NNR5 Chapter 3 remissvar

Här kommer mitt remissvar på NNR5 Chapter 3 

 This text is intended to replace lines 245 to 303 in NNR5 Chapter 3 Draft of 2011-12-12

Text in font Times New Roman (10 p) is original information in NNR5 Chapter 3

Text in font Times New Roman (12 p) is added information to NNR5 Chapter 3

 

http://www.slv.se/upload/NNR5/Background%20and%20principles%20NNR%202012.pdf 

 

245 Reference values for energy intake

The term reference value for energy intake is used in the NNR and refers to the calculated estimated energy requirement for groups of healthy individuals with normal body size, age, sex and various levels of physical activity. Setting the reference value for energy intake requires a different approach compared with the reference values for vitamins and minerals. For some vitamins and minerals RIs can be given with large margins, since the absorption can be limited or the excess broken down or secreted. The RIs may therefore exceed the defined requirements of the individual on a long-term basis.

 

For energy intake, the situation is different, because an energy intake consistently above or below the energy requirement may will result in weight gain or weight loss which may affect health adversely. As a consequence and to prevent under- or over consumption, energy intake should approximate equal energy expenditure. The reference value for energy intake is expressed as the average of energy requirement for a defined population group with various levels of physical activity (excluding competitive athletes). Thus, the reference value for energy intake should be considered as a theoretical value intended to be used as a reference for the entire population group [1].

 

Recommended intake of macronutrients

The term recommended intake of macronutrients is used to emphasise the importance of the distribution of energy between energy-providing nutrients, i.e. macronutrients.

 

The macronutrient composition of NNR4 is proven unscientific by SBU – Swedish Council on Health Technology Assessment [2] in their report ”Mat vid diabetes” from May to August 2010.

 

This means that the non-scientific and rejected NNR4  recommendations has to be completely discarded and rejected, they can not be used as a basis for NNR5. NNR5 has to use science from previous centuries to establish a scientific base from physiology, biochemistry and endocrinology to be able to recommend any intake of macronutrients.   

 

Some basic facts seem to be necessary here. There are three macronutrients, protein and fat are both of them essential and the third macronutrient is the nonessential and toxic carbohydrate.

 

We have to eat protein, preferably of animal origin, as we are unable to produce about ten out of twenty amino acids, the building blocks of protein [3].

 

We have to eat fat, preferably of animal origin, as we have a limited production of long chained polyunsaturated fatty acids of animal origin. We also need fat as the major energy source for the body as well as fat makes the structural entity of cell membranes and constitutes padding fat tissue protecting delicate organs in the body [4].

 

Proteins and fats of animal origin are non-toxic and self regulate the energy intake. Animal fat has the same properties and melting temperature as our own fats and are optimal [5]. Excess of vegetable polyunsaturated omega-6 fatty acids may be cancerous [6]

 

The background is that the current major lifestyle diseases mainly result from over consumption of nonessential carbohydrates. Already Hippocrates knew 400 B.C. that over consumption of carbohydrates had a obesity and disease creating effect. Also the old pig farmer knew how to get a pig fat until Christmas, he fed the pig coarse milled grain (“gröpe” in Swedish) together with boiled potatoes and cow’s milk.

 

An excess of carbohydrates creates havoc in the body as carbohydrate in excess increase the plasma glucose level above normal values of 3-6 mmol/L triggering the insulin response to try to normalize the plasma glucose level. As the old fashioned physiology, biochemistry and endocrinology implies [7], the body has to change energy production from fat derived production of AcetylCoenzyme A (AcCoA) to carbohydrate derived production of AcCoA in an attempt to normalize the blood glucose level. For more information about insulin response, see Fact Box 3-A below.

 

As a 70 kg person has only 1.5 to 3 grams of glucose in the whole blood volume of 5.6 L, having just five grams glucose will increase the plasma glucose level from 5 mmol/L to 15 mmol/L without any insulin. This tiny amount of glucose triggers the insulin response in an attempt to normalize blood glucose level.

 

If the blood glucose level increases above 6 mmol/L glucose is toxic to the cells and the body. The production of Advanced Glycation Endproducts (AGE), i.e. glycosylation of cell membrane proteins, can damage the function of the proteins. As an example, HbA1c is glycated haemoglobin with a fructose or glucose molecule nonenzymatically attached to the first amino acid lysine blocking sterically the oxygen uptake to the haemoglobin molecule. This means that enough glucose or fructose in the blood may block oxygen uptake to prevent enough oxygenation of parts of the body.

 

If the blood glucose level increases above 30 to 50 mmol/L the concentration of glucose is lethal. This means that the small amount of more than 15 to 25 g glucose in the blood of a 70 kg person is lethal.

 

Without a competent pancreas producing enough insulin, carbohydrate consumption is potentially lethal.

 

Still, in the rejected NNR4 the recommended amount of carbohydrates are 50-60 percent of the energy (E%). This means 400-480 grams of carbohydrates, a.k.a. glucose, fructose, sugar. 400-480 grams of carbohydrates are about twenty-fold of a lethal dose of glucose.

 

The logical measure would be limiting the consumption of carbohydrates from the rejected NNR4 recommended level of 480 grams of carbohydrates per day to less than 100 g for healthy population, the way diabetes was treated efficiently 100 years ago [8] with at least 100 years if not at least 2 500 years of practical experience.

 

This is also the same carbohydrate restriction that was used until about 1980. Then three things happened almost concerted. First, the name “sockersjuka” was in Sweden replaced by the name “diabetes”. Second, the first “Dietary goals for the United States” recommendations were issued [9] and third, unlimited amounts of human insulin became available by gene technology.

 

So the current major lifestyle diseases mainly result from nutrition and nutritional imbalances, rather than the under-nutrition and deficiency symptoms. The intention of setting the recommended intake of macronutrients is thus to derive at a dietary macronutrient composition that will provide an adequate intake of essential nutrients, associated with optimal health and a reduced risk of major lifestyle diseases (Fig 3.1).

 

The recommended intake of macronutrients is based on an overall assessment of the present knowledge about the impact of macronutrient intake on health and/or risk of disease. This requires various types of scientific data, primarily from the physiology, biochemistry and endocrinology of previous centuries [10], [11]. The research behind NNR4 is rejected by SBU already in 2010 and can thus not be used by NNR5.

 

Here the protein intake is minimum 0.5 g animal protein/kg body weight to secure essential amino acid supplies. Excess protein intake leading to amino acid excess is converted to carbohydrates.

 

The carbohydrate intake ought to be limited to a physiological level. Healthy populations ought not have more than 100 g carbohydrates per day and populations with a metabolic disease like metabolic syndrome, diabetes or obesity are to be recommended a much lower carbohydrate intake.

 

This implies that the rest of the energy requirements should be satisfied by fat intake [12]. Polyunsaturated fats of omega-6 type should be limited to less than 20 g/day [13]

 

Randomized controlled clinical trials (RCTs), prospective cohort studies and other epidemiological studies are not applicable in nutritional research. RCT can not be used as there are always at least two parameters changed at the same time, which means we can usually not tell which parameter that is causative. Prospective cohort studies are difficult to control and thus unreliable. Epidemiological studies are always unreliable and may be hypothesis generating but never give causal relationship.

 

So RCTs, prospective cohort studies and epidemiological studies can not be the basis of nutritional recommendations.

 

Where possible, studies providing evidence of a 273 causal relationship and dose-response effects are used. A direct causal relationship between 274 intake of a single nutritional factor and a specific function or selected criterion such as reduction 275 of risk of diseases is not always evident from the scientific data, due to for example interaction 276 between several energy-providing nutrients. In such cases effects due to substituting different 277 energy-providing nutrients are taken into consideration under energy-balance conditions (e.g. 278 replacing saturated fat with unsaturated fat or complex carbohydrates). [B1] 

 

Good nutritional observations and research are available from the old fashioned physiology, biochemistry and endocrinology from previous centuries [14], [15] as well as modern studies from this century [16], [17].

 

In these cases, the recommended intake of macronutrients is based on an overall assessment of the scientific, this means physiological, biochemistrical and endocrinological evidence and includes specific considerations about known patterns of intake of nutrients and foods and actual composition of available foods in the Nordic countries.

 

 On this basis, the 282 recommended intake of macronutrients should be considered as ‘optimal’ in Nordic conditions. 283 [B2] 

 

The recommended intake of macronutrients refers to average intakes for groups and should be considered as goals for dietary changes and dietary advice (planning). Using acceptable ranges for the percentage of energy provided by carbohydrate, protein, and fat and their subclasses in the diet, refers to appropriate ranges of usual intake in the majority of the population (King et al, 2007)[B3] . The recommended intake for protein also includes considerations of an average requirement (AR) level.

 

Food based dietary guidelines

Food based dietary guidelines (FBDG)are based on an overall assessment of the present knowledge about the impact of food/food groups on health and/or risk of disease. Setting food based dietary guidelines requires various types of scientific data, especially evidence from physiology, biochemistry and endocrinology instead of non-scientific prospective cohort studies and other epidemiological studies and controlled clinical trials (RCTs) including the by SBU rejected NNR4.

 

These guidelines are considered as a translation of nutrient recommendations into foods. They also take into consideration the habitual dietary patterns and scientific evidence of the effects of foods on different health outcomes. Since 150 years we know what is a cofactor in causing obesity, heart disease, diabetes, cancer and dementia. The knowledge shows that the extremely high carbohydrate Western diet is the common denominator if not the cause [18]. Also, all weight reducing diets have a common denominator, they all reduce the carbohydrate content of the food. A causal relationship between food intake and risk of diseases is not always available from the scientific data. The food based dietary guidelines are therefore based on an overall assessment of the scientific evidence and include physiology, biochemistry and endocrinological knowledge and also specific considerations about known patterns of intake of foods and food groups and actual composition of available foods in the Nordic countries. On this basis, the FBDG should be considered as ‘optimal’ in Nordic countries.

 

Mora 2013-01-14

 

Björn Hammarskjöld

M.D., Ph.D.

Nutritional scientist

 

 

Fact box 3-A

 

When eating carbohydrates (mainly glucose) the response from the body includes but is not restricted to the following events:

1.      The blood glucose level rises above 6 mmol/L which leads to

2.      the insulin level rises, which leads to

3.      slowing down the passage speed of the intestines,

4.      decreasing the uptake rate of carbohydrates,

5.      increasing the conversion of glucose to Acetyl Coenzyme A (AcCoA) and

6.      Increasing the body temperature to increase the Krebs cycle aerobic conversion of AcCoA to carbon dioxide, water and adenosine triphosphate (ATP), the cellular energy storing molecule.

7.      As the AcCoA is produced in excess insulin shuts down the lipolysis normally creating the majority of the AcCoA essential for energy production. Now the insulin demands the body to burn AcCoA from glucose in an effort to normalize blood glucose level.

8.      Excess of AcCoA is created and the liver polymerizes AcCoA into saturated fatty acids like palmitic and stearic acids, transported to fat cells by VLDL.

9.      Insulin also knocks on all cell’s insulin receptors GLUT4 asking the cells to take up another glucose molecule. So the glucose molecule enters the cell surrounded by a cloud of 190 water molecules per glucose molecule. Very soon the cell becomes swollen and is risking cell membrane rupture due to intracellular water and glucose overload. So the cell retracts the GLUT4 receptors to protect itself from membrane rupture. We usually calls this cell self protection measure insulin resistance and we usually punish the cell by injecting more insulin.

10.  If the blood glucose level is above 11-12 mmol/L the kidneys are unable to reabsorb all filtrated glucose and we get glucoseuremic.

  1. If all these measures fail to normalize the blood glucose level the body pulls the emergency brake and converts glucose anaerobically to lactic acid. This requires 19 times higher glucose consumption compared to aerobic energy production but at the cost of a lower blood pH which can be lethal, usually called ketoacidosis

 



Reference list

[1] http://www.slv.se/sv/grupp1/Mat-och-naring/Svenska-narings-rekommendationer/Referensvarden-for-energiintag-hos-grupper/

[2] SBU rapport 201 ”Mat vid diabetes” Augusti 2010.

http://www.sbu.se/upload/Publikationer/Content0/1/Mat%20vid%20diabetes/Mat_vid_diabetes_fulltext.pdf

[3] Ganong, W F, Medical physiology, Lange Medical Publications, Los Altos, CA, USA, 1971

[4] Ganong, W F, Medical physiology, Lange Medical Publications, Los Altos, CA, USA, 1971

[5] Livsmedelsverket Livsmedelsdatabasen, http://www7.slv.se/Naringssok/

[6] 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

[7] Ganong, W F, Medical physiology, Lange Medical Publications, Los Altos, CA, USA, 1971

[8] Lagerholm, Julius, sjukhusläkare, i Hemmets Läkarebok, Fröléen & Co, Stockholm, 1904-1921

[9] Dietary goals for the United States 1977 http://zerodisease.com/archive/Dietary_Goals_For_The_United_States.pdf

[10] Ganong, W F, Medical physiology, Lange Medical Publications, Los Altos, CA, USA, 1971

[11] Taubes, G, Good Calories, Bad Calories, Knopf Publishing Co N.Y., N.Y., USA2007

[12] Socialstyrelsen Kost vid diabetes http://www.socialstyrelsen.se/Lists/Artikelkatalog/Attachments/18471/2011-11-7.pdf

[13] 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

[14] Brilliat-Savarin, The physiology of taste, Paris, 1825

[15] Taubes, G, Good Calories, Bad Calories, Knopf Publishing Co N.Y., N.Y., USA2007

[16]Vesti Nielsen, J, Jönsson, E Low-carbohydrate diet in type 2 diabetes: stable improvement of bodyweight and glycemic control during 44 months follow-up

Nutrition and metabolism 2008, 5:14http://www.nutritionandmetabolism.com/content/5/1/14

[17] Jørgen V NielsenCaroline GandoEva Joensson and Carina Paulsson, Low carbohydrate diet in type 1 diabetes, long-term improvement and adherence: A clinical audit Diabetology & Metabolic Syndrome 2012, 4:23 doi:10.1186/1758-5996-4-23 Published: 31 May 2012

http://www.dmsjournal.com/content/pdf/1758-5996-4-23.pdf

[18] Taubes, G, Good Calories, Bad Calories, Knopf Publishing Co NY, NY, USA2007


 [B1]This passage is irrelevant and non-scientific and must be deleted.

 [B2]This passage is irrelevant and non-scientific and must be deleted.

 [B3]Irrelevant reference and must be deleted.


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