Discussion Board

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Jeff, thanks for that response.

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

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.

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

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.

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.

Let me put it in perspective...

The need for sodium is so low and the amount occurs so easily in foods that there is no RDA for sodium. The National Academy of Sciences says humans can survive on as little as 125 mgs/day. However, a whole plant food diet would easily provide 350-500 in what occurs naturally in foods.

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

The Upper Limit (UL) is set at 2300.

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.

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, 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?

In Health
Jeff

Absolutely, good to know the nuts and bolts.

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.

A few more recent ones..

1) Salt & health

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.


2) Salt impairs the endothelium

High dietary sodium intake impairs endothelium-dependent dilation in healthy salt-resistant humans. J Hypertens. 2012 Dec 20. [Epub ahead of print] 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.


3) Salt & blood pressure

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

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

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

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

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 and health

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.

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

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."