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.
http://www.cocoscience.com/pdf/the_oiling_of_america.pdf
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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