Low Salt Diet Part Two
by Jeffrey Dach MD
This article is part two of a series, for part one, click here.
In Part One, we discussed the medical studies showing increased mortality from salt restriction. You may have been wondering about this if you saw a recent article in the New York Times by Jane Brody extolling the virtues of a low salt diet.(1)
Jan Brody quotes a computer simulation model that predicted 500,000 lives saved by restricting dietary salt in a program similar to the one started in Finland. This was described in a New England Journal article on salt and hypertension.(2,3)
Gary Schwitzer does a good job on his blog explaining where the Jane Brody article goes wrong.(4).
Research by Jan A. Staessen, MD, PhD, of the University of Leuven in Belgium and colleagues, raises questions regarding whether population-wide sodium restriction will actually lower cardiovascular risks. (5,6) In actually clinical studies where 24 hr sodium excretion is measured in 3681 participants and followed over 8 years, this is what they found:
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.(5,6)
This type of data seems to suggest that salt restriction has been over-hyped as an intervention, and although salt restriction does reduce blood pressure slightly, this intervention does not reduce mortality or complications of cardiovascular disease over the long term.
Junk Food Diets
I would agree with Jane Brody that hypertension, heart disease and other health problems are a direct result of diets containing large amounts of processed salt (NaCl), Trans Fats, Sugars, MSG, Aspartame, GMO corn and GMO Soy, and added wheat fillers. To focus attention on the salt content alone, while ignoring the other harmful additives may be not be a valid exercise.
A Central Dogma Of Mainstream Medicine
The “low salt diet” for reducing blood pressure in the hypertensive patient is a central dogma of mainstream medicine. Indeed, popular wisdom says that the “low salt diet” is also healthy for the rest of us “normal” people who don’t have hypertension. Along with the rest of my medical school class, I was indoctrinated to believe this. Is this really true? Many studies have looked at this question. They show the “low salt diet” will in fact reduce blood pressure slightly. However, this effect is minimal, and is counteracted by compensatory mechanisms that release harmful substances into the bloodstream, that counteract the “low salt diet”. The released chemical mediators include insulin, epinephrine, norepinephrine, renin, aldosterone, etc. These are harmful and damaging to the vascular system.
In addition, a study published by John H. Laragh in the 1995 Hypertension found 4 times greater Myocardial Infarction in hypertensive men on a low salt diet. See left chart, showing linear relationship between “events” and urinary sodium excretion . He says:
“These findings conflict with widely held popular belief. However, they are consistent with the biologically plausible hypothesis that, because sodium and renin are inversely related, a low sodium diet would be associated with increased MI.“
U Shaped Curve
O’Donnell MJ, Yusuf S, Mente A, Gao P, Mann JF, Teo K, McQueen M, Sleight P, Sharma AM, Dans A, Probstfield J, Schmieder RE. Urinary sodium and potassium excretion and risk of cardiovascular events. JAMA. 2011 Nov 23; 306(20):2229-38.
“In a recent study, published in the Journal of the American Medical Association (JAMA),31 researchers found moderate salt intake to be associated with the lowest risk of cardiovascular events, whereas low intakes, equivalent to less than or equal to 3,000 mg sodium or 1.5 teaspoons (8 grams) of salt per day, were associated with an increased risk of cardiovascular death and hospitalization for congestive heart failure, and higher intakes of more than 7,000 mg sodium or three teaspoons (15 grams) of salt per day, were associated with an increased risk of stroke, heart attack and other cardiovascular events. Once again, a J-shaped curve appeared to describe the dose-response relationship.” Quote from Weston Price
For part one of this series click here.
Update Jan 2015: Optimal salt intake is between 3000-6000 mg per day.
O’Donnell, Martin, et al. “Urinary sodium and potassium excretion, mortality, and cardiovascular events.” New England Journal of Medicine 371.7 (2014): 612-623.
“In this study in which sodium intake was estimated on the basis of measured urinary excretion, an estimated sodium intake between 3 g per day and 6 g per day was associated with a lower risk of death and cardiovascular events than was either a higher or lower estimated level of intake. As compared with an estimated potassium excretion that was less than 1.50 g per day, higher potassium excretion was associated with a lower risk of death and cardiovascular events. “
Optimal Sodium intake of 2.5-6.0 g/day
Our study identified a specific range of sodium intake (2,645–4,945 mg) associated with the most favorable health outcomes, within which variation in sodium intake is not associated with variation in mortality. …Finally, an increased mortality risk was found to be associated with
intakes that violate this range. In none of the primary or supplementary
analyses was a low sodium intake associated with beneficial effects on ACM (all cause mortality) or CVD (cadiovascular mortality) . Thus, these data are consistent with the hypothesis that a U shape best describes the relationship of sodium intake to health outcomes.
One teaspoon (5 grams salt) of Celtic Sea Salt contains about 2300 sodium . Weston Price.
Jeffrey Dach MD
Links and References
Personal Health April 1, 2013, 12:02 pm Sodium, Hiding in Plain Sight By JANE E. BRODY
Hypertension. 2013; 61: 564-570 Mortality Benefits From US Population-wide Reduction in Sodium Consumption Projections From 3 Modeling Approaches
Pamela G. Coxson, Nancy R. Cook, Michel Joffres, Yuling Hong, Diane Orenstein, Steven M. Schmidt, Kirsten Bibbins-Domingo
From the Department of Medicine, University of California San Francisco (UCSF), San Francisco, CA (P.G.C., K.B-D.); Department of Epidemiology and Biostatistics, UCSF, San Francisco, CA (K.B.-D.); Division of Preventive Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA (N.R.C.); Faculty of Health Sciences, Simon Fraser University, Burnaby, BC, Canada (M.J.); and Division for Heart Disease and Stroke Prevention, Centers for Disease Control and Prevention, Atlanta, GA (Y.H., D.O., S.M.C.).
Computer simulations have been used to estimate the mortality benefits from population-wide reductions in dietary sodium, although comparisons of these estimates have not been rigorously evaluated. We used 3 different approaches to model the effect of sodium reduction in the US population over the next 10 years, incorporating evidence for direct effects on cardiovascular disease mortality (method 1), indirect effects mediated by blood pressure changes as observed in randomized controlled trials of antihypertension medications (method 2), or epidemiological studies (method 3).The 3 different modeling approaches were used to model the same scenarios: scenario A, gradual uniform reduction totaling 40% over 10 years; scenario B, instantaneous 40% reduction in sodium consumption sustained for 10 years to achieve a population-wide mean of 2200 mg/d; and scenario C, instantaneous reduction to 1500 mg sodium per day sustained for 10 years.
All 3 methods consistently show a substantial health benefit for reductions in dietary sodium under each of the 3 scenarios tested. A gradual reduction in dietary sodium over the next decade (scenario A) as might be achieved with a range of proposed public health interventions would yield considerable health benefits over the next decade, with mean effects across the 3 models ranging from 280 000 to 500 000 deaths averted. Projections of instantaneous reductions illustrate the maximum benefits that could be achieved (0.7–1.2 million deaths averted in 10 years). Under 3 different modeling assumptions, the projected health benefits from reductions in dietary sodium are substantial.
Salt in Health and Disease — A Delicate Balance
Theodore A. Kotchen, M.D., Allen W. Cowley, Jr., Ph.D., and Edward D. Frohlich, M.D. N Engl J Med 2013; 368:1229-1237March 28, 2013DOI: 10.1056/NEJMra1212606
Jane Brody’s One-Sided Take on Sodium Posted by Gary Schwitzer in Health care journalism, Limits of observational studies
Author Insights: Questioning the Benefits of Salt Restriction
By Mike Mitka on May 3, 2011
Fatal and Nonfatal Outcomes, Incidence of Hypertension, and Blood Pressure Changes in Relation to Urinary Sodium Excretion
by Katarzyna Stolarz-Skrzypek, MD, PhD; Tatiana Kuznetsova, MD, PhD; Lutgarde Thijs, MSc; Valérie Tikhonoff, MD, PhD; Jitka Seidlerová, MD, PhD; Tom Richart, MD; Yu Jin, MD; Agnieszka Olszanecka, MD, PhD; Sofia Malyutina, MD, PhD; Edoardo Casiglia, MD, PhD; Jan Filipovský, MD, PhD; Kalina Kawecka-Jaszcz, MD, PhD; Yuri Nikitin, MD, PhD; Jan A. Staessen, MD, PhD; for the European Project on Genes in Hypertension (EPOGH) Investigators Author Affiliations: Studies Coordinating Centre, Division of Hypertension and Cardiovascular Rehabilitation, Department of Cardiovascular Diseases, University of Leuven, Leuven, Belgium (Drs Stolarz-Skrzypek, Kuznetsova, Thijs, Richart, Jin, and Staessen); First Department of Cardiology and Hypertension, Jagiellonian University Medical College, Kraków, Poland (Drs Stolarz-Skrzypek, Olszanecka, and Kawecka-Jaszcz); Department of Clinical and Experimental Medicine, University of Padova, Padova, Italy (Drs Tikhonoff and Casiglia); Faculty of Medicine in Pilsen, Charles University, Pilsen, Czech Republic (Drs Seidlerová and Filipovský); Institute of Internal Medicine, Novosibirsk, Russian Federation (Drs Malyutina and Nikitin); and Department of Epidemiology, Maastricht University, Maastricht, the Netherlands (Drs Richart and Staessen).
Context Extrapolations from observational studies and short-term intervention trials suggest that population-wide moderation of salt intake might reduce cardiovascular events.
Objective To assess whether 24-hour urinary sodium excretion predicts blood pressure (BP) and health outcomes.
Design, Setting, and Participants Prospective population study, involving 3681 participants without cardiovascular disease (CVD) who are members of families that were randomly enrolled in the Flemish Study on Genes, Environment, and Health Outcomes (1985-2004) or in the European Project on Genes in Hypertension (1999-2001). Of 3681 participants without CVD, 2096 were normotensive at baseline and 1499 had BP and sodium excretion measured at baseline and last follow-up (2005-2008).
Main Outcome Measures Incidence of mortality and morbidity and association between changes in BP and sodium excretion. Multivariable-adjusted hazard ratios (HRs) express the risk in tertiles of sodium excretion relative to average risk in the whole study population.
Results Among 3681 participants followed up for a median 7.9 years, CVD deaths decreased across increasing tertiles of 24-hour sodium excretion, from 50 deaths in the low (mean, 107 mmol), 24 in the medium (mean, 168 mmol), and 10 in the high excretion group (mean, 260 mmol; P < .001), resulting in respective death rates of 4.1% (95% confidence interval [CI], 3.5%-4.7%), 1.9% (95% CI, 1.5%-2.3%), and 0.8% (95% CI, 0.5%-1.1%). In multivariable-adjusted analyses, this inverse association retained significance (P = .02): the HR in the low tertile was 1.56 (95% CI, 1.02-2.36; P = .04).
Baseline sodium excretion predicted neither total mortality (P = .10) nor fatal combined with nonfatal CVD events (P = .55).
Among 2096 participants followed up for 6.5 years, the risk of hypertension did not increase across increasing tertiles (P = .93). Incident hypertension was 187 (27.0%; HR, 1.00; 95% CI, 0.87-1.16) in the low, 190 (26.6%; HR, 1.02; 95% CI, 0.89-1.16) in the medium, and 175 (25.4%; HR, 0.98; 95% CI, 0.86-1.12) in the high sodium excretion group. In 1499 participants followed up for 6.1 years, systolic blood pressure increased by 0.37 mm Hg per year (P < .001), whereas sodium excretion did not change (–0.45 mmol per year, P = .15). However, in multivariable-adjusted analyses, a 100-mmol increase in sodium excretion was associated with 1.71 mm Hg increase in systolic blood pressure (P.<001) but no change in diastolic BP.
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.
April 4, 2013 Less sodium, longer lives. The New York Times ran an article earlier this week on the public health benefits of reduced sodium intake. Jane Brody’s piece begins this way:
For More, use this link: http://wp.me/P3gFbV-cY.
Link to this article: http://wp.me/p3gFbV-d8
Jeffrey Dach MD
Jeffrey Dach MD
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