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The Cholesterol Times, Issue #007 -- Cancer: It's Not the Meat, But How You Cook It
October 15, 2005
A Publication of
Issue #007, October 16, 2005

Dear Reader,

Welcome back to another issue of The Cholesterol Times!

In this issue, you'll be able to delve into the delectable delights of news and research I've prepared for you, which include news about genetically engineered super-viruses, the history of the discovery of vitamins, responses to a new Lancet meta-analysis claiming the safety and efficacy of statins, a new study that finally differentiates between various methods of preparing and cooking meat when analyzing its association with cancer, and much more.

While we await the publication of my new comprehensive article on dioxins in the food supply by the Weston A. Price Foundation, let me supply you with a thought to ponder: There are over 2,000 organochlorines that are produced in nature, including dioxins, which have been found in preserved soil samples preceding the advent of the chlorine industry. A gram of wood smoke contains 100-500 times the amount of chlorinated dioxins that an adult human consumes from food in a day, produced in a reaction between carbon and chloride compounds that naturally occur in wood. The burning of wood was, before the modern era, not only central to cooking and the provision of warmth, but also to maintaing soil fertility. In his epic work, Nutrition and Physical Degeneration, Weston A. Price established the necessary role of animal foods in maintaining the superb health, dental and skeletal structure, and freedom from degenerative diseases experienced by select isoated pre-modern groups, who probably were exposed to dioxins both through inhalation and through the food supply. So can anything have changed today, mandating that we forego these health-promoting animal foods, as some claim? Or is the truth very, very different? Find out as soon as this mammoth article is published.

If you are reading this issue of The Cholesterol Times in plain text rather than html format, I recommend viewing the html version by copying and pasting into your browser this URL.

This will allow you to follow all the external links by easily clicking on them, as well as to navigate much more easily through the contents of the newsletter by using the internal links.

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Have a great weekend!

--Chris Masterjohn, Editor

In This Issue

Site Updates
  • Coenzyme Q10 Distribution in Foods
    Best of the 'Net
  • Genetically Engineered Super-Flu Viruses: Made in the USA
  • Florida Farmer Not Allowed To Open His Own Freezer to Feed Himself Without Inspector Present
  • The History of the Discovery of Vitamins
  • Aspartame: Killing Us by Degrees
  • Statins Safe And Effective? Anthony Colpo Responds
  • Saturated Fat Causes Heart Disease? Dr. Ravnskov Responds
    Research Watch
  • Cancer: It’s Not the Meat - It’s How You Cook It
  • Alzheimer’s Study Takes Cheap Shot at Cholesterol
  • High-Cholesterol, High-Fat Diet Reduces Inflammation in Baboons - But You Wouldn’t Know It From the Abstract
  • Inhibiting Inflammatory Factor Reduces Atherosclerosis in Mice With No Effect on Cholesterol or Triglycerides
  • Fructose Enhances Atherosclerosis in Cholesterol-Fed Rabbits
    How to Link to This Newsletter
    Weston A. Price Foundation Conference
  • Conference Details
  • Hotel Reservations
  • Travel Accomodations
    Copyright and Disclaimer

    Site Updates

    Coenzyme Q10 Food Composition Table

    The site's article on coenzyme Q10, a nutrient with important roles as an antioxidant, in cellular respiration, as a protector of the heart and maintainer of blood pressure and inflammation, found in the highest amounts in animal foods and whose synthesis in the body is inhibited by cholesterol-lowering statin drugs, has been updated to include a food composition table. Although several more analyses have been published, the table only includes data from the two studies I have so far been able to obtain. In the future, it will be updated to provide more detailed information. However, this table, showing the CoQ10 content of 98 different foods, is probably the most detailed coenzyme Q10 food composition table available on the internet that can be freely accessed.

    Best of the 'Net

    The Deadliest Flu In the World: Made in the USA

    As if the H5N1 Spanish flu virus that killed millions worldwide wasn't enough, researchers at a semi-secure laboratory in a midwestern American university have mutated one of the genes of this virus to make it far more virulent. Full body protection suits are not required at the laboratory, and its location can easily be obtained over the internet by an interested terrorist. The intention is to research a possible vaccine, but one must question, given the obvious risks: are they out of their minds? Bill Sardi reports.

    State of Florida: Don't Dare Open Your Own Freezer Without Our Inspector Present

    In the state of Florida, the food you put into your own body isn't just your business: it's the state Department of Agriculture's business. Merely to be a thorn in his side in retribution for his provision of unpasteurized milk to those who wish to buy it and believe it to be health-promoting, Dennis Stoltzfoos of Full Circle Farm is not allowed even to open his own storage freezer -- bound by official government white tape -- to feed himself without the state's inspector making the 60-mile round trip to be present for the "operation."

    This History of the Discovery of Vitamins

    A century ago, nutrition was thought of merely as fats, proteins, and carbohydrates. The discovery of vitamins revolutionized how we think about why we eat food.

    Aspartame: Killing Us by Degrees

    Is aspartame, the sweetener also known as Nutri-Sweet or Equal, safe? Not according to Pat Thomas. Part II of a continuing series of installments provided by Dr. Mercola.

    Anthony Colpo's Response to the New Lancet Meta-Analysis Alleging the Safety and Efficacy of Statins

    A recent review in the journal The Lancet provided a meta-analysis making grand claims about the safety and efficacy of the cholesterol-lowering statin drugs. In this thoughtful article, Anthony Colpo dissects the claim, showing how the authors distorted the studies' findings by generalizing from findings in a small sub-group of patients to the general population, and explaining how many statin trials have achieved exaggerated safety by weeding out most of those susceptible to side effects during pre-screening-- people who are put on statins in the real world.

    Saturated Fat Causes Heart Disease? Dr. Ravnskov Responds

    Dr. Uffe Ravnskov provides a concise refutation of Drs. Willet's and Zotonski's recent claim from one study that saturated fat contributes to heart disease by expanding the view to include the bigger picture.

    Research Watch

    Cancer: It’s Not the Meat - It’s How You Cook It

    Pancreatic cancer is the fourth most common cause of cancer deaths in the US, and is the most fatal cancer: 5-year survival rates are less than five percent. Studies associating dietary factors with pancreatic cancer have been inconsistent. Some have found associations with animal products, while others have not. Most studies finding such an association have wrongly attributed it to fat, saturated fat, or cholesterol without justification, which is contradicted by a new study published by Nothlings and coworkers, on October 5, 2005, in the Journal of the National Cancer Institute.

    The study analyzed data from the Multiethnic Cohort Study, collected prospectively (meaning the dietary data was collected before disease occurrence) over seven years, from more than 215,000 men and women aged 45-75 years old, 190,545 of whom contracted pancreatic cancer.

    While most studies claiming to indict meats and other animal products in disease pay little attention to the quality of the meat, this study provided analysis specific to processed meats, and discussed the possibility of the confounding effects of high-temperature cooking and grilling.

    The authors wrote in the abstract that “the strongest association was with processed meat,” noting a 68% increased risk in the uppermost quintile of consumption compared to the lowest quintile, and noted that the same comparison for pork and total red meat (beef, pork, and lamb) were about 50%, while no associations were found for other animal products, fat, or saturated fat.

    Beef consumption itself had a 21% increased risk comparing the highest and lowest quintiles, but the fourth (second highest) quintile had only a two percent increased risk, only a quarter of the eight percent increased risk seen in the second lowest quintile, making the association inconsistent and unconvincing. The association with pork was not linear, but was somewhat more convincing, being much higher in the fourth and fifth quintiles (44% and 53%) than in the second and third quintiles (14% and 12%), compared to the lowest quintile. “Red meat,” which the authors considered to mean beef, pork, and lamb, had a 45% increased risk when comparing the fifth quintile to the first, yet the second-highest quintile, the fourth, had only a 3% increased risk over the first! The third quintile had a 27% increased risk, and the second quintile had a 6% increased risk. Again, the association was very inconsistent and unconvincing.

    The authors noted that “processed meats” had the highest correlation out of all meats: 68% increased risk in the highest quintile compared to the lowest. Again, consistency was lacking. The third (middle) quintile actually had the highest association at a whopping 80%, while the second (59%) and fourth (47%) quintiles both had lower associations than the middle or highest quintile. However, the association with processed meat is still the most convincing out of all associations, because the associations were relatively high in all quintiles compared to the lowest, whereas the others showed weak and negligible correlations interspersed between strong ones.

    Unfortunately, where this study failed to deliver was in providing data on non-processed meats. If a substantial portion of “red meats” were processed, then they would carry an association that might not belong to unprocessed red meats.

    Although the study did not consider cooking temperature or cooking method, they rightly noted that cooking meats at high temperatures causes the formation of heterocyclic amines, and charcoal broiling and grilling cause the formation of polycyclic aromatic hydrocarbons, both of which have been found to be carcinogenic in animals. This study cited three other studies in its discussion finding that meats - including red meats -- that were not grilled or barbecued were not associated with pancreatic cancer, while barbecued and grilled red meats were. It is relieving to see researchers paying attention to these nuances and noting that the associations they have found between meats and cancer may well be due to carcinogens formed as a result of cooking and preserving methods rather than the meats themselves. I would add an additional consideration: prolonged cooking of meats, or the cooking of meats at high temperatures may not only cause the formation of injurious compounds, but also the destruction of protective compounds.

    The study found no statistically significant correlations for poultry, fish, dairy products, or eggs. Fat, saturated fat, and cholesterol were not associated with pancreatic cancer. Thankfully, the authors emphasized these negative findings by noting them in the abstract.

    Nothlings, et al., "Meat and Fat Intake as Risk Factors for Pancreatic Cancer: The Multiethnic Cohort Study," Journal of the National Cancer Institute, Vol. 97 No. 19 (2005) 1458-1465.

    Alzheimer’s Study Takes Cheap Shot At Cholesterol

    An October study published in the Archives of Neurology found strong correlations between body mass index and cholesterol levels, and the risk of Alzheimer’s Disease (AD).

    Although the unique angle of the study was that it measured body mass index, the authors considered their measurements of cholesterol levels to be important enough to note in the abstract and discussion. The authors noted that high cholesterol levels (above 251 mg/dL) about doubled the risk of AD, and that in combination with high blood pressure and obesity, they yielded a six-fold increase in the risk of AD.

    This study constitutes nothing more than a cheap shot against cholesterol. If the authors considered their findings on cholesterol to be worth devoting half of the results section of the abstract to, then it deserved a more careful analysis. Although total cholesterol levels above 251 mg/dL showed an association with Alzheimer’s, no attempt was made to analyze a dose-response effect between cholesterol levels and AD (that is, to demonstrate a consistent effect of higher cholesterol levels yielding higher rates of Alzheimer’s). More importantly, no adjustment of cholesterol levels for the apolipoprotein E epsilon-4 allele (ApoE4) or familial hypercholesterolemia was made.

    In multivariate analysis (that is, adjusting for possible confounding factors), a body mass index (BMI) over 30 carried a 144% increased risk of AD when adjusted for age, sex, education, and follow-up time; a BMI over 30 carried a 110% increased risk of AD when adjusted for blood pressure, cholesterol level, and smoking; leastly, BMI carried a substantially reduced 88% association with AD when adjusted for ApoE4, diabetes, and myocardial infarction. Fat intake and physical activity had no effect on the association between AD and BMI.

    These figures indicate that the third model, which adjusted for ApoE4, diabetes, and myocardial infarction, contained the most important confounding factors, accounting for about half of the association with obesity.

    Despite these strong effects of confounding factors on the association with obesity, the authors made no such attempt to adjust the association with total cholesterol levels with multivariate analysis.

    As explained in Part One and Part Two of’s Alzheimer’s articles, a contributing factor to Alzheimer’s disease may be an inability to incorporate cholesterol into cell membranes, possibly due to an inefficiency of the ApoE4 allele. ApoE4 is associated with high cholesterol levels, possibly for this very reason: free cholesterol levels outside of cells are higher when the cholesterol is not properly incorporated into cells and into their membranes. Some researchers have hypothesized that the ApoE4 allele is only harmful when combined with a high-carbohydrate diet, demonstrating that the ApoE4 allele has largely been weeded out in ancestries with a long history of agriculture.

    High cholesterol levels would also include those with familial hypercholesterolemia, which is a genetic disease that involves the lack of a properly functioning LDL receptor, not a disorder merely of high cholesterol levels. Associations with cholesterol levels that do not account for this confounding factor have no validity.

    The authors of any study asserting an association between cholesterol and Alzheimer’s disease owes their readers a thoughtful analysis of that association’s significance, including adjustment for familial hypercholesterolemia, the ApoE4 allele, carbohydrate intake, and other factors hypothesized to interact with the ApoE4 allele.

    Kivipelto, et al., "Obesity and vascular risk factors at midlife and the risk of dementia and Alzheimer disease," Archives of Neurology 62 (2005) 1556-1560.

    High-Cholesterol, High-Fat Diet Reduces Inflammation in Baboons -- But You Wouldn’t Know It From the Abstract

    An October 2005 study published in the American Journal of Clinical Nutrition measured the effect of a high-cholesterol, high-fat (HCHF) diet on inflammation in baboons. The authors noted the inconsistency with which cholesterol levels are associated with heart disease in humans, and sought to examine biomolecular changes in the baboons that are difficult to study in humans. They used both blood samples and biopsies of the femoral artery.

    The study was not controlled with an untreated sample of baboons. Instead, one group of baboons was fed a “normal” diet for a period of time, and then switched to an HCHF diet. Blood samples were taken at baseline (the beginning of the study period), three weeks, and 7 weeks, while biopsies were taken from the femoral artery at baseline and seven weeks, and put through different tests.

    Although the authors didn’t mention it in the abstract, discussion, or anywhere in the text of the study, the high-cholesterol, high-fat diet contained only 0.9% of calories as omega-3 fatty acids -- which are precursors to anti-inflammatory hormones -- compared to 3.4% on the “normal” diet -- nearly 4 times lower a concentration. Similarly, the HCHF diet contained 3.3 times fewer omega-6 fatty acids, which are precursors to both inflammatory and anti-inflammatory hormones. This was shown in Table 1, but the significance of the failure to control for these inflammatory and anti-inflammatory factors in the diet in a study measuring inflammation was not discussed anywhere in the text.

    The authors referred to the changes seen on the HCHF diet as “arterial endothelial dysfunction.” Endothelial cells line the insides of arteries and are the first line of defense against injurious factors within the arteries. In the abstract, they wrote: “We found that the HCHF diet induced a high inflammatory status, as indicated by increased concentrations of interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha), and monocyte chemoatractant protein-1 (MCP-1).”

    What the authors failed to note in the abstract was that this effect was temporary, and the long-term effect of the high-fat, high-cholesterol diet was to dramatically decrease these markers of inflammation. While TNF-alpha doubled at three weeks, its concentration was eight times lower at seven weeks compared to baseline. Likewise, while IL-6 concentration was nearly tripled at three weeks, it was seven times lower at seven weeks than at baseline. MCP-1 remained 60% higher than baseline at seven weeks, and another chemical called interleukin-8 was also much higher at seven weeks than baseline, while oxidized cholesterol levels began declining between three and seven weeks, antioxidant status remained unchanged on the diet, and other endothelial dysfunction markers remained unchanged.

    The high-fat, high-cholesterol diet -- which contained 6 times the fat and 318 times the cholesterol concentrations of the “normal” diet -- produced a doubling of total cholesterol levels, while the ratio of total to HDL cholesterol remained unchanged. No changes were found in C-reactive protein, which is regarded as a better predictor of heart disease than cholesterol levels. No atherosclerotic lesions were observed, nor were any fatty streaks observed in the arteries.

    In the cultured cells -- one set taken at baseline and the other taken at seven weeks of a high-fat, high-cholesterol diet -- output of MCP-1 and several insoluble inflammatory markers were about doubled on the HFHC diet, while no difference was found in the concentrations of cytokines or other soluble inflammatory markers.

    It is difficult to know exactly what this change would mean within the living baboon, since cells normally interact with many other factors secreted by neighboring cells to which they are attached, or from far-away cells in the body. When the researchers tested how these cells reacted to stimulators of inflammation, what they found was a dramatic decrease in inflammatory response.

    The authors hypothesized that feeding an HCHF diet might precondition cells to react with a greater degree of inflammation to substances that normally induce an inflammatory response. Yet they found the opposite. Cells from HCHF-fed baboons had an 8-fold lower VCAM-1 (a chemical that helps inflammatory cells infiltrate blood vessels) and 6-fold lower mE-selectin response to TNF-alpha, and a 9-fold decreased VCAM-1 response to lipopolysacccharide. The HCHF diet completely abolished the inflammatory response to both native and oxidized LDL.

    The authors concluded: “In summary, our results clearly show that the HCHF diet resulted not only in increased serum cholesterol concentrations but also in inflammation and endothelial dysfunction.” Yet, as one can see, the results are anything but clear. The authors disingenuously cited increases in inflammatory markers in the abstract when those same inflammatory markers were actually dramatically decreased by the high-fat, high-cholesterol diet when it was allowed to be fed over seven weeks. And even seven weeks is a very short time. Were the few other inflammatory markers that didn’t eventually fall after seven weeks there to stay, or was it only a matter of a few more weeks before they also would adjust?

    What does this study tell us about how high-cholesterol, high-fat diets affect humans? Nothing. The baboons themselves are not only not human, but, as noted in the text, “the baboons selected for this study were previously classified as high responders because their serum LDL-cholesterol concentrations increased after an HCHF diet.” In other words, the baboons were selectively bred to respond to such a diet with increased cholesterol concentration, when we know that high-cholesterol feeding usually causes very little change in cholesterol levels in most humans.

    The study also failed to control for inflammatory and anti-inflammatory hormone precursors in the diet. Since the HCHF diet had several times less omega-3 fatty acids, precursors to anti-inflammatory hormones, there is no way to know what portion of the results were due to a reduced quantity of this factor. Nevertheless, most measures of inflammation were either unchanged or even declined, some dramatically.

    The ultimate lesson of this study is how an abstract can be written to tell a very different story from the one told in the tables of data within the text. Just click on the link below to read the abstract for yourself -- and then consider whether you would have the same impression of the study if the abstract had been the only piece of information about it that you had read.

    Shi, et al, “Arterial endothelial dysfunction in baboons fed a high-cholesterol, high-fat diet,” American Journal of Clinical Nutrition, 82 (2005) 751-759.

    Inhibition of Inflammatory Factor Decreases Atherosclerosis in Mice With No Effect on Cholesterol or Triglycerides

    Yet another piece of research verifies that atheroclerosis can be inhibited by substances that have no effect on cholesterol levels, strongly suggesting that the beneficial effects seen in the use of cholesterol-lowering statin drugs are coincidental to, and not because of, their ability to lower cholesterol.’s review of Dr. Duane Graveline’s Statin Drugs Side Effects and the Misguided War on Cholesterol discusses how statins inhibit nuclear factor-kappa B, a molecule that activates the inflammatory process. Statins also inhibit cholesterol synthesis independently.

    A new study published in the Journal of Physiology and Pharmacology shows that pyrrolidine dithiocarbamate (PDTC), a substance that, like statins, inhibits nuclear factor-kappa B, but, unlike statins, does not lower cholesterol levels, substantially reduces atherosclerosis in mice. Like statins, PDTC also has antioxidant effects. The experiment used mice that were genetically altered to not produce apolipoprotein E (apoE) or the LDL receptor (LDLR). These mice develop severe dyslipidemia and athersclerosis.

    Blood vessels of mice treated with PDTC had only 62% as much area affected by atherosclerosis when examined longitudinally and only 51% as much area affected by atherosclerosis when measured cross-sectionally. PDTC treatment had no effect on cholesterol or triglyceride levels.

    This study is a small part of a large body of evidence that refutes the lipid hypothesis - that is, the idea that the formation of atherosclerotic lesions and the development of arterial obstruction and heart disease is a function of the concentration of cholesterol in the blood. In Issue #005 of this newsletter, I reported on a meta-analysis that found omega-3 fatty acids to be much more effective than statins at reducing deaths from heart disease, despite having no effect on cholesterol levels. Conversely, fibrates, niacin and “diet” were effective at reducing cholesterol levels but had no effect on deaths from heart disease, and fibrates increased death from cancer. The same issue reported on a study finding that resveratrol, a component of red wine, reduced atheroclerotic obstruction of rabbit arteries without affecting cholesterol levels. In The Cholesterol Myths Dr. Uffe Ravnskov pointed out that pathogenic changes in arterial plaques tend to occur after middle-age peaks in blood cholesterol levels have begun to decline, and Issue #006 of this newsletter reported on a new hypothesis put forth by Wilbert Gamble, in which he pointed out that arteries of mammary glands, which have very high concentrations of cholesterol and triglycerides, do not develop atherosclerosis. Anthony Colpo and Shane Ellison have made numerous other very important points refuting the lipid hypothesis.

    Hopefully this study and others like it, illuminating mechanisms by which the non-cholesterol-lowering effects of statin drugs can reduce heart disease risk, will eventually help waken us from the lull of junk science that has brought us the theoretical wasteland that is the lipid hypothesis.

    Jawien, et al., “Inhibition of nuclear factor-kappa B attenuates atherolsclerosis in apoE/LDLR - double knockout mice,” Journal of Physiology and Pharmacology, Vol. 56 No. 3 (2005) 483-489.

    Fructose Enhances Atherosclerosis in Cholesterol-Fed Rabbits

    One hypothesis of heart disease considers oxidized lipoproteins, rather than lipoprotein levels themselves, to contribute to heart disease, or to be markers of other oxidative stress that cause heart disease. One process that increases oxidative stress is called glycation. Glycation is the addition of a sugar molecule to another molecule. Glycation is an important process when performed by enzymes in the body, but it is believed that random glycation occurs when blood sugar levels are elevated, which causes random damage that can increase other measures of oxidative stress such as lipid peroxides.

    Since fructose is believed to be better at enhancing glycation than glucose, a recent study published by Tokita and coworkers in the Journal of Atherosclerosis and Thrombosis tested the effect of fructose feeding on the development of atherosclerosis in cholesterol-fed rabbits.

    Unsurprisingly, the rabbit -- an herbivorous animal adapted to its herbivorous diet -- develops atherosclerotic lesions and heart disease when fed a 1% cholesterol diet, which is 34 times the concentration of cholesterol that would be consumed on a diet of pure egg yolk. Yet even in the rabbit, and even at this concentration of cholesterol that is impossible even for an animal on an exclusively carnivorous diet to encounter in nature, it appears that it is not the cholesterol that is harmful, but the increased concentration of lipoproteins that results in the blood, which carry cholesterol on the inside, but contain phospholipids on the outside of their membranes that are vulnerable to oxidative stress. Thus, as reported in an earlier issue, when rabbits are fed the antioxidant resveratrol, the atherogenic effect of a 1% cholesterol diet is radically diminished.

    The Tokita study divided male Japnese white rabbits into three groups. Each group was fed for eight weeks on their respective diets: one, a control diet; another, the control diet supplemented with 1% cholesterol; the third, the control diet supplemented with 1% cholesterol and 10% fructose water in place of plain water.

    The degree of atherosclerotic lesions formed on the cholesterol-fructose diet was 58% greater than that observed in rabbits fed cholesterol alone. Supporting the hypothesis that oxidative stress is involved in the effect of cholesterol-feeding, the cholesterol-fed rabbits had a significant increase in peroxide levels in the aorta compared to the controls. Yet the cholesterol-fructose-fed rabbits had a substantially greater level of peroxides in the aorta than did the cholesterol-fed rabbits.

    Unfortunately, this study didn’t control for caloric intake. Adding fructose to the water rather than replacing another source of energy with fructose must have increased the caloric intake of the rabbits. The value of the study would have been enhanced if a fourth group of rabbits fed a 10% glucose water was also included.

    What does this mean for humans? The connection between oxidized lipoproteins in humans isn’t very clear. In Issue #003 of this newsletter, I reported on a study that found a strong correlation between oxidized lipoproteins and coronary obstruction in persons under the age of 60, but in persons over the age of 60 there was no relationship. Since most heart disease occurs in older rather than younger individuals, the significance of the finding is questionable. On the other hand, since insulin resistance and diabetes are occurring more often, and since some young people do experience heart disease, possibly related to this trend, and since fructose is also capable of inducing insulin resistance, this may shed light on how our increasing consumption of fructose is involved in our increasing decline in many parameters of health.

    Fructose is the predominant sugar in fruit and fruit juice, constitutes half of table sugar, and constitutes an equal or much higher proportion of the sugars in high fructose corn syrup, found in many sodas and packaged foods. Consumption of fructose has dramatically increased over the past several decades. Unlike cholesterol, which is consumed in milligram per serving quantities, tends of grams of fructose can be found in single servings of foods and drinks. It is impossible to consume a 1% cholesterol diet outside of a laboratory setting, while it is very possible to eat a 10% fructose diet, or a diet much higher than that in fructose, when selecting from the typical menu of modern foods and junk foods. If the increase in oxidative stress found in this study is due to the fructose, it represents one more reason to moderate our fructose consumption and avoid excessive consumption of sugar and other junk foods.

    Tokita et al., “Fructose ingestion enhances atherosclerosis and deposition of advanced glycated end-products in cholesterol-fed rabbits,” Journal of Atherosclerosis and Thrombosis, Vol. 12, No. 5 (2005) 260-267.

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    Weston A. Price Foundation Annual Conference

    Conference Details

    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.

    If you need to make travel arrangements, we encourage you to use Price Line, with which you can search for the cheapest price according to your own specifications.

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    Please take notice that the contents of this newsletter and are copyright of Chris Masterjohn, 2005, and that this information is not to be construed or understood as any form of advice. Please visit our disclaimer page here.

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