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Coconut Oil
by Raymond Peat, Ph.D.
I have already discussed the many toxic effects of the 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 left-over 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 l920s, 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.
Immunosuppression
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
l960s, 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 demonstrated 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
l940s, 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 antithyroid 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 l940s,
it was found that the same antithyroid 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
l930s, 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 the menopause.
By
l950, 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--are
going 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, because 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 stably when they had the habit of eating large amounts of
tortilla chips fried in coconut oil, but 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 l930s, it has been clearly established that suppression of the
thyroid raises serum cholesterol (while increasing mortality from
infections, cancer, and heart disease), while 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, I 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.
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Copyright 1996
Raymond Peat
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Raymond Peat, Ph.D.
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