Faculty Peer Reviewed
January 11, 2010: The New York City Department of Health and Mental Hygiene (DOHMH) announces proposed targets for the voluntary reduction of salt found in packaged and restaurant foods. The ultimate goal of this new policy is the reduction in cardiovascular events.
Studies have shown that Americans consume roughly twice the recommended limit of salt each day which can lead to hypertension, a major risk factor for coronary artery disease (CAD) and cerebrovascular accidents (CVA). Much of the time, though, this is not a matter of choice. In fact, data from the DOHMH shows that nearly 80% of sodium is added to foods before they are sold or prepared.  Given these astonishing numbers, the National Salt Reduction Initiative (NSRI) was created. The NSRI is a coalition of local and state health authorities and health organizations that is working to help food manufacturers and restaurants voluntarily reduce the amount of salt in their products. The ultimate goal is to reduce Americans’ salt intake by 20% over a five year period. These actions are estimated to save tens of thousands of lives each year and billions of dollars in health care costs. These actions have already been implemented in a number of fast food chains.
With governments setting lower targets for salt intake and food manufacturers working diligently to remove high sodium content from their packaging, a number of large research trials are underway to get a broader understanding of the true benefits and risks of this salt reduction.
July 6, 2011. A systematic Cochrane review by Taylor et al. published in the American Journal of Hypertension discussed how cutting salt consumption leads to slight reductions in systolic blood pressure; however, this does not equate to lower risk of heart disease or death.
The authors found seven studies (three in normotensives, two in hypertensives, one in a mixed population of normo- and hypertensives, and one in heart failure patients) that together included 6,257 participants with follow-up of six months or longer. The studies compared dietary salt reduction to no intervention in order to elucidate cardiovascular morbidity and mortality data. Salt reduction was associated with reductions in urinary salt excretion (a marker of salt intake) between 27 and 39 mmol/24hr and reductions in systolic blood pressure between 1 and 4 mm Hg. Results showed no strong evidence that salt reduction reduced all-cause mortality or CVD morbidity in baseline normotensives or hypertensives (normotensives RR- 0.90, 95% confidence interval (CI): 0.58–1.40, and hypertensives RR-0.96, CI: 0.83–1.11). A single randomized-controlled trial interestingly showed an increase in the risk of all-cause death in those with congestive heart failure receiving a low-sodium diet (RR-2.59, CI: 1.04–6.44).
Despite the fact that this meta-analysis as well as previous trials have found a benefit regarding BP, no one knows if this translates into better overall heart health in the population. A meta-analysis of 13 prospective studies with 177,000 participants reported that high salt intake was associated with a greater risk of stroke (RR-1.23, 95% CI: 1.06–1.43). However, there was no association between salt intake and all CVD events, and total mortality was not reported. In fact, the relationship between salt reduction and BP control is the primary basis for the assumed belief that restriction in dietary sodium intake will prevent BP-related CVD events. Although the Taylor study did show that salt reduction was beneficial in normotensive and hypertensive patients in terms of lowering BP, it found little effect on morbidity or mortality of CVD except when evaluating patients with systolic heart failure.
A recent study published in JAMA in May went even further than the Taylor review and proposed that modest reductions in salt intake may be associated with an increased risk of CVD and death. This is a shocking claim that contradicts everything we have been taught in medical school and from the media.
This was an observational study that followed 3,681 middle-aged Europeans without known hypertension or CVD for an average of 7.9 years. The researchers assessed the participants’ sodium consumption at the study’s start via a 24hr urinary sodium excretion.
The authors found that the less sodium consumed, the more likely the study participants were to die of heart disease. For the lowest third of salt consumption, the death proportion was 4.1% (95% CI: 3.5-4.7). For the middle third, the proportion was 1.9% (1.5-2.3), and for the highest third, 0.8% (0.5-1.1%). While those eating the most salt had, on average, a slight increase in systolic blood pressure–a 1.71mm Hg increase for each 2.5-gram increase in sodium per day–they were no more likely to develop hypertension than those in the other groups.
This certainly challenges the advice of a majority of healthcare workers and public health agencies (i.e. NSRI), who have been preaching to consumers to drastically cut back on their sodium consumption. Can we take this one study and forget all we have been taught during the last 10 years? Before doing so, we need to take note of the key limitations of the study. First, this was an observational study. Observational studies can only be suggestive, not conclusive. Second, although the study quotes a sample size of 3,681, the conclusions about CVD are based solely on the 84 participants who died during the study and not the total population followed. Third, the average age of inclusion was relatively young (~40 years old) leading to a potential underestimation of the risk of excessive sodium intake. Fourth, the study consisted only of white Europeans making it hard to extrapolate the conclusions in such an ethnically diverse population such as NYC where other races might be more salt sensitive. Fifth, sodium intake was only determined for one 24-hour urine collection at the start of the study, which may be insufficient to characterize an individual’s habitual salt intake, and no calorie or other nutritional data were collected. As such, the conclusions should be interpreted in the context of these potential limitations.
Regardless of the limitations, controversies, and unanswered questions from these studies, the authors certainly opened up a can of worms. So what is left to investigate? Ultimately, should a low sodium diet, previously believed to reduce the risk of CVD, now be taken with a grain of salt?! I feel that further research, including randomized controlled trials, is definitely needed that can effectively answer this question. Until then, I will continue to urge all my patients, and myself, to limit the amount of salt on my next order of French fries.
Rachel Bond is a 3rd year resident at NYU Langone Medical Center
Peer reviewed by Ishmeal Bradley, MD, section editor, Clinical Correlations
Image courtesy of Wikimedia Commons
1. Cutting Salt, Improving Health. NYC Department of Health and Mental Hygiene. Retrieved: July 7, 2011 from http://www.nyc.gov/html/doh/html/cardio/cardio-salt-initiative.shtml
2. Taylor RS, Ashton KE, Moxham T, Hooper L, Ebrahim S. Reduced Dietary Salt for the Prevention of Cardiovascular Disease: A Meta-Analysis of Randomized Controlled Trials (Cochrane Review). The American Journal of Hypertension, advance online publication July 6, 2011. http://http://www.nature.com/ajh/journal/vaop/ncurrent/pdf/ajh2011115a.pdf
3. Strazzullo P, D’Elia L, Kandala NB, Cappuccio FP. Salt intake, stroke, and cardiovascular disease: meta-analysis of prospective studies. BMJ 2009; 339:b4567. http://www.bmj.com/content/339/bmj.b4567.full.pdf?sid=d6199964-f270-47e7-86da-73591c7120b2
4. Elliott P, Stamler J, Nichols R, Dyer AR, Stamler R, Kesteloot H, Marmot M. Intersalt revisited: further analyses of 24 hour sodium excretion and blood pressure within and across populations. Intersalt Cooperative Research Group. BMJ 1996; 312:1249–1253. http://www.bmj.com/content/312/7041/1249.full
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. Fatal and Nonfatal Outcomes, Incidence of Hypertension, and Blood Pressure Changes in Relation to Urinary Sodium Excretion. JAMA. 2011;305(17):1777-1785. http://jama.ama-assn.org/content/305/17/1777.full.pdf+html