Butter has an Undeserved Bad Reputation, According to New Analysis

Butter

Another new review of the scientific literature finds that saturated fat (like butter) has an undeserved bad reputation. There’s no reason to fear fat anymore.

I wonder if it will be read at the USDA?

Earlier about saturated fat

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149 Comments

Top Comments

  1. Murray
    These measure "risk factors". It begs the question of the causality of the risk factor. If A ( which is benign) causes higher LDL and B ( which is not benign) causes higher LDL, then higher LDL will appear to be a risk factor. However, it does not distinguish between A or B.

    I find it encouraging that since Lipitor went off patent we are beginning to see more scientists who no longer fear publication of results unwelcome to statin makers.

    Read more →
  2. Michelle
    Another shield to add to my defences when I am being told that I am killing myself and my family. Thanks doc. :)
    Read more →
1 2 3

All Comments

  1. Healthy Longevity
    I was meant to say "but still produced a pooled finding of <1.32" for the passive smoking studies, ie. lower than the estimate of Stamler's SFA-fatal CHD analysis.
  2. FrankG
    Yet more ad hominem (no surprise there 'cos it sure seems like that's all you got) but still waiting on...

    What is your explanation for my excellent health markers, apparently (according to you) despite my diet? Weight, BP, A1c, lipids etc.. etc... are these invalid tests in some way, in which case why do Doctors rely on them to assess health risks? I even have a green-light from a Lipidologist. What exactly are your qualifications?

    Should I ignore the evidence of my own body in favour of the "preponderance of evidence" -- much of which has been sponsored by drug companies and "food" manufacturers who have profited very nicely out their "conclusions"?

  3. Z.M.
    @Healthy Longevity

    You are repeating the same thing over and over with your use of selective citing, faulty analogies and double standards. It gets tedious to argue with someone who lacks any logical and scientific standards and it just adds confusion. In any case, I would like to add a few things:

    You can argue all day long about the unreliability of observational studies (while downplaying confounding which is a major issue btw) but the fact is none of your arguments or Stamler's provide any evidence that saturated fat is harmful. Arguing about errors in observational data is not equivalent to providing evidence against saturated fat. It's a massive runaround to distract from the lack of evidence. I have a simpler explanation of why numerous studies (both observational and clinical trials) have failed to find any harmful effect of saturated: maybe there is no harmful effect. You can't use failed observational studies and trials as evidence in your "definitive lines of evidence". So stop using them as if it supports your case because they do not. They are inconsistent with your position. All your arguments reek of bias.

    For Ramsden, I'll repeat that his arguments are reasonable that the trans fat intakes in both groups were similar and I'll add to his arguments that the Research Committee study is consistent with this which did not add n-6 oils. See his reply to Dr. Gutierrez. I know you like to downplay these studies because they all decreased cholesterol levels yet were still miserable failures.

    Your genetic studies are consistent with the Response to Retention and Oxidative hypothesis (which intersect to some degree). The fact that these people can have other risk factors yet still stay free from disease is a testament to their spectacular cholesterol metabolism which most of us do not possess. All this talk about lowering cholesterol and saturated fat is a distraction from things that actually have been shown lower mortality in normal humans. It is very telling that many studies which lowered cholesterol without increasing nutrient/antioxidant intake have been disappointing even with long follow up times e.g. Posch, LRC-CPPT. On the other hand you have other trials like the Lyon Diet Heart Study (which Plant Positive misinterprets btw) which used a sensible intervention of increased intakes of antioxidants (from fruits and vegetables) together with increasing ALA and reducing LA intake in the context of an omnivorous diet that produced big reductions in CHD events, total mortality and cancer in the absence of reduced cholesterol levels. The totality of the evidence is not consistent with your position though you try to make it seem so while committing many fallacies.

  4. LDLDarwinPro
    Evidence against SFA, so far presented:

    1) Experimental evidence (SFA and dietary cholesterol induces atherosclerosis in virtually any animal tested). Are humans an exception?

    2) Biochemistry; SFA elevate serum cholesterol by downregulating LDL receptor activity. And LDL cholesterol is the direct, causal agent influencing coronary artery disease, able to initiate atherosclerosis in both humans and animals in the absence of other risk factors.

    3) Trials & prospective cohorts

    Huge body of epidemiologic research demonstrating that serum cholesterol has a strong, independent and log-linear association to CHD starting from very low levels of cholesterol even among population with low cholesterol levels. And, most studies underestimate the strength of the this association because of regression dilution bias.
    http://aje.oxfordjournals.org/content/150/4/341.full.pdf

    A meta-analysis of 108 randomized controlled trials of various medical and dietary based lipid modifying interventions with around 300,000 participants found that lowering LDL cholesterol significantly decreases the risk of coronary heart disease and all-cause mortality, independent of changes to HDL cholesterol and triglycerides, and non-lipid effects of specific drugs

    Replacement of saturated fat by polyunsaturated fat is also associated with a lower risk of CHD in prospective cohort studies and with lower risk of CHD in randomized trials (See Katan et al 2010)

    4) Ecologic evidence

    Population consuming more SFA have more heart disease, the best study (a prospective cohort study) is ofcourse the 7CS with its 16 cohorts.

    5) IMPACT-models by Capewell

    These models similar to those used in econometrics have quantified the risk factors and their impact on the reduced CHD levels in industrialized countries. In Finland f.ex, the age-adjusted CHD mortality has declined over 80% in the last decades. 50% of this reduction if attributed to reduced mean cholesterol levels and 80% of the reduced cholesterol levels are explained by the decrease of SFA consumption; SFA which was replaced by carbohydrates (SFA went from 20% calories to the current 13% in Finland). Similar experiences from New Zealand, and in from all developed nations, albeit in less dramatic fashion.

    These findings presented demonstrates that the benefit of lowering LDL depends on both the timing and the magnitude of the LDL reduction, and that the benefits associated with lower LDL are largely independent of the mechanism in which LDL is lowered. This in-turn provides strong evidence indicating that dietary changes to reduce serum cholesterol will result in similar results as other medical based lipid modifying interventions (ie. the meta-analysis of 108 lipid modifying interventions), as has been observed in a number of nations that experienced some of the largest declines in cardiovascular disease mortality in the world.

    @ZM,

    you discuss the findings from Lyon -trials without any regards to cumulative exposure to cholesterol. What matters in CHD is the life-long exposure to elevated cholesterol. A measurement at the end of life-span with developed coronary disease is less irrelevant. The lack of difference in cholesterol levels between the control group and reference group is insignificant detail. Statins were used more widely in the reference group as opposed to the control arm (34% vs. 26%). Moreover, age-confounds the cholesterol numbers, because senile devitalization induces metabolic changes in the intestine leading lower absorption and synthesis of cholesterol resulting in lower cholesterol level in elderly sick people.

    As de Lorgiril put it himself:

    ”“(…) each increase of 1 mmol/L of total cholesterol increased the risk of recurrence by 20% to 30%.Epidemiological studies have consistently shown a positive correlation between plasma cholesterol levels and the incidence of (and mortality from) CHD in various populations. Thus, our population does not appear to be different from other low-risk populations. In other words, the data indicate that neither the Mediterranean dietary pattern nor any major bias has altered the usual and expected relationships between the major risk factors of CHD and recurrence.”

    The control arm in Lyon consumed less SFA (8% vs. 13% of calories, if I remember correctly) and less dietary cholesterol and more PUFA.

  5. FrankG
  6. LDLDArwinRi
    @ZM

    "The fact that these people can have other risk factors yet still stay free from disease is a testament to their spectacular cholesterol metabolism which most of us do not possess".

    What these people have is a life-long exposure to low LDL levels. Mean age at the randomization in a typical statin trial is 63. A way too old mean age to achieve optimal results with lipid-lowering therapies, at least until more potent PCSKY9 antibodies are in the market (REGN727).

    The findings from the genetic trials are very consistent with the ecologic evidence from low risk population with life-long exposure to low SFA & low cholesterol diets and low serum cholesterol levels (See f.ex the baseline stats from the Ushibuka cohort in the 7CS; mean cholesterol 143mg/dl, no heart disease even though 70% of males smoked and 40% smokers smoked over 20 fags per day). Similar findings from rural China and Central Africa. But as usual, you perceive the world in a vacuum, one data point at the time in isolation. Luckily diet-heart scientist with influence on public dietary guidelines do not have similar limitations with their scope.

  7. FrankG
    By the way Pee Pee I laughed out loud at your erudite put-down of Anthony Colpo.. boy oh boy, you have such a way with words! :-)

    "This is guy a barely made it to high-school." ??? LOLZ

  8. LDLDarwinPrp
    I reckon most people would have figured by now that "Pee Pees" first language is English, while mine is not.
  9. FrankG
    "Please, could you keep the the Aussie bodybuilders out from this discussion. I don't ask much from you. Respect me with some standards, please."

    As I believe I wrote before It is to laugh! to which I now add an Hah! :-P

    You already stated that you rely on the gullibility of others but I thought I had pointed out that you are not fooling anyone here Pee Pee.

    As for respect: my default is to show it to strangers UNLESS they show to me that they are not worthy of it, then it has to be earned. I realise that you are not the brightest candle but surely you must know where you fit in that scheme of things by now?

    And on the contrary you "ask" a great deal of me -- you expect me to take the word of someone who hides behind anonymity and slinks around using multiple pseudonyms, all the while spouting half-truths and out of context quotes from studies that it seems you don't even bother to read yourself BUT you spout them with such certainty as if to show that you know everything! It is remarkable that you say real scientists like to hedge their bets with a "maybe" every now and then... but you don't!

    AND you expect me to take all that over folks who are open and honest about who they are, make a great deal of sense to me and can back up their facts with evidence that stands up beyond superficial scrutiny.

    NOT to mention that you expect me to take the word of an anonymous shyster (you) over my personal experience WITHOUT even the vaguest attempt to explain why my health markers fly in the face of everything you assert!

    And PLEASE don't play the n=1 card with me because you know full well there are dozens, if not hundreds, or possibly even thousands of folks with similar "anecdotes" just on this one blog.

    You are not fooling me, I don't respect you, your "standards" are in the gutter and I'm not buying it so please give it a rest... Don't make me post more from Anthony Colpo!

  10. Z.M.
    No, your interpretation of the Lyon study is biased as I expected.

    The lack of difference in cholesterol levels between the control group and experimental group is very much a significant factor in its interpretation. It is absurd that you downplay this. The association you see there with cholesterol in the 19 month follow up is a combined group analysis. However, the risk was considerably different in the two groups despite the same level of cholesterol during the whole study suggesting that cholesterol could not have much of anything to do with the between-group difference. By the way, Dr. Michel de Lorgeril would agree with me on this, not you.

    The PUFA intake in the experimental group was lower than the control group. Note that LA intake was LOWERED and kept at only 3.6% of calories. They used a monounsaturated based margarine (not polyunsaturated) rich in ALA (3 times as much as the control group).

    Your implication that reduction of saturated fat benefited the experimental group is nonsense and not supported by any other clinical trial, yet we are supposed to believe that saturated fat reduction in this trial was responsible for massive benefits? Laughable. There is no evidence whatsoever that saturated fat is incompatible with such an intervention. A far more likely explanation is increases in nutrient/antioxidant intake and ALA intake. There is no need to lower cholesterol levels for a lifetime to reap the benefits of such an intervention and it is sad that people like you try to dismiss such successful interventions to promote some vegan ideology. One can also argue that if such interventions are employed from early on in childhood (yea it's a twist on the lifetime cholesterol argument) the reductions would be even greater and would provide benefits not only in regard to CHD, but every disease.

    Reply: #112
  11. LDLRichieye
    "There is no need to lower cholesterol levels for a lifetime to reap the benefits of such an intervention and it is sad that people like you try to dismiss such successful interventions to promote some vegan ideology. One can also argue that if such interventions are employed from early on in childhood (yea it's a twist on the lifetime cholesterol argument) the reductions would be even greater and would provide benefits not only in regard to CHD, but every disease"

    LOL! The diet used in the control arm in Lyon heart trial was a textbook example of low-cholesterol, low SFA, high canola-oil based margharine diets that the mainstream promotes. Most vegans think coconut- and palm oils are health foods.

    You fail to take into consideration anything I wrote. Each 1mmol/l increase in cholesterol predicted 20-30% increase in recurrence. Statins and age co-founded the issue of serum cholesterol levels here. This was about the recurrence of clinical events on people who already had the disease. Moreover, none of the individuals in the control arm showed any actual reversal of their disease. There's not a single (animal)model that has succeeded in reversing atherosclerosis in the absence of reduction in serum cholesterol levels.

    @FranG,

    you are a mislead anti-darwinist deep in the appeal-to-nature fallacy. You are no different from the religious intelligent design people. I never expected to do anything for you. I merely responded so that other people who read this blog would get "a second opinion".

    Reply: #113
  12. FrankG
    "...if such interventions are employed from early on in childhood (yea it's a twist on the lifetime cholesterol argument) the reductions would be even greater and would provide benefits not only in regard to CHD, but every disease."

    Surely you are not suggesting we feed poor defenseless babies on saturated animal fat? :-P

    "Mature human milk contains 3%--5% fat, 0.8%--0.9% protein, 6.9%--7.2% carbohydrate..."[1]

    So assuming Fat is 9 calories per gram, with carbs and protein at 4 calories per gram (quite approximate and based on a bomb-calorimeter rather than a real human being) that comes to: 27-45% of energy from fat, 3.2-3.6% of energy from protein and 27.6-28.8% of energy from carbs... maths is really not my strong suit but isn't that descriptive of LCHF?

    And what kind of fats?

    "Human milk fat is characterized by high contents of palmitic and oleic acids. the former heavily concentrated in the 2-position and the latter in the 1- and 3-positions of the triglycerides."[1]

    Palimitic? "Palmitic acid, or hexadecanoic acid in IUPAC nomenclature, is the most common fatty acid (saturated) found in animals, plants and microorganisms."[2]

    Fatty acid (saturated) found in animals? Ohhh... you mean Saturated Animal Fat?!?

    [1]The composition of human milk.
    http://www.ncbi.nlm.nih.gov/pubmed/392766

    [2]Palmitic acid
    http://en.wikipedia.org/wiki/Palmitic_acid

  13. FrankG
    "you are a mislead anti-darwinist deep in the appeal-to-nature fallacy. You are no different from the religious intelligent design people."

    If by that you mean I go where the evidence leads me, rather than letting others tell me what to think, then I guess you would be right -- but, once again, you are wrong Pee Pee!

  14. Z.M.
    Richard this is getting tedious. Again, there is no evidence that the intervention is incompatible with saturated fat. I eat saturated fat but also monounsaturated and n-3 fatty acids. You are committing the fallacy of false dichotomy. There is no either-or here unless you have some agenda (which you do). Notice also it was not a vegan diet that was used -- far from it.

    You obviously have not read what I wrote as I have responded to the association seen with cholesterol already. Don't expect me to keep responding as I've spent far too much time arguing with two vegan trolls which seem to be on a mission as if from a higher power with know-it-all arrogant attitudes with the only purpose of wanting to be right more than anything else.

    FrankG, I suggest we ignore these trolls :)

  15. LDLrichieDaewi
    @ZM,

    Thanks huge pile of tightly controlled, large scale statin trials we know that the progression of atherosclerosis halts at around 2mmol/l (see the link above)

    LDL-C and disease progression
    http://www.jussiriekki.fi/wp-content/uploads/2013/02/SATURN.jpg

    This is the background context we have to keep in mind while interpreting diet-heart trials. They are about people with pre-existing disease. Most trials did very little to achieve any meaningful outcome. For example in the Sydney Diet-Heart trials, TC cholesterol in both groups was well above 6mmol/l. The disease kept progressing at full pace with these digits. Those few trials that have been more aggressive, such as Ornish et al 1991, managed to lower LDL cholesterol for 40% (drug-free), and the healing of the atherosclerotic lesions were proportional to the LDL lowered in the patients. The patients with lowest LDLs showed reversal of the disease at highest degree. This is of course something you do not consider at all: people with pre-existing heart disease late in life are not likely to see meaningful end-outcomes next to controls with few % change in the consumption of saturated fats. When it comes chronic disease, what matters is cumulative exposure over life.

  16. LDLrichieDaewi
    We know that the progression of atherosclerosis halts when LDL-C is below 2mmol/l, that is (see the link above).
  17. Healthy Longevity
    @Z.M.

    The 4 closet to definitive types of studies I referred to were not observational studies, they were 1) Thousands of animal studies showing that saturated fat establishing that cholesterol accelerates atherosclerosis across virtually every type of vertebrate, and that they are the sine qua nons for the dietary modification of experimental atherosclerosis 2) Hundreds of rigorously controlled metabolic ward studies establishing that dietary cholesterol and saturated fat elevate LDL and total cholesterol, 3) Meta-analysis of 108 randomized controlled trials with 300,000 subjects establishing that LDL significantly reduces both coronary heart disease and all-cause mortality after controlling for other risk factors, 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.

    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. No matter the quality of evidence that is presented here you will simply refuse to accept this hypothesis. I guess that you are hoping that if you keep on chanting phrases such as “faulty analogy” and “double standards” and keep trying to take to my comments out of context that this will somehow undo all this data.

    The mendelian randomization studies demonstrate what we knew all along, that maximum benefit is achieved when LDL lowering is maintained long term, preferably lifelong before the development of atherosclerosis. Reducing cholesterol short-term, especially when atherosclerosis is already full blown (which is considered to have been the case for the diet-heart trials) may do little to decrease the risk of coronary heart disease, similar to how the smoking cessation trials failed to significantly reduce lung cancer mortality. A failed trial does carried out after the damage has already been done does not necessarily negate the hypothesis.

    It is not very meaningful to only cite a limited number of failed cholesterol lowering experiments when there are over 100 of them – all evidence should be considered. As the authors of the meta-analysis of mendelian randomization studies stated “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).” LDL lowering therefore lowers the risk independently of antioxidant intake.

    LDL is not everything, but it is still important. The highest quality mendelian randomization studies demonstrate that a 2mmol/l lower lifetime LDL cholesterol translates into an 80% lower risk of coronary heart disease, without any suggestion of a threshold effect, ie. 3mmol/l would probably further significantly lower risk if not almost eliminate risk. Coronary heart disease is the leading cause of death in many countries and these findings should not be overlooked if we are interested in saving lives. Plus I am suggesting that it would be beneficial to replace food rich in saturated fat and cholesterol with other foods very rich in fiber and antioxidants which would likely decrease the risk of coronary heart disease over-and-above the projected decrease in LDL cholesterol.

  18. Z.M.
    @Healthy Longevity

    None of your runaround changes any of my points, and yes, you do commit many logical errors to support your position and routinely cite non-supportive evidence as evidence. I have no desire to continue conversing with someone who displays such traits.

  19. Healthy Longevity
    Yes I agree that conversing with you is of little point. You have done very little to challenge the 4 main lines of evidence that I cited which is composed of thousands of rigorously controlled experiments across a wide variety of vertebrates including over one dozen different species of nonhuman primates, as well as hundreds of controlled human trials. Of course it is much easier to take a swipe at the other lines of evidence I cited as these are somewhat weaker than the main lines of evidence that I cited.
  20. Z.M.
    No, the evidence as a whole does not support your position as you try to portray. You may be able to fool others but thankfully I'm not as gullible and see through your tactics quite easily.
  21. LDLrichieDaewi
    Thanks HealthyLongevity,

    you are such a goldmine. I going to take a full advantage of the material you presented when tackling diet-heart/SFA denialism.

  22. Z.M.
    Sure he's a goldmine...a goldmine of misleading nonsense of which you are too gullible to see through.
  23. ProkdDawr
    The science is that SFA elevate cholesterol and there's not single specimen in the biosphere which is immune to the harms of elevated cholesterol.

    As Stamler (2010) showed in his response, the RR's for SFA - CHD went up in every study that used modern dietary recall methods, even though most studies were adjusted for serum cholesterol.

    Regarding item 4, the meta-analysis (2) reported its findings as independent of a quality score including diet assessment. Of the 16 CHD studies, 4 relied on one 24-h dietary recall; the SFA-CHD RR was >1.00 for only one of these studies. Seven used a food-frequency questionnaire (FFQ); the RR was >1.00 in 3 of these studies. Five used dietary history or multiday food record; the RR was >1.00 in all 5 studies, even though 3 were adjusted for serum or dietary lipids (2). These facts, which were unnoted in the meta-analysis (2), prompt the question: Did low-level reliability (reproducibility) of dietary SFA data drive RR values toward 1.00 (the regression-dilution bias problem)? No data on SFA reliability are given

  24. ptoDawrb
    Ouh,,,

    the latest stance of IOM, that is.

    "There is much evidence to indicate a positive linear trend between cholesterol intake and low density lipoprotein cholesterol concentration, and therefore increased risk of coronary heart disease"

    http://www.nap.edu/openbook.php?record_id=10490&page=542

  25. Z.M.
    Stamler is exaggerating the findings:

    In Kushi et al the RR was small and the difference in average saturated fat intake of those who had CHD events and those that didn't was a mere 0.5% of calories. Yeah, right.

    In Fehily et al which made no adjustments the RR was 1.57 but was non-significant.

    In Tucker et al the RR was 1.22 but was non-significant.

    All these studies were small. The largest one which used only 7-d diet records was Jakobsen et al and the RR was only a non-significant 1.03.

    Of course bias is a problem in observational studies and confounding is a major issue that is not sufficiently dealt with using statistical models. However, complaining about the unreliability (e.g. measurement error) of observational studies is not evidence against saturated fat. Note, one cannot prove that saturated does not cause disease -- non-causation is assumed until proven otherwise.

  26. Pro-DLDL Rich
    Z.M,

    Stamler is the most experienced diet-heart scholar and pointed that the RRs for SFA-CHD was more stronger and consistent when the quality of the dietary assessment was taken into consideration:

    "Regarding item 4, the meta-analysis (2) reported its findings as independent of a quality score including diet assessment. Of the 16 CHD studies, 4 relied on one 24-h dietary recall; the SFA-CHD RR was >1.00 for only one of these studies. Seven used a food-frequency questionnaire (FFQ); the RR was >1.00 in 3 of these studies. Five used dietary history or multiday food record; the RR was >1.00 in all 5 studies, even though 3 were adjusted for serum or dietary lipids (2) . These facts, which were unnoted in the meta-analysis (2), prompt the question: Did low-level reliability (reproducibility) of dietary SFA data drive RR values toward 1.00 (the regression-dilution bias problem)? No data on SFA reliability are given".

    Most findings in regards to passive have been non-significant. Health professionals cannot act like denialist cranks. Measures to protect public must be made even without 100% certainty. Preponderance of evidence is enough, just like in smoking; it's still not 100% certain whether the link between lung cancer and fags is causal. However, it's 100% bullet-proof that SFAs elevate LDL cholesterol levels when it replaces PUFA and carbohydrate.

    Moreover, pay attention that the studies you cited come from homogeneous, high risk population that has no overlapping of SFA consumption when compared to low-risk populations. F.ex the mean intake of SFA in the highest quartile of consumption in rural Japan (1970s) was 3g less per day compared to the SFA consumption in the lowest quartile of consumption in the Nurses Health Study cohort (1980s). The cohort studies you cited show massive SFA consumption overall with very little versatility in the sub-categories.

    Bonus:

    Saturated Fatty Acid-Mediated Inflammation and Insulin Resistance in Adipose Tissue: Mechanisms of Action and Implications

    "This review highlights the inflammatory and insulin-antagonizing effects of saturated fatty acids (SFA), which contribute to the development of metabolic syndrome"

    http://jn.nutrition.org/content/139/1/1.full

  27. Pro-DforlifeRich
    Most findings in regards to passive smoking have been non-significant, that is.
  28. ProDarwnks@gmail.com
    ZM,

    do you think that the Darwinian foundation of our biomedical research paradigm is flawed? Dietary cholesterol and SFA are utmost definitely the causal agents influencing CHD, sudden death, gangrenes, etc in non-human primates, and pretty much in every single animal specimen in the face of the planet, even in LDL receptor deficient carnivores.

    HealthyL's blog has lot of nice information. Stamler recited Kuczinskys's classic findings among Kirghiz pastorals, they subsisted mostly on organic meat and whole-milk. They were obese and cardiadic symptoms and end-points were frequent among them:

    "Kuczynski (1925) reported on an Asian population at the opposite end of the dietary spectrum - nomadic Kirghiz plainsmen who habitually consumed large amounts of meat and milk. He noted high incidence of obesity, premature extensive atherosclerosis, contracted kidney, apoplexy, and arcus senilis. Their urbanized kinsmen, subsisting on more varied fare, did not exhibit such severe vascular disease".

    http://healthylongevity.blogspot.fi/2012/08/forks-over-knives-and-hea...

    "They get arteriosclerosis in an intense degree and often at an early age as shown by cardiac symptoms, nervous disordes, typical changes of the peripheral vessels, nephrosclerosis and, finally, apoplectic attacks. Even in men thirty-two years old I frequently observed arcus senilis"

    http://healthylongevity.blogspot.fi/2012/11/traditional-diets-in-asia...

  29. FrankG
  30. Z.M.
    Richard, I couldn't care less how experienced Stamler is. His experience doesn't make him exempt from following scientific principles. I have read Stamler's paper and he's trying to make something out of nothing.

    As I said before the smoking example is a faulty analogy. That tactic is not going to work here.

    Also you say: "However, it's 100% bullet-proof that SFAs elevate LDL cholesterol levels when it replaces PUFA and carbohydrate"

    I say, so what. None of the dietary trials show that replacing saturated fat with n-6 oils would benefit anyone even though n-6 oils lowers cholesterol. In fact, n-6 oils show indications of harm, not benefit. As for n-3 fats, one can eat them with saturated fat -- they are not mutually exclusive.

    You say: "The cohort studies you cited show massive SFA consumption overall with very little versatility in the sub-categories."

    I'm not the one who cited them. Stamler is the one that brought them up so send your complaints to Stamler.

    As for the meta-regression analysis (http://www.bmj.com/content/338/bmj.b92) that vegans constantly cite, it just shows how little they care about science. A meta-regression analysis is not an experiment. It's observational in nature, yet vegans cite it as if it proves something about LDL and HDL. Garbage in, garbage out. Vegans also like to bring up the point that the Siri Tarino analysis had connections to the NDC but make no mention of the fact that the meta-regression analysis had connections to the pharmaceutical industry.

    The genetic studies do not isolate LDL-C. This should be apparent from the proposed mechanisms which usually involves increased clearance (as in loss of function PCSK9) or decreased clearance of LDL particles which would either decrease oxidation or increase oxidation (as is known in FH). All of this is also compatible with animal studies which show suppression of atherosclerosis using various substances independent of cholesterol even in the face of extremely high cholesterol.

    It's not as simple as increased LDL = increased risk or decreased LDL = decreased risk which pervades the vegan mind.

  31. Pro-DarwiniazzRicghie
    @ZM,

    a) there's not a single experimental animal model on the face of this planet where reversal of atherosclerosis would have taken place without a reduction in LDL cholesterol.

    b) All free-ranging mammalian animals have very low levels of LDL (~42mg/dl, average of 18 species). The LDL cholesterol of non-human primates is typically around 1-1,8mmol/l (40-70mg/dl).

    c) I am not aware what are the trials are you referring to? Large-scale statin trials, where mean age at the randomization is 63, show that atherosclerosis starts to regress slowly once LDL cholesterol plummets under 2mmol/l (80mg/dl). LDL above 2mmol/l allows the disease to progress.

    Reduction of CHD events have been shown in therapies that have have utilized diet, bile-acid sequestrants, statin, bypass surgery of the ileum and soon PCSKY9 inhibitors. No matter what mechanism is used, lowering LDL cholesterol will result in less cardiovascular events. Welcome to the 21th century.

    Bonus: in addition to the study which vegans love to cite, here's another one covering 62 studies and over 200 000 people; before someone touts about the connection to medical industry, I may point out that one of the co-authors of the paper (2007) is Curt Furberg who is a renown critic of the pharmaceutical industry. Gould has produced systematical analysis of all lipid-lowering therapies (hormone- and fibrate therapies included) starting from 1995. The last up-date is from 2007. The results suggest that cholesterol lowering itself is beneficial (apart from specific adverse effects of fibrates and hormones)

    Cholesterol reduction yields clinical benefits: meta-analysis including recent trials.
    http://www.ncbi.nlm.nih.gov/pubmed/17697899

    http://www.ncbi.nlm.nih.gov/pubmed/9529261
    http://www.ncbi.nlm.nih.gov/pubmed/7697857

  32. LDLrich@gmail.com
    And lest not forget that we are not dealing with CHD alone, elevated cholesterol is likely a culprit in aggressive, lethal prostate cancer as well (and probably myriad of other illness such as Alzheimer and impotence). I think it's a good idea to skip the bacon fat, coconut oil and cream.

    Cholesterol and Cancer: Answers and New Questions

    "Considerable evidence supports the plausibility of an association between low cholesterol and reduced risk of high-grade prostate cancer. Several studies have reported an association between statin use and reduced risk of advanced or high-grade prostate cancer (15, 16). In addition, an inhibitory effect of low cholesterol on prostate cancer progression is biologically plausible. Laboratory evidence suggests that lowering cholesterol levels could inhibit cell-signaling pathways that are important for prostate cancer progression (17). This hypothesis is supported by experiments in mice in which lowering serum cholesterol with dietary modification or a cholesterol-lowering drug reduced the cholesterol content, size, and vascularity of human xenograft prostate tumors" (18).

    http://cebp.aacrjournals.org/content/18/11/2805.full

    "Vegan Propaganda"
    http://www.youtube.com/watch?v=LOJKGbNYnsA&feature=c4-overview-v...

  33. FrankG
  34. ProDawrRioch@gmail.com
    @Z.M,

    moreover, Ference et al did not just look genes that work via PCSKY9, they looked 8 other genes one of them being the statin-targeted HMG-CoA. The paper suggests the effect of each of included SNPs on risk of CHD is mediated largely or entirely through effect on circulating levels of LDL-C, rather than through some other pleiotropic effect. The increased clinical benefit associated with lowering LDL-C beginning early in life appears to be independent of the mechanism by which LDL-C is lowered. Diet and exercise are probably as effective as other therapies at reducing the risk of CHD (per unit reduction in LDL-C. The authors stated:

    "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).”

  35. prodarwanianrichie@gmail.com
    My last post. I wish very good summer for DietDoc,

    Cholesterol levels at mid-life and earlier is an excellent predictor for not only mortality but quality of life as well. 46-year follow-up, not bad.

    Effect of cholesterol on mortality and quality of life up to a 46-year follow-up.

    A strong and graded relation was found between the cholesterol level and total mortality, with the men with a cholesterol level ≤4 mmol/L (154 mg/dl) having the lowest mortality. In all, the men with the lowest cholesterol gained the most life years. However, no association was found with the cholesterol level in 2000 (when 16% were using statins) and subsequent mortality. The lowest (≤4 mmol/L) cholesterol value in midlife also predicted a higher score in the physical functioning scale of RAND-36 in old age. In conclusion, a low total cholesterol value in midlife predicts both better survival and better physical functioning in old age.

    http://www.ncbi.nlm.nih.gov/pubmed/21714947

  36. FrankG
    Mitchell and Webb - A Bigger Spoon

    http://www.youtube.com/watch?v=Hu9nhExp5KI

  37. Z.M.
    @Richard

    You state: "there's not a single experimental animal model on the face of this planet where reversal of atherosclerosis would have taken place without a reduction in LDL cholesterol."

    Please remember that they are able to significantly suppress atherosclerosis in animal models even under extremely high cholesterol levels. I don't think anyone here is saying that hypercholesterolemia is a desirable state to be in but it is significant that they are able to suppress atherosclerosis with extremely high cholesterol never seen in most humans. As for reversal of atherosclerosis, I'm sure some would argue otherwise: http://www.ncbi.nlm.nih.gov/pubmed/9568732

    You state:"Reduction of CHD events have been shown in therapies that have have utilized diet, bile-acid sequestrants, statin, bypass surgery of the ileum "

    None of these trials can attribute the benefits to the concentration of cholesterol. Diet trials usually employ multiple interventions, the patients in the posch trial (the actual results of this trial were disappointing) experienced numerous changes as a result of the surgery e.g. numerous lipid changes besides LDL-C, increases in cholesterol turnover and weight loss, stains obviously have pleiotropic properties. No one knows how much the concentration of cholesterol are responsible for any of these results because it has never been isolated.

    You state: "Ference et al did not just look genes that work via PCSKY9, they looked 8 other genes one of them being the statin-targeted HMG-CoA"

    I'm fully aware of all the genes. Please look into the proposed mechanisms of all these disorders. The mechanisms may differ in some but the end result is the same: lower/higher number of particles and lower/higher oxidative stress.

    You state: "My last post. I wish very good summer for DietDoc"

    Great, I'm sure there are a lot better things to do than argue with people that don't believe a word you say. A step in the right direction!

  38. Pro-Darwin Rickye
    I take the liberty of breaking a promise. Probukol therapy reduces cholesterol and more importantly it promotes reverse cholesterol transport, so no wonder it has anti-atherogenic properties as the experimental model you quoted proved.

    Pharmacologic suppression of hepatic ATP-binding cassette transporter 1 activity in mice reduces high-density lipoprotein cholesterol levels but promotes reverse cholesterol transport.
    http://www.ncbi.nlm.nih.gov/pubmed/21859969

    So, you have no reversal of atherosclerosis unless you manipulate lipid metabolism in a way or another.

    SFA does not promote reverse cholesterol transport, quite the opposite.

    Consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins and endothelial function
    http://www.ncbi.nlm.nih.gov/pubmed/16904539

    Best,
    R

  39. ProDarwinRickye
    I take the liberty of breaking a promise. Probukol therapy reduces cholesterol and more importantly it promotes reverse cholesterol transport, so no wonder it has anti-atherogenic properties as the experimental model you quoted proved.

    Pharmacologic suppression of hepatic ATP-binding cassette transporter 1 activity in mice reduces high-density lipoprotein cholesterol levels but promotes reverse cholesterol transport.
    http://www.ncbi.nlm.nih.gov/pubmed/21859969

    So, you have no reversal of atherosclerosis unless you manipulate lipid metabolism in a way or another.

    SFA does not promote reverse cholesterol transport, quite the opposite.

    Consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins and endothelial function
    http://www.ncbi.nlm.nih.gov/pubmed/16904539

    Best,
    R

  40. FrankG
    Mitchell & Webb - Cheese Argument

    http://www.youtube.com/watch?v=vyyyh8_Afyw

  41. Z.M.
    @Richard

    You state:"Probukol therapy reduces cholesterol and more importantly it promotes reverse cholesterol transport"

    so now you are changing your argument? Reverse cholesterol transport is now important?
    Note that in the study it is not known whether the benefits were due to RCT or the other properties of probucol. So it's speculation. In fact, it's more likely due to the other properties of probucol (anti-oxidant) as seen in numerous other animal studies. In any case your assertion is irrelevant because the fact is they observed similar cholesterol levels yet attenuation of atherosclerosis, which is my point. Moving the goalposts isn't going to help.

    As for the inflammatory studies vegans like to cherry-pick, the one you cited has been analyzed already by many including vegans worst nightmare Chris Masterjohn - http://www.westonaprice.org/know-your-fats/saturated-fat-attack

    And please, no more citing of Plant Positive as he has demonstrated a complete lack of objectivity (or ignorance) in his interpretation of numerous studies (e.g. Lyon or Oslo anti-smoking trial to name a few).

  42. Pro-Darwan Rickye
    Chris "negative liver fat" Masterjohn. I like this astute observer who noticed that Safflower oil may induce negative liver fat, hey nevermind the homeostatis, veggie oils will give you negative liver fat. Also be aware you may end up with zero cholesterol levels as Masterjohn enunciates if you don't track your diet properly. This careful observer also notes how Keys cherrypicked his countries....LOL,,,,Masterjohn.....phew...what next, Ravnskov?

    22 Cholesterol Confusion 5 Cholesterol Is Necessary for Life

    "Cholesterol confusionist and Weston Price Foundation blogger Chris Masterjohn wants you to believe that if you don't eat fatty animal foods you'll be cholesterol-deficient and suffer serious health problems as a result. This is nonsense. Your body can easily make whatever cholesterol it needs. But Masterjohn's disingenuous argument does raise an interesting question: How low can cholesterol go before problems arise? In this video, you'll see that the people whose genes give them extraordinarily low cholester-ol levels mostly manage just fine. Your cells are very good at regulating how much cholesterol they take in. They need to be. Too much cholesterol would be toxic for them".

    http://www.youtube.com/watch?v=RjSmmEzxK7Y&list=PLv3QDzdxan_JkGX...

    41 PUFAs Oxidize!

    "Refined fats offer little more than empty calories, whether they originate from plants or animals. No further reason to avoid them is needed. But the Paleo promoters have fabricated an additional claim against oils to bolster their nutritional myths. They say the fats that caused heart disease all along were never the saturated fats from animals but rather the toxic vegetable oils of the mod-ern world. This is yet another Paleo belief that clashes with reality. Saturated fat can't get off the hook so easily".

    http://www.youtube.com/watch?v=WOcfxpZi6a0&list=PLv3QDzdxan_JkGX...

  43. FrankG
    Mitchell & Webb -- Abraham and Ivan

    http://www.youtube.com/watch?v=vDfoJ29CR4E

  44. Z.M.
    I warned you about posting PP videos. This video demonstrates the nonsense of PP:

    He totally misinterprets the Lyon diet heart study which is actually consistent with Guyenet's views though he tries to make it seem that it is not.

    Some of references he cites are in vitro studies like this one - http://www.nature.com/ejcn/journal/v56/n1/full/1601288a.html of which even the authors admit that "Our study was not designed to investigate the effect of the SFA-rich diet on LDL oxidizability. Therefore conclusions regarding causal relationships between diet and LDL oxidizability during this phase remain tentative".

    He cites one meta-analysis with n-3 fats but ignores a systematic review published that same year showing the benefits of n-3 fats - http://www.ncbi.nlm.nih.gov/pubmed/22591894

    The claim that PUFAs are not inflammatory are based on observational studies (prone to biases such as healthy user bias) and short term trials. Chris Masterjohn doesn't claim that pufas are bad short term.

    PP cites the HEPFAT study which found increased inflammation for only 2 out of 8 inflammatory makers on the safa diet and completely fails to provide any rebuttal to Masterjohn's article http://www.westonaprice.org/blogs/cmasterjohn/2012/05/17/ajcn-publish...

    In other words, PP is full of hot air.

  45. ProdarwiniteRicss
    Lyon -trial made a heavy use of canola oil and canola oil based margarine. According to this own words, Guyenet "loves to rip on margarine".

    The IMPACT models by Capewell & Co show that the age-adjusted CHD mortality in US has halved beginning from the 1960s levels, about 25% of this reduction in the observed CHD mortality is explained by reduced cholesterol levels, a change which took place already in the pre-statin era (from the 240s to the current 200s mg/dl). PUFAS went up, SFAs and eggs came down (Stamler 1998). Much more dramatic CHD reduction rates has been observed in Northern-Europe. In Finland, reduction in cholesterol levels explains ~50% of the observed 80% reduction in age-adjusted CHD mortality. Again PUFAs & carbs went up, SFAs came down. Similar experiences from the latest models done in Eastern European countries such as Poland, where dramatical reduction of CHD mortality took place at the same time when the consumption of veggie oils increased at the expense of animal fats beginning in the early 1990's when the communist subsidies on meat and animal fats were abolished after the breakup of the Soviet Union. I think the IMPACT-models alone are enough to refute the whole nonsense around (long-term consumption) of veggie oils that is espoused in the anti-darwinist low-carb/paleo sect.

    Decline in mortality from coronary heart disease in Poland after socioeconomic transformation: modelling study
    http://www.bmj.com/content/344/bmj.d8136

    Why have total cholesterol levels declined in
    most developed countries?
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199603/pdf/1471-2458-11-...

    I personally consume a whole-food based diet with the exception of moderate use of cold-pressed canola oil, because of its low SFA content. I do this mostly to get easily digested extra calories to fuel my active lifestyle; most people do not need extra calories, I reckon.

  46. ProdarwiniteRicss
    Zatonski W, Campos H, Willett W. Rapid declines in coronary heart disease mortality in Eastern Europe are associated with increased consumption of oils rich in alpha-linolenic acid. Eur J Epidemiol2008;23:3-10.
  47. Pro-daerwaniteRichhs
    Can dietary changes rapidly decrease cardiovascular mortality rates?

    "Thus, after steady rises through the 1970s and 1980s, CVD mortality in Poland suddenly declined sharply in the early 1990s, immediately following the profound socio-economic changes experienced after the break-up of the Soviet Union in 1989. This mortality fall was consistently attributed to diet changes. Specifically, subsidies for meat and animal fats ended and consumption fell dramatically, along with substantial increases in vegetable oils and fresh fruit.13 The subsequent 26% decrease in CVD deaths between 1990 and 1994 was one of the fastest declines ever observed. It could not be dismissed as a fluke, because corresponding changes were also observed in other central European and Baltic countries,13

    http://eurheartj.oxfordjournals.org/content/32/10/1187.full.pdf

    Capewells IMPACT-models from various countries provides strong support for the diet-heart. These are similar models that are used in econometrics. Most importantly, they illustrate what has really happened in real life by providing long-term perspective.

  48. Z.M.
    Richard states: "Lyon -trial made a heavy use of canola oil and canola oil based margarine. According to this own words, Guyenet "loves to rip on margarine""

    Guyenet is not talking about monounsaturated based margarines. He's talking about trans fat/omega-6 rich margarines and the margarine used in Lyon was low in all these things. Pufa intake was kept low (LA intake was only 3.6% of calories) and the diet was also rich in antioxidants so PP's argument about oxidation is flawed right from the very start.

  49. Z.M.
    Richard: "I think the IMPACT-models alone are enough to refute the whole nonsense around (long-term consumption) of veggie oils that is espoused in the anti-darwinist low-carb/paleo sect."

    Are you serious Richard? Impact models cannot refute anything. This just shows the type of nonsense that goes on in nutritional research these days instead of doing actual experiments on hard endpoints.

    Richard: "I personally consume a whole-food based diet with the exception of moderate use of cold-pressed canola oil, because of its low SFA content. I do this mostly to get easily digested extra calories to fuel my active lifestyle; most people do not need extra calories, I reckon."

    Well, I'm happy for you. Now let others eat their low-carb/paleo or whatever diet that they feel they do best on. I'm sure many people here did the vegan thing already and things didn't turn out so well.

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