- quote -


"Increasing alpha-linolenic acid intake results in an increase in
eicosapentaenoic acid in plasma lipids"

http://www.raysahelian.com/eicosapentaenoic.html

How Eicosapentaenoic acid is made
The main biological role of alpha-linolenic acid (18:3n-3) appears to
be as a precursor for the synthesis of longer chain n-3
polyunsaturated fatty acids (PUFA).
Increasing alphaLNA intake for a period of weeks to months results in
an increase in the proportion of eicosapentaenoic acid (EPA; 20:5n-3)
in plasma lipids, in erythrocytes, leukocytes, platelets and in breast
milk but there is no increase in docosahexaenoic acid (DHA; 22:6n-3),
which may even decline in some pools at high alphaLNA intakes.


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com


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DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk


- quote -

On Nov 10, 4:12 am, Piotr Kasztelowicz <pek...[at]am.torun.pl> wrote:
This can not directly suggest, that vegetarian diet will be effective
to block IL-6. <<

If a fatty acid has been shown to inhibit IL-6 and you ingest
NOTHING .. but .. that fatty acid .. then it wouldn't be too much of a
stretch to .. assume .. that it DOES suggest a vegetarian diet WILL ..
inhibit .. IL-6.

Kinda .. logical ..

Who loves ya.
Tom


Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com


Man Is A Herbivore!
http://tinyurl.com/a3cc3


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk


- quote -

On Thu, 8 Nov 2007, ironjustice wrote:

- quote -

This can not directly suggest, that vegetarian diet will be
effective to block IL-6. This is rather reason to think,
to project trials with monoclonal IL-6-antybodies as
possible treatment option, but from experimental trial
to clinical use is very long way.

P.
--
Piotr Kasztelowicz Piotr.Kasztelowicz[at]am.torun.pl
http://www.am.torun.pl/~pekasz
http://www.am.torun.pl
http://medycyna-i-filozofia.blog.onet.pl/
PGP Key IDs: DH/DSS:0xF3EED8AF

On Nov 9, 6:50 am, ironjustice <ironjust...[at]cashette.com> wrote:

- quote -

Inhibiting the delta-5 desaturase would also inhibit the synthesis of
Mead acid in those "blessed" with it. Not a good idea even in the
case of AA given that the people are not overloaded with it.

Taka

On Nov 9, 9:17 am, ironjustice <ironjust...[at]cashette.com> wrote:
- quote -

Chinese cuisine uses a lot of oil ... which is these days mostly the
refined unsaturated or trans-fat containing suff ...

Taka

On Nov 8, 3:41 pm, monty1...[at]lycos.com wrote:
A study you once cited on "iron overloaded" Asians who didn't have the
iron-related
diseases that were thought to occur at those levels was a clear
indication that dietary iron
is not the most important factor.
<<

Now I wonder where they would get the idea there was no iron-related
diseases when one out of two Asians in China over forty have
osteoarthritis ..

Who loves ya.
Tom


Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com


Man Is A Herbivore!
http://tinyurl.com/a3cc3


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk

"...extensive lipid peroxidation (LP) was detected..."

This seems to be the underlying cause or at least a major factor in
the majority of "diseases" in "civilized societies" today. It is an
easy hypothesis to test, but because saturated fatty acids are
considered "bad," the experiments are not conducted. I determined
that the molecular-level evidence couldn't be any clearer, and so have
eaten a diet much richer in SFAs (relative to UFAs), in terms of
overall calories consumed, for about 6 years now. I've only
experienced benefits from this diet. You seem to think that SFAs are
tied to animal products whereas UFAs are tied to vegetable ones,
though this is couldn't be further from the truth. All naturally-
occurring fat sources have at least some SFAs and some PUFAs. In
biology, what matters is whether or not a threshold is reached. A
chemist named Ottoboni wrote a book called something like, "It's the
Does that Makes the Poison," and this is true for dietary intakes. I
agree that most Westerners are consuming too much iron, but it's the
lipid peroxidation that makes this really dangerous. A study you once
cited on "iron overloaded" Asians who didn't have the iron-related
diseases that were thought to occur at those levels was a clear
indication that dietary iron is not the most important factor.

"n-3 PUFA beneficial effects on several demyelinating diseases"

J Neurosci Res. 2007 Oct 16; [Epub ahead of print] Links
Eicosapentaenoic acid stimulates the expression of myelin proteins in
rat brain.
Salvati S, Natali F, Attorri L, Di Benedetto R, Leonardi F, Di Biase
A, Ferri F, Fortuna S, Lorenzini P, Sanchez M, Ricceri L, Vitelli L.
Department of Food, Nutrition and Health, Istituto Superiore di
Sanità, Rome, Italy.

We have previously demonstrated that, in C6 glioma cells,
eicosapentaenoic acid (EPA) stimulates the expression of proteolipid
protein (PLP) via cAMP-mediated pathways. In this study, we
investigated whether n-3 polyunsaturated fatty acids can affect
myelinogenesis in vivo. A single dose of either EPA or docosahexaenoic
acid (DHA) was injected intracerebroventricularly into 2-day-old rats,
which were then killed after 3 days post-injection (p.i.). Total RNA
was isolated from the medulla, cerebellum, and cortex, and the
expression of myelin-specific mRNAs was analyzed by real-time PCR. The
levels of PLP, myelin basic protein, and myelin oligodendrocyte
protein mRNAs increased in nearly all brain regions of DHA- and EPA-
treated animals, but the effect was more pronounced in EPA-treated
rats. The enhancement in PLP transcript levels was followed by an
increase in PLP translation in EPA-treated rats. A further indicator
of accelerated myelination was the increase in 2'-3'-cyclic nucleotide
3'-phosphodiesterase (CNPase) protein levels. In EPA-treated rats, the
increased expression of myelin genes coincided with a decrease of cAMP-
response element-binding protein (CREB)-DNA binding in the cerebellum
and cortex (1 hr p.i.). After 16 hr, this effect was still present in
the same cerebral regions even though the decrease in EPA-treated rats
was less pronounced than in controls. The down-regulation of CREB
activity was due to a decrease in the levels of CREB phosphorylation.
In conclusion, our data suggest that EPA stimulates the expression of
specific myelin proteins through decreased CREB phosphorylation. These
results corroborate the clinical studies of the n-3 PUFA beneficial
effects on several demyelinating diseases. (c) 2007 Wiley-Liss, Inc.

PMID: 17941053 [PubMed - as supplied by publisher]
------------------------
"The long-chain omega-3 fatty acid eicosapentaenoic acid (EPA) is
derived from alpha-linolenic acid, a shorter-chain member of the same
family."

That means it comes from lecithin which is found in a vegetarian diet
at a high rate .. in fact it pretty much ALL that IS found in the
vegetarian diet.
Different fatty acid intakes results IN .. different fatty acid ..
contents.

It inhibits IL-6 .. which seems to also .. **trigger** ... MS.

"Can displace arachidonic acid"
"The omega-3 fatty acids inhibit the conversion of linoleic acid to
arachidonic acid, thereby reducing the biosynthesis of arachidonic
acid and its eicosanoids"
"Up to 80% of the fatty acids in leafy green plants is in the form of
Alpha-linolenic Acid"


Prostaglandins Leukot Essent Fatty Acids. 1998 Mar;58(3):185-91.
Links
Dietary alpha-linolenic acid increases TNF-alpha, and decreases IL-6,
IL-10 in response to LPS: effects of sesamin on the delta-5
desaturation of omega6 and omega3 fatty acids in mice.
Chavali SR, Zhong WW, Forse RA.
Department of Surgery, Harvard Institute of Medicine, Beth Israel
Deaconess Medical Center and Harvard Medical School, Boston, MA
02215,
USA.


Sesamin (a non-fat portion of sesame seed oil) inhibits delta-5
desaturase activity resulting in an accumulation of dihomo-gamma-
linolenic acid (DGLA) which can displace arachidonic acid (AA) and
decrease the formation of pro-inflammatory mediators. We investigated
the effects of consumption of diets containing 0.25wt% sesamin and 15
wt% safflower oil (SO) (providing 12% of the added fat as linoleic
acid) or a 15 wt% 2:1 mixture of linseed oil and SO (LOSO) (providing
6% alpha-linolenic acid and 6% linoleic acid) for 3 weeks on the
liver
membrane fatty acid composition and on the production of
prostaglandin
(PG) E2, TNF-alpha, IL-6 and IL10 in mice. Consumption of sesamin-
supplemented SO and LOSO diets resulted in a significant increase in
the levels of 20:3omega6 (DGLA), suggesting that sesamin inhibited
delta-5 desaturation of omega6 fatty acids. In animals fed LOSO
diets,
the levels of alpha-linolenic acid, eicosapentaenoic acid (EPA) and
of
docosahexaenoic acid (DHA) were elevated with a concomitant decrease
of arachidonic acid (AA) in the liver membrane phospholipids.
Further,
in animals fed LOSO diets with or without sesamin, an increase in the
circulating levels of TNF-alpha was associated with a concomitant
decrease in PGE2. Despite a lack of differences in the levels of AA,
the PGE2 levels were significantly lower in mice fed sesamin-
supplemented SO compared to those fed SO alone. Thus, these data
suggest that irrespective of the availability of a specific fatty
acid
as a substrate, through regulating the PGE2 synthesis, the production
of TNF-alpha could be modulated.


PMID: 9610840 [PubMed - indexed for MEDLINE]


-
Molecule May Drive Multiple Sclerosis-Linked Disorder
Discovery could lead to treatments for transverse myelitis and MS

WEDNESDAY, Oct. 12 (HealthDay News) -- Researchers report that a
single
molecule called IL-6 is the cause of transverse myelitis (TM), an
autoimmune disease in the central nervous system that's related to
multiple sclerosis.


The study found that levels of IL-6 are dramatically elevated in the
spinal fluid of people with TM. The finding may help in the
development
of treatments for both TM and multiple sclerosis.


"This is the first time a single culprit has been identified as
causing
a CNS (central nervous system) autoimmune disease," researcher Dr.
Adam
Kaplin, a psychiatrist and assistant professor of medicine at Johns
Hopkins University School of Medicine, said in a prepared statement.


IL-6 is a chemical messenger that immune system cells use to
communicate with each other. Most TM patients suffer a single attack,
but 15 percent to 30 percent of TM patients go on to develop full-
blown
multiple sclerosis. TM usually results in permanent impairment,
including leg and arm weakness, bowel and bladder dysfunction, pain
and
paralysis.


The researchers decided to investigate IL-6 because TM patients
suffer
from memory impairment and depression. Previous research implicated
IL-6 in mood and concentration disorders.


The study appears in the October issue of the Journal of Clinical
Investigation.


More information


The U.S. National Institute of Neurological Disorders and Stroke has
more about transverse myelitis.


-- Robert Preidt


SOURCE: Johns Hopkins Medicine, news release, news release, Sept. 22,
2005


Last Updated: Oct. 12, 2005


Copyright © 2005 ScoutNews LLC. All rights reserved
-
<<snip> >
IL6-induced BBB defect precipitates iron accumulation
<<snip> >

J Neuropathol Exp Neurol. 1998 Mar;57(3):268-82. Related Articles,
Links


Abnormal iron deposition associated with lipid peroxidation in
transgenic mice expressing interleukin-6 in the brain.


Castelnau PA, Garrett RS, Palinski W, Witztum JL, Campbell IL, Powell
HC.


Department of Pathology (Neuropathology), School of Medicine,
University of California San Diego and the Veterans Affairs Research
Service, La Jolla 92093-0612, USA.


Transgenic mice, named GFAP-IL6, that express interleukin-6 in
astrocytes in the central nervous system (CNS) have a constitutive
blood-brain barrier (BBB) defect and develop a progressive
neurodegenerative disease. Based on ultrastructural observations
showing electron-dense pigment in the brain of the GFAP-IL6 mice, we
hypothesized that iron metabolism was altered in the brains of these
animals. Enhanced histochemical methods revealed abnormal iron
deposition in the cerebellum from 1 month of age that worsened with
progression of the disease. Immunohistochemical analysis of
iron-binding proteins (IBP) showed increased ferritin
immunoreactivity
and a decreased signal from the transferrin receptor in symptomatic
animals. Atomic absorption spectroscopy revealed a 40% increase of
total iron concentration in the cerebellum at the symptomatic stage.
In
order to obtain evidence that accumulation of this oxidizing metal
was
toxic, we looked for the presence of oxidative damage. Using the
MAL-2
antibody, extensive lipid peroxidation (LP) was detected in the
neocortex and the cerebellum in symptomatic animals. Ultrastructural
analysis indicated lipofuscin deposition at the sites of neuro-axonal
degeneration and abnormal iron deposition. These results suggest that
the IL6-induced BBB defect precipitates iron accumulation in the
GFAP-IL6 mouse brain and that subsequent IBP regulation mediates
protective responses. As these defenses become overwhelmed, the iron
overload seems to promote LP, which may contribute to the
neurodegeneration that ensues. This transgenic mouse model of
IL6-mediated neurodegeneration provides a unique opportunity to
examine
several aspects of iron metabolism in the brain, including its entry
at
the site of the BBB, its distribution through the IBP, and its
mechanisms of toxicity.


PMID: 9600219 [PubMed - indexed for MEDLINE]


---------------------------------------------------------------------------*-----

http://www.flaxhealth.com/foodsources.htm


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com


Man Is A Herbivore!
http://tinyurl.com/a3cc3


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk