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  1. Nowhere in the study does it say "Asian meat eaters are healthier". It simply says they did not find a higher risk of mortality for meat intake.

    From the abstract: "Conclusions: Ecological data indicate an increase in meat intake in Asian countries; however, our pooled analysis did not provide evidence of a higher risk of mortality for total meat intake and provided evidence of an inverse association with red meat, poultry, and fish/seafood. Red meat intake was inversely associated with CVD mortality in men and with cancer mortality in women in Asian countries."

    You do know the meaning of an "inverse association" I presume?

    Getting less cancer and less heart disease should imply better health IMO. Furthermore the first paragraph of the post specifies exactly what the title refers to.

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  2. François
    I do like some controversy, when arguments are stated intelligently and people open to change their mind in face of new evidence. I'll confess here that I have written a book a few years back in which I spoke of the dangers of saturated fats, based on the research I knew at the time. Since then, I went back to school, did a masters in public health and realized that most science was crappy. I have changed my mind completely on saturated fat and cholesterol, based on science. It is nevertheless getting irritating to read comments made by vegans on this blog... Desperately trying to convert others to their religion (I call this a religion because they treat it as such). The double standard in article interpretation is rather pathetic.

    Some food for thought here...
    "Fat and cholesterol are very important components in human milk. In fact, the milk from a healthy mother has about 50 to 60 percent of its energy (kilocalories) as fat. The cholesterol in human milk supplies an infant with close to six times the amount most adults consume from their food...Some women produce milk that has a fat level similar to the Guernsey or Jersey cow (high fat) and some produce milk that more closely resembles the Holstein cow (lower fat). The higher fat is more desirable, of course, for the developing infant. The higher fat milk will have more of the fat molecules that are needed for their many functional properties, and will also supply enough energy so that all of the protein can be used by the infant for development. Fat is spoken of as "protein sparing." Without adequate fat, the protein in human milk cannot be used...
    typical milk from French mothers has an average of 44 percent saturated fatty acids, with a range from 39-47 percent. Studies of milk from Dutch mothers showed averages of 38-52 percent saturated fatty acids. Typical milk from Sudanese mothers has an average of 46 percent saturated fatty acids with a range of 36-55 percent. From Spanish mothers the average reported is 41 percent saturated fatty acids and the range is 32-51 percent."
    From: Jensen RG. Lipids in Human Milk. Lipids 1999;34:1243-1271, retrieved from http://www.westonaprice.org/childrens-health/fat-and-cholesterol-in-h...

    So wait a minute.
    Cholesterol is an essential part of the developing brain, of cell membranes and of sex hormones. Human beings naturally produce it and "human milk supplies an infant with close to six times the amount most adults consume from their food". Worse: most of the protein sparing fat in mother"s milk is saturated fat.

    Darn! Nature and God must be really cruel! They must have paired with the Devil to plant the seeds of cardiovascular disease in breast-fed infants. Maybe we should give statins to babies to save them from doom (and make idiots out of them for preventing development of their brain!)

    Come on, get real! Cholesterol is always present where there is an MI because cholesterol is one of the mechanisms used by the body to repair inflammation lesions. Getting rid of cholesterol to decrease cardiovascular risk is like getting rid of fire-fighters to stop fires (have you noted? They usually are around fires, therefore they must be the cause of these fires, of course.)

    Inflammation in vessels has clearly been shown to be caused by an excess of omega-6 fatty acids, by trans fats and by an excess of carbs, especially quick-acting carbs.

    And as far as statins are concerned, the "extraordinary" decrease in reduction of the cardiovascular risk may be due to their anti-inflammatory properties. Industry also downplays the dangerous side effects: severe myalgias due to the destruction of Ubiquinol (necessary for energy production in cell mitochondria), confusion, dementia, massive heart failure - the increase in heart failure rate occured shortly after the introduction of statins... Though it does not prove causation, the fact that statins bring down ubiquinol as much as cholesterol suggests this should be looked at seriously (but it is very unlikely the industry will subsidize a study that could prove that their product is dangerous).

    As far as the efficacy, the 36% reduction in heart attacks is due to statistical manipulation and does not reflect reality. The 10 years study on the efficacy of lipitor, a statin, in high risk middle-aged men, showed 2 heart attack deaths for each 100 patients in the lipitor group and 3.05 in the placebo group, for an absolute reduction of 1 heart attack for 10 years of treatment in 100 middle-aged men at high risk of cardio-vascular disease (men tend to have different hormones than women on average and naturaly occuring estrogen tend to protect women from heart disease). How did we get this 36% reduction number then?

    Easy! Manipulate data and present the relative reduction! The equation is the following: divide the smaller number by the bigger number, substract from 1 and voilà! A big impressive number. Let's do it for the Lipitor study: 2/3.05 = 0.64. 1 - .64 = .36. Therefore, the RELATIVE reduction of heart attacks after taking LIPITOR for 10 years (with all its side effects) is 36%. 36% does not mean that one in 3 men will be saved from doom! But it is understood that way by patients and physicians alike. The real difference is 1%, not 36%.

    I'll stick to my red meat and butter (and wild fish, and poultry, and veggies). I'm very happy that my wife breastfed our kids and I hope my daughter and my daughter-in-law will do the same when they have kids. And I hope my future grand-children will never be fed this crappy soy milk.

    People with an agenda tend to cherry-pick studies and interpret them according to their own preconceived ideas. They already have decided what was the right answer. I wonder what our vegan friends think of the EPIC study, conducted at Oxford University and of the conclusion of this study?
    Alexander D, Cushing CA, Lowe KA, Sceurman B, Roberts MA, Meta-analysis of animal fat or animal protein intake and colorectal cancer Am J Clin Nutr 2009 89: 1402-1409; their conclusion? On the basis of the results of this quantitative assessment, the available epidemiologic evidence does not appear to support an independent association between animal fat intake or animal protein intake and colorectal cancer.

    More: what about the conclusion of this other study?
    Key TJ, Appleby PN, Spencer EA, Travis RC, Roddam AW, AllenNE. Cancer incidence in vegetarians: results from the European Prospective Investigation into Cancer and Nutrition (EPIC-Oxford) Am J Clin Nutr 2009 89: 1620S-1626S; "The overall cancer incidence rates of both the vegetarians and the nonvegetarians in this study are low compared with national rates. Within the study, the incidence of all cancers combined was lower among vegetarians than among meat eaters, but the incidence of colorectal cancer was higher in vegetarians than in meat eaters."

    For a vegan, this cannot be true. Maybe these vegetarians were not true vegans. They mut have eaten some form of animal product to increase the risk of colorectal cancer... Maybe...
    Happy digestion! Hopefully, this will open a few closed minds.

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  1. Healthy Longevity
    There have been over 100 LDL-C lowering randomized controlled trials which have demonstrated that many different types of interventions that lower LDL-C reduces the risk of CHD. Even when researchers control for HDL-C, triglycerides and the pleiotropic effects of specific drugs (by controlling for drug class), lower LDL-C is still associated with a significantly decreased risk of CHD and all-cause mortality.

    Another recent meta-analysis of mendelian randomization studies with over 312,000 individuals found that inheriting any of nine studied genetic variants that modify lifelong LDL cholesterol concentrations predicted a 55% lower risk of coronary heart disease for each mmol/l (38.7 mg/dl) lower LDL cholesterol.

    “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).”
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645847/
    http://content.onlinejacc.org/article.aspx?articleid=1379036

    In regards to ZM review on red meat intake and colorectal cancer, the researchers declared no conflicts of interest even though in a previous paper they reported receiving funding from the Cattlemen's Beef Board. It is clear that the authors were trying to downplay the evidence linking red meat and colorectal cancer. Randomized controlled trials have demonstrated biologically plausible mechanisms that explain the findings for the intake of heme iron and dietary fiber and the risk colorectal cancer in cohort studies. There is little doubt that replacing red meat with foods rich in dietary fiber would decrease the risk.

    It would be easy to reword some of these claims here substituting the words “LDL” for “smoking” to produce claims that appear to be virtually identical to those who attempt to downplay the dangers of smoking. For example:
    “Amazing that even when faced with the evidence of so many hospitalised patients with diagnosed CAD but did not smoke, they seemingly are unable to even stop and consider the possibility that not smoking is NOT an effective measure of risk.”

    Of course we do not need to consider whether these CAD patients use to smoke or previously had high LDL - that is bad science isn’t it? Where is the evidence that people who have maintained a very low LDL throughout life have a high risk of CAD? Why not cite some studies that were able to assess regression dilution in long-term follow-up instead or resorting to desperate cherry picking? Unfortunately you are unable to downplay the evidence linking LDL-C to CAD without resorting to desperate cherry picking because the causal relationship has been firmly established.
    http://www.ncbi.nlm.nih.gov/pubmed/10453810

    There is no point arguing with you as you refuse to consider the evidence.

  2. Richard Mjödstånka
    Great insights HL,

    I'd like to point out that the cholesterol levels start to generally decline on people after the age of 65 due to metabolic changes in the intestine resulting in lower absorption and synthesis of cholesterol. However, cholesterol is an excellent predictor of mortality of quality of life all the way to mid-life. It works like blood pressure and BMI which also display J or U-shaped curve in relation to mortality. When people get old and sick and are at higher risk of death, their blood pressure and BMI comes down as well. Of course with serum cholesterol, statins and reverse causation (sick-quitter effect) also confounds the association in older people. People respond to high cholesterol by starting to consume cholesterol lowering foods (Becel) and dropping down SFA and dietary cholesterol. Cholesterol levels come down rather quickly on many people, however, the plaque-build-up in the artery, accumulated over time, does not disappear in just few weeks.

    Cholesterol is about cumulative exposure over time, the reason why people have "normal" cholesterol at the time of hospitalization is because they are high risk people who are already put to cholesterol lowering drugs after showing first signs of chest pain or even before. Moreover, cholesterol levels come down naturally immediately after a myocardial infarction.

    The stupidity displayed in this blog is just appalling.

  3. FrankG
    Ohh good grief.. why even bother?

    More sleight of hand? More smoke 'n mirrors?

    You may call the folks here stupid but I think what is frustrating you is that we are not the same gullible fools who you are more used to dealing with. Perhaps when a person is deprived of vital nutrients they tend to be more amenable to your vegan propaganda.

    You try to goad an unmeasured response with your insults... are you six years old?

    So now "hospitalised with diagnosed Coronary Artery Disease (CAD)" magically equals "Myocardial Infarction (MI)" Really? In which alternate dimension?

    AND having an MI magically lowers the awful LDL-C? I'd ask for a citation but I really don't trust your sources anyway and you expect me to believe the that researchers who made this observation of over 130,000 in-patients were unaware of this starling fact? They must be stoopid too I guess.... BUUUUT then if researchers cannot be trusted, why should anyone accept the evidence of all your cited studies???

    Let's see...
    Pee Pee says "the reason why people have "normal" cholesterol at the time of hospitalization is because they are high risk people who are already put to cholesterol lowering drugs"

    Study says "Before admission, only 28,944 (21.1%) patients were receiving lipid-lowering medications"

    Oh noes... I've gone cross-eyed again! LOL

  4. Healthy Longevity
    The authors of the study that Frank cited concluded "These findings may provide further support for recent guideline revisions with even lower LDL goals and for developing effective treatments to raise HDL."

    These authors do not seem to be implying that low LDL-C is not beneficial. As I pointed out in my reference before, current cholesterol levels poorly correlate with lifetime cholesterol levels. It was unlikely just lipid-lowering medication which explains why these participants had low cholesterol, other explanations including lifestyle changes and cholesterol lowering diseases.

    A number of studies have noted a paradox among patients administered to hospitals where smokers have a lower risk of mortality after acute coronary syndrome than non-smokers. This may be partly explained by smokers having a greater risk of fatality before admission to hospital than non-smokers (ie. maybe the result of selection bias). Selection bias should be considered
    http://www.biomedcentral.com/1741-7015/9/97

    Also in regards to the meat study.

    As the researchers pointed out, meat intake has increased many fold in many parts of Asia in the last few decades. The strongly suggests that the difference in high vs low intake of meat in these cohorts would have been significant smaller earlier on in these participants life. Therefore it is expected that meat intake would have only had a negligible effect on the rates of mortality of these participants with this length of follow-up.

    Similarly, we would not expect that someone who only recently started smoking would have a significant 10 year greater risk of lung cancer compared to a never smoker because the time lag between smoking and the maximum risk of developing lung cancer is likely to be several decades.

    Reply: #55
  5. Paul
    "These findings may provide further support for recent guideline revisions with even lower LDL goals and for developing effective treatments to raise HDL."

    so, which diet most effectively lowers LDL and raises HDL ?

  6. Richard Mjödstånka
    FrankG,

    Swedish cardiovascular experts gave a complete refutation for the nonsense espoused by cholesterol denialists. GWTG study was well covered, unfortunately the text is in Swedish only. But at least, Doc can browse it through. Indeed, one of the point raised by these experts was that cholesterol levels plummet temporarily after an acute infarction. No information was provided about whether the patients were at fasting state or not, the study had no control group, measurement error due to non-standardized lipid measurements is also a potential issue. The authors of the study (GWTG) simple wanted to make a point that more aggressive lipid-lowering therapies are needed. "normal" cholesterol are not a good idea in population where it is normal to die in a heart disease.

    Kolesterolhypotesen står sig
    http://ltarkiv.lakartidningen.se/2010/temp/pda37881.pdf

    @Paul,

    HDL-C is not causally related to CHD nor strokes. It's rather marker, a risk predictor like a poverty in Western epidemiology, not a causal actor, that is. Populations that were once immune to CHD had quite low levels of HDL-C (Okinawa, rural China, etc).

    An elevation of triglycerides reflecting decreased triglyceride clearance may not be pathogenic -- relevance to high-carbohydrate diets.

    Triglyceride levels are relatively high in certain Third World societies which are virtually immune to coronary disease so long as they persist in their traditional very-low-fat diets; in Ornish's celebrated study, a moderate rise in triglycerides coincided with a marked reduction in coronary events. Although the particle size of both LDL and HDL tends to decrease when triglyceride levels are high, it is questionable whether this effect has a major pathogenic impact. The one clear drawback of high-carbohydrate diets is a decrease in HDL particle number, resulting from decreased hepatic production of apoA-I; this effect is seen whether or not triglycerides increase. The very favorable effects of very-low-fat, whole food, quasi-vegan diets on LDL cholesterol, insulin sensitivity, and body weight appear to more than compensate for this decrease in HDL; it is notable that HDL levels tend to be quite low in Third World cultures at minimal risk for coronary disease. On the other hand, this decrease in HDL may be of more significance in the context of omnivore diets only moderately low in fat, as suggested by the fact that diets higher in unsaturated fats emerge as more protective in Western prospective epidemiology. The tendency of high-carbohydrate diets to boost triglycerides can be minimized by exercise training, supplemental fish oil, an emphasis on fiber-rich, low-glycemic-index whole foods, and the "spontaneous" weight loss often seen with ad libitum consumption of such diets -- measures which are highly recommendable whether or not triglycerides are a concern.

    http://www.ncbi.nlm.nih.gov/pubmed/15504577

    Reply: #57
  7. Paul
    I see.

    "The stupidity displayed in this blog is just appalling." - I am confused, to whom this statement is addressed to ?

  8. Murray
    The problem with citing umpteen studies craftily designed y ideologists and shills for pharmaceuticals is that they run counter to empirical real-world experience. I expect a good number of the people who follow this blog have had a lengthy history of being told, for example, that high fat causes weight gain. This was "proven" beyond doubt by "peer-reviewed" studies. But those pesky "denialists" kept losing weight and getting manifestly healthier on LCHF. Oh dear. Bring out the attack dogs. So in retrospect, numerous oft-cited studies appear to have flawed methods and the more credible studies are those that brought unexpected results, those counter to the pre-cooked design to promote favoured outcomes by those who review research grant applications. Clifton Leaf (Truth in Small Doeses: Why we are losing the war on cancer) does a nice survey of the problem in cancer research. When the status quo in a field, such as obesity, diabetes and cardiovascular disease, has made little progress indecades, that is almost an inductive proof that the research methods are skewed and the paradigm flawed. So, for example, I am a genetic theory of cancer denialists, sure, but only because the status quo has been empirically unsuccessful as the foundation of productive engineering and the metabic theory is more credible. Oddly, with diabesity, the engineering (manifestly successful LCHF despite being counter to dogma) is driving revision of dogma and new approaches to experimental design. Who are you gonna believe, vegan ideologues and industry shills, or personal practical experience?
  9. Z.M.
    Healthy Longevity says: "There have been over 100 LDL-C lowering randomized controlled trials which have demonstrated that many different types of interventions that lower LDL-C reduces the risk of CHD. Even when researchers control for HDL-C, triglycerides and the pleiotropic effects of specific drugs (by controlling for drug class), lower LDL-C is still associated with a significantly decreased risk of CHD and all-cause mortality."

    I repeat, none of those studies lower LDL-C alone whether you are talking about ileal bypass surgery, LDL apheresis, diet, Bile Acid Sequestrants or statins. Statistical adjustment cannot establish causation and is useless for variables that cannot be measured or are poorly measured (like the pleiotropic effects of drugs). So I suggest you stop pushing this lie.

    Healthy Longevity says: "Another recent meta-analysis of mendelian randomization studies with over 312,000 individuals found that inheriting any of nine studied genetic variants that modify lifelong LDL cholesterol concentrations predicted a 55% lower risk of coronary heart disease for each mmol/l (38.7 mg/dl) lower LDL cholesterol."

    How many times do I have to repeat myself? LDL-C is not lowered alone. What you may be seeing is lifelong lowered oxidative stress (the opposite of hypercholesterolemia): http://blog.cholesterol-and-health.com/2011/03/genes-ldl-cholesterol-...

    Healthy Longevity says: "In regards to ZM review on red meat intake and colorectal cancer, the researchers declared no conflicts of interest even though in a previous paper they reported receiving funding from the Cattlemen's Beef Board."

    So it's fine for you to post studies connected to the pharmaceutical industry but is a problem when I post a study connected to the Cattlemen's Beef Board?

    Healthy Longevity says: "It is clear that the authors were trying to downplay the evidence linking red meat and colorectal cancer."

    You have no clue what the authors did. The authors laid out how weak the evidence was in a scientific manner.

    Healthy Longevity says:"It would be easy to reword some of these claims here substituting the words “LDL” for “smoking” to produce claims that appear to be virtually identical to those who attempt to downplay the dangers of smoking."

    Starting with your faulty analogies again? You mentioning smoking is just a distraction to how weak the evidence is for the diet heart hypothesis. Smoking has no bearing on whether cholesterol or saturated fat causes anything.

    Healthy Longevity says: "that is bad science isn’t it?"

    Your views are an example of bad science: making claims in such a certain manner about something when you haven't excluded other plausible alternative hypotheses.

  10. FrankG
    "nonsense espoused by cholesterol denialists" -- oh no you have me confused with somebody else! I do actually BELIEVE in cholesterol... I realise how vital it is in the healthy functioning for so many of my body's systems

    "one of the point raised by these experts was that cholesterol levels plummet temporarily after an acute infarction"

    AGAIN with the acute infarction? Please point out to me where it says these 137,000 people were admitted for an acute MI??? Maybe it is in the full article? All I see in the abstract is the data "was analyzed for CAD hospitalizations from 2000 to 2006 with documented lipid levels in the first 24 hours of admission"

    Is this another of your nebulous links? More smoke 'n mirrors? Perhaps they did all have MI's -- in which case why not state that in the article? It seems to me more important to recognise that someone has actually had an MI rather than identifying some atherosclerosis in the coronary arteries... what do you think? Perhaps they (some/many/all) were long time CAD patients who had come in during a period of stability for a routine workup (including blood work), angiogram, angioplasty, stent or some other procedure? Let's guess shall we and base all our "science" on that? LOL

    I still suspect that "HL" and Sneakie Dickie Pee Pee are one and the same person playing tag team with himself -- probably in his Mother's basement :-P but in either case I find it quite telling that the vegan element here seems so ruffled by this study... so desperate to try and rationalise what does not fit the much proclaimed dictum that "high LDL-C causes CVD"

    Here we have a VERY large set of data from over 136,000 diagnosed CVD patients (CAD is a subset of CVD)... NOT some make believe hypothetical maybe in the future CVD but real and now AND for around 50% of them their LDL-C is low/normal! Again factual blood results, not some conclusion in a study, open to interpretation by others.. real numbers! Read 'em and weep vegans ideologues :-P

    That feeling Pee Pee, where your eyes are bulging and that vein on your forehead is throbbing..? That is called "cognitive dissonance". It is what happens when the observed data does not fit your preconceptions. A real scientist, who was not tied to the dogma, would question their preconceptions.

    I think the problem here is that you have already lost the argument Pee Pee but you don't see it yet. Perhaps you think that we are playing by kindergarten rules where the last one shouting wins! Knock yourself out bozo.

    No, you have already lost because you come from a position of ideology rather than evidence. Much like in religion where we are told that here is the one true god and that we know this to be true because the holy book says so.. and we know the holy book is right because it is the word of god. Circular reasoning that does not stand up to even the most superficial scrutiny. Maybe there is a god... I don't know and I don't see any evidence to support the claim but I remain open to new evidence if it comes along.

    You are not presenting any new evidence. You are NOT convincing me of anything except your own stupidity for persisting in this attempt.

  11. Tom Levine
    Oh China Study....Sigh.
  12. Healthy Longevity
    "I repeat, none of those studies lower LDL-C alone"
    We are meant to believe that this is just a coincidence that these LDL-C lowering interventions that have shown to lower the risk of CHD are always confounded by another factor that can low the risk of CHD to this degree? Perhaps you can cite some studies showing that this small degree of change to these other risk factors can predict the same degree of decrease in CHD with other drugs that do not significantly lower LDL-C.

    We are also meant to believe that it is the biggest coincidence of the millennium that all 9 genetic variants predict the exact same change in risk of CHD per unit change in LDL-C concentration even though all 9 genes likely modify LDL-C via different mechanisms?

    We are also meant to believe that Brown and Goldstein who were awarded a Nobel Prize for their research on the metabolism of LDL-C know nothing about LDL-C?

    We are also meant to believe that virtually every prominent health authority in the world are all in on a conspiracy that LDL-C is causally associated with CHD? They must have all been infiltrated by vegan zealots and pharmaceutical companies right?

    This list could go on an on.

    Sorry what you people are doing is just trying to desperately confuse uninformed people so you can promote a disease promoting diet that no respected health authority has said can be healthy in the long term.

    Wow lets cite WAPF! Sally Fallon and Mary Enig, the founders of the Weston A. Price Foundation claim that ‘For women, there is no greater risk for heart disease, even at levels as high as 1000 mg/d’. Of course this claim must be as true as the claims of WAPF member William Douglass aka ‘Dr. Tobacco’ who states that the consensus that smoking is disease promoting was derived from ‘prejudices based on false science and government propaganda’, that there is a ‘broad spectrum of therapeutic and preventive applications of tobacco smoking for human medicine’, and even that nicotine can ‘Help you live longer’. Of course we should not cast any doubt on what these researchers say.

  13. François
    I do like some controversy, when arguments are stated intelligently and people open to change their mind in face of new evidence. I'll confess here that I have written a book a few years back in which I spoke of the dangers of saturated fats, based on the research I knew at the time. Since then, I went back to school, did a masters in public health and realized that most science was crappy. I have changed my mind completely on saturated fat and cholesterol, based on science. It is nevertheless getting irritating to read comments made by vegans on this blog... Desperately trying to convert others to their religion (I call this a religion because they treat it as such). The double standard in article interpretation is rather pathetic.

    Some food for thought here...
    "Fat and cholesterol are very important components in human milk. In fact, the milk from a healthy mother has about 50 to 60 percent of its energy (kilocalories) as fat. The cholesterol in human milk supplies an infant with close to six times the amount most adults consume from their food...Some women produce milk that has a fat level similar to the Guernsey or Jersey cow (high fat) and some produce milk that more closely resembles the Holstein cow (lower fat). The higher fat is more desirable, of course, for the developing infant. The higher fat milk will have more of the fat molecules that are needed for their many functional properties, and will also supply enough energy so that all of the protein can be used by the infant for development. Fat is spoken of as "protein sparing." Without adequate fat, the protein in human milk cannot be used...
    typical milk from French mothers has an average of 44 percent saturated fatty acids, with a range from 39-47 percent. Studies of milk from Dutch mothers showed averages of 38-52 percent saturated fatty acids. Typical milk from Sudanese mothers has an average of 46 percent saturated fatty acids with a range of 36-55 percent. From Spanish mothers the average reported is 41 percent saturated fatty acids and the range is 32-51 percent."
    From: Jensen RG. Lipids in Human Milk. Lipids 1999;34:1243-1271, retrieved from http://www.westonaprice.org/childrens-health/fat-and-cholesterol-in-h...

    So wait a minute.
    Cholesterol is an essential part of the developing brain, of cell membranes and of sex hormones. Human beings naturally produce it and "human milk supplies an infant with close to six times the amount most adults consume from their food". Worse: most of the protein sparing fat in mother"s milk is saturated fat.

    Darn! Nature and God must be really cruel! They must have paired with the Devil to plant the seeds of cardiovascular disease in breast-fed infants. Maybe we should give statins to babies to save them from doom (and make idiots out of them for preventing development of their brain!)

    Come on, get real! Cholesterol is always present where there is an MI because cholesterol is one of the mechanisms used by the body to repair inflammation lesions. Getting rid of cholesterol to decrease cardiovascular risk is like getting rid of fire-fighters to stop fires (have you noted? They usually are around fires, therefore they must be the cause of these fires, of course.)

    Inflammation in vessels has clearly been shown to be caused by an excess of omega-6 fatty acids, by trans fats and by an excess of carbs, especially quick-acting carbs.

    And as far as statins are concerned, the "extraordinary" decrease in reduction of the cardiovascular risk may be due to their anti-inflammatory properties. Industry also downplays the dangerous side effects: severe myalgias due to the destruction of Ubiquinol (necessary for energy production in cell mitochondria), confusion, dementia, massive heart failure - the increase in heart failure rate occured shortly after the introduction of statins... Though it does not prove causation, the fact that statins bring down ubiquinol as much as cholesterol suggests this should be looked at seriously (but it is very unlikely the industry will subsidize a study that could prove that their product is dangerous).

    As far as the efficacy, the 36% reduction in heart attacks is due to statistical manipulation and does not reflect reality. The 10 years study on the efficacy of lipitor, a statin, in high risk middle-aged men, showed 2 heart attack deaths for each 100 patients in the lipitor group and 3.05 in the placebo group, for an absolute reduction of 1 heart attack for 10 years of treatment in 100 middle-aged men at high risk of cardio-vascular disease (men tend to have different hormones than women on average and naturaly occuring estrogen tend to protect women from heart disease). How did we get this 36% reduction number then?

    Easy! Manipulate data and present the relative reduction! The equation is the following: divide the smaller number by the bigger number, substract from 1 and voilà! A big impressive number. Let's do it for the Lipitor study: 2/3.05 = 0.64. 1 - .64 = .36. Therefore, the RELATIVE reduction of heart attacks after taking LIPITOR for 10 years (with all its side effects) is 36%. 36% does not mean that one in 3 men will be saved from doom! But it is understood that way by patients and physicians alike. The real difference is 1%, not 36%.

    I'll stick to my red meat and butter (and wild fish, and poultry, and veggies). I'm very happy that my wife breastfed our kids and I hope my daughter and my daughter-in-law will do the same when they have kids. And I hope my future grand-children will never be fed this crappy soy milk.

    People with an agenda tend to cherry-pick studies and interpret them according to their own preconceived ideas. They already have decided what was the right answer. I wonder what our vegan friends think of the EPIC study, conducted at Oxford University and of the conclusion of this study?
    Alexander D, Cushing CA, Lowe KA, Sceurman B, Roberts MA, Meta-analysis of animal fat or animal protein intake and colorectal cancer Am J Clin Nutr 2009 89: 1402-1409; their conclusion? On the basis of the results of this quantitative assessment, the available epidemiologic evidence does not appear to support an independent association between animal fat intake or animal protein intake and colorectal cancer.

    More: what about the conclusion of this other study?
    Key TJ, Appleby PN, Spencer EA, Travis RC, Roddam AW, AllenNE. Cancer incidence in vegetarians: results from the European Prospective Investigation into Cancer and Nutrition (EPIC-Oxford) Am J Clin Nutr 2009 89: 1620S-1626S; "The overall cancer incidence rates of both the vegetarians and the nonvegetarians in this study are low compared with national rates. Within the study, the incidence of all cancers combined was lower among vegetarians than among meat eaters, but the incidence of colorectal cancer was higher in vegetarians than in meat eaters."

    For a vegan, this cannot be true. Maybe these vegetarians were not true vegans. They mut have eaten some form of animal product to increase the risk of colorectal cancer... Maybe...
    Happy digestion! Hopefully, this will open a few closed minds.

  14. Richard Mjödstånka
    In regards to the post HL;

    there's not a single person who knows the statin drugs and who longer believes that the benefits associated with statins mediate via some other mechanism besides LDL lowering (pleiotropy). Again, a renown Swedish cardiovascular expert wrote an excellent article about the issue called "pleiotropic effects of statins, where are you?"
    http://ltarkiv.lakartidningen.se/2006/temp/pda32183.pdf

    If statins worked through some mechanism besides LDL-lowering, they ought to work in acute coronary syndrome where the LDL lowering effect of the drug has not yet kicked in. Statins do not work in acute coronary cases which have been proved without reasonable doubt in placebo controlled trial (Briel et al) which have tested the hypothesis that manufacturers of less efficient statins kept pushing. Even in acute cases, more potent statins are better, although the benefits are limited which is understandable, since LDL-lowering takes time. More potent statins have always outperformed less efficient statins and the only reasonable finding for this consistent pattern is that potent statins lower cholesterol more efficiently, lower the better.

  15. Healthy Longevity
    Cholesterol and saturated fat cannot be bad for human adults because it is in mothers milk?
    Elevated LDL-C cannot be bad because LDL-C has a critical role in the health of humans?

    Just because something is in mothers milk, it does not mean that it is health promoting after weaning. Atherosclerosis can be induced in chickens by feeding them fresh eggs and in calves by feeding them cow’s milk supplemented with or without extra cholesterol.
    http://ps.fass.org/content/65/5/979.short
    http://www.sciencedirect.com/science/article/pii/0021915074900409

    If we look at the low-carbers arguments it seems that they are suggesting that if something plays a critical role for body health (like cholesterol) it is not biologically plausible that it can be harmful at levels in excess of what is required for normal bodily function. This argument therefore suggests that it is not biologically plausible that excess body fat, hypertension and hyperglycaemia could be harmful.

    It is obvious that anyone who brings up these arguments has no interest in honest debate. It seems like people here are “desperately trying to convert others to their religion” of eating meat and butter with a bunch of misleading nonsense that no respected health authorities would fall for.

  16. FrankG
    http://www.youtube.com/watch?v=T0kRyv3RRH4

    http://www.youtube.com/watch?v=dLpCZ8g5uK8

    or if you want a real laugh, try listening to this drivel from Pee Pee (I challenge you to try even a minute of this grating voice).. apparently there is over 70 hours of it!

    http://www.youtube.com/watch?v=6bSdnQ1MKGo

    Reply: #67
  17. FrankG
    And Pee Pee it really (REALLY) is so dreary and oh so dull dull dull! I can't imagine anyone listening to hour upon hour upon hour of that drek -- especially in that droning, boring, obnoxious voice -- without reaching for a gun to blow their own brains out.. 'cept of course we already know that low cholesterol and lack of saturated animal fat leads to depression, suicidal tendencies, violence etc.. anyway so maybe it is all relative and the vegans don't notice? Or perhaps all those statins have his listeners/readers so cognitively impaired that they aren't really listening anyway, or perhaps so muscle damaged that they are bed-ridden and can't escape the torture... who knows eh? Or maybe he HAS no listeners/readers so spends hours creating alias after alias to put out positive comments praising himself for all his good works! Who knows what his sick, malnourished mind might get up to next? LOL

    But literally hours of droning on and on and on and on... in YouTube videos, several web-blog sites, haunting sites likes here... he has long and varied trail, more often unwelcome than otherwise -- all anonymous of course, juggling all those pseudonyms -- badly I might add: for someone who claims English as a second language he uses some pretty high falutin' words.. and don't even get me started on how every single alias uses the same words, same phrases, same way of putting things.. and then he praises his own posts under another alias.. pretty sick eh?!?

    Makes me wonder who is bankrolling all this effort? Must be a full-time job? I hope it pays well but then we already know that encouraging folks to keep eating their hearthealthywholegrains and keep taking their medicine is VERY good for business... whereas an LCHF diet would be bad for the bottom-line eh?

  18. Z.M.
    HL: "Perhaps you can cite some studies showing that this small degree of change to these other risk factors can predict the same degree of decrease in CHD with other drugs that do not significantly lower LDL-C."

    What small degree of change are you talking about? All the diet studies that were successful reduced trans fat, increased nutrient intakes (typically from fruits, vegetables and n-3 fatty acids), reduced consumption of processed foods and in some weight loss occurred. On the other hand those studies that replaced saturated fat with n-6 oils or simply reduced saturated fat have been miserable failures even though cholesterol was reduced.

    Stains have a ****load of effects unrelated to cholesterol and may reduce oxidation either directly or indirectly e.g. http://www.doiserbia.nb.rs/img/doi/0352-5139/2009/0352-51390910063N.pdf

    Cholestyramine is similar to statins in that it reduces cholesterol by increasing LDL receptor activity thereby increasing lipoprotein clearance which would reduce oxidative stress much like is hypothesized in the study above. Cholestyramine may have an overall antioxidant effect - http://www.ncbi.nlm.nih.gov/pubmed/11476969. This drug is also known to inhibit iron absorption.

    For the rest figure it out yourself. In genetic studies the mechanisms may be different but the end result the same. Figure out the POSCH trial for yourself.

    Since you are the one who finds it necessary to push your views down everyone's throat, it is you who have to show that the benefits are actually due to the concentration of cholesterol.

    HL: "We are also meant to believe that Brown and Goldstein who were awarded a Nobel Prize"

    Brown and Goldstein are bound to the rules of logic and science just like everyone else. I really don't care that they won a Nobel Prize. That's a non-argument.

  19. Z.M.
    Francois: "Desperately trying to convert others to their religion (I call this a religion because they treat it as such). The double standard in article interpretation is rather pathetic."

    Exactly. Why do they find the need to push their views onto others? Obviously no one here is buying it. Richard is like the disciple who spreads his propaganda every chance he gets because of course he is in the possession of the "truth".

  20. Z.M.
    It's funny that these vegans bring up the iron issue because it's possible that iron reduction through phlebotomy (which is the best treatment, not reductions in red meat) may be a far better treatment than any cholesterol lowering can achieve. Sullivan JL wrote on this possibility many years ago - http://www.ncbi.nlm.nih.gov/pubmed/8970483 Unfortunately the full text doesn't seem to be available but I can tell you it's a good read.
  21. Richard Mjödstånka
    ZM,

    one of the leading scholars in clinical CHD research, Evan Stein writes:

    Low-density lipoprotein cholesterol reduction and prevention of cardiovascular disease

    "There was little question after the first major statin trials that the reduction in CVD was related to lipid lowering and was totally consistent and supportive of the lipid hypothesis. However, stimulated by funding from the pharmaceutical industry, in which competition was fierce for market share and was driven mainly by the efficacy of lowering LDL-C levels, manufacturers of less-effective agents for lowering LDL-C levels helped propagate “beyond LDL-C” theories; these theories were that statins reduced CVD events by means other than lipid reduction, often termed pleotropic effects, usually shown in in vitro laboratory studies or small, poorly standardized surrogate marker trials. This belief culminated in an RCT by a pharmaceutical company that was designed to show that more LDL-C reduction with a competitor's statin achieved no greater benefit.13 However, the results of that study clearly and convincingly showed otherwise, with additional reduction in CVD events with the drug that lowered LDL-C levels more. Even with this evidence, and perhaps with an even more powerful statin about to be approved, the investigators suggested that the reduced events were due to pleotropic effects of the more efficacious statin. However, the trial was soon followed up with results from another head-to-head RCT, with the same drug at different LDL-C lowering doses,14 which eliminated the pleotropic potential and rein-forced that lower is better"

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2665973/

    Oxidated LDL is just one form of LDL modification that can be harmful, and very few in the business perceive it as important in the etiology of atherosclerosis anymore. Studies by Frank and Fogelman have demonstrated the generation LDL aggregates in the subendothelial space. Aggregation does not depend upon prior oxidative modification. Quite a distinct mechanism by which LDL uptake into the macrophages can be accelerated and can perhaps initiate the fatty streak lesion.

    Stephan Guyenet's colleague, Jay Heinecke, from the state of Washington happens to be one of leading HDL researchers in the world and has expressed skepticism over the whole oxification story:

    Lipoprotein oxidation in cardiovascular disease: chief culprit or innocent bystander?
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118281/

    As the IMPACT models throughout the Western world have shown, once SFA consumption goes down, so does the CHD mortality. This applies also to Eastern Finnish cohort of the 7CS which consisted of lean and fit timber men with no obesity nor diabetes. These people on a butter fat diet had the highest SFA intake in the world and the highest CHD mortality in the world (1960s). Toothless trials performed on people with existing coronary heart disease does not change this fact.

    Why have total cholesterol levels declined in most developed countries?
    http://www.biomedcentral.com/1471-2458/11/641

  22. FrankG
    Funny how whenever Sneakie Dickie Pee Pee cites a source they are a "world renowned leading expert authority in the field" but any scientist or researchers with whom he disagrees are charlatans, shysters, denialists etc.. etc... etc... :-P

    Truth be damned... must win the internet at any cost! LOL

  23. Paul
    Let me repeat myself from the other topic (after all in research we repeat i.e. we search and research)

    http://www.youtube.com/watch?v=TjxZ6MrBl9E
    P.S. If Stephan Guyenet was a geologist he would be a staunch supporter of "Young Flat Earth Facts". I am sure there are aplenty

    Reply: #74
  24. FrankG
    Well sure... and obviously the consensus, the weight of observation, ought to convince us that the Earth is stationary, with everything else revolving around us. I mean just stand outside and look for a while. If the Earth was really spinning on its axis and orbiting the Sun, while our entire Solar System moves at incredible speed in an outer spiral arm of the Milky Way galaxy, which is itself rushing though the Universe... how could we even be standing up? And just watch the Sun as it rises in the East and sets in the West.. obviously it is moving around us. Duh! :-)

    Once again Sneakie Dickie Pee Pee -- or whatever alias you may try to hide behind this time... it is NOT about consensus, NOT about having "authority", NOT about having the "weight of evidence" AND is is certainly NOT about having blind faith in anything, least of all the slimy weasel words of an obviously untrustworthy pseudonym on the internet. It IS about having the right evidence; that which makes the most sense of everything we know.

  25. Murray
    "The louder he talked of his honor, the faster we counted our spoons." Ralph Waldo Emerson

    FrankG, the more people argue from credentials, the more skeptical I become. You and I seem united in that we have only one interest in this--our own health, the health of our family and the health of as many others as might seek counsel. I get that a lot because people noticed my improvement in health since going from no processd food low fat to no processd food high fat low carb. Almost all my peers are greying, my greying reversed. Almost all my peers are getting bellies despite working out over a hour per day five days per week, they all ask me what i do. I was getting cracking in teeth but the cracking has healed and my teeth are hardening to the point my dentist says mine are now rock hard (after learning about vitamin K2). I used to need seven plus hours sleep, now five is plenty and I feel energized in the morning. My flexibility has increased. I could always touch my toes but now I can put my head between my legs, thanks to more flexible arteries. My blood pressure dropped from 120/90 to 95/65. My skin health improved noticeably. When I skip dinner, burning ketones all night, next morning my wife invariably comments my skin feels like a baby's. I have enhanced endurance, swimming 6 km around islands at the lake. I can go on.

    The point is, the engineering (change diet to high fat low carb) has produced a plethora of health improvements with zero detected downsides in terms of outcome, as opposed to hypothesized risk factors. This engineering success, according to dogma (the sad state of science) was not supposed to happen. That tells me the science is wrong. The paradigm is faulty. The engineering the dogma science has produced has yielded a diabesity epidemic. The direction of my thinking has reversed. What science can explain why LCHF engineering is so successful, at least for a good number of people?

    Hearing the same old paradigm being repeated, citing unremarkable studies, does not advance thinking. It fails to explain why LCHF is manifestly successful. Until it does that, it has little credibility, beyond the starry credentials of the rent-seeking courtiers of the status quo. And the louder they talk of their honor, the harder we look for science in other fields and for emperical anecdotal experience to help explain what is actually happening.

    The entire situation resembles Lorenzo's Oil. Even worse, it seems.

  26. Z.M.
    Richard, first of all the concentration of cholesterol has never been isolated so whatever Evan Stein or Heinecke says are their opinions, not fact. Evan Stein tries to support his case by referencing the LRC-CPPT, which was rightly criticized for its use of a one-talied test and cholestyramine has other effects as I described above. Why on earth does he mention ezetimibe, which so far has been a failed drug? Exactly how does his paper refute the evidence from both animal and human studies demonstrating that the pleiotropic effects of statins may indeed be very important? and the evidence keeps growing - http://www.esciencecentral.org/journals/JVMS/JVMS-1-e101.pdf

    As far as Heinecke goes, he focuses on probucol. However the evidence for oxidative stress goes far beyond probucol. He mentions a few interesting trials in his paper so I'm glad you brought this up:

    In the FAST trial Pravastain reduced LDL by 35.9% and probucol by 28.6% but both reduced IMT to a similar extent. In the control group LDL fell 8.5% but IMT increased. The authors stated "probucol therapy retarded the progression of IMT, independent of its LDL or HDL cholesterol-lowering effect in the present study".

    Heinecke mentions AGI-1067. There was a trial done on AGI-1067 (http://www.ncbi.nlm.nih.gov/pubmed/17214993). Although it didn't quite achieve significance (p = 0.12 ) verses placebo, a statistically significant plaque regression in the AGI-1067 group from baseline was observed even though it raised
    LDL cholesterol by 4%.

    Impact models cannot prove anything. Waste of time.

  27. FrankG
    Very well put Murray. Thanks.
  28. Nan
    Richard M lurks here because he is a closeted LFLC-er.
  29. Kaos42
    WHO about to announce that meat is just as cancerous as smoking, arsenic, asbestos and alcohol, all have the 5 star rating as being very likley to cause cancer in those who are exposed to it or consume it.

    http://www.cbc.ca/news/health/meat-cancer-1.3285858

  30. Kaos42
    " ... a landmark new article in the New England Journal of Medicine shows that choline in eggs, poultry, dairy and fish produces the same toxic TMAO as carnitine in red meat, which may help explain plant-based protection from heart disease and prostate cancer. "

    https://www.youtube.com/watch?v=x3yp0oTd1YA

  31. Kaos42
    "Cancer may use a molecule found in animal products to trick our immune system into feeding it with inflammation. Neu5GS is a molecule in meat that human tumors may use to facilitate growth. It's one of the most fascinating topics in modern day nutrition"

    https://www.youtube.com/watch?v=D42GJsV-2I4

  32. Kaos42
    The longest living and healthiest communities on Earth either eat very little meat or not meat at all.

    http://bluezones.com/

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