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.
Raymond
Peat, Ph.D.
P.O. Box 5764
Eugene, OR 97405
Dr. Mercola's Comment:
I have great respect for Dr.
Peat's work. He
is the main scientist that influenced Dr. John Lee with his work on
progesterone. Dr. Peat does a terrific job of describing some of the
many reasons why you should strongly consider replacing other oils you
use with coconut oil. He is a biochemist, however, so his writing can
be a bit difficult to understand at times.
Raw coconut is outstanding, and
I also use shredded coconut in my vegetable
juice pulp. These are other great ways to
obtain the health benefits of coconut.
You should definitely consider
switching to
coconut oil exclusively for all your sautéing and cooking needs.
It
does not form dangerous trans
fatty acids that even olive oil does, and
it is far healthier than the other vegetable oils out there.
Finally, if you are using canola
oil and are not yet aware of the problems with this oil, please click
on the link below.
Related
Articles:
Canola Oil Update
|