Posted 29 November 2014 - 20:07 PM
Posted 29 November 2014 - 20:18 PM
Luin Fogelholmin jutun pari vuotta sitten jostain naisten lehdestä. Esitteli ruokavaliotaan. Lobbasi kovasti tuolloin vähä-rasvaista maitoa ja kalaa. Omassa ruokapäiväkirjassaan joka aterialla eläinproteiinia, paljon kalaa. Tämä siis pari vuotta sitten, mutta ihmettelin jo tuolloin kovasti meininkiä. "Vegaanipropagandalle" ei ollut Fogelholm altistunut ainakaan tuolloin lainkaan. Kai se sama levy pyöriii vieläkin.
Posted 29 November 2014 - 20:28 PM
Fogelholm toteaa sen faktan, että hiilihydraatin nopeus ei todellakaan ole kovin hyvä hiilarin laadun mittari. Hyvälaatuinen hiilari ja hyvät rasvat on parempia Fogelholmin mukaan kuin kova rasva.
- Richard likes this
Posted 29 November 2014 - 20:39 PM
Aika perus tuubaahan toi koko esitys on .
Laitetaan tähän perään mun default postaus tyydyttyneistä rasvoista. Fogelholm on poliitikko.
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.
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 randomized controlled trials or prospective cohorts from homogeneous populations. The lack of statistically significant favourable 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.
When Siri-Tarino et al. considered 7 of the 11 studies included in their original meta-analysis paper that addressed the association between saturated fat and fatal coronary heart disease they found an 18% excess risk that almost reached statistical significance (0.99-1.42). When Stamler considered all 11 studies he found a 32% excess risk despite over-adjustments for serum lipids and a number of other problems addressed in his editorial that would expected to have significantly weakened this finding (regression dilution bias). The authors of the original Siri-Tarino et al. meta-anlaysis that the low-carbers love to cite actually acknowledged Stamler’s concern about a positive association between saturated fat and fatal heart disease, but instead of using all 11 studies that concerned fatal heart disease from their original meta-analysis as Stamler did in his analysis, they performed their analysis with only 7. Their pooled RR estimate was 1.18 (95% CI, 0.99–1.42). Had they included the additional 4 studies in their analysis perhaps their estimate would have shown an even stronger relationship.
Another point is that the negative findings from cohort studies do not necessarily negate other lines of evidence linking saturated fat with coronary heart disease, and are actually the results that would be expected even if a strong relationship existed. Prominent diet-heart researchers predicted over 3 decades ago, before any of the papers in the Siri-Tarino et al. meta-analysis were published that null findings in these studies would be the case. For example, in 1979 Jacobs et al. stated:
“The link of diet to coronary heart disease is presumably not direct but is through its effect on serum cholesterol. Since diet and serum cholesterol have a zero correlation cross-sectionally, a study of the relationship between diet and coronary heart disease incidence will suffer from the same difficulties as the study of diet and serum cholesterol. A corollary of the mathematical model here presented is that a correlation close to zero would likely be observed between diet and coronary heart disease incidence.”
The RR of 1.32 (Stamler 2010) is actually slightly stronger than that of meta-analyses of the association between passive (second hand) smoking and lung cancer which have produced an RR of around 1.27.
The closet to definitive types of studies supporting diet-heart are not observational, they comes from 4 independent lineages of research
1) Thousands of animal studies showing that saturated fat and dietary cholesterol accelerates atherosclerosis across virtually every type of vertebrate, and that they are the sine qua nons for the dietary modification of experimental atherosclerosis. This includes mammalian, avian and fish species- herbivores, omnivores and carnivores, and over one dozen different species of nonhuman primates. Again this cannot be attributed to the way that the animal was raised as when taking into consideration the amount of antioxidants and carotenoids as well as the lack of cholesterol, tropical plant fats high in lauric, myristic and palmitic acids will also accelerate atherosclerosis in animals to a similar degree as saturated animal fats.
2) Hundreds of rigorously controlled metabolic ward studies establishing that dietary cholesterol and saturated fat elevate LDL and total cholesterol. The cholesterol raising effects of saturated fat is not the result of how the animal was raised as tropical plant fats high in lauric, myristic and palmitic acids will also raise total and LDL cholesterol.
3) Meta-analysis of 108 randomized controlled trials with 300,000 subjects and with a mean follow-up of only three years establishing that lowering LDL significantly reduces both coronary heart disease and all-cause mortality independent of changes to HDL cholesterol and triglycerides, and non-lipid effects of specific interventions.
4) A meta-analysis of mendelian randomization studies with over 312,000 individuals demonstrated that inheriting any of nine studied genetic variants that modify lifelong LDL cholesterol concentrations, but not any other known risk factors predicted a 55% lower risk of coronary heart disease for each mmol/l (38.7 mg/dl) lower LDL cholesterol. This represents a three-fold greater reduction in coronary heart disease per lower unit of LDL cholesterol than the statins trials which lasted only 5 years and the average participant age was 63. The p-value for this finding was 0.000000000000000000843. This is also expected to also translate into a 3 fold lower risk of all-cause mortality. The authors concluded:
“We found no evidence of any heterogeneity of effect on the risk of CHD per unit lower LDL-C among any of the polymorphisms included in our study. This lack of heterogeneity of effect strongly suggests that the results of our study are unlikely to be significantly confounded by pleiotropy or linkage disequilibrium because it is unlikely that each of the included polymorphisms are acting through similar pleiotropic effects or have similar linkage disequilibrium patterns… This finding suggests that the effect of long-term exposure to lower LDL-C on the risk of CHD appears to be independent of the mechanism by which LDL-C is lowered. Therefore, the method of lowering LDL-C is likely to be less important than the magnitude and timing of LDL-C reduction. As a result, diet and exercise are probably as effective at reducing the risk of CHD as are statins or other treatments that lower LDL-C when started early in life (and when measured per unit lower LDL-C).”
These can be considered the strongest lines of evidence for the diet-heart hypothesis, with other lines of evidence simply adding confidence to the hypothesis.
Keys demonstrated mathematically that if the within-person variation is larger than the between-person variation, which is common in homogeneous populations where everyone consumes a similar diet, then this will especially bias the findings towards a null association. For example, in a homogeneous population with a between-person variation of between 2 to 6 eggs per week on average, the variation of intake of an individual consuming on average 4 eggs per week maybe between 1 to 7 eggs per week. If this person’s diet is measured at a high or low point they will be misclassified into a high or low range of intake, typically biasing the results towards a null association.
By the way, it has been pointed out in the literature that regression dilution bias dilutes the real association between serum cholesterol concentration and the risk of CHD in several large-scale prospective population studies such as the Framingham and Whitehall
Another concern is related to the fact that observational studies addressing the association between diet and blood cholesterol and cardiovascular disease dating back to at least the early 1950s have been complicated by reverse causation. It is well documented that people will lower intake of cholesterol and saturated fat in response to elevated blood cholesterol. This is known to bias studies towards finding an association between a higher intake of cholesterol and saturated fat and lower blood cholesterol levels. This would also likely similarly bias the results for the association between intake of cholesterol and saturated fat and the risk of cardiovascular disease.
The most relevant models for human atherosclerosis come from experiments done with non-human primates. 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 SFA confusion. 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”.
- Blueteam likes this
Posted 29 November 2014 - 20:52 PM
Hyvin sanoo myös sen, että vaikka kova rasva ei olisi itsenäinen haittatekijä jossain väestössä, niin ei se tarkoita, että kova rasva on haitatonta. Se tarkoittaa esim., että muut ravintoaineet voi piilottaa haittavaikutusta kyseisessä väestössä.
- Richard likes this
Posted 29 November 2014 - 21:05 PM
En ole varma oliko tossa yhtään mitään hyvää. Fogelholm tuo Suomeen tunnettujen Yhdysvaltalais pseudodenialistien juttuja (Mozaffarian, jne.). Hyvin outoa ettei Fogelholm suomalaisena tuonut lainkaan esiin sitä faktaa, että juuri Suomessa on koettu valtava ikä-vakioitu sydäntautikuolemien lasku. Mistä tämä johtui? Ei sanakaan eteenpäin suuntautuneiden väestötutkimusten ongelmista. Tämä asetelma ei välttämättä ole se optimaalisin asetelma diet-heart hypoteesin testaamiseksi. Globaali epidemiologia ja mekanismi antavatkin sitä painavinta näyttöä.
Tyydyttyneellä rasvalla on täysin itsenäinen rooli LDL kolesterolin kohottajana, jopa painostabiilissa tilassa.
- Blueteam likes this
Posted 30 November 2014 - 23:24 PM
Kummallista sekoilua: Toisaalla sanoo, että tyydyttynyt rasva olisi hyvä korvata hyvillä hiilareilla ja rasvoilla. Sitten taas toisaalla sanoo, että lihan rasva ei ole ongelma. Voinko nyt vetää huoletta rasvaista lihaa, eikä ole mitään hyötyä syödä vähärasvaista lihaa hyvien rasvojen tai hyvän hiilarin kanssa?
Posted 01 December 2014 - 12:49 PM
En ole varma oliko tossa yhtään mitään hyvää. Fogelholm tuo Suomeen tunnettujen Yhdysvaltalais pseudodenialistien juttuja (Mozaffarian, jne.).
Tossa hyvä esimerkki tuosta Mozan denialismista:
Posted 01 December 2014 - 13:39 PM
Fogelholm on poliitikko.
Joo, vihreä on.
Posted 01 December 2014 - 20:17 PM
Denise Minger on hiljattain altistunut "vegaanipropagandalle" ja siteeraa joitain tutkimuksia, jotka ehkä valoittaisivat sitä tausta-ajatusta, joka (vielä) 1970-luvulla oli noita diet-heatrt tutkimuksia tulkittaessa (siis tulkinnoista, joita Fogelholm katsoo harhaanjohtaviksi).
Posted 08 May 2015 - 00:39 AM
Siinä on samaan valioon saatu mahtumaan luomua superfuudia, ruohosyötettyä lihaa, ehtaa voita, paleota ja vähähiilaria (hiukan bataattia sentään mahtuu mukaan, onhan se "parempi peruna"). Tietty jonkun mielestä sellainen ultravähärasvainen kasvisvalio vaikuttaisi yhtä hassulta. Meitä on moneen junaan. Näistä saisi komedian.
Posted 03 September 2017 - 16:56 PM
Fogelholm on kyllä kolesteroliasioissa ihan tietämätön. Huomaa, että hänellä ei ole lääketieteen koulutusta. Varmaan jotain maitoteollisuuden sponsorointiakin on taustalla, kun mies antaa ymmärtää, että juustojen rasva on terveyden kannalta ongelmatonta.
Juusto on paha, koska se on prosessoitua, rasvaista, suolaista ja sisältää ympäristömyrkkyjä. Maitotuotteet aiheuttavat muun muassa reumaa ja astmaa.
– Lähes höpöä. Suola voi toki olla ongelma. Väestöseurantojen mukaan tosin runsas juuston käyttö on ennuste pikemminkin hyvälle kuin huonolle terveydelle.
Also tagged with one or more of these keywords: Mikael Fogelholm, Fogelholm
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