Essential Fatty Acids Archives

Dr. Peat's reply re flax oil

As some of you know I wrote a message to Dr. Peat this morning asking him to comment on Dr. Johanna Budwig's opinions and work on flax seed oil (I gave him links to the Budwig sites that Rosemarie posted recently). He replied very promptly. I have not had time to read it in full, but will post it now anyway for all those interested. Here it is (very long).

Those sites don't even report J. Budwig's writings accurately.
I have read
all of her German publications, and some of the publications
in English
that purport to be translations are just fabrications,
to make her
statements sound a little more credible. In all of Budwig's
German
publications that mention cancer, there is nothing resembling
documentation.
In 1954 a Mexican professor began advocating the use of
large amounts of
flax oil as a purgative for treating cancer patients. Laxatives
and enemas
are traditional and are physiologically very appropriate
for cancer
patients. Quark, or curd, is the part of the milk after
the whey has been
removed. Most of the tryptophan is in the whey, so the
curd is relatively
poor in tryptophan content, and this makes the curd very
appropriate food
for anyone, especially cancer patients, since tryptophan
stimulates tumor
growth, and is the only amino acid known to be carcinogenic.
That is to
say that flax oil and cottage cheese could have their proper
place in
treating cancer.
However, the American and Canadian oil merchants who use
Budwig to promote
their products are careless about everything except what
will increase
sales. The statements on the website that suggest equivalence
of soy or
rice "milk," or yogurt, with milk curd are very irresponsible;
soy products
contain a variety of cancer-promoting agents, and the protein
quality of
rice is too low to sustain life.

"...quark, which is something similar to cottage cheese
or yogurt in that
it is rich in high quality protein. Quark is difficult
to obtain in the
U.S, but either yogurt, cottage cheese, skim milk, soy
milk or rice milk is
a good substitute."

One of my articles on unsaturated oils follows:


Oils in Context

An oil researcher[0] 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.)
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.
DHEA (dehydroepiandrosterone) is known to be low in people
who are
susceptible to heart disease [1] 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,

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.[2]

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. [3]
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. [4] According
to Draper, et al., [5]

… 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.

According to Lemeshko, et al., it seems that this effect
increases with the
age of the animal. [6]
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.
Mechanisms and Essentiality: 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.
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," [7] 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, [8]
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 [9,
10] 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 [11] 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 [12, 13] 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.
Some insects that have been studied have been found not
to require the
essential fatty acids. [14]* According to reviewers, hogs
and humans have
not been shown to require the "essential" fatty acids.
[15] In vitro
studies indicate that they are not required for human diploid
cells to
continue dividing in culture. [16] According to Guarnieri,
[17]
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 [18]
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 [19] (which is a co-factor of transaminases,
for example), the
increased rate of energy production and improved digestibility
of dietary
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.
____________________________________________________________________________
____
*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.

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. [20] 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.
Temperature and Fat: 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.
Bacteria vary the kind of fat they synthesize, according
to temperature,
forming more saturated fats at higher temperatures.[21]
The same thing has
been observed in seed oil plants. [22] 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.[23] 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.
Unsaturated Fats Are Essentially Involved In Heart Damage:
The toxicity of
unsaturated oils for the heart is well established, [24,
25, 26] though not
well known by the public.
In 1962, it was found that unsaturated fatty acids are
directly toxic to
mitochondria. [27] 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 [18] 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. [29]
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, [30] the amount
of usable energy
produced by cellular respiration.
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. [31]
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
[32] 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.
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.[33] 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.

… 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. [34]

In the Shutes' research in the 1930s and 1040s, vitamin
E and estrogen
acted in opposite directions on the clot-removing enzymes.[33]
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.
Immunodeficiency and Unsaturated Fats: Intravenous feeding
with
unsaturated fats is powerfully immunosuppressive [35] (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. [36] 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.
[37] The
suppression of these anti-tumor immune factors persists
after the fish oil
treatment is stopped.
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. [38]
Several aspects of the immune system are improved by short-chain
saturated
fats. Their anti-histamine action [39] is probably important,
because of
histamine's immunosuppressive effects.[40] Unsaturated
fats have been
found to cause degranulation of mast cells.[41] The short-chain
fatty
acids normally produced by bacteria in the bowel apparently
have a local
anti-inflammatory action.[42]
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." [43] MacCallum's Pathology described
some related
work:

…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.[44]

Another comment by MacCallum suggests one way in which
unsaturated fats
could block the action of cytotoxic cells:

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. [45]

Unsaturated Fats Are Essential For Cancer: 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 acitvity 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.[46] Cancer cells
are known to have
a high level of unsaturated fats,[47] yet they have a low
level of lipid
peroxidation;[48] lipid peroxidation inhibits growth, and
is often
mentioned as a normal growth restraining factor.[49]
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. [51,
52, 53] Tumors secrete a factor which mobilizes fats from
storage, [54]
presumably guaranteeing their supply in abundance until
the adipose tissue
are depleted. Saturated fats-coconut oil and butter, for
example-do not
promote tumor growth.[55] Olive oil is not a strong tumor
promoter, but in
some experiments it does have a slightly permissive effect
on tumor growth.
[56, 57] In some experiments, the carcinogenic action
of unsaturated fats
could be offset by added thyroid, [57] 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.[58] 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.
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.[59]
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: [52}

This suggests that the optimal EFA intake might be 0.5%
or.less.
Butter and coconut oil contain significant amounts of the
short and
medium-chain saturated fatty acids, which are very easily
metabolized,[60]
inhibit the release of histamine,[39] promote differentiation
of cancer
cells,[61] tend to counteract the stress-induced proteins,[62]
decrease the
expression of prolactin receptors, and promote the expression
of the T3
(thyroid) receptor. [63] (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.)
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.
By using lethargic connective tissue cells known to have
a very low
propensity to take up unsaturated fats [65] 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.[66] Given a choice, skin fibroblasts
demonstrate a very
specific preference for oleic acid, over a polyunsaturated
fat.[67]
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
resitance, and their carcinogenicity.
Brain Damage And Lipid Peroxidation: 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 ininfant
formulas. More
recently, [68] pregnant rats and their offspring were given
soy lecithin
with their food, and the exposed offspring developed sensorimotor
defects.
Many other studies have demonstrated that excessive unsaturated
dietary
fats interfere with learning and behavior, [70, 71] 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.[72]
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.
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.
It has shown that it is probably impossible to experience
a detectable
deficiency of linoleic acid outside of the laboratory setting,[69]
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.
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).[73] 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[74] should provide new motivation
to
investigate the antistress properties of substances such
as the protective
steroids mentioned above, and the short-chain saturated
fats.
Essential for Liver Damage: Both experimental and epidemiological
studies
have shown that dietary linoleic acid is required for the
development of
alcoholic liver damage.[75] 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 inflammmation. Dietary cholesterol
at a level of 2%
was found to cause no harm,[76] 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.
Obesity: For many years studies have been demonstrating
that dietary
coconut oil causes decreased fat synthesis and storage,
when compared with
diets containing unsaturated fats. Moree recently, this
effect has been
discussed as a possible treatment for obesity.[77] 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.
Other Problem Areas: The presence of palmitate in the
lung surfactant
phospholipids[78] 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,
Balanites
aegyptica (Wall).[79] Another palm fruit also contains
sterols with
anti-androgenic and anti-edematous actions.[80, 81]
If the amount of ingested unsaturated fats (inhibitors
of protein
digestion) were lower, protein requirements might be lower.
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.
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 condtion 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.
Conclusions: 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 are
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.


Note:
A possible mitochondrial site for toxicity: 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 yelloow 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 Age Pigments
(R. S. Sohal,
ed.), pp. 1-62, Elsevier, Amsterdam, 1981.]

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