Nya forskningsrön, Okategoriserade, Tankar kring fettdebatten

03 november 2013

Vart har kostforskares kritiska tänkande tagit vägen?

För ungefär ett år sedan lade forskare ner Look AHEAD, den största studie som någonsin har genomförts av en lågfettdiet och motion som behandling av diabetes. Orsaken till nedläggningen var att livsstilsförändringen inte visade några tecken på att hjälpa hjärtat. Jag har skrivit om detta tidigare: Nya rön: lågkalorikost skyddar inte mot hjärtinfarkt (trots en ordentlig viktnedgång!)

Studien visar att dagens kostparadigm sannolikt är felaktigt. Men en del kostforskare vill inte se detta. Istället kliar de sig i huvudet och försöker förbryllade förklara resultatet. Idag har Nature Medicin en artikel, ”Are diet and exercise helpful for the heart?”, där spekulationerna är i full gång: kontrollgruppen fick mera läkemedel; viktskillnaderna var för små; det kan vara bra för personer med hjärtproblem att vara lite överviktiga.

Kostforskare har satsat på fel häst

Ingenstans i artikeln ifrågasätter forskarna om de har använt sig av rätt kost. Mot slutet skiver de till och med: ”It may no longer be feasible or sufficiently important to initiate new clinical trials of lifestyle modification where clinically significant weight loss is sustained longitudinally in subjects with type 2 diabetes mellitus.”

Den här inställningen möter jag ofta bland forskare. De har gett upp kostspåret. Om och om igen har de misslyckats att behandla patienter med en lågfettdiet. Deras slutsats är att det där med kostråd inte fungerar. Det är hopplöst. Och så tar de fram kniven och genomför istället en gastric bypass.

Slutsatsen borde istället vara att de kan ha satsat på fel häst. Biokemisk forskning talar för att diabetes borde behandlas med en kost som sänker blodsockret och insulinnivåerna. Det effektivaste sättet är att snåla på kolhydraterna. Ibland kan jag undra vart det kritiska tänkandet har tagit vägen i den del av forskarvärlden som pysslar med kost.

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Mr Big ∙ 4 november, 2013 kl. 07:50

http://sverigesradio.se/sida/artikel.aspx?programid=99&artikel=5692618

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maxiq ∙ 4 november, 2013 kl. 11:14

”Förr i tiden sökte forskarna sanningen – Nu söker de bara pengar”

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celdos ∙ 4 november, 2013 kl. 19:17

Man undrar varför dessa kostforskare inte ens tänker på sig själva, alltså på sitt eget framtida mående. Men de tror nog att de är immuna. Jag kan krasst konstatera att nu när jag är 50+ får fler och fler av mina jämnåriga problem av alla de slag. Cancer, hjärtproblem, ledvärk, allergier, proppar. Och det hämmar deras livskvalitet något så förfärligt. Det gör ont i själen att stå bredvid och se på men inte bli lyssnad på.

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Richard Arppe ∙ 6 november, 2013 kl. 08:07

Ann,

there are actually 3 such trials that I am aware of the tested the hypothesis that smoking cessation would lower the risk of lung cancer mortality. All 3 trials failed to produce statistically significant findings despite reporting significant reductions in smoking prevalence in the group that received counselling on smoking cessation. These trials include the Whitehall Study, the Lung Health Study, and MRFIT, which included in total over 20,000 participants and up to 20 years of follow-up. This makes these trials considerably larger in both in terms of participant size and length of follow-up than the trials that focused on replacing primarily saturated fats with polyunsaturated fats. The largest of these 3 trials found that the number of lung cancer deaths were actually 15% greater, albeit not statistically significant in the group that received counselling on smoking cessation.
http://onlinelibrary.wiley.com/doi/10.1002/1097-0142(20001201)89:11+%3C2422::AID-CNCR16%3E3.0.CO;2-E/full

The relative failure of these smoking cessations trials can be considered a very good example of why all forms of evidence need to be considered when evaluating a hypothesis, not just a few data points from a few randomized controlled trials. The lack of statistically significant favorable findings in the group that received counselling on smoking cessation has been explained by a lack of follow-up time sufficient to achieve the maximum benefits of smoking cessation (which is believed to be more than 2 decades), lack of participant size, a smaller than anticipated number of participants in the group that received counselling that quit smoking, and a greater than anticipated number in the group that did not receive counselling that quit smoking. These limitations are very similar to those that plague the trails that attempted to test the diet-heart hypothesis.

It has been observed that the long-term feeding of cholesterol and saturated fat has resulted in heart attacks, sudden death, development of gangrene, softening on the bones and numerous other serious complications in nonhuman primates. For example, it has been shown that when diets rich in cholesterol and saturated fat are fed to monkeys of the genus Macaca, including the rhesus monkey and the crab-eating macaque, they experience heart attacks at approximately the same rate as high-risk populations living in developed nations.

It has also been demonstrated that the cessation of a cholesterol-rich diet and the subsequent lowering of serum cholesterol results in the regression of atherosclerosis in various mammalian and avian species, including herbivores, omnivores, carnivores and nonhuman primates. In one experiment Armstrong and colleagues induced severe atherosclerosis in rhesus monkeys by feeding a diet with 40% of calories from egg yolks for 17 months. The egg yolks were then removed from the monkeys diet and replaced with a cholesterol-free diet with either 40% of calories from corn oil or low-fat chow with 77% calories from sugar for three years, resulting in a reduction of serum cholesterol to <140 mg/dl and a marked regression of atherosclerosis.

Unfortunately, these lines of evidence have been consistently neglected by the promoters of cholesterol and saturated laden diets. As noted by Stamler:

“To neglect this fact in a review about humans is to imply that the Darwinian foundation of biomedical research is invalid and/or that there is a body of substantial contrary evidence in humans. Neither is the case”.

http://ajcn.nutrition.org/content/91/3/497.full

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Henrik ∙ 12 november, 2013 kl. 08:38

Rhesus monkeys, according to Wikipedia, are ”primarily herbivorous”, and crab-eating macaques, though omnivorous, primarily feed on plant matter.

As evidenced by modern hunter-gatherers, who enjoy nowhere near the abundance of animal prey that their, and our, pre-agriculture ancestors would have had access to, humans have adapted to a diet with a greater percentage of animal fat and protein than our less hunting-savvy primate relatives.

So why would there NOT be a difference in how we react to animal fat and cholesterol as compared to our much more herbivorous furry cousins?

The time perspective can be helpful too. We separated from the ancestors of our closest living relatives, the chimpanzees, about 7 million years ago. From the ancestors of Rhesus monkeys and Macaques, much earlier. In contrast, we separated from our human hunter-gatherer lifestyle around 10-13,000 years ago. The difference in time span for differential adaptation should be obvious.

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Richard Arppe ∙ 13 november, 2013 kl. 15:26

Well, if evolution has any predictive power (which I am sure it does) then a stimulus should have similar (albeit not identical) effect on similar species. This is, after all, what refer as the Darwinian legacy. Saturated fat and dietary cholesterol are the sine qua non for experimental atherosclerosis for nearly all mammalian species, even for those carnivore specimen with inherent malfunction of LDL receptors. This is the very foundation of the diet-heart and the reason why any attack on the diet-heart is and shall remain futile.

Hunter Gatherers, beyond few artic tribes, eat a diet very low in saturated fat, and often low in cholesterol. Moreover, all HG tribes carry intestinal parasites such as tapeworms and schistosomiasis which have been documented to alter lipid metabolism of the host and shown to regress atheroma plaques in animal models.

An anti-atherogenic effect of Schistosoma mansoni infections in mice associated with a parasite-induced lowering of blood total cholesterol. Parasitology. 2002 Nov;125(Pt 5):415-21.

Although, not even the parasites could help the Inuits. In 1904, Bertelsen proved the existence of cancer in the native Inuit, diagnosing a case of breast cancer. During the following decades researchers documented that the existence of cancer was exceedingly common among the Inuit despite their relatively short life expectancy. Consistent with Bertelsen’s findings, an Inuit predating western contact who was mummified in approximately 1475, 450km north of the Arctic Circle was shown to have evidence of cancer, likely of the breast. It has also been documented that numerous preserved pre-contact Inuit who were mummified dating all the way back to 1,500 years ago had a severe degree of atherosclerosis, osteoporosis, and osteoarthritis, consistent with studies of Inuit living in the 20th century. Other evidence of poor health among the pre-contact Inuit includes iron deficiency anemia, trauma, infection, dental pathology, and children with downs syndrome and Perthes disease.