n = 274,683) showed that the risks of ACM and CVDEs were decreased in usual sodium vs. low sodium intake (ACM: HR = 0.91, 95% confidence interval (CI) = 0.82–0.99; CVDEs: HR = 0.90, 95% CI = 0.82–0.99) and increased in high sodium vs. usual sodium intake (ACM: HR = 1.16, 95% CI = 1.03–1.30; CVDEs: HR = 1.12, 95% CI = 1.02–1.24). In population representative samples adjusted for multiple confounders, the HR for ACM was consistently decreased in usual sodium vs. low sodium intake (HR = 0.86; 95% CI = 0.81–0.92), but not increased in high sodium vs. usual sodium intake (HR = 1.04; 95% CI = 0.91–1.18). Within the usual sodium intake range, the number of events was stable (high usual sodium vs. low usual sodium: HR = 0.98; 95% CI = 0.92–1.03).
CONCLUSIONS Both low sodium intakes and high sodium intakes are associated with increased mortality, consistent with a U-shaped association between sodium intake and health outcomes.
Key words
blood pressure cardiovascular disease diet hypertension meta-analysis mortality salt sodium chloride stroke.
© American Journal of Hypertension, Ltd 2014. All rights reserved. For Permissions, please email: journals.permissions@oup.com
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