So he says. In any case, anecdote (individual experience) cannot be used for
extrapolative purposes.

I'll let the National Acadamies of Science, Food and Nutrition Board of the
Institute of Medicine, speak for me. They've done an excellent job of summarizing
the available evidence.
http://books.nap.edu/books/0309085373/html/609.html#pagetop

Note, after reading this chapter (Chapter 11), be sure and read chapter 8.

I think that you are taking issue with me for exactly what you claim I do not do. I
am asking Nick to address the aspects of contradiction, explicitly.

Lar

Thats OK Nick old friend.
I remember how the story goes:
.
" I've made up my mind, you idiots  .   .   .so don't none of you go
trying to confuse me with evidence."

In pacem requiescat.

MikeV

How do you know? They do not eat any meat, diary?

It is virtually impossible to "eat no omega 3 at all".

Mirek

And what about the rest of us, who have studied the science of nutrition for much
longer than that? It is only months ago that you were calling Mead acid a MUFA.

BTW, it can take years to fully express Essential Fatty Acid Deficiency Syndrome. It
all depends on how replete your body was with the PUFAs in the beginning, diet (of
course), along with genetic regulatory factors which have not yet been fully
elucidated.

If you lost the condescending tone, you might find that people have less difficulty
trying to sort out your message.

You propose that high Mead acid is a sign of health. It is formed from delta-5 and
delta-6 desaturase activity on the substrate oleic acid, with elongation.

Given the substrate affinity sequence, that omega-3 has more affinity than does
omega-6 than does omega-9 for the delta-5 and delta-6 desturase enzymes, how is it
that evolutionary pressure has created a situation which is the absolute converse of
what you propose? Given the accessibility of omega-3 and omega-6 fatty acids in
normal human foodstuffs, how is it that your grossly manipulated diet is essential
for health? Without the knowledge provided by the "pathetic biomedical profession",
it would not even be possible for you to propose an argument for your thesis.

You have frequently said that we should read your mentor's book. Did you read the
passages of the online books which I referenced for you?

Lar

Regarding the study posted:

1: Lipids. 1999;34 Suppl:S1-3. Related Articles, Links

Essentiality of fatty acids.

Spector AA.

Department of Biochemistry, College of Medicine, University of Iowa,
Iowa City 52242, USA. arthur-spector@uiowa.edu

All fatty acids have important functions, but the term "essential"
is applied only to those polyunsaturated fatty acids (PUFA) that are
necessary for good health and cannot be completely synthesized in
the body. The need for arachidonic acid, which is utilized for
eicosanoid synthesis and is a constituent of membrane phospholipids
involved in signal transduction, is the main reason why the n-6
class of PUFA are essential. Physiological data indicate that n-3
PUFA also are essential. Although eicosapentaenoic acid also is a
substrate for eicosanoid synthesis, docosahexaenoic acid (DHA) is
more likely to be the essential n-3 constituent because it is
necessary for optimal visual acuity and neural development. DHA is
present in large amounts in the ethanolamine and serine
phospholipids, suggesting that its function involves membrane
structure. Because the metabolism of n-6 PUFA is geared primarily to
produce arachidonic acid, only small amounts of 22-carbon n-6 PUFA
are ordinarily formed. Thus, the essentiality of n-3 PUFA may be due
to their ability to supply enough 22-carbon PUFA for optimal
membrane function rather than to a unique biochemical property of
DHA.

This study is worth addressing in more detail.  First of all, where
has it ever been demonstrated that an adult human’s “cell
membranes” need 22 carbon PUFAs?  A simple experiment could be
done on dogs (since they metabolize fatty acids the way humans do).
Just get some stray dogs and feed them a diet that contains too little
PUFAs to supply all these supposed lipid bilayer membranes.  If I were
to do the experiment, the dogs would get fresh coconut oil (only 2%
PUFAs), as well as organic eggs, nutritional yeast, along with other
foods that have no more than trace amounts of PUFAs.  According to
theory, the dogs should stiffen up (due to too much saturated fatty
acids), fall apart literatly (because their cells lack structural
integrity), or something else really horrible.  The only thing that
will happen is that the dogs will live long and healthy lives.
Studies have been done on pigs and chickens fed coconut, for example.

It is likely that arachidonic acid is not metabolized to omega 6 22
carbon PUFAs because it’s so biochemically unstable.  The study
is important in that the investigator admits that there is not likely
a unique biochemical need for DHA, and since Gilbert Ling has
demolished the “cell membrane/lipid bilayer” garbage, we
have here another piece of evidence AGAINST the notion of
“essentiality.”  Some idiot nutritionist apparently
decided to include this “essentiality” notion in a
textbook, after the decades that passed with his
“profession” ignoring this idea (first advanced by Burr &
Burr, 1930, working with vitamin B deficient rats), and the PUFA oil
industry eventually figured out that they could use the claim to sell
their toxic products to an ignorant public.  Why does the idea that a
human body metabolizing its own PUFA, the Mead acid, produce so much
cognitive dissonance to the Larry Hoovers of this world?  That’s
a psychological issue, not a physiological or biochemical one, so
I’ll leave that out of this post.  But show me some evidence
that allowing your body to produce its own PUFA is such a terrible
idea – if it were, there should be plenty of studies that
demonstrate this clearly.  What about the Pellagra episodes in
history?  Why hasn’t there been a similar episode involving
so-called essential fatty acids?  If it’s so easy to obtain
these fatty acids, why even bother to talk about them?  It would be
like saying protein is essential.  How many people in the USA need to
worry about not getting enough protein?  I was a vegan for 14 years,
and ate poor quality protein, yet I played sports and didn’t
have any major health problems, until the malabsorption started, which
was apparently due to low stomach acid, which could have been related
to the vegan diet, but that is questionable, considering it took 14
years to occur.  The point is that if you are going to make an
extraordinary claim, namely that people need PUFAs in the diet in more
than trace amounts, there better be extraordinary evidence
(considering we can make our own PUFA), not just a flawed rat study
from 1930.

The idea of omega 6s being needed for signal transduction has been
refuted by Gilbert Ling, but others have all done experiments
demonstrating that this is the job of protein (though biochemically
overactive fatty acids, like arachidonic, can cause major problems).
For example:
Membrane, action, and oscillatory potentials in simulated protocells.
Przybylski AT; Stratten WP; Syren RM; Fox, S.W. Naturwissenschaften,
1982 Dec, 69:12, 561-3.
"Electrical membrane potentials, oscillations, and action potentials
are observed in proteinoid microspheres impaled with (3 M KC1)
microelectrodes. Although effects are of greater magnitude when the
vesicles contain glycerol and natural or synthetic lecithin, the
results in the purely synthetic thermal protein structures are
substantial, attaining 20 mV amplitude in some cases. The results add
the property of electrical potential to the other known properties of
proteinoid microspheres, in their role as models for protocells."

As for my relatives and others I know; if you are saying that they get
enough omega 3s from the chicken and beef they eat, then, again, why
should anyone worry about being “deficient?”  In
actuality, unless you eat beef raw, and from grass fed cows, I want to
see the evidence that there is any measurable amount of omega 3 PUFAs
from the beef they buy in the local supermarket.  Also, after cooking
the beef or chicken as most people do, many of the PUFAs will be
oxidized and then they can’t be metabolized to longer chain
PUFAs (though since there’s plenty of omega 6s, a few of them
won’t get oxidized – the ones in the middle of the steak
especially).  You’ll have a better chance finding the proverbial
needle in the haystack then finding more than a few molecules of
non-oxidized omega 3 PUFAs in the beef or chicken products my friends
and relatives are consuming.  Why is common sense so uncommon with
regard to PUFAs?
If you do just a little research, you’ll see how dangerous
arachidonic acid.  One study concluded that it’s unlikely
arachidonic acid is safe when it’s in your body, regardless of
what it’s role is at any particular time or place.  Here’s
a good quotation:
“The interior of a cell is filled with a gelatinous material
that houses the nucleus, DNA, and protein ‘transcription
factors.’  These proteins are nothing more than tiny molecular
messengers that can move to the nucleus to stimulate our DNA to
replicate RNA and make important proteins for cell function.  Here we
want to concentrate on two important transcription factors, nuclear
factor kappa B (NF-kB) and activator protein 1 (AP-1).  These
transcription factors are not active in the cell unless the redox
level of the cell changes and free radicals are about to overwhelm the
cell’s defense mechanism, a state called oxidative stress.  When
cells undergo oxidative stress, the transcription factors are
activated.  NF-kB migrates to the nucleus and attaches to the DNA,
resulting in cellular production of proinflammatory cytokines –
chemicals that are the so-called ‘serial killers’ of the
cellular world.”
Source: Page 35.  “The Perricone Prescription.” Nicholas
Perricone.  2002.

Arachidonic acid is known to promote NF-kB.  Here are some things
worth reading:

Dynamic Chiropractic
October 6, 2003, Volume 21, Issue 21
   

What Is NFkB? It Could Kill You
by David Seaman, DC, MS, DABCN, DACBN, FACC

The Saga of Inflammation

Earlier this year, I completed a six-part series on how diet drives
inflammation, pain, subluxation and a host of diseases, including
heart disease, cancer and Alzheimer's.* Nearly all of the degenerative
diseases are driven by chronic subclinical inflammation; essentially,
nearly every condition that walks into a doctor's office is driven, at
least in part, by inflammation.

The old view of inflammation is that it represents the healing
response. This is true, to a point; however, once inflammation,
becomes chronic, it becomes a disease. You will not find a statement
as clear as this in typical physiology books, or even in pathology
books. However, in pathology texts, we are led to believe that chronic
inflammation plays a role in promoting the disease process. In journal
articles, we are given more precise statements. Consider the
following:

"Recent studies on diseases which involve insulin insensitivity (e.g.
obesity, type 2 diabetes and atherosclerosis) also show increased
cytokine production and markers of inflammation. Evidence at present
favours chronic inflammation as a trigger for chronic insulin
insensitivity, rather than the reverse situation."1

You will not find this type of statement in any physiology or
pathology book anytime soon. Why? I don't know. Nonetheless, we can
see that inflammation is definitively viewed as a driver of chronic
disease.

The Reduction of Inflammation

In recent years, a massive volume of literature has supported the view
that we need to halt chronic inflammation and its induction. Aspirin,
NSAIDs and corticosteroids have been the main medical weapons against
inflammation. These days, COX2 inhibitors are also being used.

Pharmacology texts tell us that aspirin, NSAIDs, and COX2 inhibitors
act to reduce inflammation by blocking the cyclooxygenase enzyme that
converts arachidonic prostaglandin E-2 (PGE2). In other words, these
drugs inhibit inflammation by blocking PGE2. Corticosteroids work
higher up the chain, inhibiting phospholipase A2, which inhibits
arachidonic acid release from phospholipids in the cell membrane.
These mechanisms have been known about for a long time. For example,
in 1971, John Vane discovered that aspirin inhibits the COX enzyme.

In more recent years, the study of inflammation has gone deeper into
the cell, to the point that cell-signaling molecules have been
identified which stimulate genes that induce the expression of the COX
enzyme. As it turns out, aspirin, NSAIDs, and corticosteroids can
inhibit certain cell signaling molecules, such as nuclear factor kappa
binding (NFkB) - which reduces inflammation.

On the natural end of the treatment spectrum, various botanicals have
anti-inflammatory effects that work in the same manner as these drugs,
except their actions are not as pronounced. Ginger and curcumin are
the most well-known substances that possess significant
anti-inflammatory actions.

Nuclear Factor Kappa B

NFkB is the "big cheese" cell-signaling molecule for inflammation; its
activation induces the expression of COX-2, which leads to tissue
inflammation. "Intriguingly, the expression of the COX-2-encoding
gene, believed to be responsible for the massive production of
prostaglandins at inflammatory sites, is transcriptionally regulated
by NFkB."2

NFkB resides in the cytoplasm of the cell and is bound to its
inhibitor. Injurious and inflammatory stimuli, such as free radicals,
release NFkB from the inhibitor. NFkB moves into the nucleus and
activates the genes responsible for expressing COX-2. Research has
demonstrated that aspirin, NSAIDs, and corticosteroids can inhibit the
activation of NFkB, which is why people derive relief from these
drugs. Problems arise due to their nasty side-effects, which means
that alternative ways need to be pursued to reduce NFkB activity.

As mentioned earlier, free radicals are examples of substances that
activate NFkB. Cytokines such as interleukin-1 (IL-1) can also
stimulate NFkB.2 Not surprisingly, antioxidants can reduce the
activation of NFkB, including green tea polyphenols; resveratrol from
red wine; vitamins C and E; curcumin; and glutathione.2 Whenever you
see glutathione, you need to think of the substances that maintain
glutathione in its active state, which includes supplements such as
lipoic acid and coenzyme Q10.3

In all likelihood, the family of flavonoids and carotenoids found in
fruits and vegetables that have antioxidant functions is capable of
reducing free-radical activation of NFkB. So, our approach to keeping
NFkB at bay should be a fruit- and vegetable-based diet that includes
green tea, red wine, and antioxidant supplements.

Fatty acids (FAs) also need to be considered. The anti-inflammatory
omega-3 FAs reduceNFkB activity,4,5 which means we need to reduce our
grain, seed, and related oil intake. Omega-3 FAs also reduce IL-1,6
which is an activator of NFkB.2 Omega-3 fatty acids are found in green
vegetables, most fish, wild game, and grass-fed meat. (See
www.texasgrassfedbeef.com.) Supplementing with 1-2 grams of EPA/DHA
from fish oil is also a good idea.

We must also be cognizant of glycemic regulation in controlling NFkB.7
An assessment of Type 1 diabetic patients found that inefficient
glycemic control resulted in increases in NFkB activity in white cells
- which results in inflammation. This means that, as alluded to
earlier, inflammation causes diabetes,3 and the diabetic state
promotes inflammation.7 It was determined that HbA1c and NFkB were
correlated with each other, and also with hyperglycemia and lipid
peroxidation.7

Diseases Driven by NFkB

We want to reduce the inappropriate activation of NFkB because it can
drive so many seemingly unrelated diseases. We don't typically think
of asthma and neurodegenerative diseases as having similar etiologies;
however, NFkB plays a role in each disease. In fact, NFkB promotes
asthma; neurodegeneration; ischemia/reperfusion injury; hepatitis;
glomerulonephritis; inflammatory bowel disease; rheumatoid arthritis;
and probably most other diseases driven by inflammation,2 including
the subluxation complex.8,9 Consider that Faye's original model of the
subluxation complex included an inflammatory component.

On a more lethal note, I searched MEDLINE for articles related to
cancer and NFkB; 1,773 appeared. One paper stated that NFkB is
strongly linked to inflammatory and immune responses, regulation of
cell proliferation and apoptosis, suggesting its role in tumor
development and many other diseases, including atherosclerosis.10 I
suggest we adopt an anti-inflammatory diet and give ourselves a
nutritional adjustment.

References
Grimble RF. Inflammatory status and insulin resistance. Curr Opin Clin
Nutr Metab Care 2002;5:551-9.
D'Acquisto F, May MJ, Ghosh S. Inhibition of nuclear factor kappa B
(NF_B): an emerging theme in anti-inflammatory therapies. Molec Interv
2002;2:22-35.
Sen CK, Packer L. Thiol homeostasis and supplements in physical
exercise. Am J Clin Nutr 2000;72(2 Suppl):653S-69S.
Lo CJ, Chiu KC, Fu M, Lo R, Helton S. Fish oil decreases macrophage
tumor necrosis factor gene transcription by altering the NF kappa B
activity. J Surg Res 1999;82(2):216-21.
Novak TE, Babcock TA, Jho DH, Helton WS, Espat NJ.NF-kappa B
inhibition by omega -3 fatty acids modulates LPS-stimulated macrophage
TNF-alpha transcription. Am J Physiol Lung Cell Mol Physiol
2003;284(1):L84-9.
Simopoulos AP. Essential fatty acids in health and chronic disease. Am
J Clin Nutr 1999;70(3 Suppl):560S-569S.
Hofmann MA, Schiekofer S, Kanitz M, et al. Insufficient glycemic
control increases nuclear factor _B binding activity in peripheral
blood mononuclear cells isolated from patients with type 1 diabetes.
Diabetes Care 1998; 21:1310-16.
Seaman DR. Joint complex dysfunction, a novel term to replace
subluxation/subluxation complex: etiological and treatment
considerations. J Manipulative Physiol Ther 1997;20(9):634-44.
Seaman DR. The diet-induced proinflammatory state: a cause of chronic
pain and other degenerative diseases? J Manipulative Physiol Ther
2002;25 (3):168-79.
Ignatowicz E, Baer-Dubowska W. Resveratrol, a natural chemopreven-tive
agent against degenerative diseases. Pol J Pharmacol
2001;53(6):557-69.

David Seaman MS, DABCN, DACBN, FACC
Port Orange, Florida

Editor's note: Dr. Seaman's six-part series on diet and inflammation
is available online at www.chiroweb.com/archives/20/21/18.html.

Source: http://www.chiroweb.com/archives/21/21/19.html

As usual, this author never gave a second thought to the notion of the
essentiality of dietary PUFA, but a scientist is supposed to question
everything and ask for the evidence, which only a few scientists have
in the case of dietary PUFAs, unfortunately.

And here’s more, though you can find plenty more like this by
doing your own research:

Am J Physiol Cell Physiol. 2004 Oct;287(4):C1139-51.
Epub 2004 Jun 02.Related Articles,Links
 
Novel effect of NF-kappaB activation: carbonylation
and nitration injury to cytoskeleton and disruption of
monolayer barrier in intestinal epithelium.

Banan A, Zhang LJ, Shaikh M, Fields JZ, Farhadi A,
Keshavarzian A.

Rush University Medical Center, Department of Internal
Medicine, Section of Gastroenterology and Nutrition,
1725 W. Harrison, Suite 206, Chicago, IL 60612, USA.
ali_banan@rush.edu

Using monolayers of intestinal cells, we reported that
upregulation of inducible nitric oxide synthase (iNOS)
is required for oxidative injury and that activation
of NF-kappaB is key to cytoskeletal instability. In
the present study, we hypothesized that NF-kappaB
activation is crucial to oxidant-induced iNOS
upregulation and its injurious consequences:
cytoskeletal oxidation and nitration and monolayer
dysfunction. Wild-type (WT) cells were pretreated with
inhibitors of NF-kappaB, with or without exposure to
oxidant (H(2)O(2)). Other cells were transfected with
an IkappaBalpha mutant (an inhibitor of NF-kappaB).
Relative to WT cells exposed to vehicle, oxidant
exposure caused increases in IkappaBalpha instability,
NF-kappaB subunit activation, iNOS-related activity
(NO, oxidative stress, tubulin nitration), microtubule
disassembly and instability (increased monomeric and
decreased polymeric tubulin), and monolayer
disruption. Monolayers pretreated with NF-kappaB
inhibitors (MG-132, lactacystin) were protected
against oxidation, showing decreases in all measures
of the NF-kappaB --> iNOS --> NO pathway. Dominant
mutant stabilization of IkappaBalpha to inactivate
NF-kappaB suppressed all measures of the iNOS/NO
upregulation while protecting monolayers against
oxidant insult. In these mutants, we found prevention
of tubulin nitration and oxidation and enhancement of
cytoskeletal and monolayer stability. We concluded
that 1) NF-kappaB is required for oxidant-induced iNOS
upregulation and for the consequent nitration and
oxidation of cytoskeleton; 2) NF-kappaB activation
causes cytoskeletal injury following upregulation of
NO-driven processes; and 3) the molecular event
underlying the destabilizing effects of NF-kappaB
appears to be increases in carbonylation and
nitrotyrosination of the subunit components of
cytoskeleton. The ability to promote NO overproduction
and cytoskeletal nitration/oxidation is a novel
mechanism not previously attributed to NF-kappaB in
cells.

Free Radic Biol Med. 2003 Sep 15;35(6):636-47.       
 
Arachidonic acid activates a functional AP-1 and an inactive NF-kappaB
complex in human HepG2 hepatoma cells.

Becuwe P, Bianchi A, Didelot C, Barberi-Heyob M, Dauca M.

Laboratoire de Biologie Cellulaire du Developpement, EA 3446,
Universite Henri Poincare-Nancy I, Vandoeuvre-les-Nancy Cedex, France.
becuwe@scbiol.u-nancy.fr

Exogenous arachidonic acid (AA) has been shown to induce the
antioxidant manganese superoxide dismutase gene by reactive oxygen
species (ROS) derived from AA metabolism and the participation of the
p38 mitogen-activated protein kinase (MAPK) pathway in human HepG2
hepatoma cells. The goal of this study was to investigate the effect
of AA on the activation of the two redox-sensitive transcription
factors AP-1 and NF-kappaB in HepG2 cells. Using electrophoretic
mobility shift assays, DNA-binding activities of AP-1 and NF-kappaB
were markedly increased in AA-treated HepG2 cells. The c-Jun and c-Fos
proteins were identified as components of the AA-induced AP-1 complex
and their levels were increased. AA-activated NF-kappaB complex was
constituted as a p50 homodimer resulting in a nuclear translocation
for this protein only. Moreover, no degradation of IkappaBalpha was
observed. These results were contrasted to the
interleukin-1beta-activated p50/p65 complex used as a positive
control. Using 5,8,11,14-eicosatetraynoic acid and inhibitors of AA
metabolism, AP-1 and NF-kappaB activation required the
lipoxygenase/cytochrome P450 monooxygenase pathways. In addition,
antioxidants inhibited the AA-induced AP-1 and NF-kappaB activation,
suggesting a role of ROS released from the AA metabolism. In reporter
gene assays, AA induced the transcriptional activity of AP-1 but not
that of NF-kappaB. Further investigations showed that the AA-induced
transcriptional activity of AP-1 was regulated by protein kinase C and
p38 MAPK pathways. These results suggest that the functional AP-1
activated by AA and coupled to that of p38 MAPK pathway may play an
important role in response to ROS induced by AA metabolism in HepG2
cells without the involvement of the NF-kappaB pathway.

Prostaglandins Other Lipid Mediat. 2003 Jul;71(3-4):189-204.       

Platelet-type 12-lipoxygenase activates NF-kappaB in prostate cancer
cells.

Kandouz M, Nie D, Pidgeon GP, Krishnamoorthy S, Maddipati KR, Honn KV.

Department of Radiation Oncology, Wayne State University, 431
Chemistry Bldg., Detroit, MI 48202, USA.

Platelet-type arachidonate 12-lipoxygenase (12-LOX) is highly
expressed in many types of cancers and plays an important role in
cancer pathophysiology. Arachidonic acid metabolism by 12-LOX results
in the stable end product 12(S)-hydroxy eicosatetraenoic acid
(12(S)-HETE), which is a signaling molecule with effects on cell
proliferation, motility, invasiveness, angiogenesis, and inhibition of
apoptosis. The myriad biological activities manifested by 12(S)-HETE
appear to be mediated, at least in part, by the activation of
NF-kappaB. Overexpression of the 12-LOX in PC-3 prostate cancer cells
resulted in the constitutive activation of the transcription factor.
The enzymatic product of arachidonic acid metabolism, 12(S)-HETE,
mediates the activation of NF-kappaB by the 12-LOX. 12(S)-HETE
treatment of PC-3 cells induced the degradation of IkappaB by the S6
proteasomal pathway and the activated NF-kappaB translocated to the
nucleus causing kappaB-induced transcription. Specificity of the
NF-kappaB activation by 12(S)-HETE was established by the use of a
12-LOX-specific inhibitor and 13(S)-HODE, a known 12(S)-HETE
antagonist. Considering the known involvement of MAP kinase pathway in
NF-kappaB activation and that of 12(S)-HETE in MAP kinase pathway,
12-LOX present in prostate cancer tissues may contribute to the
constitutive activation of NF-kappaB in prostate cancer cells.

More of these kinds of studies are published each week, just go to
www.pubmed.com and see for yourself.

Finally, I’ve already acknowledged in a previous post that
saying Mead acid was a MUFA instead of saying it was derived from a
MUFA was a mistake.  Yes, even I make mistakes trying to write as much
as I can in the little time that I have, though I’m willing to
admit it, unlike, apparently, anyone else in this country.  Or you can
just listen to Mr. Hoover.  He’s always right, even though he
has little interest in citing evidence, and when he does, I absolutely
tear it apart, piece by piece.  He's got nothing, as they say, except
perhaps, a mountain of agressive ignorance.