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The Cholesterol Times, Issue #008 -- Steinberg Strikes Back: The Cholesterol Wars
October 31, 2005
|A Publication of Cholesterol-And-Health.com
Issue #008, October 31, 2005
Welcome back to another issue of The Cholesterol Times! And to those who celebrate it, Happy Halloween!
In this issue, the theme of the Research Watch section is how our perception of cholesterol is often affected by confounding factors. Inflammation, oxidation, receptor dysfunction -- each of these, as well as other physiological phenomena, can be confused with cholesterol levels if careful attention isn't paid to why cholesterol levels are elevated, or why they are lowered, and what is happening alongside those effects. In the Best of the 'Net section, I link to new research showing the protective effects of vegetables against lung cancer to depend on the genes of the person eating them, a more relaxed article on the glories of bacon by Brad Edmonds, and an off-topic yet fascinating article on prehistoric global warming... and more!
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--Chris Masterjohn, Editor
In This Issue
The site's article on the benfits of liver and cod liver oil has been updated to include a discussion of why cod liver oil is a better source of omega-3s than both plant oils and fish oil. It also includes a preliminary recommendation against Twin Lab cod liver oil based on information provided by the company through a third person indicating that their oil has so-called "vitamins A and D" added to it derived from soy. I will update the recommendation again, awaiting more specific information provided directly from the company.
Best of the 'Net
Many vegans argue that animal products are so polluted with dioxins -- a class of powerfully carcinogenic, reproductive-inhibiting, immune-suppressing, and endocrine-disrupting industrial pollutants -- that we must adopt a vegan diet to avoid their nasty effects. In this article, written for the Weston A. Price Foundation, I show that dioxins have been rapidly disappearing from the environment, that their toxicity is overrated, that it is mythical that dioxins are concentrated at some uniquely high level in animal foods, and that certain animal foods are rich in important nutrients that protect against the toxicity of dioxins.
We all know that "vegetables are good for you," but new research shows that the truth of that statement depends on just who "you" is. The protection against lung cancer provided by vegetables has been shown to be almost entirely attributable to the posession of certain alleles for two genes responsible for the rate of clearing of a class of compounds called "isothiocyanates." Having the right allele for one gene offers roughly 30% protection, while having the right allele for both genes offers roughly 70% protection -- yet in those without the right alleles for either, vegetables do not offer any significant protection at all.
Government Holds Vaccines Manufacturers' Hand, Protects Them From Responsibility for the Effects of Their Products
Republican Senator Richard Burr has helped to create a bill that would create a "true partnership" between government and pharmaceutical companies, the former of which will walk the latter "through the valley of the shadow of death" of responsiblity for the effects of their own products. The bill would transfer the right to acquit or find fault with a pharmaceutical company from a jury to the Secretary of the Department of Health and Human Services, protecting vaccine manufacturers from lawsuits deemed frivolous -- by the same agency with whom they are bound in a "true partnership."
To take a break from the science for a moment, it can be important to remember one of the primary reasons we eat food -- and doubtlessly one of the health-promoting effects of food as well -- because it tastes good and brings us pleasure.
Brad Edmonds extolls the gustatory glories of bacon.
A Look From the Other Side of "The Cholesterol Controversy"
Dr. Daniel Steinberg, MD, PhD, of the University of California's Department of Medicine, is publishing a series of reviews entitled "An Interpretive History of the Cholesterol Controversy," in the "Thematic Review Series" of the Journal of Lipid Research, in promotion of his upcoming book, The Cholesterol Wars.
Dr. Steinberg was one of the architects of the nation's wholesale acceptance of the lipid hypothesis -- that is, the idea that the development of heart disease is dependent upon and caused by elevation of the levels of certain lipids and lipoproteins in the blood, which creates a vicious cycle of cholesterol-raising as these lipoproteins infiltrate immune cells, resulting in the deposition of arterial plaque and the continued generation of more lipoproteins that continue to fuel this process -- having co-chaired the NIH committee that designed the landmark Coronary Primary Prevention Trial of the National Heart and Lung Institute, and having served as the Chair of the National Institute of Health's (NIH's) Consensus Development Conference, which resulted in the 1985 Journal of the American Medical Association publication that declared the full support of the nation's experts -- embodied by the official endorsement of the NIH -- behind the lipid hypothesis.
Steinberg tells the story of the "Cholesterol Wars" from the perspective of a supporter of the lipid hypothesis, reporting how the voice of a few vocal dissenters duped a well-intended Science Magazine journalist and many others into thinking there was genuine controversy, even after the landmark Coronary Primary Prevention Trial (CPPT) had "proven" the lipid hypothesis.
The CPPT was a massive project with its roots in the June 1970 establishment of the Panel on Hyperlipidemia and Athersclerosis by the National Heart and Lung Institute. The Panel launched a national network of Lipid Research Clinics that would standardize lipid and lipoprotein testing among local hospitals, physician offices, and clinics at a time when most physicians had no interest in testing lipid levels.
Yet many researchers and physicians were still unimpressed by the "evidence" for the causal role of cholesterol in heart disease. 20 of the 21 Panelists, on the other hand, believed that lowering lipids would lower heart disease, but by some unknown amount, and the Panel agreed a massive, randomized and double-blinded study was necessary to prove the case for the lipid hypothesis. "Even though the cumulative evidence was impressive, the direct clinical intervention trials were individually weak," Steinberg recalls. "What was missing was an airtight study -- a 'clincher' -- that would bring the skeptics into the fold and mobilize the medical community."
After rejecting various methods of cholesterol-lowering because of side effects or expected diffiulty with compliance, or in the case of diet, the expectation that cholesterol-lowering effects would be too limited to prove the point, the architects of the Coronary Primary Prevention Trial used cholestyramine, a resin that binds bile acids and prevents their resorption, thereby diverting cholesterol into the bile acid synthesis pathway. Cholestyramine was used because of its lack of systemic toxicity and side effects, and its effectiveness in lowering cholesterol.
In order to generate statistically powerful findings, the study would have had to enlist 3,800 men. The study would be limited to men with cholesterol levels over 265 mg/dl, and as a "primary" prevention trial, would by definition be limited to those without a prior history of heart disease. Yet after ten months of recruitment through physician referral, only 74 men had been recruited. The Lipid Research Clinics were thus mobilized to conduct mass public screenings, using gimmicks like free cholesterol tests at sports games in order to boost recruitment. Three years and 500,000 screenings later, 3,806 male participants had finally been enlisted.
To ease anxiety about ethical problems of letting men with high cholesterol go untreated, both groups were treated with dietary advice designed to lower cholesterol by 5%. Of course, Steinberg says, today such a trial would be unequivocally unethical since the lipid hypothesis has been "proven." The treatment group had to down six tablespoons of cholestyramine powder mixed with water per day, while the placebo group had to down six tablespoons of a chemically altered form of cholestyramine that did not lower cholesterol.
13 years and $150 million later, the results were in.
Compliance had failed miserably. Downing the six tablespoons of powder was so unpleasant that many of the men stopped taking the treatment or placebo within the first weeks of the years-long trial. Others took only a half-dose. While a 20-25% lowering of total cholesterol and a 30-35% lowering of LDL was expected, only a 13.4% reduction in total cholesterol and a 20.3% reduction in LDL was achieved, resulting in a 19% reduction of coronary events. The amazing clincher -- as Dr. Steinberg regards it -- within this study was the finding that those who took the full six tablespoons of cholestyramine had a 35% drop in cholesterol and a 49% reduction in coronary events.
The study was widely hailed as proof of the lipid hypothesis, although there were detractors. Geroge Mann of Vanderbilt University College of Medicine, for example, has written that "The managers at the NIH have used Madison Avenue hype to sell this failed trial in the way the media people sell an underarm deodorant."
One interesting point of the study was that, although there was a reduction from 44 coronary events in the untreated group to 32 coronary events in the treated group, with a p value of 0.05, meaning a 5% liklihood the finding is due to chance (the borderline minimum needed to consider a finding "statistically significant"), the difference in total mortality was a non-significant (likely to be due to chance) 7%. 71 untreated subjects died during the course of the study, while 68 in the treated group died.
Some researchers suggested that the large relative increase in "traumatic deaths" such as accidents, suicides, and homicides could have been due to mental effects of cholesterol-lowering. Steinberg brushes this off by reasoning that the cholesterol levels in these subjects were not "particularly low," and that in the one homicide death in the treated group, the treated participant was the victim of a burglary in which he was shot and killed, though he does not address the increase in suicides. Steinberg notes that this "small" difference in suicide and homicide deaths was also replicated in another study. The "small" effect was actually a near tripling from 4 deaths in the untreated group to 11 in the control group.
Dr. Steinberg regards the two data points in this study -- the cholesterol-lowering and coronary mortality reduction in the total treatment group, and the same figures for the minority of men who took the full dose -- as a true dose-response curve, showing that the degree of treatment and cholesterol-lowering is related to the degree of cardiac mortality reduction, strengthening a causal relationship. A more convincing dose-response would plot individual cholesterol levels or cholesterol level reductions against an effect, rather than using only two aggregated data points. Nevertheless, when viewed alone, and without looking at contradicting evidence, the results seem strongly suggestive -- or at least would have at the time.
The following year, in 1985, as Dr. Ravnskov reports here, Dr. Miettinen and colleagues from Helsinki, Finland, published another cholesterol-lowering trial in the Jounral of the American Medical Association where cholesterol-lowering resulted in a 400% increase in coronary mortality (four versus one) and a doubling of all-cause death (ten versus five). Although they were published in the very same journal, the positive CPPT trial was cited 109 times in the first year after it was published, 121 times the second year, 202 times the third year, and 180 times the fourth year, while the negative Miettinen study was cited only six times in its first year, five in its second, three in its third year, and only one time in the fourth year after it was published.
Actually, newer research on effects of cholestyramine makes it highly questionable whether any protective effect would be due to cholesterol-lowering. For example, a 2001 study by Hussein and coworkers showed that cholestyramine has a net antioxidant effect on LDL cholesterol. Cholestyramine has a variety of effects, including decreasing the absorption of dietary fat and some fat-soluble vitamins, and has contradicting effects on antioxidant status, lowering the vitamin E content of LDL, while raising the beta-carotene and lycopene content of LDL. The Hussein study found that children with familial hypercholesterolemia have a higher rate of LDL oxidation, and that cholestyramine not only lowers LDL, but abolishes the significant difference in vulnerability of LDL to oxidative damage.
In addition, if dietary fat is largely composed of polyunsaturated fatty acids, the consumption of which raises oxidative stress, then a decrease in the absorption of dietary fat could lower oxidative stress by causing a reduction in the absorption of polyunsaturated fats. Finally, a Medline search as of October 30, 2005 reveals that there is very little research conducted on the metabolic effects that lie downstream of cholestyramine's induction of the 7-alpha cholesterol hydroxylase enzyme and inhibition of certain cytochrome P450 enzymes, which could have a variety of unknown effects.
An interpretation of the cholestyramine trials attributing positive effects on cardiac mortality to their antioxidant effect is consistent with a study reported on in Issue #005 of this newsletter finding that the antioxidant resveratrol abolishes the effect of cholesterol-feeding on the development of atherosclerotic lesions in rabbits.
In the fifth issue of this newsletter I reported on a recent meta-analysis (an analysis that pools data from many studies together) that looked at all lipid-lowering trials to date that fulfilled certain objective criteria, with blinding used to protect against selection bias. The meta-analysis included the CPPT. It found statins (which are antioxidant and anti-inflammatory), resins (used in the CPPT,and which are antioxidant) and omega-3 fatty acids (which are anti-inflammatory) to be effective in lowering cardiac mortality, but not "diet", niacin, or fibrates, all of which lowered cholesterol effectively. While statins lowered cholesterol 33% more than resins, they were 27% less effective at reducing cardiac mortality. Omega-3 fatty acids were the most effective treament of the three, but had no effect on cholesterol levels. Usually p values of < 0.05 are considered statistically significant, which would have included omega-3 fatty acids (p = 0.001), but resins and statins were considered "statistically significant" with p values of 0.83 and 0.42 respectively (an 83% and 42% liklihood the effect was due to chance, respectively.)
In terms of overall mortality, resins, fibrates, niacin, and "diet" all had considerable cholesterol-lowering effects but did not significantly reduce mortality, whereas omega-3 fatty acids had the greatest reduction in overall mortality with no effect on cholesterol levels.
In the last issue of this newsletter I summarized an incomplete and by no means comprehensive, yet nevertheless compelling, group of evidences against the lipid hypothesis, including various methods of reducing atherosclerosis in animals by counteracting inflammation or oxidative stress, allowing extremely elevated cholesterol levels to result in no harm to the heart or blood vessels, the fact that the development of atherosclerotic lesions does not relate to cholesterol levels as determined by the time of life in humans in which it tends to develop, the specific arteries in which it tends to develop, and studies that have actually measured plaque and lesion levels post-mortem, and, with new technology, while the subject is alive, and shown the development of plaques and lesions to be unrelated to cholesterol levels.
Nevertheless the lipid hypothesis pushed full-steam ahead despite the vocal dissent of detractors. The NIH put together a Consensus Development Conference, Chaired by Steinberg. Richard Peto, who is credited with the introduction of the meta-analysis to epidemiology, used the first instance of this technique at this historic conference. What was, according to Steinberg, only a handful of vocal opponents to the lipid hypothesis, including Edward H. Ahrens, Jr., Michael F. Oliver, and Robert E. Olson presented opposing views.
Mary Enig and Sally Fallon report the story, as told by some of the attending dissenters, differently in "The OIling of America":
A number of clinicians and statisticians, including Michael Oliver and Richard Krommel, who participated in a 1984 Lipid Research Clinics [LRC] conference workshop, were highly critical of the manner in which the LRC results had been tabulated and manipulated. In fact, the conference went very badly for the NHLBI, [National Heart, Lung, and Blood Institute] with critics of the lipid hypothesis almost outnumbering supporters. One participant, Dr. Beverly Teter of the University of Maryland's lipid group, was delighted with the state of affairs. "It's wonderful," she remarked to Basil Rifkind [Chief of the Lipid Metabolism-Atherogenesis Branch of the NHLBI], "to finally hear both sides of the debate. We need more meetings like this." His reply was terse and sour: "No we don't."
Dissenters were again invited to speak briefly at the NHLBI-sponsored National Cholesterol Consensus Conference held later that year, but their views were not included in the panel's report for the simple reason that the report was generated by NHLBI staff before the conference convened. Dr Bev Teter discovered this when she picked up some papers by mistake just before the conference began, and found they contained the consensus report, already written, with just a few numbers left blank. Kritchevsky represented the lipid hypothesis camp with a humorous five-minute presentation full of ditties. Edward Ahrens, a respected researcher, raised strenuous objections about the "consensus", only to be told that he had misinterpreted his own data, and that if he wanted a conference to come up with different conclusions he should pay for it himself.
Whatever the nature and magnitude of the dissent, the Executive Session voted unanimously that cholesterol played a causal role in heart disease, and that efforts to reduce cholesterol levels would lower rates of heart disease. From Dr. Steinberg's perspective, the author of the Science article entitled "Heart Panel's Conclusions Questioned," was duped into believing that there was actually genuine controversy with many dissenters, when the dissenters were actually so few in number as to be insignificant. He cites a 1978 poll in which 90% of questioned experts responded, over 99% of whom believed there was a "consensus" on the role of cholesterol in heart disease and most agreeing that plasma cholesterol levels were related to heart disease, although the questions were not explicit on what that consensus was or exactly what the relationship between plasma cholesterol levels and heart disease was.
Amid this discussion, Dr. Steinberg seems to have missed the point that such a poll, even if indeed conducted in such a way as to yield accurate results, would not constitute evidence favoring the lipid hypothesis, but simply evidence that most researchers believed the lipid hypothesis. The history of scientific development reveals that what the majority of scientists believe at any given point in time has little relationship on what the truth actually is.
As part of the "vitriol" levied against the lipid hypothesis, Steinberg also cites Michael Oliver, a major figure in British cardiology, who claimed the Panel was arranged "selectively," as well as an article by journalist Thomas J. Moore in The Atlantic who claimed that "the dissenters have been overwhelmed by the extravaganza put on not just by the heart institute but by a growing coalition that resembles a medical version of the military-industrial complex. This coalition includes . . . the 'authorities' . . . the heart institute itself . . . and the American Heart Association . . . "
Dissent falling by the wayside, out of the Executive Session of the Consensus Conference was born the National Cholesterol Education Program (NCEP). An "education" program backed by the strong arm of government can have massive results: according to Steinberg, the NCEP has played a "key role" in the "sea change of cholesterol awareness," in which the percentage of physicians considering LDL an important marker for heart diseae rose from 34% to 75% over the course of 1986 to 1995.
Dr. Steinberg ends this fourth of five installments in his series with this glorious achievement. Perhaps his fifth installment will discuss some of the questionable procedures with which the NCEP has released guidelines for cholesterol-lowering drugs, such as timing the release of new guildelines with the release of new cholesterol-lowering drugs, releasing guidelines to the public weeks before doctors could view the scientific information on which the guidelines were based, the failure to open meetings to the public or keep detailed minutes of proceedings or other questionable procedures that Dr. Paul Rosch has summarized in the article linked to above.
Or perhaps Dr. Steinberg will tell us how eight of nine NCEP panel members came to the table bearing financial conflicts of interest, tied to the same pharmaceutical companies whose products they were recommending be given to ever-broader sectors of the population, as Shane Ellison reported in The Hidden Truth About Cholesterol-Lowering Drugs.
For this, we will have to wait and see.
Steinberg, Daniel, "An interpretive history of the cholesterol controversy, part IV: The Landmark 1984 Coronary Primary Prevention Trial and the Endorsement of the Lipid Hypothesis by NIH. End of the Controversy?Journal of Lipid Research (2005) Oct. 15 [Epub ahead of print.]
Lack of LDL Receptor, But Not High Cholesterol, Contributes to Alzheimer's
In the last issue of this newsletter, I reported on a study that took a cheap shot at cholesterol by discussing the increased risk of Alzheimer's experienced by those with very high cholesterol levels, without discussing the confounding effects of having certain genes such as the ApoE4 allele or familial hypercholesterolemia (lack of a properly functioning LDL receptor) that can contribute both to increased levels of blood cholesterol and to Alzheimer's by independent means.
A new study published in the journal Neurobiology of Aging by Cao and coworkers demonstrates this point. Mice were either genetically altered to express the human amyloid precursor protein (APP), which has some incompletely understood role in Alzheimer's disease, or left normal. Each of these two groups were either left normal, had the genes for their LDL receptors (LDLR) knocked out, or were a cross between those with and without an LDL receptor.
The mice who lacked both alleles for the LDLR gene had hypercholesterolemia -- highly elevated blood cholesterol levels -- similar to humans with a similar genetic defect. The half of them who were "transgenic" for the human APP gene also had 2-fold increased amyloid-beta plaque depositions over those who had functioning LDL receptors, which first began to develop at 11 months, and impaired spatial memory and learning at 13 months compared to those transgenic for APP and with functioning LDL receptors. At 10 months, before plaque deposition began, mice who were transgenic for human APP had spatial learning and memory deficits over those who were not transgenic for human APP, but the presence or absence of the LDL receptor had no effect at that point.
Does this support the cholesterol-amyloid hypothesis? In my article Myth: Cholesterol Causes Alzheimer's Disease, I described what I called the "cholesterol hypothesis of Alzheimer's disease," which holds that elevations in cholesterol cause increased production of amyloid-beta, which then form amyloid plaques, which in turn cause the memory and other mental deficits seen in Alzheimer's disease. I also presented a thorough refutation of this theory, showing that beta-amyloid levels themselves do not determine amyloid plaques, that cholesterol appears to be protective against Alzheimer's, that beta-amyloid may be an essential protein that protects against an inability to properly incorporate cholesterol into membranes, and showing that the neurobehavioral deficits found in animal models of Alzheimer's are largely independent of amyloid plaques and dependent on other factors.
In this study, the elevated blood levels of cholesterol had no relation to brain cholesterol levels. In fact, there was a very slight lowering of brain cholesterol levels in the mice who were deficient in the LDL receptor. There was also no change in brain levels of APP, which is the precursor to beta-amyloid. There was, however, an increase in insoluble beta-amyloid, but the lack of an increase in APP and in soluble beta-amyloid indicates that the beta-amyloid was probably not being produced at a higher rate, but was instead being cleared at a lower rate. Although, since it is rather questionable that low clearing of beta-amyloid itself would result in plaque formation, the LDLR could have a role in preventing plaque-formation as well.
It is known that the LDL receptor-related protein (LRP) plays a primary role in clearing beta-amyloid from the brain, and this study seems to indicate that the LDL receptor also plays such a role. Yet the lack of elevation of brain cholesterol levels shows that the elevation of blood cholesterol levels is an independent effect, unrelated to whatever causal role the lack of an LDL receptor plays in the deposition of amyloid plaques and the development of learning and memory impairment. This interpretation is strengthened by the fact that, while there was large variation in plaque deposition among those who were negative for the LDL receptor, this variation had no correlation with blood cholesterol levels.
Since cholesterol-lowering statins upregulate the LDL receptor, their supposed positive effects on Alzheimer's may be related to this effect, rather then their lowering of cholesterol. Still, the evidence on this is unclear, and I reported on a study in Issue #003 of this newsletter that seemed to indicate statins could cause dementia and Alzheimer's.
In any case, this study quite clearly demonstrates how familial hypercholesterolemia can act as a confounding factor when drawing correlations with blood cholesterol levels. Since very high blood cholesterol levels are associated with the lack of a functioning LDL receptor, the inclusion of familial hypercholesterolemics with the general population can show correlations of diseases with blood cholesterol levels that have nothing to do with the cholesterol levels and everything to do with improper receptor functioning. Any study that makes correlations of any illness with blood cholesterol levels must for the sake of intellectual honesty also provide data that examines familial hypercholesterolemics separately from those who are not familial hypercholesterolemics.
The very important effect of this seemingly subtle nuance is whether we should seek to lower our cholesterol levels or brain cholesterol levels through diet and drugs. If those with very high cholesterol levels have an increased risk for Alzheimer's because of independent genetic defects and not because of those high cholesterol levels, those who advocate a low-fat, low-cholesterol diet as "brain-healthy," may be recommending the very opposite of a truly "brain-healthy" diet.
For more complete coverage of the cholesterol-Alzheimer's controversy, see:
When considering the role of cholesterol in Alzheimer's disease, Cholesterol-And-Health.com's article on the importance of cholesterol to the brain may also be useful reading.
Oxidative Stress and Inflammation Tied to Mobility Limiation in the Elderly, LDL Protective
Although cholesterol levels, oxidative stress, and inflammation are often discussed in terms of fatal diseases, quality of life is just as important if not more important than maintaining a long life itself.
In 1956 Harman posited the "free radical theory of aging." Free radicals are any substance with an unpaired electron, which can damage the body as it seeks to rob another substance of an electron to complete the pair. Harman hypothesized that the degenerative processes of aging are due to this free radical damage.
A new study published by Cesari and coworkers in the Archives of Internal Medicine, analyzing data from the Health, Aging, and Body Composition (Health ABC) study, a 10-year prospective cohort study (prospective studies gather data on independent variables before the endpoints they are studying occur) investigating changes in body composition and health conditions on physiologic and functional status at increased ages, has found that oxidized cholesterol levels and indicators of inflammation, but not levels of cholesterol per se, are predictors of mobility limitation.
In this study, any two semiannual reports of difficulty walking 1/4 mile or climbing 10 steps without resting were considered "mobility limitation," and severe difficulty performing the same tasks was consdered "severe mobility limitation." The total level of oxidized LDL, the proportion of LDL that was oxidized, and the level of interleukin-6, an inflammatory marker, were all strong, independent, and statistically significant predictors of mobility limitation and severe mobility limitation, with correlations as strong as 43%.
Although LDL levels are associated to some degree with oxidized LDL levels, this study actually found that LDL cholesterol levels were protective, but this protective effect was not statistically significant. An increase of 100 mg/dl of LDL cholesterol carried a protective effect of 25% against severe mobility limitation and 27% against mobility limitation. Although this was not statistically significant, meaning there was some inconsistency making the finding more likely to be due to chance, the inconsistency could have been introduced by the positive correlation between LDL levels and oxidized LDL. In other words, it appeared that unoxidized LDL was protective against mobility limitation, while oxidized LDL was a predictor of mobility limitation, even though there was a moderate tendency for these opposite factors to occur together.
As an interesting side-note, in the the last issue of this newsletter I reported on a study that found that feeding a high-fat, high-cholesterol diet to baboons decreased the level of interleukin-6 by a factor of seven, even though the authors claimed the opposite effect in their abstract based on a temporary effect found at the beginning of the study.
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Weston A. Price Foundation Annual Conference
Friday, November 11, through Sunday, November 13, The Weston A. Price Foundation will be holding its Sixth Annual Wise Traditions Conference.
Conferences in the past have featured Dr. Uffe Ravnskov's presentation of his hypothesis that cholesterol protects against infectious diseases, Dr. Kilmer McCully discussing his revolutionary work on homocysteine, Dr. Russel Blaylock's presentation of his work on excitotoxins, and many other excellent presentations.
This year's conference will feature social activities, workshops on fertility awareness and fermentation of beverages, 2 main tracks on heart disease and cancer, and a long list of featured speakers, including Dr. John Cannell, President of the Vitamin D Council, and Dr. Noel Solomons, Director of the CeSSIAM International Nutrition Foundation.
For more information on the conference, click here.
Travel and Lodging.
You can get a conference-related discount at the Westfield Marriot where the conference is being held of $139/night for double, triple, and quadruple occupancy by making reservations here.
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