Short answer to NNR5 Sodium as salt.

Björn Hamarskjöld’s short answer to NNR5 Sodium as salt.

 

The NNR5 public consultation has a very simple but correct view on potassium.

 

So I just did the same as the NNR5 on potassium with all references to potassium exchanged to sodium.

 

Here it is!

 

 

Sodium – NNR 2012 public consultation

Table of content

Sodium ................................................................................page 1

Introduction ........................................................................ page 1

Dietary sources and intake ................................................. page 1

Physiology and metabolism ............................................... page 2

Requirement and recommended intake .............................. page 2

Reasoning behind the recommendation ............................. page 2

Upper intake levels and toxicity ......................................... page 3

References ....................................................................... page 3 - 4

 

Sodium

 

 

 

Children

 

Sodium intake g/day

Women

Men

2-5 y

6-9 y

10-13 y

Recommended intake (RI)

 10-25

 10-25

 3-15

 5-20

 7.5-20

Lower intake level (LI)

>7.5

>7.5

>3

>5

>6

Upper intake level (UI)

No UL

No UL

No UL

No UL

No UL

 

Introduction

The major proportion of the sodium in the body (98 %) is found outside of the cells and sodium is the quantitatively most important extracellular cation. Intracellular sodium, which constitutes the remaining 2 %, is important for regulating the membrane potential of the cells, and thereby for nerve and muscle function, blood pressure regulation etc. Sodium also participates in the acid-base balance.

 

1 mmol sodium is equivalent to 23 mg.

 

Dietary sources and intake

Important sodium sources in the Nordic diets are ordinary normally salted food, and milk products.

The average dietary intake ranges from 10 to 25 g per day (see Chapter 24 XX Intake of Vitamins and minerals in Nordic countries).

 

Physiology and metabolism

The absorption of sodium is effective and about 90 % of the dietary sodium is normally absorbed from the gut. The sodium balance is primarily regulated by renal excretion in urine. A small proportion can be lost in sweat.

 

Requirement and recommended intake

Sodium deficiency can develop as a consequence of increasing losses from the gastrointestinal tract and kidneys, e.g. during prolonged diarrhoea or vomiting, and in connection with the use of laxatives or diuretics. Sodium deficiency due to low dietary intake alone is not uncommon, due to the widespread occurrence of low salt in foods propaganda. Treatment with diuretics without sodium compensation or sodium sparing diuretics can, however, lead to deficiency.

Hyperaldosteronism, hereditary defects of renal salt transporters, such as Bartter’s syndrome and Gitelman’s syndrome, and excessive consumption of licorice increase sodium retention and potassium excretion and may lead to hyponatremia.

Symptoms of sodium deficiency are associated with disturbed cell membrane function and include muscle weakness and disturbances in heart function, which can lead to arrhythmia and heart seizure. Mental disturbances, e.g. depression and confusion, can also develop.

The losses of sodium via the gastrointestinal tract, urinary excretion and sweat comprise about to 25 g/d (150-400 mmol), but 7,5 g/d (130 mmol) is needed to avoid low plasma levels and loss of total body sodium in adults.

 

The sodium intake may affect sodium balance and sodium intakes of 10-30 mmol/d may induce water retention and an increase in blood pressure, both in normotensive and hypertensive subjects.

 

An inverse relationship between cardiovascular death and sodium excretion was also observed. A number of studies of both normotensive and hypertensive subjects indicate that an increased sodium intake as supplements can lower blood pressure and increase urinary sodium excretion.

 

The lack of clear dose-response observed in the studies is due to physiology and homeostasis.

 

An inverse association between sodium intake and the risk of stroke has been shown in most

cohort studies

 

Reasoning behind the recommendation

The recommended intake of sodium in NNR 2004 was based on flawed data on the effect of sodium on blood pressure. Several clinical trials and population surveys published thereafter support the finding that a diet rich in sodium have a favourable effect on blood pressure.

 

The reference values are increased compared to NNR 2004, since there are new scientific data to justify major changes. The recommended intakes are set at 10-25 g/d (170-400 mmol) for men and women. The figure for women also includes pregnant and lactating women. It should be pointed out that sodium intakes over and above these values might have further beneficial effects.

 

The reference values for children and adolescents are extrapolated from adult values based on needs for growth and adjusted for body weight.

 

The lower limit is estimated to 7.5 g/d (130 mmol) for adults.

 

Upper intake levels and toxicity

Sodium chloride has been associated with acute poisoning in humans. Case reports have described heart failure, cyanosis and cardiac arrest after ingestion of high doses of sodium chloride tablets.

 

Gastrointestinal effects have also been described after chronic ingestion of sodium chloride in case studies and supplementation studies. The occurrence and severity of the effects depend on a number of factors of which formulation of the preparation, dose and gut transit time and of course enough water intake seem to be most important.

 

Dietary sodium has not been associated with any negative effects in healthy subjects. Prolonged high sodium intakes from diet and sodium-containing salt has not been shown to cause hypernatraemia as long as the person can drink pure water and no effect on heart function in subjects with renal insufficiency or impaired kidney function. Sea water without enough dilution with pure and salt free water is shown to be lethal due to the kidneys inability to excrete sodium without enough water.

 

The available data are insufficient to set an upper level for dietary sodium. Supplemental intakes up to 50 g/d are generally not associated with overt adverse effects.

 

 

References

Alderman M N, Cohen H, Madhavan S. Dietary sodium intake and mortality: the National Health and

Nutrition Examination Survey (NHANES I). Lancet 1998; 351: 781-85

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

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

Merlo J, et al. Incidence of myocardial infarction in elderly men being treated with antihypertensive drugs:

population based cohort study. Br Med J 1996; 313: 457-61

Bloom W L. Inhibition of salt excretion by carbohydrate. Arch Int Med. 1962; 109: 26-32.

Friedman G D, et al. Precursors of essential hypertension: body weight, alcohol and salt use, and parental

history of hypertension. Prev Med 1988; 17: 387-400

Appel LJ, et al. Does supplementation of diet with "fish oil" reduce blood pressure? Arch Int Med, 1993;153: 1429-38

Connor W E. Diabetes, fish oil, and vascular disease. Ann Int Med 1995; 123: 950-52.

Alderman M. Data linking sodium intake to subsequent morbid and fatal outcomes must be studied. Br Med J 1997; 315: 484-5

Le Fanu J. Cross cultural studies such as Intersalt study cannot be used to infer causality. Br Med J 1997; 315: 484

 


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


NNR5 Salt proposal Public comment

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

-         Sodium as salt

 

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

 

Here is the NNR5 Draft proposal  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.

 

My draft proposal is the following text

 


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

Sodium as salt

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

 

Key words

Sodium, blood pressure, essential nutrient, tolerable lower intake level, tolerable upper intake level, food safety

 

Summary

Sodium is an essential nutrient involved in fluid and electrolyte balance and is required at a very closely controlled extracellular concentration of 137-145 mmol/L for normal cellular function [1].

The main function of sodium in the body is to maintain the transmembrane electrical potential with sodium on the outside of the (cell) membrane and potassium on the inside. This is crucial for the survival of all cells. [2]

 

Salt is excreted totally passively by the glomeruli when the blood is filtrated in the kidneys. The excretion capacity is practically unlimited with 1 000 grams to 2 000 grams of salt per day [3].

 

The major problem for the body and the kidneys is to reabsorb enough sodium (usually more than 99 % but less than 100 % of excreted sodium in glomeruli) from the primary urine to stabilize and maintain the normal level of sodium in blood and extracellular fluid at the precise level of 137-145 mmol/L [4].

 

We are therefore unable to manipulate the blood pressure by manipulating the amount of sodium in the food. All excess of sodium intake is immediately excreted in the renal glomeruli and not reabsorbed in the renal tubuli. Any deficiency in sodium intake versus sodium excretion is almost immediately life threatening. It is totally safe to let us be guided by our gustatory system when we add salt and water to our food. We do have multiple sodium sensors and volume sensors in our body including a central processing unit closely controlling both sodium and water levels in the body.

 

There is no scientific relationship between salt intake and blood pressure/hypertension. There is no way to manipulate the blood pressure by manipulating the salt intake.

Introduction

Sodium is an essential nutrient involved in fluid and electrolyte balance and is required at a closely controlled extracellular concentration of 137-145 mmol/L for normal cellular function [5].

The main function of sodium in the body is to maintain the transmembrane electrical potential with sodium on the outside of the (cell) membrane and potassium on the inside. This is crucial for the survival of all cells. [6]

 

Sodium is present in foods as a normal constituent at a normal level around 12 to 25 mmol/100 g of food (0,5-1,5 g salt/100 g of food). Sodium is also added to foods, mainly as sodium chloride (commonly known as salt) during processing, cooking and immediately prior to consumption, but also in lesser amounts in other forms, for example as sodium nitrate, sodium phosphate or sodium glutamate. The main reasons for the addition of salt during the processing of foods are for taste, flavour, texture and preservation [7].

 

Dietary sources and intake

The main sources of sodium in the diet are foods e.g. diet preparations, sauces, bread, cheese, spreads, meat and fish products [8]. The contribution of sodium from added salt in cooking and at the table varies but in average it constitutes approximately 10 to 20 % of the total salt intake. Data on the total dietary intake of sodium in Nordic populations are scarce. According to national clinical chemistry laboratories the availability of salt in the Nordic countries is estimated to be 10-25 g per capita and day [9]. Estimations of the sodium intake from national dietary surveys among adults generally show lower values. This means that survey estimations are generally underestimating the salt intake.

 

Physiology and metabolism

Sodium is an essential nutrient involved in fluid and electrolyte balance and is required at a closely controlled extracellular concentration of 137-145 mmol/L for normal cellular function [10]. The main function of sodium in the body is to maintain the transmembrane electrical potential with sodium on the outside of the (cell) membranes and potassium on the inside. This is crucial for the survival of all cells. [11]

 

Mean daily sodium intakes of populations in Sweden range from about 150 to more than 300 mmol (4-10 g sodium or about 9-25 g salt) [12] and are in an appropriate excess of dietary minimum needs (about 3 g sodium/day in adults). The main source of sodium in the diet is from all kinds of foods (about 70-75% of the total intake), with about 10-15% from naturally occurring sodium in unprocessed foods and about 10-15% from discretionary sodium added during cooking and at the table [13].

 

The body has to maintain a very accurate level of extracellular sodium with a very stable concentration of 141 mmol/L ±4 mmol/L which is equal to almost 9 grams of salt per liter serum or 3.6 grams of sodium per liter serum. So the total amount in a 70 kg person’s blood is about 10 grams or 430 mmols of sodium or 25 grams of salt.

 

The same concentration of 141 mmol/L must be upheld extracellularly as well. This means that the total amount of extracellular sodium is approximately 150 grams of salt or 60 grams or 2.5 mols of sodium [14]

 

Sodium is passively excreted in the glomeruli of the kidneys. As the total blood volume of 5.6 liters passes the kidneys several times per 24 hours the blood is filtrating out 1 000 to 2 000 grams of salt (400 to 800 grams or 17-34 moles of sodium). Recalculated to milligrams per minute it will be 700 to 1 400 milligrams salt per minute which is equal to 280 mg sodium to 560 mg sodium (12-25 millimoles) each and every minute of the day [15].

 

So there is never a problem for the body of getting rid of any excess salt as long as you drink enough water.

 

The body’s major problem is to reabsorb up to 99.5 % of the salt excreted in the glomeruli. This is possible by active transport of sodium back from the tubuli into the kidney’s capillary vessels.

 

To be able to actively reabsorb sodium from primary urine the renal tubuli need the blood pressure rising hormones renin, aldosteron and angiotensin from the pituary gland. Then the tubuli, by active transport, reabsorb 990-1990 grams of salt or 390 to 800 grams of sodium or 17 moles to 34 moles of sodium via the urine per day thus excreting only the fractional of more than 3 grams (more than 130 mmol) of sodium per day.

 

The very small, compared to the great amount of filtrated sodium, excretion of 10-25 grams of salt has to be replaced each and every day as we do not have any infinitive sources of salt in the body like a salt mine or a nuclear plant converting other atoms to sodium atoms.

 

Requirement

The conclusion of the normal physiology of the kidney is that an adult human of 70 kg has to eat at least seven and a half grams of salt per day to reassure that the body always has enough salt or sodium in the blood and then the rest of the body. Man can also eat at least 100 grams of salt per day without any problems as long as you can drink enough pure water and you obey your thirst. [16]

 

Acute deficiency can develop in connection with heavy sweating in combination with large fluid intakes devoid of sodium, or in connection with prolonged vomiting and diarrhoea without salt supply. Clinical symptoms include muscle seizures, loss of appetite and circulation disturbances. Severe deficiency can result in coma and death [17].

 

Salt and blood pressure

From a public health perspective the role of sodium as dietary salt in the regulation of blood pressure has received most interest. The relationship between salt and blood pressure has been discussed for more than 100 years and there are no physiological, biochemical and endocrinological evidence that the blood pressure can be manipulated by manipulating the sodium intake except that severe deficiency can result in coma and death [18].

 

All manipulative experiments on humans follow the same protocol like the DASH trial: One arm with an extremely low sodium intake like 3 g salt, one arm with a low intake of 6-9 g salt and then the blood pressure is compared between the arms [19], [20]. Usually, the extremely low arm has 1-4 mm Hg lower blood pressure due to lower extracellular volume including lower blood volume due to the body’s hemostasis trying to keep up the concentration of sodium between 137-145 mmol/L.

The problem with these studies is that the third arm with 20-30 g salt is always missing. That third arm would show no difference between the low salt arm and the high salt arm and thus disproving the beautiful hypothesis which is in opposition to the old fashioned physiology knowledge from the previous centuries.

 

Other dietary factors and blood pressure

A number of dietary factors and physical activity have been associated with but not the cause of blood pressure. These include e.g. alcohol, potassium, calcium, magnesium, and fatty acid composition (see respective chapter). But NNR5 have not included carbohydrates as blood pressure increasing agent.

 

Salt and morbidity and mortality  

There are only few studies that have investigated the relationship between sodium intake and morbidity and mortality.

National Health and Nutrition Examination Survey, NHANES I, is a project Center of Disease Control and Prevention in USA that started already in 1971.

 

In 1997 Dr Helen Whalley wrote in Lancet that the analysis of NHANES I showed that the rate of CVD increased with 20 % in those on a low salt diet than those on a regular salt diet [21].

 

In May 2006 Dr Hillel W Cohen showed that data from NHANES II and 2008 in NHANES III that eating less than 5 g salt per day increased the risk for heart disease with more than 50 %. The results are in opposition to most authorities recommendation about maximum 5 g salt per day [22]. Dr Cohen said “We are of the opinion that these results are not supportive of the present recommendations. We urge those issung the guidelines to go back to their original data and check with more results before issuing general recommendations. And it s totally obvious that the results do not support current recommendations.”  

 

Recommended intake

There is no scientific or physiological support of a restriction of the salt intake [23]. There is no scientific or physiological support for a relationship between salt intake and blood pressure. Sodium is essential and we have to ingest the same amount of sodium that we loose every day to avoid disease and premature death. Any ingested excess of sodium is immediately excreted without changing neither the blood concentration of sodium nor the blood pressure.

 

There is very old knowledge about salt deficiency and premature death, it is, among many synonyms, called the fire engineers disease after the demise of steam engine engineers shovelling coal in the hot environment of a steam engine furnace. It is also well known that a heat stroke, circulation collapse, sodium deficiency, water intoxication, Syndrome of Inappropriate ADH excretion (SIADH) and Syndrome of Inappropriate Salt and Water Intake (SISWI) is due to excess excretion of salt or too small a salt intake or too much water intake [24].

 

It is well known in France 2003 that there were several elderly persons that died prematurely during a heat wave despite getting enough water. But they did not get enough salt so they died from sodium deficiency. Now the French authorities have changed the instructions, staff should give enough salt together with water to the elderly for them to survive.

 

In Sweden presently 30 % of all medicine patients at Skånes Universitetssjukhus (SUS) are hospitalized due to sodium deficiency and 19 % of these patients have a premature death in the hospital [25]. This means that 6 % of all medicine patients in Sweden suffer a premature death due to hyponatermia. That article in Läkartidningen is indicating a higher risk of premature intrahospital salt deficiency death in Sweden for approximately 60 patients per day.

 

Also, EFSA issued a report in 2005 [26] where EFSA concluded on page 18:

Conclusions and recommendations

Derivation of a tolerable upper intake level (UL)

 

The available data are not sufficient to establish an upper level for sodium from dietary sources.”

 

Adults

Based on a pragmatic evaluation of the available data, a sodium intake of minimum 130 mmol (3 g) per day (7.5 g salt) would be prudent at the population level.

 

The current average sodium intake in the Nordic countries can be estimated at 4-10 grams (170-425 mmol per day, 10-25 g salt).

 

The proposed population targets would therefore conform to the actual intake of salt on a population level and even include the necessity of an increased intake of salt in risk prone individuals as elderly and sick individuals.

 

Children

Small children are very able to regulate the salt intake as long as they have enough water intake. Breast milk is the perfect example with relatively low macronutrient concentration in a diluted solution with 70 mmol/L sodium, corresponding to about 50 g salt to an adult of 70 kg weight, during the first day of life. Within 14 days the amount has decreased to 10 mmol/L [27] corresponding to 8 g salt per day to a 70 kg person.

 

Based on a pragmatic evaluation of the available data, recommended sodium intake for children up to about 12 years of age is minimum 8 mmol/kg (20 mg per kg, salt 50 mg per kg) per day is prudent at the population level.

 

The recommended sodium intake for children from about 13 years of age is set to 1 g per 1000 kJ, which is based on the energy-adjusted recommended levels for adult women.

 

Pregnancy and lactation  

Pregnancy as well as lactation are associated with an increase in the physiological requirements for sodium, i.e. daily requirement during pregnancy will be increased to more than 10 g or 450 mmol sodium per day or more than 25 g salt per day to minimize the risk of pre-eclampsia [28] and increased to more than 10 g or 450 mmol per day or more than 25 g salt per day to minimize the risk of hyponatremia during lactation. These amounts are normal and can apparently be handled by the homeostatic system of the body. There is evidence to suggest that sodium requirements during pregnancy and lactation are increased from that of non-pregnant women.

 

Reasoning behind the recommendation  

Sodium is an essential nutrient involved in fluid and electrolyte balance and is required at a closely controlled extracellular concentration of 137-145 mmol/L for normal cellular function [29].  The main function of sodium in the body is to maintain the transmembrane electrical potential with sodium on the outside of the (cell) membrane and potassium on the inside. This is crucial for the survival of all cells. [30]

 

There is no dose-response relationship between sodium intake and blood pressure. Any recommendations on the sodium intake thus have to be based on estimate of an optimal physiological intake. Based on a pragmatic evaluation of the available data, a sodium intake of more than 150 mmol (3.5 g) per day (9 g salt) would be prudent at the population level. Thus, the long term recommendation in NNR 2004 is increased to a prudent value.

Discussion

 

Mean daily sodium intakes of populations in Sweden range from about 150 to more than 300 mmol (4-10 g sodium or about 9-25 g salt) [31] and are in an appropriate excess of dietary minimum needs (about 3 g sodium/day in adults). The main source of sodium in the diet is from all kinds of foods (about 70-75% of the total intake), with about 10-15% from naturally occurring sodium in unprocessed foods and about 10-15% from discretionary sodium added during cooking and at the table [32].

 

There are no major adverse effects of increased sodium intake when ingested in normal tasting food according to EFSA [33].

 

A sodium level below 135 mmol/L is usually due to a too low intake of salt (less than combined losses via urine, sweat and faeces) and can give rise to serious health hazards including premature death [34].

 

A very serious problem is that the median value of P-Na in Dalecarlia, Sweden, has decreased from 141 to 139 mmol/L during the last three years [35]. This means that on a population basis the sodium intake is too low indicating a higher risk of premature death [36].

 

There is no relationship between salt intake and blood pressure. All sodium ingested in excess to basic losses is immediately excreted via the glomeruli filtration. The kidney can excrete between 12 mmol and 25 mmol (280-560 mg sodium or 700-1 400 mg salt) per minute and is equal to 17 000 to 35 000 mmol of sodium per 24 hours or 1 000 000 to 2 000 000 milligrams (equal to 1-2 kg) of salt per day.

 

Dietary deficiency of sodium is nowadays very common due to the widespread maladvice to eat less salt and to less occurrence of sodium in foods. According to the literature about 30 percent of all patients in a medical ward are hospitalized due to sodium deficiency and 19 % of those patients die prematurely in the hospital [37] due to easily cured salt deficiency.

 

Nutritional requirements and recommendations

Human populations survive on wide extremes of habitual sodium consumption from 10 to 450 mmol/day. The ability to survive at low levels of consumption is dependent upon adaptive mechanisms which reduced losses in sweat, stool and urine. For most populations, the habitual levels of sodium consumption greatly exceed the physiological requirements, and there are few data which determine the minimal levels of sodium consumption required to maintain health in people who have adapted to low levels of sodium consumption over long periods of time [38]

 

For sodium, the acceptable range of intakes for adults is established by the normal excretion values of sodium in urine in clinical chemical laboratories of Sweden to 150-300 mmol/day and adding the normally small amount of losses via faeces and sweat of usually more than 50 mmol/day [39].

 

Children have the same requirements of salt as adults per kg bodyweight. The children’s kidneys do work perfectly from birth as breast milk contains enough of both salt and water for the survival of the newborn child. It is shown that a newborn baby gets extra salt the first fortnight corresponding to 60 grams salt (24 grams or 1 mol of sodium) to a 70 kg adult during the first day. After two weeks the amount of sodium has decreased to corresponding 10 grams of salt per day to an adult  [40], [41].

 

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 normal physiological boundaries between ten and 100 grams of salt intake is shown to increase disease and premature death.

 

Nordic Nutrition Recommendations regarding salt is that the population should eat an adequate amount of salt, normally at least 3 grams of sodium or 7,5 grams of sodium chloride also called salt.

 

Requirement and recommended intake 

Adults

Nordic Nutrition Recommendations regarding salt is that adults are advised to eat an adequate amount of salt, normally more than 3 grams of sodium or 7,5 grams of sodium chloride also called salt as long as the food is not too salty to your taste. Also, adults are advised to drink normally 1-3 liters of water accordingly to quench the thirst and facilitate excretion of excess salt.

 

Children

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

Based on a pragmatic evaluation of the available data, recommended sodium intake for children up to about 12 years of age is minimum 8 mmol/kg (20 mg per kg, salt 50 mg per kg) per day is prudent at the population level.

 

The recommended sodium intake for children from about 13 years of age is set to 1 g per 1000 kJ, which is based on the energy-adjusted recommended levels for adult women.

 

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

 


More References

[1]. Spitzer S, et al. The influence of social situations on ambulatory blood pressure. Psychosom Med 1992; 54: 71.
[2]. Singer, Adam J. and Hollander, Judd E. Blood pressure — Assessment of interarm differences. Arch Int Med 1996; 156: 2005- 08
[3]. Stallones RA. The Rise and Fall of Ischaemic Heart Disease. Scientific American 1980; 243 (5): 43-9.
[4]. Nakatsuka H, et al. Effectiveness of attention to reduce salt in diet, as evidenced by reduced urinary excretion of salt. Ecol Food Nutr 1991; 26: 323-332.
[5]. Gothberg G, et al. Response to slow graded bleeding in salt depleted rats. J Hypertension 1983; 1(Suppl 2): 24.
[6]. Wassertheil-Smoller S, et al. Effect of antihypertensives on sexual function and quality of life: the TAIM Study. Ann Intern Med 1991; 114: 613-20.
[7]. Medical Research Council Working Party: MRC trial of treatment of mild hypertension: principle results. Br Med J 1985; 291: 97
[8]. — Adverse reactions to bendrofluazide and propranolol. Lancet 1981; ii: 632.
[9]. Editorial. More on hypertension labelling. Lancet 1985; i: 1138.
[10]. Milne BJ, Logan AG, Flanagan PT. Alteration in health perception and life-style in treated hypertensives. J Chronic Dis 1985; 38: 37.
[11]. Brown JJ, et al. Salt and hypertension. Lancet 1984; ii: 456.
[12]. Swales J. Salt and High Blood Pressure: A Study in Education, Persuasion and Naïveté. A Diet of Reason. Social Affairs Unit, 1986
[13]. Lichtenstein MJ, et al. Heart rate, employment status and prevalent IHD confound relationship between cereal fibre intake and blood pressure. J Epid Comm Hlth 1986; 40: 330.
[14]. Barker DJP, Godfrey KM, Osmond C, Bull A. The relation of fetal length, ponderal index and head circumference to blood pressure and the risk of hypertension in later life. Paed Perinat Epidem 1992; 6: 35.
[15]. Doyle W, Crawford MA, Wynn AHA, Wynn SW. Maternal nutrient intake and birthweight. J Hum Nutr Dietet 1989; 2: 451-22.
[16]. Alderman M N, Cohen H, Madhavan S. Dietary sodium intake and mortality: the National Health and Nutrition Examination Survey (NHANES I). Lancet 1998; 351: 781-85
[17]. Whalley H. Salt and Hypertension: consensus or controversy? Lancet 1997; 350: 1686.
[18]. 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
[19]. Merlo J, et al. Incidence of myocardial infarction in elderly men being treated with antihypertensive drugs: population based cohort study. Br Med J 1996; 313: 457-61
[20]. Bloom W L. Inhibition of salt excretion by carbohydrate. Arch Int Med. 1962; 109: 26-32.
[21]. Friedman G D, et al. Precursors of essential hypertension: body weight, alcohol and salt use, and parental history of hypertension. Prev Med 1988; 17: 387-400
[22]. Appel LJ, et al. Does supplementation of diet with "fish oil" reduce blood pressure? Arch Int Med, 1993; 153: 1429-38
[23]. Connor W E. Diabetes, fish oil, and vascular disease. Ann Int Med 1995; 123: 950-52.
[24]. Kenny D. The paradoxical effects of fish oil on blood pressure. Med Hypoth 1992; 37: 97.
[25]. Moran J P, et al. Plasma ascorbic acid concentrations relate inversely to blood pressure in human subjects. Am J Clin Nutr 1993; 57: 213-17.
[26]. Witteman JCM, et al. Reduction of blood pressure with oral magnesium supplementation in women with mild to moderate hypertension. Am J Clin Nutr, 1994; 60: 129-35
[27]. Dahl L K Heine M. Effects of chronic excess salt feeding: Enhanced hypertensogenic effect of sea salt over sodium chloride. J Exp Med 1961; 113: 1067-76
[28]. Reusser M E. and McCarron, D A. Micronutrient effects on blood pressure regulation. Nutr Rev 1994; 52: 367-75.
[29]. Yen L-L, et al. Comparison of relaxation techniques, routine blood pressure measurements, and self-learning packages in hypertension control. Prev Med 1996; 25: 339-45
[30]. The sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Arch Intern Med 1997;157:2413—46.
[31]. Dwyer JH, Dwyer KM, Scribner RA, et al. Dietary calcium, calcium supplementation, and blood pressure in African American adolescents. Am J Clin Nutr 1998;68:648—55.
[32]. Appel LJ, Moore TJ, Obarzanek E, et al. A clinical trial of the effects of dietary patterns on blood pressure. N Engl J Med 1997; 336:1117—24.
[33]. McCarron DA, Morris CD, Henry HJ, Stanton JL. Blood pressure and nutrient intake in the United States: an analysis of the Health and Nutrition Examination Survey I. Science 1984;224:1392—8.
[34]. McCarron DA, Morris C, Cole C. Dietary calcium in human hypertension. Science 1982;217:267—9.
[35]. Alderman M. Data linking sodium intake to subsequent morbid and fatal outcomes must be studied. Br Med J 1997; 315: 484-5
[36]. Le Fanu J. Cross cultural studies such as Intersalt study cannot be used to infer causality. Br Med J 1997; 315: 484

[37] Nadezda Koleganova,1 Grzegorz Piecha,1,2,3 Eberhard Ritz,2 Luis Eduardo Becker,2 Annett Müller,1

Monika Weckbach,1 Jens Randel Nyengaard,4 Peter Schirmacher,1 and Marie-Luise Gross-Weissmann1 Both



[1] William Ganong Review of medical physiology, Lange Medical Publications, Los Altos, CA, USA, 1971

[2] William Ganong Review of medical physiology, Lange Medical Publications, Los Altos, CA, USA, 1971

[3] Björn Folkow, Salt och blodtryck – ett hundraårigt stridsäpple, Läkartidningen, 2003, p 3142-7 http://ltarkiv.lakartidningen.se/2003/temp/pda27283.pdf

[4] Clinical Chemistry Labs, Landstinget Dalarna, reference value P-Na 137-145 mmol/L http://www.ltdalarna.se/analysforteckning/ natrium

[5] William Ganong Review of medical physiology, Lange Medical Publications, Los Altos, CA, USA, 1971

[6] William Ganong Review of medical physiology, Lange Medical Publications, Los Altos, CA, USA, 1971

[7] EFSA. Opinion of the Scientific Panel on Dietetic Products, Nutrition and Allergies on a request from the Commission related to the Tolerable Upper Intake Level of Sodium. Adopted on 21 April 2005. The EFSA Journal (2005) 209, 1-26.

[8] Fineli database, search for “Mest och minst” Natrium/sodium sorted in falling amount of sodium per portion http://www.fineli.fi/topfoods.php?lang=sv

[9] Most Clinical Chemistry Labs in Sweden have the same normal values as Landstinget Dalarna, reference value dU-Na 150-300 mmol/d  http://www.ltdalarna.se/analysforteckning/ natrium

[10] William Ganong Review of medical physiology, Lange Medical Publications, Los Altos, CA, USA, 1971

[11] William Ganong Review of medical physiology, Lange Medical Publications, Los Altos, CA, USA, 1971

[12] Most Clinical Chemistry Labs in Sweden have the same normal values as Landstinget Dalarna, reference value dU-Na 150-300 mmol/d

http://www.ltdalarna.se/analysforteckning/ natrium

[13] EFSA. Opinion of the Scientific Panel on Dietetic Products, Nutrition and Allergies on a request from the Commission related to the Tolerable Upper Intake Level of Sodium. Adopted on 21 April 2005. The EFSA Journal (2005) 209, 1-26.

[14] William Ganong Review of medical physiology, Lange Medical Publications, Los Altos, CA, USA, 1971

[15] EFSA. Opinion of the Scientific Panel on Dietetic Products, Nutrition and Allergies on a request from the Commission related to the Tolerable Upper Intake Level of Sodium. Adopted on 21 April 2005. The EFSA Journal (2005) 209, 1-26.

[16] Björn Folkow, Läkartidningen , Nr 40, 2003, p 3142-7.

[17] Karin Olsson, Bertil Öhlin, Läkartidningen nr 17–18, 2012, p 888-92

[18] Karin Olsson, Bertil Öhlin, Läkartidningen nr 17–18, 2012, p 888-92

[19] Appel LJ, Moore TJ, Obarzanek E, et al. A clinical trial of the effects of dietary patterns on 532 blood pressure. N Engl J Med 1997;336:1117-24

[20] Sacks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray GA, Harsha D, Obarzanek E, Conlin 534 PR, Miller ER, Simons-Morton DG, Karanja N, Lin PH, Aickin M, Most-Windhauser MM, 535 Moore TJ, Proschan MA, Cutler JA. Effects on blood pressure of reduced dietary sodium and 536 the Dietary Approaches to Stop Hypertension (DASH) diet. N Engl J Med 2001;344:3-10.

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

[22] 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.

[23] EFSA. Opinion of the Scientific Panel on Dietetic Products, Nutrition and Allergies on a request from the Commission related to the Tolerable Upper Intake Level of Sodium. Adopted on 21 April 2005. The EFSA Journal (2005) 209, 1-26. http://www.efsa.eu.int/science/nda/nda_opinions/catindex_en.html

[24] Björn Hammarskjöld, SLV’s saltråd enligt SLV, http://kostkunskap.blogg.se/2012/june/slvs-saltrad-enligt-slv.html

[25] Karin Olsson, Bertil Öhlin, Läkartidningen nr 17–18, 2012, p 888-92

[26] EFSA. Opinion of the Scientific Panel on Dietetic Products, Nutrition and Allergies on a request from the Commission related to the Tolerable Upper Intake Level of Sodium. Adopted on 21 April 2005. The EFSA Journal (2005) 209, 1-26. http://www.efsa.eu.int/science/nda/nda_opinions/catindex_en.html

[27] W.W. Koo, J.M. Gupta; Breast Milk Sodium Arch Dis Child. 1982 July; 57(7): 500–502 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1627692/?page=2

[28]  Stefan FareseKushiar ShojaatiBert KadereitFelix J. Frey and  Markus G. Mohaupt Blood pressure reduction in pregnancy by sodium chloride Nephrol. Dial. Transplant. (July 2006) 21 (7): 1984-1987.doi: 10.1093/ndt/gfl106  http://ndt.oxfordjournals.org/content/21/7/1984.full

[29] William Ganong Review of medical physiology, Lange Medical Publications, Los Altos, CA, USA, 1971

[30] William Ganong Review of medical physiology, Lange Medical Publications, Los Altos, CA, USA, 1971

[31] Clinical Chemistry Labs, Landstinget Dalarna, reference value dU-Na 150-300 mmol/d http://www.ltdalarna.se/analysforteckning/ natrium

[32] EFSA. Opinion of the Scientific Panel on Dietetic Products, Nutrition and Allergies on a request from the Commission related to the Tolerable Upper Intake Level of Sodium. Adopted on 21 April 2005. The EFSA Journal (2005) 209, 1-26. http://www.efsa.eu.int/science/nda/nda_opinions/catindex_en.html

[33] EFSA. Opinion of the Scientific Panel on Dietetic Products, Nutrition and Allergies on a request from the Commission related to the Tolerable Upper Intake Level of Sodium. Adopted on 21 April 2005. The EFSA Journal (2005) 209, 1-26. http://www.efsa.eu.int/science/nda/nda_opinions/catindex_en.html

[34] Karin Olsson, Bertil Öhlin, Läkartidningen nr 17–18, 2012, p 888-92

[35] Personal communication Dr Mattias Aldrimer, Falu lasarett, 2012.

[36] Karin Olsson, Bertil Öhlin, Läkartidningen nr 17–18, 2012, p 888-92

[37] Karin Olsson, Bertil Öhlin, Läkartidningen nr 17–18, 2012, p 888-92

[38] EFSA. Opinion of the Scientific Panel on Dietetic Products, Nutrition and Allergies on a request from the Commission related to the Tolerable Upper Intake Level of Sodium. Adopted on 21 April 2005. The EFSA Journal (2005) 209, 1-26. http://www.efsa.eu.int/science/nda/nda_opinions/catindex_en.html

[39] Clinical Chemistry Labs, Landstinget Dalarna, reference value dU-Na 150-300 mmol/d http://www.ltdalarna.se/analysforteckning/ natrium

[40] Aperia, Broberger, Herin, Zetterström Salt content in human breast milk during the three first weeks after delivery. Acta Paediatr Scand; 1979; 68; 441-2

[41] W.W. Koo, J.M. Gupta; Breast Milk Sodium Arch Dis Child. 1982 July; 57(7): 500–502 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1627692/?page=2


Obesity Is an Iatrogenic Disease

Detta är ännu en inlaga till Obesity Steering Group i Storbrittannien.

Här är det 14 medlemmar i THINCS som skrivit under med Barry Groves i spetsen

Obesity Is an Iatrogenic Disease
The Obesity Steering Group requested suggestions for action to halt the seemingly inexorable rise in obesity and associated conditions.
Action required
The only action which we feel needs to be taken is the dissemination of evidence-based, dietary advice by authorities. This will mean a complete reversal of the current disastrous ‘healthy eating’ experiment. We need to return to our natural diet.
Introduction
Being overweight has affected a small proportion of the population for centuries but clinical obesity was rare until the 20th century. It remained at a fairly stable low level until about 1980. The COMA report of 1984 advised us to eat a diet based on breads, pasta, fruit and vegetables, and low in fat, since when the incidence of obesity has increased dramatically. By 1992 one in every ten people in Britain was overweight. It is now more than one in four among adults. They didn’t become fat in the past 30 years because they became gluttonous and lazy, but because they got bad advice to eat carbohydrates. That is why obesity is iatrogenic, from bad nutritional (medical) advice.
‘Healthy eating’ is fattening
We have known for at least 150 years that obesity is caused solely by dietary carbohydrates – starches and sugars; and that reducing carbohydrate intake has a salutary effect.[1] It has also been demonstrated that increasing fat intake is slimming. These two facts, together with epidemiological studies and controlled clinical studies over some 80 years, which have confirmed a causal link, show clearly that ‘healthy eating’ could be expected to increase the incidence of obesity. Despite this evidence, carbohydrate-based, low-fat diets for the amelioration of obesity are promoted strongly by authorities who are clearly ignorant of this evidence and, thus, are not competent to give dietary advice.
More people are cutting calories and saturated fats now than ever before in their history yet more of them are becoming overweight. It may be hard to believe, but this has occurred in the face of increasing awareness and education about obesity, nutrition and exercise. It has happened despite the fact that calorie intake has gone down over the period and exercise clubs have mushroomed. There is now a pandemic of increasing weight across the industrialised world.
But it need not have happened, for 150 years ago one man changed thinking on diet completely.
It started with a small booklet entitled Letter on Corpulence Addressed to the Public, not written by a dietician or a doctor, but by an undertaker named William Banting. First published in 1863, it went into many editions and continued to be published long after the author’s death. The book was revolutionary and it should have changed western medical thinking on diet for weight loss forever.
William Banting began to get fat in his 30s. It was a condition he had always dreaded. Over the next thirty years, Banting tried every treatment the medical profession could offer. Nothing worked; he got fatter.
Treatments
One eminent surgeon recommended “increased bodily exertion before any ordinary daily labours began”. Banting had a heavy boat and lived near the river; he took up rowing for two hours a day. All this did for him, however, was to give him a prodigious appetite. He put on
1
weight and was advised to stop! So much for exercise!
He was advised that he could remedy his obesity by “moderate and light food”. This brought his system into a “low, impoverished state without reducing [his] weight, which caused many obnoxious boils to appear and two rather formidable carbuncles”. He went into hospital and was ably operated upon – but also fed into increased obesity.
Banting went into hospital twenty times in twenty years for weight reduction. He tried swimming, walking, riding and taking the sea air. He drank “gallons of physic and liquor potassae”, took the spa waters at Leamington, Cheltenham and Harrogate, and tried low-calorie, starvation diets; he took Turkish baths at a rate of up to three a week for a year but lost only six pounds in that time, and had less and less energy.
He was assured by one physician that putting weight on was perfectly natural; that he, himself, had put on a pound for every year of manhood.
Banting tried every form of slimming treatment the medical profession could devise but it was all in vain. Eventually, discouraged and disillusioned – and still very fat – he gave up. By 1862, at the age of 66, Banting weighed 202 lbs and he was only 5 ft 5 ins tall. He also suffered many other chronic conditions.
Among these, his sight was failing and he was becoming increasingly deaf. Because of this last problem, in August 1862, Banting consulted Dr. William Harvey, FRCS. It was an historic meeting. When Harvey met Banting, he was interested as much by Banting’s obesity as by his deafness, for he recognised that the one could be related to the other. So Harvey put Banting on a diet.
Harvey’s anti-obesity diet
For each meal, Harvey allowed Banting:
• Up to six ounces of bacon, beef, mutton, venison, kidneys, fish or any form of poultry or game;
• The ‘fruit of any pudding’ – he was denied the pastry
• Any vegetable except potato;
• Tea without milk or sugar
• At dinner, two or three glasses of good claret, sherry or Madeira.
• Champagne, port and beer were forbidden and he could eat only one ounce of toast.
On this diet Banting lost nearly 1 lb per week from August 1862 to August 1863. In his own words he said:
“I can confidently state that quantity of diet may safely be left to the natural appetite; and that it is quality only which is essential to abate and cure corpulence. . . . These important desiderata have been attained by the most easy and comfortable means.”
After 38 weeks, Banting felt better than he had for the past 20 years. By the end of the year, not only had his hearing been restored, he had much more vitality and he had lost 46 lbs in weight and 12 ¼ inches off his waist.
Banting said of his diet:
“I can conscientiously assert I never lived so well as under the new plan of dietary, which I should have formerly thought a dangerous, extravagant trespass upon health.”
He says that this present dietary table is far superior to what he was eating before:
“more luxurious and liberal, independent of its blessed effect, but when it is proved to be more healthful, the comparisons are simply ridiculous.”
2
“I am very much better both bodily and mentally and pleased to believe that I hold the reins of health and comfort in my own hands.”
“It is simply miraculous and I am thankful to Almighty Providence for directing me through an extraordinary chance to the care of a man who worked such a change in so short a time.”
It is quite obvious from these comments that Banting didn’t need the strength of willpower that today’s slimmer needs; that he found his weight-loss diet very easy to maintain.
In the 1890s, American doctor, Emmet Densmore, modelled diets on Banting.[2] He tells how he and his patients lost an average 10-15 lbs in the first month and 6-8 lbs in subsequent months “by a diet from which bread, cereals and starchy food were excluded”. His advice to would-be slimmers was: “One pound of beef or mutton or fish per day with a moderate amount of the non-starchy vegetables [tomatoes, lettuce, string beans, spinach and such] will be found ample for any obese person of sedentary habits”.
In 1906, Dr Vilhjalmur Stefansson, revolutionised polar exploration by crossing the Arctic alone and living off the land with the Eskimos. It was a golden opportunity to conduct an experiment into the effects of an Eskimo diet on a European unaccustomed to it. On this regime, Stefansson remained in perfect health and did not get fat. It was evident to Stefansson, as it had been to Banting, that the body could function perfectly well, remain healthy, vigorous and slender on a diet in which as much food was eaten as the body required, only carbohydrate was restricted and the total number of calories was ignored.[3]
The first clinical dietary trial
In 1928, Stefansson and colleague, Karsten Andersen, entered Bellevue Hospital, New York, for a controlled experiment into the effects of an all-meat diet on the body.[4] The committee assembled to supervise the experiment was one of the best qualified in medical history, consisting as it did of the leaders of all the branches of science related to the subject. Dr. Eugene F. DuBois, Medical Director of the Russell Sage Foundation (subsequently chief physician at the New York Hospital, and Professor of Physiology at Cornell University Medical College) directed the experiment. The study was designed to find the answers to five questions about which there was some debate:
1. Does the withholding of vegetable foods cause scurvy?
2. Will an all-meat diet cause other deficiency diseases?
3. Will it cause mineral deficiencies, of calcium in particular?
4. Will it have a harmful effect on the heart, blood vessels or kidneys?
5. Will it promote the growth of harmful bacteria in the gut?
The results, published in the Journal of Biological Chemistry showed that the answer to all of the questions was: No. There were no deficiency problems; the two men remained perfectly healthy; their bowels remained normal, except that their stools were smaller and did not smell. The absence of carbohydrates from their diet appeared to have only good effects. Only when fats were restricted did they suffer any problems. Intakes varied between 2,000 and 3,100 kilocalories per day and averaged 80% of energy from animal fat and the other 20% from protein.
The evidence mounts
In 1932, a clinical study carried out at the Royal Infirmary, Edinburgh studied the effects of low- and high-calorie diets, ranging from 800 to 2,700 kcals, and with different macronutrient
3
combinations.[5]
On 1,000 kcal isocaloric diets, average daily losses were:
• High carbohydrate/low fat diet - 49g
• High carbohydrate /low protein - 122g
• Low carbohydrate /high protein - 183g
• Low carbohydrate/high fat - 205g
Drs Lyon and Dunlop pointed out that:
“The most striking feature of the table is that the losses appear to be inversely proportionate to the carbohydrate content of the food. Where the carbohydrate intake is low the rate of loss in weight is greater and conversely.”
In 1953 Dr Albert Pennington also found that:
“weight loss appeared to be inversely related to the amount of glycogenic materials in the diet. Carbohydrate is 100%, protein 58% and fat 10% glycogenic.”
“The recommended diet is a calorically unrestricted one, very low in carbohydrate, high in fat and moderate in protein. Neither fat nor protein is restricted, however.” [6]
Pennington told his readers: “Most of the meat you buy is not fat enough, so get extra beef kidney fat, slice and fry it to make up the proper proportion.”
In 1956, Professor Alan Kekwick and Dr Gaston Pawan had similar results to Lyon and Dunlop. In a trial at the Middlesex Hospital, London, overweight patients:
• Lost the most weight on a high-fat, low-carbohydrate diet
• Lost the least weight on a carbohydrate-based, low-fat diet
• Lost weight even at 2,600 calories a day – but only on a high-fat diet.[7]
In 1959, Professor John Yudkin, Queen Elizabeth Hospital, University of London, confirmed Kekwick and Pawan’s findings when he showed that a diet with unlimited protein and fat, but with little or no carbohydrate was far more effective in causing weight loss than a calorie-controlled, low-fat diet.[8]
And there have been many more controlled studies this century.
Obesity is an iatrogenic disease
In 1994, Professor Susan Wooley and Dr David Gardner highlighted the role of the professional in people’s increasing weight, saying:
“The failure of fat people to achieve a goal they seem to want – and to want above all else – must now be admitted for what it is: a failure not of those people but of the methods of treatment that are used.
“We should stop offering ineffective treatments aimed at weight loss. Researchers who think they have invented a better mousetrap should test it in controlled research before setting out their bait for the entire population. Only by admitting that our treatments do not work – and showing that we mean it by refraining from offering them – can we begin to undo a century of recruiting fat people for failure.”[9]
But there is a ‘better mousetrap’. William Banting wrote of it 150 years ago.
4
All mammals naturally eat a high-fat diet
All herbivores, using microfloral activity, ferment large quantities of vegetable fibre and other carbohydrates to produce short-chain fatty acids which are absorbed for energy. Little or no carbohydrate is absorbed as glucose. Similarly, all carnivores eat and absorb saturated animal fats, and no carbohydrates. In fact, whether herbivore, omnivore or carnivore, the natural diet of all mammals is high in total fats and saturated fats and low in carbohydrates. In nature, no animal is overweight and none suffers the chronic degenerative diseases we ‘civilised’ humans do. This also applies to ‘primitive’ human cultures.
Our natural diet is a high-fat diet, just like every other mammal.[10] We disregard this fact at our peril.
And saturated fat is best
Scientists at the Faculty of Medicine, University of Geneva, found that the more saturated a fat was, the less likely it was to increase a person’s weight.[11] This is not surprising as saturated fats are lower in calories than unsaturated fats.[12, 13]
Conclusion
Current ‘wisdom’ champions high-carbohydrate, low-fat diets as optimum, while dismissing higher protein/fat, low-carbohydrate diets as dangerous. Yet the evidence from evolutionary, epidemiological and clinical trials shows conclusively that the healthiest diet for weight loss (and many other diseases) is the exact opposite: one which is high in animal fats and protein, low in carbohydrates, particularly from cereals, legumes and fruit, and where calories are unrestricted. It is no coincidence that the incidence of obesity has risen so dramatically since ‘healthy eating’ was introduced – it’s a classic example of cause and effect.
Yet, despite the overwhelming weight of evidence that ‘healthy eating’ is not healthy, unsupported dogma still rules as leaders in medicine continue to ignore science and even their own experience, and push a grotesque diet which has led to today’s gross obesity and runaway diabetes.
Let us leave the last word to Dr Sylvan Lee Weinberg, past president of the American College of Cardiology and previously a fervent supporter of ‘healthy eating’. In 2004, Weinberg wrote in the Journal of the American College of Cardiology:
“The low-fat, high-carbohydrate diet . . . can no longer be defended . . . by rejecting clinical experience and a growing medical literature suggesting that the much-maligned low-carbohydrate, high-protein diet may have a salutary effect on the epidemics in question.”[14]
Like every other mammal on Earth, we should eat a high-saturated fat, low-carbohydrate diet.
2,500 words
Barry Groves, PhD. Independent nutritional researcher and author. Oxford, UK.
Dr David Brownstein, MD, Medical Director, Center for Holistic Medicine, Michigan
Dr Robert Davidson, MD PhD. Fellow, American Institute of Stress, Internal Medicine Doctor, Texas
Marshall E. Deutsch, PhD (Physiological Sciences) Independent investigator. Sudbury, Massachusetts.
Professor David Diamond, PhD, Professor, Departments of Psychology, Molecular Pharmacology and Physiology; Research Career Scientist, Medical Research Service, Veterans Hospital, Tampa, FL, USA
Dr Duane Graveline, MD MPH. former NASA Astronaut, USAF Flight Surgeon, Space
5
Medicine Research Scientist, Family Doctor, Florida.
Professor M Canan Efendigil Karatay, Cardiologist and İnternist, İstanbul Science University Medical Department.
Dr Malcolm Kendrick, MbChB, MRCGP (exam). General practitioner in Macclesfield.
Dr Peter Langsjoen, MD, FACC, Cardiologist and Internist, private practice, Tyler, Texas.
Lt Col. Dr Luca Mascitelli, MD, Medical Service, Comando Brigata Alpina “Julia”, Udine, Italy
Carlos Monteiro, President, Infarct Combat Project.
Dr Uffe Ravnskov, MD, PhD, specialist in internal medicine and nephrology, independent researcher, Lund, Sweden
Professor Paul J. Rosch, MD, FACP. President The American Institute of Stress; Clinical Professor of Medicine and Psychiatry, New York Medical College; Honorary Vice President, International Stress Management Association
Dr Stephanie Seneff, Senior Research Scientist, MIT, Cambridge, Massachusetts.
Glyn Wainwright, MSc, MBCS, CEng, CITP. Independent Reader of Research, Leeds, UK
Correspondence to barrygroves@tiscali.co.uk
References
1. William Banting. Letter on Corpulence, 1863.
2. Emmet Densmore. How Nature Cures. 1892.
3. Vilhjalmur Stefansson. The Fat of the Land. 1946.
4. McClelland WS, du Bois EF. Clinical Calorimetry. XLV, XLVI, XLVII Prolonged meat diets with a study of kidney function and ketosis. J Biol Chem 1930-1931; 87: 651-658; 87: 669; and 93: 419.
5. Lyon DM, Dunlop DM. The treatment of obesity: a comparison of the effects of diet and of thyroid extract. Quart J Med 1932;1:331-52.
6. Pennington AW. A Reorientation on Obesity. New Eng J Med 1953;248: 959-64.
7. Kekwick A, Pawan GLS. Calorie intake in relation to body-weight changes in the obese. Lancet 1956; ii: 155-160.
8. Yudkin J. The Causes and Cure of Obesity. Lancet 1959;II(7112):1135-8.
9. Wooley SC, Garner DM. Dietary treatments for obesity are ineffective. BMJ 1994; 309: 655-6.
10. Ben-Dor M, et al. PLoS ONE 2011; 6(12): e28689.
11. Dulloo AG, et al. Metabolism 1995; 44: 273-279.
12. Lars A Carlson; Sven Lindstedt. The Stockholm prospective study. 1: The initial values for plasma lipids Almqvist & Wiksell, Stockholm, 1968.
13. Apgar JL, Shively CA, Tarka SM. Digestibility of cocoa butter and corn oil and their influence on fatty acid distribution in rats. J Nutr 1987;117: 660-665
14. Weinberg SL. The Diet-Heart Hypothesis: a Critique. J Am Coll Cardiol 2004;43:731–733.
Further reading
Volek JS, Feinman RD. Carbohydrate restriction improves the features of metabolic syndrome. Metabolic syndrome may be defined by the response to carbohydrate restriction. Nutr Metabol 2005;2:3148.
Westman EC, Yancy WS, Haub MD, Volek JS. Insulin resistance from low carbohydrate, high fat diet perspective. Metabol Syndr Relat Dis 2005;3:14-18.
Cannon MC, Nuttall FQ. Control of blood glucose in type 2 diabetes without weight loss by modification of diet composition. Nutr Metabol 2006;3:16-23.
6


Landstinget Dalarna väljer att bryta mot lag.

Vid Landstinget Dalarnas fullmäktigemöte 2013-02-18 beslöt man att fortsätta GBP-operera patienter med övervikt i stället för att ge patienterna riktiga kostråd så att de sluppe denna magstympande operation. Dessutom skulle Landstinget Dalarna spara minst 90 MSEK, i en landstingsekonomi i kris.

 

Dalarnas sjukvårdspartis oppositionsråd Lisbeth Mörk Amnelius hade lämnat in en motion i höstas.

 

Landstinget Dalarna måste följa lagen

Ge överviktiga riktiga kostråd i stället för Gastric Bypassoperation

http://www.ltdalarna.se/handling/LF/20130218/lfh20130218Bilaga204.pdf

 

Nu skulle den godkännas, anses vara besvarad eller avslås.

 

Vad som förvånar mig är svaret. Motionen var en komplett utredning som visade på Patientperspektiv mindre sjukdom

Finansiering och ekonomiska konsekvenser besparing på minst 90 MSEK

Miljö, likabehandling, barnkonsekvens och konsekvensbedömning enligt systematiskt arbetsmiljöarbete bara positiva aspekter

Juridik försäkra sig om att Landstingets personal följer lag.

Folkhälsa bara positivt

Samverkan med fackliga organisationer behövs

Uppföljning Kontrollera attLD:s medarbetare följer lag

Vi föreslår att ansvariga förtroendevalda politiker tar befälet,

  • genom att besluta att vården ska följa RF 1 kapitlet 9 §, PSL 6 kapitlet 1, 6 och 7 §§ och HSL 2 a och 2 b §§ vid behandling av övervikt, allt baserad på vetenskap och beprövad erfarenhet i enlighet med Socialstyrelsens beslut av den 16 januari 2008 och
  • genom att påbörja en förebyggande verksamhet baserad på den befintliga kunskapen om lågkolhydratkost.
  • genom att sätta medborgarnas hälsa och samhällets intressen i första rummet och följa lag.

 

Vad händer?

Motionen beslutas vara besvarad. Men landstingets ledning inklusive fullmäktige anser att

”Patientperspektiv, Finansiering och ekonomiska konsekvenser, Miljö, likabehandling, barnkonsekvens och konsekvensbedömning enligt systematiskt arbetsmiljöarbete

Dessa perspektiv bedöms inte vara relevanta i ärendet.

 

Juridik

Enligt hälso- och sjukvårdslagen (HSL) 3 § ska all hälso- och sjukvård bedrivas

utifrån vetenskap och beprövad erfarenhet. Nuvarande behandlingsmetoder

mot fetma bedrivs utifrån denna utgångspunkt.

 

Samverkan med fackliga organisationer

Motionssvar är inte föremål för facklig samverkan.

 

Uppföljning

Någon uppföljning krävs inte i detta ärende.”

 

Det är till att vara okunnig inom ledningen.

Det är till att vara arrogant inom ledningen.

Det är till att förakta patientperspektivet.

Det är till att låta bli att spara mer än 90 miljoner.

Det är till att bryta mot grundlagens 1 kapitel 9 §, Patientsäkerhetslagen och Hälso- och sjukvårdslagen.

 

Man verkar inte bry sig.

         Inte om patienter.

              Inte om ekonomi.

                Inte om kunskap. Inte om miljö

 

Man verkar vilja ha som mål att bryta lag till högsta möjliga kostnad.

 

Inte undra på att Landstinget Dalarnas sjukvård de senaste åren gått med underskott på omkring 150 MSEK per år.

 

Björn Hammarskjöld

Tjänstgörande ersättare i Landstinget Dalarnas fullmäktige.

 


Obesity steering group in Great Britain

The Obesity Sterring Group of AMRC issued recommendations yesterday.
 
http://www.aomrc.org.uk/about-us/news/item/doctors-unite-to-deliver-prescription-for-uk-obesity-epidemic.html 
 
April 2012, The Academy of Medical Royal Colleges announced that they were launching a review into the UK obesity crisis. They wanted ideas before June 2012 and they got my proposal and at least three more proposals recommending along the same lines as my letter.
 
Of course they ignored our recommendations.
 
Read more here:
 
Zoë Harcombe submitted her version to the Obesity Steering Group. You can read it here
http://www.zoeharcombe.com/2013/02/the-medical-professions-prescription-for-the-nations-obesity-crisis/ 
 
Stephanie Seneff submitted her version and here it is:
http://www.zoeharcombe.com/2013/02/the-academy-of-medical-royal-colleges-obesity-initiative-stephanie-seneffs-submission/
 
Barry Groves submitted evidence countersigned by 14 members of THINCS. http://www.lizscript.co.uk/Glyn/AoMRCSub.pdf
 
So here is my letter:
 

To The Obesity Steering Group.

obesity@aomrc.org.uk ;

academy@aomrc.org.uk ;

alastair.henderson@aomrc.org.uk

 

Dear Sirs,

You are asking how we should be tackling obesity on behalf of the MedicalRoyalColleges and Faculties.

 

This is an excellent strategy.

 

First of all we need to use established knowledge in the areas of Physiology, Biochemistry and Endocrinology.

 

We have to eat protein, preferably of animal origin, as humans are unable to produce 10 of the about 20 amino acids we need for protein production in our bodies. Therefore, proteins are essential in the diet.

 

We require animal fat to maintain our cell membranes and our fat depots. We also need fats as our primary energy source. We consist of a minimum of 10 % animal fat, and fat is used for padding to protect vital organs. Our brain and neurological systems are also mainly composed of fat. Therefore, we need to acknowledge that fat is an essential nutrient.

 

Almost all cells contain mitochondria, and the only fuel mitochondria accept is AcetylCoenzyme A, (shorthand ACoA or acetic acid) in the Krebs cycle where AcCoA is added to oxaloacetic acid to form citric acid. The citric acid is then metabolized to two CO2, two H2O and 15 ATP (adenosintriphosphate) and back to oxaloacetic acid to recycle with the next available AcCoA. Our mitochondria have to use AcCoA as fuel but it makes no difference to mitochondrial metabolism if the AcCoA comes from fat or carbohydrates.

 

Animal fat has the same composition in all warm blooded animals. Very nearly 50 % saturated fats, and 50 % monounsaturated fats.  The rest, about 5 %, are polyunsaturated fats. This composition is key to maintaining the correct melting temperature of fat for the function of cell membranes and fat depots. This is also why fish, living in a cool environment, have to have more polyunsaturated fats to produce fat with lower melting temperature. For a similar reason, horses and cows during wintertime have a higher proportion of polyunsaturated fats in their hoofs, and cloven, as their feet are colder than the rest of the body. That polyunsaturated rich oil is called hoof oil and was used to dampen nautical compasses, before the cheaper silicone oils were available.

 

Also, all essential micronutrients like vitamins and minerals we have to eat are in ample amounts in animal food, but are scarce in vegetables and carbohydrate containing food.

 

Carbohydrates are necessary in small amounts in our blood. The normal range of glucose is 3-6 mmol/L. This means that there are 1.5-3 grams glucose in the total blood volume of a 70 kg person. This amount of glucose is essential to the red blood cells (RBC) as they lack mitochondria and need glucose to anaerobically metabolize it via 2,3-diphosphoglycerate (2,3-DPG) (Rapoport-Luebring pathway) . This allows the release of oxygen from haemoglobin and also creates two molecules of ATP and two molecules of lactic acid per molecule of glucose, powering the energy requirements of the RBC.

 

If you eat 5 grams of carbohydrates then the blood glucose level will increase another 10 mmol/L from 5 mmol/L to 15 mmol/L. This glucose level will trigger the beta cells of the pancreas to release insulin to lower the toxic level of glucose.

 

Insulin’s primary effect is to restore the blood glucose level back to 3-6 mmol/L. An elevated level of glucose is toxic to the body, as glucose nonenzymatically binds to proteins causing Advanced Glycation Endproducts (AGE). The most well known AGE is HbA1c, glycated haemoglobin, where glucose or fructose sterically hindering oxygen binding to haemoglobin reducing oxygen transportation in the blood.

 

Thus, carbohydrates create havoc even in relatively small amounts. When blood sugar levels rise, insulin stops the production of AcCoA from fat. At which point the main source of AcCoA will be glucose metabolized to AcCoA. This inevitably leads to an excess of AcCoA, that can not be metabolized to two CO2, two H2O and 15 ATP in the already overloaded Krebs’s cycle. The excess of AcCoA is thus polymerized in the liver to saturated fat of up to nine AcCoA modules which will then be stored in our fat depots.

 

Insulin has many actions that will restore the normal blood glucose level of 3-6 mmol/L. So it is an ample supply and production of insulin that keeps us from dying prematurely. Patients with diabetes have insufficient insulin production to meet the demands of the extreme amounts of carbohydrates now recommended by the authorities. On the other hand, patients with diabetes fare much better on a low carbohydrate and higher fat diet, some of them can even get rid of all their drugs, including insulin. This was the regular method of diabetes treatment before the advent of insulin 1923. That method was still recommended up to about 1980 when all of a sudden it was decreed that patients with diabetes should not be treated differently from the healthy population.

 

If we have more than 30-50 mmol/L (>15-25 grams) of glucose in the blood it is a lethal concentration of glucose. Yet, the authorities recommend a diet containing 381 grams of carbohydrates per day (60 % of 2 605 kcal). Carbohydrates are neither essential nor necessary to us, as the liver can make all the carbohydrates we need. This is common scientific knowledge for more than a hundred years.

 

The old pig farmer knew how to get a fat pig for Christmas. He fed the pig boiled potatoes with fat and coarse milled grain with a lot of fibres, both good sources of carbohydrates and added fat to be stored as the old physiologists knew. Today we feed our children milled grain with a lot of fibres, now rebranded to Fibre rich pasta, and oil cooked potatoes, now rebranded to French Fries (British Chips). This is why our children get fat, we offer them the same old fashioned pig farmer’s weight gaining food. Only, rebranded with new names.

 

The modern pig farmer knows how to get a slender pig, just feed the pig protein and ample amounts of fat and small amounts of carbohydrates.

 

All weight reduction diets have one thing in common. Just look at the two extremes, 

 

  1. Standard famine diet with 600 kcal and 50 E% carbohydrates contains 75 g carbohydrates, 23 g protein (113 g meat) and 23 g fat per day.
  2. Low carbohydrate high fat (LCHF) diet with 2500 kcal and 12 E% carbohydrates contains 75 g carbohydrates, 94 g protein (470 g meat) and 203 g fat per day.

 

Both diets have the same amount of carbohydrates and give the same weight reduction in a short time perspective. This has been shown many times in the past [[1], [2], [3], [4] ] but are not reproduced in the modern clinical literature, as this would be contrary to the politically correct “conventional wisdom” of the Dietary goals from 1977. In the Mc Govern Select Committee Nick Mottern, a former labour journalist and vegetarian [[5]], almost single handed wrote the Dietary goals which are still recommended by authorities like EFSA in Europe and Livsmedelsverket in Sweden.

 

The famine diet is bound to fail and must end in a few months. The body craves more nutrients and the person is forced to start eating more food to survive or the person will die of famine due to too little energy, too little micronutrients, too little fat and too little animal protein.

 

The LCHF diet gives satisfaction, all nutrients come in ample amounts and the diet can be eaten until the person dies of old age.

 

We need a diet with high energy density as our brain requires 20 % of our basal metabolism.

 

We need a diet with high energy density as we then do not need long eating times like herbivores.

 

Fat has the energy density of approximately 9 kcal/g required to feed the brain with enough AcCoA. Natural animal fat is also shown to be non-toxic in all amounts/concentrations up to more than 400 kg body weight.

 

Protein in the form of meat has about 0.8 kcal/g meat so animal protein sources are energy scarce and excess of 0.5 g/kg bodyweight is usually deaminated to carbohydrates.

 

Carbohydrates (excluding grain) have just fractions of a kcal/g vegetable. Cucumber has just 0.14 kcal/g. Fruit has about 0.4 kcal/g fruit so they are not good enough for energy production.

 

Dried grain has maximally 3.5 kcal/gram flour but carbohydrates causes havoc in our body and can be toxic or even lethal at higher amounts. We cannot deal with too high an intake of carbohydrates without causing disease, including obesity and diabetes. The upper level of carbohydrates should not be more than 100 g carbohydrates per day or a healthy adult. Persons with a metabolic diagnosis must consume even fewer carbohydrates [[6]].

 

Also, there is an excellent article about weight loss among patients with diabetes showing that a decrease of carbohydrate from 400-500 g to 100 g gave a weight reduction of 11.5 kg in six months [7]. The control group decreased 1.8 kg during the same time. Half the control group switched over to the low carbohydrate diet and repeated the experiment within the experiment. The weight loss was stable during 44 month.

 

The main responsibilities of The Obesity Steering Group are to:

  1. Produce a strategy on the most effective and coherent way to tackle obesity

 

  1. Produce a recommendation report to form part of a wider Obesity campaign by the last quarter of 2012.

 

Ad item # 1.

There are several steps that would be recommended to try to combat the obesity epidemic, outlined below.

1.      The most important thing of all is to understand the physiological, biochemical and endocrinological background to the obesity epidemic. That background can be retrieved from the metabolic science and knowledge from before the second half of the 20th century. Most of the research before the 1950th was done in Europe, most of it in German writing countries but also both France and United Kingdom were participating in the scientific research.

2.      Next comes that The Obesity Steering Group has to educate the senior advisors in the health care system.

3.      The next step is to convey the knowledge from the senior advisors to all medical staffs

4.      The last step is to educate the whole population the new directives.

 

These steps would not take long as you can use modern video education including publishing on the Internet

 

Ad item #2

Be straight and just show that meat, fish, eggs and animal fat is good for us. Protein and fat are essential (we have to eat that kind of food) and they contain enough with minerals and vitamins. It is enough to have 0.5 g/kg (or 175 g meat or fish) per day of animal proteins. Eating vegetable proteins that often are missing some essential amino acids why you usually need at least double amounts of vegetable protein or more.

 

Eggs are very nutritious and we can have several eggs per day. Remember that a fertilized egg that is hatched under a hen contains everything (but heat, oxygen and water) inside the eggshell to produce a complete chicken in three weeks, so there is no better food for us.

 

Regarding animal fat and vegetable hard fats, a normal person needs around 200 g per day.

 

Carbohydrates, including grain, starch, sugars and High Fructose Corn Syrup (HFCS), can be eaten in moderation but they are toxic. This means a maximum of 50-100 grams of carbohydrates per day for healthy persons. You can have as much vegetables and tubers as the person want up to two kilograms per day. Limit the potatoes to 300-600 grams/day or grain products (bread, pasta, pizza, cereals and similar grain products) less than 100-200 grams per day. But potatoes and grain should be summarized as carbohydrates.

 

Industrial unsaturated trans fatty acids should be avoided as they are toxic.

 

Rumenoid trans fatty acids, also called Conjugated Linoleic acid (CLA) are safe for us and should be encouraged to eat.

 

SUMMARY

 

We need to eat essential food (animal protein, fat, minerals and vitamins) like the old French kitchen and old fashioned local food like the Swedish “husman” (“Master’s”) diet from before 1960.

 

Carbohydrates are toxic and even lethal and nonessential. So we should avoid processed modern food as they usually contain a lot of carbohydrates replacing the animal fat.  The processed food also often contain vegetable oils containing omega-6 rich fatty acids which causes inflammation and even cancer [8].

 

Avoid fiscal measures as they usually backfires, education of the population is much more efficient and cheaper.

 

Exercise is known for generations to increase the appetite, so I do not understand how the advice to “run more and eat less” actually works. That advice has been recommended to obese patients for decades and there have never been any long standing results of that piece of advice.

 

A high-level government official, preferably the prime minister, should make a public statement on a highly-visible occasion bravely admitting that we were wrong to blame the obesity epidemic on saturated fat and cholesterol in the diet, and that, instead, people should focus on reducing carbohydrates including dietary sugars and processed foods. People are going love to be allowed to have real and natural food. So there will be no problems.

 

There are three excellent books that should be required reading for all nutritionists and government personnel involved in the anti-obesity campaign:

  1. Gary Taubes, Good Calories Bad Calories by A Knopf, NY, NY, USA, 2007
  2. Barry Groves, Trick and Treat Hammersmith, London, UK, 2008
  3. Weston A. Price, Nutrition and Physical Degeneration

 

A good lecturer for each book (can be a lecture film on the Internet) can be a shortcut as these books take a considerable time to read and understand. In the first two books there are about 400 pages plus about 200 pages with references. So actually every word written in these two books are excellently referenced with both old as well as modern references.

 

Carbohydrate containing beverages should be non-recommended or at least restricted in size in public.

 

The whole population and especially our children should be educated on the benefits of real unprocessed food and the dangers of fast food including the cost and taste benefit of real food compared to carbohydrate rich food.

 

An aggressive advertising campaign should be initiated to promote foods containing healthy animal fat and cholesterol, such as meat, fish, oysters, eggs, bacon, butter and whole milk.

 Mora June 06, 2012.

 Björn Hammarskjöld

M.D.,

Former Senior Consultant in Paediatrics.

Ph.D. in Biochemistry

Independent scientist in Nutrition.

Limholsvägen 6

792 91 MORA

Sweden

 

 

 

 



[1] William Banting. Letter on Corpulence, 1863

[2] Lyon DM, Dunlop DM. Quart J Medicine 1932;1:331-52.

[3] Pennington AW. .A Reorientation on Obesity New Eng J Med 1953;248: 959-64.

[4] Kekwick A, Pawan GLS. Calorie intake in relation to body-weight changes in the obese. Lancet 1956; ii: 155-160

[5] Gary Taubes, Good Calories, Bad Calories, A Knopf, N.Y., 2007, pp 45-6

[6] Ben-Dor M, et al. PLoS ONE 2011; 6(12): e28689

[7] Jörgen V Nielsen* and Eva A Joensson, Nutrition & Metabolism 2008, 5:14 doi:10.1186/1743-7075-5-14  http://www.nutritionandmetabolism.com/content/5/1/14

[8] Wirfeldt, E, Mattisson, Irene, et al. Cancer Causes Control 2002; 13; 883-93


Livsmedelsverket, forskningsfusk och rekommendationer

Livsmedelsverkets nuvarande kostrekommendationer är baserade på forskningsfusk och fria fantasier. Det visades mycket fint av Statens beredning för medicinsk utvärdering (SBU) i dess rapport «Mat vid diabetes» som kom ut den 2, 3 och 5 maj 2010 samt slutversionen i augusti 2010. SBU fann att det helt saknades vetenskap bakom kostråden, varför de skulle behållas oförändrade (!).

Det saknas helt RCT-studier i strikt bemärkelse då det gäller kost. Det finns flera orsaker till det. Det går inte att randomisera kosten utan att försökspersonerna märker skillnaden. Ändrar man en parameter så ändrar man minst en parameter till, minskar man mängden kolhydrater så ändrar man mängden energi och man ändrar kroppens hormonbalans. Så det är alltså omöjligt att göra en RCT-studie, i strikt bemärkelse.

Däremot så kan man göra en kostförändring och se vad som händer med individen, individen är sin egen kontroll. Detta har gjorts många gånger men pillerkramarna ser inte skillnaden på nutrition och piller, utan tror att det är samma sak.

Ett av de allra snyggaste exemplen på en perfekt genomförd koststudie är doktor Jörgen Vesti Nielsens försök i Karlshamn sedan 2003. Läs mer här…

Här har 16 patienter med diabetes fått rådet att äta högst 100 g kolhydrater/dag. Det gav efter 6 månader en viktminskning på 11,5 kg i genomsnitt, tre av dem slapp alla mediciner, övriga minskade insulindosen från 60 E/dag till 18 E/dag.

Kontrollgruppen om 15 patienter tappade 1,8 kg på 6 månader, ingen medicinförändring, de hade fortfarande 60 E insulin per dag.

Åtta av kontrollgruppen gick efter 8 månader över till lågkolhydratkost och de gjorde en liknande resa in i frisklandet. Alla 24 mådde helt bra efter 44 månader, ingen progress av ”naturalförloppet”, inga dödsfall.

Av de fem som var kvar i högkolhydratkosten hade fyra fått hjärtinfarkt och två av dessa hade dött. De har alltså helt följt det ”naturalförlopp” som Socialstyrelsens Dan Andersson beskrev i Läkartidningen 1998, där 40 % av patienter med nyupptäckt diabetes hade dött inom fem år efter diagnos.

Vi ser denna undersökning som perfekt. Att få signifikanta resultat i en liten undersökning är mycket svårare än i en stor undersökning. Försöket är upprepat inom försöket med samma resultat. En sådan upprepning av försöket i försöket med samma resultat är briljant!

Beträffande långtidsstudier så har vi William Banting på 1860-talet, han som är upphovet till ordet bantning. Han gick ned i vikt och levde länge på lågkolhydratkost. Vidare finns det en studie som redogjorde för samernas kost från 1732, alltså en 280 år gammal studie. Sedan har vi Paal Røiris beskrivning av inuiternas kost som stämmer perfekt med samernas kost (länk), från 2002. Røiris slutsats är tänkvärd:

”En dokumentasjon av at gjeldende norske kostholds-retningslinjer ikke er i pakt med foreliggende forskningsresultater, og bør revideres.”

Önskan om ökad valfrihet och att laga riktig mat från grunden även i skolan är helt i överensstämmelse med våra önskemål. För att kunna laga riktig och god mat bör man följa Livsmedelsverkets kostråd i SvenskaNäringsrekommendationer Översatta till livsmedel (SNÖ).

Livsmedelsverkets SNÖ

I SNÖ står det att kolhydrater (den så kallade ”utrymmesmaten” består enligt Livsmedelsverket nästan enbart av kolhydrater) bör begränsas till maximalt 13-14 E%.

Vi vill liberalisera det något så att maximalt 100 g kolhydrater per dag till vuxna är en enkel gräns att använda. Det blir max 35 g kolhydrater per huvudmål, motsvarar 7 hg grönsaker per huvudmål om eleven orkar äta så mycket.

Men barnen slipper alla former av utrymmesmat i form av bullar, även benämnda fullkornsbröd, pasta, tårta, pizza, glass, hårt bröd och alla andra spannmålsprodukter, samt socker.

I övrigt blir det normal mängd protein (0,5 g animaliskt protein per kg kroppsvikt) som även Livsmedelsverket rekommenderar. Observera att vegetabiliska proteiner saknar den essentiells aminosyran taurin, varför vegetabiliska proteiner är mindre dugliga för människan.

Resten av energin i maten bör komma från animaliskt fett, det fett som är mest likt vårt eget fett. Man kan använda en del kokosfett och eventuellt rapsolja och olivolja.

Övriga vegetabiliska fetter innehåller abnormt höga halter av omega-6-fetter som är cancer- och inflammationsdrivande (se Livsmedelsverkets Irene Mattissons artikel från 2002 i ”Cancer Causes Control”, där hon visar att omega-6 i större mängder än 20 g leder till ökad risk för bröstcancer). Dessa oljor bör man låta bli för att fortsätta att hålla sig frisk.

Detta ger att för 2 500 kcal per dag blir det 35 g kolhydrater, 11 g protein och 77 g fett, i mat blir det 700 g grönsaker, 55 g kött och 1,5 dL riktig gräddsås.

Feta barn är undernärda barn

Det är visat i början av 1930-talet i New York att feta barn är undernärda barn. Många tvingades till soppkök under den stora depressionen och då fick barnen spannmål som ökade deras fetma, men för litet protein, fett och mikronäringsämnen i den näringsfattiga soppan och brödet.

Så som du beskriver det så ska alla överviktiga (= undernärda barn) ha rätt till mera fett och mindre kolhydrater i maten, precis som Livsmedelsverket skriver i SNÖ.

Jag anser att det strider mot Barnkonventionen och grundlagens 1 kapitel 9 § att särskilja barn och deras mat på grund av kroppsvikt.

  • Man får aldrig glömma att protein är livsnödvändigt..
  • Man får aldrig glömma att fett är livsnödvändigt..
  • Man får aldrig glömma att kolhydrater är giftiga i högre koncentration än 7 mmol/L (motsvarar mer än 7 g i blodet hos 70 kg människa)..
  • Man får aldrig glömma att kolhydrater är dödliga i koncentrationer mer än 30-50 mmol/L (motsvarar mer än 30-50 g i blodet hos 70 kg människa).

Kolhydrater ställer därför till kaos i kroppen om man äter mer än 5 g stärkelse (=5 g glukos), som höjer blodglukosnivån till 10 mmol/L. Se insulins effekter här…

Dessutom åldras proteiner i kroppen av en hög glukos- eller fruktoshalt, det blir en försockring eller kandering av proteinmolekyler som förstör funktionen av proteinet.

Den mest kända kanderingen är HbA1c eller ”långtidssockret”. Här sätter sig en sockermolekyl på hemoglobinet som då förhindras att ta upp syre. Detta kan leda till syrebrist och död i vävnaderna.

Så kolhydrater bör minimeras för att säkerställa en hälsosam blodglukosnivå. Detta uppnås genom att äta mat som innehåller protein och fett från animaliska källor, det vill säga artegen mat. Då mår man bra.

PS. Eftersom Livsmedelsverkets hemsida med ”Frågor och svar om LCHF” är behäftad med en del faktafel och med påståenden som inte är styrkta, har vi bett dem att justera sidan, eftersom de enligt lag är skyldiga att tala sanning.

Brevkonversationen med SLV och en uppdaterad korrekt version av ”Frågor och svar om LCHF” finns här… (en version baserad på ”vetenskap och beprövad erfarenhet”).


NNR 2012 makronutrienter förslag

Björn Hammarskjöld's  proposition to NNR5 macronutrient recommendation to healthy individuals ahead of official publication.

These recommendations are based on the old trustworthy sciences physiology, biochemistry and endocrinology:

 

Summary of NNR 2012 recommendations to healthy individuals

 

NNR 2012 recommend an adequate intake of essential nutrients of protein, fat, minerals and vitamins.

 

NNR 2012 recommends a normal daily intake of essential animal protein of at least 0,5 g/kg bodyweight.

 

NNR 2012 recommends a normal daily intake of essential salt of at least 10 g per day.

 

NNR 2012 recommends an upper limit of 100 g of carbohydrates/sugars per day [1].

 

NNR 2012 recommends a sufficient intake of essential fats to satisfy the energy and metabolic requirements.

 

NNR 2012 recommends an upper limit of 20 g per day of vegetable omega-6 polyunsaturated fats. [2], [3].

 

NNR 2012 recommends an upper limit of fiber intake of 25 g per day to an adult and an upper limit of 0,35 g/kg to a child.

 

NNR 2012 recommends an upper limit of one fruit per day.

 

  

The conclusion of food consumption changes between NNR4 and NNR5 to promote health in Nordic populations

                                                                            

Increase                     ..                     .

Fat, preferably animal 

Salt, at least 10 g/day     .

 

Unchanged          

Protein from meat  

Vegetables

 

Limit to per day

 Limit Carbohydrates to 100 g.

 Limit Omega-6 PUFA to 20 g

 Limit fiber to 25 g 

  Limit fruit to one

 

 Mora February 10, 2013

Björn Hammarskjöld

Independent nutritional scientist

 

 

Background information for NNR 2012 recommendations

From NNR5.org http://www.slv.se/en-gb/Startpage-NNR/ 

Recommendation for carbohydrates, fibre and added sugar

http://www.slv.se/upload/NNR5/NNR5%20Carbohydrates.pdf

 

 Mikael Fogelholm

The data on health effects of dietary fibre and fibre-rich foods are very strong.[4]

Recommendations in NNR 2012:

Adults: Intake of dietary fibre should be at least 25-35 g/d,

i.e. approximately 3 g/MJ.

Children: An intake corresponding to 2-3 g/MJ is appropriate

for children from 2 years of age. From school age the

intake should gradually increase to reach the recommended

adult level during adolescence.

 

My comment

According to present recommendations in NNR4 children should have about double the amount of fiber per kg bodyweight as an adult. Adults are recommended about 30 g/day or 0,4 to 0,6g/kg while children are supposed to have 3 g/MJ which will be 12 g fiber per day or 1,2 g/kg. This is due to recommendations are associated to the amount of energy eaten instead of kg bodyweight. Children have a higher energy intake per kg bodyweight due to the fact that they need more energy to grow and need more energy to compensate for a larger skin surface heat loss per kg bodyweight than adults.

 

As fibers are associated to an increased risk of colon cancer [5], [6], there is an increased risk that children and adults get colon cancer with the present recommendations.

 

So the new recommendations should be:

 

NNR 2012 recommends an upper limit of fiber intake of 25 g per day to an adult and an upper limit of 0,35 g/kg to a child.

 

Mikael Fogelholm

Intake of added sugars should be kept below 10 E%.

Limitation of the intake of added sugars from particularly sugar-sweetened beverages and sugar–rich foods is recommended in order to reduce the risk for type 2 diabetes, weight gain and dental caries.

•A limitation of the intake of added sugars is also necessary to ensure an adequate intake of essential nutrients and dietary fibre, especially in children and adults with a low energy intake.

 

My comment

In NNR4 there is a recommendation to keep intake of added sugars to below 10 E%.

 

It seems that the NNR4 have disregarded that carbohydrates and sugar are synonyms as they recommend a limit of carbohydrates in the form of “added sugar” but recommend 50-60 E% of carbohydrates in a day.

 

 It is good that NNR 2012 will limit the intake of sugar to ensure an adequate intake of essential nutrients. All kinds of carbohydrates consists of sugar which are nonessential and contains 1 to 1/1 000th (or less) of minerals and vitamins compared to food of animal origin [7]. Then we have to re-establish what the essential nutrients are.

 

So the new recommendations should be:

 

NNR 2012 recommend an adequate intake of essential nutrients of protein, fat, minerals and vitamins, preferable in the form of animal proteins and fats which contain enough minerals and vitamins.

 

Vegetables are insufficient in amino acids, all fatty acids including long chain polyunsaturated fatty acids, minerals and vitamins [8] but vegetables are excellent to improve the visual impression of food. Fruit with 10 % sugar content may decrease to maximum one fruit per day

 

Also, the NNR 2012 finds no justifications to include a diet-based recommendation for GI in NNR.

 

My comment

This is correct as GI is a partial and indirect measurement of carbohydrates, we are just measuring the glucose level in the blood, we are not measuring all other sugars like fructose, galactose nor are we measuring the continuous insulin level that delays the uptake of sugars in an attempt to normalize a too high blood glucose level. 

 

So an added recommendations should be:

 

NNR 2012 finds no justifications to include a diet-based recommendation for GI in NNR.

 

Also, NNR4 recommends specific “quality” of fat.

As all mammals have the same temperature of 37ºC, they all have the same animal fat composition with the same melting temperature for correct function. This means animal fat has shy of 50 % saturated fat, shy of 50 % monounsaturated fat and about 5 % polyunsaturated fat. This is the ideal mixture of fats and the fat has a correct melting temperature to support correct function of fat in tissues and cell membranes..  

 

 

 


[1] Based on old fashioned physiology, biochemistry and endocrinology, e.g. Lagerholm, J., Hemmets Läkarebok, Fröléen & Comp, Stockholm, 1921 and Ganong, W., Medical physiology, Lange Medical Publications, Los Altos, CA, USA 1971.

[2] Wirfält, Mattisson et al Postmenopausal breast cancer is associated with high intakes of omega6 fatty acids (Sweden). Cancer Causes Control. 2002 Dec;13(10):883-93.

[3] Ramsden, Zamora et al Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis. BMJ 2013;346:e8707 http://www.bmj.com/highwire/filestream/629053/field_highwire_article_pdf/0/bmj.e8707

[4] SBU rapport Mat vid diabetes 2010. No scientific support for NNR4 recommendations.

[5] Park Y, et al. Dietary fiber intake and risk of colorectal cancer: a pooled analysis of prospective cohort studies. JAMA 2005; 294: 2849-2857.

[6] Fuchs CS, et al. Dietary Fiber and the Risk of Colorectal Cancer and Adenoma in Women. New Engl J Med 1999; 340: 169-176, 223-224.

[7] Livsmedelsverkets databas http://www7.slv.se/Naringssok/

[8] Livsmedelsverkets näringssök http://www7.slv.se/Naringssok/

 

 

Damage control brukar det kallas

Damage control

eller

Omega-6-fetter i stället för mättat fett minskade överlevnad

 

I Dagens medicin står om en artikel i BMJ där man återfunnit gamla data från 1964-73. http://www.dagensmedicin.se/vetenskap/hjarta-karl/omega-6-fetter-minskade-overlevnad

Originalstudien http://www.bmj.com/highwire/filestream/629053/field_highwire_article_pdf/0/bmj.e8707.full.pdf

 

Bristen i den ursprungliga studien publicerad 1978 var att man inriktade sig på insjuknande i hjärtsjukdomar och inte på dödlighet. Nu har man återfunnit de gamla databanden och kunnat läsa av dem och bearbeta dödlighetssiffrorna.

 

Den enda ändring man gjorde i försöket var att minska mängden smör och öka mängden margarin och tistelolja (en omega-6-olja som saknar omega-3) från 6 % till 15 % omega-6.

 

I övrigt fick både kontrollgruppen och försöksgruppen inga andra instruktioner avseende kost, man fortsatte att äta sin vanliga mat som vanligt.

 

Och man finner till vissas fasa att dödligheten ökar då man ökar mängden omega-6-fetter till 15 % av energiintaget.

 

Slutsatsen blir att man anser att myndigheternas rekommendation om omega-6 bör omprövas.

 

Dagens Medicin har intervjuat professor Joep Perk, från Oskarshamn, som sitter högt i diverse europeiska kardiologföreningar.

 

Perks invändningar:

” – Av deltagarna i studien var två tredjedelar rökare och väldigt få hade diabetes, vilket är i starkt kontrast till dagens hjärtpatienter. Studien är också gjord långt innan det fanns effektiva behandlingar i form av till exempel statinläkemedel och ballongvidgning, säger Joep Perk.”

 

Men det var lika många som rökte i behandlingsgruppen som kontrollgruppen. Alltså kan det inte vara rökningen som var orsaken.

 

Att det fanns få patienter med sockersjuka runt 1970 visste vi redan och antalet sockersjuka har tredubblats sedan dess på grund av den extrema högkolhydratkosten vi rekommenderas sedan dess. Men det är ingen skillnad mellan grupperna.

 

Lyckligtvis är denna studie gjort innan statinerna gjorde sitt intåg så man kan inte skylla på statinerna heller.

 

Sedan kvarstår att den enda skillnaden mellan grupperna var just det enda man randomiserade och mätte, omega-6 ökade 7 E% och mättat fett minskade 5 E% mellan grupperna. Det gav en signifikant ökning av antalet dödsfall i interventionsgruppen som leder till slutsatsen att den nuvarande rekommendationen om omega-6 bör ifrågasättas och ändras.

 

I de allra flesta senare studier ändrar man på många fler faktorer så de studierna är totalt värdelösa.

 

” Vidare pekar han [Perk] på vad han anser vara metodologiska problem i studien. – Man hade dålig kontroll på matvanorna i kontrollgruppen där flera deltagare började äta mer margarin och mindre smör. Flera av dödsfallen i interventionsgruppen fanns dessutom bland dem där man saknade uppgifter om matvanor. Det verkar också som om kontrollgruppen minskat mer på kaloriintaget än i interventionsgruppen, vilket kan ha påverkat resultatet, säger Joep Perk.”

 

Låt oss syna Perks uttalande.

 

Dålig kontroll på matvanorna kan det inte vara eftersom man upptäckte att även kontrollgruppen åt litet mer margarin. Kontrollgruppen minskade energiintaget med 9 % och interventionsgruppen med 7 %, insignifikant skillnad. Så det verkar som om Joep Perk försöker mildra studiens implikationer på de nuvarande kostråden om ökad mängd omega-6 i maten.

 

Damage control brukar det kallas.

 

Perk synes försöka minska betydelsen av denna gamla reviderade artikel. Detta trots att denna artikel är helt klar, omega-6 ökar totala mortaliteten. Detta trots all den kunskap som transplantationskirurger har om att omega-6 ger minskat immunförsvar och därmed minskad avstötningsrisk för transplantatet och ökad cancerrisk. Detta trots att Livsmedelsverkets Irene Mattisson som andreförfattare skrev en artikel i Cancer Causes Control 2002 där man fann att det enda fettet som var skadligt var omega-6-fetter som ökade risken för bröstcancer.

 

Nu sitter Mattisson och pushar omega-6 till våra barn i skolan som den värsta omega-6-langare.

 

Joep Perks jävsdeklaration som ordförande i en programgrupp för kardiovaskulär prevention inom det europeiska kardiologisällskapet ESC står inte att återfinna på ESCs hemsida trots att de enligt uppgift ska finnas där. Men han ingår i Apotekets vetenskapliga expertråd. Alltså har han seriösa ekonomiska läkemedelsintressen.

 

Då förstår jag att han ägnar sig åt Damage comtrol.


Gräddproduktionen i Sverige

Svensk Mjölk har producerat siffror på sin gräddproduktion i Sverige.
 
Det är en kraftig ökning av vispgräddtillverkningen från 60 000 ton till 77 000 ton på fyra år. Eller från 60 till 77 kt (=kiloton eller tusen ton). Det blir en ökning med 28 % på fyra år.
 
Även smör har ökat från 14 till 15,6 kt, mejeriernas övriga matfett, Bregott, Lätt&lagom och Omega 3 harb ökat från 28 till 34 kt. Så totala matfettsproduktionen har ökat från 42 till 50 kt per år. Det är inte dåligt med animaliefett i kosten med andra ord och ökningen har varit 19 % på 4 år
 
Det tar sig sa mordbrännaren och satte eld på håret.
 
Aftonbladet är inte mycket sämre heller. I deras omröstning föredrog 10 % margarin och 90 % smör av 12 300 röstande (2013-02-04) 
 
Så nu väntar vi bara på att NNR5 inser att SBU gett de nuvarande kostråden körförbud genom sitt underkännande 2010.
 

RSS 2.0