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Coconut Oil
and Its Virtues
By Ray Peat, PhD
Excerpted from the book
From PMS to Menopause
NaturoDoc Note: Dr. Peat's refreshing
thought process is predicated upon some physiology and endocrinology
basics, so go slowly if you need to. The references alone are
worth saving this article. If you like the reasoning, buy his
books and newsletter -- they work.
I have discussed the many toxic effects of
unsaturated oils, and I have frequently mentioned that coconut oil
doesn't have those toxic effects, though it does contain a small
amount of the unsaturated oils. Many people have asked me to
write something on coconut oil. I thought I might write a
small book on it, but I realize that there are no suitable channels
for distributing such a book. If the seed-oil industry can
eliminate major corporate food products that have used coconut oil
for a hundred years, they certainly have the power to prevent
dealers from selling a book that would affect their market more
seriously. For the present, I will just outline some of the
virtues of coconut oil.
The unsaturated oils in some cooked foods become
rancid in just a few hours, even at refrigerator temperatures, and,
are responsible for the stale taste of leftover foods. (Eating
slightly stale food isn't particularly harmful, since the same oils,
even when eaten absolutely fresh, will oxidize at a much higher rate
once they are in the body, where they are heated and thoroughly
mixed with an abundance of oxygen.) Coconut oil that has been
kept at room temperature for a year has been tested for rancidity,
and showed no evidence of it. Since we would expect the small
percentage of unsaturated oils naturally contained in coconut oil to
become rancid, it seems that the other (saturated) oils have an
antioxidative effect: I suspect that the dilution keeps the
unstable unsaturated fat molecules spatially separated from each
other, so they can't interact in the destructive chain reactions
that occur in other oils. To interrupt chain reactions of
oxidation is one of the functions of antioxidants, and it is
possible that a sufficient quantity of coconut oil in the body has
this function. It is well established that dietary coconut oil
reduces our need for vitamin E, but I think its antioxidant role is
more general than that, and that it has both direct and indirect
antioxidant activities.
Coconut oil is unusually rich in short and medium
chain fatty acids. Shorter chain length allows fatty acids to
be metabolized without use of the carnitine transport system.
Mildronate, which I discussed in an article on adaptogens, protects
cells against stress partly by opposing the action of carnitine, and
comparative studies showed that added carnitine had the opposite
effect, promoting the oxidation of unsaturated fats during stress,
and increasing oxidative damage to cells. I suspect that a
degree of saturation of the oxidative apparatus by short-chain fatty
acids has a similar effect -- that is, that these very soluble and
mobile short-chain saturated fats have priority for oxidation,
because they don't require carnitine transport into the
mitochondrion, and that this will tend to inhibit oxidation of the
unstable, peroxidizable unsaturated fatty acids.
When Albert Schweitzer operated his clinic in
tropical Africa, he said it was many years before he saw any cases
of cancer, and he believed that the appearance of cancer was caused
by the change to the European type of diet. In the 1920s,
German researchers showed that mice on a fat-free diet were
practically free of cancer. Since then, many studies have
demonstrated a very close association between consumption of
unsaturated oils and the incidence of cancer.
Heart damage is easily produced in animals by
feeding them linoleic acid; this "essential" fatty acid turned
out to be the heart toxin in rape-seed oil. The addition of
saturated fat to the experimental heart-toxic, oil-rich diet
protects against the damage to heart cells.
Immuno-suppression was observed in patients who were
being "nourished" by intravenous emulsions of "essential fatty
acids," and as a result coconut oil is used as the basis for
intravenous fat feeding, except in organ-transplant patients.
For those patients, emulsions of unsaturated oils are used
specifically for their immunosuppressive effects.
General aging, and especially aging of the brain, is
increasingly seen as being closely associated with lipid
peroxidation.
Several years ago I met an old couple, who were only
a few years apart in age, but the wife looked many years younger
than her doddering old husband. She was from the Philippines,
and she remarked that she always had to cook two meals at the same
time, because her husband couldn't adapt to her traditional food.
Three times every day, she still prepared her food in coconut oil.
Her apparent youth increased my interest in the effects of coconut
oil.
In the 1960s, Hartroft and Porta gave an elegant
argument for decreasing the ratio of unsaturated oil to saturated
oil in the diet (and thus in the tissues). They showed that
the "age pigment" is produced in proportion to the ratio of oxidants
to antioxidants, multiplied by the ratio of unsaturated oils to
saturated oils. More recently, a variety of studies have shown
that ultraviolet light induces peroxidation in unsaturated fats, but
not saturated fats, and that this occurs in the skin as well as in
vitro. Rabbit experiments, and studies of humans, showed that
the amount of unsaturated oil in the diet strongly affects the rate
at which aged, wrinkled skin develops. The unsaturated fat in
the skin is a major target for the aging and carcinogenic effects of
ultraviolet light, though not necessarily the only one.
In the 1940s, farmers attempted to use cheap coconut
oil for fattening their animals, but they found that it made them
lean, active, and hungry. For a few years, an anti-thyroid
drug was found to make the livestock get fat while eating less food,
but then it was found to be a strong carcinogen, and it also
probably produced hypothyroidism in the people who ate the meat.
By the late 1940s, it was found that the same anti-thyroid effect,
causing animals to get fat without eating much food, could be
achieved by using soy beans and corn as feed.
Later, an animal experiment fed diets that were low
or high in total fat, and in different groups the fat was provided
by pure coconut oil, or a pure unsaturated oil, or by various
mixtures of the two oils. At the end of their lives, the
animals' obesity increased directly in proportion to the ratio of
unsaturated oil to coconut oil in their diet, and was not related to
the total amount of fat they had consumed. That is, animals
which ate just a little pure unsaturated oil were fat, and animals
which ate a lot of coconut oil were lean.
In the 1930s, animals on a diet lacking the
unsaturated fatty acids were found to be "hypermetabolic."
Eating a "normal" diet, these animals were malnourished, and their
skin condition was said to be caused by a "deficiency of essential
fatty acids." But other researchers who were studying vitamin
B6 recognized the condition as a deficiency of that vitamin.
They were able to cause the condition by feeding a fat-free diet,
and to cure the condition by feeding a single B vitamin. The
hypermetabolic animals simply needed a better diet than the
"normal," fat-fed, cancer-prone animals did.
G. W. Crile and his wife found that the metabolic
rate of people in Yucatan, where coconut is a staple food, averaged
25% higher than that of people in the United States. In a hot
climate, the adaptive tendency is to have a lower metabolic rate, so
it is clear that some factor is more than offsetting this expected
effect of high environmental temperatures. The people there
are lean, and recently it has been observed that the women there
have none of the symptoms we commonly associate with menopause.
By 1950, then, it was established that unsaturated
fats suppress the metabolic rate, apparently creating
hypothyroidism. Over the next few decades, the exact
mechanisms of that metabolic damage were studied. Unsaturated fats
damage the mitochondria, partly by suppressing the repiratory
enzyme, and partly by causing generalized oxidative damage.
The more unsaturated the oils are, the more specifically they
suppress tissue response to thyroid hormone, and transport of the
hormone on the thyroid transport protein.
Plants evolved a variety of toxins designed to
protect themselves from "predators," such as grazing animals.
Seeds contain a variety of toxins, that seem to be specific for
mammalian enzymes, and the seed oils themselves function to block
proteolytic digestive enzymes in the stomach. The thyroid
hormone is formed in the gland by the action of a proteolytic
enzyme, and the unsaturated oils also inhibit that enzyme.
Similar proteolytic enzymes involved in clot removal and
phagocytosis appear to be similarly inhibited by these oils.
Just as metabolism is "activated" by consumption of
coconut oil, which prevents the inhibiting effect of unsaturated
oils, other inhibited processes, such as clot removal and
phagocytosis, will probably tend to be restored by continuing use of
coconut oil.
Brain tissue is very rich in complex forms of fats.
The experiment (around 1978) in which pregnant mice were given diets
containing either coconut oil or unsaturated oil showed that brain
development was superior in the young mice whose mothers ate coconut
oil. Because coconut oil supports thyroid function, and
thyroid governs brain development, including myelination, the result
might simply reflect the difference between normal and hypothyroid
individuals. However, in 1980, experimenters demonstrated that
young rats fed milk containing soy oil incorporated the oil directly
into their brain cells, and had structurally abnormal brain cells as
a result. Lipid peroxidation occurs during seizures, and
antioxidants such as vitamin E have some anti-seizure activity.
Currently, lipid peroxidation is being found to be involved in the
nerve cell degeneration of Alzheimer's disease.
Various fractions of coconut oil are coming into use
as "drugs," meaning that they are advertised as treatments for
diseases. Butyric acid is used to treat cancer, lauric and
myristic acids to treat virus infections, and mixtures of
medium-chain fats are sold for weight loss. Purification
undoubtedly increases certain effects, and results in profitable
products, but in the absence of more precise knowledge, I think the
whole natural product, used as a regular food, is the best way to
protect health. The shorter-chain fatty acids have strong,
unpleasant odors; for a couple of days after I ate a small amount of
a medium-chain triglyceride mixture, my skin oil emitted a rank,
goaty smell. Some people don't seem to have that reaction, and
the benefits might outweigh the stink, but these things just haven't
been in use long enough to know whether they are safe. We have
to remember that the arguments made for aspartame, monosodium
glutamate, aspartic acid, and tryptophan -- that they are like the
amino acids that make up natural proteins -- are dangerously false.
In the case of amino acids, balance is everything. Aspartic
and glutamic acids promote seizures and cause brain damage, and are
intimately involved in the process of stress-induced brain aging,
and tryptophan by itself is carcinogenic. Treating any complex
natural product as the drug industry does, as a raw material to be
fractionated in the search for "drug" products, is risky, because
the relevant knowledge isn’t sought in the search for an association
between a single chemical and a single disease.
While the toxic unsaturated paint-stock oils,
especially safflower, soy, corn, and linseed (flaxseed) oils, have
been sold to the public precisely for their drug effects, all of
their claimed benefits were false. When people become
interested in coconut oil as a "health food," the huge seed-oil
industry -- operating through their shills -- is likely to attack it
as an "unproved drug." While components of coconut oil have
been found to have remarkable physiological effects (as
antihistamines, antiinfectives/ antiseptics, promoters of immunity,
glucocorticoid antagonist, nontoxic anticancer agents, for example),
I think it is important to avoid making any such claims for the
natural coconut oil. It very easily could be banned from the
import market as a "new drug" which isn't "approved by the FDA."
We have already seen how money and propaganda from the soy oil
industry eliminated long-established products from the U.S. market.
I saw people lose weight steadily when they had the habit of eating
large amounts of tortilla chips fried in coconut oil. Those
chips disappeared when their producers were pressured into switching
to other oils, in spite of the short shelf life that resulted in the
need to add large amounts of preservatives. Oreo cookies, Ritz
crackers, potato chip producers, and movie theater popcorn makers
have experienced similar pressures.
The cholesterol-lowering fiasco for a long time
centered on the ability of unsaturated oils to slightly lower serum
cholesterol. For years, the mechanism of that action wasn't
known, which should have suggested caution. Now, it seems that
the effect is just one more toxic action, in which the liver
defensively retains its cholesterol, rather than releasing it into
the blood. Large-scale human studies have provided
overwhelming evidence that whenever drugs, including the unsaturated
oils, were used to lower serum cholesterol, mortality increased from
a variety of causes including accidents, but mainly from cancer.
Since the 1930s, it has been clearly established that suppression of
the thyroid raises serum cholesterol (while increasing mortality
from infections, cancer, and heart disease), whereas restoring the
thyroid hormone brings cholesterol down to normal. In this
situation, however, thyroid isn't suppressing the synthesis of
cholesterol, but rather is promoting its use to form hormones and
bile salts. When the thyroid is functioning properly, the
amount of cholesterol in the blood entering the ovary governs the
amount of progesterone being produced by the ovary, and the same
situation exists in all steroid-forming tissues, such as the adrenal
glands and the brain. Progesterone and its precursor,
pregnenolone, have a generalized protective function:
antioxidant, anti-seizure, antitoxin, anti-spasm, anti-clot,
anti-cancer, pro-memory, pro-myelination, pro-attention, etc.
Any interference with the formation of cholesterol will interfere
with all of these exceedingly important protective functions.
As far as the evidence goes, it suggests that
coconut oil, added regularly to a balanced diet, lowers cholesterol
to normal by promoting its conversion into pregnenolone. (The
coconut family contains steroids that resemble pregnenolone, but
these are probably mostly removed when the fresh oil is washed with
water to remove the enzymes which would digest the oil.)
Coconut-eating cultures in the tropics have consistently lower
cholesterol than people in the U.S. Everyone that I know who
uses coconut oil regularly happens to have cholesterol levels of
about 160, while eating mainly cholesterol rich foods (eggs, milk,
cheese, meat, shellfish). I encourage people to eat sweet
fruits, rather than starches, if they want to increase their
production of cholesterol, since fructose has that effect.
Many people see coconut oil in its hard, white
state, and as a result of their training watching television or
going to medical school associate it with the cholesterol-rich
plaques in blood vessels. Those lesions in blood vessels are
caused mostly by lipid peroxidation of unsaturated fats, and relate
to stress, because adrenaline liberates fats from storage, and the
lining of blood vessels is exposed to high concentrations of the
blood-borne material. In the body, incidentally, the oil can't
exist as a solid, since it liquefies at 76 degrees.
(Incidentally, the viscosity of complex materials isn't a simple
matter of averaging the viscosity of its component materials;
cholesterol and saturated fats sometimes lower the viscosity of cell
components.) Most of the images and metaphors relating to
coconut oil and cholesterol that circulate in our culture are false
and misleading. I offer a counter-image, which is
metaphorical, but it is true in that it relates to lipid
peroxidation, which is profoundly important in our bodies.
After a bottle of safflower oil has been opened a few times, a few
drops that get smeared onto the outside of the bottle begin to get
very sticky, and hard to wash off. This property is why it is
a valued base for paints and varnishes, but this varnish is
chemically closely related to the age pigment that forms "liver
spots" on the skin, and similar lesions in the brain, heart, blood
vessels, lenses of the eyes, etc. The image of "hard, white
saturated coconut oil" isn't relevant to the oil's biological
action, but the image of "sticky varnish-like easily oxidized
unsaturated seed oils" is highly relevant to their toxicity.
The ability of some of the medium chain saturated
fatty acids to inhibit the liver's formation of fat very likely
synergizes with the pro-thyroid effect, in allowing energy to be
used, rather than stored. When fat isn't formed from
carbohydrate, the sugar is available for use, or for storage as
glycogen. Therefore, shifting from unsaturated fats in foods
to coconut oil involves several anti-stress processes, reducing our
need for the adrenal hormones. Decreased blood sugar is a
basic signal for the release of adrenal hormones. Unsaturated
oil tends to lower the blood sugar in at least three basic ways.
It damages mitochondria, causing respiration to be uncoupled from
energy production, meaning that fuel is burned without useful
effect. It suppresses the activity of the respiratory enzyme
(directly, 'and through its anti-thyroid actions), decreasing the
respiratory production of energy. And it tends to direct
carbohydrate into fat production, making both stress and obesity
more probable. For those of us who use coconut oil
consistently, one of the most noticeable changes is the ability to
go for several hours without eating, and to feel hungry without
having symptoms of hypoglycemia.
One of the stylish ways to promote the use of
unsaturated oils is to refer to their presence in "cell membranes,"
and to claim that they are essential for maintaining "membrane
fluidity." As I have mentioned above, it is the ability of the
unsaturated fats, and their breakdown products, to interfere with
enzymes and transport proteins, which accounts for many of their
toxic effects, so they definitely don't just harmlessly form
"membranes." They probably bind to all proteins, and disrupt
some of them, but for some reason their affinity for proteolytic and
respiration-related enzymes is particularly obvious. (I think
the chemistry of this association is going to give us some important
insights into the nature of organisms. Metchnikof's model that
I have discussed elsewhere might give us a picture of how those
factors relate in growth, physiology, and aging.)
Unsaturated fats are slightly more water-soluble
than fully saturated fats, and so they do have a greater tendency to
concentrate at interfaces between water and fats or proteins, but
there are relatively few places where these interfaces can be
usefully and harmlessly occupied by unsaturated fats, and at a
certain point, an excess becomes harmful. We don't want
"membranes" forming where there shouldn't be membranes. The
fluidity or viscosity of cell surfaces is an extremely complex
subject, and the. degree of viscosity has to be appropriate for the
function of the cell. Interestingly, in some cells, such as the
cells that line the air sacs of the lungs, cholesterol and one of
the saturated fatty acids found in coconut oil can increase the
fluidity of the cell surface. In many cases, stressful
conditions create structural disorder in cells. These
influences have been called "chaotropic," or chaos-producing.
In red blood cells, which have sometimes been wrongly described as
"hemoglobin enclosed in a cell membrane," it has been known for a
long time that lipid peroxidation of unsaturated fats weakens the
cellular structure, causing the cells to be destroyed prematurely.
Lipid peroxidation products are known to be "chaotropic," lowering
the rigidity of regions of cells considered to be membranes.
But the red blood cell is actually more like a sponge in structure,
consisting of a "skeleton" of proteins, which (if not damaged by
oxidation) can hold its shape, even when the hemoglobin has been
removed. Oxidants damage the protein structure, and it is this
structural damage which in turn increases the "fluidity" of the
associated fats.
So, it is probably true that in many cases the
liquid unsaturated oils do increase "membrane fluidity," but it is
now clear that in at least some of those cases the "fluidity"
corresponds to the chaos of a damaged cell protein structure.
(N. V. Gorbunov, "Effect of structural modification of membrane
proteins on lipid-protein interactions in the human erythrocyte
membrane," Bull. Exp. Biol. & Med 116(11), 1364-67. 1993.
Although I had stopped using the unsaturated seed
oils years ago, and supposed that I wasn't heavily saturated with
toxic unsaturated fat, when I first used coconut oil I saw an
immediate response, that convinced me my metabolism was chronically
inhibited by something that was easily alleviated by "dilution" or
molecular competition. I had put a tablespoonful of coconut
oil on some rice I had for supper, and half an hour later while I
was reading, I noticed I was breathing more deeply than' normal.
I saw that my skin was pink, and I found that my pulse was faster
than normal--about 98, 1 think. After an hour or two, my pulse
and breathing returned to normal. Every day for a couple of
weeks I noticed the same response while I was digesting a small
amount of coconut oil, but gradually it didn't happen any more, and
I increased my daily consumption of the oil to about an ounce.
I kept eating the same foods as before (including a quart of ice
cream every day), except that I added about 200 or 250 calories per
day as coconut oil. Apparently the metabolic surges that
happened at first were an indication that my body was compensating
for an anti-thyroid substance by producing more thyroid hormone;
when the coconut oil relieved the inhibition, I experienced a moment
of slight hyperthyroidism, but after a time the inhibitor became
less effective, and my body adjusted by producing slightly less
thyroid hormone. But over the next few months, I saw that my
weight was slowly and consistently decreasing. It had been
steady at 185 pounds for 25 years, but over a period of six months
it dropped to about 175 pounds. I found that eating more
coconut oil lowered my weight another few pounds, and eating less
caused it to increase.
The anti-obesity effect of coconut oil is clear in
all of the animal studies, and in my friends who eat it regularly.
It is now hard to get it in health food stores, since Hain stopped
selling it. The Spectrum™ product looks and feels a little
different to me, and I suppose the particular type of tree, region,
and method of preparation can account for variations in the
consistency and composition of the product. The unmodified
natural oil is called "76 degree melt," since that is its natural
melting temperature. One bottle from a health food store was
labeled "natural coconut oil, 92% unsaturated oil," and it had the
greasy consistency of old lard. I suspect that someone had
confused palm oil (or something worse) with coconut oil, because it
should be about 96% saturated fatty acids.
P.O. Box 5764
Eugene, OR 97405
Web:
www.efn.org/~raypeat
Top
References
The following are some recent
references that discuss the toxic effects of unsaturated fats, some
of the things that offer protection against them, and some
comparisons with saturated fats. I include a few
references on the issue of "membrane fluidity," just to show that
there is probably nothing of value in that idea.
1. Y.P. Wang and S.W.
Walsh, "Aspirin inhibits both lipid peroxides and thromboxane in
preeclamptic placentas," Free Radical Biol. Med. 18(3),585-591,1995.
2. R. Padmanabhan et al.,
"Effect of pre-treatment with aspirin on alcohol-induced neural tube
defects in the T0 mouse fetuses," Drug Alcohol Depend.
36(3),175-186, 1994. (Effect depends on time and dose.)
3. M. Puchala, ''The
interaction of alcohol radicals with human hemoglobin. 1.
Spectral properties of hemoglobin in the visible range," Radiat.
Environ. Biophys. 33(4),325-339, 1994. (Ethyl alcohol ads against
free radicals.)
4. C.L. Randall et al,
"Aspirin dose-dependently reduces alcohol-induced birth defects and
prostaglandin F levels in mice," Teratology 44, 521-529,1991.
5. C.S. Bangur, J.L.
Howland, S.S. Katyare, ''Thyroid hormone treatment alters
phospholipid compos ition and membrane fluidity of rat brain
mitochondria," Biochem. J. 305(l), 29-32, 1995. (Increases
fluidity.)
6. J.M. Gaziano et al.,
"Supplementation with beta-carotene in vivo and in vitro does not
inhibit low density lipoprotein oxidation," Atherosclerosis 112(2),
187-195, 1995. (May accelerate LPO.)
7. H.A. Kleinveld et al.,
"Vitamin E and fatty acid intervention does not attenuate the
progression of atherosclerosis in watanabe heritable hyperlipidemic
rabbits," Arterioscler. Thromb. Vasc. Biol. 15(2), 290-287, 1995.
(Linoleic acid promotes oxidation.)
8. P.S. Tappia, W.J. Man,
and R.F. Grimble, "Influence of unsaturated fatty acids on the
production of tumour necrosis factor and interleukin-6 by rat
peritoneal macrophages," Mol. Cell Biochem. 143(2), 89-98, 1995.
9. T. Gunther et al.,
"Effects of magnesium and iron on lipid peroxidation in cultured
hepatocytes," Mol. Cell Biochem. 144(2), 141-145, 1995.
(Magnesium protects against iron.)
10. C.W. Welsch, "Review
of the effects of dietary fat on experimental mammary &land
tumorigenesis: Role of lipid peroxidation," Free Radical Biol. Med.
18(4), 757-773, 1995.
11. J.P. Allard et al.,
"Effect of omega 3 fatty acids and vitamin-E supplements on lipid
peroxidation measured by breath ethane and pentane output-a
randomized controlled trial," Fatty Acids and Lipids: Biolo. 75,
162-165, 1994.
12. K.D. Croft et al.,
"Oxidation of low-density lipoproteins: Effect of antioxidant
content, fatty acid composition and intrinsic phospholipase activity
on susceptibility to metal ion-induced oxidation," BBA-Lipid Lipid
Metab. 1254(3),250-256,1995.
13. D.H. Vanpapendorp et
al., "Biochemical profile of osteoporotic patients on essential
fatty supplementation," Nutr. Res. 15(3), 325-334, 1995. (Fish
oil increased urinary calcium fish oil/evening primrose oil
increased osteocalcin and procollagen.)
14. J.H. Choi and B.P. Yu,
"Brain synaptosomal aging; Free radicals and membrane fluidity,"
Free Radical Biol. Med. 18(2), 133-139, 1995 ("...fluidity loss may
be influenced by factors other than cholesterol. We suggest
that lipid peroxidation may be a major factor in the change in
fluidity during the aging process.")
15. E. Chiarpotto et al.,
"Metabolism of 4-hydroxy-2-nonenal and aging." Biochem. Biophys.
Res. Commun. 297(2),477-484,1995. (Accumulation of unsaturated
fat breakdown produc in old animals.)
16. J.P. Allard et al.,
"Effect of omega 3 fatty acids and vitamin-E supplements on lipid
peroxidation measured by breath ethane and pentane output--a
randomized controlled trial," Fatty Acids and Lipids: Biolo 75,
162-165, 1995.
17. A. Kolling et al.,
"Membrane fluidity of microsomal and thymocyte membranes after x-ray
and UV irradiation," Radiat. Environ. Biophys. 33(4), 303-313, 1994.
(Pure lipid membranes are rigidized by ionizing radiation by
peroxidation; membranous protein lipid interface increases its
fluidity under radiation conditions.)
18. A-A. Nanji et al.,
"Markedly inhibited cyt P450 2E I and lipid peroxidation is
associated with liver injury in fish oil-ethanol fed rats," Alcohol
Clin. Exp. Res. 18(5), 1280-1285, 1994.
19. A-A Nanji et al.,
"Effect of type of dietary fat and ethanol on antioxidant enzyme
mRNA induction in rat liver," J. Lipid Res. 36(4), 736-744, 1995.
(Saturated fat and ethanol fed animals had no liver injury, fish oil
and ethanol rats had severe liver injury.)
20. C.V. Felton et al.,
"Dietary polyunsaturated fatty acids and composition of human aortic
plaques," Lancet 344(8931), 1195-1196, 1994.
21. S.C. Sahn and O.C.
Gray, "Kaempferol-induced nuclear DNA damage and lipid
peroxidation," Cancer Left. 85(2), 159-164, 1994. (Kaempferol
is a polyphenolic flavonoid which is structurally similar to
quercetin, which is sold as an antioxidant. Antioxidants often
function as pro-oxidants.)
22. S. Harel, "Oxidation
of ascorbic acid and metal ions as affected by NaCl," J. Agr, Food
Chem. 42(11), 2402-2406,1994.
23. K. Landholm et al.,
"Antiinflammatory treatment may prolong survival in undernourished
patients with metastatic solid tumors," Cancer Research 54(21),
5602-5606, 1994. (Prednisolone and indomethacin significantly
prolonged survival.)
24. J.J. Chen and B.P. Yu,
"Alterations in mitochondrial membrane fluidity by lipid
peroxidation products," Free Radical Biol. Med. 17(5), 411418, 1994.
25. J.H. Choi and B.P. Yu,
"Modification of age-related alterations of iron, ferritin, and
lipid peroxidation in rat serum," Age 17(3),93-97,1994.
26. H.J. Sipe et al., "The
metabolism of beta-estradiol by lactoperoxidase: A possible source
of oxidative stress in breast cancer," Carcinogenesis 15(11),
2637-2643, 1994.
27. N.W. Istfan et al.,
"DNA replication time accounts for tumor growth variation induced by
dietary fat in a breast carcinoma model," Cancer Lett. 86(2),
177-186, 1994.
28. A. Ishihara et al.,
":Dietary high-linoleate safflower oil is not hypocholesterolemic in
aged mice after a long-term feeding--Comparison with lard, perilla
oil and fish oil," Biol. Pharm. Bull. 18(4), 485490, 1995.
(The various unsaturated oils increased whole-body cholesterol in
the first 30 days. I consider this a defensive reaction, which
accounts for the temporary reduction of serum cholesterol.
Safflower oil, more strongly than the other oils, then produced
higher cholesterol levels in the serum as the experiment was
extended to 4 months.)
29. M.J. Endresen et al.,
"Effects of free fatty acids found increased in women who develop
pre-eclampsia on the ability of endothelial cells to produce
prostacyclin, cGMP and inhibit platelet aggregation," Scan. J. Clin.
Lab. Invest- 54(7), 549-557, 1994.
30. H. Darmani et al.,
"Interferon-gamma and polyunsaturated fatty acids increase the
binding of lipopolysaccharide to macrophages," Int. J. Exp. Pathol.
75(5), 363-368, 1994.
31. P. Yaqoob, et al.,
"Inhibition of natural killer Cell activity by dietary lipids."
Immunol. Lett. 41(2-3),241-247,1994.
32. M.H.L. Green et al.,
"Effect of diet and vitamin C on DNA strand breakage in
freshly-isolated human white blood cells," Mutat. Res.-DNA. Genet.
Aging 316(2), 91-102, 1994. (Dietary vitamin C may provide
protection against DNA breaks, though in vitro tests showed it could
also induce DNA breaks. Cells taken after eating breakfast had
fewer breaks than cells taken before breakfast; i.e., fasting
overnight seems to cause genetic damage.)
33. F. Berschauer et al.,
"Nutritional-physiological effects of dietary fats in rations for
growing pigs. 4. Effects of sunflower oil and coconut oil on
protein and fat retention, fatty acid pattern of back fat and blood
parameters in piglets," Arch. Tieremahr (East Germany) 34(l), 19-33,
1984. [Fat content in the coconut oil fed animals, after only
34 days, was 15.9%, in the control group, 18.6%; and in the
sunflower oil fed animals. 21:1%.]
34. J. Yazbech et al.,
"Effects of essential fatty acid deficiency on brown adipose tissue
activity in rats maintained at thermal neutrality," Comp. Bioch.
Physiol. A (England) 94(2), 273-276, 1989, suggested that the
observed increase in resting metabolic rate produced by using
coconut oil to create an essential fatty acid deficiency, is partly
the result of increased heat production in the brown adipose tissue.
The weight of that fat decreased by 28%, while its ability to
produce heat increased 690/0.
35. R.W. Ordway et al.,
"Direct regulation of ion channels by fatty acids," Trends Neurosci.
14, 96-100, 199 1.
36. H.G.P. Swarts et al.,
"Binding of unsaturated fatty acids to Na+,K+-ATPase leading to
inhibition and inactivation," Biochem. Biophys. Acts
1024,32-40,1990.
37. G. Autore et al.,
"Essential fatty acid-deficient diet modifies PAF levels in stomach
and duodenum of endotoxin-treated rats," J. Lipid Mediators Cell
Signalling 9. 145-153, 1994.
38. J. Rafael et al., "The
effect of essential fatty acid deficiency on basal respiration and
function of liver mitochondria in rats," J. Nutr. 114, 255-262,
1984.
39. P.H. Chan and R.A.
Fishman, "Brain edema: Induction in cortical slices by
polyunsaturated fatty acids," Science 201, 358-369, 1978.
"Ibis cellular edema was specific, since neither saturated fatty
acids nor a fatty acid containing a single double bond had such
effect."
40. C. Larsson Backstrom
et al., "Effects of dietary alpha- and gamma-linolenic acids on
liver fatty acids, lipid metabolism, and survival in sepsis," Shock
4(l), 11-20, 1995. "Dietary GLA reduced survival from sepsis."
41. D. Chemla et al.,
"Influence of dietary polyunsaturated fatty acids on contractility,
inotropy and compliance of isolated rat myocardium, J mol Cell
Cardiol 27(8), 1745-1755, 1995. "There was a trend towards a
lower peak lengthening velocity at preload in the LC (n-3) group ...
together with an unchanged peak rate of isometric force decline.
This resulted in a significant impairment of the two mechanical
indexes testing the load dependence of myocardial relaxation."
See B. Pieske, Circul. 92(5),1169-78.
42. R. Lemer et al.,
"Development and characterization of essential fatty acid deficiency
in human endothelial cells in culture," Proc Natl Acad Sci USA
92(4), 1147-1151, 1995. Oleic acid derivative 5,8,11
-eicosatrienoic acid (20:3 omega 9) (5,8,11,14,17 eicosapentaenoic,
20-5 omega 3)); 20:3 omega 9 impaired the Ca2(i) response,
indicating a suppressive effect of it. (Agonist-induced
increases in concentrations of prostacycline PGI 2, and cytosolic
Ca2+ were reduced in efad cells.)
43. K. lmaizumi et al.,
"Dissociation of protein kinase C activities and diacylglycerol
levels in liver plasma membranes of rats on coconut oil and
safflower oil diets," J. Nutr Biochem 6(10), 528-533, 1995. "The
activation of PKC is affected differently in vitro by different
fatty acids." "Rats on coconut oil ... had a markedly lower
PKC activity in liver plasma membranes with slight but significant
reduction of the activity in the cytosol than did rats fed safflower
oil…" "…Coconut oil resulted in a higher content of diacylglycerols
in these membranes than did ingestion of safflower oil, whereas the
proportions of saturated fatty acids and phospholipids and membrane
fluidity were similar between rats ingesting different fats." "It
seems likely that saturated fats exert various physiological effects
on lipid and lipoprotein metabolism, in part through PKC pathways. "
44. V. Boutard et al., "Fish oil supplementation and essential
fatty acid deficiency reduce nitric oxide synthesisby rat
macrophages," Kidney Int. 46(5), 1280-1296, 1494. "Both ...
have been shown to exert anti-inflammatory effects…"
45. A.A. Farooqui, K.
Wells, L.A. Horrocks, "Breakdown of membrane phospholipids in
Alzheimer disease --involvement of excitatory amino acid receptors,"
Mol Chem Neuropathol 25(2-3) 155-173, 1995. "Me release of
arachidonate from the sn-2 position of glycerophospholipids is
catalyzed by phospholipases and lipases. These enzymes are
coupled to EAA receptors. Overstimulation of these receptors
may be involved in abnormal calcium homeostasis, degradation of
membrane phospholipids, and the accumulation of free fatty acids,
prostaglandins, and lipid peroxides. Accumulation of the
mentioned metabolites, as well as abnormalities in signal
transduction owing to stimulation of lipases and phospholipases may
be involved in the pathogenesis of the neurodegeneration in AD."
46. P.H. Chan and R.A.
Fishman, "Transient formation of superoxide radicals in
polyunsaturated fatty acid-induced brain swelling," J. of
Neurochemistry 35, 1004-1007,1980.
47. T. Gunther et al.,
"Effects of magnesium and iron on lipid peroxidation in cultured
hepatocytes," Mol. Cell Biochem. 144(2), 141-145, 1995.
(Magnesium protects against iron.)
48. K.D. Croft et al.,
"Oxidation of low-density lipoproteins: Effect of antioxidant
content, fatty acid composition and intrinsic phospholipase activity
on susceptibility to metal ion-induced oxidation," BBA-Lipid Lipid
Metab. 1254(3),250-256,1995.
49. J.H. Choi and B.P. Yu,
"Brain synaptosomal aging: Free radicals and membrane fluidity,"
Free Radical Biol. Med. 18(2), 133-139, 1995. ("...fluidity
loss may be influenced by factors other than cholesterol. We
suggest that lipid peroxidation may be a major factor in the change
in fluidity during the aging process.")
50. J.H. Choi and B.P. Yu,
"Modification of age-related alterations of iron, ferritin, and
lipid peroxidation in rat serum," Age 17(3),93-97,1994.
51. E. Chiarpotto et al.,
"Metabolism of 4-hydroxy-2-nonenal and aging" Biochem. Biophys. Res.
Commun. 297(2),477-484,1995. (Accumulation of unsaturated fat
breakdown product in old animals.)
52. M.J. Endresen et al.,
"Effects of free fatty acids found increased in women who develop
pre-eclampsia on the ability of endothelial cells to produce
prostacyclin, oGMP and inhibit platelet aggregation," Scan. J. Clin.
Lab. Invest. 54(7), 549-557, 1994. "...levels of circulating
fire fatty acids are increased in women who later develop
pre-eclampsia long before the clinical onset of the disease."
"...linoleic acid reduced the thrombin-stimulated prostacyclin
release by 30-60% oleic acid by 10-30%, wheras palmitic acid had no
effect." "Linoleic acid reduced the endothelial cells' ability to
inhibit platelet aggregation by 10-45%...."
53. R. Sanchez Olea et
al., "Inhibition by polyunsaturated fatty acids of cell volume
regulation and osmolyte fluxes in astrocytes," Amer. J. of
Physiology--cell physiology 38(1), C96-C102, 1995. Potent
blockers of regulatory volume decrease and of the swelling-activated
efflux of taurine, D-aspartate, inositol, and 1-125 (used as marker
ofCl) ... oleic and ricinoleic acids and saturated fatty acids were
ineffective." "...polyunsaturated fatty acids directly inhibit the
permeability pathways correcting cell volume after swelling in
cultured astrocytes."
54. M. D'Aquino et al.,
"Effect offish oil and coconut oil on antioxidant defence system and
lipid peroxidation in rat liver, Free Radical Res. Commun.
(Switzerland) 12-13 (1), 147-152, 1991. The rate of lipid
peroxidation in isolated microsomes was three-fold higher in rats
fed fish oil as compared to rats with coconut oil diet." "These
results suggest that fish oil feeding at an amount compatible with
human diet, although decreasing plasma lipids, actually challenges
the antioxidant defence system, thus increasing the susceptibility
of tissues to free radical oxidative damage."
55. R. Sanchez Olea et
al., "Inhibition by polyunsaturated fatty acids of cell volume
regulation and osmolyte fluxes in astrocytes," Amer. J. of
Physiology--cell physiology 38(l), C96-CI02, 1995. "...potent
blockers ofregulatory volume decrease and of the swelling-activated
efflux of taurine, D-aspartate, inositol, and 1-125 (used as marker
of Cl). ...oleic and ricinoleic acids and saturated fatty acids were
ineffective polyunsaturated fatty acids directly inhibit the
permeability pathways correcting cell volume after swelling in
cultured astrocytes."
56. W.N. Spellacy and K.L.
Carlson, "Plasma insulin and blood glucose levels in patients
.taking oral contraceptives: Preliminary report of a prospective
study," Am. J. Obst. & Gynec. 95, 474-478, 1966.
57. M.C. Galli et al.,
Comp. Biochem. and Physiology C-Pharmacology Toxicology &
Endocrinology 107(3), 435-440, 1994. Age-related
"susceptibility was correlated with the content of polyunsaturated
fatty acids and of lipophilic chain-breaking antioxidants." [Free
radical injury)
58. Y.P. Wang and S.W.
Walsh, "Aspirin inhibits both lipid peroxides and thromboxane in
preeclamptic placentas," Free Radical Biol. Med. 18(3), 585-591,
1995.
59. C.S. Bangur, J.L.
Howland, S.S. Katyare, "Thyroid hormone treatment alters
phospholipid composition and membrane fluidity of rat brain
mitochondria," Biochem. J. 305(1),29-32, 1995. (Increases fluidity.)
60. R.S. Sohal et al.,
"Mitochondrial superoxide and hydrogen peroxide generation, protein
oxidative damage,and longevity in different species of flies," Free
Rad. Biol. & Med. 19(4),499-504, 1995. Cytochrome C oxidase protects
against free radical damage. This enzyme depends on thyroid
and light.
61. T. Gunther et al.,
"Effects of magnesium and iron on lipid peroxidation in cultured
hepatocytes," Mot. Cell Biochem. 144(2), 141-145, 1995.
(Magnesium protects against iron.)
62. K.D. Croft et al.,
"Oxidation of low-density lipoproteins: Effect of antioxidant
content, fatty acid composition and intrinsic phospholipase activity
on susceptibility to metal ion-induced oxidation," BBA-LipidLipid
Metab. 1254(3), 250-256, 1995.
63. J.H. Choi and B.P. Yu, "Brain synaptosomal aging: Free
radicals and membrane fluidity," Free RadicalBiol. Med. 18(2),
133-139, 1995 ("...fluidity loss may be influenced by factors other
than cholesterol. We suggest that lipid peroxidation may be a
major factor in the change in fluidity during the aging process.")
64. J.H. Choi and B.P. Yu,
"Modification of age-related alterations of iron, ferritin, and
lipid peroxidation in rat serum," Age 17(3),93-97,1994.
65. E. Chiarpotto et al., "Metabolism of 4-hydroxy-2-nonenal
and aging," Biochem. Biophys. Res. Commun. 297(2),477-484, 1995.
(Accumulation of unsaturated fat breakdown product in old animals.)
66. M.J. Endresen et al.,
"Effects of free fatty acids found increased in women who develop
pre-eclampsia on the ability of endothelial cells to produce
prostacyclin, cGMP and inhibit platelet aggregation,'' Scan. J.
Clin. Lab. Invest. 54(7), 549-557, 1994. "...levels of circulating
five fatty acids are increased in women who later develop
pre-eclampsian long before the clinical onset of the disease ...
.... linoleic acid reduced thethrombin-stimulated prostacyclin
release by 30-60%, oleic acid by 10-30%, whereas palmitic acid had
no effect." "Linoleic acid reduced the endothelial cells" ability to
inhibit platelet aggregation by 10-45% L. A, Norris and J. Bomar,
'Effect of oestrogen dose on whole blood platelet activation in
women taking new low dose oral contraceptives," Thromb. Haemost.
72(6), 926-930, 1994: "Increased levels of ADP and arachidonic
acid-induced aggregation were observed in women taking the 30
microgram ethinyloestradiol combination. Platelet release of
beta-thromboglobulin (bets TG) was also significantly increased.
Increased collagen-induced aggregation was observed, but this failed
to reach statistical significance for the individual treatment
groups.") Estrogen dominance is an essential factor in
preeclampsia. Women who have died of (eclamptic) convulsions
have been found to have massive clots in their brain blood vessels.
Much of this work had its origin in the 1930s (Shute and others),
and was buried by the power of the estrogen industry.
67. H. Darmani et al.,
"Interferon-gamma and polyunsaturated fatty acids increase the
binding of lipopolysaccharide to macrophages," Int. J. Exp. Pathol.
75(5), 363-368, 1994.
68. G. Autore et al.,
"Essential fatty acid-deficient diet modifies PAF levels in stomach
and duodenum of endotoxin-treated rats," J. Lipid Mediators Cell
Signalling 9, 145-153, 1994. Deficiency of "essential" fats
decreases damage from endotoxin
69. N. Auge et al.,
"Proliferative and cytotoxic effects of mildly oxidized low-density
lipoproteins on vascular smooth-muscle cells," Biochern. J. 309(Part
3), 1015-1020, 1995. "Me proliferative effect on smooth-muscle cells
is counterbalanced at high concentrations of mildly oxidized LDLs
(or at high oxidation levels) by their cytotoxic effect."
70. S.K. Clinton et al.,
"The combined effects of dietary fat and estrogen on survival,
7,12-dimethylbenz(a)anthracene-induced breast cancer and prolactin
metabolism in rats," J. Nutr. 125(5), 1192-1204, 1995. "Mortality in
controls was doubled by feeding a high fat diet...." "...the
presence of estrogen may be a prerequisite for significant dietary
modulation."
71. P.S. Tappia et al.,
"Influence of unsaturated fatty acids on the production of tumour
necrosis factor and interleukin-6 by rat peritoneal macrophages,"
Mot Cell Biochem 143(2), 89-98, 1995. at 50 micro moles all fatty
acids suppressed PKA activity, except oleic acid which increased it;
PKC activity was enhanced by linoleic acid and oleic acid. 100
me MLA enhanced PKC by 146%, while EPA and DHA suppressed PKC.
72. R. Lerner et al.,
"Development and characterization of essential fatty acid deficiency
in human endothelial cells in culture," Proc Natl Acad Sci USA
92(4), 1147-1151, 1995. Oleic acid derivative 5,8,11-eicasatrienoic
acid (20:3 omega 9) (5,8,11,14,17 eicosapentaenoic, 20-5 omega 3));
20:3 omega 9 impaired the Ca2(i) response, indicating a suppressive
effect of it. (Agonist-induced increases in concentrations of
prostacycline PGI 2, and cytosolic Ca2+ were reduced in efad cells.)
73. K. Imaizumi et al.,
"Dissociation of protein kinase C activities and diacylglycerol
levels in liver plasma membranes of rats an coconut oil and
safflower oil diets," J. Nutr Biochem 6(10), 528-533, 1995. "The
activation of PKC is affected differently in vitro by different
fatty acids." "Rats on coconut oil had a markedly lower PKC activity
in liver plasma membranes with slight but significant reduction of
the activity in the cytosol than did rats fed safflower oil
"...coconut oil resulted in a higher content of diacylglycerols in
these membranes than did ingestion of safflower oil, whereas the
proportions of saturated fatty acids and phospholipids and membrane
fluidity were similar between rats ingesting different fats." "It
seems likely that saturated fats exert various physiological effects
on lipid and lipoprotein metabolism, in part through PKC pathways."
74. V. Boutard et al.,
"Fish oil supplementation and essential fatty acid deficiency reduce
nitric oxide synthesis by rat macrophages," Kidney Int. 46(5),
1280-1286, 1994. "Both have been shown to exert anti-inflammatory
effects...."
75. M.E. Miller et al.,
"Influence of hormones on platelet intracellular calcium,"
Thrombosis Research 77(6), 515-530, 1995. "Platelet
intracellular calcium concentration and release was significantly
decreased in women ingesting tamoxifen compared to controls and
significantly increased, as was platelet adhesion, in oral
contraceptive users." "Only oral contraceptive users had increased
sensitivity to aggregating agents. ...platelet calcium levels are
closely related to the degree of platelet adhesion and aggregation
in vivo."
76. F. Mercure and G.
Vanderkmak, "Inhibition of gonadotropin-stimulated ovarian steroid
production by pufa in teleost fish," Lipids 30(6), 547-554, 1995.
-EPA and DHA inhibited gonadotropin-stimulated testosterone
production in a dose-related manner ...."
77. A.A. Farooqui, K.
Wells, L.A. Horrocks, "Breakdown of membrane phospholipids in
Alzheimer disease-involvement of excitatory amino acid receptors,"
MoiChem Neuropathol 25(2-3) 155-173,1995." The release of
arachidonate from the sn-2 position of glycerophospholipids is
catalyzed by phospholipases and lipases. These enzymes are
coupled to EAA receptors. Overstimulation of these receptors
may be involved in abnormal calcium homeostasis, degradation of
membrane phospholipids, and the accumulation of free fatty acids,
prostaglandins, and lipid peroxides. Accumulation of the
mentioned metabolites, as well as abnormalities in signal
transduction owing to stimulation of lipases and phospholipases, may
be involved in the pathogenesis of the neurodegeneration in AD."
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