THE REMARKABLE BENEFITS OF COCONUT OIL

By Ray Peat

This is a slightly modified version of Ray Peat’s article which

can be found at http://www.efn.org/~raypeat/ He does some fine paintings too!

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

Read more: The Remarkable

benefits of Coconut Oil: 2

return to top

Join Me