Montygram
Fri, Nov-04-05, 06:15
In grad. school, one of the best exercises was having students
argue the position that they were opposed to. The debate was
informal, and questions were asked and points made after a
basic presentation was done by the two "sides." This was a
good way to see all apects of an issue, and often led to a
more sophisticated understanding of the
it. In science, this is especially useful, at least for
issues that have been the focus of much research.
I have tried to construct an "essential fatty acid" (EFA)
hypothesis, since those who enjoy attacking the basic,
scientific points I make refuse to do so. At least two posters
have actually said that omega 3 and 6 polyunsaturated fatty
acids (PUFAs) are "essential" because the body cannot make
them, as if any substance the body cannot make is "essential."
Perhaps they feel that cyanide is essential, since the body
cannot make it either. If they decide to act upon this, at
least the rest of us will no longer have to read their absurd
posts and witness their dodging of basic scientific
methodology all the time.
I now see why they refuse to respond to my request to state a
basic scientific hypothesis for "EFAs" - it is impossible to
do so without making a fool of oneself. The best argument one
can make is to say that a pregnant woman or growing child
probably needs a boost in biochemical activity at some point,
but this has not been investigated in enough depth to know if
this is the case or not. Moreover, omega 3 and/or 6 PUFAs
would have to be compared to the omega 9 PUFA made by humans,
the Mead acid, and this has never been done, as far as I have
been able to determine (after years of researching it).
Moreover, it could be a matter of high quality protein intake
or some other obvious factor, and all would have to be
controlled for in experiments. Instead, researchers usually
have compared a totally fat free diet, which no animal used in
the experiments eats in its natural environment, against a fat
source that contains all classes of fatty acids.
How this is supposed to demonostrate omega 3 and 6 PUFA
"essentiality?" is the obvious question few ever ask. It may
demonstrate that some dietary fatty acids of some kind are
"essential," but biochemist Ray Peat has noted that in the
older experiments that waited for the animals to die, the ones
on the fat diets died younger, and so the researchers who
believed in "EFAs" (apparently, with a religious quality) made
note of fatty liver or reduced feeding efficiency. The latter
refers to fattening up livestock animals with as little food
as possible, and is considered a "benefit." When this happens
to people, however, it is referred to as an "obesity
epidemic," and is not thought of as a "benefit," but as a
"disease." Fatty liver has been demonstrated to be caused by
excessive glucose consumption, and in many of the experiments,
the fat free animals were given more glucose to substitute for
the fat the other animals were eating. They talk of "dry skin"
and such as well, but as I've learned, when you are
"deficient" in the "EFAs" you may need to drink more, and then
this is not a problem, so we'd need to know if the animals
were given enough water.
It is true that metabolites of a long chain PUFA are needed to
avoid problems with cutaneous barrier function, and on a
totally fat free diet, dysfunction can occur here. Because it
is assumed that the Mead acid is a sign of "deficiency"
(without evidence from properly controlled experiments to
support this notion), researchers have never done an
experiment comparing adult, non-pregnant animals fed plenty of
fresh coconut oil and a similar group fed plenty of canola and
fish oil. This is the experiment I have proposed many times
here (and nobody is interested in taking me up on the offer I
put forth). The experiment that would determine whether the
Mead acid can be as effective as the "essential" omega 3s and
6s, yet without any of the "negatives," such as cancer,
immunosupression, neurodegeneration, atheroscelrosis, etc. In
any case, if one needs to drink a bit more while being
"essential fatty acid deficient" it is a small price to pay
for the benefits, and not something to worry about, unless you
have only polluted water to drink, in which case you have
bigger problems that the "EFA" debate.
The evidence that omega 3 and 6 PUFAs are very dangerous is
overwhelming, so anyone who wants to posit that they are
"essential" had better have some very strong evidence that
this is the case. In actuality, the evidence is either
terribly flawed (as mentioned above and as examined in other
posts) or is irrelevant. The most obvious example of
irrelevant evidence is the kind that is cited very frequently,
that is, evidence demonstrating the "anti-inflammatory"
effects of omega 3 PUFAs, especially the long chain ones. The
reason why "inflammation" is there in the first place is that
too many omega 6s are being consumed. Without omega 6 PUFAs
(except in unavoidable trace amounts) there is very little
inflammation, so there is no reaon to counteract something
that doesn't exist with incredibly biochemically unstable
substances.
So let's look at the most common claim about "EFAs," since
there is nothing remotely resembling a scientific hypothesis
for these dangerous molecules:
A common and comprehensive book on nutrition today is
"Perspectives in Nutrition" by Gordon Wardlaw (see pages 120
and 135 of the fourth edition). The author claims that one
needs at least "1 tablespoon of polyunsaturated plant oil a
day," which he claims is acceptable even on a very low fat
diet. If not, "one's skin will become flaky and itchy, and
diarrhea and other symptoms such as infections often are seen.
Growth and wound healing may be retarded..." However, I have
witnessed the exact opposite in myself (with the exception of
wound healing, which is slower but involves much less
"inflammation"), and the few others I know eating similar
diets as mine report similar results. In addition, one can
examine the typical diet of the Amish in the USA, which in
many if not most cases appears to contain less than a
tablespoon of one of the kinds of oils Wardlaw mentions as
meeting the "EFA requirements." He also says that such
symptoms appear in "2 to 3 weeks" on those fed little or not
fat (due to some illness that requires that they be fed
intravenously. The idea is that metabolites generated by cells
when they are stressed require a long chain PUFA as substrate.
This is true, but the body makes its own PUFA, the Mead acid,
which is then made into metabolites that do the same thing,
only with very little "inflammation." This is because Mead
acid is much more chemically stable than long chain omega 3s
and 6s. If an experiment that meets the requirements of the
scientific method were done to determine if omega 3s and 6s
are truly essential, they would need to be compare against the
Mead acid, not against a fat free diet.
This "shell game" has been going on since 1930, and is so
obvious it is worse than the proverbial bad joke that an
obnoxious relative enjoys telling over and over again. I have
proposed experiments that would control for this, but nobody
here is interested in taking my up on any of my offers. One
individual said that he didn't want to subject the rats to
such a horrible diet - the kind that I have been eating for
about 4 years now, with no "deficiency symptoms" and many
benefits. Isn't he a great guy? Perhaps we should call him the
"rat lover," sparing the cute little rats the terrible fate of
a long life lived in great health. Presumably, this rat lover
man thinks it's better if the rats were instead used in the
more common kinds of experiments, where they would be given
cancer and then their heads would be chopped off in a few
weeks, at most.
The evidence against AA metabolites is now clear, and you can
see for yourself at www.pubmed.com - just search for LTB4
cancer, for example. Here are some of the latest:
Oncogene. 2004 Dec 9;23(57):9259-68.
Role of the BLT2, a leukotriene B4 receptor, in Ras
transformation.
Yoo MH, Song H, Woo CH, Kim H, Kim JH.
School of Life Sciences and Biotechnology, Korea University,
5-1 Anam-dong, Sungbuk-gu, Seoul 136-701, Korea.
Oncogenic Ras is known to drive both the Rac and
Raf-MAP-kinase pathways, which act in concert to cause cell
transformation. Unlike the Raf-MAP-kinase cascade, however,
the downstream elements of Rac pathway are not fully
understood. Previously, we showed that cytosolic phospholipase
A2 (cPLA2) and subsequent metabolism of arachidonic acid act
downstream of Rac to mediate the transformation signaling
induced by Ha-Ras(V12). In the present study, we observed that
leukotriene B4 (LTB4) and its synthetic enzymes as well as
BLT2, the low-affinity LTB4 receptor, are all elevated in
Ha-Ras(V12)-transformed cells. In addition, the malignant
phenotypes of Ras-transformed cells were markedly inhibited by
BLT2 blockade, as was their tumorigenicity in
vivo. Finally, in situ hybridization analysis revealed that
expression of BLT2 is significantly upregulated in a
variety of human cancers. Taken together, our results
suggest that an LTB4-BLT2-linked cascade plays a crucial
mediatory role in the cell transformation induced by
oncogenic Ha-Ras(V12), possibly acting downstream of
Rac-cPLA2.
OR:
Clin Cancer Res. 2004 Oct 1;10(19):6703-9.
Overexpression of 5-lipoxygenase in rat and human esophageal
adenocarcinoma and inhibitory effects of zileuton and
celecoxib on carcinogenesis.
Chen X, Wang S, Wu N, Sood S, Wang P, Jin Z, Beer DG, Giordano
TJ, Lin Y, Shih WC, Lubet RA, Yang CS.
Susan Lehman Cullman Laboratory for Cancer Research,
Department of Chemical Biology, Ernest Mario School of
Pharmacy, Rutgers, The State University of New Jersey,
Piscataway, New Jersey 08854, USA. xiaochen@rci.rutgers.edu
PURPOSE: Aberrant arachidonic acid (AA) metabolism, especially
through the cyclooxygenase (Cox) and 5-lipoxygenase (5-Lox)
pathways, has been suggested to play an important role in the
development of esophageal adenocarcinoma (EAC). The purpose of
this study was to investigate the expression of 5-Lox in EAC
of a rat model and in human samples as well as the
chemopreventive effects of zileuton (a specific 5-Lox
inhibitor) and celecoxib (a specific Cox2 inhibitor) in the
rat EAC model. EXPERIMENTAL DESIGN: 5-Lox expression in EAC of
a rat esophagogastroduodenal anastomosis model and of humans
was examined with immunohistochemistry. A chemoprevention
study was designed to test whether zileuton and celecoxib
could suppress aberrant AA metabolism and esophageal
adenocarcinogenesis. RESULTS: With immunohistochemistry, we
found that 5-Lox was overexpressed during esophageal
adenocarcinogenesis in our rat model and in humans. In the
chemoprevention study, EAC incidence was reduced in a
dose-dependent manner from 68.8% (11 of 16) to 44.4% (8 of 18;
P > 0.05) and 31.3% (5 of 16; P < 0.05) by 500 and 1,000 ppm
zileuton, respectively, and to
33.3% (7 of 21; P < 0.05) and 20% (3 of 15; P < 0.05) by 500
and 1,000 ppm celecoxib, respectively. With isobolographic
analysis, zileuton and celecoxib, both at a dose of 500
ppm, had an additive effect by reducing the tumor incidence
to 16.7% (3 of 18, P < 0.01). Leukotriene B4 and
prostaglandin E2 levels in the esophageal tissues were also
significantly reduced by zileuton and celecoxib.
CONCLUSIONS: This study clearly demonstrated that 5-Lox and
Cox2 play important roles in the development of EAC. Both
zileuton and celecoxib had inhibitory effects on esophageal
adenocarcinogenesis through inhibition on their respective
enzymes of AA metabolism.
OR:
Blood. 2005 Feb 1;105(3):1274-9. Epub 2004 Sep 28. Related
Articles, Links
Leukotriene B4 plays a pivotal role in CD40-dependent
activation of chronic B lymphocytic leukemia cells.
Runarsson G, Liu A, Mahshid Y, Feltenmark S, Pettersson A,
Klein E, Bjorkholm M, Claesson HE.
Department of Medicine, Microbiology and Tumor Biology Center,
Karolinska Institutet, 17177 Stockholm, Sweden.
Biosynthesis of leukotrienes (LTs) occurs in human myeloid
cells and B lymphocytes. However, the function of leukotrienes
in B lymphocytes is unclear. Here, we report that B-cell
chronic lymphocytic leukemia (B-CLL) cells produce leukotriene
B(4), and that specific leukotriene biosynthesis inhibitors
counteracted CD40-dependent activation of B-CLL cells. Studies
on the expression of the high-affinity receptor for LTB(4)
(BLT1) by flow cytometry analysis showed that the receptor was
expressed, to a varying degree, in all investigated B-CLL
clones. At a concentration of 100 nM, the drugs BWA4C (a
specific 5-lipoxygenase inhibitor) and MK-886 (a specific
5-lipoxygenase activating protein inhibitor) markedly
inhibited CD40-induced DNA synthesis (45% and 38%,
respectively) and CD40-induced expression of CD23, CD54, and
CD150. Addition of exogenous LTB(4) (150 nM) almost completely
reversed the effect of the inhibitors on DNA synthesis and
antigen expression. Taken together, the results of the present
study suggest that leukotriene biosynthesis inhibitors may
have a therapeutic role in B-CLL.
There are about 250 of these just on the LTB4 connection to
cancer at pubmed.com. Mead acid cannot be made into LTB4 and
there is no COX 2 activity if your body is ridded of AA. It
takes about 2 years to do this on the right diet. And don't
think that the evidence against "EFAs" is new, for example:
Ip, C., et al., "Requirement of essential fatty acids for
mammary tumors," Cancer Res. 45 (5) 1997-2001, 1985.
Interestingly, some authors blame the toxic effects of cod
liver oil supplmentation, which was popular several decades
ago, on the vitamin A and D it contains, yet there are plenty
of people who have been consuming megadoses of vitamin
supplements since the 1960s, and yet the toxicity of all the
supplements combined (with the few rare exceptions that are
totally unrelated to A and D, such as the tryptophan deaths)
appears to be nearly nonexistent. Rather, taking large doses
of fish oil, a substance that will generate huge amounts of
free radicals, is undeniably highly toxic, and I've proposed
on point experiments, comparing rats/mice large amounts of
fish oil or fresh coconut oil, but of course, nobody is
interested, even though I will pay for all expenses if the
fish oil group lives longer.
Almost all "diseases" in the USA today are caused or
exacerbated by omega 3 and 6 PUFAs. Bacteria, fungi, yeast,
viruses, etc. become dangerous with excess biochemical
activity is present, particularly when a great deal of free
radical generation occurs. Packing your body with saturated
fatty acids and avoiding unsaturated ones does not allow
pathogens to become dangerous. Basically, they need the
activity to "feed on." The activity damages or destroys vital
biomolecules, switches biochemical pathways on that should be
off (and vice versa), and can then lead to tissue or organ
damage or severe dysfunction. If you search this newsgroup for
montygram, you can read the evidence demonstrating how just
about every "disease" is related to this situation. "Slow
wound healing" means that pathogens are not able to take
advantage of the situation; they can't infiltrate tissues
easily, which often occurs when cellular function is being
suppressed by a prolonged inflammatory process. After having
frequent infections of the fingers for well over a decade (due
mostly to paper cuts), I have not had one for a few years now.
"Slow" or "retarded" growth means that checkpoints that stop
cancer will not be overrun. Exactly what a pregnant woman or
growing child needs has yet to be determined, but I am
addressing the obvious case of the non-pregnant adult human;
here, omega 3s and 6s are "essentially" very dangerous,
nothing more.
My critics on this newsgroup make arguments that contradict
each other all the time, which is why real scientists
insist on putting forth a hypothesis. They won't formulate
a hypothesiss, but instead make illogical statements, suich
as that anything the body can't make is essential. Some
claim that hardly any omega 3s and 6s are needed each day,
which contradicts Wardlaw and the establishment. Others
cite "researchers" who claim that there is "rapid DHA
turnover" in the normal brain, and that horrible things
will happen if this does not occur. In almost everyone I
know, "rapid DHA turnover in the brain" is physically
impossible, because the people rarely eat anything with
more than trace amounts of omega 3s (also, alpha-linolenic
acid is not metabolized into DHA efficiently and DHA is
often changed into molecules that cannot be reconverted
back before it gets out of your stomach).
Some critics say that omega 3s are "essential" because they
balance omega 6s, but if omega 6s are not essential, then the
"balancing" is not necessary. The more PUFAs you consume in
the diet, the more risks you expose yourself to, as Wardlaw
and others admit: "An upper limit of 10% of energy intake as
polyunsaturated fatty acid is often recommended, in part
because the breakdown (oxidation) of those present in
lipoproteins is linked to increased cholesterol deposition in
the arteries... This breakdown may also increase the risk of
cancer. Depression of immune function is also suspected to be
caused by an excessive intake of polyunsaturated fatty acids."
This is exactly what I have been saying, except that I point
out that there is no reason to take these risks if one can
allow one's body to make its own PUFA as it sees fit. Thus, my
hypothesis is simple and straightforward: let the body make
it's own long-chain PUFA and the animals will live longer and
be in better health. The first experiment should determine
life expectancy only, and that is what I propose, but nobody
will take me up on my offer.
In Wardlaw's book, he writes as if proper experiments were
done that established an absolute requirement for omega 3s
and 6s in adult, non-pregnant humans. He gives a minium daily
amount, articulates the deficiency syndrome and amount of
time before the symptoms of this deficiency take to appear,
and details the risks of too much omega 3 and/or 6 PUFA
consumption. There is plenty of very strong evidence
demonstrating how extreme the risks are, and thus I agree
with him on this point. However, in order for a scientific
hypothesis to be accepted as a bona fide theory, it must not
have exceptions, unless there is a scientific theory which
supersedes it. Newton's laws function in the part of the
universe which we as humans experience, but under conditions
that we would consider extreme (and be unable to exist
within), Einstein's relativity prevails. Because of my
experience with fatty acids (as well as those of several
other people), it is obvious that the "essential fatty acid"
claim for omega 3s and 6s is incorrect in the way people like
Wardlaw state it. Since the problems considered symptoms of
"essential fatty acid deficiency" disappeared when I became
"deficient" the hypothesis must be wrong. There can be no
unexplained exceptions in science. If there are, at the very
least, one must put the hypothesis aside until the
ccontradictory phenomena in question can be examined and
explained. One must not tell people to consume potentially
deadly substances until it can be sort out sufficiently. Why
this situation actually does exist involves the fact that
once a claim gets established in the biological textbooks,
those who might want to question it are often criticized and
even if they are correct, are not rewarded - some even lose
funding or are forced into retirement. As an example, I have
posted the experience of the British scientist Harold Hillman
here on more than one occasion. One can also read about a
similar example at www.gilbertling.org. It is not new, nor
unusual, but because of this situation, few biological
scientists are interested in "rocking the boat."
Interestingly, Wardlaw does not explain how humans were able
to exist for tens of thousands of years, before highly
polyunsaturated oils existed.
As I have pointed out many times, the professional literature
(going back more than 15 years), makes clear that fish oil
supplements are basically playing with fire. As Wardlaw points
out: "Fish oil supplementation is generally not advised
becauses excess omega-3 fatty acids can lead to hemorrhagic
stroke and other problems." If one eats large amounts of oily
fish, one will be at great risk for dying at young ages, as
the National Research Council noted in the late 1980s (based
upon an examination of the evidence available at that time),
and it appears that fish oil is worse than a high omega 6 PUFA
diet (in the sense of life expectancy). There is no denying
that if your body is packed with AA, then fish oil will
counteract the metabolization of AA into molecules like LTB4
to some degree, but this just means swapping one terrible
"disease" for another. There is no way a body cannot be
adversely affected by the kinds of biochemical activity,
especially the generation of free radicals, that will occur if
you eat large amounts of fish oil on top of a high omega 6
diet. It is true that if you eat massive amounts of
antioxidants you can counteract this, but nobody knows what
you should take and at what doses. You will be taking a huge
risk when all you need to do is to avoid the omega 3 and 6
PUFAs. If you are concerned about "deficiency," according to
the literature, you will experience dry skin, itchiness, and
diarrhea within 3 weeks. I have not experience any of this in
about 4 years. I had dandruff, but that is gone now. I had
very bad rosacea, but that is gone now. I've had chalazions,
but not since avoiding major sources of unsaturated fatty
acids. I had a keloid for over 20 years, but that has shrunk
considerably over the last few years. Do not allow the myth of
the "essential fatty acids" prevent you from doing one of, if
not the healthiest things you can do to prevent "chronic
disease." Follow the diet I have recommened in my previous
posts for a month and see what happens. Just remember to drink
a bit more water than usual.
If you find all of this too technical and difficult, I am here
for you, free of charge, and with no agenda. Just make a new
post with "Montygram" in it and I will attempt to determine
what you need to
iu. Describe your condition, your medical and family
history, your diet and other aspects of your lifestyle
(drink, smoke, drugs/medications, exercise, sleep,
psychological factors, etc.) in as much detail as
possible. Do not worry about your doctor telling you
that you have "high cholesterol." It is a "marker," and
doesn't mean anything by itself. The only mechanism by
which damage leading to "chronic disease" can go
undetected was put forth by Spiteller a couple of years
ago, and you can avoid this by avoiding any major source
of unsaturated fatty acids (I've cited the abstract here
several times). I'm not going to sit by while the
various kinds of "snake oil salesmen" of today try to
get rich off your suffering. And spread the word to your
friends and relatives: there is no reason to take drugs
or loads of "supplements" in almost all cases. Instead,
you just avoid certain foods, while choosing from a
large number of tasty kinds that are truly beneficial
(butter, dark chocolate, coconut, fruit, cheese, tea,
coffee, ice cream, potatoes, eggs, etc. - even bread is
okay in reasonable amounts - just make sure it is was
not made with eggs, dairy, or any oil, for example, a
French baguette should be okay). If you are overweight,
you will lose weight eating this way, but it may take a
while for your appetite to normalize. Obviously, if you
eat huge amounts of these foods, you will not lose
weight, but it will counteract to some degree the higher
"feeding efficiency" that dietary PUFAs cause.
Technical note: this is but one example of "experts" accepting
what might be best described as a rabble's chorus of
contradictory claims that appear to be connected in some basic
way. Another example is of the Perth Group of scientists'
examination of the evidence that a retrovirus called HIV
exists. When one of this group was asked how scientists could
accept the existence of a virus that causes supposedly deadly
disease and may soon reach "epidemic proportions" even though
the procedure for isolating a virus that HIV is supposed to be
was devised and considered the standard before 1980, the
response was:
"The definition of a virus and the method that follows for
proving the existence of a virus... was endorsed by the
Pasteur Institute in 1973. Nobody can deny that here is a
method which constitutes absolute proof for the existence of a
retrovirus. And what nobody can also deny is that HIV has
never been accorded reality according to this method. In other
words, in spite of AIDS being regarded as one of the gravest
conditions ever to afflict the human race, no one has deemed
it necessary to use a proven method to establish the existence
of the putative cause of this dread disease. Instead
everybody's opted for a set of non-specific criteria and
appear to imagine that if you put all these together they must
somehow metamorphose into the right answer... What if the true
cause is something unexpected? Or something of which you have
no knowledge or cannot even possibly imagine? In that case the
more clues you have to what you are expecting, or what you
want it to be, the more likely you will be misled. It all
boils down to whether you would rather deal in probabilities
rather than facts. That's what I mean about being subjective.
It's like a physician seeing a patient with fever, diarrhoea,
vomiting, weakness and shock and then declaring the cause is
cholera. Sure it might be cholera but what about the dozens of
other germs that cause a similar pattern? What if your life
depended on it?"
Source: http://groups.msn.com/ThePerthGroup-DiscussionForum/p-
apers.msnw?action=get_message&mview=0&ID_Message=13&LastModif-
ied=4675487929809925301
Compared to this incredible lapse, the "essential fatty acid"
claim seems like "small potatoes," though you can read about
the Mead acid in the Enclycopedia Britannica Book of the Year
(1948). In other words, after the 1930 EFA claim was made, it
was later discovered that humans can make their own PUFA, the
much more stable Mead acid. Yet no appropriate follow-up study
was done. Experiments that were done did not control even the
basic variables, which makes one question either the integrity
of the scientists, or their competency. This is tied to the
"HIV/AIDS" claim, and to the other "chronic diseases" because
the biochemical instability that a body packed with highly
unstable PUFAs must endures appears to predispose people to
"AIDS" and other "diseases." "AIDS" existed before the early
1980s, but was rare (see Root-Berntein's book on "AIDS" for
examples). It was only when the highly unsaturated oils became
common that "AIDS" was viewed as an "epidemic." It is highly
unlikely, given the evidence that now exists, that this is a
coincidence. And the other "epidemics" (such as obesity,
autism, diabetes) and the predictions of future "epidemics"
(I've heard scientists say that oral cancers and Alzheimer's
disease could very well reach "epidemic proportions" within
the next decade or two) have occurred along with the huge rise
in the consumption of these oils.
argue the position that they were opposed to. The debate was
informal, and questions were asked and points made after a
basic presentation was done by the two "sides." This was a
good way to see all apects of an issue, and often led to a
more sophisticated understanding of the
it. In science, this is especially useful, at least for
issues that have been the focus of much research.
I have tried to construct an "essential fatty acid" (EFA)
hypothesis, since those who enjoy attacking the basic,
scientific points I make refuse to do so. At least two posters
have actually said that omega 3 and 6 polyunsaturated fatty
acids (PUFAs) are "essential" because the body cannot make
them, as if any substance the body cannot make is "essential."
Perhaps they feel that cyanide is essential, since the body
cannot make it either. If they decide to act upon this, at
least the rest of us will no longer have to read their absurd
posts and witness their dodging of basic scientific
methodology all the time.
I now see why they refuse to respond to my request to state a
basic scientific hypothesis for "EFAs" - it is impossible to
do so without making a fool of oneself. The best argument one
can make is to say that a pregnant woman or growing child
probably needs a boost in biochemical activity at some point,
but this has not been investigated in enough depth to know if
this is the case or not. Moreover, omega 3 and/or 6 PUFAs
would have to be compared to the omega 9 PUFA made by humans,
the Mead acid, and this has never been done, as far as I have
been able to determine (after years of researching it).
Moreover, it could be a matter of high quality protein intake
or some other obvious factor, and all would have to be
controlled for in experiments. Instead, researchers usually
have compared a totally fat free diet, which no animal used in
the experiments eats in its natural environment, against a fat
source that contains all classes of fatty acids.
How this is supposed to demonostrate omega 3 and 6 PUFA
"essentiality?" is the obvious question few ever ask. It may
demonstrate that some dietary fatty acids of some kind are
"essential," but biochemist Ray Peat has noted that in the
older experiments that waited for the animals to die, the ones
on the fat diets died younger, and so the researchers who
believed in "EFAs" (apparently, with a religious quality) made
note of fatty liver or reduced feeding efficiency. The latter
refers to fattening up livestock animals with as little food
as possible, and is considered a "benefit." When this happens
to people, however, it is referred to as an "obesity
epidemic," and is not thought of as a "benefit," but as a
"disease." Fatty liver has been demonstrated to be caused by
excessive glucose consumption, and in many of the experiments,
the fat free animals were given more glucose to substitute for
the fat the other animals were eating. They talk of "dry skin"
and such as well, but as I've learned, when you are
"deficient" in the "EFAs" you may need to drink more, and then
this is not a problem, so we'd need to know if the animals
were given enough water.
It is true that metabolites of a long chain PUFA are needed to
avoid problems with cutaneous barrier function, and on a
totally fat free diet, dysfunction can occur here. Because it
is assumed that the Mead acid is a sign of "deficiency"
(without evidence from properly controlled experiments to
support this notion), researchers have never done an
experiment comparing adult, non-pregnant animals fed plenty of
fresh coconut oil and a similar group fed plenty of canola and
fish oil. This is the experiment I have proposed many times
here (and nobody is interested in taking me up on the offer I
put forth). The experiment that would determine whether the
Mead acid can be as effective as the "essential" omega 3s and
6s, yet without any of the "negatives," such as cancer,
immunosupression, neurodegeneration, atheroscelrosis, etc. In
any case, if one needs to drink a bit more while being
"essential fatty acid deficient" it is a small price to pay
for the benefits, and not something to worry about, unless you
have only polluted water to drink, in which case you have
bigger problems that the "EFA" debate.
The evidence that omega 3 and 6 PUFAs are very dangerous is
overwhelming, so anyone who wants to posit that they are
"essential" had better have some very strong evidence that
this is the case. In actuality, the evidence is either
terribly flawed (as mentioned above and as examined in other
posts) or is irrelevant. The most obvious example of
irrelevant evidence is the kind that is cited very frequently,
that is, evidence demonstrating the "anti-inflammatory"
effects of omega 3 PUFAs, especially the long chain ones. The
reason why "inflammation" is there in the first place is that
too many omega 6s are being consumed. Without omega 6 PUFAs
(except in unavoidable trace amounts) there is very little
inflammation, so there is no reaon to counteract something
that doesn't exist with incredibly biochemically unstable
substances.
So let's look at the most common claim about "EFAs," since
there is nothing remotely resembling a scientific hypothesis
for these dangerous molecules:
A common and comprehensive book on nutrition today is
"Perspectives in Nutrition" by Gordon Wardlaw (see pages 120
and 135 of the fourth edition). The author claims that one
needs at least "1 tablespoon of polyunsaturated plant oil a
day," which he claims is acceptable even on a very low fat
diet. If not, "one's skin will become flaky and itchy, and
diarrhea and other symptoms such as infections often are seen.
Growth and wound healing may be retarded..." However, I have
witnessed the exact opposite in myself (with the exception of
wound healing, which is slower but involves much less
"inflammation"), and the few others I know eating similar
diets as mine report similar results. In addition, one can
examine the typical diet of the Amish in the USA, which in
many if not most cases appears to contain less than a
tablespoon of one of the kinds of oils Wardlaw mentions as
meeting the "EFA requirements." He also says that such
symptoms appear in "2 to 3 weeks" on those fed little or not
fat (due to some illness that requires that they be fed
intravenously. The idea is that metabolites generated by cells
when they are stressed require a long chain PUFA as substrate.
This is true, but the body makes its own PUFA, the Mead acid,
which is then made into metabolites that do the same thing,
only with very little "inflammation." This is because Mead
acid is much more chemically stable than long chain omega 3s
and 6s. If an experiment that meets the requirements of the
scientific method were done to determine if omega 3s and 6s
are truly essential, they would need to be compare against the
Mead acid, not against a fat free diet.
This "shell game" has been going on since 1930, and is so
obvious it is worse than the proverbial bad joke that an
obnoxious relative enjoys telling over and over again. I have
proposed experiments that would control for this, but nobody
here is interested in taking my up on any of my offers. One
individual said that he didn't want to subject the rats to
such a horrible diet - the kind that I have been eating for
about 4 years now, with no "deficiency symptoms" and many
benefits. Isn't he a great guy? Perhaps we should call him the
"rat lover," sparing the cute little rats the terrible fate of
a long life lived in great health. Presumably, this rat lover
man thinks it's better if the rats were instead used in the
more common kinds of experiments, where they would be given
cancer and then their heads would be chopped off in a few
weeks, at most.
The evidence against AA metabolites is now clear, and you can
see for yourself at www.pubmed.com - just search for LTB4
cancer, for example. Here are some of the latest:
Oncogene. 2004 Dec 9;23(57):9259-68.
Role of the BLT2, a leukotriene B4 receptor, in Ras
transformation.
Yoo MH, Song H, Woo CH, Kim H, Kim JH.
School of Life Sciences and Biotechnology, Korea University,
5-1 Anam-dong, Sungbuk-gu, Seoul 136-701, Korea.
Oncogenic Ras is known to drive both the Rac and
Raf-MAP-kinase pathways, which act in concert to cause cell
transformation. Unlike the Raf-MAP-kinase cascade, however,
the downstream elements of Rac pathway are not fully
understood. Previously, we showed that cytosolic phospholipase
A2 (cPLA2) and subsequent metabolism of arachidonic acid act
downstream of Rac to mediate the transformation signaling
induced by Ha-Ras(V12). In the present study, we observed that
leukotriene B4 (LTB4) and its synthetic enzymes as well as
BLT2, the low-affinity LTB4 receptor, are all elevated in
Ha-Ras(V12)-transformed cells. In addition, the malignant
phenotypes of Ras-transformed cells were markedly inhibited by
BLT2 blockade, as was their tumorigenicity in
vivo. Finally, in situ hybridization analysis revealed that
expression of BLT2 is significantly upregulated in a
variety of human cancers. Taken together, our results
suggest that an LTB4-BLT2-linked cascade plays a crucial
mediatory role in the cell transformation induced by
oncogenic Ha-Ras(V12), possibly acting downstream of
Rac-cPLA2.
OR:
Clin Cancer Res. 2004 Oct 1;10(19):6703-9.
Overexpression of 5-lipoxygenase in rat and human esophageal
adenocarcinoma and inhibitory effects of zileuton and
celecoxib on carcinogenesis.
Chen X, Wang S, Wu N, Sood S, Wang P, Jin Z, Beer DG, Giordano
TJ, Lin Y, Shih WC, Lubet RA, Yang CS.
Susan Lehman Cullman Laboratory for Cancer Research,
Department of Chemical Biology, Ernest Mario School of
Pharmacy, Rutgers, The State University of New Jersey,
Piscataway, New Jersey 08854, USA. xiaochen@rci.rutgers.edu
PURPOSE: Aberrant arachidonic acid (AA) metabolism, especially
through the cyclooxygenase (Cox) and 5-lipoxygenase (5-Lox)
pathways, has been suggested to play an important role in the
development of esophageal adenocarcinoma (EAC). The purpose of
this study was to investigate the expression of 5-Lox in EAC
of a rat model and in human samples as well as the
chemopreventive effects of zileuton (a specific 5-Lox
inhibitor) and celecoxib (a specific Cox2 inhibitor) in the
rat EAC model. EXPERIMENTAL DESIGN: 5-Lox expression in EAC of
a rat esophagogastroduodenal anastomosis model and of humans
was examined with immunohistochemistry. A chemoprevention
study was designed to test whether zileuton and celecoxib
could suppress aberrant AA metabolism and esophageal
adenocarcinogenesis. RESULTS: With immunohistochemistry, we
found that 5-Lox was overexpressed during esophageal
adenocarcinogenesis in our rat model and in humans. In the
chemoprevention study, EAC incidence was reduced in a
dose-dependent manner from 68.8% (11 of 16) to 44.4% (8 of 18;
P > 0.05) and 31.3% (5 of 16; P < 0.05) by 500 and 1,000 ppm
zileuton, respectively, and to
33.3% (7 of 21; P < 0.05) and 20% (3 of 15; P < 0.05) by 500
and 1,000 ppm celecoxib, respectively. With isobolographic
analysis, zileuton and celecoxib, both at a dose of 500
ppm, had an additive effect by reducing the tumor incidence
to 16.7% (3 of 18, P < 0.01). Leukotriene B4 and
prostaglandin E2 levels in the esophageal tissues were also
significantly reduced by zileuton and celecoxib.
CONCLUSIONS: This study clearly demonstrated that 5-Lox and
Cox2 play important roles in the development of EAC. Both
zileuton and celecoxib had inhibitory effects on esophageal
adenocarcinogenesis through inhibition on their respective
enzymes of AA metabolism.
OR:
Blood. 2005 Feb 1;105(3):1274-9. Epub 2004 Sep 28. Related
Articles, Links
Leukotriene B4 plays a pivotal role in CD40-dependent
activation of chronic B lymphocytic leukemia cells.
Runarsson G, Liu A, Mahshid Y, Feltenmark S, Pettersson A,
Klein E, Bjorkholm M, Claesson HE.
Department of Medicine, Microbiology and Tumor Biology Center,
Karolinska Institutet, 17177 Stockholm, Sweden.
Biosynthesis of leukotrienes (LTs) occurs in human myeloid
cells and B lymphocytes. However, the function of leukotrienes
in B lymphocytes is unclear. Here, we report that B-cell
chronic lymphocytic leukemia (B-CLL) cells produce leukotriene
B(4), and that specific leukotriene biosynthesis inhibitors
counteracted CD40-dependent activation of B-CLL cells. Studies
on the expression of the high-affinity receptor for LTB(4)
(BLT1) by flow cytometry analysis showed that the receptor was
expressed, to a varying degree, in all investigated B-CLL
clones. At a concentration of 100 nM, the drugs BWA4C (a
specific 5-lipoxygenase inhibitor) and MK-886 (a specific
5-lipoxygenase activating protein inhibitor) markedly
inhibited CD40-induced DNA synthesis (45% and 38%,
respectively) and CD40-induced expression of CD23, CD54, and
CD150. Addition of exogenous LTB(4) (150 nM) almost completely
reversed the effect of the inhibitors on DNA synthesis and
antigen expression. Taken together, the results of the present
study suggest that leukotriene biosynthesis inhibitors may
have a therapeutic role in B-CLL.
There are about 250 of these just on the LTB4 connection to
cancer at pubmed.com. Mead acid cannot be made into LTB4 and
there is no COX 2 activity if your body is ridded of AA. It
takes about 2 years to do this on the right diet. And don't
think that the evidence against "EFAs" is new, for example:
Ip, C., et al., "Requirement of essential fatty acids for
mammary tumors," Cancer Res. 45 (5) 1997-2001, 1985.
Interestingly, some authors blame the toxic effects of cod
liver oil supplmentation, which was popular several decades
ago, on the vitamin A and D it contains, yet there are plenty
of people who have been consuming megadoses of vitamin
supplements since the 1960s, and yet the toxicity of all the
supplements combined (with the few rare exceptions that are
totally unrelated to A and D, such as the tryptophan deaths)
appears to be nearly nonexistent. Rather, taking large doses
of fish oil, a substance that will generate huge amounts of
free radicals, is undeniably highly toxic, and I've proposed
on point experiments, comparing rats/mice large amounts of
fish oil or fresh coconut oil, but of course, nobody is
interested, even though I will pay for all expenses if the
fish oil group lives longer.
Almost all "diseases" in the USA today are caused or
exacerbated by omega 3 and 6 PUFAs. Bacteria, fungi, yeast,
viruses, etc. become dangerous with excess biochemical
activity is present, particularly when a great deal of free
radical generation occurs. Packing your body with saturated
fatty acids and avoiding unsaturated ones does not allow
pathogens to become dangerous. Basically, they need the
activity to "feed on." The activity damages or destroys vital
biomolecules, switches biochemical pathways on that should be
off (and vice versa), and can then lead to tissue or organ
damage or severe dysfunction. If you search this newsgroup for
montygram, you can read the evidence demonstrating how just
about every "disease" is related to this situation. "Slow
wound healing" means that pathogens are not able to take
advantage of the situation; they can't infiltrate tissues
easily, which often occurs when cellular function is being
suppressed by a prolonged inflammatory process. After having
frequent infections of the fingers for well over a decade (due
mostly to paper cuts), I have not had one for a few years now.
"Slow" or "retarded" growth means that checkpoints that stop
cancer will not be overrun. Exactly what a pregnant woman or
growing child needs has yet to be determined, but I am
addressing the obvious case of the non-pregnant adult human;
here, omega 3s and 6s are "essentially" very dangerous,
nothing more.
My critics on this newsgroup make arguments that contradict
each other all the time, which is why real scientists
insist on putting forth a hypothesis. They won't formulate
a hypothesiss, but instead make illogical statements, suich
as that anything the body can't make is essential. Some
claim that hardly any omega 3s and 6s are needed each day,
which contradicts Wardlaw and the establishment. Others
cite "researchers" who claim that there is "rapid DHA
turnover" in the normal brain, and that horrible things
will happen if this does not occur. In almost everyone I
know, "rapid DHA turnover in the brain" is physically
impossible, because the people rarely eat anything with
more than trace amounts of omega 3s (also, alpha-linolenic
acid is not metabolized into DHA efficiently and DHA is
often changed into molecules that cannot be reconverted
back before it gets out of your stomach).
Some critics say that omega 3s are "essential" because they
balance omega 6s, but if omega 6s are not essential, then the
"balancing" is not necessary. The more PUFAs you consume in
the diet, the more risks you expose yourself to, as Wardlaw
and others admit: "An upper limit of 10% of energy intake as
polyunsaturated fatty acid is often recommended, in part
because the breakdown (oxidation) of those present in
lipoproteins is linked to increased cholesterol deposition in
the arteries... This breakdown may also increase the risk of
cancer. Depression of immune function is also suspected to be
caused by an excessive intake of polyunsaturated fatty acids."
This is exactly what I have been saying, except that I point
out that there is no reason to take these risks if one can
allow one's body to make its own PUFA as it sees fit. Thus, my
hypothesis is simple and straightforward: let the body make
it's own long-chain PUFA and the animals will live longer and
be in better health. The first experiment should determine
life expectancy only, and that is what I propose, but nobody
will take me up on my offer.
In Wardlaw's book, he writes as if proper experiments were
done that established an absolute requirement for omega 3s
and 6s in adult, non-pregnant humans. He gives a minium daily
amount, articulates the deficiency syndrome and amount of
time before the symptoms of this deficiency take to appear,
and details the risks of too much omega 3 and/or 6 PUFA
consumption. There is plenty of very strong evidence
demonstrating how extreme the risks are, and thus I agree
with him on this point. However, in order for a scientific
hypothesis to be accepted as a bona fide theory, it must not
have exceptions, unless there is a scientific theory which
supersedes it. Newton's laws function in the part of the
universe which we as humans experience, but under conditions
that we would consider extreme (and be unable to exist
within), Einstein's relativity prevails. Because of my
experience with fatty acids (as well as those of several
other people), it is obvious that the "essential fatty acid"
claim for omega 3s and 6s is incorrect in the way people like
Wardlaw state it. Since the problems considered symptoms of
"essential fatty acid deficiency" disappeared when I became
"deficient" the hypothesis must be wrong. There can be no
unexplained exceptions in science. If there are, at the very
least, one must put the hypothesis aside until the
ccontradictory phenomena in question can be examined and
explained. One must not tell people to consume potentially
deadly substances until it can be sort out sufficiently. Why
this situation actually does exist involves the fact that
once a claim gets established in the biological textbooks,
those who might want to question it are often criticized and
even if they are correct, are not rewarded - some even lose
funding or are forced into retirement. As an example, I have
posted the experience of the British scientist Harold Hillman
here on more than one occasion. One can also read about a
similar example at www.gilbertling.org. It is not new, nor
unusual, but because of this situation, few biological
scientists are interested in "rocking the boat."
Interestingly, Wardlaw does not explain how humans were able
to exist for tens of thousands of years, before highly
polyunsaturated oils existed.
As I have pointed out many times, the professional literature
(going back more than 15 years), makes clear that fish oil
supplements are basically playing with fire. As Wardlaw points
out: "Fish oil supplementation is generally not advised
becauses excess omega-3 fatty acids can lead to hemorrhagic
stroke and other problems." If one eats large amounts of oily
fish, one will be at great risk for dying at young ages, as
the National Research Council noted in the late 1980s (based
upon an examination of the evidence available at that time),
and it appears that fish oil is worse than a high omega 6 PUFA
diet (in the sense of life expectancy). There is no denying
that if your body is packed with AA, then fish oil will
counteract the metabolization of AA into molecules like LTB4
to some degree, but this just means swapping one terrible
"disease" for another. There is no way a body cannot be
adversely affected by the kinds of biochemical activity,
especially the generation of free radicals, that will occur if
you eat large amounts of fish oil on top of a high omega 6
diet. It is true that if you eat massive amounts of
antioxidants you can counteract this, but nobody knows what
you should take and at what doses. You will be taking a huge
risk when all you need to do is to avoid the omega 3 and 6
PUFAs. If you are concerned about "deficiency," according to
the literature, you will experience dry skin, itchiness, and
diarrhea within 3 weeks. I have not experience any of this in
about 4 years. I had dandruff, but that is gone now. I had
very bad rosacea, but that is gone now. I've had chalazions,
but not since avoiding major sources of unsaturated fatty
acids. I had a keloid for over 20 years, but that has shrunk
considerably over the last few years. Do not allow the myth of
the "essential fatty acids" prevent you from doing one of, if
not the healthiest things you can do to prevent "chronic
disease." Follow the diet I have recommened in my previous
posts for a month and see what happens. Just remember to drink
a bit more water than usual.
If you find all of this too technical and difficult, I am here
for you, free of charge, and with no agenda. Just make a new
post with "Montygram" in it and I will attempt to determine
what you need to
iu. Describe your condition, your medical and family
history, your diet and other aspects of your lifestyle
(drink, smoke, drugs/medications, exercise, sleep,
psychological factors, etc.) in as much detail as
possible. Do not worry about your doctor telling you
that you have "high cholesterol." It is a "marker," and
doesn't mean anything by itself. The only mechanism by
which damage leading to "chronic disease" can go
undetected was put forth by Spiteller a couple of years
ago, and you can avoid this by avoiding any major source
of unsaturated fatty acids (I've cited the abstract here
several times). I'm not going to sit by while the
various kinds of "snake oil salesmen" of today try to
get rich off your suffering. And spread the word to your
friends and relatives: there is no reason to take drugs
or loads of "supplements" in almost all cases. Instead,
you just avoid certain foods, while choosing from a
large number of tasty kinds that are truly beneficial
(butter, dark chocolate, coconut, fruit, cheese, tea,
coffee, ice cream, potatoes, eggs, etc. - even bread is
okay in reasonable amounts - just make sure it is was
not made with eggs, dairy, or any oil, for example, a
French baguette should be okay). If you are overweight,
you will lose weight eating this way, but it may take a
while for your appetite to normalize. Obviously, if you
eat huge amounts of these foods, you will not lose
weight, but it will counteract to some degree the higher
"feeding efficiency" that dietary PUFAs cause.
Technical note: this is but one example of "experts" accepting
what might be best described as a rabble's chorus of
contradictory claims that appear to be connected in some basic
way. Another example is of the Perth Group of scientists'
examination of the evidence that a retrovirus called HIV
exists. When one of this group was asked how scientists could
accept the existence of a virus that causes supposedly deadly
disease and may soon reach "epidemic proportions" even though
the procedure for isolating a virus that HIV is supposed to be
was devised and considered the standard before 1980, the
response was:
"The definition of a virus and the method that follows for
proving the existence of a virus... was endorsed by the
Pasteur Institute in 1973. Nobody can deny that here is a
method which constitutes absolute proof for the existence of a
retrovirus. And what nobody can also deny is that HIV has
never been accorded reality according to this method. In other
words, in spite of AIDS being regarded as one of the gravest
conditions ever to afflict the human race, no one has deemed
it necessary to use a proven method to establish the existence
of the putative cause of this dread disease. Instead
everybody's opted for a set of non-specific criteria and
appear to imagine that if you put all these together they must
somehow metamorphose into the right answer... What if the true
cause is something unexpected? Or something of which you have
no knowledge or cannot even possibly imagine? In that case the
more clues you have to what you are expecting, or what you
want it to be, the more likely you will be misled. It all
boils down to whether you would rather deal in probabilities
rather than facts. That's what I mean about being subjective.
It's like a physician seeing a patient with fever, diarrhoea,
vomiting, weakness and shock and then declaring the cause is
cholera. Sure it might be cholera but what about the dozens of
other germs that cause a similar pattern? What if your life
depended on it?"
Source: http://groups.msn.com/ThePerthGroup-DiscussionForum/p-
apers.msnw?action=get_message&mview=0&ID_Message=13&LastModif-
ied=4675487929809925301
Compared to this incredible lapse, the "essential fatty acid"
claim seems like "small potatoes," though you can read about
the Mead acid in the Enclycopedia Britannica Book of the Year
(1948). In other words, after the 1930 EFA claim was made, it
was later discovered that humans can make their own PUFA, the
much more stable Mead acid. Yet no appropriate follow-up study
was done. Experiments that were done did not control even the
basic variables, which makes one question either the integrity
of the scientists, or their competency. This is tied to the
"HIV/AIDS" claim, and to the other "chronic diseases" because
the biochemical instability that a body packed with highly
unstable PUFAs must endures appears to predispose people to
"AIDS" and other "diseases." "AIDS" existed before the early
1980s, but was rare (see Root-Berntein's book on "AIDS" for
examples). It was only when the highly unsaturated oils became
common that "AIDS" was viewed as an "epidemic." It is highly
unlikely, given the evidence that now exists, that this is a
coincidence. And the other "epidemics" (such as obesity,
autism, diabetes) and the predictions of future "epidemics"
(I've heard scientists say that oral cancers and Alzheimer's
disease could very well reach "epidemic proportions" within
the next decade or two) have occurred along with the huge rise
in the consumption of these oils.