This was posted on sci.med.nutrition (by me) a while back, but I'd like to post it here so that it doesn't get deleted there.
On the Weston Price web site
(http://www.westonaprice.org/knowyourfats/essentialfattyaciddef.html )
we are presented with an essay by "fatty acid expert" Mary Enig,
who disputes the proposal that Mead acid is what nature intended for
organisms like humans, contradicting biochemist Ray Peat's view that
omega 3s and 6s are basically "nothing but trouble," to put it
colloquially. Interestingly, she speaks in the tone of an authority
figure who is not to be questioned, and cites no evidence, though she
has criticized other scientists for doing the exact same things. For
example, in Science 2002 295: 1464-1465, there is the following
statement:
"IN HIS LETTER ABOUT THE ARTICLE "THE
soft science of dietary fat" (News Focus,
G. Taubes, 30 Mar. 2001, p. 2536), Scott
M. Grundy says that saturated fatty acids
(SFA) are the main dietary cause of coronary
heart disease (CHD) ("Dietary fat: at
the heart of the matter," 3 Aug., p. 801),
and he cites two reviews in support (1, 2).
In one of the reviews, there are no references
(1); in the other, of which Grundy is a
co-author, most of the references do not appear
to be supportive of his statement."
I must admit that though she has done much good work (for example, her
book on "traditional diets" and her essay on canola oil were
excellent, though of course I don't agree with everything she says),
and until now I just thought she was simply unfamiliar with the
literature (which she may be), there is something else. There is an
arrogance, which is fine with me, if she is willing to think clearly
and address the relevant evidence. Since she does not, there is
nothing but the arrogance and a load of misleading statements; this is
an example of "establishment science" at its worst. I have lost a
great deal of respect for her, intellectually (I don't know her
personally). She fought the "good fight" against the
anti-cholesterol crowd, but now it seems that her ignorance of general
biochemical principles has taken its toll on her ability to understand
the underlying mechanism involved here.
Below this paragraph is her essay, with my comments in brackets,
followed by two studies to which she alludes, but for some reason does
not cite directly, followed by my comments on the studies, and then
some concluding remarks. Note that this is not a "minor" point.
If Mead acid is what "nature intended," and if the huge amount of
evidence demonstrating the dangers of more than trace amounts of omega
3 and 6 PUFAs (polyunsaturated fatty acids) in the diet is even
somewhat true, then we are dealing with something like a combination of
genocide and suicide - suigenocide? "Chronic disease" and the
consumption of highly unsaturated oils have risen with the exact same
curve (if graphed out), yet it is only recently that molecular-level
evidence is available in abundance to support this claim, but
apparently because people like Enig want to "defend their turf"
(notice the snide remark about who has the "expertise" even though
fatty acids are among the simplest biological molecules and the
experiments needed for verification comprehensible to children), there
is a sense among such people that the dogma must be defended at all
costs and without regard for the scientific method.
"A Reply to Ray Peat
on Essential Fatty Acid Deficiency"
By Mary G. Enig, PhD
Ray Peat, PhD, is an influential health writer who
claims that there is no such thing as essential fatty
acid (EFA) deficiency. According to Peat, the body can
make its own EFAs; furthermore, he claims that EFAs in
the body become rancid and therefore cause cancer.
Unfortunately, Peat does not understand the use of EFA
by the human body. He is trained in hormone therapy
and his training in fats and oils has been limited to
misinformation as far as the polyunsaturated fats and
oils are concerned.
Research on EFAs is voluminous and consistent: EFAs
are types of fatty acids that the body cannot make,
but must obtain from food. We do not make them because
they exist in virtually all foods, and the body needs
them only in small amounts. The body does make
saturated and monounsaturated fatty acids because it
needs these in large amounts and cannot count on
getting all it needs from food.
[then where are all the dead people who didn't consume
omega 3s in decades, such as my relatives who lived to be 100, or are
still alive and in their 90s? Also, the body does make a PUFA, the
Mead acid. And why can't she cite one on point experiment that is
not terribly flawed?]
There are two types of EFAs, those of the omega-6
family and those of the omega-3 family. The basic
omega-6 fatty acid is called linoleic acid and it
contains two double bonds. It is found in virtually
all foods, but especially in nuts and seeds. The basic
omega-3 fatty acid is called linolenic acid and it
contains three double bonds. It is found in some
grains (such as wheat) and nuts (such as walnuts) as
well as in eggs, organ meats and fish if these animals
are raised naturally, and in green vegetables if the
plants are raised organically.
[The claim that only organically grown green vegetables can contain
some omega 3s is extraordinary, almost supernatural, but without any
citations, I will not pursue this tangential point here.]
Essential fatty acids have two principal roles. The
first is as a constituent of the cell membrane. Each
cell in the body is surrounded by a membrane composed
of billions of fatty acids. About half of these fatty
acids are saturated or monounsaturated to provide
stability to the membrane. The other half are
polyunsaturated, mostly EFAs , which provide
flexibility and participate in a number of biochemical
processes. The other vital role for EFAs is as a
precursor for prostaglandins or local tissue hormones,
which control different physiological functions
including inflammation and blood clotting.
[The "cell membrane" claims have been refuted decisively by Gilbert
Ling, but
if it is true, "EFAD" animals should literally fall apart, but they
do not - the major effect is to slow growth, which is not
detrimental, but beneficial to adults humans. Furthermore, one should
need more than small amounts of omega 3s and 6s if they are needed to
hold cells together, and this would lead people to eat more than the
threshold amount for cancer, as the NRC and other scientists have
determined. The intelligent thing to do would be to avoid any major
source of omega 3s and 6s and wait until one's body showed deficiency
signs, then supplement. I have done this for about 4 years, Peat about
a decade - we only see benefits at this point. In my own experience,
the reverse has been observed: my blood clots better now - healing is
a little slower, but there is little in the way of "inflammation"
and there is no itchy feeling. Also, a nasty case of rosacea that I
had for over a decade went away. This is consistent with biochemical
activity as the underlying mechanism, not some special need for
particular unsaturated fatty acids. However, she has no excuse for
ignoring the many studies which reach such conclusions as: "COX-2
derived prostaglandin E2 (PGE2) can promote tumor growth by binding its
receptors and activating signaling pathways which control cell
proliferation, migration, apoptosis, and/or angiogenesis. However, the
prolonged use of high dosages of COX-2 selective inhibitors (COXIBs) is
associated with unacceptable cardiovascular side effects." Source:
Gut. 2005 Aug 23; [Epub ahead of print] "Prostaglandins and
cancer."
Wang D, Dubois RN. As I've said, with Mead acid, there is no COX-2
problem because there is no COX-2 expression, due to the lower level of
biochemical activity involved. Enig acts as if these kinds of studies,
as well as the many studies that show benefits from Mead acid, along
with others that have observed things like Mead acid in healthy young
cartilage but arachidonic acid (AA) in old, arthritic cartilage, do not
exist! For example: "n-9 20:3 acid [Mead acid] in cartilage may be
important for maintaining normal cartilage structure." Source: The
FASEB Journal, Vol 5, 344-353, Copyright © 1991 by The Federation of
American Societies for Experimental Biology.
Enig's presentation is irresponsible and demonstrates a serious
breach of scholarly integrity - there is no excuse for it. I, on the
other hand, try to read every relevant study, and will respond directly
and clearly to any study which appears to contradict the points I make
here. If I am wrong or mistaken, I admit it, and learn from it]
Scientists have induced EFA deficiency in animals by
feeding them fully hydrogenated coconut oil as their
only fat. (Full hydrogenation gets rid of all the
EFAs; coconut oil is used because it is the only fat
that can be fully hydrogenated and still be soft
enough to eat.) The animals developed dry coats and
skin and slowly declined in health, dying prematurely.
(Interestingly, representatives of the vegetable oil
industry blame the health problems on coconut oil, not
on fatty acid deficiency!)
[A citation here is crucial, but this claim about coconut oil makes no
sense and is misleading. Fresh coconut oil is natural, hydrogenated
coconut oil introduces complicating factors that a scientist tries to
eliminate from experiments, such as toxic nickel from the hydrogenation
process. Since fresh coconut oils contains no omega 3s, there is no
reason to use the unnatural hydrogenated stuff, which may indeed act as
a strong inhibitor of what is truly needed in pregnant animals, that
is, biochemical activity. Without omega 3s, the animals would be
"deficient" and should not produce viable offspring. There are all
kinds of claims these days about the need for omega 3s in pregnancy,
and so the fresh coconut oil should be used if one wants to do a more
scientifically consistent experiment. Yet the best idea would be to
feed mice that ate only fresh coconut oil as their fat source to a
carnivorous animal like cats, both pregnant ones and adult males. The
cats should be allowed to eat as many mice as they want, in whatever
way they want, so that nature would dictate the diet, with the one
exception of Mead acid being substituted for omega 3 and 6 PUFAs. This
would demonstrated whether omega 3s and 6s are special, or whether
it's a matter of a threshold amount of biochemical activity.]
In a situation of fatty acid deficiency, the body
tries to compensate by producing a fatty acid called
Mead acid out of the monounsaturated oleic acid. It is
a 20-carbon fatty acid with three double bonds named
after James Mead, a lipids researcher at the
University of California at Los Angeles who first
identified it. An elevated level of Mead acid in the
body is a marker of EFA deficiency.
According to Peat, elevated levels of Mead acid
constitute proof that your body can make EFAs.
However, the Mead acid acts as a "filler" fatty acid
that cannot serve the functions that the original EFA
are needed for. Peat claims that Mead acid has a full
spectrum of protective anti-inflammatory effects;
however, the body cannot convert Mead acid into the
elongated fatty acids that the body needs for making
the various anti-inflammatory prostaglandins.
[this is really perplexing, because if AA "overdose" is
the cause of "inflammation," one would not need
anti-inflammatory substances if there was no substance
that caused inflammation in the first place. And how does she know
that Mead acid is a "filler?" What is a "filler,
scientifically?" She seems to make things up as she goes along,
without any regard for scientific principles. Ironically, much of her
essay is what we used to call "filler" in grad school. ]
Peat also asserts that polyunsaturated fatty acids
become rancid in our bodies. This is not true; the
polyunsaturated fatty acids in our cell membranes go
through different stages of controlled oxidation. To
say that these fatty acids become "rancid" is
misleading. Of course, EFAs can become rancid through
high temperature processing and it is not healthy to
consume these types of fats. But the EFAs that we take
in through fresh, unprocessed food are not rancid and
do not become rancid in the body. In small amounts,
they are essential for good health. In large amounts,
they can pose health problems which is why we need to
avoid all the commercial vegetable oils containing
high levels of polyunsaturates.
[Here, Enig should be clear about what she means. A google search for
"in vivo lipid peroxidation" produced 14,100 results. She appears to
be far outside the scientific mainstream on this point, but if she does
not explain how she came to this conclusion - as I always do about my
claims - her claim cannot be taken seriously. Moreover, there are
some phenomena that is undeniable: what about food that is not
completely digested? I
ate foods that came out of me looking the same way they did when I ate
them, when I had the terrible bout of malabsorption. There would have
been at least some in vivo lipid peroxidation going on under such
circumstances. I sped up the aging of my gastrointestinal track by my
diet high in nuts, seeds, beans, flax, etc., but it is known that many
people produce less stomach acid and enzymes as they age, meaning that
even if they don't eat too much, there will likely be some undigested
food in their guts. And it is the ease with which the highly unstable
omega 3s and 6s are changed in the body, or during cooking, into very
dangerous molecules such as 4-HNE that may do the most damage. The
omega 3s and 6s don't just "stand around" waiting for "good
things" to happen to them.]
Peat's reasoning has led him to claim that cod liver
oil causes cancer because cod liver oil contains
polyunsaturated fatty acids. Actually, the main fatty
acid in cod liver oil is a monounsaturated fatty acid.
The two main polyunsaturated fatty acids in cod liver
oil are the elongated omega-3 fatty acids called EPA
and DHA, which play many vital roles in the body and
actually can help protect against cancer. Furthermore,
cod liver oil is our best dietary source of vitamins A
and D, which also protect us against cancer.
[Enig's reasoning here is incomprehensible: Peat has argued that
high-quality olive oil, a great source of oleic acid, is much better
than oils such as safflower (unless you want to paint with it). Almost
everything with fat contains some oleic acid. Oleic acid is not the
issue, and she should know this. If you mixed cyanide with olive oil
and fed them to mice and the mice died, we would all agree that the
cyanide was to blame. The issue is susceptibility to free radical
degradation, and that is where the very unstable EPA and DHA molecules
are a major cause of concern. If fish oil protects against cancer and
has no "down side," then she or those who agree with her should
take me up on my offer, which the evidence suggests will demonstrate
that biochemical activity is the mechanism involved. The idea that
omega 3s and 6s are essential is inconsistent with basic biochemical
principles, because cells need the stress from excess biochemical
activity to grow, not any particular fatty acid. Experiments should
substitute an amount of Mead acid that has the equivalent biochemical
potency of the amount of arachidonic acid that is considered necessary
for proper growth. This would be settle the issue once and for all
(assuming the experiment was conducted properly), and provide a
scientific basis for accepting or discarding what up to this point have
been grand pronouncements based upon opinions about what the supposed
results of terribly flawed experiments mean.
And again, there are no citations for these remarkable claims about
EPA/DHA.]
Actually, Peat's argument that polyunsaturated fatty
acids become harmful in the body and hence cause
cancer simply does not make sense. It is impossible to
avoid polyunsaturated fatty acids because they are in
all foods.
[Does she realize that Mead acid is a PUFA - apparently not.
Moreover, this demonstrates a lack of knowledge of the relevant
literature, which suggests that there is a threshold
amount that causes much higher rates of cancer - the
NRC saw this about 15 years ago, and I have quoted them on this point
on this newsgroup several times over the years.]
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