In a recent thread, "MMu" cited a statement of mine:

"The "experts" are

then stated:

"Hmm.. if that is so: who makes the actual new research? Amateurs?"

What a "nutritinal expert" actually is may be worth some consideration.
It's easy to take for granted what one knows, but what others do not.
Many scientists who conduct actual research may be "experts" in a very
narrow field, and this field is often nearly impossible to explain to
non-scientists.  Some of these research scientists are asked questions
by reporters, and are portrayed by the media as "an expert," regardless
of whether he or she likes such a designation.  Others, with no
academic credentials of any kind, proclaim themselves "experts," and
then often try to sell some sort of health product.  Thus, there is a
wide range of people who may be classified as "experts," depending up
who is doing the classifying.  I have often criticized "experts"
because many of those so classified act as if everything is known about
a particular subject, when in fact there is a great deal that is not
known, and much that is in dispute.  Some "experts" make remarks that
demonstrate ignorance of their own subject of expertise or refuse to
answer questions about statements they made in the past.  Many have
obvious conflicts of interest.

I would make one point here that I think is very important, especially
in the context of the MMu remark: "experts" often try to make
generalizations about a subject, while researchers tend to be very
specific.  I will give a good example.  There is a new book making the
rounds called "The Fat Resistance Diet," and the author, a medical
doctor, makes argument that chronic inflammation often causes leptin
resistance, which often leads to obesity.   Now this sounds like it
could be accurate.  The old farm literature is clear: if you want to
fatten an animals up, feed it food that is high in omega 6
polyunsaturated fatty acids (PUFAs).  If you want them to be thin
(something few, if any farmers want) you feed them coconut oil.  On the
diet high in omega 6 PUFAs, the cells of the person's or animal's body
become filled up with arachidonic acid, which causes chronic
inflammation.  Without the arachidonic acid there (technically, in the
sn-2 position of phospholipids), there can be no chronic inflammation,
nor a host of other "diseases."  This doctor does not appear to know
this, but he provides some advice that would have the effect of
blocking the body's use of arachidonic acid in this way ("antioxidants"
do this, for example).  A researcher, on the other hand, may understand
the actual biochemical phenomenon, down to the molecular level, but he
or she is too focused on just that, and rarely tries to generalize, or
to work out the dietary implications of the phenomenon studied.  Thus,
there is a void that exists between the "expert," as I am defining
him/her, and the "researcher," and this is the role I am attempting to
fill on this newsgroup.  Because generalizations were made many years
ago that were based on assumptions and "models," many "experts" simply
do not consider the possibility that the evidence - taken as a whole -
does not suggest what they have been advising people to do for many
years, but instead in some ways suggests the opposite.  In some cases,
such as claims against "saturated fat," the phrase itself has no
scientific meaning that is consistently applied, and therefore one
cannot say anthing scientific about it until "it" is defined precisely.

Below is an abstract (summary) of a study that was just published.  I
cite it because it is a great example of a researcher who has appears
to have no interest in being an "expert," as I have described him/her
here.  Notice how there is no mention of how one can change one's diet
to prevent the disorders describe.  Instead, they just talk about the
specific scientific phenomenon that was studied.  In academia, it used
to be much more common for scholars/researchers to have formal debates.
In these debates, the scholars would make arguments about the meaning
of the evidence, instead of leaving that to all kinds of people, many
trying to make money or enhance their careers by advocating a
particular position.  I have challenged those who criticize my posts
(it's basically the same people saying the same nonsensical things,
over and over again) to such a formal, moderated debate, but they have
all refused.  I made several offers of different experimental
propositions (the "loser" would pay for the expenses), but they show no
interest in this.  I also asked them simply to state their positions as
scientific hypotheses, which is the basis of the scientific method, but
they never have.  Instead, they make all kinds of excuses why they
won't, or else they attack me for asking for such a statement.   I have
explained to these people, down to the molecular level, exactly what my
argument is (based upon the evidence, as well as the clear statements
made by scientists like JoAnn Braganza, Spiteller, Peat, Gower, and
many others), but instead they cite studies that contradict their own
arguments, and actually support my points.  In general, they appear to
have severe reading comprehension problems, but a formal debate would
remedy the situation, because the moderator would be able to say to
that person, "wait a minute, he is saying that he agrees with you that
omega 3s can interfere with arachidonic acid metabolization, but that
this will result in the person or animal not living as long, because of
the free radical damage and the disruptions caused by the excess
biochemical activity.  Do you agree or disargee that this is possible?
And if you disagree, would you be willing to take him up on his
experimental offer, which would settle the issue?"

Here is the abstract:

Free Radic Biol Med. 2006 Feb 1;40(3):376-87. Epub 2005 Nov 21.
Phospholipase A(2), reactive oxygen species, and lipid peroxidation in
cerebral ischemia.

Muralikrishna Adibhatla R, Hatcher JF.

Department of Neurological Surgery, University of Wisconsin, Madison,
WI 53792, USA; Cardiovascular Research Center, University of Wisconsin,
Madison, WI 53792, USA; Veterans Administration Hospital, Madison, WI,
USA.

Ischemic stroke is caused by obstruction of blood flow to the brain,
resulting in energy failure that initiates a complex series of
metabolic events, ultimately causing neuronal death. One such critical
metabolic event is the activation of phospholipase A(2) (PLA(2)),
resulting in hydrolysis of membrane phospholipids and release of free
fatty acids including arachidonic acid, a metabolic precursor for
important cell-signaling eicosanoids. PLA(2) enzymes have been
classified as calcium-dependent cytosolic (cPLA(2)) and secretory
(sPLA(2)) and calcium-independent (iPLA(2)) forms. Cardiolipin
hydrolysis by mitochondrial sPLA(2) disrupts the mitochondrial
respiratory chain and increases production of reactive oxygen species
(ROS). Oxidative metabolism of arachidonic acid also generates ROS.
These two processes contribute to formation of lipid peroxides, which
degrade to reactive aldehyde products (malondialdehyde,
4-hydroxynonenal, and acrolein) that covalently bind to
proteins/nucleic acids, altering their function and causing cellular
damage. Activation of PLA(2) in cerebral ischemia has been shown while
other studies have separately demonstrated increased lipid
peroxidation. To the best of our knowledge no study has directly shown
the role of PLA(2) in lipid peroxidation in cerebral ischemia. To date,
there are very limited data on PLA(2) protein by Western blotting after
cerebral ischemia, though some immunohistochemical studies (for cPLA(2)
and sPLA(2)) have been reported. Dissecting the contribution of PLA(2)
to lipid peroxidation in cerebral ischemia is challenging due to
multiple forms of PLA(2), cardiolipin hydrolysis, diverse sources of
ROS arising from arachidonic acid metabolism, catecholamine
autoxidation, xanthine oxidase activity, mitochondrial dysfunction,
activated neutrophils coupled with NADPH oxidase activity, and lack of
specific inhibitors. Although increased activity and expression of
various PLA(2) isoforms have been demonstrated in stroke, more studies
are needed to clarify the cellular origin and localization of these
isoforms in the brain, their responses in cerebral ischemic injury, and
their role in oxidative stress.

Let us now either formally debate or negotiate an offer to do an
experiment that would settle the matter.  It is clear, however, that
MMu simply does not understand what he is saying, nor what I (and many
scientists) are suggesting.  For example: " it has been shown,
repeatedly, that at the time mead acid is built
in the body (which only happens in case of w3/w6 deficiency) a lot of
very
bad things start to happen."  You ask for evidence, but you don't seem
to be in any hurry to supply some for your own assertions.  I have
repeatedly examined this rather scant body of evidence, and no such
conclusion can be drawn.  You also fail to mention the positive studies
about Mead acid "buildup" that I have cited on this newsgroup.
Moreover, I have avoided all major sources of omega 6s and nearly any
amount of omega 3s since 2001 yet I have better health than ever
before, with several "chronic disease" no longer bothering me.  Where
is the evidence?  As I have shown, the experiments use a mixed fat diet
versus a no-fat diet, such experiments are short term.  In the old
animal experiments, the no fat animals lived longer and rarely got
cancer.

"Tell me a single food that contains large ammounts of mead acid
please."

This is my point: you don't want PUFAs in your diet - you want your
body to make them as it sees fit, because all PUFAs are biochemically
unstable.  However, if animals weren't fed a high omega 6 diet, they
would have Mead acid PUFAs rather than omega 6 in their cells.  You
seem to be totally unaware of the studies that have been conducted that
have shown how much fatty acid content can vary in animals people like
to eat (such as chickers).  The amount can be considerable.

"If mead acid is so much better than w3 / w6 fatty acids there should
have
been a selection against animals that consume w3 / w6 fatty acids"

Yes, that is exactly what is happening now.  As people eat more omega 6
PUFAs, they diet of "chronic diseases" at young ages.  Take a look in
the newspaper obituaries some day.  Look at the "heart disease,"
"prostate cancer," colo-rectal cancer," etc. deaths.  Do you know that
in the early twentieth century, these "diseases" were very rare?  Or
are you ignorant of that basic knowledge as well?

"...its NF-kB; and the "genetic machinery" is hopefully *always* turned
on..
otherwise we would be dead very soon- protein synthesis, cell cycle,
metabolism.. they all depend on the "genetic machinery"

Once again, you enjoy attacking obvious typographical errors - hope you
had a lot of fun with it, at least.  On to the point in question.  I
will cite a source that believes in the "essentiality" of omega 3s and
6s, actually (they sum it up well):

"The transcription factor NFB is involved in regulating expression of
a large number of genes involved in inflammation including COX-2, TNF,
IL-1, and adhesion molecules. NFB exists as an inactive trimer in the
cell cytosol; one of its subunits is termed inhibitor of NFB (IB).
Upon cellular activation, a signalling process leads to activation of
kinase enzymes (IB kinases) that phosphorylate IB. Upon
phosphorylation IB dissociates from the trimer and is degraded. The
remaining NFB dimer is able to translocate to the cell nucleus where
it binds to regulatory elements in the promoter regions of target
genes, inducing their transcription.
Cell culture studies have shown that arachidonic acid activates NFB
in monocytic cells (14). This might be the mechanism by which
arachidonic acid induces COX-2 and inflammatory cytokines."

Source: http://www.fatsoflife.com/article.asp?i=a&id=197

"The bad properties of saturated fats have, in contrast to your theory,
not
ever been asociated with any kind of free radical damage- but if you
have
literature that indicates otherwise please be kind enough to post a
citation."

First, you will need to define "saturated fat."  You seem to ignore the
point I have made over and over again: to classify lard at 39%
saturated with coconut oil at 92% saturated as the same "kind" of fat
is beyond ludicrous.  I have no idea what you are talking about in this
statement.  Lard, if one is to call it a "saturated fat," which is
common among "nutritional experts," is used in Rancimat tests because
of the ease with which lipid peroxidation occurs if you just expose it
to oxygen.  This is very different with coconut oil.  Thus, depending
how one defines "saturated fat," as well as how the food is prepared,
etc., free radical damage can be minimal or severe.

What makes you and your kind especially disingenuous is your
non-responses or diversionary remarks when I make my simple
experimental offer:  we will feed a couple dozen dogs two diets: the
only difference between them is that half will get 30% fish and canola
oil and the other half will get fresh coconut oil at 30% daily
calories.  And we will see which group lives longer.  According to you
and your kind, the fish and canola oil group will be gettin optimal
nutrition, while the coconut oil dogs will be deprived of "essential
fatty acids," especially omega 3s (since coconut oil contains none).
Thus, the fish and canola oil group should live much longer.  But even
if they live just a bit longer, I would pay for the expenses.  Instead,
you and your kind cite studies that do not address the central
question, but either look for "signs of deficiency" in animals fed no
fat, or something equally ridiculous.