Knockout. Much appreciated.
Good work. Her grant list shows she has received hundreds of thousands of dollars from the Cattleman's Beef Association, and from Dairy Management. Too bad the NYT didn't require a disclosure of financial ties.
In March 2010, Dr. Campbell gave a less than one star rating to the "New Atkins Diet" book. 2690 posts later, last night, I linked, plus quoted, your excellent blogs countering the animal-based low carb nonsense diet. It would be good to have votes for "Useful" for the counters. Here is the location:http://www.amazon.com/review/R2W7KWZKQY6BGJ/ref=cm_cr_rev_detup_redir?_encoding=UTF8&cdForum=FxZJ813G2J60B7&cdPage=1&asin=1439190275&store=books&cdSort=newest&cdThread=TxCB0L17B0KXSQ&newContentID=Mx14DLVPRU1D8UH#Mx14DLVPRU1D8UHThe "Gang of Nine" supporting the Atkins/Paleo/Etc. diet are a mean-spirited lot. "D.M." and I continue to post because the arguments against low carb-high fat/high protein are compelling. You are going in depth in providing further justification for plant-based nutrition as optimal for human health.Yes, you can reveal who you are. Thanks for the solid material! I have 10 years of good vegan nutrition results. Some education items are posted at http://chinaoneorcutt.com
I read the comments that you and D.M. post from time to time and understand what you are up against. Keep up the good work.
Sorry, that should have been WSJ, not NYT.
Do you have any proof for this? Where van I find it?
Scroll down to the grants section from the following link.http://www.cag.uconn.edu/nutsci/nutsci/hpg/nrr.html
You are doing a fantastic work. A much appreciated addition to the dietary blogosphere. A big thank you!
I wish your blog entry could only generate as much traffic as Minger's. I guess quality is the trade-off for confirmation bias. Keep up the good work!
Prediction: high LDL on a diet of refined carbohydrates, with all their associated toxins (both natural and added), is BAD whether you eat meat or not.high LDL on a diet free from refined carbs, grains and toxins is meaningless with regard to CVD risk and protective against cancer and sepsis.You are mistaking two different things which give the same sign.A knock on the door from the Gestapo is not the same as a knock on the door from the Jehovah's Witnesses.Low Serum LDL Cholesterol Levels and the Risk of Fever, Sepsis, and Malignancyhttp://www.annclinlabsci.org/content/37/4/343.fullLipid lowering therapy of serum LDL cholesterol (LDL) has proved beneficial in reducing cardiovascular morbidity and mortality. Lately the recommended target LDL level in very high risk patients was reduced to <70 mg/dl, raising the question of what the price of such a low level will be. To elucidate this concern, we investigated the associations of low serum LDL cholesterol levels (≤ 70 mg/dl) and the incidences of fever, sepsis, and malignancy. Retrospective analysis of 203 patients’ charts was carried out. Patients were divided into 2 groups: Group 1 (n = 79) had serum LDL levels ≤ 70 mg/dl, while Group 2 (n = 124) had levels >70 mg/dl. The first group demonstrated increased odds of hematological cancer by more than 15-fold (OR 15.7, 95% CI 1.78–138.4, p = 0.01). Each 1 mg/dl increase in LDL was associated with a relative reduction of 2.4% in the odds of hematological cancer (OR 0.976, 95% CI 0.956–0.997, p = 0.026). Low LDL levels also increased the odds of fever and sepsis between the groups (OR 5.3, 95% CI 1.8–15.7, p = 0.02). In summary, low serum LDL cholesterol level was associated with increased risks of hematological cancer, fever, and sepsis.Hey, it's your body man, I guess you can choose the way you want to go. No-one is immortal, that's cool.
@George Phew....cholesterol denialist confuse the cause and effect. Try reverse Causation. The idea that physiological cholesterol concentration, the levels observed in free ranging mammalians, healthy neonates and people in socities where chronic disease is near absent, would cause cancer is really far-fetched. Campbell & Junshi (1994) reported that elevated serum cholesterol concentrations within a population with low-cholesterol as a baseline was a chief correlate to all diseases of affluence (p = 0.01) including cancers."These findings suggest that even small intakes of foods of animal origin are associated with significant increases in plasma cholesterol concentrations, which are associated, in turn, with significant increases in chronic degenerative disease mortality rates".http://ajcn.nutrition.org/content/59/5/1153S.abstract?related-urls=yes&legid=ajcn;59/5/1153SMoreover, LDL -cholesterol is identified as the causal factor influencing coronary artery disease based on multiple lines of evidence. There's absolutely zero evidence showing that the risk associated with elevated LDL could be offset by choosing a diet free of refined carbohydrates. In fact such postulation seems ridiculous given the data at hand.
In other words, the negative effects CAUSED by elevated LDL cholesterol are likely to accrue independent of the scheme used (carbohydrate deprived athrogenic diet, LDL receptor inactivity, etc).
@Peter'..There's absolutely zero evidence showing that the risk associated with elevated LDL could be offset by choosing a diet free of refined carbohydrates. ..'So your idea is that elevated LDL is caused entirely by eating animal products? Deficiencies of nutrients removed from refined carbs plays no role at all? Well you are in good company. I have corresponded with both Colin Campbell and Richard Peto about this and it seems they have absolutely no idea about the role of various minerals in heart disease. The literature on this subject is enormous. If I were them I'd be pretty embarrassed.
I provided evidence from over 100 randomized controlled trials demonstrating 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. I further provided evidence from very large genetic studies demonstrating virtually the exact same thing and that the benefits of lowering LDL cholesterol are largely independent of the mechanism in which LDL is lowered.It is important to take into account that pre-contact Inuit and nomadic Kirghiz plainsmen who subsisted primarily on organic animal foods and had little or no access to refined foods developed severe premature atherosclerosis. Furthermore, it has been observed that among free-ranging non-human primates consuming only foods found in their natural habitat, higher cholesterol concentrations have been associated with atherosclerosis. Your prediction is merely wishful thinking and endangers other uninformed people.I also demonstrated that statins do have certain dangerous side effects, but there is scant evidence for the specific side affects mentioned in this small observational study you cited. For example the Cholesterol Treatment Trialists’ Collaboration including 27 randomized trials with >174,000 participants found that statins had no effect on the incidence of, or mortality from, hematological cancer. This suggests that findings from this observational study that you cited may have reflected reverse-causation, such as an undiagnosed cancer causing a reduction in cholesterol levels.
The National Cholesterol Education Panel are FRAUDS who hold stock in statin drug companies ( Dr. Berz) and get payments anywhere from $ 100,000 to a MILLION dollars such as Dr. Scott Grundy.Eight our of the nine have DIRECT ties to statin drugs pharmacuetical companies.They set arbitrary invalid guidelines. THEY MUST BE FIRED IMMEDIATELY.Atherosclerosis does NOT form uniformly, NOR does it for "willy nilly" WE ONLY see it at KINKSA and areas of DAMAGE to the artery. The cholesterol hypothesis has major problems.
The National Institutes of Health came to the conclusion that total and LDL cholesterol is causally linked to coronary heart disease in 1984, at a time when the statin industry was virtually non-existent. These conclusions cannot be explained by conflicts of interest.If you are suggesting that virtually all the major health authorities are participating in some worldwide conspiracy then cite quality studies from peer review journals that challenges evidence from over one hundred randomized controlled trials. Imaginary science, denialism and spam (that you post elsewhere as well) will not be tolerated here.
@Healthy Longevity Wonderful stuff. I am not entirely sure about the pre-contact Inuit. Yes it seems there were individuals with atherosclerosis, you gave us a picture. But how common was it? I would like to think it was very common, because otherwise I can't understand how they could eat such a lot of meat and not get iron overload. But there are accounts of them being very healthy. For instance 'The Eskimos are also exceptionally healthy. "The fact that the Eskimos of this polar tribe have such excellent physique, hair, and teeth, and such superb health without any trace of scurvy, rickets, or other evidence of malnutrition," write McCollum and Simmonds, "is interesting in the light of their restricted and simple diet."'It is also interesting as a counterweight to Hindhede and other nutritionists who plump for the excellent lacto-vegetarian diet. There are other excellent diets, and the wholecarcase one of the polar Eskimos is one of them.' - The Wheel of Health (1938), Chapter 6
In addition to this mummy dating back 1,600 years, atherosclerosis has also been observed in a number of Eskimo mummies dating back between the 14th and 18th century. For references and more details on atherosclerosis and other chronic and degenerative diseases in the pre-contact and early contact Eskimo’s please see my post here.In regards to your hypothesis about iron overload, yes there is evidence that iron aggravates atherosclerosis, but it is not required to produce experimental atherosclerosis, nor does there appear to be sufficient evidence that iron overload alone can induce experimental atherosclerosis. The "materia peccans" for the induction of experimental atherosclerosis is dietary cholesterol, which can induce atherosclerosis in virtually any animal model that it elevates serum cholesterol in, even when the elevation is considered to be small. I briefly reviewed this here. Therefore in regards to atherosclerosis, the studies on pre-contact and early contact Eskimo mummies merely demonstrate what was to be expected, although findings of iron deficiency anemia are surprising.
@Healthy LongevityThanks, that's very helpful indeed. Your Zimmerman paper has convinced me.Do you know whether cholesterol that hasn't been oxidised can cause atherosclerosis? My impression is that it's oxidised cholesterol that's the problem, and that it gets oxidised with the help of free/loosely bound iron. Yes, anemia seems to be very common among today's Inuit and I think it cannot be due to iron deficiency. In China (Jiangsu province) anemia is not associated with a low iron intake but a low magnesium intake. Manganese deficiency is also supposed to cause anemia, and I think this is the most likely explanation for Inuit anemia. Meat is very low in manganese and so are the refined foods they now eat. I suspect manganese deficiency may also be the explanation for atherosclerosis and osteoporosis in Inuit mummies.You will be aware that lots of people think iron deficiency was common among ancient people because of porotic hyperostosis/cribra orbitalia in their skeletons. Have you seen the work showing these disorders could not have been due to iron deficiency?'The causes of porotic hyperostosis and cribra orbitalia: a reappraisal of the iron-deficiency-anemia hypothesis.'http://www.ncbi.nlm.nih.gov/pubmed/19280675
My only comment is THANK YOU FOR YOUR EFFORTS!!!
It is highly unlikely that only oxidised LDL-C can induce atherosclerosis. Meta-analyses of randomized controlled trials of various different lipid modification intervention’s controlling for non-lipid effects of specific drug specific and mendalian randomization studies of various different genetic polymorphisms have generally shown consistent reductions in the risk of CHD per unit lower LDL-C despite lowering LDL-C through a number of different mechanisms. Here is an interview with SteinbergPasswater: Is it accurate to say that only oxidized-LDL starts the plaque process?Steinberg: No, it seems to me very likely that other modified forms of LDL are involved in plaque formation. What we know so far is that the use of antioxidants can decrease the rate of progression of lesions by 50-80%. That would speak to a major involvement of oxidation, but other things can also lead to foam cell formation. Studies by Dr. John C. Khoo in my laboratory have shown that aggregation of LDL with itself markedly increases the rate of uptake by macrophages.  The uptake in that case occurs by way of the native LDL receptor, not the acetyl LDL receptor or oxidized LDL receptor.Studies by Drs. J. S. Frank and A. M. Fogelman at UCLA have demonstrated the generation LDL aggregates in the subendothelial space.  Aggregation does not depend upon prior oxidative modification. So here is a quite distinct mechanism by which LDL uptake into the macrophages can be accelerated and can perhaps initiate the fatty streak lesion.Studies by Dr. Joseph L. Witztum and others in our laboratory have shown that minor modifications in the structure of LDL can render it immunogenic. Autoantibodies against oxidized LDL have been demonstrated in rabbits and in humans as well. Therefore, a complex of a modified LDL particle and an antibody against it can be taken up into macrophages by way of a completely different receptor, the receptor for immunoglobulins (the FC receptor).So, there are at least two or three alternative modifications of LDL that could account for foam cell formation. These have not yet been studied in vivo as intensively as oxidative modification, and so we are not in a position to say with any confidence how important they may be.http://www.healthy.net/scr/interview.aspx?Id=197There are over 100 hundred experiments demonstrating that dietary cholesterol induces experimental atherosclerosis in a variety of species, including non-human primates. This persisted even when researchers made sure that micronutrient intake requirements were being met. Intake of dietary cholesterol is a much more plausible explanation as to why the pre-contact Inuit/Eskimo developed atherosclerosis. Please let me know if you are aware of any studies where micronutrient deficiencies alone were adequate to induce experimental atherosclerosis.
@Healthy LongevityYes, copper deficiency will do it. Cholesterol feeding actually induces copper deficiency, according to Leslie Klevay. Here's what he said about it in 2010. 'That cholesterol feeding can induce copper deficiency has been confirmed several times (22–24, 28, 29, 31) since the phenomenon was reported two decades ago (16). ...Metabolism of cholesterol and copper were linked in 1973 (17); hypercholesterolemia from deficiency has been confirmed many times (7, 12, 20, 27, 30). Hypertriglyceridemia also occurs (1, 26, 27).'http://ajpendo.physiology.org/content/298/1/E138.shortHere's his ref 23: 'Dietary copper supplementation reduces atherosclerosis in the cholesterol-fed rabbit'http://www.ncbi.nlm.nih.gov/pubmed/10487484?dopt=AbstractAnd here's a paper about what copper deficiency does.'Marginal copper deficiency and atherosclerosis'http://www.ncbi.nlm.nih.gov/pubmed/11314977AbstractCopper is an essential trace element in the maintenance of the cardiovascular system. Copper-deficient diets can elicit, in animals, structural and functional changes that are comparable to those observed in coronary heart disease. In this study, the effect of dietary-induced copper deficiency on aortic lesion development was measured by quantitative image analysis in C57BL/6 mice that are susceptible to diet-induced aortic lesions. The diets administered were severely copper deficient (0.2 mg/kg diet), marginally deficient (0.6 mg/kg diet), or copper adequate (6.0 mg/kg diet). Similarly, increased aortic lesion areas and elevated serum cholesterol were demonstrated in both deficient groups, compared with the copper-adequate group. Evidence for graded differences in copper status among the dietary groups was shown by the dose-response increase in liver copper concentration, copper-zinc superoxide dismutase and cytochrome-c oxidase activities, together with serum caeruloplasmin oxidase with increasing intakes of dietary copper. Despite the difference in copper status between the copper marginal and severely deficient groups, similar lesions found in both groups of mice suggest a threshold effect of copper deficiency on lesion formation.
Yes, these studies show that copper deficiency can aggravate the atherosclerosis process, at least in certain animal models, but do not necessarily demonstrate that copper deficiency by itself can actually initiate the atherosclerosis process without cholesterol feeding or using rodents that are genetically prone to atherosclerosis. Feeding 43µg/kcal cholesterol to rhesus monkeys receiving micronutrient supplements would unlikely have resulted in copper deficiency, yet it resulted in the induction of significant amounts atherosclerosis in a period of only 18 months. It is therefore unlikely that copper deficiency is the only or primarily mechanism by which cholesterol feeding induces experimental atherosclerosis, in particular in the non-human primate model.Yes, micronutrient deficiencies are a cause for concern, but it would take a leap of faith to assume that sufficient intake of micronutrients will undo all the harm caused by dietary cholesterol and other disease promoting dietary constituents. Care also needs to be taken to ensure that copper is not consumed in excess due to the adverse effects, such as being a possible risk factor for Alzheimer’s disease.
How do you know the cholesterol fed to the monkeys wasn't oxidised? My understanding of the literature is that it's either oxidised cholesterol that's the problem or a deficiency of antioxidant nutrients. Same thing really.BTW it's copper deficiency that's the problem in Alzheimer's. It looks like the copper gets stuck in lysosomes and can't get to where it's needed. Intracellular trafficking is dependent on an enzyme called Class III PI3 kinase or Vps34, which in vitro will not work without manganese. This enzyme also controls autophagy, whose failure is now thought to be the ultimate cause of neurodegenerative diseases like Alzheimer's. Meat is very low in manganese and most or all of it gets removed from refined carbs. In other words, Alzheimer's is arguably caused by a diet of meat and refined carbs. Not excess copper.
@Healthy LongevityI forgot to comment on what you said about LDL aggregation, sorry. I looked up Khoo's work and it seems LDL aggregates when its hydrophobic core is exposed. If this can happen without oxidation I think there would have to be some other source of instability. Could be manganese deficiency. '...Because manganese is involved in the activation of glycosyl transferases (13), glycosylation of VLDL may be impaired. ...Manganese may also be essential to lipoprotein structure (14) due to its high affinity for complexing with the polar heads of phospholipids, thereby stabilising the lipoprotein particle (15). ...'http://www.ncbi.nlm.nih.gov/pubmed/6822906
You need to follow similar changes in LDL from more than one type of diet, then see whether these different diets have the same effect on disease. This has never been done in any study I've seen.In which case, you're just guessing when you extrapolate from studies to actual diets. The Rose Corn oil study, prudent diet study, and Israeli paradox all illustrate that HOW LDL is lowered may make more difference than WHETHER it is lowered or not.http://www.ncbi.nlm.nih.gov/pubmed/8960090?dopt=Abstract
Such postulation is not addressed at all by the data at hand. "free ranging mammalians, healthy neonates and people in socities where chronic disease is near absent" eat diets free of refined carbohydrates.Campbell is comparing high-carbohydrate diets; there was no low-carb or even grain-free cohort in the China study.
In 1908, Williams referred to the cancer rates of a nomadic population that lived predominantly or organic pasture raised animal foods:“Cancer is commoner in Argentina which comprises the pampas region inhabited by the Gauchos, who for months subsist entirely on beef, and never touch salt than in other parts of South America. On the other hand, among the natives of Egypt, who are of vegetarian habits, and consume immense quantities of salt, cancer is almost unknown”Similar to the nomadic Kirghiz plainsmen example I provided, this should satisfy the definition of a comparison between a carbohydrate restricted diet consisting of predominantly organic pasture raised animal foods and a carbohydrate rich diet high in grains, in particular wheat which was the Egyptian staple.
As dietary cholesterol is prone to LDL oxidation, this could in part explain why it is atherogenic, however it is likely that any oxidation caused by the very small amounts of dietary cholesterol fed to these monkeys would have been mitigated by the antioxidant vitamin supplements provided.1 2 Blood cholesterol is associated with atherosclerosis in free-ranging primates even though they are known to consume very large amounts of antioxidants including manganese, suggesting the likelihood of an independent effect of blood cholesterol.3 4Several studies have also found suggestive evidence that excess copper consumption increases the risk of Alzheimer’s and other degenerative diseases disease.5 6
But do we know whether the cholesterol was oxidised before the monkeys ate it? The authors don't seem to have taken precautions to prevent this. And your first reference says 'It seems likely that it is oxidized cholesterol in the diet that is harmful.'If blood cholesterol is associated with atherosclerosis even in wild animals, might it not mean that the liver is using lipoproteins to transport fat-soluble vitamins to the lesions to help them heal? There is only one study showing high copper consumption associated with cognitive decline, and you need to look at it very carefully. The authors did not 'subtract from baseline'. Their Table 1 shows cognitive function in relation to copper intake, and you may be surprised to hear that the highest quintile of copper intake had a cognitive score SIX TIMES HIGHER than the lowest quintile. http://www.ncbi.nlm.nih.gov/pubmed/16908733I have emailed the lead author about this, and so has a senior Alzheimer researcher I know who was as shocked as I was.
I read a information about this from one of health related site-high cholesterol can cause a buildup of plaque along the arteries that can cause thickening and hardening of the arterial walls, constricting the flow of blood.http://reduce-blood-pressure.gnbo.com.ng/
In the article about Nancy Rodriguez debating Colin Campbell, you've misspelled her name several times in the first two paragraphs. Misspellings do not add to your credibility.
Thanks for informing me of this. I hope you at least found the references to be informative.
One of the big differences in food consumption in Europe in WW2 was a decreased reliance on wheat as this was earmarked for occupying forces and exported to Germany (or, in Britain's case, imported in valuable shipping). The cause of celiac disease was first identified in the Netherlands after wheat supplies were resumed. Decreased butter consumption was often compensated for by the consumption of fat and offal that was previously discarded. Many more sick people died of respiratory diseases in occupied countries during the war, skewing any reportage of other diseases.
I have already cited several pieces evidence which you appear to be ignorant of suggesting that the decrease in cardiovascular disease mortality in a number of nations in during the World Wars was likely real and not obscured by deaths from other causes. In Sweden the decrease in all-cause mortality demonstrate that the observed decrease in cardiovascular mortality was likely real. As I stated:”In Sweden where mortality from infectious diseases actually decreased during the war, there was a record decline in both cardiovascular disease and all-cause mortality during the war years when animal food intake decreased”In Sweden, intake wheat did not appear to have decreased, but the extraction rate actually increased during the war years. In Norway evidence from changes in post-operative thrombosis demonstrate that the observed decrease in cardiovascular mortality was likely real. As I stated:”Minger appears to be either ignorant or unaware that Strom and Jensen provided additional data demonstrating that from over 15,000 operations carried out in Norway that were complicated by danger of thrombosis, the same surgeons found that the occurrence of these complications declined significantly during the period of deprivation of foods rich in animal fats, which then sharply increased after the resumption of intake. These findings provided strong evidence of actual improved cardiovascular health in Norway during the period of deprivation of animal foods.”In Norway intake of bread was actually increased, especially from black-market sources.In Finland and Germany changes in severity of atherosclerosis at autopsy demonstrate that the observed decrease in cardiovascular mortality was likely real. As I stated:”Other researchers also observed a striking decline in advanced atherosclerosis in Finland and Western Germany during the periods of deprivation of animal foods that returned to near pre-war levels after increasing intake.”In Finland the wartime diet was based around grains and potatoes.It is clear from all the dietary surveys I cited from these nations that the decreases in cardiovascular mortality during the war period paralleled the decrease in intake of animal protein, saturated fat and cholesterol. In regards to people with gluten intolerance, it is clear that they should refrain from consuming gluten rich foods, but this does not mean that they should be replacing such foods with the cholesterol laden foods you appear to be advocating.References can be found from the post in link below: http://www.healthylongevity.blogspot.com/2012/08/forks-over-knives-and-healthy-longevity.html
I wonder if the improvement in cardiovascular health in wartime Norway might have been due in part to the reduction in refined carbs?'Dental caries in Norwegian children during and after the last world war'http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2081187/?page=1'...the caries frequency decreased steadily from year to year during the war. ...From 1946 the caries frequency has increased again...'Nearly all food articles were rationed. ...Meat and pork were rarely obtainable on coupons. ...The flour was of 95% extraction... As a consequence of strict rationing, sweet marmalade, pastry, cookies, candy and other sweets were very seldom to be had during the war. ..'
Sugar and tobacco consumption significantly declined in both Denmark and the UK, but there were no significant changes in the consumption of cholesterol laden foods, and coincidentally no significant changes in the rate of cardiovascular disease mortality. In Sweden it appears that sugar intake did not appreciably decline until towards the end of the war, after the significant decline in cardiovascular mortality had already occurred. (See my post for references)Obviously the changes in cardiovascular mortality during the wars was likely multifactorial, and refined carbohydrate rich foods should not be made into a scapegoat (which at least you do not seem to be implying), but should be treated as just one factor of many.
Maybe the Gauchos had low cholesterol. What does Williams say?None of this addresses the effect of high LDL on refined carb diets. It's not cholesterol denialism to say that such high LDL might be harmful. Or is it? Who knows what the lipid hypothesis said today.
Yeah I suppose tobacco was not restricted in Sweden due to the generosity of the blockading powers.Tobacco was restricted everywhere, and this alone gives the first significant health input.The second is that rationing and full employment meant that the very poor often had enough to eat for the first time ever. What food there was more evenly distributed, this was definitely the case in Britain. The lower cvd rate could represent those very poor people who finally got enough protein to keep them alive.Remember, the previous, baseline stats were the great depression, high unemployment.
About the nomads - why might a diet of milk be harmful?Check out galactose. High serum galactose levels throughout one's life may be even more harmful that high glucose or fructose levels.http://www.ncbi.nlm.nih.gov/pubmed/19859980In most organisms, productive utilization of galactose requires the highly conserved Leloir pathway of galactose metabolism. Yet, if this metabolic pathway is perturbed due to congenital deficiencies of the three associated enzymes, or an overwhelming presence of galactose, this monosaccharide which is abundantly present in milk and many non-dairy foodstuffs, will become highly toxic to humans and animals. Despite more than four decades of intense research, little is known about the molecular mechanisms of galactose toxicity in human patients and animal models. In this contemporary review, we take a unique approach to present an overview of galactose toxicity resulting from the three known congenital disorders of galactose metabolism and from experimental hypergalactosemia.
Arcus senilis could be this: http://en.wikipedia.org/wiki/Galactosemic_cataractReasons for cancer in gauchos include ulcers from long rides on horseback and similar injuries; these types of injury-related cancers killed Rimbaud and Bob Marley. Also, high UV exposure, smoking patterns, alcohol and its contaminants, or use of the wrong herbs as teas or medicine are other possible non-dietary explanations.In fact, there is no real mechanism for their diet causing the cancer, all we can say is, in the case of the gauchos diet didn't cure cancer.
As I noted in one of my posts:Since 1984 evidence accumulated from over 100 randomized controlled trials of various medical and dietary based lipid modifying interventions has further established 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.http://healthylongevity.blogspot.com/2012/10/diet-blood-cholesterol-blood-pressure.htmlAs noted by Jeremiah Stamler:In fact, the decisive dietary modification for experimental atherogenesis, the sine qua non or materia peccans (Anitschkow's term), is cholesterol ingestion. This has been the prerequisite since the 1908–1912 breakthrough by Anitschkow et al (a centennial anniversary meriting celebration and discussion) in thousands of experiments in mammalian and avian species—herbivorous, carnivorous, and omnivorous—including nonhuman primates. To neglect this fact in a review about humans is to imply that the Darwinian foundation of biomedical research is invalid and/or that there is a body of substantial contrary evidence in humans. Neither is the case. Dietary cholesterol (as well as SFA) adversely influences human serum lipid concentrations, per cited equations. And several prospective epidemiologic studies found direct relations of dietary cholesterol to CHD independent of serum total cholesterol.http://ajcn.nutrition.org/content/91/3/497.fullThis enormous amount of data demonstrates that the severe vascular disease experienced by these nomadic plainsmen at a young age is far more likely the result of their diet that was rich in dietary cholesterol and saturated fat and a poor in minimally processed plant foods.
You cited no references showing that the Gaucho consumed large quantities of tobacco and alcohol well over a century ago when these observations were made. If the Gaucho had the ability to trade for large amounts of tobacco and alcohol it is unlikely that they would have had to subsist entirely on beef for several months at a time.It is clear that a diet rich in red meat and poor in dietary fiber and fruits and vegetables increases the risk of cancer. I already cited data regarding plausible mechanisms as to how red meat increases cancer risk:A number of tightly controlled feeding trials with human participants have established that heme iron from the protein portion of meat increases the production of NOCs (N-nitroso compounds) in the digestive tract to concentrations similar to that found in cigarette smoke, of which most are cancerous. Furthermore, a controlled feeding trial found that NOCs arising from heme iron in meat forms DNA adducts in the human digestive tract, and DNA adducts are a well-established marker of cancer. These findings are consistent with recent meta-analyses of prospective studies that found that intake of both fresh red meat and heme from meat is associated with a significant increased risk of colorectal cancer.Based partly on these lines of evidence, in 2011 the expert panel from the World Cancer Research Fund reviewed 749 publications on colorectal cancer and concluded that there is convincing evidence that both fresh and processed red meats are a cause of colorectal cancer. Furthermore, a more recent prospective study with over 2.24 million men and women found that compared to participants who consumed less than 1 serving per week, consuming 2 or more servings of meat significantly increased the risk of colorectal cancer.http://www.healthylongevity.blogspot.com/2012/08/forks-over-knives-and-healthy-longevity.htmlIt is clear that you are simply making up half of your claims or rely merely on wishful thinking in order to confuse other readers to resort to nutritional stupidity, and demonstrate no interest in considering the evidence from the hundreds of studies that I have cited.As Diethelm and McKee quoted in regards to denialism:The normal academic response to an opposing argument is to engage with it, testing the strengths and weaknesses of the differing views, in the expectations that the truth will emerge through a process of debate. However, this requires that both parties obey certain ground rules, such as a willingness to look at the evidence as a whole, to reject deliberate distortions and to accept principles of logic. A meaningful discourse is impossible when one party rejects these rules.http://eurpub.oxfordjournals.org/content/19/1/2.full
It is clear from numerous dietary surveys that I cited that protein intake either significantly decreased or was largely unchanged in the Scandinavian countries that experienced an observed decrease in CVD mortality. Furthermore I documented a number of populations that consumed significantly lower amounts of protein than what the Scandinavians consumed prior to World War II that had a very low incidence of atherosclerosis, coronary heart disease and stroke. Indeed in Britain during WWII there were no significant changes in intake of cholesterol laden foods, and also no significant changes in CVD mortality.http://www.healthylongevity.blogspot.com/2012/08/forks-over-knives-and-healthy-longevity.htmlhttp://healthylongevity.blogspot.com/2012/11/traditional-diets-in-asia-pacific-and.htmlIt is clear that you have not carefully read my posts and the studies I have cited or that you are just being ignorant.
As Jeremiah Stamler noted:In fact, the decisive dietary modification for experimental atherogenesis, the sine qua non or materia peccans(Anitschkow's term), is cholesterol ingestion. This has been the prerequisite since the 1908–1912 breakthrough by Anitschkow et al (a centennial anniversary meriting celebration and discussion) in thousands of experiments in mammalian and avian species—herbivorous, carnivorous, and omnivorous—including nonhuman primates. To neglect this fact in a review about humans is to imply that the Darwinian foundation of biomedical research is invalid and/or that there is a body of substantial contrary evidence in humans. Neither is the case.1Indeed oxidised dietary cholesterol is a cause for concern, however this alone probably does not explain the consistent findings from hundreds of experiments in which the researchers were not intentionally using oxidized dietary cholesterol, and many such experiments included antioxidant vitamins supplements which would have helped to mitigate such a problem if it existed. The adverse effects of dietary cholesterol may be partly explained by the down-regulation of the LDL receptor.2 3You seem to be suggesting that the association between blood cholesterol and atherosclerosis is caused by reverse causation, and cast doubt on the findings cited throughout my posts from large clinical trials and mendelian randomization studies on humans and experiments in non-human primates which have produced convincing evidence of a causal association between total cholesterol/LDL and atherosclerosis/coronary heart disease. What is your basis for such suggestions? You seem to be suggesting that these cited findings are irrelevant and that the primary cause of chronic diseases is micronutrient deficiencies.One of the reviews I cited also provided evidence that both low and high intakes of copper promote what the researchers refer to as “disease of aging”, such as atherosclerosis.4 Several prospective studies have found that serum copper and copper supplements were associated with an increased risk of all-cause mortality.5 6
Thanks for the link to your Forks Over Knives post, I'd read it before but I needed to read it again. I have to say, your work is very impressive. All I am suggesting is that refined carbs synergise with animal products to cause disease, and that the common factor is minerals. Cholesterol feeding for example causes copper deficiency, according to Klevay. Saturated fat does the same, by inhibiting copper absorption. Beef is very low in copper, and dairy products are even lower, so low that milk has been used in the lab to make animals copper-deficient. Refined carbs have had much or all of their copper removed. So it follows that animal products will act together with refined carbs to cause copper-deficiency diseases, which include cardiovascular disease. Much the same can be said for manganese and magnesium. All three of these metals are higher in plant foods than in animal foods, sometimes much higher, and most significantly, all have their specific antagonists which are very high in animal foods. Iron antagonises manganese, zinc antagonises copper, and calcium antagonises magnesium. The conventional view is that modern diets are too low in iron, zinc and calcium, but in 30 years of studying the biomedical literature I have not found evidence for this, rather the reverse.
I see the denialists and spindoctors have finally found this blog, very good. In his university textbook Stewart Truswell (Cholesterol & Beyond) pretty much closes the whole sugar nonsense case. The evidence linking sugar to CHD is extremely weak, it's ridulous idea that have never even bothered to conduct a trial about. In animal models plain sucrose open the arteries of monkeys. For diabetics table sugar actually improves insulin sensitity. Even cultures with traditionally huge table sugar consumption (Cuba, Costa Rica, Equador) have traditionally displayed low CHD rates, atleast compared to UK & US. PlantyPositive covers in to an extent, slides from Truswells book included. Denialists will look any excuse to keep up with their LDL elevating diet, it must be the sugar, it's the wheat. LOLThe Futility of Cholesterol Denialism, Part 3: A Process of Eliminationhttp://www.youtube.com/watch?v=SD48EGuP0QY&list=PLDBBB98ACA18EF67C&index=4&feature=plpp_video
Yes, serum copper is associated with disease, because copper is sent from the liver to the damaged tissue to help repair it. Yes copper supplements can make animals sick, if the amount is high enough (20mg/day for a rabbit???) and if it's inorganic copper which is a powerful oxidising agent and very toxic. If I might make a suggestion, it would be to read Klevay and not Brewer. Brewer's review has mistakes, which Klevay's work does not.
Your effects are really very appreciable that you wrote beneficiary thing related to traditional diets
Thanks a lot for the very well researched information.I'm German and had the opportunity to visit a lecture of professor zur Hausen, who won the Nobel price in medicine, he is from the university of Heidelberg and afterwards spoke personally to him.He clearly states that there is no doubt anymore in scientific research: it is absolutely clear that read meat consumption promotes cancer.regards Daniel
RED MEAT OF COURSE, sorry.
Charles Grashow, are you trying to say something?
read the article
I did. What are "you" trying to say?
That the diet-heart hypothesis doesn't hold up - for every study you find that "proves" it I can find one that "disproves" it.According to this site with my diet and blood lipid profile I should be dead!!
From your posted link, It clearly states that diet will not reverse Atherosclerosis. Do you believe that? Do you have High Elevated LDL Cholesterol levels?Do you have Atherosclerosis?How do you know that you don't have Atherosclerosis?
Charles Grashow, if you found out today that you had Atherosclerosis, what would you do?
Give me your definition of atherosclerosis and atherosclerotic progression
Charles Grashow, from your posted link, It clearly states that diet will not reverse Atherosclerosis. Do you believe that? You sidestepped that extremely important question. You also ignored my other questions.There's nothing else to talk about. Take care and good luck.
Berkeley Heart Lab test results - blood drawn on 10/18/12TC 242 mg/dLLDL-C 158 mg/dLHDL-C 76 mg/dLTriglycerides 41 mg/dLAp- B 104 mg/dL Reference Range <115 mg/dLLP(a) <2 mg/dL Reference Range 0-30 mg/dLLipid SubClass DetailBerkeley Lab analyzes LDL for 7 sub classes from large buoyant to small denseLDL I, IIa and IIb are considered large buoyant - As a % these 3 totalled 82.5% - LDL I=51.1%, LDL IIa=16.2% and LDL IIb=15.2%LDL IIIa+b, LDL IVa and LDL IVb are considered small dense with IVb being the smallest. As a % these totalled 17.5% - LDL IIIa=11.2%, LDL IIIb=3.8%, LDL IVa=1.8% and LDL IVb=0.7%LDL IIIa+b=15% Reference Range=13.6-43%LDL IVb=0.7% Reference Range=1.7-9.8%LDL IIIa=B = 17.9 mg/dL Reference Range=12.0-32.1 mg/dLLDL IVb=1.0 mg/dL Reference Range=1.5-11.2 mg/dLHDL is analyzed for 5 subclassesHDL2b=34%, HDH2a=24%, HDL3a=20%, HDL3b=14% and HDL3c=8%HDL2b Reference Range 7-30%Collected 10/5/12 - Shiel Medical Lab - day 14 (before Testosterone injection)HA1C - 5.6Fasting Glucose - 100mg/dL Ref Range 65-99 mg/dLEstimated Average Glucose - 114.5 mg/dLLDL-P 1430 nmol/LSmall LDL-P 132 nmol/LHDL-C 69mg/dLTriglycerides 31 mg/dLTrig/HDH ratio - .45LDL-C (Calculated) 199 mg/dLLDL-C (Iranian Formula) 146 mg/dLTC - 274 mg/dLEstradiol, LC/MS/MS - 4 pg/mL S/B <= 29 pg/mLEnhanced Estradiol - 22.7 pg/mL Ref Range <39.8 pg/mLSHBG - 39 nmol/L Ref Range 11 - 80 nmol/L Thyroid PanelThyroxine (T4) - 10.9 ug/dL Ref Range 4.5 - 10.9 ug/dLT3-Uptake - 34.0% Ref Range 22.5 - 37%TSH - 3rd Generation Ultra - 1.47 uIU/mL Ref Range 0.40 - 4.50 uIU/mLReverse T3, LC/MS/MS - 34ng/dL Ref Range 9 - 28 ng/dLT3, Total 81 ng/dL - Ref Range 60 - 181 ng/dLT4, Free 1.43 ng/d/L - Ref Range 0.80 - 1.80 ng/dLVitamin D (25 hydroxy) - 74 ng/dL Ref Range 30 - 100 ng/dLCardiac Homocysteine - 10.0 umol/L Ref Range <11.4 umol/LPSA - 0.42 ng/d/L Ref Range <4.00 ng/dLQuest Diagnostics - collected 10/8/12 (3 days AFTER the testosterone shot)Just to show how different labs get different resultsBerkley Heart Labs TestLDL PAttern Size A (Large)Triglycerides - 41 mg/dLHDL-C 76 mg/dLTrig/HDL ratio .54Apolipoprotein B - 104 mg/dL Ref Range <115 mg/dL
as to your questions - if you mean will a LOW FAT PLANT BASED diet reverse atherosclerosis look at this studyhttp://circ.ahajournals.org/content/121/10/1200.longDietary Intervention to Reverse Carotid AtherosclerosisConclusions — Two-year weight loss diets can induce a significant regression of measurable carotid VWV. The effect is similar in low-fat, Mediterranean, or low-carbohydrate strategies and appears to be mediated mainly by the weight loss–induced decline in blood pressure.DiscussionThe main findings in this study are as follows: (1) Diet-mediated weight loss over a 2-year period induced a significant regression of carotid VWV; (2) carotid IMT and 3DUS VWV changes are mainly predicted by diet-induced changes in blood pressure over 2 years compared with the changes in lipoprotein levels; and (3) all diets provided a similar benefit, suggesting that the low-carbohydrate diet is at least as effective as the others and may be considered an alternative to low-fat and Mediterranean diets. However, our power to detect moderate differences in the effect of the 3 diets was limited.In our intervention trial of 3 popular weight loss diets, moderate weight loss per se, whether from a low-fat, Mediterranean, or low-carbohydrate diet, was the main modifiable predictor of carotid VWV regression among moderately obese individuals, and this effect appears to be mediated primarily by reductions in blood pressure.As in a previous drug study,we found that systolic but not diastolic blood pressure or serum cholesterol was associated with alterations in carotid IMT. Because a significant dose-response relationship was found between the status of hypertension and the severity of carotid atherosclerosis, as measured by thicker IMT, hypertension is suggested to have a major role in the pathogenesis of atherosclerosis.http://stroke.ahajournals.org/content/32/10/2265.fullHypertension Status Is the Major Determinant of Carotid AtherosclerosisA Community-Based Study in Taiwanhttp://www.ncbi.nlm.nih.gov/pubmed/11204308?dopt=Abstract
Charles Grashow. Based on the Study, "Dietary Intervention to Reverse Carotid Atherosclerosis" you just posted, do you believe that a LOW FAT PLANT BASED diet will reverse Atherosclerosis?
Plant Positive has addressed the study you referred to regarding reversal of carotid atherosclerosis:http://www.youtube.com/watch?v=sZAP47e-NPc&list=PLCC2CA9893F2503B5This paper was funded by the Atkins Foundation. The low carb group "were counseled to choose vegetarian sources of fat and protein" and consumed on average only 1281 calories per day. Furthermore, there were problems with the randomization of the participants in a way that would favor atherosclerosis reversal in the low-carb group.
Charles is simply not someone that can be reasoned with. He is a sick minded person who goes around calling vegetarians evil because Hitler consumed less meat than the general German population. This reminds me of what Diethelm and McKee mentioned in regarding one of five characteristics of denilism:“The fifth is the use of misrepresentation and logical fallacies. For example, pro-smoking groups have often used the fact that Hitler supported some anti-smoking campaigns to represent those advocating tobacco control as Nazis (even coining the term nico-nazis)”http://donmatesz.blogspot.com/2012/08/still-not-weaned.html?commentPage=2http://eurpub.oxfordjournals.org/content/19/1/2.full
Assuming that your high TC and LDL-C is not genetic, I assume that you agree that many of the low-carb and Paleo promoters who claim that saturated fat does not raise TC/LDL-C are being dishonest? I also assume that you are already aware that the very high risk people with familial hypercholesterolemia also have mainly large LDL particles? http://www.lipidjournal.com/article/S1933-2874%2811%2900672-6/abstract
That is true. Charles Grashow actually posted a study that proved that a Low Carb VEGAN diet could reverse Atherosclerosis. Sheeeesh :-) I could have told him that :-)
Thanks for the "heads up". I was actually concerned about his unnaturally High LDL levels.
@H-L You said of me"He is a sick minded person who goes around calling vegetarians evil because Hitler consumed less meat than the general German population. This reminds me of what Diethelm and McKee mentioned in regarding one of five characteristics of denilism:“The fifth is the use of misrepresentation and logical fallacies. For example, pro-smoking groups have often used the fact that Hitler supported some anti-smoking campaigns to represent those advocating tobacco control as Nazis (even coining the term nico-nazis)”I simply mentioned that Adolf Hitler was a Vegetarian Megalomaniac Mass Murderer - which BTW is true.@ Goinglite I do not need your concern - How old are you - how much exercise do you get in a typical week - what were the results of your last blood testLet's compareAs to me being a denialist - would that also mean that ALL of the doctors and/or scientists who publish peer-reviewed articles that do not agree with the cholesterol CVD theory that you and other vegans espouse are also denialists??
@Charles Grashow, Do you have High Elevated LDL Cholesterol levels? That is a question that only requires a "Yes" or "No" answer. I did not ask for proof that you have elevated LDL. My main concern is about reversing the #1 Killer, Heart disease. You posted this link - "http://circ.ahajournals.org/content/121/10/1200.longDietary Intervention to Reverse Carotid Atherosclerosis"You clearly provided the proof that a LOW FAT PLANT BASED diet AND a LOW CARB VEGAN diet will reverse Atherosclerosis. I am well aware of that study, but thanks anyway.If I have Atherosclerosis, then I really need to be on a LOW FAT PLANT BASED diet or a LOW CARB VEGAN diet.You have provided the proof that a vegan plant based diet will save lives. Thank you.
It is painly obvious that your comment about Hitler was ill-intentioned. There are many accounts of Hitler consuming meat as well as vegetarian societies being oppressed by the Nazi’s. At the most Hitler could have been considered by todays standards as flexitarian.http://www.vegsource.com/berry/hitler.htmlI certainly doubt the validity of the claims of researchers who suggest that serum lipids, including LDL cholesterol play very little or no role in the development of cardiovascular disease. You seem to be implying that mainly only vegans are in agreement with the lipid-hypothesis (which should be considered separate from the diet-heart hypothesis), and not by the medical community as a whole. Back in 1977 a survey of 193 prominent researchers answered the question “Do you think there is a connection between plasma cholesterol level and the development of coronary heart disease?”. 189 answered yes, 2 no, and 2 were uncertain. Today an even greater % of researchers would probably answer yes.http://onlinelibrary.wiley.com/doi/10.1111/j.1753-4887.1978.tb03753.x/abstract
One thing I am certain of is there are no Clinical Trials that show a reversal of Atherosclerosis based on a High Animal Protein, High Animal Saturated Fat and Low Carb Diet.If you go to a Low Carb Paleo Doctor with Atherosclerosis, ALL he can do is put you on STATINS and various supplements with the target of getting your LDL Level down to 60 mg/dl.Well, with the proper diet, your LDL levels should had been at 60 to 80 mg/dl in the first place.The Cure for Heart Disease is a simple Low Fat Plant Based Diet.In a Land where Heart Disease is the NUMBER ONE Killer, most folks would rather spend their lives RUNNING FROM THE CURE.
http://www.nba.com/lakers/community/1213_fitforlife_featuresKobe Bryant's Diet Helps Maintain Elite Level Of Play"Part of that changed diet and those healthy eating tips come from Dr. Cate Shanahan, a team consultant who has her own practice in Napa Valley. Pasture-fed foods - pasture-grazed beef from a pasture-fed cow, eggs from a free-range chicken (not a cage chicken) - are just some of the main staples of Bryant's diet. Sugars, specifically anything with corn syrup, should be avoided, and the intake of carbohydrates has been scaled down, consumed in moderation."What happens is the athlete consumes one of these products high in carbohydrates and sugar, they get a spike of energy and feel really good," Vitti said. "Your body knows that, sends insulin and then they crash. As soon as they crash, they need another sugar fix, and they're yo-yoing up and down. If we get them off that stuff and get them into more of protein and the right kind of fats, then they'll have a higher level of energy without the lows or the dips."More findings examine the ratio of high-density lipoproteins (HDL's) and low-density lipoproteins (LDL's), better known as "good" cholesterol and "bad" cholesterol, which can be monitored. The common thought was the ratio for of HDL's to be high and LDL's to be low. But according to Vitti, new findings are changing that perception."We're finding out now that a higher level of LDL's, which we thought was bad, doesn't necessarily mean it's bad," he continued, "because within that category, there are good LDL's and bad LDL's. Even though you might have an elevated level of LDL's, it might be the right kind of LDL's."For example, eating fats, when they're the right kind of fats, can be packed with nutrients.""All this fat free stuff and all these things we've been doing has been the biggest proponent of it," Vitti said. "When they strip the fat, they strip all the nutrients with it. We don't necessarily want to stay away from fats, but it has to be the right kind of fat."Vitti acknowledges they have created, not only for Bryant, but also all their players, food groups that are red, yellow and green. The traditional food pyramid is not what they're preaching to the players. In fact, it's the inverse."The current science reverses the pyramid," Vitti said. "The base of the pyramid is on the top. We're not telling them to just eat fat - it has to be the right kind of fat. Pasture-grazed beef and products from that; you can eat butter, but it has to be pasture-fed. Not pasteurized, pasture-fed. There's a big difference. Milk from a pasture-fed cow, cheese from a pasture-fed cow."Altogether, the shift in dietary habits is one of the reasons why the five-time champion has performed at such an effective and efficient level this late into his career. No guard in NBA history has averaged over 15 points in his 17th season or later, but Bryant ranks second in the league in scoring at 29.2 points per game, while also shooting at a 46.5 percent clip."What I've done really is just train really hard and watch my diet," Bryant said. "I think that's the thing that catches guys most. They don't do self-assessing. They feel like they can go out there and do some of the things that they did when they were younger and eat some of the things that they've been (eating) and not accept the fact that what you put in has an impact."
This is not exactly a link to a peer-reviewed journal showing that elevated levels of certain LDL’s are beneficial. This again reminds me of what Diethelm and McKee mentioned in regarding one of five characteristics of denialism:”The second is the use of fake experts. These are individuals who purport to be experts in a particular area but whose views are entirely inconsistent with established knowledge.”I am guessing that Vitti has confused Bryant into falsely believing that his diet is safe, just as you and the rest of the WAPF brigade spam all over the internet trying to confuse the general population.
It's the protocal that participants are asked to consume veggie fats instead of animal fats. Doing otherwise would be unethical. Anyways, as Plant pointed out in the Shai et al study around 30% of the patients in the intervention arm was on blood-pressure medication which have shown to improve carotid thickness status alone. Moreover over 20% of the patients were on statins.
Healthy, please ban Charles Grashow. He is most likely an anti-darwinian, intelligent design -troll. Moreover, it can be legitimately asked whether Charles has the IQ even to make it through high-school. If Charles G was correct and lipid theory was not valid it would follow that: a) Human is the only mammalian specimen in the biosphere that would immune to dyslipidemia, elevation of LDL cholesterol in particular. b) LD-lipoproteins would be the only substance found in the human body that could not cause harm in excess. Makes sense. NOT!
Thanks for your concerns. I am considering allowing the denialists a chance state their opinion but will see that they are banned when they take their denialism too far.
Thanks for adding those points Peter!
@Peterand what are you??
@Healthy Longevity. I just want to thank you for your very detailed and outstanding research. I was a Low Carb Paleo for many years. I am now a vegan. Your research has answered many of my questions. I will continue to promote your blog.
Thanks, I really appreciate your support.
http://www.bmj.com/content/346/bmj.e8707Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysisAbstractObjective To evaluate the effectiveness of replacing dietary saturated fat with omega 6 linoleic acid, for the secondary prevention of coronary heart disease and death.Design Evaluation of recovered data from the Sydney Diet Heart Study, a single blinded, parallel group, randomized controlled trial conducted in 1966-73; and an updated meta-analysis including these previously missing data.Setting Ambulatory, coronary care clinic in Sydney, Australia.Participants 458 men aged 30-59 years with a recent coronary event.Interventions Replacement of dietary saturated fats (from animal fats, common margarines, and shortenings) with omega 6 linoleic acid (from safflower oil and safflower oil polyunsaturated margarine). Controls received no specific dietary instruction or study foods. All non-dietary aspects were designed to be equivalent in both groups.Outcome measures All cause mortality (primary outcome), cardiovascular mortality, and mortality from coronary heart disease (secondary outcomes). We used an intention to treat, survival analysis approach to compare mortality outcomes by group.Results The intervention group (n=221) had higher rates of death than controls (n=237) (all cause 17.6% v 11.8%, hazard ratio 1.62 (95% confidence interval 1.00 to 2.64), P=0.05; cardiovascular disease 17.2% v 11.0%, 1.70 (1.03 to 2.80), P=0.04; coronary heart disease 16.3% v 10.1%, 1.74 (1.04 to 2.92), P=0.04). Inclusion of these recovered data in an updated meta-analysis of linoleic acid intervention trials showed non-significant trends toward increased risks of death from coronary heart disease (hazard ratio 1.33 (0.99 to 1.79); P=0.06) and cardiovascular disease (1.27 (0.98 to 1.65); P=0.07).Conclusions Advice to substitute polyunsaturated fats for saturated fats is a key component of worldwide dietary guidelines for coronary heart disease risk reduction. However, clinical benefits of the most abundant polyunsaturated fatty acid, omega 6 linoleic acid, have not been established. In this cohort, substituting dietary linoleic acid in place of saturated fats increased the rates of death from all causes, coronary heart disease, and cardiovascular disease. An updated meta-analysis of linoleic acid intervention trials showed no evidence of cardiovascular benefit. These findings could have important implications for worldwide dietary advice to substitute omega 6 linoleic acid, or polyunsaturated fats in general, for saturated fats.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2937583/Diet quality and weight gain among black and white young adults: the Coronary Artery Risk Development in Young Adults (CARDIA) Study (1985–2005)Conclusions: Our findings do not support the hypothesis that a diet consistent with the 2005 DGA benefits long-term weight maintenance in American young adults. Greater need for attention to obesity prevention in future DGAs is warranted.http://www.health.gov/dietaryguidelines/dga2005/document/
Please do not use this thread just to dump abstracts of your favorite studies.
@H-LPoint out why these studies are wrong
The following link is a reply to Ramsden’s previous meta-analysis which still largely applies to this recent paper:http://journals.cambridge.org/action/displayFulltext?type=6&fid=8376168&jid=BJN&volumeId=106&issueId=06&aid=8376167&bodyId=&membershipNumber=&societyETOCSession=&fulltextType=LT&fileId=S0007114511004466 "The most important determinant of event reductions was the length of the intervention; and the studies using ALA-rich oil were much longer in duration than the LA-only studies. If only participants who had been on the diet for 1 year or more in the Minnesota experiment were to be assessed, then the ratio of total coronary events was fifty-four in the treatment group and fifty-eight in the control group." "Trans-fatty acids may also play a role – the experimental polyunsaturated fat diet which incorporated soft margarines containing trans-fats would have increased trans-fat intake as was the case in both the Sydney study and the Minnesota study"Here are some replies to Ramsden’s latest paper:http://www.smc.org.au/2013/02/round-up-dietary-fats-and-heart-disease-bmj-experts-respond/"Although dismissed by the authors trans fats are likely to be responsible for the lack of benefit. The margarine would have contained at least 20% trans fatty acids and if the participants were eating 25g/day of margarine then they would be consuming 5g of trans which might represent about 2% of calories. From the Nurses Health study this could reduce heart disease by 40-50% which would almost completely remove the apparent increased risk from the N6 margarines. The more margarine eaten the greater the risk. The test margarine would have mostly supplanted butter rather than other margarines. The fall in total cholesterol seen not only reflects a fall in LDL cholesterol but also a trans induced fall in HDL cholesterol."Although I am not entirely sure whether miracle margarine actually did contain such a high amount of trans fat, Ramsden et al. should have not dismissed the likelihood of a high intake of trans fat in the experimental group. The only biomarker that Ramsden et al. used for linoleic acid intake was a decrease in serum cholesterol, but some of this drop can be caused by trans-fat induced fall in HDL. Ramsden et al. either ignored or tried to downplay the contrasting evidence from prospective cohort studies, animal studies as well as the proved benefits of lowering LDL-C. Studies on non-human primates have consistently shown significant benefits of replacing saturated fat with linoleic acid in preventing and reversing atherosclerosis which would seem to refute Ramsden’s suggested mechanism of linoleic acid having adverse effects on atherosclerosis.
I do find it disturbing to see this Low Carb Paleo pattern of dumping worthless "Studies" in order to create confusion. http://www.bmj.com/content/346/bmj.e8707 was clearly taken apart and debunked by Prof Tom Sanders, Head of Diabetes & Nutritional Sciences Division, King’s College London. (Seehttp://www.sciencemediacentre.org/expert-reaction-to-research-into-dietary-fats-and-heart-disease/)
I have linked to your blog. Let me know if you want me to change the name of the link. Thanks again for your support.
Here is another response to the reanalysis of the Sydney Diet Heart Study: http://www.bmj.com/content/346/bmj.e8707/rr/629609”Participants in the intervention group consumed “Miracle” Margarine, a product based on safflower oil. Hydrogenation of safflower oil itself creates a grainy product low in linoleic acid, so high-linoleic safflower oil margarine products were created by blending liquid safflower oil with another hydrogenated oil stock (3). Miracle Margarine used in the original study was either low in linoleic acid (due to hydrogenation of the safflower oil itself) or the oil was blended with another commercially hydrogenated fat to create a plastic margarine product. An investigation by Bernfeld, Homburger, & Kelley, published in 1962, indicated that the fatty acid composition of most margarines of the time were about 50-60% 18:1 monounsaturated fats (including oleic and trans isomers) and about 20-30% 18:2 linoleic acid, even in those products having high-PUFA claims on the label (4). None of the 22 margarines studied had a majority of fatty acids coming from PUFA. Another report from the same time period indicates that commercially produced hydrogenated fats, like those added to safflower oil to make margarine, were generally composed of about 25-40% trans fats (5). Fatty acid composition of margarines in the 1960s investigation were not comparable to liquid vegetable oil, despite package claims. The only reference supporting the healthful content of Miracle Margarine is a very general press release from the company who made the product (6). It is probable that Miracle Margarine had significant trans fatty acid content.”
That's perfect. Thanks.
@Healthy Longevity. I have a future request. Many Low Carbers with extremely high TC and LDL Levels take great comfort in their Zero Calcium Scores. I think this can be a false sense of security. A Zero Calcium Score does not mean a person does not have Atherosclerosis. (Jimmie Moore brags about his Zero Calcium Score with his TC around 400+) Undetectable Atherosclerosis kills a lot of people. (See http://plantbasedlinks.blogspot.com/2012/12/the-most-dangerous-form-of.html)If you could cover this in the future, I would deeply appreciate it.
Thanks for the links. The low carbers are desperate to find risk factors that their diet does not have an adverse effect on. To the low carbers the only risk factors that they consider important entirely depends on which risk factors their diet does not necessarily have an adverse effect on.
Interesting new study:Diet and risk of chronic diseases: results from the first 8 years of follow-up in the EPIC-Potsdam study."Subjects/Methods: We used data from 23 531 participants of the EPIC-Potsdam study to analyse the associations between 45 single food groups and risk of major chronic diseases, namely, cardiovascular diseases (CVD), type 2 diabetes and cancer using multivariable-adjusted Cox regression...Results: During follow-up, 363 incident CVD, 837 type 2 diabetes and 844 cancer cases were identified. Higher intakes of whole-grain bread, raw vegetables, coffee and cakes and cookies were found to be significantly associated with a lower risk of chronic diseases. Conversely, higher intakes of low-fat dairy, butter, red meat and sauce were associated with higher risks of chronic diseases."http://www.ncbi.nlm.nih.gov/pubmed/23388667
My kind of study :-) Cakes and Cookies :-) Yummy :-)
Stephan Guyenet responds http://wholehealthsource.blogspot.com/2009/07/diet-heart-hypothesis-stuck-at-starting.html1) This person is conflating the effect of PUFA with the effect of SFA. The long-term trials cited in which circulating cholesterol were durably reduced either involved a large increase in linoleic acid intake, or multiple dietary changes besides SFA. There are several long-term trials including the Women's Health Initiative and MRFIT where the expected long-term reduction in circulating cholesterol with SFA reduction was either absent or very small in the absence of a large increase in PUFA (0-3% reduction in TC or LDL).2) This person refers to the meta-analysis of Siri-Tiriano as "misleading". The reality is that the meta-analysis is the same thing anyone would conclude if they read the primary literature, since very few prospective studies have found a direct association between SFA intake and heart attack risk. The counterargument usually offered for the Siri-Tarino meta-analysis is that some of the studies it was based on adjusted for circulating cholesterol ("overadjustment"). However, Siri-Tarino responded to this critique by re-analyzing the data only including the studies that did not adjust for cholesterol, and found the exact same result (which is what one would expect, considering that little or no association is found between diet and circulating cholesterol in these studies). It is a fact that the best observational studies ever conducted have almost all reported no association between SFA intake and heart attack risk. This is frequently muddled by making PUFA-to-SFA ratios and the like, but I find this sort of argument unconvincing.3) This person cites the Health Professionals Follow-Up Study as if it supports the diet-heart hypothesis. Here is one of the key findings of the study:"The results of mutivariate analyses, with or without correction for measurement errors, however, indicated that intake of fiber is more strongly related to risk of coronary disease than intake of saturated fat or cholesterol, and that this largely accounts for the observed association with saturated fat""Benefits of reducing intakes of saturated fat and cholesterol are likely to be modest unless accompanied by an increased consumption of foods rich in fiber"In other words, when you correct for fiber intake, the effect of SFA on heart attack risk basically disappears. Their words, not mine.They analyzed the data in various ways, and after maximum adjustment, they found that SFA intake was not associated with overall heart attack risk or fatal heart attack, and in fact some of the trends were inverse (which would have suggested a protective association if it had been significant). Rather than acknowledge these findings, this person focuses on one single number, which is the barely significant elevated risk of fatal MI in the highest quintile of SFA intake. However, the association between the two variables was not significant overall (p = 0.09). It is therefore not correct to suggest that this paper supports the idea that SFA is associated with heart attack risk, when nearly all of the data it contains do not support this conclusion.
Stephan Guyenet has clearly not considered many of my main points, although he states “That's all I want to write about it for now”, suggesting that there may be more to come.1 In regards to 1)Guyenet ignores one of my main points of my posts in his statement “This person is conflating the effect of PUFA with the effect of SFA.” As I pointed out in my posts, “First, the notion that there exists such a thing as “the effect of saturated fat” is flawed. A lower intake of saturated fat implies an increased intake of some other source of calories to maintain caloric balance. Different substitutions for saturated fat have different effects on risk of coronary heart disease (CHD) and need to be discussed separately.” Guyenet needs to be clear as to which sources of calories he is comparing SFA to. For example, I stated “Metabolic ward experiments have also demonstrated that isocaloric substitution of saturated fat for monounsaturated fat and carbohydrates also raises serum cholesterol but less appreciatively than when replaced for linoleic acid.”Guyenet claimed that the Women’s Health Initiative and MRFIT (and also Lyon Diet-Heart trial in this main post) only reduced serum LDL and total cholesterol in the intervention group by 0-3% “in the absence of a large increase in PUFA”. It appears that Guyenet has not carefully considered the design and findings of these trials.Indeed in the Lyon Diet-Heart trial there was no difference in serum cholesterol even though saturated fat intake was 8% and 11.7% of total calories in the intervention and control groups respectively. However, Guyenet conveniently failed to mention that lipid-lowering drugs were used by 26.5% and 34% in the intervention and control groups respectively.2 According to Guyenet’s hypothesis it would have been expected that serum cholesterol would have been significantly lower in the control group due to a much greater use of lipid-lowering drugs.In the Multiple Risk Factor Interventional Trial (MRFIT) dietary trial, compared to baseline serum cholesterol actually decreased on average by 7.5% in the intervention group. As the MRFIT researchers stated “Participants with lower food record rating scores, which indicate better adherence, demonstrated greater reductions in serum total cholesterol, plasma total cholesterol, and low-density lipoprotein fraction cholesterol determinations on a group basis.”3 Furthermore, MRFIT researchers stated “Comparison with earlier population data suggests that the overall responses to the MRFIT eating pattern were limited by the apparent fact that participants had already made self-initiated changes toward the fatcontrolled dietary pattern before they entered the study.”4 Compared to the control group however, the difference in cholesterol was only 3%. This was partly explained by the control group making voluntary dietary changes in order to improve their lipid profile and thus obscuring the difference between the groups.
The focus of the Women’s Health Initiative (WHI) Diet Modification trial was to determine the effects that lowering total fat intake has on the rates of developing breast and colorectal cancer, not to lower serum LDL and total cholesterol. Furthermore, there was no formal advice to lower saturated fat intake, resulting in only a small decrease in intake and only a small decline in LDL and non-HDL cholesterol. As the WHI researchers stated “The differences in the changes in LDL cholesterol between the DM-I and DM-C groups of 1.2, 2.8, and 0.9 mg/dL after 1, 3, and 6 y were consistent with what would be predicted given the small decline in reported saturated fat intake and an accompanying decline in reported polyunsaturated fats… Changes in LDL cholesterol and non-HDL cholesterol were greater in those who reported lower levels of saturated (P , 0.001) and trans (P , 0.05) fats, and, in the case of LDL cholesterol, had the greatest change in Katan score (P , 0.001).”5I will respond to 2) and 3) soon. However, I would like to note that Guyenet failed to mention anything about Jeremiah Stamler’s meta-analysis which found that SFA intake was associated with a 32% increase risk of fatal coronary heart disease, even though this was based off the same studies that included in the Siri-Tarino et al. meta-analysis that Guyenet is defending.
http://www.nmsociety.org/docs/aboutfat/Skeaff-Dietary-Fat-and-Coronary-Heart-Disease.pdfDietary Fat and Coronary Heart Disease: Summary of Evidence from Prospective Cohort and Randomised Controlled TrialsC. Murray Skeaff Jody MillerDepartment of Human Nutrition, University of Otago, Dunedin , New ZealandThe cohort study endpoints reviewed were CHD death, CHD events, and non-fatal CHD. Cohort studies that did not report a RR associated with intakeof dietary fats were excluded from the meta-analyses. In all cases the differences were not multivariable-adjusted comparisons and therefore subject to potential confounding; accordingly we have presented the results in the supplementary tables but excluded them from this review.Meta-Analysis of Cohort Studies of Total Fat andCHDIntake of total fat was not significantly associated withCHD mortality, with a RR for highest compared with thelowest category of 0.94 (95% CI 0.74–1.18, p = 0.583; fig. 1 ).Intake of total fat was also unrelated to CHD events (RR0.93, 95% CI 0.84–1.03, p = 0.177). Meta-Analysis of Cohort Studies of SFA and CHDIntake of SFA was not significantly associated withCHD mortality, with a RR of 1.14 (95% CI 0.82–1.60, p =0.431) for those in the highest compared with the lowestcategory of SFA intake ( fig. 6 ). Similarly SFA intake wasnot significantly associated CHD events (RR 0.93, 95% CI0.83–1.05, p = 0.269 for high vs. low categories). Moreover,there was no significant association with CHDdeath (RR 1.11, 95% CI 0.75–1.65, p = 0.593) per 5% TEincrement in SFA intake ( fig. 8 ).Conversely, high compared with low PUFA intake was not associated with CHD events (RR 0.97, 95%CI 0.74–1.27, p = 0.825, for high compared with low category).A 5% incremental increase in PUFA intake wasassociated with a significantly lower risk of CHD events(RR 0.84, 95% CI 0.70–1.00, p = 0.049), but not with CHDmortality (p = 0.669; fig. 14 ).
Randomised Controlled Trials of Dietary Fat and CHDMeta-Analysis of Randomised Controlled Trials of Fat-Modified Diets and CHDThe results of the meta-analyses showed that the RR of fatal CHD was not reduced by either the low-fat diets(1.00, 95% CI 0.80–1.24, p = 0.317) or the high P/S diets(0.84, 95% CI 0.62–1.12, p = 0.867), respectively ( fig. 20 ;21 ). High P/S diets reduced the risk of total CHD events(RR 0.83, 95% CI 0.69–1.00, p = 0.050), whereas the lowfatdiets did not affect CHD events (RR 0.93, 95% CI 0.84–1.04, p = 0.072; fig. 20 ; 21 ). According to the classic ‘diet-heart’ hypothesis, high intakeof SFAs and cholesterol and low intake of PUFAs increaseserum cholesterol levels and risk of CHD. However, fewwithin-population studies have been able to demonstrateconsistent associations with any specific dietary lipids,with the exception of trans fats and n–3 fatty acids. Theavailable evidence from cohort and randomised controlledtrials is unsatisfactory and unreliable to makejudgement about and substantiate the effects of dietary faton risk of CHD. There is probably no direct relation between total fatintake and risk of CHD. The strongest evidence in supportof this judgement comes from the Women’s HealthInitiative that showed that CHD risk was not reduced after8 years of a low-fat diet. The observational evidence,summarised in the meta-analysis, showed no associationbetween total fat intake and CHD risk, although therewas heterogeneity between the study results.In this regard, the meta-analysis of trials in which serumcholesterol concentrations in the high P/S diet groupwere significantly lower than in the control group, revealedthat a diet higher in PUFA and lower in SFA decreasedthe risk of fatal CHD; however, this was significantonly after inclusion of results from the Oslo studywhich included smoking cessation as part of the treatment.The evidence from metabolic ward studies clearly shows thatdiets low in SFA reduce total cholesterol and should thereforereduce the risk of CHD. However, the meta-analysisof results from cohort studies – albeit from a limitednumber of studies – showed no association between SFAintake and CHD, demonstrating their unreliability.
I copypasted your reply on Stephan "intelligent design, TC cholesterol of 250 is healthy" Guyenet's blog. We'll see whether he will publish it.
@Charles Grashow. What is the difference between http://www.nmsociety.org/docs/aboutfat/Skeaff-Dietary-Fat-and-Coronary-Heart-Disease.pdfDietary Fat and Coronary Heart Disease: Summary of Evidence from Prospective Cohort and Randomised Controlled TrialsC. Murray Skeaff Jody Miller and Am J Clin Nutr. 2010 Mar;91(3):535-46. doi: 10.3945/ajcn.2009.27725. Epub 2010 Jan 13.Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease.Siri-Tarino PW, Sun Q, Hu FB, Krauss RM ???
@Peter -please show the link to your comment
Also in regards to 1)First in regards to Guyenet’s statement, “The long-term trials cited in which circulating cholesterol were durably reduced either involved a large increase in linoleic acid intake, or multiple dietary changes besides SFA”. Of course there is going to be an increase of other sources of calories when saturated fat intake is reduced in order to maintain caloric balance. It is not clear what Guyenet is trying to suggest or whether he is just trying to confuse the topic. If the participants reduced intake of saturated fat by decreasing total caloric intake without making any other significant dietary changes then the cholesterol skeptics would probably attribute any decrease in serum cholesterol to a decrease in caloric intake. This is because they always try to create a win-win situation for themselves.In regards to Guyenet’s statement in this same post, “According to Keys' interpretation of the trials, saturated fat raised, and to a lesser extent polyunsaturated fat lowered, blood cholesterol. But there were serious flaws in the data from the very beginning, which were pointed out in this searing 1973 literature review in the American Journal of Clinical Nutrition”. The 1973 literature review that Guyenet refers to is an absolutely appalling paper authored by Raymond Reiser. Keys et al. responded to this paper demonstrating that Reiser completely misinterpreted and distorted the data and that Reiser lied multiple times throughout the paper in regards to the changes in the participants serum cholesterol, changes in body weight and the nutrient composition of foods used in these experiments.6 I would rather not say this, but this paper was one of the lowest forms of cholesterol skeptic propaganda that one could cite.
In regards to 2)”The reality is” that major health authorities consider the Siri-Tarino et al. meta-analysis as being uninformative and that the evidence supporting the reduction of saturated fat intake as being convincing, often citing Stamler’s editorial.7In regards to Guyenet’s statements about overadjustment for serum cholesterol, Siri-Tarino et al. calculated that the association between saturated fat intake and the incident of coronary heart disease increased from a relative risk of 1.07 to 1.13 after excluding studies that adjusted for serum lipids but not necessarily dietary lipids.8 Although this finding did not quite reach statistical significance, it would be incorrect to claim as Guyenet did that Siri-Tarino et al. “found the exact same result”. When limiting the studies to only those that did not include adjustments for either serum or dietary lipids the relative risk ranged from 1.22 to 2.77, ie. >1.13. Furthermore, Guyenet claimed that Siri-Tarino et al. “found the exact same result” because this is “what one would expect, considering that little or no association is found between diet and circulating cholesterol in these studies”. As I have explained in great detail in my posts, it has been proved beyond plausible doubt that diet can significantly influence serum lipids. If a study fails to find an association between diet and serum lipids then this is likely due in part to imprecise dietary measurement methods, and would therefore be expected that such a study would also fail to find a strong association between diet and coronary heart disease, even if one existed. This brings me to my next point.I addressed a number of other limitations of the Siri-Tarino meta-analysis, not only the inclusion of overadjustment for serum lipids. For example I suggested that the findings could have been obscured by the use of imprecise dietary assessment methods, by participants voluntarily reducing saturated fat intake in response to unfavorable serum lipids, and the lack of comparing saturated fat with appropriate substitutes. Guyenet does not define as to which studies he considers are the “best observational studies ever conducted” and for what reasons, and is therefore difficult to comment on.
In regards to 3)In regards to the findings from the Health Professionals Follow-up Study, the findings across each fifth of the distribution of intake of saturated fat and fatal coronary heart disease were: 1, 1.41, 1.38, 1.32 and 1.72 respectively. Although the findings across ranges of intake did not reach statistical significant, it did show a trend towards an increased risk of fatal coronary heart disease. Furthermore, these findings could have been obscured by measurement error, bringing me to my next point.One of the reasons it is important to consider the association for the highest compared to lowest ranges of distribution of dietary intake, rather than across all ranges of intake is because of the relatively low chance of misclassifying a significant portion of participants between extreme ranges of usual dietary intakes (due to measurement error in the dietary assessment methods). This maybe one of the main reasons that the authors of the Health Professionals Follow-up Study only mentioned the findings for highest compared to lowest intakes of saturated fat in the abstract of this paper. Measurement error may cause a significant portion of participants being misclassified into the medium range of intake, when according to their usual intake they should have actually been classified as being in the highest or lowest range of intake. It is less likely however that measurement error would cause such a significant portion of the participants being misclassified into the lowest range of intake, when according to their usual intake they should have actually been classified in the highest range of intake and vice-versa.9 Of course this is unless for example the participants in the highest range of intake voluntary lower intake of saturated fat in response to unfavorable serum lipid concentrations, which would expect to bias the findings towards null or even an inverse association.These findings for high compared to low intake of saturated fat, which was associated with a significant increased risk of fatal coronary heart disease should be acknowledged, especially as it can be explained by a plausible mechanism (ie. elevated LDL cholesterol). It is Guyenet that incorrectly stated in regards to this study that “there was no statistically significant association between SFA intake and any measure of CHD after maximum adjustment”, not me. I agree with these authors key message “Benefits of reducing intakes of saturated fat and cholesterol are likely to be modest unless accompanied by an increased consumption of foods rich in fibre”. However, I believe that Guyenet has misinterpreted this key message. In reality it would be difficult to increase intake of both foods rich in saturated fat and dietary fiber simultaneously without increasing total caloric intake. This is particularly true for animal sources of saturated fat which contains zero fiber. The take home message from this paper and my posts should be that foods rich in saturated fat, particularly saturated animal fat should be replaced with foods rich in dietary fiber, such as fruit, vegetables, whole grain, legumes and nuts in order to significantly lower the risk of coronary heart disease.
Murray Skeaff, one of the primary authors of this systematic review from New Zealand has demonstrated strong agreement with the diet-heart hypothesis in a more recent paper.1 This is of particular interest considering that Skeaff has declared receiving funding from Fonterra which represents the dairy industry in NZ.In the review from NZ, Skeaff and Miller included only 6 separate cohort studies that addressed the association between saturated fat intake and fatal coronary heart disease (excluding the additional studies included in Fig. 7. which were not included in the analyses you referred to), which of half included overadjustments for serum LDL or total cholesterol. In comparison, Stamler included 11 cohorts in his meta-analysis. Nevertheless, Skeaff and Miller still found a positive association for fatal coronary heart disease, albeit non-significant.In regards to the isocaloric substitution of PUFA for SFA, you failed to mention what Skeaff and Miller stated in their post-script regarding the pooled analysis of 11 large cohort studies which they considered of higher quality than their previous analysis. “In the judgement of the Expert Consultation, the results of the ‘Pooling Project of Cohort Studies on Diet and Coronary Disease’ were a significant advance in quality on the update, undertaken by the Consultation, of the published meta-analyses of observational trials. The Pooling Project combined the results from 11 cohort studies – each meeting criteria for quality of dietary assessment, years of follow-up, and ascertainment of events – to examine the effect on CHD death and CHD events of replacing SFA with MUFA, PUFA or carbohydrate. The main finding was a significantly decreased risk of CHD death and CHD events when PUFA replaces SFA. The multivariate-adjusted hazard ratio for CHD death per 5% TE incremental substitution of PUFA for SFA was 0.87 (95% CI 0.77–0.97);for CHD events, the hazard ratio for the same fat substitution was 0.74 (95% CI 0.61–0.89). This result from the pooling of observational studies, along with supportive evidence from clinical trials of lower CHD risk in high P/S diets, and the effects of PUFA to lower LDL cholesterol and the total:high-density lipoprotein ratio, led the Consultation to conclude there was convincing evidence of lower CHD risk when PUFA replaces SFA.”
In regards to the Cochrane meta-analysis, the part where the researchers stated “the meta-analysis of results from cohort studies – albeit from a limited number of studies – showed no association between SFA intake and CHD, demonstrating their unreliability”, they were referring to the Siri-Tarino et al. meta-analysis that I have already covered. In regards to the Women’s Health Initiative (WHI), the researches stated: “Because there are no apparent changes that would have mitigated a potentially favorable effect on CVD, the lack of an appreciable CVD effect maybe attributable to the limited decrease(only 2.7 mg/dL [0.07 mmol/L]) in LDL-C level, as well as the modest differences in other potentially favorable dietary components. Based on a large body of evidence from LDL-C–lowering trials, this magnitude of change in LDL-C level would be predicted to produce only a small (2%-4%) decrease in CVD risk, a value far below the power for detection in the current study. As delivered, the dietary intervention was not expected to have substantial effects on lipoprotein levels, but it is possible that a diet specifically lower in saturated and trans fat combined with increased intakes of vegetables ,fruits, and grains might have led to a decrease in CVD risk.”The researchers of the WHI also stated: “Compared with those in the entire comparison group, a trend was observed oward reduction of CHD risk among those in the intervention group who reached the lowest levels of saturated fat (HR, 0.81; 95% CI, 0.69-0.96 in the group that consumed <6.1% energy; P<.001 [adjusted HR, 0.82; 95%CI, 0.67-0.99; P=.05])... While these additional analyses are subject to residual confounding because of reporting bias or the lack of a comparable comparison group, some confidence in their validity is supported by parallel patterns of LDL-C reductions in participants stratified by changes in saturated fat at year 1 (−10.1; 95% CI, −13.5 to −6.6 mg/dL[0.26; 95% CI, −0.36 to −0.17 mmol/L]in the quartile with the greatest reduction;P=.005 for trend)”1
Charles, I am welcoming your recent comments because I feel that they contribute in at least some way to the topic at hand. However, please make sure in the future that when you post comments here that you carefully consider what I have already covered on this site. I will not tolerate for example what you did on Don Matesz’s blog, where you kept on spamming the same copy-and-paste of studies that we already addressed and tried to compare vegetarians to Hitler.
Long-Term Consumption of a Raw Food Diet Is Associated with Favorable Serum LDL Cholesterol and Triglycerides but Also with Elevated Plasma Homocysteine and Low Serum HDL Cholesterol in Humans"In conclusion, the present study indicates that a strict raw food diet may result in remarkably low serum total cholesterol and triglyceride concentrations. However, the elevated tHcy as well as the low HDL cholesterol concentrations in participants in this study could provide a mechanistic explanation of the higher mortality from coronary heart disease in vegans compared with ovo-lacto-vegetarians, which was reported in a recent meta-analysis of prospective studies (16). A high tHcy concentration accompanied by a low HDL level may result in endothelial dysfunction via impaired bioavailability of NO. In contrast, studies of moderate ovo-lacto-vegetarian diets suggest that well-planned vegan and other types of vegetarian diets are appropriate for all stages of the life-cycle including during pregnancy, lactation, infancy, childhood, and adolescence and reduce risk for diseases (49). Changing the ratio of raw food intake toward an extreme regimen with a very low intake of vitamin B-12 may be harmful in the prevention of coronary heart disease rather than providing additional benefits as occurs with milder dietary regimens.
Do you mean this from study #2 (Siri-Tarino)Disclosure Dr. Krauss is a member of the Merck Global Atherosclerosis Advisory Board. He has received grants from the National Dairy Council, National Cattleman’s Beef Association, Robert C. and Veronica Atkins Foundation, and the National Institutes of Health. He is the co-inventor of two licensed patents for lipoprotein particle analysis and receives royalties from their use. Dr. Siri-Tarino has received an honorarium and has been supported by a grant from the National Dairy Council. No other potential conflicts of interest relevant to this article were reported.
http://circ.ahajournals.org/content/98/9/935.fullAHA Science AdvisoryVery Low Fat DietsAlice H. Lichtenstein, DSc; Linda Van Horn, PhD, RD; for the Nutrition Committe"Blood Triglyceride LevelsTG levels consistently increase in response to short-term consumption of a very low fat diet.25 28 29 31 32 33 34 35 36 The magnitude of the response is highly variable among subjects and can represent a 70% increase from initial TG levels. Cross-country epidemiological comparisons support these observations.37 Higher TG levels are frequently accompanied by lower HDL-C levels and higher total cholesterol/HDL-C ratios28 29 33 34 36 38 39 as well as increased levels of small, dense LDL particles.40 41 Very low fat diets increase TG levels regardless of whether the diet is high in simple or complex carbohydrates,30 42 but the increase may be attenuated by high dietary fiber intake43 or weight loss.29 Increased TG and decreased HDL-C levels due to increased carbohydrate intake are most likely in people with hypertriglyceridemia or hyperinsulinemia, especially those who are older, male, or inactive.36 An additional concern is the atherogenic postprandial lipemia associated with very low fat diets44 45 46 and the palmitate enrichment of circulating TG induced by increased fatty acid synthesis.47 Weight loss attenuates the HDL-C–lowering effect of very low fat diets and is related in part to blunting the increase in TG levels.24 26 28 29 The long-term effect of very low fat diets on blood lipid levels after weight stabilization has yet to be determined."
It is clear in this study that a significant portion of these raw-foodists were not supplementing vitamin B-12 which is a cause for concern. A relatively low HDL would not seem to be such a cause for concern if the dieters can sufficiently lower their LDL, especially considering that raising HDL has failed to produce benefit in randomized controlled trials [reviewed previously].It is important not to over-interpret the results from this meta-analysis as the number of vegans was small. Information is required for a larger number of vegans and for length of adherence to a vegan diet in order to make an informed conclusion. Also, it is likely important to exclude deaths during the early follow-up period in order to control for reverse causality, ie. to try and exclude participants who adopted a vegan diet due to a pre-existing illness or unfavorable risk factors that would ultimately become life-threatening.
From these researchers conclusions:There is overwhelming evidence that reductions in saturated fat, dietary cholesterol, and weight offer the most effective dietary strategies for reducing total cholesterol, LDL-C levels, and cardiovascular risk. Decreases in saturated fat should come at the expense of total fat because there is no biological requirement for saturated fat. Essential fatty acids can be adequately derived from unsaturated sources even if total fat intake is <15% of calories, but the appropriate types and amounts of these dietary fat sources must be selected (ie, highly polyunsaturated vegetable oils).I suggest referring to the post below for information regarding the concerns of low HDL-C and high triglycerides.http://healthylongevity.blogspot.com/2012/08/forks-over-knives-and-healthy-longevity_17.html
@Charles. Are you concerned with elevated levels of Homocysteine?http://www.ncbi.nlm.nih.gov/pubmed/12091753The effect of high-, moderate-, and low-fat diets on weight loss and cardiovascular disease risk factors.Here's a quote from this link -"Only patients following HF (High Fat) diets showed a worsening of each cardiovascular disease risk factor (LDL-C, TG, TC, HDL-C, TC/HDL ratio, Ho(Homocysteine), Lp(a), and fibrinogen), despite achieving statistically significant weight loss."
@Charles,I am blocking that last comment you posted. It is a link to an article by someone who is obviously trying to promote themselves by focusing on sex appeal and the male ego. This person states that they “hate vegans”, strongly suggesting a bias. The take home message from the article would appear to be that an inappropriately designed vegetarian diet could result in nutrient deficiencies. The author of that article also refers to Dr. Fuhrman as being "scrawny". If the author showed a picture Dr. Fuhrman flexing his muscles then his statement would not have likely convinced his audience. For example see the picture of Dr. Fuhrman in the link below:http://www.mensjournal.com/magazine/joel-fuhrman-the-doctor-is-out-there-20121107
@GoingliteFrom my last blood testCardiac Homocysteine - 10.0 umol/L Ref Range <11.4 umol/LApo B 104 mg/dL Reference Range <115 mg/dLLP(a) <2 mg/dL Reference Range 0-30 mg/dL
@H-LThe ‘science’ on nutrition is so contradictory, one can make a case for ANY viewpoint by pulling up thousands of studies that support your beliefs. Of course, it’s just as easy to pull up thousands of contradictory studies as well, just as legitimate.
Yes, I agree that anyone can make a case for any viewpoint by distorting the data. This is what you and your peers continue to do. I have not seen you or anyone produce a reference to a meta-analysis of over 100 metabolic ward experiments demonstrating that substituting saturated fat for carbohydrate, polyunsaturated fat and monounsaturated fat does not raise LDL, or a meta-analysis of over 100 randomized controlled trials demonstrating that lowering LDL cholesterol does not lower the risk of coronary heart disease and all-cause mortality. Where is this contradictory ‘science’ that you refer to?
@H-Lyou should be interested in these 2 papershttp://nature.berkeley.edu/miltonlab/pdfs/backbasics.pdfBack to Basics: Why Foods of Wild Primates have Relevance for Modern Human Healthhttp://ajcn.nutrition.org/content/71/3/665.fullHunter-gatherer diets—a different perspective"There is general agreement that the ancestral line (Hominoidea) giving rise to humans was strongly herbivorous (14, 15). Modern human nutritional requirements (eg, the need for a dietary source of vitamin C), features of the modern human gut (haustrated colon), and the modern human pattern of digestive kinetics (similar to that of great apes) suggest an ancestral past in which tropical plant foods formed the basis of the daily diet, with perhaps some opportunistic intake of animal matter.""However, because some hunter-gatherer societies obtained most of their dietary energy from wild animal fat and protein does not imply that this is the ideal diet for modern humans, nor does it imply that modern humans have genetic adaptations to such diets. It does, however, indicate that humans can thrive on extreme diets as long as these diets contribute the full range of essential nutrients."
I find Milton’s work quite informative, but am concerned with what she is implying by the word ‘thrive’. If she means that humans have the ability to maintain relatively decent health up until child bearing age, but not necessarily into very old age on extreme diets, then I agree. I believe in this case the word ‘survive’ may have been more appropriate than ‘thrive’.
@Charles,Sorry I do not think that Zoe Harcombe’s statement contributes to this discussion. In the link you presented Harcombe claims that saturated fat does not raise LDL, and that elevated LDL does not increase the risk of coronary heart disease, but provides little explanation for the vast amount of contradictory evidence from randomized controlled trials that I had in question. In the link you sent me she appears to be exploiting the WHO data to suggest that elevated serum cholesterol does not increase the risk of CVD and all-cause mortality, but fails to mention that the trend she is showing can probably be explained by the fact that higher serum cholesterol typically acts as a marker of a nation’s wealth. Plant Positive has addressed this in his video “A Poverty of Animal Fat”.Typical of cholesterol sketpics, Harcombe suggests that cholesterol feeding can only induce atherosclerosis in obligate herbivores such as rabbits, and only with extremely large doses of dietary cholesterol. As you should already know from reading my blog, it has been demonstrated that cholesterol feeding can induce atherosclerosis in a range of omnivorous species. Furthermore, it has been demonstrated that even small amounts of dietary cholesterol can induce atherosclerosis in non-human primates. If the cholesterol skeptics have to resort to such misleading claims, it seems highly unlikely that they actually believe in what they are saying.http://www.healthylongevity.blogspot.com/2012/08/forks-over-knives-and-healthy-longevity.html
HealthyL:an online friend run a regression curve on the WHO MONICA data the cholesterol skeptics use to show that there's no association of cholesterol to mortality. He showed that low BMI and blood pressure is associated with very high mortality. That's because people with low BMI's and blood pressure (and low cholesterol) tend to live in the third world. In fact, Walter Willett made a good point recently in regards to a weight-study. He concluded that BMI is an excellent predictor of long-term health all the way to the age 65. This applies to cholesterol as well. After the age of 60+ the cholesterol levels starts to come down due to metabolic changes in the intestine caused by senile devitalization, a condition that is automatically associated with higher mortality. If these associations are not controlled for, spurious associations may emerge. The best kept secret of creationists is this study from Helsinki. Pay attention to the very long-follow up and the fact that the authors were not just looking CHD but total mortality and quality of life. Moreover, the cohort in this study was based on people of high social status which functioned as an effective barrier for comorbidities such as homelessness, heroin use, alcoholism and other conditions (involving liver disturbances) that are associated with low cholesterol levels. TC cholesterol is an excellent predictor of mortality and quality of life for healthy people all the way to late mid-life.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”.
I am not surprised that the WHO MONICA data showed that, and I am guessing that an intake of a number of foods that the cholesterol skeptics really dislike, including perhaps sugar would also be associated with a lower risk of CVD and all-cause mortality due to the high intake in developed nations.In the Adventist Health Study and Adventist Mortality Study, the researchers examined whether the attenuation in risk of death due to excess body fat at old age was due to confounding, and found that people aged 75 to 99 who maintained a stable BMI of >22.3 had a shorter life expectancy.http://www.ncbi.nlm.nih.gov/pubmed/21649624Thanks for the data from Helsinki. Studies on the Finnish population have contributed greatly to our current understanding of cardiovascular disease, much more that the cholesterol skeptics would like to admit.
@Peter, H-Lwith regard to Finlandhttp://tilastokeskus.fi/til/ksyyt/2010/ksyyt_2010_2011-12-16_kat_003_en.htmlWhile Age-standardised ischaemic heart disease mortality fell between 1969-2010 deaths from Breast Cancer, Prostate Cancer and Age-standardised dementia mortality (incl. Alzheimer's disease) has gone WAY upSO - DIET RELATED OR NOT?
The statistics you provided for breast and prostate cancer mortality in Finland were not actually age-standardised. As stated by the authors in the link you provided:“In Finland, breast cancer mortality among working-age women has fallen during the last twenty years by around one fifth. The age-standardised figures also show that mortality from breast cancer is falling.”This time lag between a decline in saturated fat intake and a decline in age-adjusted mortality from breast cancer in the Finland resembles the time lag between an increase in saturated fat intake and an increase in age-adjusted mortality from breast cancer in Japan. I am not however suggesting that changes in breast cancer mortality in either of these populations can be explained by diet alone.http://www.ncbi.nlm.nih.gov/pubmed/17215198In Finland, the upwards trend of deaths classified as being caused by breast cancer and prostate cancer has remained largely unchanged since the late 1940s, long before Government intervention to improve the quality of fat intake in the Finnish population. As outlined from a paper addressing the Finnish cancer registry, this increase likely not only reflects an increase in the mean age of the population, but also improved diagnostic methodology.Problems in the completeness of cancer registrationUndiagnosed cancers. Since the development of cancer takes years (if not decades), a large number of cancers will never be diagnosed during the life-time of individuals. Thus, the higher the autopsy rates, the more undiagnosed cancers will be found. A similar effect on the numbers of cancer cases and, consequently, on cancer trends is to be expected when new diagnostic methods are introduced or when mass screenings (such as mammography screening for breast cancer) are organized: ever smaller cancers will be detected. The incidence of cancer means the incidence of diagnosed cancer. Thus, while the increase in the number of cancers due to improvements in diagnostic methodology is technically correct, the increasing incidence trend does not indicate increase in the real occurrence of the cancer in questionhttp://informahealthcare.com/doi/pdf/10.3109/02841869409098430In regards to deaths from dementia, the authors in the link you provided stated:The growth is partly caused by improved diagnostics, but also clearly by the ageing of the population.It appears that either you did not bother to read this link you posted or you were just trying to confuse the topic.
Charles, the population-wide health of Finns have dramatically improved from the 1960's due to changes in dietary habits; the most important being the change from organic butter to canola-oil based margarine, a change from organic, non-pasteurized whole-milk to low-fat milk and higher intake of vegetables and fruits. Moreover, the intake of sugar has dramatically increased in Finnish diet while at the same time significant improvements in cardiovascular health has occurred ( I am not implying that these two changes that happened the same time are causally related). Sugar consumption in Sweden was significantly higher than in Finland in the 1960's, yet cardiovascular mortality in Sweden was about 1/2 of Finland's rate. That is food for thought for the creationist/cholesterol skeptic online echo-chamber.
Plant based hunter-gatherershttp://en.wikipedia.org/wiki/Yanomamihttp://www.survivalinternational.org/tribes/yanomami/wayoflifehttp://www.livestrong.com/article/314666-yanomamo-diet/Traditional Yanomami --- those not living near missions and trading goods with outsiders --- have a diet that is low in fat and sugar, high in fiber and complex carbohydrates and adequate in protein. Their dietary staples are plantains, bananas, cassavas, nuts, small game and insects, including giant grubs that they harvest inside logs. According to anthropologists Marvin Harris and Eric Ross, who documented Yanomami eating patterns, about 75 percent of their diet comes from plant-based foods.
@H-Lhttp://www.heartattackproof.com/reversal01.htmPlease address the high triglyceride levels - levels of 100 or higher usually indicate LDL-C type B - small and dense particles which are supposedly more arthrogenic?
Well in your link of Dr. Esselstyn’s study many of the participants had triglyceride levels over 100, and possibly mainly small and dense LDL-C particles, yet either halted the progression of or experienced regression of atherosclerosis. Clinical utility of inflammatory markers and advanced lipoprotein testing: Advice from an expert panel of lipid specialistsStudies have linked large LDL particles to atherosclerosis in nonhuman primates, in patients with familial hypercholesterolemia (who have an elevated concentration of predominantly large LDL particles), in participants of the population-based MESA study, in normolipidemic men with CHD, and among patients after MI in the Cholesterol And Recurrent Events (CARE) study.Many studies document links between small dense LDL particles and atherosclerotic CVD. However, these statistical associations between small, dense LDL and CV outcomes are either significantly attenuated or abolished when the analyses are adjusted for the overall number of circulating LDL particles (LDL -P) either by adjustment for Apo B levels or by adjustment for nuclear magnetic resonance–derived LDL- P.All lipoprotein particles in the LDL fraction are atherogenic, independent of size. LDL particles become trapped in the arterial wall and are internalized by macrophages through scavenger receptors on the macrophage surf ace, resulting in foam cell formation, activation of these foam cells and expansion of the inflammatory response.The NLA Biomarkers Expert Panel was unable to identify any patient subgroups in which LDL subfractionation is recommended.http://www.ncbi.nlm.nih.gov/pubmed/21981835
New paper from what is the perhaps largest cohort study on a Japanese population addressing saturated fat and the risk of coronary heart disease and stroke.Dietary intake of saturated fatty acids and incident stroke and coronary heart disease in Japanese communities: the JPHC Study.Conclusions In this Japanese population, SFAs intake was inversely associated with deep intraparenchymal haemorrhage and lacunar infarction and positively associated with myocardial infarction.http://www.ncbi.nlm.nih.gov/pubmed/23404536In prospective cohort studies, serum cholesterol has been inversely associated with certain subtypes of stroke among participants with above-optimal blood pressure, but either not associated or positively associated with most subtypes of stroke in participants with near optimal blood pressure. It is not clear from the abstract of this paper whether like in the Nurses’ Health Study the inverse association between saturated fat and certain subtypes of stroke was confined to participants with above-optimal blood pressure. Given the findings from other cohort studies, I strongly believe that it is important to consider whether blood pressure contributes to the association between SFA and stroke in order to make an informed conclusion.http://healthylongevity.blogspot.com/2012/10/diet-blood-cholesterol-blood-pressure.html
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3075799/Relationship of Dietary Cholesterol to Blood Pressure: The INTERMAP StudyConclusionINTERMAP found a low-order, positive relationship of dietary cholesterol intake to SBP with control for multiple possible confounders. Reduction of dietary cholesterol intake may contribute to prevention and control of adverse blood pressure levels in general populations.FYI - I've started taking my blood pressure after consuming a virtually cholesterol free meal - a smoothie containing 1/2 avocado, the other components were unflavored whey protein isolate and fruit(1 kiwi, 1 banana, 1 cup frozen blueberries and 1 cup frozen cherries) - and after consuming a high cholesterol meal - a 4 egg omelet cooked in butter with mashed sweet potatoes - after the egg meal the blood pressure was much higher(129/72 vs 109/69). I will continue measuring this for several days and if the pattern holds true I will have to make dietary alterations. This is very significant.Your thoughts
That paper from the INTERMAP study also describes several other studies that found an association between dietary cholesterol and increased blood pressure. Also, a very recent paper from the Caerphilly Prospective Study found that saturated fat was associated with increased blood pressure. I would not completely rule out the possibility that these nutrients act as markers of a low intake of blood pressure lowering plant based foods.http://www.ncbi.nlm.nih.gov/pubmed/23415455That is an impressive drop in blood pressure assuming that it was not the result of measurement error. Obviously as you modified many nutrients simultaneously the observed drop in blood pressure may also be explained by an increase in fiber, vitamin C and other plant based nutrients. I have provided references to a number of systematic reviews and meta-analysis addressing the association between micronutrients and blood pressure in the post below. http://healthylongevity.blogspot.com/2012/10/diet-blood-cholesterol-blood-pressure.html
@Charles GrashowInstead of copying and pasting sections of studies, especially studies that I have already addressed to some extent, please provide a reason as to why you may believe that these studies challenge what I have previously covered or challenge whether a whole foods plant-based diet is most optimal for health. As I am often not entirely sure what you are suggesting when you simply copy and paste sections from studies without commenting as to why you believe these studies contribute to the discussion, it makes it difficult to respond without resorting to trying to guess what you are suggesting.
@Healthy LongevityYour thoughts on oxidixed LDL vs regular LDLhttp://northdenvernews.com/content/view/2424/2/"A 98-year-old researcher argues that, contrary to decades of clinical assumptions and advice to patients, dietary cholesterol is good for your heart – unless that cholesterol is unnaturally oxidized (by frying foods in reused oil, eating lots of polyunsaturated fats, or smoking).The researcher, Fred Kummerow, an emeritus professor of comparative biosciences at the University of Illinois, has spent more than six decades studying the dietary factors that contribute to heart disease. In a new paper in the American Journal of Cardiovascular Disease, he reviews the research on lipid metabolism and heart disease with a focus on the consumption of oxidized cholesterol – in his view a primary contributor to heart disease."Oxidized lipids contribute to heart disease both by increasing deposition of calcium on the arterial wall, a major hallmark of atherosclerosis, and by interrupting blood flow, a major contributor to heart attack and sudden death," Kummerow wrote in the review.Over his 60-plus-year career, Kummerow has painstakingly collected and analyzed the findings that together reveal the underlying mechanisms linking oxidized cholesterol (and trans fats) to heart disease.Many of Kummerow's insights come from his relentless focus on the physical and biochemical changes that occur in the arteries of people with heart disease. For example, he has worked with surgeons to retrieve and examine the arteries of people suffering from heart disease, and has compared his findings with those obtained in animal experiments."http://ajcd.us/files/ajcd1211005.pdfInteraction between sphingomyelin and oxysterols contributes to atherosclerosis and sudden death
"Abstract: Despite major public health efforts, coronary heart disease continues to be the leading cause of death in the United States. Oxidized lipids contribute to heart disease both by increasing deposition of calcium on the arterial wall, a major hallmark of atherosclerosis, and by interrupting blood flow, a major contributor to heart attack and sudden death. Oxidized cholesterol (oxysterols) enhances the production of sphingomyelin, a phospholipid found in the cellular membranes of the coronary artery. This increases the sphingomyelin content in the cell membrane, which in turn enhances the interaction between the membrane and ionic calcium (Ca2+), thereby increasing the risk of arterial calcification. Patients undergoing bypass surgery had greater concentrations of oxysterols in their plasma than cardiac catheterized controls with no stenosis, and had five times more sphingomyelin in their arteries than in the artery of the placenta of a newborn. The oxysterols found in the plasma of these patients were also found in the plasma of rabbits that had been fed oxidized cholesterol and in frying fats and powdered egg yolk intended for human consumption. Together these findings suggest that oxysterols found in the diet are absorbed and contribute to arterial calcification. Oxidized low-density lipoprotein (OxLDL) further contributes to heart disease by increasing the synthesis of thromboxane in platelets, which increases blood clotting. Cigarette smoke and trans fatty acids, found in partially hydrogenated soybean oil, both inhibit the synthesis of prostacyclin, which inhibits blood clotting. By increasing the ratio of thromboxane to prostacyclin, these factors interact to interrupt blood flow, thereby contributing to heart attack and sudden death. Levels of oxysterols and OxLDL increase primarily as a result of three diet or lifestyle factors: the consumption of oxysterols from commercially fried foods such as fried chicken, fish, and french fries; oxidation of cholesterol in vivo driven by consumption of excess polyunsaturated fatty acids from vegetable oils; and cigarette smoking. Along with the consumption of trans fatty acids from partially hydrogenated vegetable oil, these diet and lifestyle factors likely underlie the persistent national burden of heart disease."
From what I have gathered it appears that Kummerow is suggesting that the oxidation hypothesis refutes the lipid hypothesis. His opinion differs from that of Steinburg who while accepting the oxidation hypothesis also accepts that elevated cholesterol in itself is sufficient to induce atherosclerosis. As I stated previously:Passwater: Is it accurate to say that only oxidized-LDL starts the plaque process?Steinberg: No, it seems to me very likely that other modified forms of LDL are involved in plaque formation. What we know so far is that the use of antioxidants can decrease the rate of progression of lesions by 50-80%. That would speak to a major involvement of oxidation, but other things can also lead to foam cell formation. Studies by Dr. John C. Khoo in my laboratory have shown that aggregation of LDL with itself markedly increases the rate of uptake by macrophages.  The uptake in that case occurs by way of the native LDL receptor, not the acetyl LDL receptor or oxidized LDL receptor.Studies by Drs. J. S. Frank and A. M. Fogelman at UCLA have demonstrated the generation LDL aggregates in the subendothelial space.  Aggregation does not depend upon prior oxidative modification. So here is a quite distinct mechanism by which LDL uptake into the macrophages can be accelerated and can perhaps initiate the fatty streak lesion.Studies by Dr. Joseph L. Witztum and others in our laboratory have shown that minor modifications in the structure of LDL can render it immunogenic. Autoantibodies against oxidized LDL have been demonstrated in rabbits and in humans as well. Therefore, a complex of a modified LDL particle and an antibody against it can be taken up into macrophages by way of a completely different receptor, the receptor for immunoglobulins (the FC receptor).I would recommend that people who have been confused by the oxidation hypothesis to watch the following videos below by Plant Positive:Anything but LDL, Part II PUFAs Oxidize!As I have already pointed out, there is irrefutable evidence from over 100 randomized controlled trials and large mendelian randomization studies that lowering LDL cholesterol will lower the risk of CHD. For example, a 2-mmol/l (77 mg/dl) lower lifetime exposure to LDL cholesterol can lower the risk of CHD by 80%. Focusing on lowering LDL which has actually been proven to lower the risk of CHD may also in-turn lower oxidized LDL.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645847/http://content.onlinejacc.org/article.aspx?articleid=1379036
@Healthy Longevity1) Can you provide a link to the Steinburg study2) This is most interesting to me - I've emailed the lead author to see if I can get a copy of the full study - your thoughts would be appreciatedhttp://www.ncbi.nlm.nih.gov/pubmed/21353104Comparison of atorvastatin 5 and 20 mg/d for reducing F-18 fluorodeoxyglucose uptake in atherosclerotic plaques on positron emission tomography/computed tomography: a randomized, investigator-blinded, open-label, 6-month study in Japanese adults scheduled for percutaneous coronary intervention.CONCLUSION:Six months of treatment with atorvastatin 20 mg, but not 5 mg, was associated with a significant reduction in TBR in the ascending aorta and femoral artery in these Japanese adults with dyslipidemia undergoing PCI for stable angina pectoris.
the link is broken
Here is the link:http://www.healthy.net/scr/interview.aspx?Id=197Here is reference  and  mentioned in the interview:15. Enhanced macrophage uptake of low density lipoprotein after self-aggregation. Khoo, J. C.; Miller, E.; McLoughlin, P. and Steinberg, D. Arteriosclerosis 8:348-58 (1988)16. Ultrastructure of the intima in WHHL and cholesterol-fed rabbit aortas prepared by ultra-rapid freezing and freeze-etching. Frank, J. S. and Fogelman, A. M.J. Lipid Res. 30:967-78 (1989)
http://www.nytimes.com/2013/03/10/science/earth/ct-scans-find-vascular-disease-in-ancient-mummies.html?hp&_r=0"Indeed, this study, published online Sunday in The Lancet, found atherosclerosis in 29 of the 76 Egyptian mummies examined.But the researchers also found the disease in 13 of 51 Peruvian remains dated between A.D. 200 and 1500, two of five ancestral Pueblans who lived between 1500 B.C. and A.D. 500, and three of five Aleutian Islanders who lived in the 19th and early 20th centuries.Over all, 38 percent of the Egyptians and 29 percent of the other mummies had definite or probable evidence of atherosclerosis, the scientists concluded.The senior author, Dr. Gregory S. Thomas, a cardiologist and medical director at Long Beach Memorial Medical Center in Long Beach, Calif., said that among the mummies of people age 40 and older, 50 percent had atherosclerosis.Diet and climate varied among these four groups. The Egyptians may have eaten a diet high in saturated fat. The Peruvians farmed corn, potatoes and beans, and they kept domestic animals. Ancestral Pueblans grew corn and hunted rabbits, deer and sheep, while the Aleutian Islanders subsisted on a diet of fish, shellfish, seals, sea otters and whale."
Numerous large autopsy studies including the International Atherosclerosis Project that was based on data from 23,207 cases in 19 geographic and ethnic groups demonstrated the existence of a great variation in raised atherosclerotic lesions between populations, with a significantly lower rate in populations that had lower serum cholesterol and consumed predominantly plant based diets.1 These findings are consistent with the findings from other autopsy studies I previously cited demonstrating that the Okinawans and Papua New Guineans had a near absence of severe atherosclerosis. These findings are also consistent with a recent large mendelian randomization study which demonstrated that elevated lifetime concentrations of LDL cholesterol is a strong predictor of atherosclerosis.2There have been hundreds of experiments carried out on animals, including non-human primates that have demonstrated that severe atherosclerosis can be induced by the feeding of cholesterol and saturated fat and that the process can be reversed by removing these atherogenic components. Regression has even been demonstrated in non-human primates consuming 77% energy from sucrose in the presence of a cholesterol-free diet.3 Also as previously mentioned, it has been consistently demonstrated in intervention studies that significantly lowering LDL in humans by dietary changes or drugs results in either inhibiting or reversing the atherosclerosis process.4 5This enormous body of research was largely ignored by the researchers of this study on mummies who suggested that diet and exercise may have little appreciable effect on the development of atherosclerosis, and that atherosclerosis is an avoidable result of aging.6 These researchers ignorance of the medical literature is further demonstrated by their suggestion that only animal foods are sources of protein. Interestingly the authors suggest that ‘None of the cultures were known to be vegetarian’, yet still cast doubt as to whether diet can have a significant effect on the development of atherosclerosis. It is not surprising that all of these populations had atherosclerosis as it has been demonstrated in a number of animals, including non-human primates that long-term feeding of small amounts of dietary cholesterol induces atherosclerosis.7
Typically those who were mummified in ancient societies were the elites of society and consumed diets richer in animal foods than the lower class. An obvious exception to this rule is the preserved bodies from people such as the Inuit living in the polar circle who were accidently frozen were unlikely to have been elites (but consumed a diet predominantly based on marine foods). As I previously pointed out in regards to David et al.:It is important to point out that there was a marked difference between the mainly vegetarian diet most Egyptians ate and that of royalty and priests and their family members whose daily intake would have included these high levels of saturated fat. Mummification was practised by the elite groups in society, ensuring that their remains have survived to provide clear indications of atherosclerosis; by contrast, there is a lack of evidence that the condition existed among the less well-preserved remains of the [mainly vegetarian] lower classes.Although the authors suggested that there was insufficient data to make an informative comparison between the four studied populations, the data suggested that the Peruvians who perhaps had the greatest tendency towards a plant based diet had the lowest rates of atherosclerosis despite having the highest mean age. Confidence of this comparison can be increased by including additional samples of Inuit mummies studied by Zimmerman who mostly had gross atherosclerosis.8 While this data should not be extrapolated as the authors of this study on mummies did to suggest that diet has little appreciable effect on the development of atherosclerosis, the data nevertheless suggests that the diets of hunger-gatherers, especially those rich in cholesterol laded foods did not protect ancient humans against atherosclerosis as certain proponents of Paleo and Primal diets often suggest.
An interpretive history of the cholesterol controversy "The first four reviews in this series tracedthe gradual accumulation of evidence, evidence of severaldifferent kinds, supporting the lipid hypothesis. Theytracked the history from Anitschkow’s 1913 classic workon the cholesterol-fed rabbit model to the breakthrough1984 Coronary Primary Prevention Trial, the first large, randomized, double-blind primary intervention trial showingthat decreasing blood cholesterol (using cholestyramine) significantly reduces coronary heart disease events. At thatpoint, for the first time, decreasing blood cholesterol levelsbecame an official national public health goal. Still, only asmall fraction of patients at high risk were getting appropriate cholesterol-lowering treatment, and a number of important clinical questions remained unanswered. Thisfinal review in the series traces the early studies thatled to the discovery of the statins and briefly reviews the nowfamiliar large-scale clinical trials demonstrating their safetyand their remarkable effectiveness in reducing coronaryheart disease morbidity and mortality" Part 1 - http://www.jlr.org/content/45/9/1583.full Part 2 - http://www.jlr.org/content/46/2/179.full Part 3 - http://www.unicityscience.com/images/Files/steinberg%20III.pdf Part 4 - http://www.jlr.org/content/47/1/1.full Part 5 - http://www.jlr.org/content/47/7/1339.full.pdf+html
http://www.pnas.org/content/106/36/15418.fullVascular effects of a low-carbohydrate high-protein diet"Although caution is warranted in extrapolating from such animal studies, these data at least raise concern that low-carbohydrate high-protein diets could have adverse vascular effects not adequately reflected in serum risk markers. Moreover, these observations demonstrate important pathophysiological vascular effects of nonlipid macronutrients that are dissociated from weight gain. These features provide a unique model for understanding mechanisms of atherogenesis and neovascularization that may have implications for efforts to combat obesity and reduce its complications."http://mygreendiet.com/wp-content/uploads/2010/02/2286.pdf"Traditionally, the atherosclerotic risk profile that is associated with specific diets is determined by measuring intermediate risk factors, such as levels of low-density lipoprotein cholesterol, blood pressure, and C-reactive protein. The work of Foo et al.1 suggests that the HPLC diet might increase the risk of cardiovascular disease through mechanisms that have nothing to do with these “usual suspects” and so provides a note of caution against reliance on the traditional cardiovascular risk factors as a gauge of safety
George, do you have some peer-reviewed evidence that "refined carb diets" containing no animal products or cholesterol can produce high LDL?
Maybe it's NOT the fat or cholesterol - maybe it's the cholinehttp://www.sciencedaily.com/releases/2011/04/110406131814.htmThe study shows that people who eat a diet containing a common nutrient found in animal products (such as eggs, liver and other meats, cheese and other dairy products, fish, shellfish) are not predisposed to cardiovascular disease solely on their genetic make-up, but rather, how the micro-organisms that live in our digestive tracts metabolize a specific lipid -- phosphatidylcholine (a component of lecithin). Lecithin and its metabolite, choline, are also found in many commercial baked goods, dietary supplements, and even children's vitamins.The study examined clinical data from 1,875 patients who were referred for cardiac evaluation, as well as plasma samples from mice. When fed to mice, lecithin and choline were converted to a heart disease-forming product by the intestinal microbes, which promoted fatty plaque deposits to form within arteries (atherosclerosis); in humans, higher blood levels of choline and the heart disease forming microorganism products are strongly associated with increased cardiovascular disease risk.In studies of more than 2,000 subjects altogether, blood levels of three metabolites of the dietary lipid lecithin were shown to strongly predict risk for cardiovascular disease: choline (a B-complex vitamin), trimethylamine N-oxide (TMAO, a product that requires gut flora to be produced and is derived from the choline group of the lipid) and betaine (a metabolite of choline).
This study was published by the same research group which has just published a study linking intake of carnitine found in animal foods, particularly red meat to cardiovascular disease.New Link Between Heart Disease and Red Meat: New Understanding of Cardiovascular Health Benefits of Vegan, Vegetarian Dietshttp://www.sciencedaily.com/releases/2013/04/130407133320.htmCharles, if you have carefully read through my new posts and watched Plant Positive’s video and still believe that I have not addressed the contents of those two comments you tried to post the other day, then please repost and I will respond when I can find some time. I feel that I have already addressed the contents of your comments in my new posts and that you simply attempted to copy-and-paste some text from your favorite egg studies without carefully reading my posts.
Please analyze this rebuttalhttp://www.westonaprice.org/blogs/cmasterjohn/2011/04/13/does-dietary-choline-contribute-to-heart-disease/
Thanks for all of your hard work, and comments on The Food Way blog. Your help is greatly appreciated. I said as much at the end of the post I just published, which also is a photo essay of my transformation from paleo to sanity, clarity, and lightness of being!http://thefoodway.blogspot.com/2013/04/fruit-makes-you-fat-not-me-see-for.html
I also appreciate the hard work you have put into your blog. Don has also produced some very valuable work and I am looking forward to his possible upcoming projects.
Don was referring to Nanacy Rodriguez and not Denise Minger in his comment. Sorry if this has caused any confusion.
LOL, woah, those low-carbers are fanatical.
Dr. Michael Gregor has just released a very informative video addressing the recent findings on carnitine, choline and TMAO:http://nutritionfacts.org/video/carnitine-choline-cancer-and-cholesterol-the-tmao-connection/
Hats off.You did an amazing job, keep on doing so.I admire and respect you.Greetings from Greece.
Are you ever going to learn how to spell Dr. Greger's name right? :)
http://drbganimalpharm.blogspot.com/2013/05/the-great-cholesterol-fairy-tale.htmlThe Mistaken Implication of FHC and Elevated Blood CholesterolAbstract Following their Nobel Prize-winning discovery of the defective gene causing familial hypercholesterolaemia, Brown and Goldstein misunderstood the mechanism involved in the pathogenesis of the associated arterial disease. They ascribed this to an effect of the high levels of cholesterol circulating in the blood. In reality, the accelerated arterial damage is likely to be a consequence of more brittle arterial cell walls, as biochemists know cholesterol to be a component of them which modulates their fluidity, conferring flexibility and hence resistance to damage from the ordinary hydrodynamic blood forces. In the absence of efficient receptors for LDL cholesterol, cells will be unable to use this component adequately for the manufacture of normally resilient arterial cell walls, resulting in accelerated arteriosclerosis. Eating cholesterol is harmless, shown by its failure to produce vascular accidents in laboratory animals, but its avoidance causes human malnutrition from lack of fat-soluble vitamins, especially vitamin D.Unfortunate consequences of Brown and Goldstein’s mistakeBrown and Goldstein’s burst of fascinating information dazzled the medical profession, most of whom consequently accepted the false cholesterol hypothesis. This has led to unfortunate consequences that include:Waste of money on misdirected research.Waste of money on blood cholesterol tests.Waste of money on statins.Malnutrition from lack of fat-soluble vitamins (A,D,K,E) present in butter, full-cream milk and animal fat but lacking in margarine and skim milk (green-top bottles in New Zealand).Fear of eating eggs, contributing to unhealthy, starchy diets.Ricketts in middle-aged men from lack of vitamin D due to use of margarine and skim-milk.Distortion of the Dairy Industry, causing unnecessary marketing of skim milk.Distortion of the Meat Industry with unnecessary production of lean meat.The author concludes 'The fact that of the thousands of people involved in achieving this spurious result did not include a single elementary mathematician with intellectual independence is in accord with the whole sorry story of the great cholesterol myth, starting with the false statistics used in analysing the Framingham data.10 The meta-analysis of Ray et al.,13 showing no prolongation of life by use of statins in randomized controlled trials involving 65 229 participants, is the final nail in the coffin of the great cholesterol myth.'http://qjmed.oxfordjournals.org/content/104/10/867.longAtheromatous plaques contain cholesterol. Accordingly, research workers have repeatedly fed laboratory animals large amounts of cholesterol in their diets,1 expecting this to produce vascular accidents. It never has, which shows that despite the presence of cholesterol in atheromatous plaques these lesions are not caused by eating cholesterol. Before describing the strong evidence that hydrodynamic stresses cause the arterial degeneration responsible for ischaemic heart disease and strokes, we shall recount description2 of the spectacular deviation from reality caused by a mistaken interpretation made by Goldstein and Brown after they had brilliantly discovered the defective gene that causes familial hypercholesterolaemia (FH).
Here is a Swiss study from pubmed with numerous references that claims low carb diets improve health and can be used to treat a host of diseases including metabolic syndrome. It also claims cholesterol in food does not enter the bloodstream.http://www.ncbi.nlm.nih.gov/pubmed/?term=Diets+for+body+weight+control+and+health%3A+the+potential+of+changing+the+macronutrient+composition.+Acheson+KJ.I don't have the analytical tools to evaluate this study and would appreciate some help.
Here is part of a response to this article:“What evidence can Adams adduce to show that membrane composition and physical properties are impaired in FH in the manner that he states and that this is the basis of the atherosclerosis? Does he propose that the mechanism for atherosclerosis in FH is fundamentally different from that in individuals at the upper end of the serum cholesterol distribution who have no defect in LDL receptor function? Adams criticizes the authors of the Lipid Research Clinics Trial of cholestyramine over their statistical treatment but omits to mention that partial ileal bypass, which is much more potent than cholestyramine at interrupting the entero-hepatic circulation of bile acids, significantly reduces coronary events2 and that an aggregate analysis of pre-statin secondary prevention lipid-lowering trials also showed significant reduction in fatal and non-fatal coronary events.All in all Adams presents his hypothesis with a certainty that belies his inability to cite any substantial evidence in support. His eclectic criticism of a few papers supportive of the lipid hypothesis fails to take account of the totality of the published evidence. Brown and Goldstein should lose no sleep.”http://qjmed.oxfordjournals.org/content/105/3/291.fullIn regards to Adams claim about the Ray et al. meta-analysis finding of a lack of statistically significantly decreased risk of all-cause mortality by use of statins in primary prevention trials being “the final nail in the coffin of the great cholesterol myth”, these trials found a significantly decreased risk of cardiovascular events and a near-significant decreased risk of all-cause mortality which approached significance. A more recent and significantly larger meta-analysis of primary prevention trials found a statistically significant decreased risk of all-cause mortality. A recent Cochrane review also similarly found a statistically significant decreased risk of all-cause mortality.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3437972http://summaries.cochrane.org/CD004816/statins-for-the-primary-prevention-of-cardiovascular-diseaseIn regards to FHC, a meta-analysis of mendelian randomization studies with over 312,000 individuals demonstrated that inheriting any of nine studied genetic variants (including FHC) 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. The researchers also noted “We found no evidence of any heterogeneity of effect on the risk of CHD per unit lower LDL-C among any of the polymorphisms included in our study. This lack of heterogeneity of effect strongly suggests that the results of our study are unlikely to be significantly confounded by pleiotropy or linkage disequilibrium because it is unlikely that each of the included polymorphisms are acting through similar pleiotropic effects or have similar linkage disequilibrium patterns... This finding suggests that the effect of long-term exposure to lower LDL-C on the risk of CHD appears to be independent of the mechanism by which LDL-C is lowered. Therefore, the method of lowering LDL-C is likely to be less important than the magnitude and timing of LDL-C reduction. As a result, diet and exercise are probably as effective at reducing the risk of CHD as are statins or other treatments that lower LDL-C when started early in life (and when measured per unit lower LDL-C).” These findings also represent 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 in which the mean age at time of randomization was already 63 years. The p-value for this finding was 0.000000000000000000843. There is probably less than a one in quintillion chance the Brown and Goldstein were wrong.http://www.ncbi.nlm.nih.gov/pubmed/23083789
Thank you for the plethora of great information! We just shared your newest article on eggs (part II) on www.fb.com/GreenTidings.
Please tell me if you have an article, or research, or know where to find it, on why grass-fed, free-range, organic animal flesh/eggs is bad for health. The comments I always read after posting one of your articles (or other similar articles) is "What was the diet of the animal? the fat ratios are different in free-range, grass fed... The diet of the animal is the reason for this result."
Sorry for the late reply, I have been busy or away for a bit over a month. Plant Positive explains many of the flaws in the low-carb dietary trials. Advocates of low-carb diets will use this as evidence to downplay the recommendations to consume diets rich in minimally refined carbohydrates foods even those these studies were looking at diets dominated by refined carbohydrates. http://www.plantpositive.com/38-cherry-picked-research-by-a/As I previously pointed out, it has been demonstrated in thousands of animal experiments that the feeding of cholesterol, including in the form of fresh egg yolk accelerates the development of atherosclerosis in virtually every vertebrate species that has been sufficiently challenged. This includes mammalian, avian and fish species- herbivores, omnivores and carnivores, and over one dozen different species of nonhuman primates.The problems with dietary cholesterol is probably not as simple as dietary cholesterol entering the bloodstream but via more complex mechanisms such as the down-regulation of the LDL receptor.http://healthylongevity.blogspot.com/2013/04/cracking-down-on-eggs-and-cholesterol_7.html
Sorry for the late reply, I have been either busy or away for a bit over a month.I can understand it when someone argues that a study looking at refined carbohydrate rich foods cannot be extrapolated to minimally refined carbohydrate rich foods as the benefits of minimally refined carbohydrate rich foods have been well established. However there is scant evidence that free-range grass fed meat is healthy. Certainly it is lower in artery clogging saturated fat than conventional meat, but I am guessing these people who challenge my articles have been misled to believe that saturated fat is health promoting.I have already posted several articles describing the poor health of populations who subsisted predominantly on naturally raised animal foods which you can find below:http://healthylongevity.blogspot.com/2012/11/traditional-diets-in-asia-pacific-and.htmlhttp://healthylongevity.blogspot.com/2012/08/forks-over-knives-and-healthy-longevity_17.htmlIt is well established that saturated fat (in specific lauric, myristic and palmitic acids) raises total and LDL cholesterol, and that LDL cholesterol is an established cause of cardiovascular disease. The cholesterol raising effects of saturated fat is not the result of how the animal was raised as tropical plant fats high in lauric, myristic and palmitic acids will also raise total and LDL cholesterol.http://healthylongevity.blogspot.com/2013/01/diet-heart-problematic-revisit-part-ii.htmlAs I previously pointed out, it has been demonstrated in thousands of animal experiments that the feeding of cholesterol and saturated fat, including in the form of fresh egg yolk accelerates the development of atherosclerosis in virtually every vertebrate species that has been sufficiently challenged. This includes mammalian, avian and fish species- herbivores, omnivores and carnivores, and over one dozen different species of nonhuman primates. Again this cannot be attributed to the way that the animal was raised as when taking into consideration the amount of antioxidants and carotenoids as well as the lack of cholesterol, tropical plant fats high in lauric, myristic and palmitic acids will also accelerate atherosclerosis in animals to a similar degree as saturated animal fats. http://healthylongevity.blogspot.com/2013/04/cracking-down-on-eggs-and-cholesterol_7.htmlIt has been shown in controlled feeding trials that heme iron from meat causes the production of NOCs (N-nitroso compounds) in the digestive tract which in-turn causes DNA adducts in the human digestive tract. Therefore the heme iron content in meat rather than how the animal was raised can partly explain the positive association between red meat and colorectal cancer.http://healthylongevity.blogspot.com/2012/08/forks-over-knives-and-healthy-longevity.htmlI am well aware what the criticisms of my posts are and I would like to cover this subject more in possible future posts.
First, a personal disclosure: I am a somewhat low-carber-cholesterol-lover myself. I am not moved by any population level argument about anything because for me that only means more research is needed to isolate the actual underlying causes. Being that the case and with all-over-the-place mean values such as those of Figure 1 in Diet-Heart: Saturated Fat and Blood Cholesterol, I will keep my diet as it is today. I think that everyone of us should take his/her health as his/her responsibility, look at the evidence (of the kind you personally consider valuable) and take a personal decision. It seems it is not going to be the same for everyone, though.Second, about refined carb diets driving serum cholesterol up. There is clinical experience of Drs. like Eades, Davis and Rosedale. There is ecological data linking refined carbs with insulin resistance and insulin resistance with increased cholesterol too (sorry, a quick search hasn't come up with any direct link, certainly my fault). There is even a physiological mechanism at work.
Are you trying to suggest because these values in Figure 1 were scattered that this somehow negates a causal relationship? Did you even bother to read the text or did you just look at the pictures?It is not even debated anymore that there is a significant interinvidual variability of serum lipids in response to dietary lipids. Therefore it would be expected that the values would indeed be scattered to some degree. It would also be expected that seasonal trends and laboratory error would cause some scattering of the values. I am not one to take the word of authors of fad diet books as gospel without considering the published evidence. There are a number of concerns about refined carbohydrates but an increases in serum cholesterol is generally not one of them. Compared to other carbohydrates you would typically need to consume very large amounts of refined carbohydrates in order to experience modest increases in total and LDL cholesterol.http://www.ncbi.nlm.nih.gov/pubmed/23825185
http://www.svherald.com/content/opinion/2013/08/08/357636Easier Said Than Done:Health care giant endorses plant-based diet for allGreat news! A major American managed care company and hospital system is recommending their 15,000 doctors advise “…a plant-based diet to all their patients, especially those with high blood pressure, diabetes, cardiovascular disease, or obesity.”That recommendation was presented by Kaiser Permanente (KP) in their Spring 2013 Journal, as “Concerns about the rising cost of health care are being voiced nationwide …”http://www.thepermanentejournal.org/issues/2013/spring/5117-nutrition.htmlAbstractThe objective of this article is to present to physicians an update on plant-based diets. Concerns about the rising cost of health care are being voiced nationwide, even as unhealthy lifestyles are contributing to the spread of obesity, diabetes, and cardiovascular disease. For these reasons, physicians looking for cost-effective interventions to improve health outcomes are becoming more involved in helping their patients adopt healthier lifestyles. Healthy eating may be best achieved with a plant-based diet, which we define as a regimen that encourages whole, plant-based foods and discourages meats, dairy products, and eggs as well as all refined and processed foods. We present a case study as an example of the potential health benefits of such a diet. Research shows that plant-based diets are cost-effective, low-risk interventions that may lower body mass index, blood pressure, HbA1C, and cholesterol levels. They may also reduce the number of medications needed to treat chronic diseases and lower ischemic heart disease mortality rates. Physicians should consider recommending a plant-based diet to all their patients, especially those with high blood pressure, diabetes, cardiovascular disease, or obesity.
Hi Healthy Longevity,I just wanted to thank you for your amazing work on this blog.It really does make a difference, adds balance back to the universe and most likely saves lives.
Fantastic work HL. Terrific scholarship, bringing desperately needed clarity to a topic the paleo crowd have succeeded in making appear very murky. The whole pasture-reared issue is such a red-herring. I live in New Zealand where all the beef,lamb and dairy is pasture raised and we have some of the highest colon cancer, obesity, heart disease and diabetes rates in the developed world.I can't believe your patience with Charles Grashow but you seem to have won him round!I look forward to your future posts.
Good news indeed.
HeLo,I have been making a point of eating an average of around 2500mg of cholesterol per day for 1.5 years now. I'm 57 years old.Tell me, how long do you think it will take me to get heart disease?
Even if we were to agree that dietary cholesterol is causally associated with heart attacks it would not necessarily mean that one would ever experience a heart attack throughout their lifetime, it would only mean that the person is at an increased risk of having one. Depending on the person the response of adding dietary cholesterol on serum cholesterol can range from near null to >100%. http://ajcn.nutrition.org/content/55/6/1060.full.pdf+htmlThe adverse effects of on blood lipids may only be one of the adverse effects that increased intake of cholesterol confers. A daily intake of around 2,500mg of cholesterol suggests a dietary pattern very high in animal foods and poorer in whole plant foods which maybe an even bigger cause for concern.http://healthylongevity.blogspot.com/2013/04/cracking-down-on-eggs-and-cholesterol_7.html/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3751676/Longitudinal analysis of short-term high-fat diet on endothelial senescence in baboons"...our results clearly established that 1) even a short-term exposure (7 weeks) to a high-fat diet can have devastating pathological effects on vascular endothelial cells, and 2) physiological responses during the first 3 weeks of high-fat diet may have lasting effects that are manifested in endothelial cells at a later time. These conclusions significantly impact the traditional perception that a high-fat diet is detrimental only if exposure to it is of long duration. They also have important implications for the design of experiments aimed at understanding the progression of events that lead to diet-induced atherogenesis. Assessment of physiological effects of diet after 3 weeks of exposure may be essential to understanding mechanisms of atherogenesis as well as individual variation in extent and severity of atherosclerosis years after the initiation of the dietary challenge."
"A daily intake of around 2,500mg of cholesterol suggests a dietary pattern very high in animal foods and poorer in whole plant foods which maybe an even bigger cause for concern."Point well taken. I agree that there are plant foods that are good for health. Indeed, the bulk of my diet is vegetation. I like eating purple sweet potatoes as a carb source. Definitely a functional food. There is research...Having said that, I get about 50% of calories from fat, of that maybe 20% coconut oil, 15% olive oil and the rest animal fat, mostly dairy. As for meat, I lean towards organs - rich in zoonutraceuticals . Green lipped mussels are good too.So where does the 2500mg cholesterol come from? I eat pork brain, 3000mg cholesterol/100g most days. Why deliberately eat a highly concentrated source of cholesterol? To get my TC back up to a more reasonable level of 150 mg/dl. As the standard formula predicts, a 0.01mg/dl increase in blood cholesterol per 1mg increase in dietary cholesterol.My cholesterol dropped from 180 to 115mg/dl when I restricted my carbs to about 25% of calories and upped my fat to 50% of calories 15 years ago. I consider a TC of 115 to be pathological, not physiological. Even 150 is well below the optimal range. Maybe I should increase my cholesterol intake to 5000mg/day ;-)Notwithstanding your meta-analyses of hundreds of studies, I'm concerned with all cause mortality. There have been studies that specifically eliminated the effect of reverse causation, and the fact remains that for people my age and older, morbidity and mortality is lowest at a TC of 200-230. This is true for both people in one geographical area and internationally.Besides, I would rather keel over suddenly from a heart attack than suffer a lingering and painful death from cancer or sepsis, or get depressed to the point of suicide.
Hi Charles, nice to hear from you again - it's been a year.Thank you for your concern. Please rest assured that I haven't been devastated by "pathological effects on my vascular endothelial cells".I used to live in Bend Oregon 22 years ago and walk up Pilot Butte most days. It is a 1 mile road with a 500 foot elevation rise. I moved away and have done very little endurance exercise since then. A few months ago, 15 years after switching to a high fat diet and 1.5 years of eating 2500mg cholesterol a day, I visited there and decided to test myself to see how well I have held up over the years. I walked the 1700m 10% grade in 15 minutes with no more stress than I experienced 22 years ago.Last year, on Don's blog, the anti zoonutrient folks said that what matters is not your fasting cholesterol, but the post prandial cholesterol rise. I took that comment seriously enough to spend $50 to test it. I had a fasting blood draw, and a few days later had a blood draw 2 hours after eating 50g saturated fat and 4000 mg of cholesterol. The cholesterol level was the same both times - 150mg/dl. That did not exactly increase the credibility of the vegans' arguments in my mind.Maybe it's because I'm not a baboon, or because I'm an example of "individual variation in extent and severity of atherosclerosis years after the initiation of the dietary challenge", but rest assured Charles, I'm doing fine and expect to go on doing so to a ripe old age. I'm betting with my life that what I'm doing is not a challenge to my health, but rather an optimization of it. I no longer have the hubris to think I can save the world, but I know that I can change my own self for the better.
@Jack"My cholesterol dropped from 180 to 115mg/dl when I restricted my carbs to about 25% of calories and upped my fat to 50% of calories 15 years ago. I consider a TC of 115 to be pathological, not physiological. Even 150 is well below the optimal range. Maybe I should increase my cholesterol intake to 5000mg/day ;-)"Obviously you need a substantial amount of cholesterol to function properly BUT obviously everyone is not you.
Such a dietary pattern is not only excessively rich in dietary cholesterol, but also excessively rich in heme iron and perhaps some other heavy metals and toxins. I have previously presented evidence showing that dietary cholesterol may confer harm over-and-above the adverse effects it has on serum cholesterol, and that heme iron even at increments of 1 mg/day may significantly increase the risk of chronic diseases.http://healthylongevity.blogspot.com/2013/08/asian-paradox-low-carb-diets.htmlhttp://healthylongevity.blogspot.com/2013/04/cracking-down-on-eggs-and-cholesterol_7.htmlThe suggestion that a low cholesterol concentration is dangerous is not consistent with the preponderance of evidence. An analysis of 18 mammalians species showed a mean LDL concentration of 42 mg/dl, and these animals appear to be doing just fine. People with hypobetalipoproteinemia show perfectly normal growth and development and actually live longer. A number of clinical trials suggest that lowering LDL cholesterol well below 70 mg/dl is unlikely to cause significant harm, and is likely to actually confer benefit. A recent review suggested that the use of statins for primary prevention in elderly subjects (>65) resulted in a significantly decreased risk of heart attacks and stroke. It even showed a trend towards a decreased risk of all-cause mortality.http://circ.ahajournals.org/content/118/6/672.longhttp://www.ncbi.nlm.nih.gov/pubmed/23954343Prospective cohort studies cannot fully eliminate reverse causality, but can attempt to remove some of the reverse causality. The Prospective Studies Collaboration of 61 cohorts provided strong evidence that lower concentrations serum cholesterol is associated with a decreased risk of all-cause mortality after excluding the first 5 years of the follow-up to attempt to remove some of the reverse causation. However, 5 years may be far from insufficient to eliminate reverse causality because it can take many decades before slowly developing chronic diseases become clinically significant. For example, the greatest risk of excess death from radiation-related solid cancers among the atomic bomb survivors of Hiroshima and Nagasaki was more than half a century after exposure.http://www.ncbi.nlm.nih.gov/pubmed/18061058http://www.ncbi.nlm.nih.gov/pubmed/22171960
In regards to cancer, plant based nutrients and dietary patterns known to lower serum cholesterol have been consistently associated with a decreased risk of cancer. Several prospective studies with up to 37 and 40 years follow-up found that lower serum cholesterol measured in the pre-statin era was associated with a decreased risk of prostate cancer. These findings are supporting by observational studies which suggest that statins lower the risk of prostate cancer.http://www.wcrf-uk.org/cancer_prevention/recommendations/plant_foods_and_cancer.phphttp://www.ncbi.nlm.nih.gov/pubmed/23169929http://www.ncbi.nlm.nih.gov/pubmed/22677895http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3226949/http://www.biomedcentral.com/1471-2407/12/25http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23049713/In regards to depressive symptoms, a recent review of clinical trials found that cholesterol lowering statins are associated with improvements in mood scores. Furthermore, several clinical trials have found that vegetarian diets, also known to lower serum cholesterol have favorable effects on measures of mood and stress. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3568015/http://www.nutritionj.com/content/11/1/9http://www.ncbi.nlm.nih.gov/pubmed?term=8205407http://www.ncbi.nlm.nih.gov/pubmed/3783150
@JackYou also stated that increasing cholesterol intake raised your total cholesterol by about 35 mg/dl or 25%. That degree of increase could be potentially very dangerous for someone who does not naturally have low serum cholesterol concentrations.
Hi Travis HL, this a bit off subject, but in the future, could you do a section on Insulin Resistance and Low Carb Diets. I know that the Low carbers make a big deal out of this, referring people over to Dr. Richard Feinman's Blog.