Essential Fatty Acid Metabolism

The more interesting issue is who in the world decided that these
extremely dangerous substances are "essential?" Fortunately, I
learned to stay away from dietary polyunsaturated fatty acids a few
years back. To all those who haven't, good luck - you're going to
need it.

"MikeV" <[email hidden]> wrote in message news:<[email hidden]>...

Quoted message said:

Another in depth review for anyone interested. (44 pages; 300+ refs)

http://www.ub.rug.nl/eldoc/dis/medicine/e.n.smit/c1.pdf

MikeV

Certain polyunsaturated fatty acids are essential but
one doesn't need large amounts. One does well to
avoid fats in general unless it is with the seed, grain,
nut, or meat it comes in. Both human infants and
lab animals can be deficient in linoleic acid which results
in dermatitis, poor growth, reproductive failure, and fatty
livers. Deficiency in linolenic acid results in adverse
changes in nervous system function. Omega 3 deficiency
can result in learning deficits and impaired vision.

One textbook says the 'optimal intake of omega-3 fatty
acids is 1.1 to 1.5 grams per day with a ratio of 4 to 10
times more of the omega 6 fatty acids'. If you suspect that
the ratio is better closer to 4 to 1 the amount are rather small.
Trans fatty acids impair the desaturation and elongation of
linoleic and linolenic acid into other critical fatty acids.
So eat some walnuts, filbert, sunflower seeds, pumpkin
seeds, almonds, flax seed, and then some oily deep sea fish,
legumes, green leafy vegetables and you'll be fine.
Cooking with oils, lard, bacon fat, hydrogenated grease
is not a wise idea. Often one heats the oils and fat to high
heat which oxidizes the fats, results in some trans fats, and forms
some toxic chemicals in the food. Oil are often stripped
of a large share of the related antioxidants found in unrefined
fatty foods.

I suspect I do better when I avoid too regular consumption of
beef and pork. I doubt baked goods with unsaturated fatty acids
are that good. Fish at least several time a week is good.
Freshly shelled nuts are much better than raw nuts which are
much better than roasted nuts.

Skip the griddle cakes and bacon in the morning.
Minimize the mayo on the lunch time sandwich.
Don't deep fry dinner.

Boil and poach when you can.
Raw is good.
I suspect the occasional use of saturated fats in some
cooking is moderately less dangerous the cooking with
high polyun oils provided the former isn't a daily habit.

"montygram" <[email hidden]> wrote in message
news:[email hidden]...

Quoted message said:

The more interesting issue is who in the world decided that these
extremely dangerous substances are "essential?" Fortunately, I
learned to stay away from dietary polyunsaturated fatty acids a few
years back. To all those who haven't, good luck - you're going to
need it.

"MikeV" <[email hidden]> wrote in message

news:<[email hidden]>...

Quoted message said:

Quoted message said:

Another in depth review for anyone interested. (44 pages; 300+ refs)

http://www.ub.rug.nl/eldoc/dis/medicine/e.n.smit/c1.pdf

MikeV

Thanks for the tip.
You should tell the creator, so that she/he will not make any more
brains with DHA, nor put it into the milk of young mothers feeding
their infants all over the world.
What do your brain cells use?
Have you found a reliable substitute for membranes? If so it is your
duty to pass it on to us all.!
After many years ingesting these HAZMATS my doctor insists that I am
still fit and healthy and refuses to treat me for it. Please tell
him too. He and "Big Pharma" may need a whole new approach.

Hurry....Hurry.......wife ..and...I ...late
.....sixties.....not....much.....time......left.
(Exits quickly stage left).

MikeV

Sorry, People, my aging sense of humor has been critically damaged
by gorging on black walnuts.
Can't you see the headlines?
"Omega 3 police raid Wal-Mart seeking Christmas Nuts."
"Osama shipping Hazardous Flax-seed Materials (HFM) to US.
Undetected in shipping Container."
"Nuts banned on Nutrition news-group."
Maybe Ashcroft should come back. :-(

MikeV
(Just like old times, Nick :-))

"montygram" <[email hidden]> wrote in message
news:[email hidden]...

Quoted message said:

The more interesting issue is who in the world decided that these
extremely dangerous substances are "essential?" Fortunately, I
learned to stay away from dietary polyunsaturated fatty acids a
few
years back. To all those who haven't, good luck - you're going to
need it.

"MikeV" <[email hidden]> wrote in message
news:<[email hidden]>...

Quoted message said:

Another in depth review for anyone interested. (44 pages; 300+
refs)

http://www.ub.rug.nl/eldoc/dis/medicine/e.n.smit/c1.pdf

MikeV

"montygram" <[email hidden]> wrote in message
news:[email hidden]...

Quoted message said:

The more interesting issue is who in the world decided that these
extremely dangerous substances are "essential?" Fortunately, I
learned to stay away from dietary polyunsaturated fatty acids a few
years back. To all those who haven't, good luck - you're going to
need it.

Why don't you tell us all about Mead's acid again? First, explain how
5,8,11-eicosatrienoic (20:3?9), also known as Mead's acid, is a MUFA (as you have
repetitively asserted), and how it is that this marker of essential fatty acid
deficiency is beneficial for health?

Lar

"montygram" <[email hidden]> wrote in message
news:[email hidden]...

Quoted message said:

who in the world decided that these extremely dangerous
substances are "essential?" >

Quoted message said:

"MikeV" <[email hidden]> wrote in message
news:<[email hidden]>...

Quoted message said:

Another in depth review for anyone interested. (44 pages; 300+
refs)

http://www.ub.rug.nl/eldoc/dis/medicine/e.n.smit/c1.pdf

MikeV

Look it up. There are plenty of references out there.
People like: AA Spector, and LS Harbige, I imagine:

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. [email hidden]

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.

Publication Types:
a.. Review
b.. Review, Tutorial

MeSH Terms:
a.. Animals
b.. Dietary Fats
c.. Fatty Acids, Essential/pharmacology
d.. Fatty Acids, Essential/physiology*
e.. Fatty Acids, Unsaturated/pharmacology
f.. Fatty Acids, Unsaturated/physiology*
g.. Human
h.. Signal Transduction
i.. Support, U.S. Gov't, P.H.S.

Substances:
a.. Dietary Fats
b.. Fatty Acids, Essential
c.. Fatty Acids, Unsaturated

Grant Support:
a.. CA 66081/CA/NCI
b.. HL 49264/HL/NHLBI

PMID: 10419080 [PubMed - indexed for MEDLINE]

Lipids. 2003 Apr;38(4):323-41. Related Articles, Links

Fatty acids, the immune response, and autoimmunity: a question of
n-6 essentiality and the balance between n-6 and n-3.

Harbige LS.

School of Chemical and Life Sciences, University of Greenwich at
Medway, Chatham Maritime, Kent ME4 4TB, United Kingdom.
[email hidden]

The essentiality of n-6 polyunsaturated fatty acids (PUFA) is
described in relation to a thymus/thymocyte accretion of arachidonic
acid (20:4n-6, AA) in early development, and the high requirement of
lymphoid and other cells of the immune system for AA and linoleic
acid (1 8:2n-6, LA) for membrane phospholipids. Low n-6 PUFA intakes
enhance whereas high intakes decrease certain immune functions.
Evidence from in vitro and in vivo studies for a role of AA
metabolites in immune cell development and functions shows that they
can limit or regulate cellular immune reactions and can induce
deviation toward a T helper (Th)2-like immune response. In contrast
to the effects of the oxidative metabolites of AA, the longer-chain
n-6 PUFA produced by gamma-linolenic acid (18:3n-6, GLA) feeding
decreases the Th2 cytokine and immunoglobulin (Ig)G1 antibody
response. The n-6 PUFA, GLA, dihomo-gamma-linolenic acid (20:3n-6,
DHLA) and AA, and certain oxidative metabolites of AA can also
induce T-regulatory cell activity, e.g., transforming growth factor
(TGF)-beta-producing T cells; GLA feeding studies also demonstrate
reduced proinflammatory interleukin (IL)-1 and tumor necrosis factor
(TNF)-alpha production. Low intakes of long-chain n-3 fatty acids
(fish oils) enhance certain immune functions, whereas high intakes
are inhibitory on a wide range of functions, e.g., antigen
presentation, adhesion molecule expression, Th1 and Th2 responses,
proinflammatory cytokine and eicosanoid production, and they induce
lymphocyte apoptosis. Vitamin E has a demonstrable critical role in
long-chain n-3 PUFA interactions with immune functions, often
reversing the effects of fish oil. The effect of dietary fatty acids
on animal autoimmune disease models depends on both the autoimmune
model and the amount and type of fatty acids fed. Diets low in fat,
essential fatty acid deficient (EFAD), or high in long-chain n-3
PUFA from fish oils increase survival and reduce disease severity in
spontaneous autoantibody-mediated disease, whereas high-fat LA-rich
diets increase disease severity. In experimentally induced T
cell-mediated autoimmune disease, EFAD diets or diets supplemented
with long-chain n-3 PUFA augment disease, whereas n-6 PUFA prevent
or reduce the severity. In contrast, in both T cell- and
antibody-mediated autoimmune disease, the desaturated/elongated
metabolites of LA are protective. PUFA of both the n-6 and n-3
families are clinically useful in human autoimmune-inflammatory
disorders, but the precise mechanisms by which these fatty acids
exert their clinical effects are not well understood. Finally, the
view that all n-6 PUFA are proinflammatory requires revision, in
part, and their essential regulatory and developmental role in the
immune system warrants appreciation.

a..

PMID: 12848277 [PubMed - indexed for MEDLINE]

MikeV

Go ahead and cite any evidence you want. I'll take a look at it. One
guy put up a web site with over 300 studies supposedly "proving" that
PUFAs are essential. All he actually did demonstrate is that omega 3s
interfere with omega 6s. But it is true that pregnant women may need
small amounts, which would explain the strange dietary urges. I'm
talking about adults who don't want to get pregnant (or like men,
can't). Aside from researching the evidence for the past 4 years, I
have my family history. Nobody eats omega 3s. My great grandfather
lived to be over 100, and my great grandmother was 97. My grandfather
is in his early 90s now, and my grandmother in her mid 80s. They eat
no omega 3s at all. They only eat at home, and I've gone through
everything they've eaten for their entire lives. They are in very
good health. If PUFAs are essential, they appear to be selectively
so. Only a few people I know eat even small amounts of omega 3s. The
whole thing goes back to a flawed experiment, Burr & Burr, 1930. Just
another example of the pathetic biomedical "profession." How's the
war on cancer going? It's past the thirty years war, and now going
for the hundred year's war. I have no doubts it will pass that
milestone by plenty. These people are really trustworthy - in my
dreams, perhaps.

"MikeV" <[email hidden]> wrote in message news:<[email hidden]>...

Quoted message said:

"montygram" <[email hidden]> wrote in message
news:[email hidden]...

Quoted message said:

who in the world decided that these extremely dangerous
substances are "essential?" >

Quoted message said:

"MikeV" <[email hidden]> wrote in message
news:<[email hidden]>...

Quoted message said:

Another in depth review for anyone interested. (44 pages; 300+
refs)

http://www.ub.rug.nl/eldoc/dis/medicine/e.n.smit/c1.pdf

MikeV

Look it up. There are plenty of references out there.
People like: AA Spector, and LS Harbige, I imagine:

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. [email hidden]

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.

Publication Types:
a.. Review
b.. Review, Tutorial

MeSH Terms:
a.. Animals
b.. Dietary Fats
c.. Fatty Acids, Essential/pharmacology
d.. Fatty Acids, Essential/physiology*
e.. Fatty Acids, Unsaturated/pharmacology
f.. Fatty Acids, Unsaturated/physiology*
g.. Human
h.. Signal Transduction
i.. Support, U.S. Gov't, P.H.S.

Substances:
a.. Dietary Fats
b.. Fatty Acids, Essential
c.. Fatty Acids, Unsaturated

Grant Support:
a.. CA 66081/CA/NCI
b.. HL 49264/HL/NHLBI

PMID: 10419080 [PubMed - indexed for MEDLINE]

Lipids. 2003 Apr;38(4):323-41. Related Articles, Links

Fatty acids, the immune response, and autoimmunity: a question of
n-6 essentiality and the balance between n-6 and n-3.

Harbige LS.

School of Chemical and Life Sciences, University of Greenwich at
Medway, Chatham Maritime, Kent ME4 4TB, United Kingdom.
[email hidden]

The essentiality of n-6 polyunsaturated fatty acids (PUFA) is
described in relation to a thymus/thymocyte accretion of arachidonic
acid (20:4n-6, AA) in early development, and the high requirement of
lymphoid and other cells of the immune system for AA and linoleic
acid (1 8:2n-6, LA) for membrane phospholipids. Low n-6 PUFA intakes
enhance whereas high intakes decrease certain immune functions.
Evidence from in vitro and in vivo studies for a role of AA
metabolites in immune cell development and functions shows that they
can limit or regulate cellular immune reactions and can induce
deviation toward a T helper (Th)2-like immune response. In contrast
to the effects of the oxidative metabolites of AA, the longer-chain
n-6 PUFA produced by gamma-linolenic acid (18:3n-6, GLA) feeding
decreases the Th2 cytokine and immunoglobulin (Ig)G1 antibody
response. The n-6 PUFA, GLA, dihomo-gamma-linolenic acid (20:3n-6,
DHLA) and AA, and certain oxidative metabolites of AA can also
induce T-regulatory cell activity, e.g., transforming growth factor
(TGF)-beta-producing T cells; GLA feeding studies also demonstrate
reduced proinflammatory interleukin (IL)-1 and tumor necrosis factor
(TNF)-alpha production. Low intakes of long-chain n-3 fatty acids
(fish oils) enhance certain immune functions, whereas high intakes
are inhibitory on a wide range of functions, e.g., antigen
presentation, adhesion molecule expression, Th1 and Th2 responses,
proinflammatory cytokine and eicosanoid production, and they induce
lymphocyte apoptosis. Vitamin E has a demonstrable critical role in
long-chain n-3 PUFA interactions with immune functions, often
reversing the effects of fish oil. The effect of dietary fatty acids
on animal autoimmune disease models depends on both the autoimmune
model and the amount and type of fatty acids fed. Diets low in fat,
essential fatty acid deficient (EFAD), or high in long-chain n-3
PUFA from fish oils increase survival and reduce disease severity in
spontaneous autoantibody-mediated disease, whereas high-fat LA-rich
diets increase disease severity. In experimentally induced T
cell-mediated autoimmune disease, EFAD diets or diets supplemented
with long-chain n-3 PUFA augment disease, whereas n-6 PUFA prevent
or reduce the severity. In contrast, in both T cell- and
antibody-mediated autoimmune disease, the desaturated/elongated
metabolites of LA are protective. PUFA of both the n-6 and n-3
families are clinically useful in human autoimmune-inflammatory
disorders, but the precise mechanisms by which these fatty acids
exert their clinical effects are not well understood. Finally, the
view that all n-6 PUFA are proinflammatory requires revision, in
part, and their essential regulatory and developmental role in the
immune system warrants appreciation.

a..

PMID: 12848277 [PubMed - indexed for MEDLINE]

MikeV

"Larry Hoover" <[email hidden]> wrote in message news:<[email hidden]>...

Quoted message said:

"montygram" <[email hidden]> wrote in message
news:[email hidden]...

Quoted message said:

The more interesting issue is who in the world decided that these
extremely dangerous substances are "essential?" Fortunately, I
learned to stay away from dietary polyunsaturated fatty acids a few
years back. To all those who haven't, good luck - you're going to
need it.

Why don't you tell us all about Mead's acid again? First, explain how
5,8,11-eicosatrienoic (20:3?9), also known as Mead's acid, is a MUFA (as you have
repetitively asserted), and how it is that this marker of essential fatty acid
deficiency is beneficial for health?

Lar

Well lets see. He has eliminated "essential fatty acids" from his
diet and has for several years yet he is not only not dead (which you
would assume would be the case since they are supposedly essential)
but he is in better health than he was before. It seems like you are
the one who has some explaining to do. Then again you do not address
realities that contradict your assumptions do you.

"montygram" <[email hidden]> wrote in message
news:[email hidden]...

Quoted message said:

Go ahead and cite any evidence you want. I'll take a look at it.
One
guy put up a web site with over 300 studies supposedly "proving"
that
PUFAs are essential. All he actually did demonstrate is that
omega 3s
interfere with omega 6s. But it is true that pregnant women may
need
small amounts, which would explain the strange dietary urges. I'm
talking about adults who don't want to get pregnant (or like men,
can't). Aside from researching the evidence for the past 4 years,
I
have my family history. Nobody eats omega 3s. My great
grandfather
lived to be over 100, and my great grandmother was 97. My
grandfather
is in his early 90s now, and my grandmother in her mid 80s. They
eat
no omega 3s at all. They only eat at home, and I've gone through
everything they've eaten for their entire lives. They are in very
good health. If PUFAs are essential, they appear to be
selectively
so. Only a few people I know eat even small amounts of omega 3s.
The
whole thing goes back to a flawed experiment, Burr & Burr, 1930.
Just
another example of the pathetic biomedical "profession." How's
the
war on cancer going? It's past the thirty years war, and now
going
for the hundred year's war. I have no doubts it will pass that
milestone by plenty. These people are really trustworthy - in my
dreams, perhaps.

"MikeV" <[email hidden]> wrote in message
news:<[email hidden]>...

Quoted message said:

"montygram" <[email hidden]> wrote in message
news:[email hidden]...

Quoted message said:

who in the world decided that these extremely dangerous
substances are "essential?" >

Quoted message said:

"MikeV" <[email hidden]> wrote in message
news:<[email hidden]>...
> Another in depth review for anyone interested. (44 pages; 300+
> refs)
>
> http://www.ub.rug.nl/eldoc/dis/medicine/e.n.smit/c1.pdf
>
> MikeV

Look it up. There are plenty of references out there.
People like: AA Spector, and LS Harbige, I imagine:

Quoted message said:

Quoted message said:

PMID: 10419080 [PubMed - indexed for MEDLINE]

PMID: 12848277 [PubMed - indexed for MEDLINE]

MikeV

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

I should have mentioned that if you go to www.pubmed.com and look up
arachidonic, lipid peroxidation, oxidative stress, etc., you'll see
how dangerous PUFAs can be. I've haven't seen any evidence that
demonstrates that allowing your body to make it's own PUFA, the Mead
acid, will harm an adult human. On the contrary, Mead acid, a very
stable fatty acid relative to dietary PUFAs, has been shown to
attenuate conditions caused by excess arachidonic acid. Recently, AD
researchers have drained the CSF out of AD patients, and found
isoprostanes in very high amounts. Then you read studies such as the
following, and you realize that the high dietary PUFA consumption of
the past 30 years or so is likely the root cause of so many "chronic
diseases."

Journal of Neurochemistry
Volume 72 Issue 2 Page 734 - February 1999
doi:10.1046/j.1471-4159.1999.0720734.x

F4 - Isoprostanes as Specific Marker of Docosahexaenoic Acid
Peroxidation in Alzheimer's Disease
Jaffar Nourooz-Zadeh, Edwin H. C. Liu*, B. Yhlen, Erik E. Änggåard &
Barry Halliwell*

Abstract : F2-isoprostanes are prostaglandin-like compounds derived
from free radical-catalysed peroxidation of arachidonic acid.
Peroxidation of eicosapentaenoic acid produces F3-isoprostanes,
whereas peroxidation of docosahexaenoic acid would give
F4-isoprostanes. This study demonstrates the presence of esterified
F4-isoprostanes in human brain and shows that levels are elevated in
certain brain cortex regions in Alzheimer's disease. Our data with
Alzheimer's disease suggest that analysis of F4-isoprostanes will
provide new opportunities to study lipid peroxidation in the
neurodegenerative diseases.

"MikeV" <[email hidden]> wrote in message news:<[email hidden]>...

Quoted message said:

"montygram" <[email hidden]> wrote in message
news:[email hidden]...

Quoted message said:

who in the world decided that these extremely dangerous
substances are "essential?" >

Quoted message said:

"MikeV" <[email hidden]> wrote in message
news:<[email hidden]>...

Quoted message said:

Another in depth review for anyone interested. (44 pages; 300+
refs)

http://www.ub.rug.nl/eldoc/dis/medicine/e.n.smit/c1.pdf

MikeV

Look it up. There are plenty of references out there.
People like: AA Spector, and LS Harbige, I imagine:

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. [email hidden]

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.

Publication Types:
a.. Review
b.. Review, Tutorial

MeSH Terms:
a.. Animals
b.. Dietary Fats
c.. Fatty Acids, Essential/pharmacology
d.. Fatty Acids, Essential/physiology*
e.. Fatty Acids, Unsaturated/pharmacology
f.. Fatty Acids, Unsaturated/physiology*
g.. Human
h.. Signal Transduction
i.. Support, U.S. Gov't, P.H.S.

Substances:
a.. Dietary Fats
b.. Fatty Acids, Essential
c.. Fatty Acids, Unsaturated

Grant Support:
a.. CA 66081/CA/NCI
b.. HL 49264/HL/NHLBI

PMID: 10419080 [PubMed - indexed for MEDLINE]

Lipids. 2003 Apr;38(4):323-41. Related Articles, Links

Fatty acids, the immune response, and autoimmunity: a question of
n-6 essentiality and the balance between n-6 and n-3.

Harbige LS.

School of Chemical and Life Sciences, University of Greenwich at
Medway, Chatham Maritime, Kent ME4 4TB, United Kingdom.
[email hidden]

The essentiality of n-6 polyunsaturated fatty acids (PUFA) is
described in relation to a thymus/thymocyte accretion of arachidonic
acid (20:4n-6, AA) in early development, and the high requirement of
lymphoid and other cells of the immune system for AA and linoleic
acid (1 8:2n-6, LA) for membrane phospholipids. Low n-6 PUFA intakes
enhance whereas high intakes decrease certain immune functions.
Evidence from in vitro and in vivo studies for a role of AA
metabolites in immune cell development and functions shows that they
can limit or regulate cellular immune reactions and can induce
deviation toward a T helper (Th)2-like immune response. In contrast
to the effects of the oxidative metabolites of AA, the longer-chain
n-6 PUFA produced by gamma-linolenic acid (18:3n-6, GLA) feeding
decreases the Th2 cytokine and immunoglobulin (Ig)G1 antibody
response. The n-6 PUFA, GLA, dihomo-gamma-linolenic acid (20:3n-6,
DHLA) and AA, and certain oxidative metabolites of AA can also
induce T-regulatory cell activity, e.g., transforming growth factor
(TGF)-beta-producing T cells; GLA feeding studies also demonstrate
reduced proinflammatory interleukin (IL)-1 and tumor necrosis factor
(TNF)-alpha production. Low intakes of long-chain n-3 fatty acids
(fish oils) enhance certain immune functions, whereas high intakes
are inhibitory on a wide range of functions, e.g., antigen
presentation, adhesion molecule expression, Th1 and Th2 responses,
proinflammatory cytokine and eicosanoid production, and they induce
lymphocyte apoptosis. Vitamin E has a demonstrable critical role in
long-chain n-3 PUFA interactions with immune functions, often
reversing the effects of fish oil. The effect of dietary fatty acids
on animal autoimmune disease models depends on both the autoimmune
model and the amount and type of fatty acids fed. Diets low in fat,
essential fatty acid deficient (EFAD), or high in long-chain n-3
PUFA from fish oils increase survival and reduce disease severity in
spontaneous autoantibody-mediated disease, whereas high-fat LA-rich
diets increase disease severity. In experimentally induced T
cell-mediated autoimmune disease, EFAD diets or diets supplemented
with long-chain n-3 PUFA augment disease, whereas n-6 PUFA prevent
or reduce the severity. In contrast, in both T cell- and
antibody-mediated autoimmune disease, the desaturated/elongated
metabolites of LA are protective. PUFA of both the n-6 and n-3
families are clinically useful in human autoimmune-inflammatory
disorders, but the precise mechanisms by which these fatty acids
exert their clinical effects are not well understood. Finally, the
view that all n-6 PUFA are proinflammatory requires revision, in
part, and their essential regulatory and developmental role in the
immune system warrants appreciation.

a..

PMID: 12848277 [PubMed - indexed for MEDLINE]

MikeV

Quoted message said:

is in his early 90s now, and my grandmother in her mid 80s. They eat
no omega 3s at all.

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

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

Mirek

"Wolfbrother" <[email hidden]> wrote in message
news:[email hidden]...

Quoted message said:

"Larry Hoover" <[email hidden]> wrote in message
news:<[email hidden]>...

Quoted message said:

"montygram" <[email hidden]> wrote in message
news:[email hidden]...

Quoted message said:

The more interesting issue is who in the world decided that these
extremely dangerous substances are "essential?" Fortunately, I
learned to stay away from dietary polyunsaturated fatty acids a few
years back. To all those who haven't, good luck - you're going to
need it.

Why don't you tell us all about Mead's acid again? First, explain how
5,8,11-eicosatrienoic (20:3?9), also known as Mead's acid, is a MUFA (as you have
repetitively asserted), and how it is that this marker of essential fatty acid
deficiency is beneficial for health?

Lar

Well lets see. He has eliminated "essential fatty acids" from his
diet and has for several years yet he is not only not dead (which you
would assume would be the case since they are supposedly essential)
but he is in better health than he was before.

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

Quoted message said:

It seems like you are
the one who has some explaining to do.

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.

Quoted message said:

Then again you do not address
realities that contradict your assumptions do you.

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

"montygram" <[email hidden]> wrote in message
news:[email hidden]...

Quoted message said:

Go ahead and cite any evidence you want. I'll take a look at it. One
guy put up a web site with over 300 studies supposedly "proving" that
PUFAs are essential.

http://books.nap.edu/books/0309085373/html/609.html#pagetop

Such studies as the one you cited below does not address the central
issue: can you have better health if you avoid PUFAs in the diet and
allow your body to make the Mead acid PUFA out of the MUFAs that are
already there (and which can be made intially from SFAs). No
experiment has been done to demonstrate this, but plenty of studies
show that Mead acid has beneficial effects, whereas arachidonic acid
is like a slow poison, which really begins to rip your body up once
your body loses the antioxidant protection of young adulthood. Don't
believe me or the thousands of studies? Who cares - go ahead and deal
with the consequences.

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. [email hidden]

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.

"MikeV" <[email hidden]> wrote in message news:<[email hidden]>...

Quoted message said:

"montygram" <[email hidden]> wrote in message
news:[email hidden]...

Quoted message said:

Go ahead and cite any evidence you want. I'll take a look at it.
One
guy put up a web site with over 300 studies supposedly "proving"
that
PUFAs are essential. All he actually did demonstrate is that
omega 3s
interfere with omega 6s. But it is true that pregnant women may
need
small amounts, which would explain the strange dietary urges. I'm
talking about adults who don't want to get pregnant (or like men,
can't). Aside from researching the evidence for the past 4 years,
I
have my family history. Nobody eats omega 3s. My great
grandfather
lived to be over 100, and my great grandmother was 97. My
grandfather
is in his early 90s now, and my grandmother in her mid 80s. They
eat
no omega 3s at all. They only eat at home, and I've gone through
everything they've eaten for their entire lives. They are in very
good health. If PUFAs are essential, they appear to be
selectively
so. Only a few people I know eat even small amounts of omega 3s.
The
whole thing goes back to a flawed experiment, Burr & Burr, 1930.
Just
another example of the pathetic biomedical "profession." How's
the
war on cancer going? It's past the thirty years war, and now
going
for the hundred year's war. I have no doubts it will pass that
milestone by plenty. These people are really trustworthy - in my
dreams, perhaps.

"MikeV" <[email hidden]> wrote in message
news:<[email hidden]>...

Quoted message said:

"montygram" <[email hidden]> wrote in message
news:[email hidden]...

> who in the world decided that these extremely dangerous
> substances are "essential?" >

> "MikeV" <[email hidden]> wrote in message
> news:<[email hidden]>...
>> Another in depth review for anyone interested. (44 pages; 300+
>> refs)
>>
>> http://www.ub.rug.nl/eldoc/dis/medicine/e.n.smit/c1.pdf
>>
>> MikeV
Look it up. There are plenty of references out there.
People like: AA Spector, and LS Harbige, I imagine:

Quoted message said:

Quoted message said:

PMID: 10419080 [PubMed - indexed for MEDLINE]

PMID: 12848277 [PubMed - indexed for MEDLINE]

MikeV

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

"montygram" <[email hidden]> wrote in message
news:[email hidden]...

Quoted message said:

Such studies as the one you cited below does not address the
central
issue: can you have better health if you avoid PUFAs in the diet
and
allow your body to make the Mead acid PUFA out of the MUFAs that
are
already there (and which can be made intially from SFAs). No
experiment has been done to demonstrate this, but plenty of
studies
show that Mead acid has beneficial effects, whereas arachidonic
acid
is like a slow poison, which really begins to rip your body up
once
your body loses the antioxidant protection of young adulthood.
Don't
believe me or the thousands of studies? Who cares - go ahead and
deal
with the consequences.

Obviously you do! You care about being right, and being some sort of
guru.
I care about the best route to the truth. At the moment, the
preponderance of the evidence does not appear to support you.

Having made it to my age in close to perfect health, perhaps you can
advise me when I should expect the dreadful consequences to be
visited upon me? 80? 90? 105? (Naturally, I would like to get my
affairs in order).

Speaking of central issues, is it your position that your brain (and
most other peoples) is not largely formed of DHA? That there is not
an optimal level of DHA in the phospholipids of your muscle cell
membranes to minimize diabetes risk? That there is not a level of
DHA at which fetuses and babies thrive optimally?
I have seen and cited evidence for all of those. None from you in
rebuttal.

Can you cite evidence that I absorb excessive quantities of w6?

Somehow you always seem to avoid the issue of how humans survived
pre-farming diets which included much higher than present day levels
of 'poisonous' ALA, DHA, EPA. etc. if you and Gilbert are correct.
If you want to educate us, the ignorant masses, explain that first.

There are not too many of us who argue against the propositions that
modern diets contain excessive vegetable oils, or that excessive
amounts, especially of w6 will bias the immune system towards
inflammation, or that they can become oxidized, and produce free
radicals. These are established.
Nick, the world does not only come in black and white. The real one
has finely graded shades of gray, and a whole lot of other hues
besides.
Nature has dealt with PUFAs for 20 million years. How come you
can't?

MikeV

"montygram" <[email hidden]> wrote in message
news:[email hidden]...

Quoted message said:

Aside from researching the evidence for the past 4 years, I
have my family history.

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.

Quoted message said:

Just another example of the pathetic biomedical "profession."

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

"Larry Hoover" <[email hidden]> wrote in message
news:[email hidden]...

Quoted message said:

"montygram" <[email hidden]> wrote in message
news:[email hidden]...

Quoted message said:

Aside from researching the evidence for the past 4 years, I
have my family history.

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.

Quoted message said:

Just another example of the pathetic biomedical "profession."

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

Larry:
Thanks a bundle for the book references. I have just skimmed them,
and they provide an excellent baseline for an amateur (me) to start
from. Fortunately they confirm much of what I have struggled to pick
up from studies and other sources.
When you get time I would like to ask that you attempt to summarize
Nick's (Monty's) philosophy, and show what (if any parts of it are
soundly based, and where he starts going wrong. I need help! On
second thoughts, I doubt it could be worth your time.
Thanks again
MikeV

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. [email hidden]

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

Journal of the American College of Nutrition, Vol. 21, No. 6,
495-505 (2002)
Published by the American College of Nutrition

--------------------------------------------------------------------------

REVIEW

Omega-3 Fatty Acids in Inflammation and Autoimmune Diseases
Artemis P. Simopoulos, MD, FACN
The Center for Genetics, Nutrition and Health, Washington, D.C

Address correspondence to: Artemis P. Simopoulos, M.D., FACN, The
Center for Genetics, Nutrition and Health, 2001 S Street, N.W.,
Suite 530, Washington, D.C., 20009. E-mail: [email hidden]

Conclusions
TOP
ABSTRACT
Introduction
Omega-6 and Omega-3 Fatty...
Omega-3 Fatty Acids, Interleukin...
Other Inflammatory Markers,...
Fatty Acids, Cytokines, and...
Rheumatoid Arthritis
Inflammatory Bowel Disease
Asthma
Psoriasis
Conclusions
REFERENCES

The anti-inflammatory properties of 3 fatty acids, especially EPA,
are due to competition with arachidonic acid (AA) as a substrate for
cyclooxygenases and 5-lipoxygenase. The eicosanoids from the 6 and 3
fatty acids have opposing properties. The eicosanoids are considered
a link between PUFA, inflammation and immunity. In addition to their
effects on prostaglandins, thromboxanes and leukotrienes, 3 fatty
acids suppress the production on interleukin 1 (IL-1ß) by
suppressing the IL-1ß mRNA, as well as the expression of Cox2
(cytooxygenase) mRNA that is induced by IL-1ß. Cox2 is overexpressed
in colon cancer cells. Both ALA, and EPA and DHA are involved in
immune function. The precise effect of ALA depends on the level of
linoleic acid (LA) and total PUFA content of the diet. A high dose
of ALA (about 15 g/day) will suppress human IL-1 and TNF (tumor
necrosis factor). It is unclear whether ALA itself exerts these
effects or whether they are the result of its conversion to EPA.
Excessive intake of 6 fatty acids characteristic of Western diets
produces an imbalance of 6 to 3 PUFAs which leads to an
overproduction of the proinflammatory prostaglandins of the 6 series
and cytokines. Supplements of LA rich vegetable oils increase IL-1
and TNF. Humans given 3-rich flax seed oil or fish oil supplements
have sharply reduced stimulated production of IL-1, IL-2 and TNF, as
well as suppressed mononuclear cell proliferation and expression of
IL-2 receptors. Thus, in humans, LA increases proinflammatory
cytokine secretion, whereas fish oil reduces proinflammatory
cytokine secretion.
*************************************
1: Lipids. 2001 Nov;36(11):1183-93. Related Articles, Links

Influence of dietary supplementation with long-chain n-3 or n-6
polyunsaturated fatty acids on blood inflammatory cell populations
and functions and on plasma soluble adhesion molecules in healthy
adults.

Thies F, Miles EA, Nebe-von-Caron G, Powell JR, Hurst TL, Newsholme
EA, Calder PC.

Department of Biochemistry, University of Oxford, United Kingdom.

Greatly increasing the amounts of flaxseed oil [rich in
alpha-linolenic acid (ALNA)] or fish oil (FO); [rich in
eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)] in the
diet can decrease inflammatory cell functions and so might impair
host defense. The objective of this study was to determine the
effect of dietary supplementation with moderate levels of ALNA,
gamma-linolenic acid (GLA), arachidonic acid (ARA), DHA, or FO on
inflammatory cell numbers and functions and on circulating levels of
soluble adhesion molecules. Healthy subjects aged 55 to 75 yr
consumed nine capsules per day for 12 wk. The capsules contained
placebo oil (an 80:20 mix of palm and sunflowerseed oils) or blends
of placebo oil with oils rich in ALNA, GLA, ARA, or DHA or FO.
Subjects in these groups consumed 2 g ALNA; approximately 700 mg
GLA, ARA, or DHA; or 1 g EPA plus DHA (720 mg EPA + 280 mg DHA)
daily from the capsules. Total fat intake from the capsules was 4 g
per day. None of the treatments affected inflammatory cell numbers
in the bloodstream; neutrophil and monocyte phagocytosis or
respiratory burst in response to E. coli; production of tumor
necrosis factor-alpha, interleukin-1beta, and interleukin-6 in
response to bacterial lipopolysaccharide; or plasma concentrations
of soluble intercellular adhesion molecule-1. In contrast, the ALNA
and FO treatments decreased the plasma concentrations of soluble
vascular cell adhesion molecule-1 (16 and 28% decrease,
respectively) and soluble E-selectin (23 and 17% decrease,
respectively). It is concluded that, in contrast to previous reports
using higher amounts of these fatty acids, a moderate increase in
consumption of long-chain n-6 or n-3 polyunsaturated fatty acids
does not significantly affect inflammatory cell numbers or
neutrophil and monocyte responses in humans and so would not be
expected to cause immune impairment. Furthermore, we conclude that
moderate levels of ALNA and FO, which could be incorporated into the
diet, can decrease some markers of endothelial activation and that
this mechanism of action may contribute to the reported health
benefits of n-3 fatty acids.

Publication Types:
a.. Clinical Trial
b.. Randomized Controlled Trial

PMID: 11795850 [PubMed - indexed for MEDLINE]
****************************************

1: Nutr Metab Cardiovasc Dis. 2004 Aug;14(4):180-5. Related
Articles, Links

Soluble adhesion molecules in healthy subjects: a dose-response
study using n-3 fatty acids.

Eschen O, Christensen JH, De Caterina R, Schmidt EB.

Department of Cardiology, Aalborg Hospital, Aalborg, Denmark.
[email hidden]

BACKGROUND AND AIM: Long-chain n-3 polyunsaturated fatty acids
(PUFA) may protect against atherosclerotic disease, and serum levels
of soluble cellular adhesion molecules (sCAMs) possibly reflect the
inflammatory process underlying atherosclerosis. We studied the
effect of n-3 PUFA dietary supplementation on the serum levels of
sP-selectin, soluble intercellular adhesion molecule-1 (sICAM-1) and
soluble vascular adhesion molecule-1 (sVCAM-1), and the correlation
between sCAMs and the fatty acid composition of granulocyte
membranes. METHODS AND RESULTS: Sixty healthy volunteers were
randomly assigned to receive a daily supplement of n-3 PUFA 6.6 g,
n-3 PUFA 2.0 g, or olive oil for 12 weeks in a double blind design.
A significant negative correlation was found between serum sICAM-1
levels and the DHA content of granulocyte membranes at entry. After
supplementation with 6.6 g of n-3 PUFA, there was a significant
decrease only in sP-selectin, which a gender subanalysis showed to
be more marked in men. Among the women, there was a significant
decrease in sICAM-1 in the PUFA 2.0 g group and a significant
increase in sVCAM-1 in the PUFA 6.6 g group. CONCLUSIONS: The
results indicate that high-dose supplementation with n-3 PUFA
decreases sP-selectin levels in healthy subjects, thus suggesting a
decrease in platelet reactivity or endothelial activation. However,
the effect of n-3 PUFA on sCAMs is complex and may depend on gender
and n-3 PUFA dose.

PMID: 15553594 [PubMed - in process]

[email hidden] (montygram) wrote in message news:<[email hidden]>...

Quoted message said:

Regarding the study posted:

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

Quoted message said:

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?

Or indeed Mead's acid.

Quoted message said:

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 there aren't enough PUFAs others will be used for membranes.

Quoted message said:

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),

Membrane stiffness is not the same as whole body stiffness. Maybe you
think joints and tendons are made of fat?

Quoted message said:

fall apart literatly (because their cells lack structural
integrity),

Bizarre. Now you're suggested saturated fats have less structural role
than PUFAs, despite packing closer. Or did you mean fall apart like a
book?

Quoted message said:

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.

So the experiment by Burr and Burr using rats is nonsense (your
words), because rats aren't humans, but ones with chickens are fine.
You do realise rats are closer to humans than chickens, right?

Quoted message said:

It is likely that arachidonic acid is not metabolized to omega 6 22
carbon PUFAs because it’s so biochemically unstable.

Define biochemically unstable, for once.

Quoted message said:

The study
is important in that the investigator admits that there is not likely
a unique biochemical need for DHA,

Biochemical is the key word there. DHA is more important as a
structural membrane component than a source of metabolites. EPA on the
other hand has biochemical activity, which is why levels affect mood.

Quoted message said:

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.

I guess you never bothered to read the reference that MikeV started
the thread with. That gives citations of human studies on the effects
of EFA deficiency. This golden fallacy you cling to just doesn't wash.
To save you the effort you never seem to put in anyway, here's a
quote:

"Thirty years later, Hansen et al. [140] were the first to describe
EFAD in
humans. They observed unsatisfactory growth rates and dryness of the
skin in many infants on low LA intakes. EFAD has been most extensively
described in subjects on fat-free total parenteral nutrition (TPN)
[141-147]. For example, O'Neill et al. [142] reported on 28 patients,
ranging from newborns to 66 years old, who received fat-free TPN. LA
levels fell rapidly, followed by AA. In most of the patients the
20:3ω9/20:4ω6 ratio (a biochemical marker for EFAD) had
increased after a few weeks above the 0.4 criterion [148], followed
approximately one week later by clinical signs of a scaly and thin
skin, and hair loss. In addition to these classical EFAD symptoms,
many other biological and behavioural changes have been documented
[149-151]"

Just in case you missed it they said that when the Mead
acid:Arachidonic acid ratio increased (more Mead acid) it led to
clinical signs of scaly thin skin and hair loss. Oh dear.

Quoted message said:

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?

It doesn't, it's the idea that it can do all the things the
metabolites of omega 6 and 3 can do that is the problem. Why has
evolution preserved all the enzymes that make the series 2/3
prostaglandins and series 4/5 leukotrienes (plus their receptors) if
there's no need for them - as you claim?

Quoted message said:

But show me some evidence
that allowing your body to produce its own PUFA is such a terrible
idea –

No-one's ever said that. As usual you're attacking assertions that
haven't been made.

Quoted message said:

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

Who's ever claimed AA was a signal transducer? It's the *result* of
signal transduction (i.e. a 2nd messenger).

Quoted message said:

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:

You think it's good?

Quoted message said:

“The interior of a cell is filled with a gelatinous material
that houses the nucleus, DNA, and protein ‘transcription
factors.’

The nucleus houses the DNA, not the gelatinous material (cytoplasm).

Quoted message said:

These proteins are nothing more than tiny molecular
messengers that can move to the nucleus to stimulate

Or inhibit

Quoted message said:

our DNA to
replicate RNA

RNA isn't replicated it's synthesised (transcribed) from a DNA
template.

Quoted message said:

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.

So would Mead's acid oxidation. All sorts of oxidative stress
stimulate it.

Quoted message said:

"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."
You will not find this type of statement in any physiology or
pathology book anytime soon. Why? I don't know.

Because there's always a lag time between research being published and
it ending up in textbooks. Nothing new there.

Quoted message said:

Nonetheless, we can
see that inflammation is definitively viewed as a driver of chronic
disease.

The Reduction of Inflammation

<snip>

Quoted message said:

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.

Did you miss this paragraph? Hardly supports your view.

Quoted message said:

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.

You've never torn anything apart. Feel free to quote one of your
devastating rebuttals though, if you can find one.

MattLB