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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