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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.
© Ray Peat 2006. All Rights Reserved. www.RayPeat.com