De kallas LOBbare

De kallas för Key Opinion Leader (KOL) eller på svenska Ledande OpinionsBildare (LOB), dessa professorer som sitter på sin universitetsstol och samtidigt på flera andra stolar tillhörande myndigheter, livsmedelsföretag och läkemedelsföretag.

 

Dessa LOBbare, har en stor påverkan på hur sjukvården behandlar olika sjukdomstillstånd. De behandlingsanvisningar vid olika sjukdomar som finns är nästan alltid utgivna av läkare som är LOBbare och samtidigt använder sig av läkemedelsbolagens information. Samma information som de själva har skrivit ihop på läkemedelsföretaget inför lanseringen av läkemedlet.

 

På livsmedelssidan finns det också mycket intressanta intressekonflikter.

 

Ta exempelvis området kost vid diabetes.

 

Här har vi en professor i diabetologi som sitter som expert i Livsmedelsverkets Expertgrupp för Kost och Hälsa. Professorn har varit med om att utforma Livsmedelsverkets kostråd. Det var två stolar.

 

Samme professor satt som expert i Livsmedelsverkets Expertgrupp för Samordnad Sjukhuskost (ESS-gruppen). Det var tre stolar.

 

Professorn får ett uppdrag av Socialstyrelsen att som expert gå igenom vetenskapen i ett tillsynsärende och beslutet kommer i januari 2008. En lågkolhydratkost är i enlighet med vetenskap och beprövad erfarenhet vid behandling av diabetes och övervikt. Någon intressekonfliktdeklaration har inte presenterats vid redovisningen. Det var fyra stolar

 

Socialstyrelsen, som under 2007 fick överta Livsmedelsverkets kostråd för sjuka, finner under våren 2008 att någon bör utreda vilken vetenskaplig grund som finns för kostråden då det gäller diabetes. Socialstyrelsen kontaktade Statens beredning för medicinsk utvärdering (SBU) som har resurser att gå igenom och utvärdera vetenskapen bakom kostråden.

 

Vår professor får sedan under våren 2008 i uppdrag att för SBUs räkning utreda vilken vetenskap som finns bakom Livsmedelsverkets kostråd. Professorn låter SBU städsla ytterligare experter under sommaren och hösten 2008. I professorns intressekonflikts- eller jävsdeklaration till SBU uppges inte att professorn är en av Livsmedelsverkets experter, ej heller att han varit expertutredare åt Socialstyrelsen. Det var fem stolar.

 

Nåväl, vår professor har fått nya uppdrag. Denna gång som LOBbare, förlåt expert ska det vara, då det gäller Socialstyrelsens nya kostråd för patienter med diabetes. I professorns jävsdeklaration till Socialstyrelsen uppges inte att professorn är en av Livsmedelsverkets experter, ej heller att han varit expertutredare åt Socialstyrelsen och SBU. Han sitter nu på sex intressekonfliktstolar.

 

Professorn har sedan blivit LOBbare hos SBU vid rapporten om fetma. Han sitter nu på sju intressekonfliktstolar.

 

Detta var myndighetsstolarna vår professor sitter på. Men professorn sitter också på tio stolar från industrin enligt egen uppgift i jävsdeklarationen till SBU. Dessutom har professorn under flera år suttit på stolen från ILSI (International Life Science Institute, ett internationellt lobbyföretag vars medlemmar kommer från de största livsmedelsproducenterna).

 

Räknar man nu ihop alla stolarna blir det till minst aderton stolar. Men det är inte Svenska akademins stolar han har ockuperat, det är aderton stolar med en mjuk sits av ekonomisk kompensation.

 

Detta är bara de av mig hittills kända stolarna som en av våra LOBbare lyckas sitta på.

 

Livsmedelsverket har vid min genomgång omkring 29 experter/LOBbare av samtliga 49 personer som jag funnit associerade till Livsmedelsverkets expertgrupper enligt protokoll. Så ytterligare 28 stycken LOBbare sitter på mer än två stolar. Sedan finns det ett tjugotal personer med anknytning till Livsmedelsverket och sexton av dem är knutna till andra myndigheter eller organisationer.

 

Men vi får aldrig veta vilka konferenser som myndigheternas tjänstemän åker på. Vi får aldrig veta hur mycket som myndigheternas tjänstemän blir bjudna på av konferenser och företag.

 

Det är ett närmast incestuöst nätverk av LOBbare som verkar styra inte bara Livsmedelsverket utan andra myndigheter liksom hälso- och sjukvården.

 

Vi kan lösa problematiken med jäv.

Det är enkelt.

 

Låt en myndighet sköta samtliga jävsdeklarationer inom hälso- och sjukvården och relaterad forskning genom att alla är skyldiga att uppge samtliga jäv till myndigheten. Ett utdrag från myndighetens databas bifogas samtliga handlingar där det behövs jävsdeklarationer som (vetenskapliga) artiklar, expertuppdrag och liknande situationer där det är viktigt att jäv deklareras.

 

Den lämpligaste myndigheten torde vara Socialstyrelsen som redan har ett färdigt register över samtliga legitimerade utövare och då bara behöver lägga till fler fält i databasen och behöver bara lägga till de myndigheters  tjänstemän som har någon form av koppling till hälso- och sjukvården.

 

Sedan kan var och en gå in på Socialstyrelsens hemsida och se vilka jäv en expert eller författare har och därmed kan man själv bedöma trovärdigheten hos experten/författaren.

 

Finner något ett jäv som saknas i databasen behöver detta kontrolleras med den jävige och om det stämmer ska det tillföras en rad med 
Undanhållet jäv Expert i xxxxxxxxxxxxxxxxx

Detta torde minimera situationer som i SBUs rapport Mat vid diabetes där en expert hade "två eventuella jäv" i de första två versionerna men uppgav 24 jäv i de två följande upplagorna. Likväl uppgavs inte att vederbörande satt som expert i en av Livsmedelsverkets expertgrupper.

 

Minimera LOBbarnas i inflytande!

 

 


Begäran om mat till skolelev och patienter

Här kommer en blankett för att elever och även patienter/vårdade inom vården få en korrekt kost.


I ATL stod i början av juni 2013 en artikel om att föräldrar lyckats få riktig mat som specialkost. 

http://www.atl.nu/lantbruk/svensk-mat-som-specialkost-i-skolan

ATL fixade sedan att finna det perfekta citatet:

”Vi tröttnade på att kommunerna serverar våra barn mat som vi skulle bli polisanmälda för om det var vi som producerade den.”

Så det är bara att kopiera det jag skrivit nedan och skicka till berörd offentlig förvaltning!

 

 

Begäran om mat

 

Av etiska skäl, miljöskäl och hälsoskäl begär vi att vårt barn

 

________________________________ född ______________ och är elev vid

 

_______________________________________ skola får mat enligt skollagens, Livsmedelsverkets, Socialstyrelsens samt Jordbruksverkets bestämmelser jämte Miljöstyrningsrådets baskrav.

 

Vi begär att skolan serverar vårt barn mat som svenska bönder som producerade maten slipper bli polisanmälda för.

 

Kosten ska enligt Skollagen vara näringsriktig [1]. Den enda kost som enligt Socialstyrelsens beslut om vetenskap och beprövad erfarenhet inom kostområdet är godkänd är en lågkolhydratkost [2]. Därför måste mängden kolhydrater begränsas till maximalt 100 g per dygn i enlighet med gammal beprövad forskning från 1900-talet [3].

 

Skollunchen bör enligt Livsmedelsverket innehålla 25-35 % av dagens energi. Därför får skollunchen innehålla maximalt 25-35 g kolhydrater.

 

Vad som serveras i övrigt bör följa Nordiska Näringsrekommendationers remissvar om kött, fisk och ägg samt animaliskt fett från mejeriprodukter och djurfett. Samtliga djurprodukter ska komma från miljöer som har uppfödnings- och djurhållningsregler som är minst lika omfattande som de svenska djurhållningsreglerna.

 

Grönsaker innehåller i stort sett enbart vatten samt smärre mängder kolhydrater, protein, fett, mineraler och vitaminer jämfört med animalisk mat [4]. Så grönsaker kan serveras utan tvång, vare sig uppåt eller nedåt.

 

 

 

Ort___________________________________   Datum 201__ - ____ - ____

 

 

 

______________________________________  ___________________________

Vårdnadshavare                                                     Vårdnadshavare

 

 

 

Ytterligare informationsbakgrund

Se baksidan


Begäran om mat

 

Ytterligare informationsbakgrund med referenser

 

Animaliskt protein innehåller samtliga livsnödvändiga proteinbyggstenar, aminosyror, i hög mängd. Mängden kött bör uppgå till minst 40 g protein per dag, det motsvarar minst 60 g kött eller fisk till lunchen

 

Vegetabiliskt protein saknar oftast tillräckliga mängder av livsnödvändiga aminosyror samt har låga mängder protein jämfört med animaliska proteiner. Växtdelar innehåller många gånger gifter för att skydda växten mot att bli uppäten av alla växtätare. Soja innehåller exempelvis växtöstrogener som kan påverka könsutvecklingen hos sojakonsumenten. Spannmål innehåller fytiner som förhindrar upptag av mineraler till kroppen.

 

För att få 14 g protein från exempelvis gurka med en femfaldig säkerhetsmarginal behöver man äta 8,75 kg gurka till lunch.

 

Animaliskt fett är nyttigt och saknar sjukdomsframkallande egenskaper [5]. Vi består till mer än 10 % av kroppsvikten av samma material utan att få sjukdomssymtom.

 

Vegetabiliska fetter som kan ätas kan komma från oliv-, raps-, palm- eller kokosolja samt i små mängder från linolja. Övriga vegetabiliska oljor har enligt forskning för stor halt av inflammationsdrivande och cancerframkallande fleromättade fetter av omega-6-typ [6].

 

Kolhydrater från spannmål och socker är giftiga om man äter mer än 100 g per dag utan insulin, eget eller tillfört via spruta. Kroppen drivs av ättiksyra från i första hand fett. Om man äter kolhydrater måste kroppen ställa om sin ämnesomsättning från fettförbränning till förbränning av kolhydrater nedbrutet till ättiksyra för att undgå att man dör i sockerförgiftning. Hos en 70 kg person så innehåller den totala blodmängden om 5,6 L endast 1,5-3,0 g glukos. Äter man 5 g kolhydrater så kan blodglukosvärdet stiga till 15 mmol/L. Tillför man snabbt mer än 25 g glukos till blodet så dör man i akut glukosförgiftning.

 

Livsmedelsverkets kostråd är helt underkända av Statens beredning för medicinsk utvärdering (SBU) i dess rapport från maj 2010 [7]. SBU fann att Livsmedelsverkets kostråd helt saknade vetenskaplig grund.

 

Livsmedelsverkets kostråd är rekommendationen på populationsnivå och får ej användas på individnivå . Livsmedelsverkets kostråd är därför olagliga att använda inom sjuk- och äldrevård, offentliga institutioner och därmed även inklusive skolan.

 

Mora den 17 juni 2013

Björn Hammarskjöld

F.d. överläkare i barn- och ungdomsmedicin

Filosofie licentiat i Biokemi

Oberoende senior vetenskapsman i näringslära



[1] Skolverket och Livsmedelsverket saknar definition av näringsriktig mat. Alltså måste man gå till gamla kunskaper i fysiologi, biokemi och endokrinologi från 1900-talet.

[2] Socialstyrelsens beslut av 2008-01-16 Dnr 44-112267/2005

[3] Julius Lagerholm, Hemmets Läkarebok, Fröléen & comp, Stockholm 1921

[4] Livsmedelsverkets matdatabas.

[5] Holmberg, Thelin High dairy fat intake related to less central obesity: A male cohort study with 12 years’ follow-up Scandinavian Journal of Primary Health Care June 2013, Vol. 31, No. 2 , Pages 89-94 (doi:10.3109/02813432.2012.757070)

[6] Wirfält, Mattisson, Irene (arbetar nu på Livsmedelsverket) et al Postmenopausal breast cancer is associated with high intakes of omega-6 fatty acids (Sweden). Cancer Causes Control. 2002 Dec;13(10):883-93.


Lågkolhydratmat på flyget

Läste på nätet att man inte kan få lågkolhydratkost på flyget. Fast det är en sanning med modifikation, portionsstorleken är så liten att det blir inte många gram kolhydrater trots hög procenthalt kolhydrater. Det är samma kost som Livsmedelsverket har som svältkost

 

Om alla bara sitter och knappar på datorn händer inget. 

 

Ring flygbolaget och meddela att du av etiska skäl äter specialkost, svenskt kött och svenska mejeriprodukter och svenska grönsaker. Sedan begär man att få den mat man behöver. "Man ska väl inte behöva svälta hela långa resan."

 

Det här fungerar på kommunal skolmatsnivå.

 

http://www.atl.nu/lantbruk/svensk-mat-som-specialkost-i-skolan

 

Det är bra att Land Lantbruk lyckas finna den viktigaste meningen i reportaget.

 

”Vi tröttnade på att kommunerna serverar våra barn mat som vi bönder skulle bli polisanmälda för, om det var vi som producerade den”

 

http://www.atl.nu/ledare/dubbelmoralen-blev-solklar-i-en-mening

 

 

Tillbaka till flygbolagen och deras mat.

 

Når man inte det önskade resultatet den vanliga normala vägen nerifrån så börjar man uppifrån.

 

Ring huvudkontoret och be att få prata med verkställande direktören (VD) (generaldirektören då det gäller myndigheter).

 

Vanligtvis hamnar man hos VDs sekreterare som alltid vet allt och omedelbart kopplar dig till den lägsta beslutsmyndiga personen.

 

Problemet löst!

 

Med du måste kontakta flygbolaget själv, det är du som är kunden och kunden har alltid rätt.

 

Om alla som äter lågkolhydratkost ringer detta lilla samtal så blir det snabbt resultat. Men det hänger som alltid på mig själv om jag vill ha resultat.


NNR5 remissvar om matens sammansättning

Jag hann med att kommentera även matens sammansättning i NNR5
 
Nu väntar vi bara på att den sista remissomgången om fett och kolhydrater kommer ut under juni.
 
Men NNR5 remissen om mat här http://www.slv.se/upload/NNR5/NNR%202012%20FBDG.pdf 
 
Och här mitt svar tpå remissen. Det blev mycket struket och en del tillagt.
 

NNR 2012 –Foods, food patterns and health outcomes: Guidelines for a healthy diet

 

Public consultation answer

By

Björn Hammarskjöld

M.D., Ph.D. in Biochemistry

Independent senior scientist in nutrition

C.E.O. of Minivent AB

 

13.              Foods, food patterns and health outcomes - Guidelines for a

14.              healthy diet

15.               

16.               

17.               

18.              Introduction

19.               

Lines 37- 48 should be replaced with the following text.

 

Much new original data from both observational and experimental studies on the impact of foods, whole diets and food patterns on health have been published during the last centuries. Several reports, reviewing the scientific basis for linking food intake and food consumption patterns with chronic disease are available. This chapter mainly summarizes information from some hundred years ago.

 

The first scientific report of the food, food patterns and health outcomes from Nordic countries is from 1732 when Carl von Linné described the Sami diet and also the health outcome [1]. In his report he described vividly that the Sami had reindeer meat, reindeer milk, fish and fowl. In season the Sami had egg and berries. Linné described that the Sami in their sixties still could roam around in the mountains in contrast to the fat, breadeating farmers from Scania

 

To follow a diet is good for loosing weight and to avoid diabetes and obesity. There is no controverse which diet is the best. Already the old pig farmer knew how get a pig fat for Christmas. Just give the pig coarse milled grain, potatoes and some fat. NNR4 recommend coarse milled grain, rebranded fibre rich bread and fibre rich cereals, oil cooked potatoes, rebranded French fries/chips.  Also the Japanese Sumo wrestlers had a more than 1 400 year of experience in weight gain, eating 3.3 kg rice, 50 fat and 250 g meat per day.

 

NNR’s have more than 35 years of experience of the effect of an extreme high carbohydrate diet. The number of persons having diabetes is at least 397 548 persons on 2012-12-31 [2] That is an increase since 2006-12-31 of 79 649 cases. It’s an increase of 13 275 cases per year.

 

The obesity rate increase is similar. Just look at pony jumping shows. In 1990ies the girls were slender all of them. Nowadays, 25 % of those pony jumping show girls are, despite much harder physical training, overweight to obese.

 

So the NNRs have the perfect method, well proven during millennia, how to increase obesity and diabetes frequencies. Recommend extreme amounts of carbohydrates. 

 

The conclusion is obvious. The NNRs (a.k.a. pig fodder) generate obesity and disease including diabetes.

 

The modern pig farmer knows how to get a slender pig for Christmas. The pig has to eat protein and fat. Then the farmer adds enough carbohydrates for the pig to convert excess of carbohydrates to stored fat.

 

This is since millennia a wellknown technology and physiology.

 

 

Lines 57-162 should be replaced with the following text.

 

for which human requirements have been less well defined. The description of major food groups
and their nutrient contributions given below is largely based on information provided by the old fashioned physiology from previous centuries.

 

First of all we have to identify the essential components of the food for humans.

 

AcCoA is the central molecule in our metabolism.

We can make AcCoA from proteins via amino acid deamination.

We can make AcCoA from fats

We can make AcCoA from carbohydrates

We can use AcCoA as an energy source

We can use AcCoA to make amino acids

We can use AcCoA to make fats

We can use AcCoA to make some carbohydrates.

We can use AcCoA to make a lot of essential molecules like cholesterol

 

So AcCoA is THE kingpin molecule in our metabolism.

 

Among essential components of our food there are:

 

  1. protein or rather the amino acids, the building stones of proteins, are partly essential as humans can produce about ten of the 20 amino acids. This means that we have to eat the remaining amino acids to survive.
  2. Fats are essential as an energy source and as building material to convert different fatty acids to other fatty acids. Also, we have a very limited processing facility for the long chain polyunsaturated animal fats so they are regarded as essential. Most of the other fats we can synthesize from smaller fatty acids, mainly from AcCoA. But we have to have fat to be able to rebuild fat and for energy production.
  3. Minerals are essential as we can not produce elementary atoms.
  4. Vitamins are mostly essential. We are unable to produce most of them.
     

Carbohydrates are nonessential as humans can produce all necessary sugars in the liver in enough amounts.

 

The brain does have mitochondria in all cells and is thus using only AcCoA as fuel. But red blood cells (RBC) need 3-6 mmol/L glucose in the blood as they lack mitochondria. Then glucose is metabolized along a RBC specific pathway to degrade glucose via the Rapoport-Luebring pathway producing 2,3-diphosphoglycerate (2,3-DPG) and then to lactic acid and energy. The 2,3-DPG is required to release the oxygen from the haemoglobin molecule. So with a too low blood concentration of glucose the brain can not get enough oxygen to oxidize citric acid in the Krebs cycle. And there is a too low concentration of glucose for the brain cells to anaerobically produce energy from glucose. So the brain does die within minutes when the glucose level in the blood goes too low. 

 

Protein

Our protein sources are from animal or vegetable origin. We need at least 0,5 g animal protein per kg per day.

 

Our best sources of animal protein is from herbivores like cattle, elk, horse and other herbivores. Also, pig, fowl, fish, egg and game are animal sources of protein as well as fat.

 

Vegetable proteins are always deficient in one or more amino acids so we have to eat several times more vegetable protein to satisfy the needs of all amino acids.

 

Free ranging herbivores are excellent carbohydrate-to-fat-and-protein converters. They eat enough minerals and vitamins for their own needs. The only thing we have to do is to eat the meat and inner organs to satisfy all our needs regarding protein, fat, minerals and vitamins in perfect amounts.

 

Fat

Free ranging herbivores are excellent carbohydrate-to-fat-and-protein converters. The fat in most animal fat have the same composition, shy of 50 % saturated fat (SFA), shy of 50 % monounsaturated fat (MUFA) and about 5 % polyunsaturated fat (PUFA). So the best fat we can eat is animal fat as it is abut the same composition as our own fat stores. They all have the same melting temperature and thus we have to process the fats minimally to save energy.

 

The only fats that have been proven harmful are trans fats and PUFA of omega-6-type [3]. SAT fats and MUFA fats are harmless and essential.

 

Sources of food

The best sources of food are of animal origin like egg, meat, fish and milk. Then we get all we need of protein, fat, minerals and vitamins. And our liver can make all necessary carbohydrates.

 

Milk from ruminants is both a food in itself and raw material for different dairy products (like cheese, butter, fermented milk, yoghurt or cream). Milk and milk products are important sources of animal fat, protein, vitamin A, riboflavin, vitamin B12, calcium, and iodine. Fat soluble vitamins are often added to skim and low fat milk as the cows are not receiving enough sunshine to produce enough vitamin D3. Two thirds of the fat in whole milk is SFA but there are shorter SFAs to keep the melting temperature constant. The major unsaturated  fatty acid is oleic acid (C18:1). Milk also contains short chain fatty acids and the odd-chain fatty acids C 15:0 and C17:0. Fat content varies from 0.1 to around 4 g/100g, protein about 3.0-3.5 gram per 100 gram; and an animal carbohydrate (lactose) about 4-5 gram per 100 gram. Whole milk and low fat milk contain about the same amounts of calcium. Cheese has a high calcium content. It is shown several times that a high intake of dairy fat (butter as spread and high fat milk and whipping cream) was associated with a lower risk of central obesity (OR 0.52, 95% CI 0.33–0.83) and those children having full fat milk are not as obese as the children having low fat milk [4], [5].

 

So the drinkers and eaters of dairy products should have high fat milk and full fat butter to stay slim.

Egg is relative to its energy content high in protein, riboflavin, vitamin A and D. Egg is low in fat, and the egg yolk contributes together with dairy products, meat and fish to the dietary intake of cholesterol. One normal egg contains about 0,2 g cholesterol. An adult of 70 kg has about 200-400 g of cholesterol in the body. So the cholesterol amount of an egg may increase the total cholesterol by less than one tenth of a percent. The cholesterol in food is totally neglible, cholesterol in food can never alter the total amount of cholesterol, the amount is too tiny.

 

Meat from beef, pork, mutton and game (e.g. reindeer and moose) is generally defined as “red” meat, while meat from chicken and turkey are defined as “white”. Processed meat has undergone some preservation process like smoking; salting or use of other chemicals for preservation (likes nitrites). Examples of such processed meats are ham, bacon, salami, different kinds of sausages, and smoked meat. Meat that is boiled, fried, dried, fermented or frozen is usually not categorized as processed.

 

Meat and meat products contain 20-35 % protein, and are usually good sources of vitamin B6, vitamin B12, iron, zinc and selenium. The content of energy, fat, fatty acids and salt may vary  considerably between types. Fat content may vary from less than one per cent to more than 40%. Also, types of fatty acids vary between different animals; typical proportion of SFA is 30% in chicken, 35-40% in pork, and 40-55% in beef and mutton. The level of conjugated linoleic acid (CLA) is less than 1 % in chicken and pork, but 3-5% in ruminants (like beef and mutton). The salt content is low in raw, unprocessed meat but much higher in processed meat. Game meat usually has lower fat content.

 

Pure meat, fresh or preserved the way our ancestors did, has never been shown to harm. On the contrary, pure carnivorous people like Sami, Eskimoos, American Indians like the Pima Indians were totally healthy as long as they stuck to their traditional diet.

 

 

Fish and seafood contain 20-35 % protein. Lean fish like cod and plaice contain less than 2 grams of fat per 100 gram, medium fat fish like winter-mackerel and tuna contain 2-8 grams of fat per 100 gram, and fatty fish like herring, summer-mackerel, trout, salmon and eel contain more than 8 grams of fat per 100 gram. Medium fat and fatty fish are the major dietary sources of marine omega-3-fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Fatty fish is also a major source of dietary vitamin D, but some lean fresh-water fish (e.g. pike-perch) also contain high amounts. Fatty fish and especially cod liver contain high amounts of vitamin A (retinol). Fish and seafood are also good sources of vitamin B12, iodine and selenium. However, the nutrient content may vary between wild fish and farmed fish depending of the feed.

 

Fish and seafood may contain different environmental toxins. In general fish captured in the open sea has lower concentrations of pollutants than fish from the Baltic Sea or Norwegian fjords. Some marine fish, e.g. large tuna and halibut, and freshwater fish from certain areas may contain elevated levels of methyl mercury. Lean fish generally contain low levels of persistent organic pollutants (POPs). Finnish studies indicate that fish consumption is related to higher blood concentration of dioxins, polychlorinated biphenyls and methyl mercury, as well as of omega-3-fatty acids (Turunen AW, Männistö S et al. 2010). However, the lower mortality of cardiovascular diseases and type 2 diabetes among fishermen indicates that the benefits of fish consumption seem to overcome the potential hazards (Turunen, Verkasalo et al. 2008).

 

Pork fat in bacon has about the same amount of animal omega-3 fatty acids as fat fish like salmon when you compare the absolute amount, not percent. So we don’t have to empty the seas from fish to get enough animal omega-3 fats. There is another way to normalize the ratio of omega-6 PUFA to omea-3 PUFA. Decrease the intake of omega-6 to below cancer causing levels and intakes. 

 

 

Vegetables, fruits and berries usually contain low amounts of food energy, plenty of water and dietary fibre, small amounts of vitamins like ascorbic acid (vitamin C), carotenoids (pre vitamin A), folate, vitamin E (tocopherol) and vitamin K, and minerals like potassium and magnesium.

 

But fibres are irritating the intestines [6] and are cancer causing [7]. Fibres contain phytates that minimise mineral uptake [8]. Carotenoids are not degradable by humans to vitamin A.

 

Beans and peas are not very good sources of protein, minerals (iron, zinc, magnesium and potassium), B-vitamins (except B12). But beans and peas contain large amounts of fibre and starch, a.k.a. sugar, carbohydrates. So they may be eaten in small amounts.

 

Nuts and seeds contain plenty of monounsaturated (MUFA) and polyunsaturated fatty acids (PUFA) (as well as some vegetable protein, magnesium, zinc, copper, potassium, vitamin E, B6, niacin and several antioxidants). Nuts and seeds also contain large amounts of carbohydrates and intake should be minimized

 

Potatoes are comparatively rich in carbohydrates (starch), but is lower than meat in several minerals (like potassium and magnesium) and vitamins. Traditionally, potatoes were sources of vitamin C and protein among high consumers.

 

We need at least 0,5 g animal protein per kg per day. Vegetable proteins are always deficient in one or more amino acids so we have to eat several times more vegetable protein to satisfy the needs of all amino acids.

 

Carbohydrate intake in physiological amounts (less than 1 hg) are very low in vitamin C.

 

Wholegrain is defined as intact and processed grain or cereal where the fractions endosperm, bran and germ are present in the same proportion as in the intact grain. Cereals are to be eaten in low amounts as they contain very large amounts of carbohydrates in the form of polymerized glucose easily digested to glucose and thus increases the glucose level very fast in the blood. Grain, a.k.a. cereals, flour, especially wheat, contain large amounts of gluten.

 

The large increase of grain consumption during the last three decades may be the cause of IBS, gluten entropathy, morbus crohn, cholitis ulcerosa and “wheat belly”. All these diseases improve on a grain free diet and may even be states free from symptoms as long as the patient totally refrain from eating grain.

 

Whole grain products do provide fibers and contain phytates that minimise mineral uptake [9]. Resistant starch is a minor part of (less than 10 % of total starch) in cooked and hydrogenated starches and the amount is usually too low to make any difference at the blood glucose level.

 

Cereals, especially those that are processed into a variety of products, should be avoided as much as possible. Because micro-nutrients and other bioactive compounds mostly are very scarcely found only in the germ and bran fractions, refined cereal products generally have very low nutrient content, and often high amounts of added sugar (see below). They are often correctly called empty calories and should be avoided.

 

All plant foods (like vegetables, root vegetables, fruits, berries and nut and seeds, and whole-grains) naturally contain a wide variety of phyto-chemicals like polyphenols, salicylates, phytosterols, saponines, glucosinolates, monoterpenes, phytoeostrogenes, sulphides, terpenes and lectins. Most of these have important functions in the plant cells and may also negatively influence biological functions in the human body via a large number of defence mechanisms. Many are antioxidants with the potential to reduce the production of our own more efficient antioxidants, others may influence our signal systems, cell cycles, repair systems and inflammation reactions. The number of bioactive phyto-chemicals has been estimated to around 100,000. A single plant based meal may provide around 25,000 different phyto-chemicals, but luckily comparatively small amounts of each. The observed ill health effects associated with vegetable, fruit, berry and whole grain consumption may likely be explained by the combined action of many phyto-chemicals and other nutrients. All plants try to defend themselves from being eaten as they can not run away from a plant eater. That is why plants always have toxins.

 

So there are more than 100 000 reasons to minimize the food from the plant kingdom.

 

Butter and some vegetable oils are used in cooking and with small amounts of bread. Margarine, spreads and vegetable oils are used by the food industry to produce foods like mayonnaise, dressings, baked goods and soups. Vegetable oils are manufactured by pressing oil from seeds or plants like rapeseeds, olives, palm fruit and coconuts. But there is also oil manufactured by omega-6 rich soya beans, maize kernels, sunflower and safflower seeds.

 

Butter is made from the fat of cow’s milk. Margarine and spreads are mixtures of different fats. Milk fats and vegetable oils, margarine and spreads contribute dietary energy, fat (essential and non-essential fatty acids) and fat soluble vitamins (i.e., A, D, E and K). Vitamins A and D are usually added to margarines and spreads. Vegetable oils contain fat (100%), while margarines and spreads contain varying amounts of fat due to dilution of fat with water and chemicals. The fatty acids composition may vary considerably depending on the fat source used in manufacturing. Soy bean, maize and sunflower seed oil are rich in omega-6 PUFA, while rapeseed oil and especially olive oil is rich in MUFA. Rapeseed and soybean oils have comparatively high content of omega-3 fatty acids but soybean oil has too much omega-6 to be classified as human food. Vegetable oils and fat from marine sources, e.g. fish oils, contain a lot more unsaturated fatty acids than fat from land living animals, e.g. lard and tallow. However, palm and coconut oils have high content of SFA. Fish oils as well as lard are generally rich in very long animal omega-3 PUFA. Fat from ruminants, e.g. tallow, have the same content of SFA, and animal fats contain tiny amounts of cholesterol. Butter and ruminant fat contain 3-5% CLA. Processed fats like margarines and spreads were previously sources of TFA, depending on the raw material used in manufacturing. However, the TFA content has during the last decade decreased considerably in the Nordic countries due to changes in raw material and processing. But still most of the vegetable oils are cheap but unhealthy. Then choose palm, coconut, canola (rapeseed) or olive oils when you choose an oil. All other oils contain much too high amounts of inflammatory and cancer causing omega-6.

 

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Energy dense and ultra-processed food products

 

Many food products in Westernized societies are manufactured from refined cereals/white bread and with additional sugar. Biomarker studies have demonstrated that Westernized dietary patterns are associated with extremely high carbohydrate concentration and low concentrations of micro-nutrients (Kant 2010) (Román-Viñas, Ribas Barba et al. 2009), and will likely provide less of other health enhancing substances found in plant-foods. The energy content is increased mainly as carbohydrates and disproportionate to the content of natural and essential animal protein, animal fat, vitamins and minerals and to other bio-active substances of health importance in ultra-processed food products (e.g. soft drinks, confectionary, candy bars, desserts, bakery goods, sugared cereals, sugared milk-products, powdered sauces and soups, snacks, deep-fried potatoes et cetera). Many refined and processed foods may also contribute components with potential adverse health effects, added during the manufacturing process (e.g. carbohydrates), or formed during prolonged heat treatment (like heterocyclic amines or so called advanced glycation/lipidoxidation end-products, AGE/ALE). Studies within EPIC (European Prospective Investigation into Cancer and Nutrition) indicate that the use of manufactured food products currently (i.e., data collected in the 1990s) is higher in northern and central European countries than in Mediterranean countries (Slimani, Deharveng et al. 2009) (Chajès, Biessy et al. 2011).

 

 

The health impact of specific foods

 

Observed associations between single nutrients and health outcomes may be difficult to interpret, because of the complexity of diet. Also, diet-related chronic diseases are caused by carbohydrates, especially fructose [10], and also excess of omega-6 rich oils [11]. Therefore a search for the health effect of single nutrients may be misleading (Slattery 2010) (Jacobs Jr and Tapsell 2007) (Appel 2008). In recognition of these complexities we have to revert to old fashioned physiology, biochemistry and endocrinology instead of reading biased research from the last decades.

 

As stated above, animal protein, animal and a few vegetable fats are essential. Carbohydrates, especially glucose, very quickly increases the blood glucose level which triggers a fast insulin response for the person to survive the massive glucose challenge. The old fashioned physiology tells us that a 70 kg person has 3-6 mmol/L or 1,5 to 3,0 grams of glucose in the whole blood volume. Having just 5 g glucose will rise the blood glucose level from 5 mmol/L to 15 mmol/L. If that person has more than 30 mmol/L - 50 mmol/L or 15-25 g glucose in the blood, that amount of glucose is lethal.

 

Then NNR4 recommends that male person to eat 480 g of carbohydrates per day, a more than 20-fold lethal dose of carbohydrates per day.

 

Fructose is 5-10 times more efficient to nonenzymatically glycate proteins than glucose. The most well known Advanced Glycated Endproduct (AGE) is HbA1c where glucose or fructose attaches to the lysine residue of haemoglobin. This sugar molecule sterically blocks the oxygen to attach to the haemoglobin molecule. Thus a high blood glucose level increases the HbA1c. Fructose is much more efficient in blocking oxygen transport. But we never measure the fructose level in blood so usually we have not a clue how much fructose there is in the blood.

 

Another problem is that fructose normally is metabolized in the liver to saturated fatty acids and increases the rate of non alcohol fatty liver disease (NAFLD) and even non alcohol fatty liver cirrhoses (NAFLC).

 

Excess carbohydrates are converted to SFA and stored in the fat depots and locked up by the high insulin levels.

 

Several studies have shown a long time weight reduction by limiting only the carbohydrates [12], [13].

 

There is no convincing evidence that consumption of milk or dairy products is related to increased risk of cardiovascular disease (Beck, Hoppe et al. 2010; Nasjonalt råd for ernaering 2011). However, studies have shown that high animal fat intake decreases the obesity rate of children [14], [15].

 

Some reports indicate that milk consumption is related to a reduced risk of metabolic syndrome, type-2 diabetes, hypertension and stroke (Beck, Hoppe et al. 2010; Nasjonalt råd for ernaering 2011). The WCRF/AICR (2007) concludes that milk consumption probably reduce the risk of colorectal cancer. No conclusion can be made on the link between milk and breast cancer.

 

 

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Macronutrients, foods and weight maintenance

 

The old fashioned physiology, biochemistry and endocrinology implies that carbohydrates are toxic to us in larger amounts than 100 g per day in metabolically healthy individuals and may reduce the symptoms in metabolically deranged persons like metabolic syndrome, diabetes and overweight/obesity.

 

Still, carbohydrates increase the blood glucose level that increases the insulin response that increases the fat deposition in fat tissue. Increased level of insulin also halts fat metabolism.

 

Animal protein is not giving a weight gain according to all old studies from previous centuries.

 

Animal fat and selected vegetable fats do not increase the blood glucose level and insulin which means fat are not making us fat, fat is making us satisfied for long.

 

Just reread the old books in physiology, biochemistry and endocrinology. Those old books reveal the truth about metabolism.

 

 

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Conclusion

 

The overall scientific evidence show that the old fashioned physiology, biochemistry and endocrinology still rules.

 

As long as humans eat their species specific food as carnivores with normal amounts of animal protein, an enough amount of animal fat and a very limited ability to eat carbohydrates, the individuals as well as the populations will keep healthy.

 

Just look at a newborn human baby. Human breast milk has evolved for millennia to be

the ultimate food for babies. The milk is diluted to ensure that all children, regardless of living in arctic region or tropical region, will have enough water. The amount of animal protein, 8 percent of total energy (E%), is enough for a newborn child to increase 50 % in length during the first year. The amount of carbohydrates, 36 E% of animal carbohydrates a.k.a. lactose, is enough for a newborn child to increase 300 % in weight during the first year. The amount of animal fat, 56 E% of animal fats, is enough for a newborn child’s brain to develop normally during the first year.

 

The same conditions apply for adults. So just decrease the amount of carbohydrates to a level that does give the endocrinological condition of normal low insulin response to stay healthy and keep the normal body weight.

 

 

 



[1] C. v. Linne, Linnés lappländska resa, 1732

[2] Socialstyrelsen’s statistical database downloaded 2013-06-02

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

[4] Holmberg, Thelin High dairy fat intake related to less central obesity: A male cohort study with 12 years’ follow-up Scandinavian Journal of Primary Health Care June 2013, Vol. 31, No. 2 , Pages 89-94 (doi:10.3109/02813432.2012.757070)

[5] S. Eriksson a,*, B. Strandvik Food choice is reflected in serum markers and anthropometric measures in healthy 8-yr-olds e-SPEN, the European e-Journal of Clinical Nutrition and Metabolism 5 (2010) e117ee124

[6] Miake K, et al. Disruption-induced mucus secretion: repair and protection. PLoS Biol 2006; 4: e276

[7] Wasan HS, Goodland RA. Fibre-supplemented foods may damage your health. Lancet 1996;348:319-20

[8] Sandstead HH Fiber, phytates and mineral nutrition. Nutr Rev 1992; 50: 30-31

[9] Sandstead HH Fiber, phytates and mineral nutrition. Nutr Rev 1992; 50: 30-31

[10] Robert H. Lustig, Laura A. Schmidt, Claire D. Brindis,Public health: The toxic truth about sugar. Nature 2012; 482: 27–29 doi:10.1038/482027a

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

[12] W Banting, A letter on corpulence, 1865, London

[13] J Vesti Nielsen, A Jönsson, Low-carbohydrate diet in type 2 diabetes: stable improvement of bodyweight and glycemic control during 44 months follow-up. Nutrition & Metabolism 2008, 5:14 doi:10.1186/1743-7075-5-14

[14] Holmberg, Thelin High dairy fat intake related to less central obesity: A male cohort study with 12 years’ follow-up Scandinavian Journal of Primary Health Care June 2013, Vol. 31, No. 2 , Pages 89-94 (doi:10.3109/02813432.2012.757070)

[15] S. Eriksson a,*, B. Strandvik Food choice is reflected in serum markers and anthropometric measures in healthy 8-yr-olds e-SPEN, the European e-Journal of Clinical Nutrition and Metabolism 5 (2010) e117ee124


NNR5 och kalcium, remissvar

Här är NNR5 kalcium remissvar.
 
Remissen finns här http://www.slv.se/upload/NNR5/Calcium%20NNR%202012.pdf 
 
Mitt svar 

NNR 2012 –Calcium

 

Public consultation answer

By

Björn Hammarskjöld

M.D., Ph.D. in Biochemistry

Independent senior scientist in nutrition

C.E.O. of Minivent AB

 

 

Introduction 42

 

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half is bound to albumin. Parathyroid hormone and 1,25(OH)2D are the most important hormones in the regulation of calcium homeostasis. They contribute to maintenance of constant calcium concentration in plasma by regulating the influx and efflux of calcium in intestine, bone and kidney. Maintenance of a constant concentration of ionised calcium is of vital importance and calcium homeostasis is probably the most tightly regulated homeostatic mechanism in the body

 

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or by an active energy requiring process. The latter is dependent on the action of 1,25-dihydroxyvitamin D3 (1,25(OH)2D), the hormonal form of vitamin D. Calcium absorption

is thus decreased in vitamin D deficiency. This means that we can not increase the uptake of calcium unless we have at least the physiological level of at least 125 nmol/L. See the Public consultation answer on Vitamin D3. The difference between dietary calcium and that

 

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(Guéguen et al. 2000). The net calcium absorption in infants is reported to range from about 30 % to 60 %, and between 25-40 % in older children, depending on absolute intake (Abrams 2010). The net absorption is relatively high during puberty (found to be about 34 % on an intake of 925 mg/d (5)) and then declines to 25-20 % in adulthood and even lower at advanced age (Guéguen et al. 2000; Schaafsma 1997). This indicates that the amount of net absorption is about 300 mg per day independent of the oral intake.

 

Calcium is lost from the body via faeces, urine and skin. Non-absorbed calcium is lost with faeces. In adults on intakes of about 1000 mg the loss amounts to about 70 to 80 % of the intake. This indicates that the amount of net absorption is about 300 mg per day independent of the oral intake. An appreciable amount is excretes via faeces as calcium soaps. Loss via skin and sweat is generally small, about 20-50 mg/d (6,7). Under warm conditions or high physical activity the loss may be appreciably greater.

 

Loss via urine may vary appreciably from person to person, generally between 100 and 400 mg/d in adults, but is relatively constant within individuals even if the intake varies. In the balance study by Malm (1) the urinary loss decreased from 231 to 201 mg/d (not significant) upon reduction of the intake from 940 mg/d to 450 mg/d. This experiment shows that a decrease of calcium intake is independent of the intake as long as the intake is higher than the uptake/urinary excretion and that the level of vitamin D3 is above 125 nmol/L. The calcium balance is very tightly regulated as long as the intake exceeds urinary excretion. The intestinal uptake is limited to 100-400 mg per day and the blood level of calcium is very tightly regulated by a free urinary excretion and a regulated uptake from the primary urine, again with a little help from my friends vitamin D3 derivates [1] So the intestines regulate the uptake of calcium and serum level is very tightly regulated by the kidneys as any excess is excreted.

 

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Requirement and recommended intake

 

The old fashioned physiological, biochemical and endocrinological knowledge shows us that the calcium intake, uptake and excretion is strictly regulated in the body.

 

By eating more calcium than excreted in the urine and that the level of vitamin D3 is above the physiological level of 125 nmol/L the body will maintain calcium homeostasis.

 

The minimum intake of 500 mg calcium applies to all ages and sexes and is then ample for most individuals as long as the level of vitamin D3 is above the physiological level of 125 nmol/L.

 

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Reasoning behind the recommendation  

The recommendations for calcium are maintained and can be decreased in NNR 2012 since no strong scientific evidence to change has emerged. This is under the condition that the level of vitamin D3 is above the physiological level of 125 nmol/L.

 



[1] Johnson JAKumar R. Vitamin D and renal calcium transport. Curr Opin Nephrol Hypertens. 1994 Jul;3(4):424-9.


Vitamin D3 till NNR5

Här kommer mitt remissvar till NNR5 rörande vitamin D3.
 
Det blev en hel del ändringar.
 
Läs remissen här http://www.slv.se/upload/NNR5/Vitamin%20D%20NNR%202012.pdf 
 
Mitt remissvar 
 

 Vitamin D – NNR 2012 Public consultation

By

Björn Hammarskjöld

2013-06-02

 

Vitamin D

50

 

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Recommendation table

Vitamin D3                                                                                  

Age group                            Minimum µg/d        Maximum µg/d

Recommended intake               RI

Children below age 10                    75 µg                       250 µg

Children above age 10                  125 µg                       500 µg

Adults                                           125 µg                       500 µg

Pregnancy and lactation                 250 µg                       500 µg

Elderly                                          125 µg                       500 µg

Average requirements             AR        125 µg                       500 µg

Lower intake level adult            LI        125 µg

Upper intake level                                                                500 µg

 

 

 

 

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Introduction

 

Vitamin D3, a seco-steroid hormone, is a prehormone essential to animals including man. The existence of a substance now named vitamin D is reported to have been known since early antiquity. The first scientific description of rickets as a deficiency was reported in the 17th century by Dr. Daniel Whistler (1645) and Professor Francis Glisson (1650).

 

Nutrition was acknowledged as an experimental science in the period 1910th – 1930th and one of the major breakthroughs in the science of nutrition was the understanding of the causative factors of rickets and the development and the appreciation of the existence of vitamins [1].

 

Traditionally, vitamin D3 is regarded as an anti rickets vitamin that is used exclusively to prevent rickets and osteoporosis. Recent research has shown that most cells in the body has Vitamin D Receptors (VDR) in the plasma membrane as well as in the cellular nuclei and that there are several hundreds of cellular reactions that are vitamin D3 dependent [2]. Also, vitamin D3 has a profound involvment in the immune systems, the endocrinological systems and a lot of other vital systems in the body [3]. Vitamin D deficiency has been linked to inflammatory and long latency diseases, such as multiple sclerosis, rheumatoid arthritis, lupus, tuberculosis, diabetes, cardiovascular disease, and various cancers, to name just a few.

 

The view of regarding vitamin D3 as a calcium regulator and rickets preventer only is an oversimplification and disregarding of true and modern science. The authorities have to have a better knowledge basis otherwise we are unable to make any decisions.

 

 

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Normal levels of vitamin D3 in the blood.

 

There has been much debate about the normal level of the vitamin D3. Clinical chemical laboratories in Sweden usually defines less than 25 nmol/L as vitamin D3 deficiency, 25-75 nmol/L as vitamin D3 insufficiency, 75-250 nmol/L as optimal level of vitamn D3 and more than 250 nmol/L as potentially toxic level of vitamin D3 [4].

 

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Physiological level of vitamin D3

There has been large debates over the physiological level of vitamin D3.

 

It is quite simple in reality.

 

There are several reports supporting that there is a linear relationship between intake of vitamin D3 and level of vitamin D3 in the blood.

 

When you increase the intake by 10 µg then the level of vitamin D3 will increase by 10 nmol/L, there is a linear relationship [5]. Also, lactating women need to have 125 nmol/L to give enough vitamin D3 in the breast milk to her baby. Parathyroid hormones are elevated when the vitamin D3 level is below 125 nmol/L. Darked skinned people living in the sun of Africa usually have a vitamin D3 level of 125-250 nmol/L

 

This shows that the physiological level of vitamin D3 is more than 125 nmol/L and that levels below 125 nmol/L must be considered as deficiency.

 

This means that the clinical chemical laboratories have to change their normal values as well.

 

Toxicity

Brohult and Jonsson showed in the beginning of 1970th that 2 500 µg vitamin D2/day for one year was without any toxic symptoms [6].

 

All toxic incidents but one is showing very large doses of vitamin D2, not vitamin D3

 

1 000 µg daily to infants gave toxicity in one to four months [7]. That is equal to 25 000 µg/day (1 000 000 IU) to an adult.

 

In Finland in 1950th up to 1964 they recommended giving 125 µg to newborns without any symptoms of toxicity [8]. 125 µg to a newborn of 2,8 kg is equivalent to 3 125 µg to a 70 kg adult per day.

 

In USA there was an accidental oversupplementation of Vitamin D in milk in the middle of 1990. The dose was up to 6 000 µg/day for half a year. The researcher found no signs of toxicity [9]

 

There are differences between vitamin D3 (animal vitamin D3 or cholecalciferol) and vitamin D2 (vegetable vitamin D2 or ergocalciferol) [10]

 

In 2008 G Jones [11] showed that an upper level of 750 nmol/L is safe.

 

In Poland the recommendation is vitamin D3 at 2,5 µgkg bodyweight, equals an adult dose of 175 µg to an adult [12].

 

In Sweden NNR4 recommends infants to have 10µg/day which equals an adult dose of 250 µg/day.

 

There is scientific information by R Vieth [13] from 1999 where the recommendation is t least 125 µg per day and a toxic dose is estimated to more than 1250 µg per day.

 

 

This means that the tolerable upper level of vitamin D3 intake is safe by a factor of at least 2, maybe a safety factor of 8, when the daily intake is below 3 500 µg/day or 50 µg*kg-1*day-1 (or 140 000 IU per day or 2 000 IU per kg and day).

 

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Vitamin D3 status in Nordic populations

According to various reports the majority of the populations in many countries have levels of vitamin D3 below the “optimal” level of minimum 75 nmol/L [14], also found in Norway by NNR5 and in Sweden [15]. But there are no reports of vitamin D3 levels below the higher physiological level of 125 nmol/L. This is embarrassing as there must be an even larger proportion of the populations that are deficient I vitamin D3. Also, the levels of vitamin D in Norway is shown to be too low, just 40 nmol/L [16]

 

 

A Finnish study giving 50 µg to newborns in 1966 reduced the incidence of diabetes type 1 by 78 % up to 30 years after birth [17]. 50 µg to a newborn of 2,8 kg is equivalent to 1 250 µg (or 50 000 IU) vitamin D3 per day to a 70 kg adult.

 

It should be remembered that the Finnish authorities in 1964 had changed the previous recommendations of 125 µg vitamin D3 from 1950th down to 50 µg per day. The recommendations previous to 1964 is equivalent to 3 125 µg (or 125 000 IU) vitamin D3 per day to an adult.

 

Now, since the Finnish recommendation was reduced to 10 µg in 1996, the number of patients with diabetes type 1 has soared in Finland.

 

 

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Summary

In most of the recent studies the results are indicating that the majority of the Nordic populations are severely deficient in vitamin 3.

 

The results of the present deficiency we are starting to see in increasing rates of diabetes type 1, multiple sclerosis, rheumatoid arthritis, lupus, tuberculosis, diabetes type 2, cardiovascular disease, and various cancers, to name just a few.

 

 

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factors such as skin surface exposed, season, latitude. Dermal
production of vitamin D3 is not affected by pigmentation. [18].

 

But the production of vitamin D3 is negatively correlated to the baseline vitamin D3 level so those with a low vitamin D3 level synthesises more vitamin D3 than those with a higher vitamin D3 level. Those with a higher S-cholesterol had a higher synthesis rate than those with a lower S-cholesterol level.

 

24 % body surface irradiated with 1.1 J/m2 10 minutes every two to three days with a total irradiation time of 40 minutes gave a mean increase of 25 nmol/L.

 

Taking in account that the half life of vitamin D3 is one to two months then the level of vitamin D3 should be well above the physiological 125 nmol/L at the beginning of autumn/fall. Otherwise the supplies formed during summer sun exposure will be insufficient during winter and spring until the summer sun can replenish the supplies.

 

 

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Supplements

 

The recommended level of vitamin D3 as more than 125 nmol/L is difficult to reach on food alone. The best source of vitamin D3 is the UVB-rays of the sun. The problem with the sun’s UVB-rays is that the sun has to be at least 35º above the horizon for the UVB to penetrate the dense atmosphere at sea level to reach the skin. At a lower inclination angle the UVB-rays are absorbed by the atmosphere and can not induce the synthesis of vitamin D3 from cholesterol. So the UVB is producing vitamin D3 only about 2-3 months before and after the summer solstice here in the Northern latitudes. The rest of the year the population has to rely on enough vitamin D3 acquired during the summer or on enough vitamin D3 in food and vitamin D3 supplementation.

 

The amount of vitamin D3 in fortified milk is 0.45 µg/dL. This means that you have to drink 277 dL milk per day. This will mean 12 500 kcal per day to obtain 125 µg vitamin D3 per day.

 

Also eating fish, salmon, then it’s necessary to eat 10 hg salmon per day to reach 125 µg

 

This means that you have to be out in the sun at least 1 h every day during summer without sunscreen or covering clothes or have a vitamin D3 supplement with at least 125 µg vitamin D3 per day year around.

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with 50 µ/d. This indicates that also children of any age must have supplement of at least 125 µg of vitamin D3 to reach the physiological level of at least 125 nmol/L.

 

 

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There seem to be a nice linear relationship between supplements of the number of µg giving about the same number of nmol/L in serum/plasma.

It should be remembered that the level of vitamin D3 on serum/plasma does not mirror the total amount of vitamin D3 in the storage volume of fat as we do not measure the concentration of vitamin D3 in fat or other tissues. This implies that obese persons will need a higher intake than lean persons until the fat tissue is saturated with vitamin D3. Then the obese person can revert to normal amounts of supplements or sunshine. We should always remember that the homeostasis in the body always will keep the body within normal limits unless we disturb the homeostasis due to sheer ignorance and maltreatment.

 

 

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osteomalacia in adults.

 

By solely focussing on vitamin D3 and bone health is a way to simplify and disregard the last decades of scientific research. We now know that vitamin D3 is indeed vital to maintain general health and that a physiological level of at least 125 nmol/L is important to breast feeding and to prevent and even treat diseases like diabetes type 1, multiple sclerosis, rheumatoid arthritis, lupus, tuberculosis, diabetes type 2, cardiovascular disease, muscle strength and various cancers, to name just a few.

 

We now know that most cells are having VDRs both at membrane levels as well as nuclear levels. This means that we do need vitamin D3 in much higher concentrations and doses than previously assumed.

 

 

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Most studies regarding vitamin D3 and mortality compares placebo (no vitamin D3 supplement) with a tiny supplement (5-40 µg) of vitamin D3 and extra calcium. You can not see any differences when you compare almost nothing with almost nothing. Previously it is shown that the physiological level of vitamin D3 is at least 125 nmol/L which means that the minimal supplement amount should be at least 125 µg of vitamin D3.

 

Most studies regarding vitamin D are using vitamin D2 (ergocalciferol). Erocalciferol is a vegetable vitamin D analogue that is not working in animals except competitively blocking the VDR thus preventing vitaminD3 (cholcecalcferol) reacting with the VDR. Also, vitamin D3 can react with sulphate thus improving the transport of vitamin D3-sulfate through cellular membranes by a factor of about 300 times [19]. Ergocalciferol can (luckily) not react with sulfate. The effect of ergocalciferol on bone health is described a hundred years ago when the knowledge was less than now. But ergocalciferol is toxic at lower levels than vitamin D3 [20].

 

What is shown is that low levels of vitamin D3 increases the mortality rate.

 

 

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A too low serum 25(OH)D3 concentration increase the risk of rickets and increase the level of parathyroid hormone. As long as the level of parathyroid hormone is above normal range is just one of several indicators of vitamin D3 deficiency. This is just one more indicator of the physiological level of 125 nmol/L o vitamin D3.

 

To try to establish a specific “fracture prone level” is just another attempt to disregard the power of homeostasis. Just follow the physiological level of vitamin D3 and there are no worries. Falls are decreased and muscle strength is improved when the level of vitamin D3 is above the physiological level of 125 nmol/L.

 

 

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In Finland it is shown that an intake of 125-50 µg per day to infants was giving a very low incidence of diabetes type 1 [21]. When the vitamin D3-supplementation decreased in 1975 to 25 µg and in 1992 to a meagre 10 µg then diabetes type 1 has soared

 

 

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Vitamin D deficiency impairs insulin secretion and induces glucose intolerance. Several vitamin D related genes are associated with different pathogenetic traits of the disease [22].

 

 

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A previously known already known in 1947 Obermer recommended: “Until further experimental evidence, adequate and incontrovertible, is made available, I submit that we should play for safety. In a climate like that of England every pregnant woman should be given a supplement of vitamin D in doses of not less than 10,000 IU per day in the first 7 months, and 20,000 IU (per day) during the 8th and 9th months.” [23]

 

Hiherto, there are no experimental evidence, adequate and incontrovertible, is published.

 

The conclusion is that pregnant women should have 250-500 µg per day to have the physiological level of at least 125 nmol/L. This secures that the child will have enough vitamin D3 via the mother’s breast milk.

 

 

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The NNR5 finds it easy to establish a physiological level of at least 125 nmol/L of vitamin D3 as shown above.

Pregnancy and lactation

E. Obermere, a British gynaecologist, issued in 1947 the following statement [24]: “Until further experimental evidence, adequate and incontrovertible, is made available, I submit that we should play for safety. In a climate like that of England every pregnant woman should be given a supplement of vitamin D in doses of not less than 10,000 IU per day in the first 7 months, and 20,000 IU (per day) during the 8th and 9th months.”

 

This is equal to 250 µg per day during the first 7 months of pregnancy and 500 µg per day the last two months of pregnancy. No experimental evidence, adequate and incontrovertible, is made available hitherto to change the recommendations from 1947. Rather, the Finnish experiences from 1950th to 1975 had shown that children should have between 125 and 50 µg vitamin D3 is not only safe but helps preventing diabetes type 1 [25]. This is approximately 4 to 8 µg vitamin D3 per day and kg bodyweight.

 

During lactation the mother’s viamin D3 level should be maintained at or more than 125 nmol/L during lactation to ensure the vitamin D3 transfer via breast milk to he child.

 

Children

The information above shows incontrovertible that children of age less than 10 years of age are recommended to have at least 125 µg Vitamin D3 as a supplement to maintain an adequate level of at least 125 nmol/L.

 

Adults

Children above 10 years age can use the same recommendations as the adults or at least 125 µg vitamin D3 per day. The safe upper limit is at least 3 500 µg per day.

 

Elderly

Elderly above 65 years of age can use the same recommendations as the adults or at least 125 µg vitamin D3 per day. The safe upper limit is at least 3 500 µg per day. This will prevent a majority of falls and bone fractures as the physiological level of vitamin D3 is maintained throughout the whole life.

 

 

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and falls and CVD outcomes. The level of vitamin D3 in NNR2004 of more than 50 nmol/L is inadequate according to both old and especially new knowledge. Many studies have shown that the physiological level of vitamin D3 is above 125 nmol/L. Also, many studies have shown that vitamin D3 levels below the physiological level of 125 nmol/L increases the risk of disease.

 

The sun induced production of vitamin D3 is limited by physical laws to about four months during summer in the Nordic countries.

 

Another limitation is the use of sunblock (contains cancer causing benzene derivates to absorb UVA and UVB) and covering clothes that blocks the synthesis of vitamin D3.

 

These sun blocking advice are not protecting against skin cancer [26], [27].

 

The supplementation level is thus set to at least 125 µg per day.

 

 

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Upper limit of vitamin D3 intake

The American IOM (Institute of Medicine) and EFSA has established an upper limit of 100 µg vitamin D3 to adults.

 

These ULs settled by IOM and EFSA seem to be too low as there are a lot of toxicity and physiological knowledge recommending a much higher Tolerable Upper Limit of vitamin D3 . See the part on toxicity.

 

Also, EFSA have recommends an upper limit intake of vitamin D3 to newborn of 25 µg per day. That is equal to 625 µg or 25 000 IU per day to an adult [28]. This mean that EFSA has settled two different upper limits, one that is 25 times higher than the next.

 

The proposed upper level of vitamin D3 intake of 500 µg is safe by a factor of at least 2, probably a safety factor of 8, when the daily intake is below 3 500 µg/day or 50 µg*kg-1*day-1 (or 140 000 IU per day or 2 000 IU per kg and day).

 

 

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Summary

Man seems, according to old and modern scientific research, to need a physiological level of at least 125 nmol/L vitamin D3 to stay healthy.

 

As sun induced synthesis of vitamin D3 has decreased due to the recommendations of the Swedish Irradiation safety authority to avoid vitamin D3 producing sunshine the proportion of individuals with vitamin D3 deficiency have increased compared to 1992.

 

The information presented here shows that the physiological level of vitamin D3 should be maintained at more than 125 nmol/L and that levels below 125 nmol/L must be considered as deficiency.

 

The sources of vitamin D3 in food are scarce so we are forced to rely on supplements of vitamin D3.

 

It is well known and established that there is a direct linear relationship between intake in µg per day and level of vitamin D3 in plasma.

 

The recommendation is therefore according to the table below to reach the population level of at least 125 nmol/L.

 

The safe upper limit of vitamin D3 intake is more than 3 125 µg per day or more than 50 µg/kg/day.

 

The recommendations to the population should thus be as shown below:

 

Recommendation table

Vitamin D3                                                                                  

Age group                            Minimum µg/d        Maximum µg/d

Recommended intake               RI

Children below age 10                    75 µg                       250 µg

Children above age 10                  125 µg                       500 µg

Adults                                           125 µg                       500 µg

Pregnancy and lactation                 250 µg                       500 µg

Elderly                                          125 µg                       500 µg

Average requirements             AR        125 µg                       500 µg

Lower intake level adult            LI        125 µg

Upper intake level                                                                500 µg

 

 

 

 

 

 



References

[1] A. Norman, University of California-Riverside, UCR, History of vitamin D 

http://vitamind.ucr.edu/about/ Accessed 2013-05-01.

[2] Vitamin D, 3rd Ed. Edited by Feldman, D., Pike, J.W, Adams, J.S. San Diego, Academic Press, pp. 1-2081 (2011).

[3] C.L. Wagner Vitamin D Recommendations during Pregnancy, Lactation and Early Infancy

http://media.clinicallactation.org/2-1/CL2-1Wagner.pdf . Accessed 2012-05-01

[4] Uppsala akademiska hospital, Akademiska laboratoriet  downloaded 2013-05-09 http://www.akademiska.se/sv/Verksamheter/Provtagningsanvisningar/

[5] R. Vieth / Journal of Steroid Biochemistry & Molecular Biology 89–90 (2004) 575–579http://www.direct-ms.org/pdf/VitDVieth/VIETH%20More%20vit%20D%20needed.pdf

[6] Brohult J, Jonson B. Effects of large doses of calciferol on patients with rheumatoid arthritis. A doubleblind clinical trial. Scand J Rheumatol. 1973;2(4):173-6.

[8] Hyppönen E, Läärä E, Reunanen A, Järvelin MR, Virtanen SM. Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study. Lancet 2001;358:1500 –3.

[9] Scanlon et al Subclinical effects in a population exposed to excess vitamin D in milk. Am J Public Health 1995 85(10): 1418-22

[10] Lisa A Houghton and Reinhold Vieth  The case against ergocalciferol (vitamin D2) as a vitamin supplement Am J Clin Nutr 2006;84:694 –7. http://www.ajcn.org/content/84/4/694.full.pdf  

[11]  G Jones Am J Clin Nutr 2008;88(suppl):582S– 6S. http://ajcn.nutrition.org/content/88/2/582S.full.pdf

[12] Pludowski P, et al, Vitamin d supplementation and status in infants: a prospective cohort observational study.  J Pediatr Gastroenterol Nutr. 2011 Jul;53(1):93-9.

[13] Vieth, R, Vitamin D supplementation, 25-hydroxyvitamin D concentrations, and safety. Am J Clin Nutr 1999;69:842–56.

[14] John H. Lee, MD,* James H. O’Keefe, MD,* David Bell, MD,† Donald D. Hensrud, MD, MPH,‡ Michael F. Holick, MD, PHD§, Vitamin D Deficiency An Important, Common, and Easily Treatable Cardiovascular Risk Factor? Journal of the AmericanCollege of Cardiology Vol. 52, No. 24, 2008

[15] Landin-Wilhelmsen K, Wilhelmsen L, Wilske J, Lappas G, Rosén T, Lindstedt G, Lundberg PA, Bengtsson BÅ. Sunlight increases serum 25(OH) vitamin D concentration whereas 1,25(OH)2D3 is unaffected. Results from a general population study in Göteborg, Sweden (The WHO MONICA Project). Eur J Clin Nutr. 1995;49(6):400-7.

[16] Brustad et al. Photochem. Photobiol. Sci., 2007, 6, 903–908http://www.nnc2012.is/programme.aspx

[17] Hyppönen E, Läärä E, Reunanen A, Järvelin MR, Virtanen SM. Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study. Lancet 2001;358:1500 –3.

[18] Morten K.B. Bogh1, Anne V. Schmedes2, Peter A. Philipsen1, Elisabeth Thieden1 and Hans C. Wulf Vitamin D Production after UVB Exposure Depends on Baseline Vitamin D and Total Cholesterol but Not on Skin Pigmentation Journal of Investigative Dermatology (2010), Volume 130 p 546-53

[19] Stephanie Seneff, MIT, personal communication in 2011.

[20] Lisa A Houghton and Reinhold Vieth  The case against ergocalciferol (vitamin D2) as a vitaminsupplement Am J Clin Nutr 2006;84:694 –7.

[21] Hyppönen E, Läärä E, Reunanen A, Järvelin MR, Virtanen SM. Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study. Lancet 2001;358:1500 –3.

[22]  Krishna G Seshadria, Bubblu Tamilselvana, Amarabalan Rajendran. Role of Vitamin D in Diabetes Journal of Endocrinology and Metabolism Volume 1, Number 2, June 2011, pages 47-56 (DOI):10.4021/jem23w http://jofem.org/index.php/jofem/article/view/23/32

[23] Obermer, E. Vitamin-D requirements in pregnancy. Br Med J. 1947 Dec 6;2(4535):927

[24] Obermer, E. Vitamin-D requirements in pregnancy. Br Med J. 1947 Dec 6;2(4535):927

[25] Hyppönen E, Läärä E, Reunanen A, Järvelin MR, Virtanen SM. Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study. Lancet 2001;358:1500 –3.

[26] Elwood JMJopson J. Melanoma and sun exposure: an overview of published studies. Int J Cancer. 1997 Oct 9;73(2):198-203.

[27] Social and welfare board of Sweden, statistical data base, showing a sudden increase in malignant melanoma rate from 2003. There is almost no malignant melanoma cases below age 20, a steady level since 1970.

[28] Scientific Opinion on the Tolerable Upper Intake Level of vitamin D. EFSA Panel on Dietetic Products, Nutrition and Allergies (NDA). EFSA Journal 2012;10(7):2813

http://www.efsa.europa.eu/en/efsajournal/doc/2813.pdf


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