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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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This is the second part:
EFAs are, however, harmful in large amounts and the
many research papers cited by Peat showing immune
problems, increased cancer and premature aging from
feeding of polyunsaturates simply corroborate this
fact. But Peat has taken studies indicating that large
amounts of EFAs are bad for us (a now well-established
fact) and used them to argue that we don't need any at
all.
[According to the NRC, these "large amounts" are less than most
Americans are consuming these days, which means this is a kind of
dietary national emergency.]
Finally, it should be stressed that certain components
of the diet actually reduce (but do not eliminate) our
requirements for EFAs. The main one is saturated fatty
acids which help us conserve EFAs and put them in the
tissues where they belong. Some studies indicate that
vitamin B6 can ameliorate the problems caused by EFA
deficiency, possibly by helping us use them more
efficiently.
[AA in your tissues means it will be released upon minor stressors.
Is this good? "...lethal injuries sustained by cells during short
exposures to AA were caused by the fatty acid itself..." Biochem
Pharmacol. 2004 Mar 1;67(5):903-9. "Ca2+ influx is not involved in
acute cytotoxicity of arachidonic acid." Doroshenko N, Doroshenko P.
Apparently, she is referring to the "antioxidant" effect of eating
plenty of SFAs have, as Peat has said specifically, since SFAs are
resistant to oxidation and can act as a "buffer" to free radical
reactions, and hence, to AA metabolization.]
About the Author
Mary G. Enig, PhD is the author of Know Your Fats: The
Complete Primer for Understanding the Nutrition of
Fats, Oils, and Cholesterol, Bethesda Press, May 2000.
Order your copy here: www.enig.com/trans.html.
IMPORTANT CORRECTION
In the Winter 2004 "Know Your Fats" column we stated
that Siberian pinenut oil was a good source of
gamma-linolenic acid (GLA). This was indicated from
fatty acid analyses performed in Siberia. We have
since performed further tests on the oil and found
that it does not contain significant amounts of GLA
but rather a fatty acid called pinoleic acid, an
18-carbon fatty acid with three double bonds but with
the first double bond on the fifth carbon, not the
sixth, as in GLA. We are sorry for any inconvenience
this may have caused.
[she is supposed to be a "fatty acid expert," and yet was unable to
do a simple analysis of this pinenut oil - makes one wonder about her
competency even in her area of "expertise"]
Now here are some abstracts that she seems to use in the above essay.
Because she did not cite her sources, as is "essential" in a
scientific paper, one cannot be sure what she was alluding to:
Br J Nutr. 1996 Feb;75(2):237-48.
Protein utilization, growth and survival in
essential-fatty-acid-deficient rats.
Henry CJ, Ghusain-Choueiri A, Payne PR.
School of Biological and Molecular Sciences, Oxford
Brookes University.
The relationship between essential fatty acids (EFA)
deficiency and the utilization of dietary protein,
growth rate and survival of offspring was investigated
in rats during development and reproduction. EFA
deficiency was induced by feeding a 200 g
casein/kg-based diet containing 70 g hydrogenated
coconut oil (HCO)/kg as the only source of fat. The
conversion efficiency of dietary protein was assessed
as net protein utilization (NPU), using a 10 d
comparative carcass technique. Consumption of the
deficient diet during the 10 d assay period induced
biochemical changes characteristic of mild EFA
deficiency in humans (triene:tetraene 0.27 (SD 0.04)
compared with 0.026 (SD 0.004) for non-deficient
controls), but there were no significant changes in
growth rate or protein utilization. These variables
were also unchanged when the deficient diet was fed
for an additional 7 d before the assay, although
triene:tetraene increased to 0.8 (SD 0.02). Feeding
the deficient diet for 63 d before assay produced
severe EFA deficiency (triene:tetraene 1.4 (SD 0.3) v.
0.036 (SD 0.005) for controls), a fall in growth rate
(25% during assay period), and NPU (31.5 (SD 0.63) v.
39.0 (SD 0.93) for controls). These
severely-EFA-deficient animals had a 30% higher
fasting-resting rate of energy metabolism than that of
age-matched controls. However, there was no change in
the rate of endogenous N loss. Voluntary energy
consumption was increased in animals fed on deficient
diets, either with 200 g protein/kg, or protein free.
The reduced efficiency of protein utilization could be
entirely accounted for by the restricted amount of
energy available for growth and protein deposition.
Consumption of an EFA-deficient diet during pregnancy
and lactation resulted in high mortality (11% survival
rate at weaning compared with 79% for controls) and
retarded growth in the preweaning offspring. It is
concluded that animals are particularly sensitive to
EFA deficiency during reproduction and pre- and
post-natal stages of development. However, after
weaning only severe EFA deficiency retarded growth,
primarily through changes in energy balance.
I agree with this study in some ways, though I think the underlying
mechanism is not correct. It is not omega 3 and 6 PUFAs that are
"essential," but a certain amount of biochemical activity
stimulation, which all agree occurs when a threshold amount of
unsaturated fatty acids are consumed. As they say, "EFA deficiency
retarded growth," and this is my point: that is, you want what they
call "retarded growth" if you are a grown human being who is not
pregnant - otherwise, you are flirting with cancer and other
"chronic diseases." Notice that some of the offspring did survive,
even with no unsaturated fatty acids at all. This is strong evidence
that omega 3s and 6s are not "essential," because if they were
there should have been no survivors. Their results are consistent with
Peat's claim that oxidative stress, often from excess PUFA
consumption, leads to thyroid suppression and more energy, which
requires more energy/calories. They probably did not feed the
hydrogenated coconut oil mice enough food, because their "normals"
were based on mice with suppressed thyroids. Farmers have known for
decades that soy and corn cause farm animals to "fatten up" -
this is not news. The key point is that the only possible
"negative" in "essential fatty acid deficiency" is less growth,
exactly what I, as a grown adult human, want at this point, and as
I've mentioned in past posts, I was able to recover fully from severe
osteoporosis (as well as a nasty bout of tendonosis) on a diet with
only trace amounts of omega 3s and 6s, so the "no growth" claim
must be false or overemphasized to such a degree as to be laughable.
High quality protein in larger amounts seems to have made a big
difference in my case, not omega 3 and 6 PUFAs, which are for fast
plant growth or for animals swimming around in very cold waters.
Now here's another such study (one that we must assume Enig is
alluding to):
J Nutr. 1996 Apr;126(4 Suppl):1081S-5S.Related
Articles,Links
Is dietary arachidonic acid necessary for feline
reproduction?
Pawlosky RJ, Salem N Jr.
National Institute on Alcoholism and Alcohol Abuse,
Division of Intramural Clinical and Biological
Research, Rockville, MD 20852, USA.
A study was carried out to determine whether corn
oil-based diets devoid of arachidonic acid, 20:4(n-6),
are capable of supporting feline reproduction. One
group of four adult female felines were acclimated to
a 10 weight% (wt%) fat diet consisting of 1 wt% corn
oil and 9 wt% hydrogenated coconut oil for 1 mo before
mating. One female produced two live offspring, and
the other three females delivered either stillborn
fetuses or offspring that were severely deformed and
died shortly after birth. Two of these females were
subsequently placed on a 1 wt% corn oil diet that was
supplemented with 20:4(n-6) (200 mg/ kg of diet), and
after 2 mo they were mated. Offspring resulting from
the second mating were healthy. A third group of
females that were maintained on a 10 wt% fat diet
consisting of 3 wt% corn oil were also mated. The
offspring from these matings appeared healthy at
birth. Neonates from each diet group were killed, and
the fatty acyl composition of the livers, plasma and
brains was analyzed. In the offspring livers and
plasma, the level of 20:4(n-6) from both the 1 wt% or
3 wt% corn oil diet groups was about half that of
offspring from those receiving 20:4(n-6) in the diet.
There were no differences in the level of 20:4(n-6) in
the neonate brains among any of the groups. This study
suggests that nutritional factors unrelated to the
tissue accumulation of arachidonic acid in the
offspring may be responsible for the high percentage
of stillbirths and deformities associated with
maternal diets containing low amounts of essential
fatty acids but that diets that contain a higher
percentage of corn oil can support feline
reproduction.
Four animals are not enough, obviously, but this experiment is
revealing because even consuming a diet in an anti-growth substance
like hydrogenated coconut oil (HCO) one of f the four produced healthy
kittens. Once again, this experiment demonstrates that "EFAs" are
not "essential," even during pregnancy. The animals may not have
been fed enough, and thus could not produce enough Mead acid to meet
the special needs of pregnancy. Rosemary and other powerful
antioxidant herbs and spices are in some ways similar to HCO in their
anti-growth effects. If the animals were force fed foods rich in
oregano, basil, rosemary, etc. (I doubt that they would voluntarily eat
it), my guess is that no offspring would have been viable. Yet nobody
is telling pregnant women not to eat such foods, which is good advice,
unless they want a miscarriage (most would likely be revolted by the
thought of eating such foods due to instincts). The underlying
mechanism is biochemical activity. You need plenty of it in pregnancy,
but not in adulthood. People are being told to consume such substances
(antioxidants, "phytonutrients," etc.), and yet they are also being
told to consume omega 3s and 6s, which have the opposite effects.
There is nothing special about omega 3s and 6s, except that they are
much more unstable/biochemically active than the Mead acid PUFA, yet
"experts" talk of omega 3s and 6s as if they are endowed with
supernatural qualities. If they want to claim that there is no
equivalency in biochemical activity (for example, 1 arachidonic acid
molecule might be as biochemically active as 5 Mead acid molecules) but
that there is some special quality to AA, and not Mead acid, then it is
their responsibility to demonstrate this in a controlled experiment.
The experiments they point to do not demonstrate what they say they do.
Their claims resemble religious doctrines more than anything else.
I will propose an experiment that does meet the criteria: take mice
that have been fed fresh coconut oil as their only major fat source
their entire lives and feed them to pregnant cats. The mice will have
Mead acid in them, but nothing more than trace amounts of omega 3s and
6s (if any). Allow the cats to eat all the mice they want, so that
caloric intake and unnatural diets will not be a factor. Probably 30
or 40 cats will be better than 4, and if enough cats are studied, we
will know if the issue is biochemical activity in general, or some
special quality of omega 3s and 6s which has yet to be determined by
science (biochemical activity, on the other hand, is a basic principle,
and can be measured), but we can start with several and see what
results. If they all produce viable offspring, there would be no need
to go further: it would be clear that the EFA claim is as nonsensical
as can be.
One point that seems to elude people like Enig is that two scientific
models can, and often do, exist at the same time, but one must be more
accurate than the other. The way to determine which is more accurate
is to do on point experiments, not experiments that can be explained by
both models.
In the absence of such experiments, there are other sources that are
suggestive, such as the demographic data showing hardly any "chronic
disease" among those who eat large amounts of fresh coconut. There
are epidemiological studies, most of which are flawed in the
dietary/nutrition context because they begin with faulty assumptions
rather than gathering data and looking at all the factors in play. A
few have done this, and have found that "red meat" and "processed
meat" are associated with higher rates of "heart disease," due to
the free radical damage that occurs to these food items, as well as to
the high arachidonic acid, iron, and cholesterol content. As Dr.
Richard Stein said a few months, it's only the oxidized cholesterol
that is a problem (page B17 of New York's Newsday newspaper, March 1,
2005), though I have been saying this here for a few years or so.
Thus, the fact that beef has a bit more saturated fatty acids than
chicken is irrelevant. In fact, if beef was as high in saturated fatty
acids as coconut oil, it might be a much safer food (due to the
resistance of saturated fatty acids to oxidation), and yet because it
is a bit higher in SFAs, the "saturated fat," which has no precise
definition in this context anyway, gets all the blame.
And this brings us to molecular level evidence, which is overwhelmingly
supportive of the points I make here. For example, a recent
experiment found that "When mildly oxidized, liposomes containing
either linoleic acid or arachadonic acid increased monocyte chemotaxis
and monocyte adhesion to endothelial cells nearly 5-fold, demonstrating
that oxidation products of both these polyunsaturated fatty acids are
bioactive," whereas "In contrast, when liposomes were enriched in
oleic acid, monocyte chemotaxis and monocyte adhesion were nearly
completely inhibited. These results suggest that enriching
lipoproteins with oleic acid may reduce oxidation both by a direct
"antioxidant"-like effect and by reducing the amount of linoleic acid
available for oxidation." Source:
http://www.jlr.org/cgi/content/abstract/39/6/1239 The body makes
palmitic acid (an SFA) and also oleic acid, which can then be made into
Mead acid (not to get too technical). In light of hundreds of these
kinds of molecular level experiments, it is remarkable that anyone
would suggest that allowing the human body to make its own PUFA, the
Mead acid, is the most intelligent thing a person can do for long-term
health.
If anyone feels that the evidence for omega 6 and 3 "essentiality"
is incontrovertible, then you have a responsibility to those people who
you think are being "misled" by me to take me up on my offer and
demonstrate the flaws in my reasoning. I am willing to put up as much
as $50,000 of my own money to demonstrated the correctness of my
thinking, but no one among the many critics are willing to put up a few
thousand dollars of their own money. I'm not suggesting anything
strange, just a verification of the 1930 Burr & Burr experiment, but
done with proper scientific controls. Most non-scientists believe that
verification experiments are done routinely, and yet the opposite is
often the case, and instead what happens is that a dogma gets
established that is based upon flawed experimental designs, incomplete
knowledge, or incorrect assumptions. If anyone wants to contact Enig
and propose my offer, I would appreciate it. I tried to contact her
via her email address at least twice over the last several years but
got no response, and I only asked a question that one would think is
within her field of "expertise." I did not make any experimental
offers to her.
If you make a claim that you want to be regarded as scientific, then
you must subject it to the scientific method. This method requires
that your claim is always true, every time confirmatory experiments
are conducted. In the case of "essential fatty acids" and pregnant
animals, some offspring did survive, which means the essential fatty
acid is incorrect, and that it is likely a matter of a threshold of
biochemical activity being required for the quick growth that a fetus
needs. The way to know for sure is to do the experiment that I
suggested, with mice fed fresh coconut oil, that are then fed to
pregnant mice (allowing the cats to eat as many mice as they want, or
whatever parts of the mice they choose). In fact, such an experiment
might show that there is an equivalency (at least in pregnant cats);
for example, 1 arachidonic fatty acid may be equivalent to 5 Mead fatty
acids, in terms of the biochemical activity involved in fetal
development. Why anyone would attack such basic, sensible,
intellectually consistent, and scientifically necessary criticisms and
proposals is incomprehensible, and implies gross incompetence,
conflicts of interest, "low self esteem," or "knee jerk
reactions" that demonstrate psychological instability (and I've
known a few professors who fit this description very well) in a
mistaken desire to "defend" one's "turf" and save the
"ignorant masses."
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There were some responses to my original post on sci.med.nutrition. I copied and pasted some of my responses to those responses below. A study that is referenced in my responses is the following:
QUOTE: J Nutr. 1983 Jul;113(7):1422-33.
Role of linoleate as an essential fatty acid for the cat independent of
arachidonate synthesis.
MacDonald ML, Rogers QR, Morris JG.
To determine the essential fatty acid (EFA) requirements of the cat,
specific pathogen-free kittens were fed either a linoleate-deficient
diet or one of two diets containing 5% safflower seed oil (SSO) with or
without 0.2% tuna oil. The diets were fed for 82-101 weeks beginning at
3 months of age. The results showed that linoleate is an essential
fatty acid for the cat. Linoleate deficiency resulted in reduced feed
efficiency (in males), high rates of transepidermal water loss, poor
skin and coat condition, and fatty liver. These manifestations of EFA
deficiency were prevented by SSO. Tuna oil had no additional effect.
Analyses of the fatty acid composition of plasma, erythrocytes and
liver lipids revealed that linoleate deficiency caused changes that
were qualitatively, but not quantitatively similar to EFA deficiency in
the rat. When SSO was provided, linoleate was elongated and desaturated
at the delta 5 position to form 20:2n6 and 20:3(5,11,14). However,
there was negligible conversion of linoleate to arachidonate. These
results indicate that linoleate has specific functions as an EFA,
independent of arachidonate synthesis and prostaglandin formation.
PMID: 6408230 [PubMed - indexed for MEDLINE]
UNQUOTE.
At least you've actually cited an experiment. Notice that they said a
linoleate free diet, but they did not tell us if the cats were fed any
fat at all. This is not science, and it makes no sense to compare to
humans anyway. If you think this makes sense, then take me up on my
offer. Cats are rather special mammals in some ways, but dogs, pigs,
monkeys are good for comparison. I'd be willing to do a mouse or rat
experiment, which would be cheaper and easier than the cats. My point:
if you feed these animals fresh coconut oil, or a diet of safflower
oil around 15 to 25%, which is a mimimum of the amount of fat most
Americans have in their diets, the fresh coconut oil animals will live
longer. You can cite all the flawed studies you like, but I will
continue to point out where they are going wrong. You can name-call
all you like, but I will continue to propose on point experiments that
cannont be "massaged" or manipulated. Common sense does not appear to
be your strong suit, so you might as well stick to the cheap insults.
Other worthwhile points to the objective reader who has not read some
of my other posts:
1. Notice they don't tell you which group of cats lived longer.
2. Notice the signs of "deficiency:" "reduced feed
efficiency (in males)" and "fatty liver." These are signs of toxic
exposure, to fumonisins and aflatoxins, probably due to whatever the
alternative feed was. "High rates of transepidermal water loss." This
is interesting, because after being "essential fatty acid deficienty"
for a few years or so, I notice that I drink more water. What this has
to do with health needs to be made clear, but until we know what the
alternative diet actually was, there's no way this study can be
examined scientifically beyond a superficial level. "Poor skin and
coat condition." This is typical "seek and ye shall find" nonsense.
When you look for signs of "deficiency" you find them. This claim is
likely due to researcher bias.
3. Why not feed the cats a diet high in top-quality olive oil as a
control, since then there would be an unsaturated fatty acid control?
This study is actually very good, because it shows once again how much
these "scientists" take for granted and don't know.
4. There is nothing special about linoleic acid. I have never seen a
claim that it is "essential" in and of itself. The claim is always
that it's needed for PG synthesis, even though non-omega 6 PUFAs can be
metabolized into substances that do the same thing, only without the
negative effects of AA. What the "scientists" here are saying makes no
sense at all, but it would be nice if they would mention exactly what
hypothesis they think their results support, because it doesn't even
exist. Again, it is like a claim that linoleic acid has magical
qualities.
5. Thus, I again ask: what is the "essential fatty acid" hypothesis,
exactly? In science, you put forth your hypothesis and you cite the
relveant evidence. With "EFAs" there is no hypothesis, only vague
claims or ones that are undeniably false, along with evidence that
contracts the claim or terribly flawed "studies." This sort of thing
is a mockery or charicature of science.
For those who don't know:
1. "Reduced feed efficiency" means they eat more but don't gain as much
weight, something a lot of Americans would like to have, not avoid.
2. Points about "fatty liver" in humans:
The basic cause of non alcoholic fatty liver disease is insulin
resistance, a condition in which the effects of insulin on cells within
the body are reduced. The most frequent risk factor for insulin
resistance is obesity, especially abdominal obesity.
Fatty liver is itself quite harmless, disappears rapidly with loss of
weight, and infrequently progresses to non alcoholic steatohepatitis,
which is the next stage of non alcoholic fatty liver disease.
http://www.medicinenet.com/script/main/art.asp?articlekey=46582&page=2
And:
Although some drugs or genetic abnormalities can cause NAFLD, the
majority of cases are associated with obesity, insulin resistance, and
type 2 diabetes.
http://www.jci.org/cgi/content/full/115/5/1139
Since we don't know what the cats were fed, there's nothing that can be
said about the experiment. We do know that insulin resistance problems
are nearly unheard of in Asian populations that consume coconut as
their major form of fat. Recently, oxidative stress has been
demonstrated to be the primary cause of "insulin resistance," and since
fresh coconut oil resists oxidative stress, while safflower oil is very
susceptible to it, this is a different way of making a mockery of
scientific understanding.
Let's do the experiment with proper controls and see what happens. |
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Hans,
you say that your wounds heal without any scar tissue (keloid). This is very interesting and may be the "holy grail" sought by the regenerative medicine. There is a mouse strain, which can regenerate organs without any scar tissue like salamanders and it has some mutation or abnormally in immunity (autoimmunity?). Given that the immune system is repairing our tissues and that the repair is driven by fatty acid metabolites (eicosanoids) this mouse can perhaps incorporate the "right fatty acids" like mead acid preferentially into its cells despite of the omega-6 rich laboratory feed ...
Philos Trans R Soc Lond B Biol Sci. 2004 May 29;359(1445):785-93.
The scarless heart and the MRL mouse.
Heber-Katz E, Leferovich J, Bedelbaeva K, Gourevitch D, Clark L.
The Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104, USA. [email protected]
The ability to regenerate tissues and limbs in its most robust form is seen in many non-mammalian species. The serendipitous discovery that the MRL mouse has a profound capacity for regeneration in some ways rivalling the classic newt and axolotl species raises the possibility that humans, too, may have an innate regenerative ability. The adult MRL mouse regrows cartilage, skin, hair follicles and myocardium with near perfect fidelity and without scarring. This is seen in the ability to close through-and-through ear holes, which are generally used for lifelong identification of mice, and the anatomic and functional recovery of myocardium after a severe cryo-injury. We present histological, biochemical and genetic data indicating that the enhanced breakdown of scar-like tissue may be an underlying factor in the MRL regenerative response. Studies as to the source of the cells in the regenerating MRL tissue are discussed. Such studies appear to support multiple mechanisms for cell replacement.
It's a miracle: mice regrow hearts
29aug05
SCIENTISTS have created "miracle mice" that can regenerate amputated limbs or damaged vital organs, making them able to recover from injuries that would kill or permanently disable normal animals.
The experimental animals are unique among mammals in their ability to regrow their heart, toes, joints and tail.
And when cells from the test mouse are injected into ordinary mice, they too acquire the ability to regenerate, the US-based researchers say.
Their discoveries raise the prospect that humans could one day be given the ability to regenerate lost or damaged organs, opening up a new era in medicine.
Details of the research will be presented next week at a scientific conference on ageing titled Strategies for Engineered Negligible Senescence, at Cambridge University in Britain.
The research leader, Ellen Heber-Katz, professor of immunology at the Wistar Institute, a US biomedical research centre, said the ability of the mice at her laboratory to regenerate organs appeared to be controlled by about a dozen genes.
Professor Heber-Katz says she is still researching the genes' exact functions, but it seems almost certain humans have comparable genes.
"We have experimented with amputating or damaging several different organs, such as the heart, toes, tail and ears, and just watched them regrow," she said.
"It is quite remarkable. The only organ that did not grow back was the brain.
"When we injected fetal liver cells taken from those animals into ordinary mice, they too gained the power of regeneration. We found this persisted even six months after the injection."
Professor Heber-Katz made her discovery when she noticed the identification holes that scientists punch in the ears of experimental mice healed without any signs of scarring in the animals at her laboratory.
The self-healing mice, from a strain known as MRL, were then subjected to a series of surgical procedures. In one case the mice had their toes amputated -- but the digits grew back, complete with joints.
In another test some of the tail was cut off, and this also regenerated. Then the researchers used a cryoprobe to freeze parts of the animals' hearts, and watched them grow back again. A similar phenomenon was observed when the optic nerve was severed and the liver partially destroyed.
The researchers believe the same genes could confer greater longevity and are measuring their animals' survival rate. However, the mice are only 18 months old, and the normal lifespan is two years so it is too early to reach firm conclusions.
Scientists have long known that less complex creatures have an impressive ability to regenerate. Many fish and amphibians can regrow internal organs or even whole limbs.
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| | | From: J-P | Sent: 5/8/2008 3:35 PM |
Hello, I read your text, good work, but when I see this article of mary enign, and ask to Dr. Peat if he have news from her. He tell that somes friends of Enign tell that Mary was very sick and dosen't write anymore article since 5 years.
Who write this article???? |
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J.P.
I don't know, but I have tried to contact Enig at least twice that I can remember (3-5 years ago) and never got any response at all. However, the evidence is what it is, and so you don't really need someone to tell you, so long as you understand the situation on a basic level. One of the reasons I decided to create this site was to try and help people (both scientists and non-scientists) understand the issues involved and to see a lot of evidence that they won't likely ever hear about from the "mainstream media" (for whatever reason). |
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| | | From: J-P | Sent: 5/8/2008 8:28 PM |
| But did you thrust Dr. Peat???? |
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| I guess you mean do I trust Ray Peat. For me, science isn't about trust, and more importantly, anyone can make a mistake, so even an honest person can make a bogus claim. He made his case, she made her case, and I examined both arguments for myself. I also been "experimenting" on myself (as several famous scientists have done) for years. I think Enig's argument makes no sense, in light of the evidence when viewed as a whole as well as my "experimenting." If she has been ill for several years, this would explain some things, but it would also mean that we should probably move on and just examine the evidence, rather than concern ourselves with what she was arguing for several years ago. |
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J-P, I have read some reports that Mary Enig had cancer and she underwent chemotherapy. I saw a video of her recently on YouTube, from the Fat-Head movie, and she looked very bad. Watch the video "Big Fat Lies" on this page..
http://youtube.com/user/FatHeadMovie
-or-
http://www.youtube.com/watch?v=v8WA5wcaHp4 |
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| Ancel Keys (in his Seven Countries book) found that overall mortality is lowest when one's cholesterol (that is, middle aged men) is in the 200 to 220 range, which is something that has been ignored by those pushing the "lipid hypothesis." Instead, almost all doctors in the USA would tell you that you had "high cholesterol" (as if it's a "disease") if you had cholesterol around 215 to 220. |
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| In women, Ancel Keys's rule doesn't apply, based on what I've read. Women live longer, the higher their cholesterol levels. I think Uffe Ravnskov pointed this out in his book, too. The lipid hypothesis is pure junk science and we shouldn't worry about our cholesterol intake or level, but rather what type of fats and foods we're eating. They're not all the same, as you've pointed out. Some are lethal, esp in the modern dietary context. |
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| It looks like people with low cholesterol die of cancer while people with high cholesterol die of heart disease. Only a small percentage of people make it to the "natural" death. Mary Enig criticized Ray Peat for denying the essentiality of Omega-3/6 PUFAs and she has been probably ingesting them as the politically correct fat researcher ... Just wondering from what disease will Ray Peat suffer when he gets old. |
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| | | From: J-P | Sent: 6/23/2008 4:49 PM |
Yes, thank you! Im from Montreal and I want to wrote a article about fat and cholesterol, if anyone have research that prove the relation that cholesterol do not contribute to heart desease or any research about high cholestrol was good.
Could you send me by email at [email protected]
Thank to everyone!
Keep taking saturated fat high as possible! |
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| If you go to a bookseller, like amazon.com, and search for cholesterol myths, you'll see some books that might interest you. Also, a good book on this subject is "Heart Failure," by Thomas J. Moore. And if you have not noticed, there's plenty of good evidence on this site. Another site you might want to take a look at is: raypeat.com |
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