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<head><title>Oils in Context</title></head>
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<h1>
Oils in Context
</h1>
<p>
An oil researcher<sup>[0]</sup>
spent 100 days eating what he considered to be the "Eskimo diet," seal blubber and mackerel paste. He
observed that his blood lipid peroxides (measured as malondialdehyde, MDA) reached a level 50 times higher
than normal, and although MDA is teratogenic, he said he wasn't worried about fathering deformed children,
because his sperm count had gone to zero. Evidently, he didn't have a very thorough understanding of the
Eskimo way of life. In most traditional cultures, the whole animal is used for food, including the brain and
the endocrine glands. Since unsaturated fats inhibit thyroid function, and since Eskimos usually have a high
caloric intake but are not typically obese, it seems that` their metabolic rate is being promoted by
something in their diet, which might also be responsible for protecting them from the effects experienced by
the oil researcher. (According to G. W. Crile, the basal metabolic rate of Eskimos was 125% of that of
people in the United States.)
</p>
<p>
People who eat fish heads (or other animal heads) generally consume the thyroid gland, as well as the brain.
The brain is the body's richest source of cholesterol, which, with adequate thyroid hormone and vitamin A,
is converted into the steroid hormones pregnenolone, progesterone, and DHEA, in proportion to the quantity
circulating in blood in low-density lipoproteins. The brain is also the richest source of these very
water-insoluble (hydrophobic) steroid hormones; it has a concentration about 20 times higher than the serum,
for example. The active thyroid hormone is also concentrated many-fold in the brain.
</p>
<p>
DHEA (dehydroepiandrosterone) is known to be low in people who are susceptible to heart disease <sup
>[1]</sup> or cancer, and all three of these steroids have a broad spectrum of protective actions. Thyroid
hormone, vitamin A, and cholesterol, which are used to produce the protective steroids, have been found to
have a similarly broad range of protective effects, even when used singly. For example, according to
MacCallum,
</p>
<p>
It has been shown that certain lipoid substances, especially cholesterine, can act as inhibiting or
neutralizing agents toward such haemolytic poisons as saponin, cobra poison, etc., through forming with them
an innocuous compound. Hanes showed that the relative immunity of puppies from chloroform poisoning is due
to the large amount of cholesterin esters in their tissues. When artificially introduced into the tissues of
adult animals a similar protection is conferred.<sup>[2]</sup>
</p>
<p>
A high level of serum cholesterol is practically diagnostic of hypothyroidism, and can be seen as an
adaptive attempt to maintain adequate production of the protective steroids. Broda Barnes' work clearly
showed that hypothyroid populations are susceptible to infections, heart disease, and cancer. <sup>[3]</sup>
</p>
<p>
In the 1940s, some of the toxic effects of fish oil (such as testicular degeneration, softening of the
brain, muscle damage, and spontaneous cancer) were found to result from an induced vitamin E deficiency.
Unfortunately, there isn't much reason to think that just supplementing vitamin E will provide general
protection against the unsaturated fats. The half-life of fats in human adipose tissue is about 600 days,
meaning that significant amounts of previously consumed oils will still be present up to four years after
they have been removed from the diet. <sup>[4]</sup>
According to Draper, et al., <sup>[5]</sup>
</p>
<p>
<strong>, , , </strong>
enrichment of the tissues with highly unsaturated fatty acids results in an increase in lipid peroxidation
in vivo even in the presence of normal concentrations of vitamin E. Fasting for more than 24 hours also
results in an increase in MDA excretion, implying that lipolysis is associated with peroxidation of the
fatty acids released.
</p>
<h2 align="justify">
According to Lemeshko, et al., it seems that this effect increases with the age of the animal. <sup>[6]</sup
>
</h2>
<p>
Commercial advertising (including medical conferences sponsored by pharmaceutical companies) and
commercially sponsored research are creating some false impressions about the role of unsaturated oils in
the diet. Like the man who poisoned himself with the "Eskimo diet," many people focus so intently on
avoiding one problem that they create other problems. Since I have discussed the association of unsaturated
fats with aging, lipofuscin, and estrogen elsewhere, I will outline some of the other problems associated
with the oils, especially as they relate to hormones.
</p>
<p>
<strong>Mechanisms and Essentiality:
</strong> When something is unavoidable, in ordinary life, talking about "essentiality," or the minimum
amount required for life or for optimal health, is more important as an exploration into the nature of our
life than as a practical health issue. For example, how much oxygen, how many germs (of what kinds), how
many cosmic rays (of what kinds), would produce the nicest human beings? The fact that we have adapted to
something---oxygen at sea level, microbes, or vegetable fats, for example--doesn't mean that we are normally
exposed to it in ideal amounts.
</p>
<p>
Animals contain desaturase enzymes, and are able to produce specific unsaturated fats (from oleic and
palmitoleic acids) when deprived of the ordinary "essential fatty acids," <sup>[7]</sup> so it can be
assumed that these enzymes have a vital purpose. The high concentration of unsaturated fats in
mitochondria--the respiratory organelles where it seems that these lipids present a special danger of
destructive oxidation--suggests that they are required for mitochondrial structure, or function, or
regulation, or reproduction. Unsaturated fats have special properties of adsorption, <sup>[8]</sup> and are
more soluble in water than are saturated fats. The movement and modulation of proteins and nucleic acids
might require these special properties. As the main site of ATP production, I suspect that their
water-retaining property might be crucial. When a protein solution (even egg-white) is poured into a high
concentration of ATP, it contracts or "superprecipitates." This condensing, water-expelling property of ATP
in protein solutions is similar to the effect of certain concentrations of salts on any polymer. It would
seem appropriate to have a substance to oppose this condensing effect, to stimulate swelling <sup>[9,
10]</sup> and the uptake of precursor substances. Something that has an intrinsic structure-loosening or
water-retaining effect would be needed. The ideas of "chaotropic agents" and "structural antioxidants" have
been proposed by Vladimirov <sup>[11]</sup> to bring generality into our understanding of the mitochondria.
Lipid peroxides are among the chaotropic agents, and thyroxin is among the structural antioxidants. The
known oxygen-sparing effects of progesterone <sup>[12, 13]</sup> would make it appropriate to include it
among the structural antioxidants. The incorporation of the wrong unsaturated fats into mitochondria would
be expected to damage the vital respiratory functions.
</p>
<p>
Some insects that have been studied have been found not to require the essential fatty acids. <sup>[14]</sup
>* According to reviewers, hogs and humans have not been shown to require the "essential" fatty acids. <sup
>[15]</sup> In vitro studies indicate that they are not required for human diploid cells to continue
dividing in culture. <sup>
[16]
</sup> According to Guarnieri, <sup>[17]</sup> EFA-deficient animals don't die from their deficiency. The
early studies showing "essentiality" of unsaturated fats, by producing skin problems and an increased
metabolic rate, have been criticized <sup>[18]</sup> in the light of better nutritional information, e.g.,
pointing out that the diets might have been deficient in vitamin B6 and/or biotin. The similar skin
condition produced by vitamin B6 deficiency was found to be improved by adding unsaturated fats to the diet.
A fat-free liver extract cured the "EFA deficiency." I think it would be reasonable to investigate the
question of the increased metabolic rate produced by a diet lacking unsaturated fats (which inhibit both
thyroid function and protein metabolism) in relation to the biological changes that have been observed.
Since diets rich in protein are known to increase the requirement for vitamin B6 <sup>[19]</sup> (which is a
co-factor of transaminases, for example), the increased rate of energy production and improved digestibility
of dietary protein on a diet lacking unsaturated fats would certainly make it reasonable to provide the
experimental animals with increased amount of other nutrients. With increasing knowledge, the old
experiments indicating the "essentiality" of certain oils have lost their ability to convince, and they
haven't been replaced by new and meaningful demonstrations. In the present state of knowledge, I don't think
it would be unreasonable to suggest that the optional dietary level of the "essential fatty acids" might be
close to zero, if other dietary factors were also optimized. The practical question, though, has to do with
the dietary choices that can be made at the present time.
</p>
<hr />
<p>
*If we followed Linus Pauling's reasoning in determining optimal vitamin C intake, this study of the
linoleic acid content of the tissues of an animal which can synthesize it would suggest that we are eating
about 100 times more "EFA" than we should.
</p>
<p>
In evaluating dietary fat, it is too often forgotten that the animals' diet (and other factors, including
temperature) affect the degree of saturation of fats in its tissues, or its milk, or eggs. The fat of wild
rabbits or summer-grazing horses, for example, can contain 40% linolenic acid, about the same as linseed
oil. Hogs fed soybeans can have fat containing over 30% linoleic acid. <sup>[20]</sup>
Considering that most of our food animals are fed large amounts of grains and soybeans, it isn't accurate to
speak of their fats as "animal fats." And, considering the vegetable oil contained in our milk, eggs, and
meat, it would seem logical to select other foods that are not rich in unsaturated oils.
</p>
<p>
<strong>Temperature and Fat:</strong> The fact that saturated fats are dominant in tropical plants and in
warm-blooded animals relates to the stability of these oils at high temperatures. Coconut oil which had been
stored at room temperature for a year was found to have no measurable rancidity. Since growing coconuts
often experience temperatures around 100 degrees Fahrenheit, ordinary room temperature isn't an oxidative
challenge. Fish oil or safflower oil, though, can't be stored long at room temperature, and at 98 degrees F,
the spontaneous oxidation is very fast.
</p>
<p>
Bacteria vary the kind of fat they synthesize, according to temperature, forming more saturated fats at
higher temperatures.<sup>[21]</sup> The same thing has been observed in seed oil plants. <sup>[22]</sup>
Although sheep have highly saturated fat, the superficial fat near their skin is relatively unsaturated; it
would obviously be inconvenient for the sheep if their surface fat hardened in cool weather, when their skin
temperature drops considerably. Pigs wearing sweaters were found to have more saturated fat than other
pigs.<sup>[23]</sup>
Fish, which often live in water which is only a few degrees above freezing, couldn't function with hardened
fat. At temperatures which are normal for fish, and for seeds which germinate in the cold northern
springtime, rancidity of fats isn't a problem, but rigidity would be.
</p>
<p>
<strong>Unsaturated Fats Are Essentially Involved In Heart Damage:
</strong>
The toxicity of unsaturated oils for the heart is well established, <sup>
[24, 25, 26]</sup> though not well known by the public.
</p>
<p>
In 1962, it was found that unsaturated fatty acids are directly toxic to mitochondria. <sup>[27]</sup> Since
stress increases the amount of free fatty acids circulating in the blood (as well as lipid peroxides), and
since lack of oxygen increases the intracellular concentration of free fatty acids, stored unsaturated fats
would seem to represent a special danger to the stressed organism. Meerson and his colleagues <sup>
[18]</sup> have demonstrated that stress liberates even local tissue fats in the heart during stress,
and that systematic drug treatment, including antioxidants, can stop the enlargement of stress-induced
infarctions. Recently, it was found that the cardiac necrosis caused by unsaturated fats (linolenic acid, in
particular) could be prevented by a cocoa butter supplement. <sup>[29]</sup> The author suggests that this
is evidence for the "essentiality" of saturated fats, but points out that animals normally can produce
enough saturated fat from dietary carbohydrate or protein, to prevent cardiac necrosis, unless the diet
provides too much unsaturated fat. A certain proportion of saturated fat appears to be necessary for
stability of the mitochondria. Several other recent studies show that the "essential" fatty acids decrease
the P/O ratio, or the phosphorylation efficiency, <sup>[30]</sup> the amount of usable energy produced by
cellular respiration.
</p>
<p>
There has been some publicity about a certain unsaturated fat, eicosapentaenoic acid, or EPA, which can have
some apparently protective and anti-inflammatory effects. A study in which butter was added to the animals'
diet found that serum EPA was elevated by the butter. The investigator pointed out that other studies had
been able to show increased serum EPA from an EPA supplement only when the animals had previously been fed
butter.<sup> [31]</sup>
</p>
<p>
Intense lobbying by the soybean oil industry has created the widespread belief that "tropical oils" cause
heart disease. In a comparison of many kinds of oil, including linseed oil, olive oil, whale oil, etc., palm
oil appeared to be the most protective. The same researcher <sup>
[32]</sup> more recently studied palm oil's antithrombotic effect, in relation to platelet aggregation.
It was found that platelet aggregation was enhanced by sunflowerseed oil, but that palm oil tended to
decrease it.
</p>
<p>
Much current research has concentrated on the factors involved in arterial clotting. Since the blood moves
quickly through the arteries, rapid processes are of most interest to those workers, though some people do
remember to think in terms of an equilibrium between formation and removal of clot material. For about 25
years there was interest in the ability of vitamin E to facilitate clot removal, apparently by activating
proteolytic enzymes.<sup>[33]</sup> Unsaturated fats' ability to inhibit proteolytic enzymes in the blood
has occasionally been discussed, but seldom in the U.S. The equilibrium between clotting and clot
dissolution is especially important in the veins, where blood moves more slowly, and spends more time.
</p>
<p>
<strong>. . . </strong>
the slower blood flows the greater its predisposition to clotting. However, this intrinsic process, leading
to fibrin production, is slow, taking up to a minute or more to occur. Thrombosis as a result of stasis,
therefore, occurs in the venous circulation; typically in the legs where"venous return is slowest. In fact,
many thousands of small thrombi are formed each day in the lower body. These pass via the vena cava into the
lungs where thrombolysis occurs, this being a normal metabolic function of the organ. <sup>[34]</sup>
</p>
<p>
In the Shutes' research in the 1930s and 1040s, vitamin E and estrogen acted in opposite directions on the
clot-removing enzymes.<sup>[33]</sup>
Since estrogen increases blood lipids, and increases the incidence of strokes and heart attacks, it would be
interesting to expand the Shutes' work by considering the degree of saturation of blood lipids in relation
to the effects of vitamin E and estrogen on clot removal. Estrogen's effect on clotting is very complex,
since it increases the ratio of unsaturated to saturated fatty acids in the body, and increases the tendency
of blood to pool in the large veins, in addition to its direct effects on the clotting factors.
</p>
<p>
<strong>Immunodeficiency and Unsaturated Fats:
</strong>Intravenous feeding with unsaturated fats is powerfully immunosuppressive <sup>[35]</sup> (though
it often was used to give more calories to cancer patients) and is now advocated as a way to prevent graft
rejection. The deadly effect of the long-chain unsaturated fats on the immune system has led to the
development of new products containing short and medium-chain saturated fats for intravenous feeding. <sup
>[36]</sup> It was recently reported that the anti-inflammatory effect of n-3 fatty acids (fish oil) might
be related to the observed suppression of interleukin-1 and tumor necrosis factor by those fats. <sup
>[37]</sup> The suppression of these anti-tumor immune factors persists after the fish oil treatment is
stopped.
</p>
<p>
As mentioned above, stress and hypoxia can cause cells to take up large amounts of fatty acids. Cortisol's
ability to kill white blood cells (which can be inhibited by extra glucose) is undoubtedly an important part
of its immunosuppressive effect, and this killing is mediated by causing the cells to take up unsaturated
fats. <sup>[38]</sup>
</p>
<p>
Several aspects of the immune system are improved by short-chain saturated fats. Their anti-histamine action
<sup>[39]</sup> is probably important, because of histamine's immunosuppressive effects.<sup>[40]</sup>
Unsaturated fats have been found to cause degranulation of mast cells.<sup>[41]</sup>
The short-chain fatty acids normally produced by bacteria in the bowel apparently have a local
anti-inflammatory action.<sup>[42]</sup>
</p>
<p>
A recent discussion of "tissue destruction by neutrophils" mentions "a fascinating series of experiments
performed between 1888 and 1906," in which "German and American scientists established the importance of
neutrophil proteinases and plasma antiproteinases in the evolution of tissue damage in vivo." <sup>[43]</sup
>
MacCallum's <em>Pathology </em>described some related work:
</p>
<p>
<strong>. . . </strong>
Jobling has shown that the decomposition products of some fats--unsaturated fatty acids and their
soaps--have the most decisive inhibiting action upon proteolytic ferments, their power being in a sense
proportional to the degree of unsaturation of the fatty acid. So universally is it true that such
unsaturated fatty acids can impede the action of proteolytic ferments that many pathological conditions
(such as the persistence of caseous tuberculous material in its solid form) can be shown to be due to their
presence. If they are rendered impotent by saturation of their unsaturated group with iodine, the
proteolysis goes on rapidly and the caseous tubercle or gumma rapidly softens.<sup>[44]</sup>
</p>
<p>
Another comment by MacCallum suggests one way in which unsaturated fats could block the action of cytotoxic
cells:
</p>
<p>
This function of the wandering cells is, of course, of immediate importance in connection with their task of
cleaning up the injured area to prepare it for repair. While the proteases thus produced are active in the
solution of undesirable material, their unbridled action might be detrimental. As a matter of fact, it is
shown by Jobling and Petersen that the anti-ferment known to be present in the serum and to restrict the
action of the ferment is a recognizable chemical substance, usually a soap or other combination of an
unsaturated fatty acid. It is possible to remove or decompose this substance or to saturate the fatty acid
with iodine and thus release the ferment to its full activity. <sup>[45]</sup>
</p>
<p>
<strong>Unsaturated Fats Are Essential For Cancer:
</strong>
The inhibition of proteolytic enzymes by unsaturated fats will act at many sites: digestion of protein,
"digestion" of clots, "digestion" of the colloid in the thyroid gland which releases the hormones, the
activity of white cells mentioned above, and the normal "digestion" of cytoplasmic proteins involved in
maintaining a steady state as new proteins are formed and added to the cytoplasm. It has been suggested that
inhibition of the destruction of intracellular proteins would shift the balance toward growth.<sup>[46]</sup
>
Cancer cells are known to have a high level of unsaturated fats,<sup>[47]</sup>
yet they have a low level of lipid peroxidation;<sup>[48]</sup> lipid peroxidation inhibits growth, and is
often mentioned as a normal growth restraining factor.<sup>[49]</sup>
</p>
<p>
In 1927, it was observed that a diet lacking fats prevented the development of spontaneous tumors.[50] Many
subsequent investigators have observed that the unsaturated fats are essential for the development of
tumors. <sup>[51, 52, 53]</sup> Tumors secrete a factor which mobilizes fats from storage, <sup>[54]</sup>
presumably guaranteeing their supply in abundance until the adipose tissues are depleted. Saturated
fats--coconut oil and butter, for example--do not promote tumor growth.<sup>[55]</sup> Olive oil is not a
strong tumor promoter, but in some experiments it does have a slightly permissive effect on tumor growth.
<sup>[56, 57]</sup> In some experiments, the carcinogenic action of unsaturated fats could be offset by
added thyroid, <sup>[57]</sup>
an observation which might suggest that at least part of the effect of the oil is to inhibit thyroid. Adding
cystine to the diet (cysteine, the reduced form of cystine, is a thyroid antagonist) also increases the
tumor incidence.<sup>[58]</sup> In a hyperthyroid state, the ability to quickly oxidize larger amounts of
the toxic oils would very likely have a protective effect, preventing storage and subsequent peroxidation,
and reducing the oils' ability to synergize with estrogen.
</p>
<p>
Consumption of unsaturated fat has been associated with both skin aging and with the sensitivity of the skin
to ultraviolet damage, Ultraviolet light-induced skin cancer seems to be mediated by unsaturated fats and
lipid peroxidation.<sup>[59]</sup>
</p>
<p>
In a detailed study of the carcinogenicity of different quantities of unsaturated fat, Ip, et al., tested
levels ranging from 0.5% to 10%, and found that the cancer incidence varied with the amount of "essential
oils" in the diet. Some of their graphs make the point very clearly:<sup>
[52}</sup>
</p>
<p>
This suggests that the optimal EFA intake might be 0.5% or less.
</p>
<p>
Butter and coconut oil contain significant amounts of the short and medium-chain saturated fatty acids,
which are very easily metabolized,<sup>[60]</sup>
inhibit the release of histamine,<sup>[39]</sup> promote differentiation of cancer cells,<sup>[61]</sup>
tend to counteract the stress-induced proteins,<sup>[62]</sup> decrease the expression of prolactin
receptors, and promote the expression of the T3 (thyroid) receptor. <sup>[63] </sup>
(A defect of the thyroid receptor molecule has been identified as an "oncogene," responsible for some
cancers, as has a defect in the progesterone receptor.)
</p>
<p>
Besides inhibiting the thyroid gland, the unsaturated fats impair intercellular communication,[64] suppress
several immune functions that relate to cancer, and are present at high concentrations in cancer cells,
where their antiproteolytic action would be expected to interfere with the proteolytic enzymes and to shift
the equilibrium toward growth. In the free fatty acid form, the unsaturated fats are toxic to the
mitochondria, but cancer cells are famous for their compensatory glycolysis.
</p>
<p>
By using lethargic connective tissue cells known to have a very low propensity to take up unsaturated fats
<sup>[65]</sup> as controls in comparison with, e.g., breast cancer cells, with a high affinity for fats, it
is possible to show a "selective" toxicity of oils for cancer cells. However, an in vivo test of an
alph-linolenic acid ester showed it to have a stimulating effect on breast cancer.<sup>[66]</sup>
Given a choice, skin fibroblasts demonstrate a very specific preference for oleic acid, over a
polyunsaturated fat.<sup>[67]</sup>
</p>
<p>
Even if unsaturated fats were (contrary to the best evidence) selectively toxic for cancer cells, their use
in cancer chemotherapy would have to deal with the issues of their tendency to cause pulmonary
embolism,their suppression of immunity including factors specifically involved in cancer resistance, and
their carcinogenicity.
</p>
<p>
<strong>Brain Damage And Lipid Peroxidation:
</strong>
When pregnant mice were fed either coconut oil or unsaturated seed oil, the mice that got coconut oil had
babies with normal brains and intelligence, but the mice exposed to the unsaturated oil had smaller brains,
and had inferior intelligence. In another experiment, radioactively labeled soy oil was given to nursing
rats, and it was shown to be massively incorporated into brain cells, and to cause visible structural
changes in the cells. In 1980, shortly after this study was published in Europe, the U.S. Department of
Agriculture issued a recommendation against the use of soy oil in infant formulas. More recently, <sup
>[68]</sup> pregnant rats and their offspring were given soy lecithin with their food, and the exposed
offspring developed sensorimotor defects.
</p>
<p>
Many other studies have demonstrated that excessive unsaturated dietary fats interfere with learning and
behavior, <sup>[70, 71]</sup> and the fact that some of the effects can be reduced with antioxidants
suggests that lipid peroxidation causes some of the damage. Other studies are investigating the involvement
of lipid peroxidation in seizures.<sup>[72]</sup>
</p>
<p>
The past use of soy oil in artificial milk (and in maternal diets) has probably caused some brain damage.
The high incidence of neurological defects (e.g., 90%) that has been found among violent criminals suggests
that it might be worthwhile to look for unusual patterns of brain lipids in violent people.
</p>
<p>
There have been a series of claims that babies' brains or eyes develop better when their diets are
supplemented with certain unsaturated oils, based on the idea that diets may be deficient in certain types
of oil, Some experimenters claim that the supplements have improved the mental development of babies, but
other researchers find that the supplemented babies have poorer mental development. But the oils that are
added to the babies' diets are derived from fish or algae, and contain a great variety of substances (such
as vitamins) other than the unsaturated fatty acids, and the researchers consistently fail to control for
the effects of such substances.
</p>
<p>
It has shown that it is probably impossible to experience a detectable deficiency of linoleic acid outside
of the laboratory setting,<sup>[69]</sup> but the real issue is probably whether the amount in the normal
diet is harmful to development. Until the research with animals has produced a better understanding of the
effects of unsaturated oils, experimenting on human babies seems hard to justify.
</p>
<p>
Marion Diamond, who has studied the improved brain growth in rats given a stimulating environment (which,
like prenatal progesterone, produced improved intelligence and larger brains), observed that in old age the
"enriched" rats' brains contained less lipofuscin (age pigment).<sup>[73]</sup>
It is generally agreed that the unsaturated oils promote the formation of age pigment. The discovery that
stress or additional cortisone (which, by blocking the use of glucose, forces cells to take up more fat)
causes accelerated aging of the brain<sup>[74]</sup> should provide new motivation to investigate the
antistress properties of substances such as the protective steroids mentioned above, and the short-chain
saturated fats.
</p>
<p>
<strong>Essential for Liver Damage:</strong> Both experimental and epidemiological studies have shown that
dietary linoleic acid is required for the development of alcoholic liver damage.<sup>[75] </sup>
Animals fed tallow and ethanol had no liver injury, but even 0.7% or 2.5% linoleic acid with ethanol caused
fatty liver, necrosis, and inflammation. Dietary cholesterol at a level of 2% was found to cause no
harm,<sup>[76]</sup>
but omitting it entirely from the diet caused leakage of amino-transferase enzymes. This effect of the
absence of cholesterol was very similar to the effects of the presence of linoleic acid with ethanol.
</p>
<p>
<strong>Obesity: </strong>
For many years studies have been demonstrating that dietary coconut oil causes decreased fat synthesis and
storage, when compared with diets containing unsaturated fats. More recently, this effect has been discussed
as a possible treatment for obesity.<sup>[77]</sup>
The short-chain fats in coconut oil probably improve tissue response to the thyroid hormone (T3), and its
low content of unsaturated fats might allow a more nearly optimal function of the thyroid gland and of
mitochondria. A survey of other tropical fruits' content of short and medium chain fatty acids might be
useful, to find lower calorie foods which contain significant amounts of the shorter-chain fats.
</p>
<p>
<strong>Other Problem Areas:
</strong> The presence of palmitate in the lung surfactant phospholipids<sup>[78]</sup> suggests that
maternal overload with unsaturated fats might interfere with the formation of these important substances,
causing breathing problems in the newborn. The bone-calcium mobilizing effect of prostaglandins suggests
that dietary fats might affect osteoporosis; the absence of osteoporosis in some tropical populations might
relate to their consumption of coconut oil and other saturated tropical oils. The steroids which occur in
association with some seed oils might be nutritionally significant, in the way animal hormones in foods
undoubtedly are. For example, soy steroids can be converted by bowel bacteria into estrogens. R. Marker, et
al., found diosgenin (the material in the Mexican yam from which progesterone, etc., are derived) in a palm
kernel, <em>Balanites aegyptica (Wall)</em>.<sup>[79]</sup>
Another palm fruit also contains sterols with anti-androgenic and anti-edematous actions.<sup>[80, 81]
</sup>
</p>
<p>
If the amount of ingested unsaturated fats (inhibitors of protein digestion) were lower, protein
requirements might be lower.
</p>
<p>
The similar effects of estrogen and of polyunsaturated fats (PUFA) are numerous. They include antagonism to
vitamin E and thyroid, to respiration and proteolysis; promotion of lipofuscin formation and of clot
formation, promotion of seizure activity, impairment of brain development and learning; and involvement in
positive or negative regulation of cell division, depending on cell type.
</p>
<p>
These parallels suggest that the role of PUFA in reproduction might be similar to that of estrogen, namely,
the promotion of uterine and breast cell proliferation, water uptake, etc. Such parallels should be a
caution in generalizing from the conditions which are essential for reproduction to the conditions which are
compatible with full development and full functional capacity. If a certain small amount of dietary PUFA is
essential for reproduction, but for no other life function, then it is analogous to the brief "estrogen
surge," which must quickly be balanced by opposing hormones. The present approach to contraception through
estrogen-induced miscarriage might give way to fertility regulation by diet. A self-actualizing
pro-longevity diet, low in PUFA, might prolong our characteristically human condition of delayed
reproductive maturity, and, if PUFA are really essential for reproduction, unsaturated vegetable oils could
temporarily be added to the diet when reproduction is desired.
</p>
<p>
<strong>Conclusions:</strong>
Polyunsaturated fats are nearly ubiquitous, but if they are "essential nutrients," in the way vitamin A, or
lysine, is essential, that has not been demonstrated. It seems clear that they <em>are </em>
essential for cancer, and that they have other properties which cause them to be toxic at certain levels. It
might be time to direct research toward determining whether there is a threshold of toxicity, or whether
they are, like ionizing radiation, toxic at any level.
</p>
<p><strong>Note:</strong></p>
<p>
<strong>A possible mitochondrial site for toxicity:
</strong>
In 1971 I was trying to combine some of the ideas of Albert Szent-Gyorgyi, Otto Warburg, W. F. Koch, and L.
C. Strong. I was interested in the role of ubiquinone in mitochondrial respiration. In one experiment, I was
using paper chromatography to compare oils that I had extracted from liver with vitamin E and with
commercially purified ubiquinone. Besides using the pure substances, I decided to combine vitamin E with
ubiquinone for another test spot. As soon as I combined the two oils, their amber and orange colors turned
to an inky, greenish black color. I tested both bacterial and mammalian ubiquinone, and benzoquinone, and
they all produced similar colors with vitamin E. When I ran the solvent up the paper, the vitamin E and the
ubiquinone traveled at slightly different speeds. The black spot, containing the mixture, also moved, but
each substance moved at its own speed, and as the materials separated, their original lighter colors
reappeared. Charge-transfer bonds, which characteristically produce dark colors, are very weak bonds. I
think this must have been that kind of bond. Years later, I tried to repeat the experiment, using
"ubiquinone" from various capsules that were sold for medical use. Instead of the waxy yellow-orange
material I had used before, these capsules contained a liquid oil with a somewhat yellow color. Very likely,
the ubiquinone was dissolved in vegetable oil. At the time, I was puzzled that the color reaction didn't
occur, but later I realized that a solvent containing double bonds (e.g., soy oil or other oil containing
PUFA) would very likely prevent the close association between vitamin E and ubiquinone which is necessary
for charge-transfer to occur. Since I think Koch and Szent-Gyorgyi were right in believing that electronic
activation is the most important feature of the living state, I think the very specific electronic
interaction between vitamin E and ubiquinone must play an important role in the respiratory function of
ubiquinone. Ubiquinone is known to be a part of the electron transport chain which can leak electrons, so
this might be one of the ways in which vitamin E can prevent the formation of toxic free-radicals. If it can
prevent the "leakage" of electrons, then this in itself would improve respiratory efficiency. If unsaturated
oils interfere with this very specific but delicate bond, then this could explain, at least partly, their
toxicity for mitochondria. ["Electron leak" reference: B. Halliwell, in <em>Age Pigments</em> (R. S. Sohal,
ed.), pp. 1-62, Elsevier, Amsterdam, 1981.]
</p>
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