|
*Weil recommends eating "oily fish"--"wild Alaskan
salmon, mackerel, sardines, or herring"--. "If you do take
supplements, fish oil is a better source of DHA than algae"
When a group of people in government and industry decide on a policy,
they can use carrots (good jobs, grants, and prestige) and sticks (loss
of jobs and grants, organized slander, and worse) to make their guidelines
clear, and most people will choose to follow those cues, even if they
know that the policy is wrong. Historically, policy makers have told
the public that "radiation is good for you," "estrogen
will make you fertile (or safely infertile) and feminine and strong
and intelligent," "starchy foods will prevent diabetes and
obesity," "using diuretics and avoiding salt will make pregnancy
safer," and that the polyunsaturated fatty acids are "nutritionally
essential, and will prevent heart disease."
The original "essential fatty acids" were linoleic,
linolenic, and arachidonic acids. Now that the toxic effects of those
are coming to be recognized, new "essential fatty acids,"
the omega-3 fatty acids, including those with long chains, found in
fish oils, are said to make babies more intelligent, to be necessary
for good vision, and to prevent cancer, heart disease, obesity, arthritis,
depression, epilepsy, psychosis, dementia, ulcers, eczema and dry skin.
With just a normal amount of vitamin E in the diet, cod liver oil is
certain to be highly oxidized in the tissues of a mammal that eats a
lot of it, and an experiment with dogs showed that it could increase
their cancer mortality from the normal 5% to 100%. Although fish oils
rapidly destroy vitamin E in the body, some of them, especially the
liver oils, can provide useful vitamins, A and D. In studies comparing
fish oil diets with standard diets, these nutrients, as well as any
toxins besides fatty acids (Huang, et al., 1997; Miyazaki, et al., 1998)
in either type of oil, should be taken into account, but they seldom
are.
Despite the nutritional value of those vitamins, fish oils are generally
much more immunosuppressive than the seed oils, and the early effects
of fish oil on the "immune system" include the suppression
of prostaglandin synthesis, because the more highly unsaturated long
chain fats interfere with the conversion of linoleic acid into arachidonic
acid and prostaglandins. The prostaglandins are so problematic that
their suppression is helpful, whether the inhibition is caused by aspirin
or vitamin E, or by fish oil.
Some of the important antiinflammatory effects of fish oil result from
the oxidized oils, rather than the unchanged oils (Sethi, 2002; Chaudhary,
et al., 2004). These oils are so unstable that they begin to spontaneously
oxidize even before they reach the bloodstream.
In experiments that last just a few weeks or months, there may not be
time for cancers to develop, and on that time scale, the immunosuppressive
and antiinflammatory effects of oxidized fish oil might seem beneficial.
For a few decades, x-ray treatments were used to relieve inflammatory
conditions, and most of the doctors who promoted the treatment were
able to retire before their patients began suffering the fatal effects
of atrophy, fibrosis, and cancer. (But a few people are still advocating
x-ray therapy for inflammatory diseases, e.g., Hildebrandt, et al.,
2003.) The fish oil fad is now just as old as the x-ray fad was at its
peak of popularity, and if its antiinflammatory actions involve the
same mechanisms as the antiinflammatory immunosuppressive x-ray treatments,
then we can expect to see another epidemic of fibrotic conditions and
cancer in about 15 to 20 years.
Around 1970 researchers reported that animals given fish oil in their
food lived longer than animals on the standard diet. Alex Comfort, who
was familiar with the research showing that simple reduction of food
intake increased longevity, observed that the animals were very reluctant
to eat the food containing smelly fish oil, and were eating so little
food that their longevity could be accounted for by their reduced caloric
intake. Even when "fresh" deodorized fish oil is added to
the diet, its spontaneous oxidation before it reaches the animal's tissues
reduces its caloric value. Without antioxidants, fish oil is massively
degraded within 48 hours, and even with a huge amount of antioxidant
there is still considerable degradation (Gonzalez, 1988; Klein, et al.,
1990).
Fish oil has been used for hundreds of years as varnish or for fuel
in lamps, and the fatty fish have been used as fertilizer and animal
feed, and later the hydrogenated solid form of the oil, which is more
stable, has been used in Europe as a food substitute for people. When
whale hunting was reduced around 1950, fish oil was substituted for
whale oil in margarine production. Like the seed oils, such as linseed
oil, the fish oils were mostly replaced by petroleum derivatives in
the paint industry after the 1960s.
Although by 1980 many animal diseases were known to be caused by eating
oily fish, and the unsaturated oils were known to accelerate the formation
of the "age pigment," lipofuscin, many "beneficial effects"
of dietary fish oil started appearing in research journals around that
time, and the mass media, responding to the industry's public relations
campaign, began ignoring studies that showed harmful effects from eating
fish oil.
When reviewers in professional journals begin to ignore valid research
whose conclusions are harmful to the fish oil industry, we can see that
the policy guidelines set by the industry and its agents in government
have become clear. Around the end of the century, we begin to see a
strange literary device appearing, in which research reports on the
toxic effects of omega-3 oils are prefaced by remarks to the effect
that "we all know how great these oils are for good health."
I think I detect groveling and shuffling of the feet by authors who
want to get their work published. If you are willing to say that your
work probably doesn't mean what it seems to mean, maybe they will publish
it.
For more than 50 years, the great majority of the medical publications
on estrogen were part of the drug industry's campaign to fraudulently
gain billions of dollars, and anyone who cared to analyze them could
see that the authors and editors were part of a cult, rather than seekers
of useful knowledge. Likewise, the doctrine of the harmlessness of x-rays
and radioactive fallout was kept alive for several decades by demonizing
all who challenged it. It now looks as though we are in danger of entering
another period of medical-industrial-governmental cultism, this time
to promote the universal use of polyunsaturated fats as both drugs and
foods.
In 2004, a study of 29,133 men reported that the use of omega-3 oil
or consumption of fish didn't decrease depression or suicide, and in
2001, a study of 42,612 men and women reported that after more than
9 years the use of cod liver oil showed no protective effect against
coronary heart disease (Hakkarainen, et al., 2004; Egeland, et al.,
2001).
The most popular way of arguing that fish oil will prevent heart disease
is to show that it lowers blood lipids, continuing the old approach
of the American Heart Association's "heart protective diet."
Unfortunately for that argument, it's now known that the triglycerides
in the blood are decreased because of the fish oil's toxic effects on
the liver (Hagve and Christophersen, 1988; Ritskes-Hoitinga, et al.,
1998). In experiments with rats, EPA and DHA lowered blood lipids only
when given to rats that had been fed, in which case the fats were incorporated
into tissues, and suppressed mitochondrial respiration (Osmundsen, et
al., 1998).
The belief that eating cholesterol causes heart disease was based mainly
on old experiments with rabbits, and subsequent experiments have made
it clear that it is oxidized cholesterol that damages
the arteries (Stapran, et al., 1997). Since both fish oil and oxidized
cholesterol damage rabbits' arteries, and since the lipid peroxides
associated with fish oil attack a great variety of biological materials,
including the LDL lipoproteins carrying cholesterol, the implications of
the rabbit experiments now seem very different.
Another way of arguing for the use of fish oil or other omega-3 fats
is to show a correlation between disease and a decreased amount of EPA,
DHA, or arachidonic acid in the tissues, and to say "these oils
are deficient, the disease is caused by a deficiency of essential fatty
acids." Those oils are extremely susceptible to oxidation, so they
tend to spontaneously disappear in response to tissue injury, cellular
excitation, the increased energy demands of stress, exposure to toxins
or ionizing radiation, or even exposure to light. That spontaneous oxidation
is what made them useful as varnish or paint medium. But it is what
makes them sensitize the tissues to injury. Their "deficiency"
in the tissues frequently corresponds to the intensity of oxidative
stress and lipid peroxidation; it is usually their presence, rather
than their deficiency, that created the disposition for the disease.
One of the earliest harmful effects of polyunsaturated fatty acids,
PUFA, to be observed was their acceleration of the formation of lipofuscin
or ceroid, the "age pigment," during oxidative stress or vitamin
E deficiency. Associated with the formation of lipofuscin, the PUFA
were discovered to cause degeneration of the gonads and brain, and the
fact that vitamin E could prevent some of their toxic effects led to
the idea that vitamin E was essentially an antioxidant. Unfortunately,
the protective effect of vitamin E against the PUFA is only partial
(Allard, et al., 1997).
The degenerative diseases are all associated with disturbances involving
fat metabolism and lipid peroxidation. Alzheimer's disease, alcoholic
and nonalcoholic liver disease, retinal degeneration, epilepsy, AIDS,
diabetes, and a variety of circulatory problems involve breakdown products
of the PUFA. The products of PUFA decomposition include acrolein, malondialdehyde,
hydroxynonenal, crotonaldehyde, ethane, pentane, and the neuroprostanes,
which are prostaglandin-like molecules formed from DHA by free radical
lipid peroxidation products, especially in the brain and at a higher
level in Alzheimer's disease.
The reactions of three types of cell--vascular endothelium, nerve cells,
and thymus cells--to the PUFA will illustrate some of the important
processes involved in their toxicity.
When the body doesn't have enough glucose, free fatty acids are released
from the tissues, and their oxidation blocks the oxidation of glucose
even when it becomes available from the breakdown of protein caused
by cortisol, which is released during glucose deprivation. Cells of
the thymus are sensitive to glucose deprivation, and even in the presence
of glucose, cortisol prevents them from using glucose, causing them
to take up fatty acids. The thymic cells die easily when exposed either
to excess cortisol, or deficient glucose. The polyunsaturated fatty
acids linoleate, arachidonate, and eicosapentaenoic, are especially
toxic to thymic cells by preventing their inactivation of cortisol,
increasing its action. (Klein, et al., 1987, 1989, 1990). Lymphocytes
from people with AIDS and leukemia are less able to metabolize cortisol.
An extract of serum from AIDS patients caused lymphocytes exposed to
cortisol to die 7 times faster than cells from healthy people. AIDS
patients have high levels of both cortisol and free polyunsaturated
fatty acids (Christeff, et al., 1988).
The cytotoxicity caused by EPA and its metabolites (15 mg. of EPA per
liter killed over 90% of a certain type of macrophage) isn't inhibited
by vitamin E (Fyfe and Abbey, 2000). Immunological activation tends
to kill T cells that contain PUFA (Switzer, et al., 2003).
When animals are fed fish oil and then exposed to bacteria, their immunosuppressed
thymic (T) cells cause them to succumb to the infection more easily
than animals fed coconut oil or a fat free diet. Natural killer cells,
which eliminate cancer cells and virus infected cells, are decreased
after eating fish oil, and T suppressor cells are often increased. More
subtle interference with immunity is produced by the actions of PUFA
on the "immune synapse," a contact between cells that permits
the transmission of immunological information. The immunosuppressive
effect of fish oil is recognized as a useful aid in preventing the rejection
of transplanted organs, but some studies are showing that survival a
year after transplantation isn't improved.
Polyunsaturated fatty acids, especially those that can be turned into
prostaglandins, are widely involved in causing inflammation and vascular
leakiness. EPA and DHA don't form ordinary prostaglandins, though the
isoprostanes and neuroprostanes they produce during lipid peroxidation
behave in many ways like the more common prostaglandins, and their enzymically
formed eicosanoids have some functions similar to those of the common
prostaglandins. The brain contains a very high concentration of these
unstable fatty acids, and they are released in synapses by ordinary
excitatory process.
Chan, et al., 1983, found that polyunsaturated fats caused brain swelling
and increased blood vessel permeability. In 1988, Chan's group found
that DHA and other polyunsaturated fatty acids added to cultured cells
from the cerebral cortex produced free radicals and stimulated production
of malondialdehyde and lactate, and inhibited the uptake of glutamic
acid, which suggests that they would contribute to prolonged excitation
of the nerves (Yu, et al., 1986). In brain slices, the polyunsaturated
fatty acids caused the production of free radicals and swelling of the
tissue, and the saturated fatty acids didn't (Chan and Fishman, 1980).
The PUFA inhibited the respiration of mitochondria in brain cells (Hillered
and Chan, 1988), and at a higher concentration, caused them to swell
(Hillered and Chan, 1989), but saturated fatty acids didn't produce
edema. Free radical activity was shown to cause the liberation of free
fatty acids from the cellular structure (Chan, et al., 1982, 1984).
The activation of lipases by free radicals and lipid peroxides, with
the loss of potassium from the cells, suggests that excitation can become
a self-stimulating process, leading to cellular destruction.
DHA itself, rather than its decomposition products, facilitates excitatory
(glutamate) nerve transmission (Nishikawa, et al., 1994), and that excitatory
action causes the release of arachidonic acid (Pellerin and Wolfe, 1991).
Considering just one of the products of fish oil peroxidation, acrolein,
and a few of its effects in cells, we can get an idea of the types of
damage that could result from increasing the amount of omega-3 fats
in our tissues.
The "barrier" between the brain and blood stream is one of
the most effective vascular barriers in the body, but it is very permeable
to oils, and lipid peroxidation disrupts it, damaging the ATPase that
regulates sodium and potassium (Stanimirovic, et al., 1995). Apparently,
anything that depletes the cell's energy, lowering ATP, allows an excess
of calcium to enter cells, contributing to their death (Ray, et al.,
1994). Increasing intracellular calcium activates phospholipases, releasing
more polyunsaturated fats (Sweetman, et al., 1995) The acrolein which
is released during lipid peroxidation inhibits mitochondrial function
by poisoning the crucial respiratory enzyme, cytochrome oxidase, resulting
in a decreased ability to produce energy (Picklo and Montine, 2001).
(In the retina, the PUFA contribute to light-induced damage of the energy
producing ability of the cells [King, 2004], by damaging the same crucial
enzyme.) Besides inhibiting the ability of nerve cells to produce energy
from the oxidation of glucose, acrolein inhibits the ability of cells
to regulate the excitatory amino acid glutamate (Lovell, et al., 2000),
contributing to the excitatory process. High levels of acrolein (and
other products of PUFA degradation) are found in the brain in Alzheimer's
disease (Lovell, et al., 2001).
The "prion" diseases, CJD and TSE/BSE (mad cow disease) have
many features in common with Alzheimer's disease, and several studies
have shown that the "prion" protein produces its damage by
activating the lipases that release polyunsaturated fatty acids and
produce lipid peroxides (Bate, et al., 2004, Stewart, et al., 2001).
Acrolein reacts with DNA, causing "genetic" damage, and also
reacts with the lysine in proteins, for example contributing to the
toxicity of oxidized low density lipoproteins (LDL), the proteins that
carry cholesterol and that became famous because of their involvement
in the development of atherosclerosis that was supposedly caused by
eating saturated fats.
My newsletter on mad cow disease discussed the evidence incriminating
the use of fish meal in animal feed, as a cause of the degenerative
brain diseases, and earlier newsletters (glycemia, and glycation) discussed
the reasons for thinking that inappropriate glycation of lysine groups
in proteins, as a result of a lack of protective carbon dioxide/carbamino
groups, produces the amyloid (or "prion") proteins that characterize
the dementias. Acrolein, produced from the decomposing "fish oils"
in the brain, is probably the most reactive product of lipid peroxidation
in the brain, and so would be likely to cause the glycation of lysine
in the plaque-forming proteins.
These toxic effects of acrolein in the brain are analogous to the multitude
of toxic effects of the omega-3 fatty acids and their breakdown products
in all of the other organs and tissues of the body. Cancer cells are
unusual in their degree of resistance to the lethal actions of the lipid
peroxides, but the inflammatory effects of the highly unsaturated fatty
acids are now widely recognized to be essentially involved in the process
of cancerization (my newsletters on cancer and leakiness discuss some
of the ways the fats are involved in tumor development).
The fats that we synthesize from sugar, or coconut oil, or oleic acid,
the omega-9 series, are protective against the inflammatory PUFA, in
some cases more effective even than vitamin E.
In Woody Allen's 1973 movie, Sleeper, the protagonist
woke up after being frozen for 200 years, to find that saturated fats
were health foods. At the time the movie was made, that had already
been established (e.g., Hartroft and Porta, 1968 edition of Present
Knowledge in Nutrition, who showed that adequate saturated fat in
the diet helped to protect against the formation of lipofuscin).
PS:
Royal Society for the Protection of Birds says 2004 has been the most
catastrophic breeding season on record for seabirds along UK coasts.
It says industrial fishing to supply fish meal and oil is barely sustainable
and imperils the whole marine food web.
"The UK has suffered serious seabird disasters this year already.
In Shetland and Orkney, entire colonies of birds failed to produce any
young because of severe food shortages. "On top of that, hundreds
of seabirds have been washing ashore having perished at sea. Again,
lack of food is thought to be one of the reasons." The report,
Assessment Of The Sustainability Of Industrial Fisheries Producing Fish
Meal And Fish Oil, was compiled for the RSPB by Poseidon Aquatic Resource
Management Ltd and the University of Newcastle-upon-Tyne.
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