Comments to the Public consultation on salt in NNR5

Public consultation on the draft proposal for the first part of the Nordic Nutrition Recommendations 2012

-         Sodium as salt

 

Comments to the Public consultation on the draft proposal for the first part of the Nordic Nutrition Recommendations 2012 the part of Sodium as salt

 

The text in the Public consultation on the draft proposal for the first part of the Nordic Nutrition Recommendations 2012 the part of Sodium as salt is definitely wrong from a scientific standpoint and must be replaced.

 

The parts in lines 24-488 needs to be rephrased to be correct from the points of views in physiology, biochemistry and endocrinology.

 

So the proposed wordings are in the added proposition.

 

Comments regarding the NNR5 about salt

It is interesting that the NNR5 experts are referring to an older EFSA report from 1993 [1] (lines 492-4) instead of the EFSA report of 2005 in the reference list above. This clearly shows that the NNR5 experts seems to avoid modern and relevant references that oppose the experts hypothesis that salt is a health hazard

 

It seems that the NNR5 experts looking into the salt issue seems to be lacking fundamental knowledge in human physiology, biochemistry and endocrinology as they seem to be totally ignorant in these areas of knowledge.

 

The NNR5 experts must also, if they had done their homework properly, know that the nutrition experts of the US Department of Agriculture already 1999 knew that salt reduction had no positive effect on blood pressure. This is according to a transcribed taped discussion readable on the Health departments web site [2]

 

Also, in an article Stolarz-Skrzypek K et al write in their Conclusions :

 

“Conclusions In this population-based cohort, systolic blood pressure, but not diastolic pressure, changes over time aligned with change in sodium excretion, but this association did not translate into a higher risk of hypertension or CVD complications. Lower sodium excretion was associated with higher CVD mortality.”

 

“Lower sodium excretion was associated with higher CVD mortality” is interpreted by associated professor Wulf Becker in Livsmedelsverkets Protokoll nr 51 (Minutes number 51) at a meeting with expertgruppen för Kost- och hälsofrågor on 2011-09-20 §7 page 3 [3] 

 

“En annan meta-analys av Stolarz-Skrzypek K et al visar att högt saltintag är associerat med ökad risk för stroke och hjärt-kärlsjukdom. [4] http://jama.ama-assn.org/content/305/17/1777.full.pdf+html?etoc

”(Another meta analysis by Stolarz-Skrzypek K et al shows that a high salt intake is associated to increased risk for stroke and cardio-vascular diseases)”

 

Becker here seems to violate the Swedish Constitution 1st chapter 9th §, both the matter of factness and the objectivity criteria.

 

I’d rather see Becker declare other reasons than infringement of the Swedish Constitution for his statement. But the facts remains, Becker told the expert group a conclusion contrary to the conclusions in the article.

 

Also, there are quite a few articles stating that a low salt intake increases the CVD mortality, e.g. Alderman et al [5], Whalley [6] and Cohen [7].

 

Dr Helen Whalley wrote in Lancet that the analysis of NHANES I showed that eating a low salt diet showed a 20 % increase in CVD.

 

In May 2006 Dr Hillel Cohen showed data from NHANES II and 2008 data from NHANES III describing that eating less than five grams of salt increased the risk of coronary disease more than 50 %.

 

Again, some of the crucial articles regarding salt and hypertension are missing, e.g. the Cochrane review from 2011 [8].

 

The conclusion in the Cochrane abstract is:

“Sodium reduction resulted in a 1 % decrease in blood pressure in normotensives, a 3,5 % decrease in hypertensives, a significant increase in plasma renin, plasma aldosterone, plasma adrenalin and plasma noradrenalin, a 2,5 % increase in cholesterol and a 7 % increase in triglycerides. In general these effects were stable in studies lasting for 2 weeks or more.”

 

This means that the decrease in blood pressure is nonsignificant but there are significant increase in hypertensive and also sodium resorption hormones like plasma renin, plasma aldosterone, plasma adrenalin and plasma noradrenalin as the sodium level in the blood decreases while eating too low amounts of salt. When the salt level in the blood decreases below 125 mmol/L the kidneys try to restore a higher salt concentration by decreasing the blood volume and then the extra cellular volume decreases as well thus lowering the blood pressure. The homeostasis of the body tries to restore the volume by increasing ADH which dilutes the blood again by lowering sodium concentration threatening the homeostasis and life of the patient.

 

This condition is called SIADH or SISWI, easily corrected by letting the patient eat salt and drink water and the body will restore homeostasis.

 

I.V. infusion of salts is another alternative but that usually takes longer time and is more dangerous than the oral route.

 

A third option is to use ADH receptor blockers like tolvaptan, a vasopressin antagonist. But there are not much of an effect as 60 % of the patients treated with tolvaptan had normal sodium excretion after 30 days while 26 % in the placebo group had normal sodium excretion. According to Läkartidningen 2012 [9] about 19 % of all patients with hyponatremia died of sodium deficiency despite treatment with tolvaptan. But they did not get enough sodium in their diet.

 

The first National Health and Nutrition Examination Survey (NHANES I) established baseline information during 1971-75 in a representative sample of 20,729 American adults aged twenty-five to seventy-five. Of these, 11,348 underwent medical and nutritional examination.

They were rechecked in 1992. By then there had been 3,923 deaths, of which 1,970 were due to a cardiovascular disease. Comparing salt intakes, this study found that all-cause mortality was inversely related to salt intake. In other words, those who ate the most salt had the fewest deaths — from any cause. And the same was found for cardiovascular deaths. Dr Helen Whalley writing a feature in the Lancet, talks of the continuing debate on the supposed association between salt and hypertension. She points out that an analysis of the NHANES I survey shows that 'the heart attack fatality rate among those on low-sodium diets was 20% higher that those on normal diets.'[10]  She goes on to report a study on the Salt Institute's website on the impact of long-term salt reduction. It found 'a four-fold increase in heart attacks among those on low-salt diets'.

 

In 1998 a large meta-analysis was published in an attempt to resolve the controversy [11]. Fifty-eight trials published between 1966 and the end of 1997 were reviewed to estimate the effects of reduced sodium intake on systolic and diastolic blood pressure, particularly as in recent years the debate has been extended by studies indicating that reducing sodium intake has adverse effects. They found that reducing salt intake did reduce blood pressure slightly, but that it increased LDL cholesterol, the so-called 'bad' cholesterol. They conclude that 'These results do not support a general recommendation to reduce sodium intake.

 

Salt restriction research is biased

All those studies showing a decreased blood pressure with decreased salt intake are biased. They all have one arm with a low salt level like 6-9 gram salt per day and another arm with extremely low salt, around 3 grams per day. The findings are a slight decrease in blood pressure due to hypovolemia despite increase in the levels of hypertensive hormones like renin, aldosterone, adrenalin and noradrenalin. But all trials have seemingly actively forgotten the third arm, giving patients 20-30 g salt per day. That third arm will have the same blood pressure as the one with 6-9 g salt. This is because the glomeruli are filtering out about 1 g salt per minute and thus the blood pressure can not increase due to the fact that there is no salt retention, everything is filtered out. Still, the main problem for the kidneys is the reabsorption of sodium using at least three blood pressure increasing and sodium retention hormones.

 

But it is also interesting that patients with diabetes having the highest intake of salt have less insulin resistance.

 

According to physiological research from 1970th it is shown that newborn children in the colostrums gets very high concentrations of sodium during the first day of life corresponding to more than 60 grams salt for a 70 kg adult [12]. Within a fortnight the breastmilk contains sodium according to 10 grams of salt to an adult.

 

Conclusion

The old fashioned physiology, biochemistry and endocrinology shows that salt is an essential micronutrient in the human body. Normal salt intake in the Swedish population is normally at least nine and more than eighteen grams of salt per day according to daily urine excretion. Manipulation of salt intake outside the physiological normal boundaries between ten and 100 grams of salt intake is shown to increase disease and premature death.

 

Requirement and recommended intake 

Adults

Adults are advised to eat at least ten grams of salt as long as the food is not too salty to your taste. Also, drink normally 1-3 liters of water accordingly to quench the thirst.

Children

Children are advised to eat the same food as parents do, as always have been the case.

 

Reasoning behind the recommendation

Normal physiology has shown that salt is an essential micronutrient that has to be replenished in excess for the body’s homeostasis. Also, enough pure water is recommended to support the excretion of excess sodium.

 

Lower intake levels

There are severe dangers of serious disease or even premature death of salt deficiency if the intake is lower than recommended above.

Upper intake levels and toxicity

As has been shown above there is no need to issue an upper intake level from dietary sources as salt is excreted passively and the level of salt in the body is maintained actively by the kidneys and hormones.

 

There has not been shown any toxicity when sodium is ingested from dietary sources

 

 

Mora November 25, 2012

 

Björn Hammarskjöld

M.D., former consultant in Pediatics

Ph.D. in Biochemistry

Independent scientist in Nutrition



[1] Commission of the European Communities. Reports of the Scientific Committee for Food 492 (Thirty-first series). Nutrient and energy intakes for the European Community. Luxembourg, 493 1993.

[2] http://www.health.gov/dietaryguidelines/dgac/pdf/dg0908.pdf pp 412 ff  

This site is coordinated by the Office of Disease Prevention and Health Promotion, Office of the Assistant Secretary for Health, Office of the Secretary, U.S. Department of Health and Human Services.

[5] Michael H. Alderman; Shantha Madhavan; Hillel Cohen; Jean E. Sealey; John H. Laragh Low Urinary Sodium Is Associated With Greater Risk of Myocardial Infarction Among Treated Hypertensive Men Hypertension. 1995;25:1144-1152.

[6] Whalley H. Salt and Hypertension: consensus or controversy? Lancet 1997; 350: 1686

[7] Cohen HWHailpern SMFang JAlderman MH. Sodium intake and mortality in the NHANES II follow-up study. Am J Med. 2006 Mar;119(3):275.e7-14.

[8] Cochrane Database Syst Rev. 2011 Nov 9;(11):CD004022

[9] Olsson, Öhlin, ABC om hyponatremi, Läkartidningen No 17-18, 2012, p 888-92

[10] Whalley H. Salt and Hypertension: consensus or controversy? Lancet 1997; 350: 1686

[11] Graudal N A, Gallee A M, Garred P. Effects of Sodium Restriction on Blood Pressure, Renin, Aldosterone, Catecholamines, Cholesterols, and Triglyceride : A Meta-analysis. JAMA 1998; 279:1383-1391

[12] Aperia, Broberger, Zetterström i Acta Paediatr Scand; 1979; 68; 441-51

Kommentera här: