UPDATED!! Time to end the war on Salt?

A place to get your questions answered from McDougall staff dietitian, Jeff Novick, MS, RDN.

Moderators: JeffN, carolve, Heather McDougall

Re: Time to end the war on Salt?

Postby Spiral » Fri Sep 02, 2011 7:11 pm

)
Today, no matter where you live in the USA, your food comes from a variety of sources around the world.

Also, contrary to popular myth, we have some of the richest soils ever.

In Health
Jeff


Jeff, thanks for that response.

I too was concerned about a possible iodine deficiency (I admit, I am a bit of a worry wart :D ).

So, I purchased some iodized salt and figured I would sprinkle a 1/4 teaspoon of it on my food once each day to make sure I wasn't deficient.

That lasted about 2 days before I figured it was unnecessary.
User avatar
Spiral
 
Posts: 3005
Joined: Sat Dec 18, 2010 8:18 pm
Location: Indianapolis, Indiana

Re: Time to end the war on Salt?

Postby JeffN » Fri Oct 21, 2011 8:02 pm

Nutrition, Metabolism & Cardiovascular Diseases (2011) 21, 617e619

New evidence relating to the health impact of reducing salt intake

Abstract: This paper is a Position Statement from an ‘ad hoc’ Scientific Review Subcommittee of the PAHO/WHO Regional Expert Group on Cardiovascular Disease Prevention through Dietary Salt Reduction. It is produced in response to requests from representatives of countries of the Pan-American Region of WHO needing clarification on two recent publications casting doubts on the appropriateness of population wide policies to reduce salt intake for the prevention of cardiovascular disease. The paper provides a brief background, a critical appraisal of the recent reports and explanations as why the implications have been misinterpreted. The paper concludes that the benefits of salt reduction are clear and consistent, and reinforces the recommendations outlined by PAHO/WHO and other organizations worldwide for a population reduction in salt intake to prevent strokes, heart attacks and other cardiovascular events.

Strong and consistent evidence shows that a diet high in salt is harmful to health and that reducing its intake is among the most cost effective possible means to reduce disease risk [1e5]. Excess dietary salt causes an increase in blood pressure, the leading risk for premature death in the developed and developing world. In addition, a high dietary salt intake is strongly associated with stroke and cardiovascular outcomes [6], gastric cancer, loss of calcium in urine and the ensuing risks of calcium-containing kidney stones and osteoporosis [7]. There are also strong associations and a pathophysiological basis for high dietary sodium intake to contribute to obesity [8].

Recently two highly publicized reports have been used by public and scientific media to suggest that high dietary sodium intake does not adversely affect health [9,10]. The critical appraisal that follows seeks to put these studies in the broader scientific and methodological context, and shows that these studies do not form a rational basis upon which to make changes to existing public health efforts to reduce population dietary salt intake.

The background to these studies is fifty years of intensive animal and human research that has seen a vast array of studies conducted on dietary sodium intake and health [1e5]. The human research program has been particularly extensive including migration studies, cross sectional studies, cohort studies, randomized trials and meta-analyses and has involved hundreds of thousands of individuals. Like most research programs it is comprised of pieces of work of varying quality and significance and the interpretation of any one project requires careful consideration of both its indi- vidual strengths and weaknesses and the broader scientific context. When taken overall, the message is very clear e salt causes high blood pressure and vascular disease. This consensus is widely accepted by national and international governmental, scientific and health organizations.

Discovering truth in science is dependent upon two key aspects of research design e precision and validity. Preci- sion describes the capacity of a piece of work to determine exactly what is going on by controlling for random errors (the play of chance) and mostly it relates to the size of the studies done. Small projects provide poor precision and are at high risk of turning up findings just by chance, or missing real effects because the study was unlucky. Even then science compromises because to be absolutely precise is usually impractical. So we settle on the notion that ‘truth’ is defined by studies that have a 90% chance of picking up a real effect if it does exist (90% power) and only a one in 20 change of showing a chance positive finding that isn’t really there (p Z 0.05). It is very important to look at every study in this context and to interpret the reported findings in light of what the study was actually able to show.

Validity describes a different concept, that of control- ling for systematic (or non-random) errors and truly understanding the cause and effect relationship. Con- founding of associations is a particular problem in nutri- tional epidemiology and has been a major cause of the debate in the salt field. Caution is required in interpreting the findings reported by cohort studies with very close examination of the mechanisms that the researchers have put in place to control for potential confounding factors and the extent to which these methods are likely to have been successful. In particular, if the observed effects in the observational data do not fit with what the results of the unconfounded randomized trials they need to be treated with extreme caution.

Recently JAMA published an article by Stolarz-Skrzypek and colleagues [10]. This cohort study examined urinary sodium excretion in relation to hypertension and fatal and non-fatal outcomes and concluded that low sodium diets increased cardiovascular disease and should not be rec- ommended on a population basis. The key problem with this trial is residual confounding. The data from the Stolarz- Skrzypek’s study show that the group consuming low salt diets were very different from the group consuming high salt in many more ways than just their level of salt consumption. They had higher levels of many known risks for CVD that would be expected to result in a poor outcome regardless of their salt intake e the lowest educational attainment, higher baseline systolic blood pressure, older age and higher total cholesterol. While the investigators sought to adjust for these confounders statistical models mostly fail to achieve full correction for such imbalances. The very large changes produced by statistical adjustment in this study are a cause for concern because this suggests that confounding was substantial and that under-correction may therefore also have been substantial. Similar imbal- ances were a feature of 2 previous cohort studies by Alderman and Cohen et al. and statistical adjustment in that case resulted in the conclusion of no significant rela- tionship between high dietary salt and adverse outcomes [11,12]. In the examples of Alderman and Cohen, the data was from a cohort derived from the NHANES in the United States, and notably two studies by different groups of investigators examining salt consumption using NHANES data refuted their findings, confirming high salt intake was associated with cardiovascular disease [13,14].
The lower sodium excretion group in the Stolarz- Skrzypek study also had lower urinary creatinine, urinary potassium, and urine volumes suggesting concurrent illness or non adherence to the collection of the full 24 h urine sample. In diverse research studies poor adherence, even to placebo, is a strong marker of bad outcomes [15,16]. The Stolarz-Skrzypek data are also unusual in that lower sodium intake is almost always also associated with a higher potassium intake and excretion because the main mecha- nism for reducing dietary sodium is to eat unprocessed foods that are high in potassium (such as vegetables and fruits) [17].
In addition to major concerns about validity, the study had very limited precision. The study population was young with a low cardiovascular disease event rate and the conclusions were based on just a small number of events. Statistical power was negligible and there is a very high risk of this being a spurious finding. When the study of Stolarz- Skrzypek is included in an updated meta analysis of all the prospective cohort studies addressing this question the overall finding is that high dietary sodium is associated with an increased incidence of stroke with a corresponding trend toward higher total cardiovascular events [18].

The second, more recent report derives from the Cochrane Collaboration and examined the impact of high dietary salt consumption on death and disability in a meta analysis of randomized controlled trials [9]. The overview found no strong evidence that salt reduction through indi- vidual dietary advice reduced all-cause mortality or CVD morbidity in normotensive persons or hypertensive patients. The media have widely misreported the findings and a false sense of controversy has been broadcast, confusing the public on important health messages. The key issue here was the study power. The overview simply did not have large enough numbers of people studied, long enough trials or large enough reductions in dietary salt to adequately assess the question being addressed. The study also separated trials of people with normal blood pressure and those with high blood pressure further limiting the studies statistical power. Another major limitation of this study is their decision to truncate follow-up in the TOHP studies to just the trial period [19]. Extended follow-up documented a significant reduction in cardiovascular events over the long-term (not evident in the trial phase alone) [19]. In contrast to the media reports, the Cochrane meta analysis results were absolutely consistent with large reductions in death and disability from lower salt diets with clear effects of salt reduction on blood pressure that were exactly in line with what would have been anticipated.

A further limitation of the Cochrane overview was the decision to include a trial done in people with severe heart failure on very high doses of diuretic. This is an inappro- priate group in which to study the effects of salt reduction, since the high doses of diuretic will have left many already substantially salt depleted. The adverse findings in this study are therefore not entirely unsurprising and the small size of the study also makes the findings prone to the play of chance. Interestingly, repeating the Cochrane meta analysis and combining the studies of people with normal and high blood pressure together results in an overall estimate of effect showing a substantive reduction in cardiovascular events [20].

Perhaps as important as the science which over- whelmingly supports the health and economic benefits of reducing dietary salt is the media attention and controversy it has generated. Many headlines have been generated that confuse the public and health care professionals. The new studies should not deter efforts to reduce dietary salt and do not change our understanding, regarding the adverse impact of salt on health. In conclusion, the benefits of salt reduction are clear and consistent, the recent studies do not indicate that salt does not affect hypertension or CVD, their publication does not change the priorities outlined by PAHO/WHO and worldwide for a population reduction in salt intake to prevent heart attacks and strokes.

In Health
Jeff
User avatar
JeffN
 
Posts: 9412
Joined: Tue Jan 08, 2008 5:56 am

Re: Time to end the war on Salt?

Postby Spiral » Thu May 03, 2012 3:53 am

My daily sodium intake has been below 2,000 milligrams. I do add a small amount of soy sauce and some mustard to my rice and vegetable and/or potato dishes. These do contain significant amounts of sodium on a per calorie basis. However, this is mostly outweighed by the calories in the rice/potatoes.

I also use Mrs. Dash seasonings quite often.
User avatar
Spiral
 
Posts: 3005
Joined: Sat Dec 18, 2010 8:18 pm
Location: Indianapolis, Indiana

Re: Time to end the war on Salt?

Postby Acura » Wed Jun 20, 2012 11:15 am

Jeff,

I have read article on salt and stroke on your facebook page. Just so I get it right. There are couple of recommendations, AHA recommends salt consumption <= 1500 mg, US department of Agriculture recommends salt consumption <=2300 mg. I believe your recommendation is <1500 mg. Is that correct?

When we talk about these limits, we are strictly talking about added salt notwithstanding the naturally occurring salt in some foods. If you account for everything, the overall salt consumption could be higher.

1 tsp is like 2300 mg just to get some perspective. So you should consume less than a tsp a day.
CC
Acura
 
Posts: 868
Joined: Wed Aug 18, 2010 8:07 am

Re: Time to end the war on Salt?

Postby JeffN » Wed Jun 20, 2012 11:27 am

Let me put it in perspective... :)

There is no RDA for sodium or chloride although the 10th edition of the Recommended Dietary Allowances states "the minimum average requirement for adults ... [is]... 115 mg of Sodium...per day. In consideration of the wide variation of patterns of physical activity and climate exposure, a safe minimum intake might be set at 500 mg/day."

In February of 2004 the Food and Nutrition Board of the Institute of Medicine (IOM) released the “Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate”. They stated that a Recommended Dietary Allowance (RDA) for sodium and chloride "could not be derived.” “Hence an Adequate Intake (AI) is provided.”

This report also set a toxic Upper Limit (UL) for sodium at 2300mg per day, which means most Americans are consuming what they consider a toxic dose of sodium (mostly all from salt) nearly every day.

The IOM set what is called an adequate intake (AI) which is <1200-1500 mg/day (based on age and health) which is used by the AHA and others.

Some of the national health organizations, like the USDA, just default to the Upper Limit and not the AI as it is more politically correct. However they have been publicly blasted by the AHA and IOM for doing so.

A whole plant food diet would easily provide 350-500 in what occurs naturally in foods

So, that's the recommendations.

In regard to intake...

The average sodium intake is estimated to be about 4000 mgs/day. Of that 4000, 10-12% occurs naturally in food, 5% is added at the table to the surface of the food, 5% is added during cooking, and about 75-80% is hidden in packaged processed foods and restaurant foods with the majority of that coming from packaged/processed foods.

So, if we eliminate the 75-80% of packaged/processed foods and the 5% we add during cooking that is 80-85% of the 4000, which leaves 600- 800 mgs per day which is way below the recommended intakes. And, that includes the 5% added at the table to the surface of the food.

Or if you look at it this way... you will get in about 350-500 mg of sodium from what occurs naturally in whole plant foods. Let say 500 to make math easier. The AI is <1200-1500 so lets use the 1500 to make math easier. And the UL is 2300. Subtract what occurs naturally in food from the AI (1500 minus 500) and from the UL (2300-500) and you get 1000- 1800 mgs.

As a tsp of salt is around 2200 - 2300 mg, that would allow for up to 1/2 to 3/4 tsp per day.

If you choose to do this, it would be best to add it to the surface of the food at the table as you will get the most flavor for the least amount. Right now, they estimate what we add at the table to be about 5% of the 4000 (which is 200). So, add the 200 to the 500 which occurs naturally and you are at 700 and safe.

Make sense?


The really good news is that we down regulate our taste buds to salt, very quickly and low salt to salt-free food begins to taste great.

http://ajcn.nutrition.org/content/36/6/1134.abstract

"These results demonstrate that the preferred level of salt in food is dependent on the level of salt consumed and that this preferred level can be lowered after a reduction in sodium intake. The implications of these findings for the maintenance of low sodium diets are discussed."

http://www.ncbi.nlm.nih.gov/pubmed/3728360

"Reduction in sodium intake and excretion accompanied a shift in preference toward less salt"

And the best way to get to reduce our intake is to get it out of all the food and if desired, sprinkle it on the food at the table.

http://www.ncbi.nlm.nih.gov/pubmed/3682116

"A substantial reduction in dietary sodium is possible if lowered-sodium foods are consumed in conjunction with ad libitum table salt."

In Health
Jeff
User avatar
JeffN
 
Posts: 9412
Joined: Tue Jan 08, 2008 5:56 am

Re: Time to end the war on Salt?

Postby Acura » Wed Jun 20, 2012 11:53 am

JeffN wrote:Make sense?

In Health
Jeff


Absolutely, good to know the nuts and bolts.
CC
Acura
 
Posts: 868
Joined: Wed Aug 18, 2010 8:07 am

Re: Time to end the war on Salt?

Postby JeffN » Tue Jul 10, 2012 8:01 am

There have been many articles of late questioning whether lowering sodium is a good idea and stating that higher intakes of sodium do not increase the risk for hypertension, cardiovascular disease, and stroke.

Most of this comes from a few recent studies that were poorly designed and several were funded by the Salt Institute.

In addition, a recent NY Times article by Gary Taubes, really contributed to the confusion.

http://www.nytimes.com/2012/06/03/opini ... wanted=all

However, three recent studies add further support for the role of high sodium intake in stroke.

From the first....

"Over a mean follow-up of 10 years, ... Of 2657 participants [age 69± 10 years] with dietary data, the mean sodium intake was 3031±1470 mg/day (median, 2787; interquartile range, 1966–3815 mg/day). Participants who consumed ≥4000 mg/day sodium had an increased risk of stroke (hazard ratio, 2.59; 95% CI, 1.27–5.28) versus those who consumed ≤1500 mg/day with a 17% increased risk of stroke for each 500-mg/day increase (95% CI, 1.07–1.27) ... using Cox models adjusting for sociodemographics, diet, behavioral/lifestyle, and vascular risk factors."(1)

From the second...

"A prospective cohort study with a 3-year follow-up was conducted in 14 721 olmesartan-naive outpatients (mean age: 64.9 years, 49.6% women) with essential hypertension. ... The mean baseline blood pressure was 157.4/88.8 mm Hg, which decreased to 134.0/76.1 mm Hg during [olmesartan] treatment (P<0.0001). ... Higher salt intake was associated with a significantly higher risk of stroke than lower salt intake (hazard ratio, 1.897; 95% confidence interval, 1.003-3.590). "(2)

From the third

"There were 19 independent cohort samples from 13 studies, with 177 025 participants (follow-up 3.5-19 years) and over 11 000 vascular events. Higher salt intake was associated with greater risk of stroke (pooled relative risk 1.23, 95% confidence interval 1.06 to 1.43; P=0.007) and cardiovascular disease (1.14, 0.99 to 1.32; P=0.07), with no significant evidence of publication bias. For cardiovascular disease, sensitivity analysis showed that the exclusion of a single study led to a pooled estimate of 1.17 (1.02 to 1.34; P=0.02). The associations observed were greater the larger the difference in sodium intake and the longer the follow-up."

In addition, a fourth study confirmed the role of excess sodium in gastric cancer.

Shake the salt habit!

In Health
Jeff

1: Gardener H, Rundek T, Wright CB, Elkind MS, Sacco RL. Dietary sodium and risk of stroke in the Northern Manhattan study. Stroke. 2012 May;43(5):1200-5. Epub 2012 Apr 12. PubMed PMID: 22499576; PubMed Central PMCID: PMC3347890.
http://stroke.ahajournals.org/content/43/5/1200.full

2. Relationship between achieved blood pressure, dietary habits and cardiovascular disease in hypertensive patients treated with olmesartan: the OMEGA study. Teramoto T, Kawamori R, Miyazaki S, Teramukai S, Shirayama M, Hiramatsu K, Kobayashi F; the OMEGA Study Group. Hypertens Res. 2012 Jul 5. doi: 10.1038/hr.2012.93. [Epub ahead of print] PMID: 22763478 [PubMed - as supplied by publisher]

3: Strazzullo P, D'Elia L, Kandala NB, Cappuccio FP. Salt intake, stroke, and cardiovascular disease: meta-analysis of prospective studies. BMJ. 2009 Nov 24;339:b4567. doi: 10.1136/bmj.b4567. Review. PubMed PMID: 19934192; PubMed Central PMCID: PMC2782060. http://www.bmj.com/content/339/bmj.b4567.full

4: D'Elia L, Rossi G, Ippolito R, Cappuccio FP, Strazzullo P. Habitual salt intake and risk of gastric cancer: A meta-analysis of prospective studies. Clin Nutr. 2012 Jan 30. [Epub ahead of print] PubMed PMID: 22296873.
User avatar
JeffN
 
Posts: 9412
Joined: Tue Jan 08, 2008 5:56 am

Re: Time to end the war on Salt?

Postby JeffN » Wed May 15, 2013 7:48 am

A few more on the problems with salt...

1) Salt & health

a) Effect of lower sodium intake on health: systematic review and meta-analyses. BMJ. 2013 Apr 3;346:f1326. doi: 10.1136/bmj.f1326.
PMID: 23558163

Free Article
http://www.bmj.com/content/346/bmj.f132 ... d=23558163

Abstract

OBJECTIVE: To assess the effect of decreased sodium intake on blood pressure, related cardiovascular diseases, and potential adverse effects such as changes in blood lipids, catecholamine levels, and renal function.

DESIGN: Systematic review and meta-analysis.

DATA SOURCES: Cochrane Central Register of Controlled Trials, Medline, Embase, WHO International Clinical Trials Registry Platform, the Latin American and Caribbean health science literature database, and the reference lists of previous reviews.

STUDY SELECTION: Randomised controlled trials and prospective cohort studies in non-acutely ill adults and children assessing the relations between sodium intake and blood pressure, renal function, blood lipids, and catecholamine levels, and in non-acutely ill adults all cause mortality, cardiovascular disease, stroke, and coronary heart disease. STUDY APPRAISAL AND SYNTHESIS: Potential studies were screened independently and in duplicate and study characteristics and outcomes extracted. When possible we conducted a meta-analysis to estimate the effect of lower sodium intake using the inverse variance method and a random effects model. We present results as mean differences or risk ratios, with 95% confidence intervals.

RESULTS: We included 14 cohort studies and five randomised controlled trials reporting all cause mortality, cardiovascular disease, stroke, or coronary heart disease; and 37 randomised controlled trials measuring blood pressure, renal function, blood lipids, and catecholamine levels in adults. Nine controlled trials and one cohort study in children reporting on blood pressure were also included. In adults a reduction in sodium intake significantly reduced resting systolic blood pressure by 3.39 mm Hg (95% confidence interval 2.46 to 4.31) and resting diastolic blood pressure by 1.54 mm Hg (0.98 to 2.11). When sodium intake was <2 g/day versus =/>2 g/day, systolic blood pressure was reduced by 3.47 mm Hg (0.76 to 6.18) and diastolic blood pressure by 1.81 mm Hg (0.54 to 3.08). Decreased sodium intake had no significant adverse effect on blood lipids, catecholamine levels, or renal function in adults (P>0.05). There were insufficient randomised controlled trials to assess the effects of reduced sodium intake on mortality and morbidity. The associations in cohort studies between sodium intake and all cause mortality, incident fatal and non-fatal cardiovascular disease, and coronary heart disease were non-significant (P>0.05). Increased sodium intake was associated with an increased risk of stroke (risk ratio 1.24, 95% confidence interval 1.08 to 1.43), stroke mortality (1.63, 1.27 to 2.10), and coronary heart disease mortality (1.32, 1.13 to 1.53). In children, a reduction in sodium intake significantly reduced systolic blood pressure by 0.84 mm Hg (0.25 to 1.43) and diastolic blood pressure by 0.87 mm Hg (0.14 to 1.60).

CONCLUSIONS: High quality evidence in non-acutely ill adults shows that reduced sodium intake reduces blood pressure and has no adverse effect on blood lipids, catecholamine levels, or renal function, and moderate quality evidence in children shows that a reduction in sodium intake reduces blood pressure. Lower sodium intake is also associated with a reduced risk of stroke and fatal coronary heart disease in adults. The totality of evidence suggests that most people will likely benefit from reducing sodium intake.


b) Salt in health and disease--a delicate balance.
N Engl J Med. 2013 Mar 28;368(13):1229-37. doi: 10.1056/NEJMra1212606.

CONCLUSIONS
Although it has been difficult to separate salt need from salt preference, current levels of salt consumption exceed salt need and are associated with adverse clinical outcomes. High salt intake is associated with high blood pressure and increased rates of cardiovascular disease. Experimental studies continue to provide information about mechanisms for these adverse effects of salt. In clinical trials, a reduction in salt intake is associated with reduced blood pressure, more so in persons with hypertension than in those with normal blood pressure. Although not discussed in the present review, it should be noted that reduced salt intake is associated with greater blood-pressure responses to antihypertensive drug therapy, including drug therapy in patients with resistant hypertension.85,86 Most, but not all, clinical trials have shown that reduced salt intake is also associated with decreased risks of cardiovascular events and death. Consequently, recommendations for reducing the currently high levels of salt consumption in the general population seem justifiable, although in terms of safety, the lower limit of salt consumption has not been clearly identified. It may be premature to dis-count the apparently paradoxical cardiovascular outcomes associated with low salt intake, particularly in specific clinical conditions (e.g., type 1 or type 2 diabetes and congestive heart failure that is aggressively treated with diuretic agents). Less-rigorous targets for salt reduction may be appropriate for these and other patient groups.


2) Salt impairs the endothelium

a) Effects of a low-salt diet on flow-mediated dilatation in humans. Am J Clin Nutr. 2009 Feb;89(2):485-90. doi: 10.3945/ajcn.2008.26856. Epub 2008 Dec 23. PMID:19106240

Abstract

BACKGROUND:

The effect of salt reduction on vascular function, assessed by brachial artery flow-mediated dilatation (FMD), is unknown.

OBJECTIVE:

Our aim was to compare the effects of a low-salt (LS; 50 mmol Na/d) diet with those of a usual-salt (US; 150 mmol Na/d) diet on FMD.

DESIGN:

This was a randomized crossover design in which 29 overweight and obese normotensive men and women followed an LS diet and a US diet for 2 wk. Both diets had similar potassium and saturated fat contents and were designed to ensure weight stability. After each intervention, FMD, pulse wave velocity, augmentation index, and blood pressure were measured.

RESULTS:

FMD was significantly greater (P = 0.001) with the LS diet (4.89 +/- 2.42%) than with the US diet (3.37 +/- 2.10%), systolic blood pressure was significantly (P = 0.02) lower with the LS diet (112 +/- 11 mm Hg) than with the US diet (117 +/- 13 mm Hg), and 24-h sodium excretion was significantly lower (P = 0.0001) with the LS diet (64.1 +/- 41.3 mmol) than with the US diet (156.3 +/- 56.7 mmol). There was no correlation between change in FMD and change in 24-h sodium excretion or change in blood pressure. No significant changes in augmentation index or pulse wave velocity were observed.

CONCLUSIONS:

Salt reduction improves endothelium-dependant vasodilation in normotensive subjects independently of the changes in measured resting clinic blood pressure. These findings suggest additional cardioprotective effects of salt reduction beyond blood pressure reduction. The trial is registered with the Australian and New Zealand Clinical Trials Registry (unique identifier: ANZCTR12607000381482; http://www.anzctr.org.au/trial_view.aspx?ID=82159).



b) Low dietary sodium intake is associated with enhanced vascular endothelial function in middle-aged and older adults with elevated systolic blood pressure. Ther Adv Cardiovasc Dis. 2009 Oct;3(5):347-56. doi: 10.1177/1753944709345790. Epub 2009 Sep 1.

Abstract
BACKGROUND: Age and increasing systolic blood pressure (BP) are associated with vascular endothelial dysfunction, but the factors involved are incompletely understood. We tested the hypothesis that vascular endothelial function is related to dietary sodium intake among middle-aged and older adults (MA and O) with elevated systolic BP.

METHODS: Data were analyzed on 25 otherwise healthy adults aged 48-73 years with high normal systolic BP or stage I systolic hypertension (130-159 mmHg). Self-reported sodium intake was <100 mmol/d in 12 (7 M) subjects (low sodium, 73+/-6 mmol/d) and between 100 and 200 mmol/d in 13 (9 M) subjects (normal sodium, 144+/-6 mmol/d).

RESULTS: Groups did not differ in other dietary factors, age, body weight and composition, BP, metabolic risk factors, physical activity and maximal aerobic capacity. Plasma concentrations of norepinephrine, endothelin-1, oxidized low-density lipoproteins (LDL), antioxidant status and inflammatory markers did not differ between groups. Brachial artery flow-mediated dilation (FMD) was 42% (mm Delta) to 52% (% Delta) higher in the low versus normal sodium group (p < 0.05). In all subjects, brachial artery FMD was inversely related to dietary sodium intake (FMD mm Delta r =-0.40, p < 0.05; %Delta r =-0.53, p < 0.01). Brachial artery FMD was not related to any other variable. In contrast, endothelium-independent dilation did not differ between groups (p >or= 0.24) and was not related to sodium intake in the overall group (p >or= 0.29).

CONCLUSIONS: Low sodium intake is associated with enhanced brachial artery FMD in MA and O with elevated systolic BP. These results suggest that dietary sodium restriction may be an effective intervention for improving vascular endothelial function in this high-risk group.



c) Endothelial function is impaired after a high-salt meal in healthy subjects. Am J Clin Nutr. 2011 Mar;93(3):500-5. doi: 10.3945/ajcn.110.006155. Epub 2011 Jan 12. PMID: 21228265

Abstract

BACKGROUND:

Dietary salt is related to blood pressure (BP), and cardiovascular disease and increased sodium intakes have been shown to impair vascular function. The effect of salt on endothelial function postprandially is unknown.

OBJECTIVE:

The aim was to investigate the postprandial effect of dietary salt on endothelial function as measured by flow-mediated dilatation (FMD) and peripheral arterial tonometry in healthy subjects.

DESIGN:

Sixteen healthy, normotensive subjects received a meal with added salt (HSM; 65 mmol Na) and a control low-salt meal (LSM; 5 mmol Na) on 2 separate occasions in a randomized order. Endothelial function was measured while fasting and postprandially at 30, 60, 90, and 120 min by using FMD and reactive hyperemia peripheral arterial tonometry. BP was also measured.

RESULTS:

Baseline FMD, reactive hyperemia index (RHI), and BP values were similar across interventions. Overall FMD was reduced 2 h postprandially. FMD was significantly more impaired after the HSM than after the LSM at 30 min [HSM (mean ± SD): 3.39 ± 2.44%; LSM: 6.05 ± 3.21%; P < 0.01] and at 60 min (HSM: 2.20 ± 2.77%; LSM: 4.64 ± 2.48%; P < 0.01). No significant differences in BP or RHI were observed between meals.

CONCLUSIONS:

An HSM, which reflects the typical amount of salt consumed in a commonly eaten meal, can significantly suppress brachial artery FMD within 30 min. These results suggest that high salt intakes have acute adverse effects on vascular dilatation in the postprandial state. This trial was registered at http://www.anzctr.org.au/trial_view.aspx?ID=335115 as ACTRN12610000124033.



d) High dietary sodium intake impairs endothelium-dependent dilation in healthy salt-resistant humans. J Hypertens. 2012 Dec 20. [Epub ahead of print] PMID:23263240. J Hypertens. 2013 Mar;31(3):530-6. doi: 10.1097/HJH.0b013e32835c6ca8. PMID 23263240

Abstract

BACKGROUND:: Excess dietary sodium has been linked to the development of hypertension and other cardiovascular diseases. In humans, the effects of sodium consumption on endothelial function have not been separated from the effects on blood pressure. The present study was designed to determine if dietary sodium intake affected endothelium-dependent dilation (EDD) independently of changes in blood pressure.

METHOD:: Fourteen healthy salt-resistant adults were studied (9M, 5F; age 33 ± 2.4 years) in a controlled feeding study. After a baseline run-in diet, participants were randomized to a 7-day high-sodium (300-350 mmol/day) and 7-day low-sodium (20 mmol/day) diet. Salt resistance, defined as a 5 mmHg or less change in a 24-h mean arterial pressure, was individually assessed while on the low-sodium and high-sodium diets and confirmed in the participants undergoing study (low-sodium: 85 ± 1 mmHg; high-sodium: 85 ± 2 mmHg). EDD was determined in each participant via brachial artery flow-mediated dilation on the last day of each diet.

RESULTS:: Sodium excretion increased during the high-sodium diet (P < 0.01). EDD was reduced on the high-sodium diet (low: 10.3 ± 0.9%, high: 7.3 ± 0.7%; P < 0.05). The high-sodium diet significantly suppressed plasma renin activity (PRA), plasma angiotensin II, and aldosterone (P < 0.05).

CONCLUSION:: These data demonstrate that excess salt intake in humans impairs endothelium-dependent dilation independently of changes in blood pressure.



e) Dietary sodium restriction reverses vascular endothelial dysfunction in middle-aged/older adults with moderately elevated systolic blood pressure. J Am Coll Cardiol. 2013 Jan 22;61(3):335-43. doi: 10.1016/j.jacc.2012.09.010. Epub 2012 Nov 7. PMID 23141486

Abstract
OBJECTIVES: This study sought to determine the efficacy of dietary sodium restriction (DSR) for improving vascular endothelial dysfunction in middle-aged/older adults with moderately elevated systolic blood pressure (SBP) (130-159 mm Hg) and the associated physiological mechanisms.

BACKGROUND: Vascular endothelial dysfunction develops with advancing age and elevated SBP, contributing to increased cardiovascular risk. DSR lowers BP, but its effect on vascular endothelial function and mechanisms involved are unknown.

METHODS: Seventeen subjects (11 men and 6 women; mean age, 62 ± 7 years) completed a, randomized crossover study of 4 weeks of both low (DSR) and normal sodium intake. Vascular endothelial function (endothelium-dependent dilation; EDD), nitric oxide (NO)/tetrahydrobiopterin (BH(4)) bioavailability, and oxidative stress-associated mechanisms were assessed following each condition.

RESULTS: Urinary sodium excretion was reduced by ≈ 50% (to 70 ± 30 mmol/day), and conduit (brachial artery flow-mediated dilation [FMD(BA)]) and resistance (forearm blood flow responses to acetylcholine [FBF(ACh)]) artery EDD were 68% and 42% (peak FBF(ACh)) higher following DSR (p < 0.005). Low sodium markedly enhanced NO-mediated EDD (greater ΔFBF(ACh) with endothelial NO synthase inhibition) without changing endothelial NO synthase expression/activation (Ser 1177 phosphorylation), restored BH(4) bioactivity (less ΔFMD(BA) with acute BH(4)), abolished tonic superoxide suppression of EDD (less ΔFMD(BA) and ΔFBF(ACh) with ascorbic acid infusion), and increased circulating superoxide dismutase activity (all p < 0.05). These effects were independent of ΔSBP. Other subject characteristics/dietary factors and endothelium-independent dilation were unchanged.

CONCLUSIONS: DSR largely reversed both macro- and microvascular endothelial dysfunction by enhancing NO and BH(4) bioavailability and reducing oxidative stress. Our findings support the emerging concept that DSR induces "vascular protection" beyond that attributable to its BP-lowering effects.


3) Salt & blood pressure

a) Long-term effects of salt substitution on blood pressure in a rural North Chinese population. J Hum Hypertens. 2012 Dec 20. doi: 10.1038/jhh.2012.63. [Epub ahead of print] PMID:23254595

Abstract

Dietary sodium and potassium intake can influence blood pressure. The effects of salt substitution on patients with hypertension and normotensive family member controls, however, have not been evaluated in a rural Chinese population.

The objective of this study, accordingly, was to assess the long-term effects of salt substitution on blood pressure.

We conducted a double-blind, randomized controlled trial among 200 families in rural China to establish the 2-year effects of a reduced-sodium, high-potassium salt substitute (65% sodium chloride, 25% potassium chloride, 10% magnesium sulfate) compared with normal salt (100% sodium chloride) on blood pressure.

Of the 462 individuals in the trial, 372 completed the study (81%). For normotensive subjects, the mean overall difference in systolic and diastolic blood pressure between the two groups at the 24-month follow-up was 2 mm Hg (95% confidence interval (CI) 0-4 mm Hg, P<0.05) and 2 mm Hg (95% CI 1-3 mm Hg, P<0.05), respectively. For subjects with hypertension, the mean overall decrease in systolic blood pressure showed a 4-mm Hg (95% CI 2-6 mm Hg, P<0.05) decrease between the two groups. Diastolic blood pressure was not affected by salt use in the hypertensive group.

Salt substitution lowers systolic blood pressure in hypertensive patients and lowers both systolic and diastolic blood pressure in normotensive controls. Salt substitution, therefore, may be an effective adjuvant therapy for hypertensive patients and the potential efficacy in preventing hypertension in normotensive individuals.


4) Salt now linked to auto-immune disease

a) Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1.Nature. 2013 Apr 25;496(7446):513-7. doi: 10.1038/nature11984. Epub 2013 Mar 6.

http://www.ncbi.nlm.nih.gov/pubmed/23467085

b) Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. Nature. 2013 Apr 25;496(7446):518-22. doi: 10.1038/nature11868. Epub 2013 Mar 6.

http://www.ncbi.nlm.nih.gov/pubmed/23467095

c) Immunology Exacerbating Autoimmune Disease with Salt
Sci. Signal., 30 April 2013 Vol. 6, Issue 273, p. ec97
[DOI: 10.1126/scisignal.2004284]
EDITORS' CHOICE

http://stke.sciencemag.org/cgi/content/ ... a051ac6c83

d) Science Volume 339, Number 6124, Issue of 8 March 2013
Dietary Salt Linked to Autoimmune Diseases

http://news.sciencemag.org/sciencenow/2 ... iseas.html

Salt in food may increase the risk of autoimmune diseases, according to provocative results reported this week in Nature. Immunobiologist David Hafler of the Yale School of Medicine and colleagues determined that a pinch of salt triggered cultures of unspecialized T cells to produce large numbers of destructive TH17 cells, which have been implicated in diseases such as psoriasis, rheumatoid arthritis, and multiple sclerosis. They also showed that a salt-rich diet makes mice more susceptible to experimental autoimmune encephalomyelitis (EAE), a rodent illness similar to multiple sclerosis.

A salt connection also crystallized when computational biologist Aviv Regev of the Broad Institute in Cambridge, immunologist Vijay Kuchroo of Harvard Medical School in Boston, and colleagues pieced together the molecular circuit that controls specialization of TH17 cells. An influential gene was SGK1, which helps cells manage sodium levels. And mice on high-salt rations developed a milder form of EAE if they lacked SGK1. The work doesn't establish that salt drives human autoimmune diseases, but "the stage is set to do precise experiments to test the hypothesis," Kuchroo says.


5) Salt & Stroke

a) The mediating effect of the Mediterranean diet on the role of discretionary and hidden salt intake regarding non-fatal acute coronary syndrome or stroke events: case/case-control study.

Atherosclerosis.
2012 Nov;225(1):187-93.
doi: 10.1016/j.atherosclerosis.2012.08.004. Epub 2012 Aug 27.

Abstract

OBJECTIVES: The aim of the present work was to evaluate the association between salt and salty food consumption on the development of an acute coronary syndrome (ACS) or ischemic stroke, under the context of adherence to the Mediterranean diet.

METHODS: During 2009-2010, 1000 participants were enrolled; 250 were consecutive patients with a first ACS, 250 were consecutive patients with a first ischemic stroke and 500 population-based, control subjects, one-for-one matched to the patients by age and sex. Socio-demographic, clinical, psychological, dietary and other lifestyle characteristics were measured. Consumption of foods with high salt concentration was evaluated with a special score (range 0-10). Adherence to the Mediterranean diet was assessed by the validated MedDietScore (theoretical range: 0-55).

RESULTS: After adjustment for potential confounding factors, use of salt added in table was associated with 81% higher likelihood of stroke (95% Confidence Interval: 1.03-3.20), whereas no association was observed regarding the development of ACS. Salt use during cooking was not associated with the development of ACS or stroke. Each unit increase of the score evaluating total salty food consumption was associated with 33% higher likelihood of stroke development (95% Confidence Interval: 1.08-1.64), but not with ACS. The effect of salt and salty food consumption regarding stroke presence was more evident for participants with lower adherence to the Mediterranean diet.

CONCLUSION: Simple dietary changes, with emphasis on reducing salt and salty food consumption, along with better adherence to the Mediterranean diet, should be incorporated in public health strategies for the primary prevention of stroke.

PMID: 22975231


b) High salt intake and stroke:
meta-analysis of the epidemiologic evidence.
CNS Neurosci Ther. 2012 Aug;18(8):691-701.
doi: 10.1111/j.1755-5949.2012.00355.x. Epub 2012 Jun 28.

Abstract

Research on the potential impact of high salt intake on health has grown rapidly over the last decades. Recent studies have suggested that high salt intake could also be associated with adverse effects on cardiovascular system. The review evaluated the current level of epidemiologic evidence on the association between the level of habitual salt intake and stroke outcome. We also suggest further research direction. There were 21 independent samples from 12 studies, with 225,693 participants (follow-up, 3-19 years) and 8135 stroke events. High salt intake was associated with risk of stroke event (pooled odd ratio [OR], 1.34; 95% confidence interval [CI], 1.19-1.51), stroke death (1.40; 1.21-1.63) and stroke onset (1.11; 1.00-1.24), ischemic stroke death (2.15; 1.57-2.95), not associated with risk of ischemic stroke onset (1.07, 0.95-1.2), with no significant evidence of publication bias. High salt intake is associated with significantly increased risk of stroke event. Further research should be directed toward clarifying and quantifying these possible effects and generating testable hypotheses on plausible biologic mechanisms.


c) Dietary Sodium and Risk of Stroke in the Northern Manhattan Study. Stroke. 2012; 43: 1200-1205
http://stroke.ahajournals.org/content/43/5/1200.long

Abstract

Background and Purpose—The American Heart Association recommends limiting sodium intake to ≤1500 mg/day for ideal cardiovascular health. Although sodium intake has been linked to vascular disease by direct relationship with hypertension, few studies have supported an association with stroke risk.

Methods—Participants were from the Northern Manhattan Study (mean age 69± 10 years, 64% women, 21% white, 53% Hispanic, 24% black), a population-based cohort study of stroke incidence. Sodium intake was assessed with a food frequency questionnaire at baseline and evaluated continuously and categorically: ≤1500 mg/day (12%), 1501 to 2300 mg/day (24%), 2301 to 3999 mg/day (43%), and ≥4000 mg/day (21%). Over a mean follow-up of 10 years, we examined the association between sodium consumption and 235 strokes using Cox models adjusting for sociodemographics, diet, behavioral/lifestyle, and vascular risk factors.

Results—Of 2657 participants with dietary data, the mean sodium intake was 3031±1470 mg/day (median, 2787; interquartile range, 1966–3815 mg/day). Participants who consumed ≥4000 mg/day sodium had an increased risk of stroke (hazard ratio, 2.59; 95% CI, 1.27–5.28) versus those who consumed ≤1500 mg/day with a 17% increased risk of stroke for each 500-mg/day increase (95% CI, 1.07–1.27).

Conclusions—High sodium intake was prevalent and associated with an increased risk of stroke independent of vascular risk factors. The new American Heart Association dietary sodium goals will help reduce stroke risk.

6) Salt & Arteriosclerosis

The authors "suggest that excessive salt intake may be an important direct pathogenic factor for cardiovascular disease". These results suggest that an excessive salt intake promotes the overgrowth of fibrous tissue in the arteries, arterioles and other tissues and this fibrosis gradually over time makes the blood vessels increasingly stiff and eventually makes them more resistant to the flow of blood

a) Improved arterial distensibility in normotensive subjects on a low salt diet.
Arteriosclerosis. 1986 Mar-Apr;6(2):166-9.

http://www.ncbi.nlm.nih.gov/pubmed/3954670
http://atvb.ahajournals.org/content/6/2/166.long

Abstract
Arterial pulse wave velocity (PWV), a noninvasive index of arterial distensibility, was measured in 57 normotensive subjects who followed a voluntary low salt diet for a period ranging from 8 months to 5 years (mean, 24.8 months). Subjects who followed a regular diet were matched for age and mean arterial pressure with the low salt (LS) sample and were used as controls (C). For both samples, subjects were divided into three age groups: Group 1 (aged 2 to 19 years, n = 16), Group 2 (29 to 44 years, n = 26), and Group 3 (45 to 66 years, n = 15). There was a marked increase in aortic PWV with age in the control sample but not in the LS sample. There was no significant difference in aortic PWV for Group 1, but in Groups 2 and 3, the LS subjects showed a decrease of 21.8% and 22.7%, respectively, compared to C subjects. Aortic PWV (cm/sec) was: Group 1: C = 581 (SE44), LS = 614 (SE31); Group 2: C = 942 (SE46); LS = 737 (SE27) (p less than 0.001); Group 3: C = 958 (SE77), LS = 741 (SE25) (p less than 0.05]. Arm and leg PWV were also significantly lower in the older age groups. These findings suggest that normotensive adult subjects who follow a low salt diet (mean intake, 44 mmol Na/24 hours) have reduced arterial stiffness and that the effect is independent of blood pressure. This is prima facie evidence that reduced salt intake has a beneficial effect in improving distensibility of the central aorta and large peripheral arteries, which is independent of its antihypertensive action.
PMID: 3954670

b) Salt induces myocardial and renal fibrosis in the normotensive and hypertensive rats.
Circulation. 1998 Dec 8;98(23):2621-8.

Abstract

BACKGROUND:
The detrimental effects of high dietary salt intake may not only involve effects on blood pressure and organ hypertrophy but also lead to tissue fibrosis independently of these factors.

METHODS AND RESULTS:
The effect of a normal (1%) or high (8%) sodium chloride diet on myocardial and renal fibrosis was assessed by quantitative histomorphometry in spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto rats (WKYs). The effect of salt on transforming growth factor-beta1 (TGF-beta1) gene expression was assessed by Northern blot hybridization. A high-salt diet from 8 to 16 weeks of age resulted in increased blood pressure and left ventricular and renal hypertrophy in both WKYs and SHRs. Marked interstitial fibrosis was demonstrated in the left ventricle (LV), glomeruli, and renal tubules and in intramyocardial arteries and arterioles but not in the right ventricle. The collagen volume fraction increased significantly after high-salt diet in the LV, intramyocardial arteries and arterioles, glomeruli, and peritubular areas in both WKYs and SHRs. In the kidneys, glomerular and peritubular type IV collagen was also increased. There was overexpression of TGF-beta1 mRNA in the LV and kidneys in both rat strains after a high-salt diet (all P<0.001).

CONCLUSIONS:
High dietary salt led to widespread fibrosis and increased TGF-beta1 in the heart and kidney in normotensive and hypertensive rats. These results suggest a specific effect of dietary salt on fibrosis, possibly via TGF-beta1-dependent pathways, and further suggest that excessive salt intake may be an important direct pathogenic factor for cardiovascular disease.
PMID: 9843472

c) Effects of a low-salt diet on flow-mediated dilation in humans.
Am J Clin Nutr 2009;89:485-90

http://www.ncbi.nlm.nih.gov/pubmed/19106240

Abstract

BACKGROUND:
The effect of salt reduction on vascular function, assessed by brachial artery flow-mediated dilatation (FMD), is unknown.

OBJECTIVE:
Our aim was to compare the effects of a low-salt (LS; 50 mmol Na/d) diet with those of a usual-salt (US; 150 mmol Na/d) diet on FMD.

DESIGN:
This was a randomized crossover design in which 29 overweight and obese normotensive men and women followed an LS diet and a US diet for 2 wk. Both diets had similar potassium and saturated fat contents and were designed to ensure weight stability. After each intervention, FMD, pulse wave velocity, augmentation index, and blood pressure were measured.

RESULTS:
FMD was significantly greater (P = 0.001) with the LS diet (4.89 +/- 2.42%) than with the US diet (3.37 +/- 2.10%), systolic blood pressure was significantly (P = 0.02) lower with the LS diet (112 +/- 11 mm Hg) than with the US diet (117 +/- 13 mm Hg), and 24-h sodium excretion was significantly lower (P = 0.0001) with the LS diet (64.1 +/- 41.3 mmol) than with the US diet (156.3 +/- 56.7 mmol). There was no correlation between change in FMD and change in 24-h sodium excretion or change in blood pressure. No significant changes in augmentation index or pulse wave velocity were observed.

CONCLUSIONS:
Salt reduction improves endothelium-dependant vasodilation in normotensive subjects independently of the changes in measured resting clinic blood pressure. These findings suggest additional cardioprotective effects of salt reduction beyond blood pressure reduction.
PMID: 19106240

d) Endothelial function is impaired after a high-salt meal in healthy subjects.
Am J Clin Nutr 2011;93:500-5.

http://www.ncbi.nlm.nih.gov/pubmed/21228265

Abstract

BACKGROUND:
Dietary salt is related to blood pressure (BP), and cardiovascular disease and increased sodium intakes have been shown to impair vascular function. The effect of salt on endothelial function postprandially is unknown.

OBJECTIVE:
The aim was to investigate the postprandial effect of dietary salt on endothelial function as measured by flow-mediated dilatation (FMD) and peripheral arterial tonometry in healthy subjects.

DESIGN:
Sixteen healthy, normotensive subjects received a meal with added salt (HSM; 65 mmol Na) and a control low-salt meal (LSM; 5 mmol Na) on 2 separate occasions in a randomized order. Endothelial function was measured while fasting and postprandially at 30, 60, 90, and 120 min by using FMD and reactive hyperemia peripheral arterial tonometry. BP was also measured.

RESULTS:
Baseline FMD, reactive hyperemia index (RHI), and BP values were similar across interventions. Overall FMD was reduced 2 h postprandially. FMD was significantly more impaired after the HSM than after the LSM at 30 min [HSM (mean ± SD): 3.39 ± 2.44%; LSM: 6.05 ± 3.21%; P < 0.01] and at 60 min (HSM: 2.20 ± 2.77%; LSM: 4.64 ± 2.48%; P < 0.01). No significant differences in BP or RHI were observed between meals.

CONCLUSIONS:
An HSM, which reflects the typical amount of salt consumed in a commonly eaten meal, can significantly suppress brachial artery FMD within 30 min. These results suggest that high salt intakes have acute adverse effects on vascular dilatation in the postprandial state. This trial was registered at http://www.anzctr.org.au/trial_view.aspx?ID=335115 as ACTRN12610000124033.
PMID: 21228265


E) Postprandial effects of a high salt meal on serum sodium, arterial stiffness, markers of nitric oxide production and markers of endothelial function. Dickinson KM1, Clifton PM2, Burrell LM3, Barrett PH4, Keogh JB5. Atherosclerosis. 2014 Jan;232(1):211-6. doi: 10.1016/j.atherosclerosis.2013.10.032. Epub 2013 Nov 20.

Abstract
AIM: The aim of the study was to determine if a high salt meal containing 65 mmol Na causes a rise in sodium concentrations and a reduction in plasma nitrate/nitrite concentrations (an index of nitric oxide production). Secondary aims were to determine the effects of a high salt meal on augmentation index (AIx) a measure of arterial stiffness and markers of endothelial function.

METHODS AND RESULTS: In a randomised cross-over study 16 healthy normotensive adults consumed a low sodium soup containing 5 mmol Na and a high sodium soup containing 65 mmol Na. Sodium, plasma nitrate/nitrite, endothelin-1 (ET-1), C-reactive protein (CRP), vasopressin (AVP) and atrial natriuretic peptide (ANP) concentrations before and every 30 min after the soup for 2 h. Blood pressure (BP) and AI were also measured at these time points. There were significant increases in serum sodium, osmolality and chloride in response to the high sodium meal. However plasma nitrate/nitrite concentrations were not different between meals (meal p = 0.812; time p = 0.45; meal × time interaction p = 0.50). Plasma ANP, AVP and ET-1 were not different between meals. AI was significantly increased following the high sodium meal (p = 0.02) but there was no effect on BP.

CONCLUSIONS: A meal containing 65 mmol Na increases serum sodium and arterial stiffness but does not alter postprandial nitrate/nitrite concentration in healthy normotensive individuals. Further research is needed to explore the mechanism by which salt affects vascular function in the postprandial period. This trial was registered with the Australian and New Zealand Clinical Trials Registry Unique Identifier: ACTRN12611000583943http://www.anzctr.or ... ?ID=343019.


7) Salt, sodium, calcium & osteoporosis

https://www.drmcdougallforums.com/viewt ... =22&t=6508

8 ) Salt and Calcium Oxalate Stones


Effects of a low-salt diet on idiopathic hypercalciuria in calcium-oxalate stone formers: a 3-mo randomized controlled trial.
Nouvenne A, Meschi T, Prati B, Guerra A, Allegri F, Vezzoli G, Soldati L, Gambaro G, Maggiore U, Borghi L.
Am J Clin Nutr. 2010 Mar;91(3):565-70. doi: 10.3945/ajcn.2009.28614. Epub 2009 Dec 30.
PMID:20042524
http://ajcn.nutrition.org/content/91/3/565.long
http://ajcn.nutrition.org/content/early ... l.pdf+html
http://ajcn.nutrition.org/content/suppl ... pp_1-2.doc

Abstract

BACKGROUND: A direct relation exists between sodium and calcium excretion, but randomized studies evaluating the sustained effect of a low-salt diet on idiopathic hypercalciuria, one of the main risk factors for calcium-oxalate stone formation, are still lacking.

OBJECTIVE: Our goal was to evaluate the effect of a low-salt diet on urinary calcium excretion in patients affected by idiopathic calcium nephrolithiasis.

DESIGN: Patients affected by idiopathic calcium stone disease and hypercalciuria (>300 mg Ca/d in men and >250 mg Ca/d in women) were randomly assigned to receive either water therapy alone (control diet) or water therapy and a low-salt diet (low-sodium diet) for 3 mo. Twenty-four-hour urine samples were obtained twice from all patients: one sample at baseline on a free diet and one sample after 3 mo of treatment.

RESULTS: A total of 210 patients were randomly assigned to receive a control diet (n = 102) or a low-sodium diet (n = 108); 13 patients (2 on the control diet, 11 on the low-sodium diet) withdrew from the trial. At the follow-up visit, patients on the low-sodium diet had lower urinary sodium (mean +/- SD: 68 +/- 43 mmol/d at 3 mo compared with 228 +/- 57 mmol/d at baseline; P < 0.001). Concomitant with this change, they showed lower urinary calcium (271 +/- 86 mg/d at 3 mo compared with 361 +/- 129 mg/d on the control diet, P < 0.001) and lower oxalate excretion (28 +/- 8 mg/d at 3 mo compared with 32 +/- 10 mg/d on the control diet, P = 0.001). Urinary calcium was within the normal range in 61.9% of the patients on the low-salt diet and in 34.0% of those on the control diet (difference: +27.9%; 95% CI: +14.4%, +41.3%; P < 0.001).

CONCLUSION: A low-salt diet can reduce calcium excretion in hypercalciuric stone formers.
User avatar
JeffN
 
Posts: 9412
Joined: Tue Jan 08, 2008 5:56 am

Re: Time to end the war on Salt?

Postby JeffN » Thu May 16, 2013 8:48 am

In regard to the new IOM report.

I am receiving many emails reflecting concern over liming salt/sodium as the news media is saying this report says that limiting salt/sodium is dangerous.

So, let's put this in perspective...

Most Americans, "say" the take in around 3500 mg/day, which is 34% more than the Upper Limit of what is recommended, which is 2300. However, in reality, most Americans probably get more like 6-10K which is 70% more than the Upper Limit. Just check out typical restaurant meals and packaged foods and we can see how easy it is to take in that much. Regardless of whether we use the 3500 or the higher amount, over 90% of Americans already exceed the Upper Limit of 2300 on a daily basis

http://www.ncbi.nlm.nih.gov/pubmed/22854410

Sodium and potassium intakes among US adults: NHANES 2003-2008.
Am J Clin Nutr. 2012 Sep;96(3):647-57. doi: 10.3945/ajcn.112.034413. Epub 2012 Aug 1.

"Overall, 99.4% of US adults consumed more sodium daily than recommended by the AHA (<1500 mg), and 90.7% consumed more than the IOM Tolerable Upper Intake Level (2300 mg)."

"In US adults who are recommended by the Dietary Guidelines to further reduce sodium intake to 1500 mg/d (ie, African Americans aged ≥51 y or persons with hypertension, diabetes, or chronic kidney disease), 98.8% overall consumed >1500 mg/d, and 60.4% consumed >3000 mg/d-more than double the recommendation. "


As you can see, most people are at no risk of getting in too little sodium. :)

Now how many people are actually salt sensitive and can benefit from a reduction in sodium?

About 31% of American adults have high blood pressure & another 30% of American adults have prehypertension—blood pressure measurements that are higher than normal, but not yet in the high blood pressure range, which raises your risk of developing high blood pressure. So, 61% of Americans are most likely salt sensitive and that is not counting all the ones who have not yet developed hypertension or prehypertension.

Now, lets adjust "normal" down to 110/70 and pre-HTN to >110/>70, as it should be from my perspective, & the percentage of Americans who are most likely salt sensitive, is even higher than 61%.

In addition, it is estimated that over 90% of all Americans will develop high blood pressure in their lifetime.

For all of these people, it is time to shake the salt habit and cut back!

Also, why does salt reduction often appear to fail in the general population? Many people with HTN come to me and say they are not "salt responders" and they have tried a low salt diet and it did not work.

The reason why many people think they are not salt responders is because they never really understand how to get the salt out of their diet. Without understanding where it is all coming from and how best to eliminate it and how to understand salt density, most American will fail at it. This is why so many of those who come to us say they have tried to eliminate salt and are just not salt responders and three days later, they are off their medications.

So, who is at risk of to little salt?

This "at risk population" discussed in the report are people on massive doses of diuretics and other BP-meds with failing hearts. In these very ill people, drastically lowering their salt intake (without changing their meds!) can indeed be the final straw.

It would be like taking someone on a high dose of insulin and drastically reducing their CHO intake and then when they die from a hypoglycemic shock concluding the problem was too little CHO - rather than too much injected insulin and other drugs to push blood glucose lower.

And, this is what the report said..

"Specifically, in some studies, low sodium intakes apparently appeared to show an association with risk of disease, when, in fact, the relationship may have been that the disease itself led to low or incomplete measures of sodium among those with pre-existing disease."

"The committee found that the evidence from multiple randomized controlled trials (RCTs) that were conducted by a single investigative team indicated that low sodium intake (e.g., to 1,840 mg/day) may lead to greater risk of adverse events in congestive heart failure (CHF) patients with reduced ejection fraction and who are receiving certain aggressive therapeutic regimens."

As Dr McDougall has always said, "aggressive treatments kill."

This is just another example of it.

As far as I know, the only data anywhere showing people not on BP-drugs are harmed by reducing sodium to less than 1500mg/day would only be the case for those with untreated Addison's Disease. In these people the lack of aldosterone production makes them lose lot's of salt. People with normal adrenal glands and in reasonable healthy kidneys simply reduce salt excretion when salt intake is reduced so there is no health risk at all. Instead there is only the benefit of reduced BP & CVD, etc..

A review of this thread will highlight all the other health concerns of too much sodium, including the amounts currently consumed by most people.

Also, in regard to endurance athletes and those who work out in high temperatures, if they have been consuming a high sodium diet and have adapted to it, they can lose sodium though their sweat. However, when one adapts to a low sodium diet, which can take about a week or so, they will lose much less sodium through their sweat and this will not be an issue. This is covered in some of the previous discussions on sodium

viewtopic.php?f=22&t=16465&p=149767

Lastly, for those who want to read more on salt and health, I would also recommend reading this Continuing Education course on the topic of salt and health

http://foodandhealth.com/cpecourses/salt_new.php

In Health
Jeff
User avatar
JeffN
 
Posts: 9412
Joined: Tue Jan 08, 2008 5:56 am

Re: UPDATED!! Time to end the war on Salt?

Postby JeffN » Sat May 18, 2013 7:11 am

The AHA weighs in on the IOM report and agrees with my above comments

In health
Jeff

http://newsroom.heart.org/news/new-iom- ... ssociation

"Much of the research suggesting that decreasing sodium intake has no effect on or leads to increased heart disease and death has been conducted among sick patients, rather than the general population. “The research that the IOM partially based their conclusions on showed inconsistencies in the relationship between sodium intake and health outcomes. Yet these studies were not designed to assess the impact of various levels of sodium intake on cardiovascular health."

"Although the scientific community continues to debate the use of biomarkers in general and surrogate indicators of health outcomes, recent evidence attributes 35 percent of heart attack and stroke events, 49 percent of heart failure episodes, and 24 percent of premature deaths to high blood pressure."

"A recent review of current research conducted by the American Heart Association concluded that people who don’t currently have high blood pressure will benefit from consuming less than 1,500 mg of sodium daily, because less dietary sodium will significantly reduce the rise in blood pressure that occurs as we age. Ninety percent of all Americans are expected to develop high blood pressure in their lifetime. Independent of its effects on blood pressure, excess sodium intake adversely affects the heart, kidneys and blood vessels."
User avatar
JeffN
 
Posts: 9412
Joined: Tue Jan 08, 2008 5:56 am

Re: UPDATED!! Time to end the war on Salt?

Postby JeffN » Thu May 23, 2013 8:55 am

The Pritikin Center and my colleague, Jay Kenney, PhD, RD, weighs in on the IOM report.

http://www.pritikin.com/your-health/hea ... newsletter

In Health
Jeff
User avatar
JeffN
 
Posts: 9412
Joined: Tue Jan 08, 2008 5:56 am

Re: UPDATED!! Time to end the war on Salt?

Postby JeffN » Sun May 26, 2013 8:11 am

Salt: friend or foe?
Lancet Volume 381, Issue 9880, 25–31 May 2013, Pages 1790
Editorial

Dietary guidelines advise against the consumption of too much salt. A high intake of sodium causes raised blood pressure—an established risk factor for heart disease, stroke, and kidney disease. But how much salt is too much? And could a very low salt intake also be detrimental?

The effects of salt consumption on health are controversial, but reduced salt intake is mostly believed to decrease the risk of cardiovascular disease. The 2010 Dietary Guidelines for Americans recommend a maximum daily consumption of 2300 mg salt for healthy adults and 1500 mg for people at raised risk of heart disease (eg, those older than 51 years, people with diabetes, and black people). The American Heart Association even advises that everyone adheres to the 1500 mg limit, irrespective of age or race. However, most people still eat too much salt—on average, US adults consume 3400 mg (about 1·5 teaspoons) daily.

In May, 2013, the Institute of Medicine reviewed recent evidence (39 studies) and reported that a very low salt intake might not be as beneficial as was previously thought, at least for those at increased risk of heart disease. Less than 2300 mg salt daily could even increase some cardiovascular risk factors, such as blood lipids and insulin resistance, potentially triggering heart problems. Moreover, no evidence suggested a benefit of an ultra-low sodium intake (<1500 mg daily) in any population.

High study heterogeneity, and the fact that the effects of reduced sodium intake on health outcomes cannot always be distinguished from those of overall diet changes, make accurate conclusions difficult. The report concludes that more trials are needed to address gaps in the data, especially studies of the effects of a 1500–2300 mg daily salt intake in different groups.

The report needs cautious interpretation—it does not suggest that people use salt freely. The Institute agrees that a link between high salt consumption and increased risk of cardiovascular disease persists, and that average intake needs to be reduced. However, the findings about very low sodium levels will help to clarify public health messages (eg, updated US dietary guidelines, due in 2015) and hopefully improve health outcomes.
User avatar
JeffN
 
Posts: 9412
Joined: Tue Jan 08, 2008 5:56 am

Re: UPDATED!! Time to end the war on Salt?

Postby JeffN » Thu Jun 06, 2013 1:38 pm

Sodium Reduction in Populations:
Insights From the Institute of Medicine Committee.
JAMA. 2013;():1-2.
doi:10.1001/jama.2013.7687.
Strom BL, Anderson CM, Ix JH.

http://jama.jamanetwork.com/article.asp ... F06%2F2013


"After release of the IOM report, several news outlets highlighted disagreement among health agencies about targets for dietary sodium intake and reported that experts disagreed about the importance of blood pressure. Focusing the debate on specific targets misses the larger conclusion with which all are in agreement and may hinder implementation of important public health policy. Rather than focusing on disagreements about specific targets that currently affect less than 10% of the US population (ie, sodium intake of <2300 mg/d vs <1500 mg/ d), the IOM, AHA, WHO, and DGA are congruent in suggesting that excess sodium intake should be reduced, and this is likely to have significant public health effects. Accomplishing such a reduction will require efforts to decrease sodium in the food environment10 and provide individual consumers more choice in their dietary consumption of sodium."
User avatar
JeffN
 
Posts: 9412
Joined: Tue Jan 08, 2008 5:56 am

Re: UPDATED!! Time to end the war on Salt?

Postby JeffN » Sat Aug 24, 2013 11:21 am

Look what happens when a community makes a concerted effort over time to reduce the salt intake in their population.

Finland has aggressively reduced salt in food over 3 decades by requiring foods that are high in salt to carry a "high salt content" warning & has seen a 40% decline in average sodium intake, which helped produce a large reduction in BP levels & an 80% drop in deaths due to stroke.

http://www.worldactiononsalt.com/worlda ... 53774.html

Also, it is important to note that they did this not just by removing animal products but by reducing the amount of salt in many of the animal products, which gives more evidence to the point that it is not just the animal products but the salt that is causing the problems. Bread products, including those marketed as being "whole" grain and/or healthy, are one of the leading contributors of added salt to our diets.

"It is estimated that industry has reformulated some product groups, such as bread, meat products, cheeses and ready meals to reduce their salt content by about 20-25%."

In Health
Jeff
User avatar
JeffN
 
Posts: 9412
Joined: Tue Jan 08, 2008 5:56 am

Re: UPDATED!! Time to end the war on Salt?

Postby JeffN » Sun Sep 08, 2013 7:27 am

It is up to you!

The strongest action you can take is your own by limiting/eliminating sodium at home & especially in processed & restaurant foods!

"Between 2005 and 2011, the sodium content in 402 processed foods declined by approximately 3.5%, while the sodium content in 78 fast-food restaurant products increased by 2.6%. Although some products showed decreases of at least 30%, a greater number of products showed increases of at least 30%. The predominant finding is the absence of any appreciable or statistically significant changes in sodium content during 6 years.

... Reductions in sodium levels in processed & restaurant foods are inconsistent & slow. These findings are in accord with other data indicating the slow pace of voluntary reductions in sodium levels in processed & restaurant foods. Stronger action is needed to lower sodium levels & reduce the prevalence of HTN & CVD diseases.

Excess consumption of sodium is an important cause of hypertension, a major risk factor for heart disease & stroke. The higher the level of consumption, the greater is a person’s likelihood of developing hypertension. Numerous organizations have recommended reductions in sodium intake in the United States. Roughly 80% of the sodium consumed by Americans has been added by food manufacturers and restaurants."

http://www.actiononsalt.org.uk/news/Sal ... /99468.pdf

In Health
Jeff
User avatar
JeffN
 
Posts: 9412
Joined: Tue Jan 08, 2008 5:56 am

PreviousNext

Return to Jeff Novick, RD

Who is online

Users browsing this forum: No registered users and 18 guests


cron

Welcome!

Sign up to receive our regular articles, recipes, and news about upcoming events.