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Polyunsaturated and trans-fats are bad

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BIOLOGICAL RANCIDIFICATION  --  Lancet 1969 Volume 294, Issue 7622, 27 September 1969, Pages 684–688   http://www.sciencedirect.com/science/article/pii/S0140673669903900

Autoxidation, a destructive interaction between unsaturated fats and molecular oxygen, accounts for many industrial and natural-decay processes. The possibility that the body fats might undergo a similar kind of degradation is still largely ignored—perhaps because the irregular irreversible pattern of this type of process seems at odds with the enzyme-controlled reversible pathways of traditional biochemistry. Yet work with mitochondria and other biological preparations has shown that the processes commonly grouped together as " degeneration ", " fatigue ", and " ageing " (none of which have a basis in classical enzymology) develop in close parallel with evidence of rancidification.


Rancidification, the product of which can be described as rancidity, is the process which causes a substance to become rancid, that is, having a rank, unpleasant smell or taste. Specifically, it is the  hydrolysis and/or autoxidation of fats into short-chain aldehydes and ketones which are objectionable in taste and odor.[Hydrolytic   . rancidity refers to the odor that develops when triglycerides are hydrolyzed and free fatty acids are released. This reaction of lipid with water sometimes requires a catalyst, but results in the formation of free fatty acids and salts of free fatty acids. In particular, short-chain fatty acids, such as common butter fats, are odorous….. Oxidative rancidity is associated with the degradation by oxygen in the air. Via a free radical process, the double bonds of an unsaturated fatty acid can undergo cleavage, releasing volatile aldehydes and ketones. Oxidation primarily occurs with unsaturated fats. For example, even though meat is held under refrigeration or in a frozen state, the poly-unsaturated fat will continue to oxidize and slowly become rancid…. Rancidification can produce potentially toxic compounds associated with long-term harmful health effects concerning advanced aging, neurological disorders, heart disease, and cancer.… The effectiveness of water-soluble antioxidants is limited in preventing direct oxidation within fats, but is valuable in intercepting free radicals that travel through the aqueous parts of foods. A combination of water-soluble and fat-soluble antioxidants is ideal, usually in the ratio of fat to water.  http://en.wikipedia.org/wiki/Rancidification  




Malonyldialdehyde (MDA) formation, a measure of polyunsaturated fat autoxidation, was estimated in normal human red cells incubated in vitro. Exposure to oxygen under a variety of conditions did not induce autoxidation. Exposure to hydrogen peroxide was either by the addition of a hydrogen peroxide solution or by incubation in an atmosphere saturated with hydrogen peroxide vapour. A pattern of MDA formation was established with both methods…. A number of recognized antioxidants inhibited peroxide-induced MDA formation. Inhibition was proportional to the logarithm of the antioxidant concentration.

The Autoxidation of Human Red Cell Lipids induced by Hydrogen Peroxide, 1971  http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2141.1971.tb00790.x/abstract


Lipid peroxidation refers to the oxidative degradation of lipids. It is the process in which free radicals "steal" electrons from the lipids in cell membranes, resulting in cell damage. This process proceeds by a free radical chain reaction mechanism. It most often affects polyunsaturatedfatty acids, because they contain multiple double bonds in between which lie methylene bridges (-CH2-) that possess especially reactive hydrogens. As with any radical reaction, the reaction consists of three major steps: initiation, propagation, and termination.  Initiation is the step in which a fatty acid radical is produced. The most notable initiators in living cells are reactive oxygen species (ROS), such as OH· and HO2, which combines with a hydrogen atom to make water and a fatty acid radical.  The fatty acid radical is not a very stable molecule, so it reacts readily with molecular oxygen, thereby creating a peroxyl-fatty acid radical. This radical is also an unstable species that reacts with another free fatty acid, producing a different fatty acid radical and a lipid peroxide, or a cyclic peroxide if it had reacted with itself. This cycle continues, as the new fatty acid radical reacts in the same way.[1]  The end products of lipid peroxidation are reactive aldehydes, such as malondialdehyde (MDA) and 4-hydroxynonenal(HNE), the second one being known also as "second messenger of free radicals" and major bioactive marker of lipid peroxidation, due to its numerous biological activities resembling activities of reactive oxygen species. http://informahealthcare.com/toc/fra/44/10  In addition, end-products of lipid peroxidation may be mutagenic and carcinogenic.[3] For instance, the end-product malondialdehyde reacts with deoxyadenosine and deoxyguanosine in DNA, forming DNA adducts to them, primarily M1G.[3]  Certain diagnostic tests are available for the quantification of the end-products of lipid peroxidation, to be specific, malondialdehyde (MDA).[3] The most commonly used test is called a TBARS Assay (thiobarbituric acid reactive substances assay). Thiobarbituric acid reacts with malondialdehyde to yield a fluorescent product. However, there are other sources of malondialdehyde, so this test is not completely specific for lipid peroxidation.[5] In recent years development of immunochemical detection of HNE-histidine adducts opened more advanced methodological possibilities for qualitative and quantitative detection of lipid peroxidation in various human and animal tissues (http://informahealthcare.com/toc/fra/44/10) as well as in body fluids, including human serum and plasma samples (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3757688/).  Wiki.


I have included two sections from the 41 page article,--the parts with the blue ink.  The link is to the entire article. 


The Oiling of America

by Mary Enig, PhD, and Sally Fallon, © 1999 Mary G. Enig, PhD and Sally Fallon.

First published in Nexus Magazine, Dec '98-Jan '99 and Feb '99-Mar '99.

 Table of Contents

• Rise of Coronary Heart Disease in the 20th Century

• The "Evidence" for the Lipid Hypothesis

• Hydrogenation and Trans Fats

• Shenanigans at the AHA

• Shenanigans at the FDA

• Shenanigans in Congress

• Enig Speaks Out

• The Food Giants Fight Back

• How Much Trans Fat Is "Normal"?

• Cat and Mouse Games in the Journals

• Lipid Research Clinics Trial

• National Cholesterol Consensus Conference

• Cholesterol Screening for Everyone

• National Food Processors Association Conference

• Other Research on Trans Fats

• '90s See the Nation Well Oiled

Dangers of Polyunsaturates  this section copied page 29 and ff. from the

Benefits of Animal Fats

• Coming Full Circle--And Yet Learning Nothing

• References

Dangers of Polyunsaturates

The irony is that these trends have persisted concurrently with revelations about the dangers of polyunsaturates. Because polyunsaturates are highly subject to rancidity, they increase the body's need for vitamin E and other antioxidants. Excess consumption of vegetable oils is especially damaging to the reproductive organs and the lungs—both of which are sites for huge increases in cancer in the US. In test animals, diets high in polyunsaturates from vegetable oils inhibit the ability to learn, especially under conditions of stress; they are toxic to the liver; they compromise the integrity of the immune system; they depress the mental and physical growth of infants; they increase levels of uric acid in the blood; they cause abnormal fatty acid profiles in the adipose tissues; they have been linked to mental decline and chromosomal damage; they accelerate aging. Excess consumption of polyunsaturates is associated with increasing rates of cancer, heart disease and weight gain; excess use of commercial vegetable oils interferes with the production of prostaglandins leading to an array of complaints ranging from autoimmune disease to PMS. Disruption of prostaglandin production leads to an increased tendency to form blood clots, and hence myocardial infarction, which has reached epidemic levels in America.41

Vegetable oils are more toxic when heated. One study reported that polyunsaturates turn to varnish in the intestines. A study by a plastic surgeon found that women who consumed mostly vegetable oils had far more wrinkles than those who used traditional animal fats. A 1994 study appearing in the Lancet showed that almost three quarters of the fat in artery clogs is unsaturated. The "artery clogging" fats are not animal fats but vegetable oils.42

Those who have most actively promoted the use of polyunsaturated vegetable oils as part of a Prudent Diet are well aware of their dangers. In 1971, William B. Kannel, former director of the Framingham study, warned against including too many polyunsaturates in the diet. A year earlier, Dr. William Connor of the American Heart Association issued a similar warning, and Frederick Stare reviewed an article which reported that the use of polyunsaturated oils caused an increase in breast tumors. And Kritchevsky, way back in 1969, discovered that the use of corn oil caused an increase in atherosclerosis.43

As for the trans fats, produced in vegetable oils when they are partially hydrogenated, the results that are now in the literature more than justify concerns of early investigators about the relation between trans fats and both heart disease and cancer. The research group at the University of Maryland found that trans fatty acids not only alter enzymes that neutralize carcinogens, and increase enzymes that potentiate carcinogens, but also depress milk fat production in nursing mothers and decrease insulin binding.44 In other words, trans fatty acids in the diet interfere with the ability of new mothers to nurse successfully and increase the likelihood of developing diabetes. Unpublished work indicates that trans fats contribute to osteoporosis. Hanis, a Czechoslovakian researcher, found that trans consumption decreased testosterone, caused the production of abnormal sperm and altered gestation.45 Koletzko, a German pediatric researcher found that excess trans consumption in pregnant mothers predisposed them to low birth weight babies.46 Trans consumption interferes with the body's use of omega-3 fatty acids found in fish oils, grains and green vegetables, leading to impaired prostaglandin production.47 George Mann confirmed that trans consumption increases the incidence of heart disease.48 In 1995, European researchers found a positive correlation between breast cancer rates and trans consumption.49

Until the 1995 study, only the disturbing revelations of Dutch researchers Mensink and Katan, in 1990, received front page coverage. Mensink and Katan found that margarine consumption increased coronary heart disease risk factors.50 The industry—and the press—responded by promoting tub spreads, which contain reduced amounts of trans compared to stick margarine. For the general population, these trans reductions have been more than offset by changes in the types of fat used by the fast food industry. In the early 1980's, Center for Science in the Public Interest campaigned against the use of beef tallow for frying potatoes. Before that they campaigned against the use of tallow for frying chicken and fish. Most fast food  concerns switched to partially hydrogenated soybean oil for all fried foods. Some deep fried foods have been tested at almost 50% trans. 51

Epidemiologist Walter Willett at Harvard worked for many years with flawed data bases which did not identify trans fats as a dietary component. He found a correlation with dietary fat consumption and both heart disease and cancer. After his researchers contacted Enig about the trans data, they developed a more valid data base that was used in the analysis of the massive Nurses Study. When Willett's group separated out the trans component in their analyses, they were able to confirm greater rates of cancer in those consuming margarine and vegetable shortenings—not butter, eggs, cheese and meat.52 The correlation of trans fat consumption and cancer was never published, but was reported at the Baltimore Data Bank Conference in 1992.

In 1993 Willett's research group at Harvard found that trans contributed to heart disease,53 and this study was not ignored, but received much fanfare in the press. Willett's first reference in his report was Enig's work on the trans content of common foods.

The industry continues to argue that American trans consumption is a low six to eight grams per person per day, not enough to contribute to today's epidemic of chronic disease. Total per capita consumption of margarine and shortening hovers around 40 grams per person per day. If these products contain 30% trans (many shortenings contain more) then average consumption is about 12 grams per person per day. In reality, consumption figures can be dramatically higher for some individuals. A 1989 Washington Post article documented the diet of a teenage girl who ate 12 donuts and 24 cookies over a three day period. Total trans worked out to at least 30 grams per day, and possibly much more. The fat in the chips that teenagers consume in abundance may contain up to 48% trans which translates into 45.6 grams of trans fat in a small ten-ounce bag of snack chips—which a hungry teenager can gobble up in a few minutes. High school sex education classes do not teach American teenagers that the altered fats in their snack foods may severely compromise their ability to have normal sex, conceive, give birth to healthy babies and successfully nurse their infants.

Benefits of Animal Fats

Foods containing trans fat sell because the American public is afraid of the alternative—saturated fats found in tallow, lard, butter, palm and coconut oil, fats traditionally used for frying and baking. Yet the scientific literature delineates a number of vital roles for dietary saturated fats—they enhance the immune system,54 are necessary for healthy bones,55 provide energy and structural integrity to the cells,56 protect the liver57 and enhance the body's use of essential fatty acids.58 Stearic acid, found in beef tallow and butter, has cholesterol lowering properties and is a preferred food for the heart.59 As saturated fats are stable, they do not become rancid easily, do not call upon the body's reserves of antioxidants, do not initiate cancer, do not irritate the artery walls.

Your body makes saturated fats, and your body makes cholesterol—about 2000 mg per day. In general, cholesterol that the average American absorbs from food amounts to about 100 mg per day. So, in theory, even reducing animal foods to zero will result in a mere 5% decrease in the total amount of cholesterol available to the blood and tissues. In practice, such a diet is likely to deprive the body of the substrates it needs to manufacture enough of this vital substance; for cholesterol, like saturated fats, stands unfairly accused. It acts as a precursor to vital corticosteroids, hormones that help us deal with stress and protect the body against heart disease and cancer; and to the sex hormones like androgen, testosterone, estrogen and progesterone; it is a precursor to vitamin D, a vital fat-soluble vitamin needed for healthy bones and nervous system, proper growth, mineral metabolism, muscle tone, insulin production, reproduction and immune system function; it is the precursor to bile salts, which are vital for digestion and assimilation of fats in the diet. Recent research shows that cholesterol acts as an antioxidant.60 This is the likely explanation for the fact that cholesterol levels go up with age. As an antioxidant, cholesterol protects us against free radical damage that leads to heart disease and cancer. Cholesterol is the body's repair substance, manufactured in large amounts when the arteries are irritated or weak. Blaming heart disease on high serum cholesterol levels is like blaming firemen who have come to put out a fire for starting the blaze.

Cholesterol is needed for proper function of serotonin receptors in the brain.61 Serotonin is the body's natural "feel-good" chemical. This explains why low cholesterol levels have been linked to aggressive and violent behavior, depression and suicidal tendencies.  

Mother's milk is especially rich in cholesterol and contains a special enzyme that helps the baby utilize this nutrient. Babies and children need cholesterol-rich foods throughout their growing years to ensure proper development of the brain and nervous system. Dietary cholesterol plays an important role in maintaining the health of the intestinal wall,62 which is why low-cholesterol vegetarian diets can lead to leaky gut syndrome and other intestinal disorders.

Animal foods containing saturated fat and cholesterol provide vital nutrients necessary for growth, energy and protection from degenerative disease. Like sex, animal fats are necessary for reproduction. Humans are drawn to both by powerful instincts. Suppression of natural appetites leads to weird nocturnal habits, fantasies, fetishes, bingeing and splurging.

Animal fats are nutritious, satisfying and they taste good. "Whatever is the cause of heart disease," said the eminent biochemist Michael Gurr in a recent article, "it is not primarily the consumption of saturated fats."63 And yet the high priests of the lipid hypothesis continue to lay their curse on the fairest of culinary pleasures—butter and Bernaise, whipped cream, souffles and omelets, full-bodied cheeses, juicy steaks and pork sausage.

41. A general review of citations for problems with polyunsaturate consumption is found in E R Pinckney, and C Pinckney, The Cholesterol Controversy, 1973, Sherbourne Press, Los Angeles, pp127-131

42. C V Felton, et al, "Dietary Polyunsaturated Fatty Acids and Composition of Human Aortic Plaques," Lancet, 1994, 344:1195 43. D Kritchevsky, Medical Counterpoint, March 1969

44. B B Teter, et al, "Milk Fat Depression in C57B1/6J Mice Consuming Partially Hydrogenated Fat," Journal of Nutrition, 1990, 120:818-824; Barnard, et al, "Dietary Trans Fatty Acids Modulate Erythrocyte Membrane Fatty Acid Composition and Insulin Binding in Monkeys," Journal of Nutritional Biochemistry, 1990, 1:190-195

45. T Hanis, et al, "Effects of Dietary Trans Fatty Acids on Reproductive Perforamnce of Wistar Rats," British Journal of Nutrition, 1989, 61:519-529

46. B Koletzko and J Muller, "Cis- and Trans-Isomeric Fatty Acids in Polasma Lipids of Newborn Infants and Their Mothers," Biology of the Neonate, 1990, 57:172-178

47. D Horrobin, "The Regulation of Prostaglandin Biosynthesis by Manipultion of Essential Fatty Acid Metabolism," Reviews in Pure and Applied Pharmacological Sciences, 1983, 4:339-383

48. G V Mann, "Metabolic Consequences of Dietary Trans Fatty Acids," The Lancet, 1994, 343:1268-1271

49. L Kohlmeier, et al, "Stores of Trans Fatty Acids and Breast Cancer Risk, "Am J Clin Nutr, 1995, 61:896;A25

50. R P Mensink and M Katan, "Effect of Dietary Trans Fatty Acids on High-Density and Low-Density Lipoprotein Cholesterol Levels in Healthy Subjects," N Eng J Med, 1990, 323:439-445

51. M G Enig, et al, "Isomeric Trans Fatty Acids in the U.S. Diet," J Am Coll Nutr, 1990, 9:471-486

52. W C Willett, et al, "Consumption of Trans-Fatty Acids in Relation to Risk of Coronary Heart Disease Among Women," Society for Epidemiology Research, June 1992, Annual Meeting, Abstract 249

53. W C Willett, et al, "Intake of Trans Fatty Acids and Risk of Coronary Heart Disease Among Women," Lancet, 1993, 341:581-585

54. J J Kabara, The Pharmacological Effects of Lipids, J J Kabara, ed, The American Oil Chemists' Society, Champaign, IL, 1978, 1-14; L A Cohen, et al, J Natl Cancer Inst, 1986, 77:43

55. B A Watkins, et al, "Importance of Vitamin E in Bone Formation and in Chrondrocyte Function" Purdue University,

Lafayette, IN, AOCS Proceedings, 1996; B A Watkins, and M F Seifert, "Food Lipids and Bone Health," Food Lipids and Health, R E McDonald and D B Min, eds, Marcel Dekker, Inc. New York, NY, p 101

56. J F Mead, et al, Lipids: Chemistry, Biochemistry and Nutrition, Plenum Press, 1986, New York

57. A A Nanji, et al, Gastroenterology, Aug 1995, 109(2):547-

54; Y S Cha, and D S Sachan, J Am Coll Nutr, Aug 1994, 13(4):338-43

58. M L Garg, et al, The FASEB Journal, 1988, 2:(4):A852; R M Oliart Ros, et al, Meeting Abstracts, AOCS Proceedings, May 1998, p 7, Chicago, IL

59. L D Lawson and F Kummerow, "B-Oxidation of the Coenzyme A Esters of Vaccenic, Elaidic and Petroselaidic Acids by Rat Heart Mitochondria," Lipids, 1979, 14:501-503

60. E M Cranton and J P Frackelton, "Free Radical Pathology in Age-Associated Diseases: Treatment with EDTA Chelation, Nutrition and Antioxidants," Journal of Holistic Medicine, Spring/Summer 1984, pp 6-37

61. H Engelberg, "Low Serum Cholesterol and Suicide," Lancet, March 21, 1992, 339:727-728

62. R B Alfin-Slater, and L Aftergood, "Lipids," Modern Nutrition in Health and Disease, 6th ed, 1980, R S Goodhart and M E Shils, eds, Lea and Febiger, Philadelphia, p 134 .

Evolutionary patterns in production of saturated and unsaturated fats


Evolution operates to maximize survival, and thus the type of energy storage is balanced by costs.  For a variety of reasons animals and plants use carbohydrates and fats for energy.  Major factors for which is stored include durability, ease of conversion to the energy molecule ATP, bulk of material stored, and energy expended in their synthesis. 


So why do animals store fats?  In the form of glycogen, carbohydrates are six times as bulky per calorie of energy; thus fats offer a survival advantage over glycogen.  But for plants they don’t move, thus carbohydrates are the preferred source of energy storage, except for seeds where size matters.  Secondly, most insects prefer for food carbohydrates thus reducing the number of seeds lost to insects.


So why animals make and store saturated fats.  They are stable; i.e., they are not subject to rancidity, while polyunsaturated fats have the highest rate and monounsaturated a modest rate.  The rate of oxidation increases with number of double bonds.  Just like the unnatural trans-fats, rancid fats cannot be metabolized for energy; thus they clog up cells.  Rancid and trans-fats have major negative health consequences including that they are atherogenic.  Animals are long lived, and the damage is cumulative, thus saturated fats provide a survival advantage over polyunsaturated fats. Scientists have demonstrated that saturated fats are much better for you than unsaturated fats. But what we are told repeatedly about fats is the opposite to what has been convincingly demonstrated. 


So why do we hear from the opinion leaders and government that polyunsaturated fats are better than saturated fats?    The lie is a product of tobacco science and corporate influence.  It is the manufactured foods and grain producing industries that promote plant derived oils and a high sugar diet.  Prof Miller accurately summarizes how tobacco science has come to dominate.  Watch his graphically entertaining lecture to an audience of physicians on YouTube.  The voice and financial clout of corporations follows the pattern of tobacco ethics, which operates counter to the public’s best interest.  And it gets worse.  Eating less fat entails eating more carbs for energy.  Another chorus of scientist has gone public about the health disaster caused by the Western diet which includes in the U.S. an average of over 150 pounds of sugar per year per person.  Yet the health harm by sugar has also been marginalized.    


So why for their seeds do plants make mostly make polyunsaturated fats (with the exception of trees)?  Saturated fats require more energy to produce, thus under certain conditions they are favored.  Most seeds will under normal moist condition germinate only during the first year or two.  These plants are short lived compared to trees.  With trees their long life entails much different evolutionary forces:  the number of oak trees is far less than for corn and soya bean, and the replacement rate is in decades versus a year.  The survival pressures for trees entails that their seeds need to survival for years.  Thus trees make the more stable saturated and monounsaturated fats for their seeds.  This is why cocoanuts make a high level of saturated, there seeds are relatively long live, while plants such as soya beans, sunflowers, and canola make mostly polyunsaturated fats, their seeds are short live, and thus oxidation of the oil in the seed is not a major loss. 

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