Posts Tagged ‘Sodium Chloride’

Science 1998; 281(14): 898-907. “The (Political) Science of Salt”

Sunday, August 1st, 2010
The (political) science of salt
Gary Taubes. Science. Washington: Aug 14, 1998. Vol. 281, Iss. 5379; pg. 898, 9 pgs

Abstract (Summary)

Taubes discusses the debate over the benefits of salt reduction, which shows how the demands of good science clash with the pressures of public health policy.

Quotes from the full article:

The last 5 years have also seen two studies published-the latest this past March in The Lancet-suggesting that low-salt diets can increase mortality. Both studies were done by Michael Alderman, a hypertension specialist at New York City’s Albert Einstein College of Medicine and president of the American Society of Hypertension. Epidemiologists-and Alderman himself-caution against putting too much stock in the studies. “They are yet more association studies,” says Swales. “Any insult you make of Intersalt you can make of those as well.” But Alderman also notes that only a handful of such studies comparing salt intake to mortality have ever been done, and none have come out definitively negative. “People just rely upon statements that [salt reduction] can’t really do any harm,” says Swales. “It may or may not be true. Individual harmful effects can be as small as beneficial effects, and you can’t detect those in clinical trials either.”

After publication of his second study, Alderman recruited past and present presidents of hypertension societies and the American Heart Association and wrote to Lenfant at the NHLBI “urging prompt appointment of an independent panel of qualified medical and public health scientists to review existing recommendations [on salt consumption] in light of all available data.” In April Lenfant told Science that he had agreed to proceed with the review. If such a panel should convene, Hennekens has one observation worth keeping in mind: “The problem with this field is that people have chosen sides,” he says. “What we ought to do is let the science drive the system rather than the opinions.”

[Sidebar]
TOUCHSTONES OF THE SALT DEBATE
[Sidebar]

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Am J Clin Nutr. 1972 Feb;25(2):231-44. “Salt and hypertension”

Sunday, August 1st, 2010

-::- Note: The below is published here for archival purposes -::-

Am J Clin Nutr. 1972 Feb;25(2):231-44.

Salt and hypertension.

Dahl LK.

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PMID: 5009786 [PubMed - indexed for MEDLINE]Free Article

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Am J Clin Nutr. 1997 Feb;65(2 Suppl):708S-711S. “Dietary sodium and blood pressure: interactions with other nutrients”

Sunday, August 1st, 2010

-::- Note: The below is published here for archival purposes -::-

Am J Clin Nutr. 1997 Feb;65(2 Suppl):708S-711S.

Dietary sodium and blood pressure: interactions with other nutrients.

Kotchen TA, Kotchen JM.

Department of Medicine, Medical College of Wisconsin, Milwaukee 53226, USA.

Abstract

This paper reviews the evidence that salt sensitivity of blood pressure is related both to the anion ingested with sodium as well as to other components of the diet.

In several experimental models of salt-sensitive hypertension and in humans, blood pressure is not increased by a high sodium intake provided with anions other than chloride. Salt-induced increase of blood pressure depends on the concomitant ingestion of both sodium and chloride.

Both epidemiologic and clinical evidence suggest that sodium chloride-induced increases of blood pressure are augmented by diets deficient in potassium or calcium. In experimental animals, a high intake of simple carbohydrates also augments sodium chloride sensitivity of blood pressure.

These observations indicate that the effect of dietary sodium on blood pressure is modulated by other components of the diet.

PMID: 9022570 [PubMed - indexed for MEDLINE]

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Acta Cardiol. 1987;42(3):187-206. “Does sodium play an adverse role in hypertension?”

Sunday, August 1st, 2010

Acta Cardiol. 1987;42(3):187-206.

Does sodium play an adverse role in hypertension?

Singh RB, Singh NK, Mody R, Cameron EA.

Medical Hospital and Research Centre, Moradabad.

Abstract

It is clear that salt is known to be a health hazard from the ancient times. Sodium intake, which was minimal during evolution, increased significantly with the civilization. The rise in prevalence of hypertension in populations with increased consumption of salt suggested a casual relationship. However, several of these studies showed conflicting results.

Many investigators agree that salt-sensitive persons often have a family history of hypertension. Such individuals possess a sodium transport inhibitor in the arterial smooth muscle cells, which affects their sodium handling (as compared to other persons).

However, many of the putative defects related to sodium can be dissociated from blood pressure and sodium consumption status. It is possible that calcium defects of deficiency of potassium and magnesium follow hypertension and sodium status. For example, the pressure response to sodium chloride may be dissociated from sodium, which may be secondary to adverse effects of chloride on calcium homeostasis. Clinical studies also indicate that the role of sodium is controversial in hypertension.

Sodium restriction can benefit salt-sensitive persons and might not otherwise. However, most authorities believe that moderation of salt intake to a relevant extent is justifiable.

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Calcium, Magnesium, Potassium, Phosphate, Vitamin D and Hypertention in Dahl Rats – Sources

Sunday, August 1st, 2010

Clin Exp Hypertens. 1998 Oct;20(7):795-815.

Hypertension development in Dahl S and R rats on high salt-low potassium diet: calcium, magnesium and sympathetic nervous system.

Wu X, Ackermann U, Sonnenberg H.

Department of Physiology, University of Toronto, Ontario, Canada.

Abstract

Dietary combination of high salt with low potassium (HSLK) exacerbates hypertension development in Dahl salt-sensitive (S) rats, and produces a mild degree of hypertension in otherwise salt-resistant (R) rats. Increased blood pressure in both strains is associated with increased urinary excretion of calcium and magnesium. The objective of this study was to determine the effect of blood pressure on body balance of these ions in Dahl rats on HSLK diet. Two groups of S and two groups of R weanlings were all placed on HSLK diet (NaCl=8%, K=0.2%) for eight weeks. One group of each strain was subjected to chemical sympathectomy with 6-hydroxydopamine (6-OHDA) to counteract hypertension development. Urinary norepinephrine was used to determine efficacy of 6-OHDA treatment. Systolic blood pressures of conscious animals were measured daily throughout the study. The last three days on the diet were used to determine total dietary intake and urinary as well as fecal excretion of sodium, calcium and magnesium. At the end of the study, extracellular fluid volume, serum aldosterone and parathyroid hormone were analyzed. Final systolic blood pressures in the 4 groups were as follows: S=235+/-9 mmHg (n=9); R=155+/-3 mmHg (n=8); 6-OHDA S=151+/-6 mm Hg (n=8); 6-OHDA R=117+/-6 mm Hg. Chemical sympathectomy decreased blood pressure in both S and R rats. There was no indication of sodium accumulation in S rats. Associated with reduced parathyroid hormone levels the S strain had significantly less positive balance for calcium than the R strain, primarily due to increased urinary excretion. A less positive balance for magnesium was also observed, due mainly to relatively reduced intestinal absorption of the ion. We conclude that the HSLK diet is associated with inappropriate activation of the sympathetic nervous system and increased arterial pressure in both strains. In addition, since divalent cations may influence blood pressure, we suggest that the observed abnormalities in calcium and magnesium metabolism might independently promote hypertension development in the S strain.

Clin Exp Hypertens. 1995 Aug;17(6):989-1008.

Potassium depletion and salt-sensitive hypertension in Dahl rats: effect on calcium, magnesium, and phosphate excretions.

Wu X, Ackermann U, Sonnenberg H.

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J Natl Med Assoc. 1990 Dec;82(12):837-40. “Hypertension induction in Dahl rats”

Sunday, August 1st, 2010

J Natl Med Assoc. 1990 Dec;82(12):837-40.

Hypertension induction in Dahl rats.

Flowers SW, Jamal IA, Bogden J, Thanki K, Ballester H.

University of Medicine and Dentistry of New Jersey, Maplewood.

Abstract

There is experimental and epidemiologic evidence that some minerals and trace elements play a role in hypertension. We designed an experiment in which salt and water sources were manipulated to examine the possible impact of this relationship. A strain of rats (Dahl rats) known to become hypertensive with sodium chloride ingestion was used to study the effect of salt source and water source on the induction of hypertension.

The group on tap water and table salt had blood pressures (184 mmHg +/- 19) significantly higher than every other group in the experiment. The experimental animals receiving tap water plus table salt had the highest blood pressure levels, although they consumed the lowest quantity of sodium.

Analysis of the tap water samples showed “soft water” by analysis of calcium and magnesium concentration. This could adversely affect blood pressure.

The relatively high magnesium concentration in sun evaporated sea salt may play a protective role in hypertension induction. The zinc and copper present in tap water may play an exacerbating role.

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Clin Sci (Lond). 2009 Jun 2;117(1):1-11. “Salt and high blood pressure”

Sunday, August 1st, 2010

Clin Sci (Lond). 2009 Jun 2;117(1):1-11.

Salt and high blood pressure.

Mohan S, Campbell NR.

Departments of Medicine and Community Health Sciences, University of Calgary, Calgary, Alberta, Canada.

Abstract

HBP (high blood pressure) is the leading risk of death in the world. Unfortunately around the world, blood pressure levels are predicted to become even higher, especially in developing countries. High dietary salt is an important contributor to increased blood pressure. The present review evaluates the association between excess dietary salt intake and the importance of a population-based strategy to lower dietary salt, and also highlights some salt-reduction strategies from selected countries. Evidence from diverse sources spanning animal, epidemiology and human intervention studies demonstrate the association between salt intake and HBP. Furthermore, animal studies indicate that short-term interventions in humans may underestimate the health risks associated with high dietary sodium. Recent intervention studies have found decreases in cardiovascular events following reductions in dietary sodium. Salt intake is high in most countries and, therefore, strategies to lower salt intake could be an effective means to reduce the increasing burden of HBP and the associated cardiovascular disease. Effective collaborative partnerships between governments, the food industry, scientific organizations and healthcare organizations are essential to achieve the WHO (World Health Organization)-recommended population-wide decrease in salt consumption to less than 5 g/day. In the milieu of increasing cardiovascular disease worldwide, particularly in resource-constrained low- and middle-income countries, salt reduction is one of the most cost-effective strategies to combat the epidemic of HBP, associated cardiovascular disease and improve population health.

PMID: 19476440 [PubMed - indexed for MEDLINE]

Prog Cardiovasc Dis. 2010 Mar-Apr;52(5):363-82. “Reducing population salt intake worldwide”

Sunday, August 1st, 2010

Prog Cardiovasc Dis. 2010 Mar-Apr;52(5):363-82.

Reducing population salt intake worldwide: from evidence to implementation.

He FJ, MacGregor GA.

Wolfson Institute of Preventive Medicine, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK. f.he@qmul.ac.uk

Abstract

Raised blood pressure is a major cause of cardiovascular disease, responsible for 62% of stroke and 49% of coronary heart disease. There is overwhelming evidence that dietary salt is the major cause of raised blood pressure and that a reduction in salt intake lowers blood pressure, thereby, reducing blood pressure-related diseases.

Several lines of evidence including ecological, population, and prospective cohort studies, as well as outcome trials, demonstrate that a reduction in salt intake is related to a lower risk of cardiovascular disease. Increasing evidence also suggests that a high salt intake may directly increase the risk of stroke, left ventricular hypertrophy, and renal disease; is associated with obesity through soft drink consumption; is related to renal stones and osteoporosis; is linked to the severity of asthma; and is probably a major cause of stomach cancer.

In most developed countries, a reduction in salt intake can be achieved by a gradual and sustained reduction in the amount of salt added to foods by the food industry. In other countries where most of the salt consumed comes from salt added during cooking or from sauces, a public health campaign is needed to encourage consumers to use less salt. Several countries have already reduced salt intake. The challenge now is to spread this out to all other countries. A modest reduction in population salt intake worldwide will result in a major improvement in public health. Copyright 2010 Elsevier Inc. All rights reserved.

PMID: 20226955 [PubMed - indexed for MEDLINE]

diovasc Dis. 1999 Jul-Aug;42(1):23-38. “Dietary salt reduction in hypertension”

Sunday, August 1st, 2010

diovasc Dis. 1999 Jul-Aug;42(1):23-38.

Dietary salt reduction in hypertension–what is the evidence and why is it still controversial?

Chrysant GS, Bakir S, Oparil S.

University of Alabama at Birmingham, Department of Medicine, Vascular Biology and Hypertension Program, 35294-0012, USA. gsc5@yahoo.com

Abstract

The link between sodium intake and hypertension remains controversial because of inconsistency between early epidemiologic studies, which showed a strong positive relationship between salt intake and blood pressure/incidence of hypertension, and more recent studies, which showed only modest decreases in blood pressure with sodium reduction, particularly in the normotensive population. In addition, there is clinical evidence that sodium is related to target organ damage such as left ventricular hypertrophy and renal disease.

Although the evidence available linking sodium intake and blood pressure in the general population is weak, sodium reduction has been shown to be useful in hypertensive patients, particularly salt-sensitive patients.

Whether dietary sodium reduction should be recommended for the general population remains questionable because of marginal benefit and the suggestion of possible deleterious effects on cardiovascular outcomes independent of blood pressure.

This paper will review the definition and methods used in determining salt sensitivity, the evidence linking sodium intake and target organ damage, and modern studies of salt and blood pressure.

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