May 3rd, 2011
Study Challenges Efforts to Lower Salt in the General Population
Larry Husten, PHD
A new study challenges the conventional wisdom that lowering salt intake in the general population will result in fewer cardiovascular events. In a paper in JAMA, Katarzyna Stolarz-Skrzypek and colleagues report the results of the study, in which they followed 3,681 European people without cardiovascular disease after measuring their blood pressure and urinary sodium excretion.
After adjusting for other variables, the researchers found that systolic (but not diastolic) blood pressure was independently correlated with sodium excretion, and that systolic blood pressure changed in accord with changes in sodium excretion. However, higher sodium excretion was not associated with more cardiovascular complications. In fact, the investigators reported “a weak but consistent inverse association between cardiovascular mortality and the 24-hour urinary sodium excretion at baseline.”
The authors note that most salt studies have measured salt intake, and no previous study has examined the “longitudinal association between changes in blood pressure on a continuous scale in relation to changes in 24-hour urinary sodium excretion.”
The authors conclude that their findings “refute the estimates of computer models of lives saved and health care costs reduced with lower salt intake. They do also not support the current recommendations of a generalized and indiscriminate reduction of salt intake at the population level. However, they do not negate the blood pressure−lowering effects of a dietary salt reduction in hypertensive patients.”
This concept has been evaluated in paired opposing articles ever since Lancet’s dual editorials about 12 years ago. It means we really don’t understand the role of renin vis-a-vis low salt excretion in the urine. The advantage of this study is that a measurement of the salt excretion in the urine is more accurate than an estimate of the salt consumed in a diet. There was also an interesting blog article published on the questionable value of a low salt diet by Dr. George Thomas at http://www.ghthomas.blogspot.com
There is a substantial movement against population-based sodium restriction, which includes many well-healed food manufacturers, reactionary believers, and a few scientists. Each of their arguments may have some merit, and most certainly this study needs larger replication with tightened limitations and simultaneous 24 hr K, Ca, ph, Mg, creat, together with scrupulous, verified, adherence to intakes and urine collection. On balance the preponderance of the evidence, from many venues, supports temperance in sodium intake. Until low sodium intakes are confirmed to raise deaths, changing practice is premature. Are we, like readers of newsmagazines, to flip every time one study disagrees with most of those known to be of substantial merit? This is not the place to go through the problems in this study, or the ones before with similar conclusions. But they are there.
Over 35% of Americans have hypertension, with more undiagnosed. Heart failure is one of the most frequent admission Dx to the hospital, an
d repeats, with the leading cause: excess salt intake in the diet. Pediatric obesity, hypertension, dyslipidemia is on the rise… is it prudent to allow them all 6000+mg daily, and train them to crave more through life. All of them will track their risk to adulthood unless changes are made in the interim–and that is spontaneously uncommon.
There is definitely a subgroup, particularly the elderly in the South, who stay low on fluids, bake in the hot sun by day, but burn their tibial skin in front of belly furnaces by night. When they are given potent diuretics and not monitored, they become dehydrated. Lower their salt intake and there is trouble. This population is fortunately not large, and is becomming less common.
In summary, there are more patients with CHD, HF, HTN, diabetes, liver,
kidney disease diagnosed, and others with pediatric and pre-clinical syndromes in adults that would benefit from sodium intake in physiological ranges. It is also well known that potassium, commonly deficient in Americans (average intake 2000 less than the IOM recommendation of 4700mg, when in reality more like 7000 is proper, since it should match calories and sodium consume, offsets many molecular and physiological effects of sodium. Patients and doctors ideas about potassium contents of foods, consumption are extremely poor.
So while large RCTs are needed, they will not be done for the usual reasons. Meantime, the most successful diets–Mediterranean, Paleolithic, DASH, and those of the very long-lived peoples–all have a moderate salt intake. If it is not, they compensatory situations protect. This should be food for thought. Observations studies totally 800000 people do say something when RCTS are unavailable… EBM says use the best evidence available, not settle politically under pressure without them.
Most people just dont want to be bothered reading labels and they like the taste of salt in everything. It is not chic to say this, so studies take the place. Truth is, they dont want to change even when it limits their health. They want you to do it for them…
Richard Kones MD
can someone tell me how urinary excretion of Na is a more accurate reflection of salt intake? Couldn’t it just be that those who had lower urinary salt excretion had decreased ability to secrete urinay na, and that these people indeed would be more prone to salt retention from excess salt intake, and be more prone to HTN and CV complications thereof, and thereby prove both concepts simultaneously?
I am confused at the jump in conclusion….
The certainty is that Na intake equals Na excretion in a steady state. As we have no reservoir for Na or other disposal mechanism aside from sweating, the intake and output must be equal.
That said, it may be that this studies conclusions based on Na excretion are not accurate.
The kidney’s ability to excrete Na may be variable and determine the individuals consumption tendencies. Na intake beyond the individuals capacity to effectively excrete may be contribute to hypertension; however one individual may be able to consume large amounts of Na without consequence while another may not.
The Na story like most medical stories will never be told with RCTs. I think it is rational to suggest that hypertensive patients reduce their Na intake. I do not think that we have crossed the threshold of knowledge to tell everyone to limit Na intake.
Competing interests pertaining specifically to this post, comment, or both:
None
Enough evidence exists to make salt reduction strategies a best buy in the prevention of NCDs says a newly published WHO report:
http://www.who.int/nmh/publications/ncd_report_chapter4.pdf
“Priority actions for the non-communicable disease crisis”
R Beaglehole, R Bonita, R Horton, C Adams, et al.
The Lancet 2011; published online 6 April 2011 (open access)
http://bit.ly/hCplSF
Competing interests pertaining specifically to this post, comment, or both:
None
The implications of this paper are perplexing: a higher amount of sodium intake correlates with prevention of cardiac events, and that this level may be on the order of 2600 mg in a general population with a suboptimal potassium intake.
In some subpopulations following a Mediterranean diet, larger amounts of salt are consumed, but in these instances other variables, such as potassium intake, body weight, etc. are favorable, and it is plausable, though unproven, that these beneficial features may offset relatively higher Na intakes.
In the JAMA paper under consideration, it is postulated that low sodium intake activates the renin-angiotensin-aldosterone system, associated with a rise in insulin resistance.
Paleolithic man consumed 200-300 mg Na daily, along with about 7000 mg potassium. In contemporary hunter-gatherer societies who maintain this ratio, CVD is remarkably low. The reversal of this enormous dietary K to Na ratio is a recent event. Classically a physiological need of only about 500 mg is recognized.
Richard Kones