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By Ray Peat
This is a slightly modified version of Ray
Peat's article which can be found at
http://www.efn.org/~raypeat/
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 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 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 the lab.
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.
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 reparatory 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 protein digestive enzymes in the stomach.
The thyroid hormone is formed in the gland by the action of a protein
digestive enzyme, and the unsaturated oils also inhibit that enzyme. Similar
protein digestive enzymes involved in clot removal and immune function
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 immune function, 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 oxidation occurs during seizures, and antioxidants such as vitamin E
have some anti-seizure activity. Currently, lipid oxidation 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.
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).
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, anticancer, 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.
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 oxidation 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 oxidation, 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 in coconut
oil 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).
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 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 oxidation of unsaturated fats weakens the cellular structure,
causing the cells to be destroyed prematurely.
Lipid oxidation products lower 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, 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.
Raymond
Peat, Ph.D.
P.O. Box 5764
Eugene, OR 97405
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