The American Heart Association misrepresented data on saturated v. polyunsaturated fats

The American Heart Association misrepresented data on saturated v. polyunsaturated fats: According to the paper... http://fb.me/CDBem1kd

Thank You Weston A Price for this information!
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Some Quotes:

"Peer review is critical for ensuring that evidence assembled in a meta-analysis is complete and impartial. Regrettably, the recent AHA Advisory [1] relied heavily upon a one-line meta-analysis cited in a non peer-reviewed book chapter [2] to support its position that high intakes of omega-6 fatty acids reduce CHD. Unfortunately, the credibility of this advisory is undermined by four additional critical errors."

1) The AHA Advisory mistakenly cited the Sydney Diet-Heart Study...

2) Although the AHA Advisory [1] criticizes other studies for failing to distinguish between “distinct effects” of omega-3 and omega-6 fatty acids, it commits this error throughout.

3) The AHA Advisory imprecisely contends that its analysis pertains to trials that “evaluated the effects of replacing saturated fatty acids with PUFAs” [1] despite its citation of trials where experimental diets displaced large quantities of trans fatty acid-rich partially hydrogenated oils.

4) The AHA Advisory failed to indicate that the Rose Corn Oil Trial [5] gives a rare opportunity to evaluate the specific effects of increased LA, because corn oil has little omega-3 ALA.

 

 

The advisory fails to inform the public that an important tissue indicator of CVD risk the ‘Omega-3 Index’5, reflects the proportion of EPA and DHA in erythrocytes, a representative phospholipid eicosanoid precursor pool. The Omega-3 Index is regarded5 as superior to LDL as a biomarker predicting cardiovascular mortality. Paradoxically, the advisory reports that increasing LA intakes decreases EPA accretion, (i.e. lowers the Omega-3 Index and increases CVD risk), but implies without comparative quantitation that lowering LA intakes would elevate LDL levels and increase net CVD risk. However, lowering LA by LNA substitution could maintain PUFA intakes and result in a more favorable Omega-3 Index.

The advisory unfortunately moves from suggestive and highly conditional interpretations to the

unsupported clinical admonition that “To reduce omega-6 PUFA intakes from their current levels would be more likely to increase than to decrease risk for CHD.”
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Please read the complete paper here.



 

High fat diet during pregnancy leads to severe liver disease - Kresser

More silly shenanigans against saturated fat

 Seriously. I cannot believe the stuff that gets published in medical journals these days. I don’t know which is the scarier possibility: that the researchers are really so poorly trained that they consistently violate the most basic principles of medical research (that you probably learned in your 8th grade science class), or that they are so dishonest that they intentionally and blatantly lie about their results.

A prime example of this is an article that came across my newsfeed a couple of days ago. The headline read “High fat diet during pregnancy leads to severe liver disease“. I’m always very, very suspicious when I see articles like this because of my previous experience evaluating such studies. All too often researchers make basic (and frankly, inexcusable) mistakes like lumping all fat types together (i.e. combining saturated fat with polyunsaturated fat, although the two fatty acids have completely different effects on human physiology).

I didn’t have time to review the study and write about it, so I emailed Chris Masterjohn, a researcher pursuing a PhD in Nutritional Sciences with a concentration in Biochemical and Molecular Nutrition at the University of Connecticut. Chris has a blog called The Daily Lipid where he writes about the benefits of saturated fat and the dangers of polyunsaturated fat. Turns out Chris had seen the article on ScienceDaily too and was planning to write a critique. Here’s what he wrote. I encourage you to check out his blog, and also his website, both of which have some great information about the health benefits of cholesterol and saturated fat.

According to a recent article on ScienceDaily, scientists have discovered that mothers who eat too much saturated fat during pregnancy will give their future child severe fatty liver disease once he or she becomes an adult.

The use of words in this article like “mother,” “child,” and “adulthood” suggests that the researchers performed some type of scientific research in humans. In fact, ScienceDaily goes so far as to claim that the researchers were studying the consumption of high-fat diets during “a woman’s pregnancy.”
Nowhere in the article do the authors inform the reader that the research was performed in mice. This is the first time I have ever read of a mouse referred to as a “woman.”

The most egregious distortion of the study, however, comes from one of the researchers himself:
Professor Christopher Byrne, with colleagues Dr Felino Cagampang and Dr Kim Bruce, of the University’s School of Medicine and researchers at King’s College London, conducted the study, funded by the BBSRC. Prof Byrne explained: “This research shows that too much saturated fat in a mother’s diet can affect the developing liver of a fetus, making it more susceptible to developing fatty liver disease later in life. An unhealthy saturated fat-enriched diet in the child and young adult compounds the problem further causing a severe form of the fatty liver disease later in adult life.”
Really, “saturated fat” causes liver disease? This stands in surprising contrast to other rodent studies showing that saturated fat prevents liver disease:

• A 1995 paper in the journal Gastroenterology lauded “dietary saturated fatty acids” as “a novel treatment for alcoholic liver disease” after showing that substitution of saturated palm oil for polyunsaturated fish oil reduced alcohol-induced liver damage.
• A more recent paper published in the Journal of Nutrition 2004 showed that saturated fat from MCT oil (medium-chain fats similar to those in coconut oil) and beef tallow reduced alcohol-induced liver damage when substituted for polyunsaturated corn oil. In fact, they replaced 20 percent, 45 percent, or two-thirds of the corn oil with saturated fat and found that the more saturated fat they used, the greater the protective effect.
• An even more recent paper published in the journal Hepatology in 2005 found that rats fed corn oil readily developed liver damage when fed over a quarter of their calories as alcohol, but rats fed saturated cocoa butter were virtually immune to liver damage when consuming the same amount of alcohol.
• A 2007 study published in the journal Nutrition and Metabolism found that although corn oil-based high-fat diets can induce non-alocholic fatty liver disease in rodents, long-term feeding of high-fat diets based on coconut oil or butter cannot.

So how is it that “saturated fat” wound up causing liver disease in the offspring of these mice?
If we look at “supplementary table 1,” we find that the “saturated fat” used in this study was mostly monounsaturated and polyunsaturated fat. In fact, 22 percent of the fat on the low-fat diet was saturated, while only 15 percent of the fat on the high-fat diet was saturated!

That means that less than seven percent of the calories from the “unhealthy saturated-fat-enriched diet” actually came from saturated fat.

The “unhealthy saturated fat-enriched diet” actually contained 44 percent of its fat as polyunsaturated fatty acids (PUFA) and almost twenty percent of its total calories as PUFA. This is in great excess of the PUFA consumption seen even in the Standard American Diet (SAD), loaded in processed PUFA-rich vegetable oils.

Apparently “saturated fat” consumed during a “woman’s pregnancy” leads to liver disease once the “child” reaches “adulthood” only when the “saturated fat” is the highly polyunsaturated kind one would find in corn oil and the “woman” is a light, fluffy critter no one would ever mistake for a human.

What can we learn from this study? Perhaps that we can never trust the news account of a research study. Unfortunately we cannot even trust the quotes in those news account taken from the researchers themselves.
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Read the full article here.

Good Fats, Bad Fats: Separating Fact from Fiction

Written by Chris Masterjohn    March 24 2012

Few driving factors have had such a profound influence on the transition from traditional to modern industrial diets as the campaign against animal fats and tropical oils. We have responded to this campaign not only by depriving ourselves of the nutrient-dense animal foods so important to human health, but also by replacing these traditional fats with processed foods laden with refined vegetable oil, flour, and sugar. Since its inception, this campaign has been based on a series of myths. These include the myths that saturated fat is the “bad fat” while polyunsaturated fat is the “good fat,” that arachidonic acid is the “bad fat,” and that so-called “solid fats” are empty calories with no nutritional value. We will consider each of these myths in the pages that follow. MYTH 1: SATURATED FAT IS BAD, POLYUNSATURATED FAT IS GOOD The myth that saturated fatty acids are “bad fat” while polyunsaturated fatty acids (PUFA) are “good fat” emerged in the 1950s as the dietheart hypothesis. This hypothesis stated that the saturated fat found in animal fats and tropical oils would contribute to heart disease by raising blood cholesterol levels while the PUFA found in vegetable oils would do just the opposite. If the nutritional and medical establishments had taken the approach of Weston Price and endeavored to begin unraveling the causes of heart disease by studying the diets and lifestyles of populations that were immune to the disease, it is unlikely the diet-heart hypothesis would ever have emerged. The traditional diets of Pacific islanders free of heart disease, for example, vary widely in their proportions of fat and carbohydrate, but as can be seen in Figure 1, they are all rich in saturated fat and low in PUFA when compared to the standard American diet.1,2,3 Each of these traditional diets is based primarily on starches, fruits, coconut and fish, so the PUFA comes mostly from fish rather than from vegetable oils. The foundation of the establishment’s approach to the riddle of heart disease featured no such investigation of traditional diets, and the result of this negligence was the diet-heart hypothesis. Advocates of this hypothesis supported it in the early 1950s with two key pieces of evidence. The first was that blood cholesterol levels were statistically associated with heart disease risk.4 The second was that, in highly controlled laboratory experiments, replacing saturated fats like butter, lard or coconut oil with polyunsaturated oils like corn or safflower oil would lower blood cholesterol levels.5,6 Playing a game of connect the dots, they argued that substituting vegetable oils for traditional animal fats and tropical oils would lower the risk of heart disease. In 1957, the American Heart Association called the hypothesis “highly speculative,” and concluded that “the evidence at present does not convey any specific implications for drastic dietary changes, specifically in the quantity or type of fat in the diet of the general population, on the premise that such changes will definitely lessen the incidence of coronary or cerebral artery disease.”7 Four years later, the state of the evidence remained the same but three members of the committee were dropped and replaced by four new members, including Ancel Keys, a leading proponent of the hypothesis. The updated report recommended that men who are overweight, have high blood pressure or high cholesterol, lead “sedentary lives of relentless frustration,” or have a strong family history of heart disease should replace part of the saturated fat in their diets with PUFA.8 The hypothesis nevertheless remained controversial in the scientific community for decades. The tide turned in 1984 when the Coronary Primary Prevention Trial showed that cholestyramine could prevent heart attacks.9 Cholestyramine is a drug that binds bile acids in the intestine and causes their excretion in the feces. As a result, the liver takes cholesterol in from the blood in order to make more bile acids and the concentration of cholesterol in the blood falls. Time magazine hailed the trial as a vindication of the American Heart Association’s twenty-three-year-old stance against animal fats. Butter, eggs, and bacon were all conspicuously absent from the treatment protocol of this trial, but Time nevertheless ran a cover story entitled “Hold the Eggs and Butter,” which artfully featured a frowning face with eyes of sunnyside up eggs and a downturned mouth of a slice of fried bacon. The article declared, “cholesterol is proved deadly, and our diet may never be the same.”10 In our own day, the American Heart Association continues to promote the hypothesis with vigor. In 2009, it updated its official stance, recommending at least 5 to 10 percent of calories as omega-6 PUFA with additional PUFA coming from omega-3 sources, and concluded that intakes even higher than this “appear to be safe and may be even more beneficial (as part of a low-saturated fat, low-cholesterol diet).”11 It was one thing to promote this hypothesis in 1961 when it had never been tested, but to throw a PUFA party in 2009 and suggest we all wash away our cardiovascular concerns with swigs of soybean oil is to ignore with callow abandon all the lessons we have learned from clinical trials published in the intervening decades. Six randomized, controlled trials specifically testing the effect of the substitution of polyunsaturated vegetable oils for animal fats on heart disease have been published.12-17 These trials were all published between 1965 and 1989. Two of them found that vegetable oils increased the risk of heart disease,12, 14 although one of these creatively concluded from this that “men who have had myocardial infarction are not a good choice for testing the lipid hypothesis.”14 Two of them reported no effect of vegetable oil.13, 15 The authors of one of these two trials, however, only reported the results half-way through the study.15 In the final report, they pooled the two groups together and compared them to a new control group that had not received any dietary advice at all.18 As a result, we have no way of knowing the true effect of vegetable oil in that study. Two of the six trials were double-blind, and deserve special attention.16, 17 These are the Minnesota Coronary Survey and the Los Angeles Veterans Administration Hospital Study. The Minnesota Coronary Survey tested the effect of substituting vegetable oils for animal fats in hospital patients who were on the diets for an average duration of only one year.16 As shown in Figure 2, vegetable oil had no effect on cardiovascular disease. While its effect on total mortality was not statistically significant, however, total survival was nevertheless better in the group eating saturated fat. We naturally must wonder what would have happened to total mortality had the subjects been on the diets for longer than one year. The Los Angeles Veterans Administration Hospital Study lasted over eight years, and most of the subjects were enrolled for at least six years.17 It is the only one of these six studies where the mean age of the subjects was greater than sixty, so it allows us to better see the effect of vegetable oils on the risk of cancer, if such an effect exists. Subjects eating the diet rich in vegetable oils had a lower risk of cardiovascular mortality, but a higher risk of mortality from other causes. As a result, diet had no effect on total mortality. This is clearly shown in Figure 3. As shown in Figure 4, deaths from cancer began to increase in the vegetable oil group after two years, and the increase became much larger after five years.19 As shown in Figure 5, the difference in the incidence of all deaths from non-cardiovascular causes began to increase in the vegetable oil group only after four years and remained extremely small until seven years.17 After seven years, non-cardiovascular mortality began to increase rapidly. The disturbing possibility that the true harms of vegetable oils take years to emerge did not escape the authors, and they concluded that “future clinical trials of diets rich in unsaturated fat must be planned for periods well in excess of eight years, rather than for the five-year periods that have been the usual goal.” Such longer trials have never been conducted. Although a superficial analysis of this study would suggest that vegetable oils decrease the risk of heart disease while increasing the risk of cancer and other diseases, this may not be the case. Even though the investigators randomly allocated the subjects to each group, the randomization failed to equally balance rates of smoking between the two groups. There were twice as many heavy smokers and 60 percent more moderate smokers in the group consuming traditional animal fats, while there were more light smokers and non-smokers in the group consuming vegetable oils.17 The diet rich in animal fats, moreover, was deficient in vitamin E. Animal experiments suggest that we should obtain 0.6 milligrams of vitamin E for every gram of PUFA we consume. The vegetable oil diet came close to this requirement, supplying a ratio of over 0.5, but the animal fat diet fell miserably short of it, supplying a ratio of less than 0.2.20 Animal fats are not intrinsically deficient in vitamin E, however. The average store-bought butter, for example, easily meets the vitamin E requirement, and a high-quality pastured butter can provide more than double this requirement. 21,22 It is thus unclear why the animal fat diet was so deficient in the vitamin, but this deficiency in combination with the higher rate of smoking may have contributed to the greater risk of cardiovascular disease in the animal fat group. It appears from these studies, then, that vegetable oils promote cancer while animal fats protect against it even in the presence of smoking and vitamin E deficiency. Vegetable oils may promote heart disease as occurred in two studies,12, 14 but the results of the LA Veterans Administration Hospital Study make this unclear. The authors of this study themselves concluded as follows: “. . . we consider our own trial, with or without the support of other published data, to have fallen short of providing a definitive and final answer concerning dietary prevention of heart disease.” These studies leave many questions to be answered. Are the effects of vegetable oils with different proportions of omega-6 and omega-3 fatty acids different from one another? What is the effect of vegetable oils over a lifetime, beginning in youth? Are there certain dietary contexts that make vegetable oils harmful, and others that make them safe? The larger question, however, is whether, given all this uncertainty, we should make ourselves guinea pigs for these newfangled foods. No one has yet offered a better summary of the issue than that offered by the late endocrinologist Broda Barnes in his 1976 book, Solved: The Riddle of Heart Attacks: Everyone should have the privilege of playing Russian Roulette if it is desired, but it is only fair to have the warning that with the use of polyunsaturated fats the gun probably contains live ammunition.23 MYTH 2: ARACHIDONIC ACID IS A "BAD FAT" The second myth is that animal fats promote inflammation because they contain a small amount of the omega-6 PUFA arachidonic acid, found primarily in liver and egg yolks with smaller amounts in butter and meat fats. This hypothesis emerged in the scientific literature in the 1980s and 1990s as researchers began attributing the low rate of heart disease among traditional Inuit to their consumption of large amounts of omega-3 fatty acids from marine oils.24 Researchers argued that these omega-3 fatty acids were protective precisely because they counteracted the inflammatory effects of arachidonic acid. Barry Sears popularized this idea in his best-selling 1995 book The Zone Diet.25 Therein, he proclaimed excess arachidonic acid “your worst biological nightmare.” Not only is it inflammatory, he wrote, but it “is so potent and so dangerous that when you inject it into the bloodstream of rabbits the animals die within three minutes.” Despite these sensational claims, arachidonic acid is not inherently inflammatory. Its deficiency, in fact, produces a number of inflammatory symptoms, including dandruff, hair loss, infertility and irritated, red, sore, swollen, and scaly skin.26,27 Inhibiting supposedly “inflammatory” products made from arachidonic acid such as prostaglandin E2 using over-the-counter nonsteroidal anti-inflammatory drugs (NSAIDs) can produce a number of inflammatory outcomes. These drugs induce intestinal pathologies that closely resemble celiac disease in laboratory animals in response to gluten or even egg white,28,29 and they interfere with the resolution of autoimmune conditions.30 Although it is true that our bodies use arachidonic acid to initiate inflammation—a vital process if we want to survive to adulthood without being wiped out by pathogenic microbes —our bodies also use this fatty acid to suppress inflammation or to resolve inflammation once it has run its course. We use arachidonic acid to make cell-to-cell junctions that form physical barriers against toxins and pathogens,31-33 to create a unique environment in the gut that causes our immune system to react to food proteins with tolerance instead of intolerance,34 and to make important molecules called lipoxins that help resolve existing inflammation.30,35 We even use arachidonic acid to signal the conversion of omega-3 fatty acids to resolvins, another class of molecules that help resolve inflammation.30 It makes little sense to characterize this fatty acid as singularly inflammatory in nature when it has so many anti-inflammatory functions, and when it is present in so many traditional foods consumed by populations free of inflammatory diseases. MYTH 3: SOLID FATS = EMPTY CALORIES The third myth, that “solid fats” are empty calories with no nutritional value, has emerged more recently with the latest revision of the USDA’s Dietary Guidelines for Americans. This document defines a “nutrient-dense” food as one whose “nutrients and other beneficial substances . . . have not been 'diluted' by the addition of calories from added solid fats, added sugars, or added refined starches, or by the solid fats naturally present in the food.”36 This peculiar definition of “nutrient-dense” allows the addition of liquid oils but requires the removal of natural solid fats. “Solid fats” are defined as “fats with a high content of saturated and/or trans fatty acids, which are usually solid at room temperature.” Using this definition, one could ostensibly make milk more “nutrient-dense” by replacing its natural butterfat with corn oil. The natural fats present in foods carry all of their fat-soluble vitamins, and added fats further increase their bioavailability. Human trials, for example, have clearly shown that butterfat increases the absorption of vitamin E,37 and that canola oil increases the absorption of carotenoids from salad.38 The more fat one adds, according to these studies, the greater the absorption of fatsoluble nutrients. This can hardly be considered a decrease in nutrient density! Animal experiments, moreover, suggest that fats and oils low in PUFA provide the best absorption of fat-soluble nutrients. When compared to corn oil, for example, olive oil roughly doubles the absorption of lycopene and astaxanthin in rats.39 If the lower absorption seen with corn oil is a result of its higher PUFA content, then socalled “solid fats” might prove superior even to olive oil, and certainly to canola oil. THE TRUTH SHALL SET US FREE Clinical trials have failed miserably to support the hypothesis that replacing saturated animal fats with polyunsaturated vegetable oils would prevent heart disease. They have shown instead that vegetable oils likely promote cancer and perhaps even heart disease. Arachidonic acid in animal fat is not "deadly," but is necessary for our bodies to initiate, suppress, or resolve inflammation as needed. These are all vital processes that allow us to respond appropriately to our environment. “Solid fats” do not “dilute” the nutrient density of our food. On the contrary, they carry fat-soluble nutrients and provide for their absorption. When we observe the ease with which these myths arise and the vigor with which they are promulgated to the public, it is important for us not to create our own equal and opposite myths. We should keep in mind that traditional diets varied widely in their fat and carbohydrate contents. Nutritional needs vary from person to person, and from one stage of life to another. Any health-promoting component of the diet, including animal fat, can become harmful if it displaces other health-promoting components. It is thus entirely plausible that some people under some circumstances may benefit by reducing their intakes of animal fat and increasing their intakes of other traditional foods. We should thus beware of promoting any “correct” amount of animal fat to consume. We should instead look upon the earth’s menu of natural, traditional foods without fear, and choose those foods we need and enjoy in freedom. REFERENCES 1. Lindeberg S, et al. Age relations of cardiovascular risk factors in a traditional Melanesian society: the Kitava study. Am J Clin Nutr. 1997;66(4):845-52. 2. Prior IA, et al. Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau island studies. Am J Clin Nutr. 1981;34(8):1552-61. 3. USDA Agricultural Research Service.What We Eat in America, NHANES 2007-2008. Table 5. Energy Intakes: Percentages of Energy from Protein, Carbohydrate, Fat, and Alcohol, by Gender and Age, in the United States, 2007- 2008 http://www.ars.usda.gov/SP2UserFiles/Place/12355000/pdf/0708/Table_5_EIN_GEN_07.pdf Accessed December 29, 2011. 4. Keys A. Atherosclerosis: a problem in newer public health. J Mt Sinai Hosp NY. 1953;20(2):118-39. 5. Kinsell LW, et al. Dietary modification of serum cholesterol and phospholipid levels. J Clin Endocrinol. Metab. 1952;12(7):909-13. 6. Ahrens EH Jr., et al..Effect on human serum lipids of substituting plant for animal fat in diet. Proc Soc Exp Biol Med. 1954;86(4):872-8. 7. Page IH, et al. Atherosclerosis and the Fat Content of the Diet. Circulation. 1957;16:163-178. 8. Dietary fat and its relation to heart attacks and strokes: report by the Central Committee for Medical and Community Program of the AHA. 1961;23:133-6. 9. The Lipid Research Clinics Coronary Primary Prevention Trial results. II. The relationship of coronary heart disease to cholesterol lowering. JAMA. 1984;251(3):365-74. 10. Wallis C, Crook C, Delaney P, Gribben S. Hold the Eggs and Butter. Time magazine. March 26, 1984. 11. Harris WS, et al. Omega-6 fatty acids and risk for cardiovascular disease: a science advisory from the AHA Nutrition Subcommittee of the Council on Nutrition, Physical Activity, and Metabolism; Council on Cardiovascular Nursing; and Council on Epidemiology and Prevention. Circulation. 2009;119(6):902- 7. 12. Rose GA, et al. Corn oil in treatment of ischaemic heart disease. Br Med J. Jun 12 1965;1(5449):1531- 1533. 13. Controlled trial of soya-bean oil in myocardial infarction. Lancet. Sep 28 1968;2(7570):693-699. 14. Woodhill JM, et al. Low fat, low cholesterol diet in secondary prevention of CHD. Adv Exp Med Biol. 1978;109:317-330. 15. Bierenbaum ML, et al. Modified-fat dietary management of the young male with CD. A five-year report. JAMA. Dec 25 1967;202(13):1119-1123. 16. Frantz ID, Jr., et al. Test of effect of lipid lowering by diet on cardiovascular risk. Minnesota Coronary Survey. Arteriosclerosis. Jan-Feb 1989;9(1):129-135. 17. Dayton S, et al. A Controlled Clinical Trial of a Diet High in Unsaturated Fat in Preventing Complications of Atherosclerosis. Circulation. 1969;150(1 Suppl 2):II-1-II-2. 18. Bierenbaum ML, et al. Ten-year experience of modified-fat diets on younger men with coronary heartdisease. Lancet. 1973;1(7817):1404-7. 19. Pearce ML and Dayton S.Incidence of Cancer in Men on a Diet High in Polyunsaturated Fat. Lancet. 1971;297(7697):464-467. 20. Dayton S, et al. Vitamin E Status of Humans During Prolonged Feeding of Unsaturated Fats. J Lab Clin Med. 1965;65:739-47. 21. NutritionData: know what you eat. Butter, without salt. http://www.nutritiondata.com/facts/dairy-andegg- products/133/2 Accessed April 21, 2009. 22. Searles SK, et al. Vitamin E, Vitamin A, and Carotene Contents of Alberta Butter. J Dairy Sci. 1970;53(2):150-5. 23. Barnes BO, Solved: The Riddle of Heart Attacks. Fries Communications, 1976. 24. Mann NJ, et al. Arachidonic Acid Content of the Australian Diet Is Lower than Previously Estimated. J Nutr. 1995;125:2528-35. 25. Sears B. The Zone Diet. HarperCollins, 1995. 26. Burr GO, Burr MM. A New Deficiency Disease Produced by the Rigid Exclusion of Fat From the Diet. J Biol Chem. 1929;LXXXII(2):345-67. 27. Turpeinen O. Further Studies on the Unsaturated Fatty Acids Essential in Nutrition. J Nutr. 1938;15(4):351-66. 28. Newberry RD, Stenson WF, Lorenz RG. Cyclooxygenase-2-dependent arachidonic acid metabolites are essential modulators of the intestinal immune response to dietary antigen. Nat Med. 1999;5(8):900-6 29. D'Arienzo R, Stefanile R, Maurano F, Luongo D, Bergamo P, Mazzarella G, Troncone R, Auricchio S, David C, Rossi M. A deregulated immune response to gliadin causes a decreased villus height in DQ8 transgenic mice. Eur J Immunol. 2009;39(12):3552-61. 30. Chan MM, Moore AR. Resolution of Inflammation in Murine Autoimmune Arthritis Is Disrupted by Cyclooxygenase-2 Inhibition and Restored by Prostaglandin E2-Mediated Lipoxin A4 Production. J Immunol. 2010;184(11):6418-6426. 31. Agrawal R, Daniel EE. Control of gap junction formation in canine trachea by arachidonic acid metabolites. Am J Physiol. Mar 1986;250(3 Pt 1):C495-505. 32. Civitelli R, Ziambaras K, Warlow PM, et al. Regulation of connexin43 expression and function by prostaglandin E2 (PGE2) and parathyroid hormone (PTH) in osteoblastic cells. J Cell Biochem. Jan 1 1998;68(1):8-21. 33. Blikslager AT, Roberts MC, Rhoads JM, Argenzio RA. Prostaglandins I2 and E2 have a synergistic role in rescuing epithelial barrier function in porcine ileum. J Clin Invest. Oct 15 1997;100(8):1928-1933 34. du Pre MF, Samson JN. Adaptive T-cell responses regulating oral tolerance to protein antigen. Allergy. 2011;66(4):478-90. 35. Banneberg G, Serhan CN. Specialized pro-resolving lipid mediators in the inflammatory response: An update. Biochim Biopys Acta. 2010; 1801(12):1260-73. 36. U.S. Department of Agriculture, U.S. Department of Health and Human Services. Dietary Guidelines for Americans 2010. www.dietaryguidelines.gov. Accessed December 30, 2012. 37. Bruno RS, Leonard SW, Park SI, Zhao Y, Traber MG. Human vitamin E requirements assessed with the use of apples fortified with deuterium-labeled alpha-tocopheryl acetate. Am J Clin Nutr. 2006;83(2):299- 304. 38. Brown MJ, Ferruzzi MG, Nguyen ML, Cooper DA, Eldridge AL, Schwartz SJ, White WS. Carotenoid bioavailability is higher from salads ingested with full-fat than with fat-reduced salad dressings as measured with electrochemical detection. Am J Clin Nutr. 2004;80(2):396-403. 39. Clark RM, Yao L, She L, Furr HC. A comparison of lycopene and astaxanthin absorption from corn oil and olive oil emulsions. Lipids. 2000;35(7):803-6. This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly magazine of the Weston A. Price Foundation, Spring 2012. ==================================================================================================== Read the full article here.