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Kolesterolsenkende margarin er farlig for helsa
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Publisert: 13.08.2012
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Uffe Ravnskov har meldt Unilever, en gigant innen blant annet produksjon av margarin, for villedende markedsføring. Her følger hele anmeldelsen og grunnlaget bak den. Dette er svært viktig informasjon som bør spres til flest mulig.
Ärende: Vilseledande reklam och ojust marknadsföring
Meddelande: Vilseledande reklam för livsmedel innehållande växtsteroler
Unilever har i många år marknadsfört sitt margarin Becel pro-activ och vissa yoghurtprodukter med argumentet att de sänker kolesterolet. Samma är fallet med Carlshamns margarin Benecol. Denna sänkning uppnår man genom att ersätta normalt kolesterol med växtsteroler utvunna ur soja och finskt timmer med extraktionsbensin. Resultatet blir att upptaget av normalt kolesterol i tarmen minskar till fördel för upptaget av växtsteroler. Därmed minskar halten av normalt kolesterol i blodet medan halten av växtsteroler ökar.
Nu till problemet. Åtskilliga vetenskapliga studier har visat, att en förhöjd halt av växtsteroler ökar risken för åderförkalkning, hjärtinfarkt och för tidig död. I det följande skall jag helt kort redovisa för de viktigaste av dessa studier. Jag har även infogat länkar till originalartiklarna.
Det finns en sällsynt medfödd sjukdom som kallas sitosterolemi. Patienter med denna sjukdom har kraftigt förhöjda halter av växtsteroler i blodet och utvecklar tidigt i livet xantomer, dvs kolesterolrika knutor i huden av samma typ som man finner hos människor med familjär hyperkolesterolemi (referens 1).
Andra forskare har visat, att patienter med sitosterolemi blir åderförkalkade i ung ålder och kan dö redan i tonåren av en hjärtkärlsjukdom (referens 2 - 5).
Att växtsterolerna har en skadlig effekt på cellväggarna har visats på råttor som utfodrats med växtsteroler. Detta hade dessutom till effekt att råttornas livslängd förkortades (referens 6).
I en senare analys av ett av de första statinexperiment, kallat 4S, fann forskarna med Tatu Miettinen i spetsen att 25 procent av patienterna hade förhöjd halt av växtsteroler i blodet. Dessa patienter hade ingen nytta av statinbehandlingen; tvärtom ökade risken för hjärtkärlsjukdom i denna grupp (referens 7).
Det tycks alltså vara skadligt att ha förhöjda halter av växtsteroler i blodet. Både Becel pro-activ och Benecol höjer halterna och är alltså potentiellt skadlig.
I en översiktsartikel från 2003 (referens 8), där man hade analyserat alla studier som använt växtsteroler i behandlingen, påstår författarna att växtsterolerna är oskadliga. Studien har finansierats av Unilever, huvudförfattarens forskning är även betald av Unilever; två av författarna har patent på margarin med tillsatta av växtsteroler; en av dessa har aktier i det finska företag Raisio som producerar Benecol och som tidigare ägde Carlshamns mejerier. I artikeln hänvisar författarna till djurexperiment, som inte skulle ha visat några skadliga effekter, men de ignorerar den nämnda råttstudien (referens 6), som publicerats tre år tidigare. Studierna, som visat att patienter med sitosterolemi drabbas av åderförkalkning och hjärtkärl-sjukdom, avvisas med följande argument: ”Denna risk är huvudsakligen hypotetisk och den lilla ökningen av blodets halt av växtsteroler mer än övervägs av den minskade LDL-halt i blodet” (This risk is believed to be largely hypothetical, and any increase due to the small increase in plasma plant sterols may be more than offset by the decrease in plasma LDL). Man påstår också, att en studie har visat, att patienter med sitosterolemi kan äta växtsteroler utan risk (referens 9). Denna studie har emellertid endast studerat växtsterolernas effekt på blodets halt av kolesterol och växtsteroler. Aven Miettinens tidigare studie (referens 7) som visat, att statinbehandling ökar risken för hjärtkärl-sjukdom hos människor med förhöjd halt av växtsteroler i blodet, ignoreras, trots att Miettinen står som medförfattare till översiktsartikeln.
Möjligen kommer Unilever och Carlshamns mejerier att hänvisa till en rapport från European Food Safety Authority, som publicerades 2008 (referens 10), men här har man inte tagit ställning till eventuella biverkningar. Man konkluderar, att växtsterolerna sänker kolesterolet, men påpekar samtidigt, att inga experiment har visat, att de även minskar risken för hjärtkärlsjukdom. Det bör också tilläggas, att många studier har visat, att effekten av statinerna, de preparaten som fram för allt används i kolesterolsänkande syfte, inte beror på själva kolesterolsänkningen; nyttan är den samma vare sig kolesterolet sänks maximalt eller blott lite grand. Härmed bortfaller industrins huvudargument, att växtsterolerna minskar blodets halt av kolesterol. Fenomenet förklarar även, varför patienterna i 4S-studien med hög halt av växtsteroler i blodet inte fick någon nytta av behandlingen trots att deras kolesterol minskade lika mycket eller mer än hos de övriga.
Ett minimikrav är att Unilever och Carlshamns mejerier åläggs att bevisa att förhöjda halter av växtsteroler i blodet är ofarligt. I väntan på detta bör den gravt vilseledande annonseringen om påstådda hälsoeffekter stoppas. Frågan är väl också om man över huvud tagit får sälja produkter, som innehåller växtsteroler.
Jag har tidigare påpekat detta i en artikel i Dagens Medicin (http://www.dagensmedicin.se/debatt/annu-en-myt--det-hjartvanliga-becel)
utan att några myndigheter har reagerat, möjligen för att jag glömde nämna, att det endast gällde Becel pro-activ, inte vanligt Becel.
Uffe Ravnskov, med dr, docent
Magle Stora Kyrkogata 9, 22350 Lund
tel +46 46145022 eller +46-702580416
Exempel på vilseledande reklam:
Becel pro-activ: http://www.becel.se/proactiv/?gclid=COirl7HT5LECFeQumAodCA8AMg
Här kommer referenserna till de vetenskapliga artiklarna:
1. Bhattacharyya and Connor 1974. Sitosterolemia and Xanthomatosis. A newly described lipid storage disease in two sisters.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC333088/pdf/jcinvest00641-0079.pdf
Utdrag av abstract: Although the usual diet may contain 150-250 mg of plant sterols, chiefly f8-sitosterol, only trace amounts of these sterols have heretofore been found in human or animal blood and tissues. We now report elevated plant sterol levels in the blood and tissues of two sisters with extensive tendon xanthomas but normal plasma cholesterol levels. Besides. P-sitosterolemia and xanthomatosis, no other physical, mental, or biochemical abnormalities were detected..... We suggest that increased absorption of P-sitosterol must be considered as one cause of this disease. The reason for the extensive xanthomatosis in these two patients remains unknown. Perhaps in some way plant sterols initiated the development of xanthomas with otherwise normal plasma cholesterol levels. Clinical atherosclerosis has not yet occurred.”
2. Beaty et al 1986. Genetic Analysis of Plasma Sitosterol, Apoprotein B, and Lipoproteins in a Large Amish Pedigree with Sitosterolemia
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1684791/pdf/ajhg00153-0088.pdf
”We previously reported the finding of phytosterolemia, xanthomatosis, and hyperapobetalipoproteinemia (hyperapoB) in five siblings in a large Amish pedigree ascertained through a 13-year-old boy who died suddenly from advanced coronary atherosclerosis…..The plasma levels of total and low density lipoprotein (LDL) sterol remain normal or moderately elevated in sitosterolemia [1-9]. Each of the 16 reported cases developed tendon xanthomas before the age of 10 years, and atherosclerosis of the coronary arteries,aorta,and aortic valve (producing aortic stenosis) occurred as early as the second decade of life [1-9].”
3. Salen et al. 1985: Lethal atherosclerosis associated with abnormal plasma and tissue sterol composition in sitosterolemia with xanthomatosis.
http://www.jlr.org/content/26/9/1126.full.pdf
”These results indicate that cholesterol, plant sterols, and 5a-stanols are deposited prematurely and are associated with accelerated atherosclerosis in subjects with sitosterolemia with xanthomatosis.”
4. Assman G. et al. 2006: Plasma sitosterol elevations are associated with an increased incidence of coronary events in men: Results of a nested case-control analysis of the Prospective Cardiovascular Münster (PROCAM) study.
http://www.nmcd-journal.com/article/S0939-4753(05)00081-5/abstract
“Conclusions: Elevations in sitosterol concentrations and the sitosterol/cholesterol ratio appear to be associated with an increased occurrence of major coronary events in men at high global risk of coronary heart disease.”
5. Weingärtner et al. 2009. Controversial role of plant sterol esters in the management of hypercholesterolaemia
http://eurheartj.oxfordjournals.org/content/30/4/404.full.pdf
”Summary points: Currently there are no data available indicating that functional foods supplemented with plant sterol esters reduce cardiovascular events. Findings in patients with the hereditary disease of sitosterolaemia, data from epidemiological studies, as well as recently published in vitro and in vivo data suggest that plant sterols potentially induce negative cardiovascular effects. Prospective clinical studies testing relevant clinical endpoints are needed, before a diet supplementation with plant sterol esters can be recommended.”
6. Walisundera et al. 2000. Vegetable Oils High in Phytosterols Make Erythrocytes Less Deformable and Shorten the Life Span of Stroke-Prone Spontaneously Hypertensive Rats.
http://jn.nutrition.org/content/130/5/1166.full.pdf
”This study suggests that the high concentration of phytosterols in CA and the addition of phytosterols to other fats make the cell membrane more rigid, which might be a factor contributing to the shortened life span of SHRSP rats.”
7. Miettinen TA et al. 1998. Baseline serum cholestanol as predictor of recurrent coronary events in subgroup of Scandinavian simvastatin survival study.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC28514/pdf/1127.pdf
“The risk of recurrence of major coronary events increased 2.2-fold (P<0.01) by multiple logistic regression analysis between the lowest and highest quarter of cholestanol.
Conclusions: Measurement of serum cholestanol concentration revealed a subgroup of patients with coronary heart disease in whom coronary events were not reduced by simvastatin treatment.”
8. Katan MB et al. 2003. Efficacy and Safety of Plant Stanols and Sterols in the Management of Blood Cholesterol Levels
http://download.journals.elsevierhealth.com/pdfs/journals/0025-6196/PIIS0025619611631443.pdf
9. Stalenhoef AFH et al. 2001. Effect of plant sterol-enriched margarine on plasma lipids and sterols in subjects heterozygous for phytosterolaemia
http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2796.2001.00788.x/full
10. European Food Safety Authority 2008. SCIENTIFIC OPINION. Plant stanol esters and blood cholesterol
http://www.efsa.europa.eu/en/efsajournal/doc/825.pdf
”There are no human intervention studies demonstrating that plant stanols reduce the risk of coronary heart disease.”
” The product may not be nutritionally appropriate for pregnant and breastfeeding women and children under the age of five years. Patients on cholesterol lowering medication should only consume products with added plant stanol esters under medical supervision.”
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Kolesterol er sunt
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Publisert: 22.07.2012
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Uffe Ravnskov, lege og uavhengig forsker har skrevet og publisert en mengde viktige og interessante artikler i anerkjente tidsskrifter. Han har også gitt ut en rekke bøker på ulike språk. Hans hovedfokus er på at naturlig mettet fett og kolesterol ikke er farlig for oss, men snarere inngår i molekyler som er viktige for kroppens totale immunforsvar. Lærdommen fra Uffe burde være obligatorisk læring for alt helsepersonell som jobber med pasienter. Legger med et utdrag av boka hans, Cholesterol is good for you.
The benefits of high cholesterol
(A shortened excerpt from Fat and Cholesterol are GOOD for You!)
Most people ‘know’ that high cholesterol is something to be afraid of and that the most important thing to do to avoid a heart attack is to lower one’s cholesterol as much as possible. But did you know that high cholesterol protects you against infectious diseases, which most probably explain that high cholesterol is associated with longevity? With these facts min mind, why should we care about high cholesterol?
Old people with high cholesterol live the longest. This statement seems so incredible that it takes a long time to clear one´s brainwashed mind, at least for those who haven’t read this book, to fully understand its importance. Yet the fact that people with high cholesterol live the longest emerges clearly from many scientific papers.1
Why High Cholesterol Is Good
In certain aspects low cholesterol is worse than high cholesterol. Already fifteen years ago American researchers found that low cholesterol predicts an increased risk of dying from diseases of the stomach, the intestines and the lungs.2
Most of such diseases are infectious. Therefore, a relevant question is whether it is the infection that lowers cholesterol or the low cholesterol that predisposes to infectious diseases You have probably already guessed what the directors of the cholesterol campaign have said, but is it true?
To answer that question the same researchers followed more than 100,000 healthy individuals in the San Francisco area for fifteen years. At the end of the study they noted that those who had low cholesterol at the start of the study had been admitted more often to hospital because of an infectious disease.3,4 This finding cannot be explained away with the argument that the infection had caused cholesterol to go down, because how could low cholesterol, recorded when these people had no evidence of infection, be caused by a disease they had not yet encountered? Isn’t it much more likely that low cholesterol in some way made them more vulnerable to infection? Much evidence exists to support that interpretation.
Low Cholesterol Predisposes To HIV And AIDS
Young, unmarried men with a previous sexually transmitted disease or liver disease run a much greater risk of becoming infected with HIV virus than other people. This was what a group of Minnesota researchers found by following such people for several years. Those who had low cholesterol at the beginning of the study were twice as likely to test positive for HIV compared with those with the highest cholesterol.5
Similar results came from another study of more than 300,000 young and middle-aged men. After sixteen years four times more in the low-cholesterol group had died from AIDS compared with the high-cholesterol group.6
Smith-Lemli-Opitz Syndrome
The benefit of high cholesterol also appears from studies of children with the Smith-Lemli-Opitz syndrome. They are born with very low cholesterol because an enzyme that is necessary for the body’s synthesis of cholesterol does not function properly. Most children with this syndrome are either stillborn or they die early because of serious malformations of the brain. Those who survive are imbecile or autistic, they have extremely low cholesterol, and they suffer from frequent and severe infections. However, if they are given extra cholesterol or eggs in their diet, their cholesterol goes up, their infections become less serious and less frequent, and their autistic and aggressive behavior improves.7
The lipoproteins
One of the many reasons not to name LDL as bad is that the lipoproteins have other important functions. One of them is to take care of microorganisms and their toxic products.
Staphylococcus aureus a-toxin is the most toxic substance produced by strains of the disease-promoting bacteria called staphylococci. It is able to destroy all kinds of human cells, including red blood cells. For instance, if minute amounts of the toxin are added to a test tube with red blood cells dissolved in salt water, the blood is hemolyzed, that is, the membranes of the red blood cells burst and hemoglobin from the interior of the cells leaks out into the solvent. Dr. Bhakdi and his team mixed purified a-toxin with human serum (the fluid in which the blood cells reside) and now the toxic effect of a-toxin almost disappeared. By various complicated methods they identified the protective substance in human serum as LDL, the carrier of the “bad” cholesterol. In accordance, nothing happened when they mixed a-toxin with purified human LDL.
Dr. Willy Flegel and his co-workers at Heidelberg University in Germany studied bacterial toxins in another way. As mentioned above, one of the effects of bacterial toxins is that they stimulate white blood cells to produce cytokines, hormones that start the inflammatory processes. The German researchers found that this effect disappeared almost completely if the toxin was mixed with purified LDL before they added the white blood cells to the test tubes.8,9 Obviously, LDL was able to neutralize the bacterial toxins.
Animal Experiments
The immune systems in various mammals including human beings have many similarities. Therefore, it is interesting to see what experiments with rats and mice can tell us. Professor Kenneth Feingold and his group at the University of California have published some interesting studies. In one of them they lowered LDL-cholesterol in rats by drugs with the result that they died much easier after an injection of bacterial toxins. The high mortality was not due to the cholesterol-lowering drug because, if they gave the animals an injection of human lipoproteins just before the experiment, they survived10
In another experiment, researchers from the Netherlands injected bacteria or their toxins into normal mice, and into mice with high cholesterol. Whereas all normal mice died, most of the mice with high cholesterol survived.11
Many of the roles played by the lipoprotein LDL are shared by HDL as well. This should not be too surprising considering that high HDL-cholesterol is associated with cardiovascular health and longevity. But there is more.
Triglycerides, molecules consisting of three fatty acids linked to a molecule named glycerol, are insoluble in water and are therefore carried through the blood inside lipoproteins, just as cholesterol. All lipoproteins carry triglycerides, but most of them are carried by the VLDL, the largest lipoprotein in our blood.
For many years it has been known that patients suffering from sepsis, a life-threatening condition caused by bacterial growth in the blood, have high levels of triglycerides. The serious symptoms of sepsis are due to bacterial toxins, most often produced by gut bacteria. Now to the interesting point. Solutions rich in triglycerides are also able to protect experimental animals from the dangerous effects of bacterial toxins, which means that the high level of triglycerides seen in sepsis is not a bad thing, but a normal response to infection.12 Usually sepsis bacteria come from the guts. It is therefore fortunate that the blood draining the guts is especially rich in triglycerides.
High cholesterol protects against allergy
Children with allergic problems, such as asthma and hay fever, have lower cholesterol than healthy children. As allergic diseases have become more common and is still increasing in the Western world it is tempting to suggest that the cause is the increasing consumption of the polyunsaturated vegetable oils of the omega-6 type, because these oils are known to stimulate inflammatory processes, and allergy is a kind of inflammation. But there is room for another explanation.
At the Skin and Allergy Hospital in Helsinki, Finland Dr.Maria Pesonen and her co-workers followed 200 children from their birth to their 20 year anniversary.13 They found that the children with allergic disorders had lower total and LDL cholesterol than the others. The difference was obvious already at a time where all the children were breastfed. Thus, the difference could not be explained by their dietary habits. The researchers had no explanation for their observation, but if the lipoproteins are able to bind microbial products, it seems not too far-fetched to assume that they can bind other molecules as well, for instance allergens, those molecules that starts the allergic reactions.
Is familial hypercholesterolemia a disease?
“The more LDL there is in the blood, the more rapidly atherosclerosis develops.”
This was the main conclusion of the American Nobel Price-winners, Joseph Goldstein and Michael Brown.14 They discovered that the cells of people with familial hypercholesterolemia had difficulties taking in cholesterol from the blood because of a defect in the LDL-receptor, the mechanism that transports these vital molecules into the cells. This was the reason why cholesterol was much higher than normal in these people. People with familial hypercholesterolemia also have more atherosclerosis than normal and some of them do die early in life from heart disease. It was therefore not too far-fetched for Goldstein and Brown to draw the conclusion they did, and also to assume that it was applicable to the rest of mankind. They were awarded the Nobel Prize in 1985 for their discovery, and many other researchers share their view.
Their finding is certainly interesting, a result of careful scientific work. Unfortunately, the conclusion they drew was too hasty. In fact, there are benefits associated with this condition, which is why I deliberately refer to individuals with familial hypercholesterolemia as people, not as patients. What is even more surprising is that the reason why some of them die at a young age from heart disease is not their high cholesterol, but something else. I shall come back to that.
In England The Simon Broome Familial Hyperlipidaemia Register Group have followed almost 3000 people with familial hypercholesterolemia for many years. At the most recent control they found that 102 of them, or 3.6 % had died from a heart attack. By analyzing mortality of the same age group in the English population they calculated that the expected number should have been 40, or 1.4 %. On the other hand, fewer had died from other causes, 112 against the expected number 193, or 4 % against 6.8 %. For instance, only half as many had died from cancer.30 If you add the figures and compare them you will see that people with familial hypercholesterolemia live at least as long as other people, if not longer. A little more die from heart disease, but fewer die from cancer and other diseases.
The authors of the scientific report stressed that the participants in their study were admitted because all of them had close relatives who had died at a young age. Cholesterol screening often identifies old people with familial hypercholesterolemia who have no such relatives. The authors therefore suggested that if the participants had been representative for all people with familial hypercholesterolemia, their mortality would have been even lower.
In Finland, Professor Tatu Miettinen and Dr. Helena Gylling studied about one hundred individuals with familial hypercholesterolemia.16 Fourteen to seventeen years later, 30 had died, 26 because of a heart attack and four of other causes. On average, initial LDL cholesterol was the same among those who had died and those who still were alive. If high LDL cholesterol was the most important cause of atherosclerosis and heart disease, as postulated by Nobel Award winners Goldstein and Brown, then we should have expected higher cholesterol in those who died, but that wasn’t the case. Many other researchers have confirmed the Finnish findings.17-23
Another conflicting observation is the fact that people with familial hypercholesterolemia have normal cerebral arteries, even though the same cholesterol-rich blood flows through their brain as through the rest of their body.25
A missing link
The genetic aberrations in people with familial hypercholesterolemia are more complicated than Brown and Goldstein assumed. For instance, in a study of 2400 such individuals, Dr. Angelique Jansen at the University of Amsterdam found that variations of the prothrombin gene were associated with an increased risk of heart disease in these people.26 Prothrombin is a substance necessary for blood coagulation and an abnormal prothrombin gene may lead to the production of too much of this substance. The result is an increased tendency to coagulation and clot formation. Thus, some individuals with familial hypercholesterolemia may form arterial clots more easily than other people, not because of their high cholesterol, but because of an abnormal coagulation system.
Heart patients with familial hypercholesterolemia more often have high concentrations of fibrinogen and factor VIII in their blood than healthy people with familial hypercholesterolemia. Also these substances participate in the coagulation process, and too much of them may stimulate to clot formation. And again, whereas the heart patients had much higher concentrations of fibrinogen and factor VIII, their total and LDL cholesterol did not differ from those measured in healthy people with familial hypercholesterolemia.27
In earlier times, people with familial hypercholesterolemia lived longer than other people! Dutch researchers tracked the ancestors of people with familial hypercholesterolemia and identified 412 individuals with a 50 percent chance of having this genetic abnormality. They also searched official records of deaths and found that the longevity of those with a family history of this genetic aberration was not lower before the year 1900; in fact, on average they lived longer than other people. As the most common cause of death at that time was infectious disease, the authors suggested that high cholesterol protects against infection.28
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Av: korsstingdama, 22.07.2012
Huff nei, noen som gidder å oversette?
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Fettskatt er farlig
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Publisert: 28.10.2011
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Den nye fedtskat vil forværre situationen. Fedmeepidemien vil fortsætte og diabetikernes antal øges. De penge, den nye skat vil indbringe, vil blive slugt af øgede udgifter til behandling af diabetikeres sygdomme.
Af Uffe Ravnskov, dr. med, docent
På kort sigt vil den nye fedtskat øge statens indtægter; på længere sigt kan det blive en menneskelig og økonomisk katastrofe. Flere og flere forskere har nemlig indset, at det er kulhydraterne, som er skyld i fedmeepidemien, og ikke fedtet. Fed mad er simpelthen det bedste middel mod fedme.
Følger politikernes medicinske rådgivere ikke med i den videnskabelige litteratur? Ved de ikke, at verdens førende kosteksperter er ved at vende om på hælen?
En af dem er Walter Willett, professor i næringslære ved Harvard og chef for verdens største og længste koststudier. Han har i mange år advaret os mod det mættede fedt, til trodsfor, at ingen af hans talrige videnskabelige studier har kunnet bevise, at infarktpatienter har spist mere mættet fedt end andre. I et interview i Los Angeles Times sidste år udtalte han følgende:
»Fedt er ikke problemet. Hvis amerikanerne kunne eliminere de søde drikkevarer, kartoflerne, det hvide brød, pastaen, den hvide ris og alt det søde slik, så skulle vi kunne fjerne næsten alle de problemer vi har haft med overvægt og diabetes.«
Også Arne Astrup, en af Danmarks ledende kostforskere, har ændret opfattelse, og Tine Tholstrup, en anden af vore verdenskendte eksperter, har længe peget på mejeriprodukternes uskyld. Forklaringen på fedmeepidemien i den vestlige verden er ikke, som mange tror, at vi spiser for meget mættet fedt. Det er, som Walter Willett påpeger, kulhydraterne, der er de skyldige.
Statistikken viser entydigt, at forbruget af kulhydrater begyndte at stige, da kolesterolkampagnens kostråd blev introduceret i USA i begyndelsen af firserne. Kort efter startede fedmeepidemien i USA og den har siden fortsat i uforandret takt, også i mange andre lande.
Men i samme periode er forbruget af mættet fedt gået ned. Statistikken viser ganske vist, at tilgangen af mættet fedt har været uforandret i mange år, men tilgang er ikke det samme som forbrug.
For at få en bedre opfattelse af forbruget er man nødt til fra den tilgængelige mængde at trække det fra, der forsvinder under lagring og transport, det, der bliver kasseret i butikkerne, og det, der skæres væk i køkkenet og på tallerkenen. De to sidste størrelser er ikke ubetydelige, fordi de fleste mennesker i dag er overbevist om, at det fede er roden til alt ondt. Den, der plejer at spise ude, ved også, hvor svært det er at få ægte smør på brødet og piskefløde i kaffen.
Trods disse fakta påstår kolesteroleksperterne, at vi bliver fede af at spise for meget mættet fedt. Hvor er logikken?
Nogen vil sikkert indvend,e at »jeg fråser i kulhydrater og er slank som en ål«. Protesten er relevant, fordi alle mennesker er forskellige, også når det drejer sig om stofskiftet. Tykke, men raske mennesker, kan slanke sig udmærket med en kulhydratrig, men kaloriefattig kost. Tykke mennesker med diabetes eller dets forstadium, det metaboliske syndrom, gør det bedst med en fedtrig og kulhydratfattig, den såkaldte LCHF-kost (LCHF = LowCarb/HighFat).
Tykke og raske mennesker er imidlertid sjældne. De fleste har metabolisk syndrom, og mere end halvdelen udvikler før eller senere diabetes. I USA udgør de kraftigt overvægtige mere end 30 procent af befolkningen og i andre lande er det ikke meget bedre. I Danmark er det endnu »kun« 12-13 procent.
Men der er hjælp forude. Der findes nu mere end 20 eksperimenter af høj kvalitet, som har vist, at man kan få alle problemerne til at forsvinde, hvis man spiser sig mæt i fedt og mindsker kraftigt på kulhydraterne. Vægten går ned, blodtrykket ligeså, alle laboratorietegn på diabetes bliver normale, og de fleste kan lægge insulinsprøjten og diabetestabletterne på hylden.
Men hvad med kolesterolet? Vi ved jo, at kolesteroltallet går op, når vi spiser mættet fedt. At mættet fedt får kolesteroltallet til at stige, er også en myte. Alle forsøg med LCHF-diæten har vist, at kolesteroltallet i gennemsnit ligger stille. Derimod stiger det »gode« HDL kolesterol en smule og triglyceriderne, »det nye kolesterol«, mindsker kraftigt.
Påstanden om fedtets kolesterolforhøjende effekt blev allerede modbevist for 50 år siden af den amerikanske medicinprofessor George Mann, som havde studeret Masaierne i Afrika. På den tid bestod de mandlige masaiers føde stort set blot af kød og fed zebumælk blandet med lidt blod fra kvæget. Trods dette var deres kolesteroltal det laveste, man nogensinde havde målt hos raske mennesker og adskillige lignende studier har vist det samme.
I Framingham, kolesterolkampagnens vugge, blev 1.000 personer omhyggeligt udspurgt om deres spisevaner i tresserne, uden at man kunne se nogen sammenhæng med kolesteroltallet.
Jeg fik en kopi af rapporten fra George Mann, som deltog i begyndelsen af projektet. Her kan man læse at »kolesteroltallet varierede betydeligt. Noget må forklare denne variation, men det kan ikke være kosten.«
Rapporten blev imidlertid aldrig publiceret; den ligger stadigvæk i en kælder i Washington.
Fedthysteriet startede allerede i 1953, da den amerikanske fysiolog Ancel Keys påstod, at vi får hjerteinfarkt, hvis vi spiser for meget fedt. Som bevis publicerede han et diagram, der viste en perfekt sammenhæng mellem hjertedødeligheden og fedtforbruget i seks lande.
Keys snød imidlertid. Han havde valgt de lande, hvor tallene passede med hans hypotese.
Den britiske forsker Peter Elwood publicerede for nylig en analyse af 15 befolkningsstudier, som i alt omfattede næsten en kvart million mennesker. Den viste, at risikoen for at få hjerteinfarkt, slagtilfælde eller diabetes var mindst i den gruppe, der havde det største forbrug af fede mejeriprodukter.
De tungeste argumenter i medicinsk videnskab er resultaterne fra kontrollerede eksperimenter på mennesker. Det er et faktum, at der ikke findes et eneste korrekt udført kosteksperiment, hvor det er lykkedes at forlænge livet ved at mindske på det mættede fedt. I flere af studierne øgedes dødeligheden til og med.
Tilbage til fedmeproblemet. Det er jo et faktum, at fedt indeholder dobbelt så mange kalorier per vægtenhed end kulhydraterne. Vore kosteksperter og sundhedsmyndigheder har tilsyneladende logikken på sin side. Hvad de glemmer er, at man bliver mere mæt af fedt, og mætheden holder sig længere. Den, der spiser sig mæt i brød, kartofler, ris og kager og skyller det ned med Coca-Cola eller andre søde drikkevarer, bliver hurtigt sulten igen. Mange udvikler til og med et sug efter søde sager.
I flere sammenligninger af de to kosttyper har det vist sig, at den gruppe, der anvender LCHF-diæten taber lettere i vægt, selvom de får lov til at spise ubegrænsede mængder af den fede mad. Maden mætter og ’sød-suget’ forsvinder mirakuløst.
Jeg ved af mange års erfaring, at det ikke er let at sætte spørgsmålstegn ved det, man mener er en videnskabelig sandhed. Science is religion, som The William Blakes synger.
Men som min svenske kollega Christer Enkvist skrev engang: Det er lige så dumt at tro, at man bliver fed af at spise fedt, som at tro, at man bliver grøn af at spise grøntsager.
Den nye fedtskat vil forværre dagens situation. Fedmeepidemien vil fortsætte og diabetikernes antal vil øges. De penge, som den nye skat vil indbringe staten, vil blive slugt af de øgede udgifter til behandling af diabetessygdommens mange komplikationer.
Koldbrand, blindhed og dialysekrævende nyresygdom kræver milliarder. De mange fedmeoperationer er heller ikke billige. Vore politikere har påtaget sig et stort ansvar.
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