I have excruciatign arthritis running thruout my body and I'm in the late
beginning stages of multiple sclerosis.

Can people guide me how to treat these things. The doctors have not been
too helpful.

Thank you.

"fkissam" <fkissam@bellsouth.net> wrote in message
news:bsSke.6859$6k7.4976@bignews4.bellsouth.net...
I'm on so many pain pills, my dentist won't give me anything when he's done
with me. Naproxen is what they give me for it, I think it's available over
the counter as "Aleve". Might want to check to see if it's ok with whatever
else you're taking though.

Gary

fkissam wrote:
Arthritis is closely related to elevated iron levels .. in fact one of
the most
recent studies has found iron in the joints of those with rheumatoid
arthritis.

Annals of the Rheumatic Diseases 2002;61:741-744


Iron deposits may damage joint tissue in RA


Our understanding of the role of iron in rheumatoid arthritis (RA) has
improved
with a recent study showing where iron accumulates in the synovial
membranes
of affected joints. The researchers speculate how iron might build up
to toxic
amounts.
Ferritin, both light and heavy subunits , was found in the lining layer
and
subintimal zone of the synovium and in synovial macrophages and
fibroblasts.
Transferrin receptor appeared only in the lining layer .
Non-specific resistance associated macrophage proteins (Nramp) were
also found
.. These are proteins that span membranes and transport divalent
cations. Nramp
2 occurred in the macrophages and fibroblasts. Nramp 1 was present in
macrophages and neutrophils, in the synovial lining layer and the
subintimal
zone, and in infiltrating inflammatory cells, but not in fibroblasts.
The study used synovial membranes from arthroplasties of 20 patients
with RA.
Thin sections were stained cytochemically for ferritin, transferrin
receptor ,
and Nramp 1 with monoclonal or polyclonal antibodies. Macrophages and
fibroblasts were isolated from collaginase digests of synovial
membranes.
Neutrophils were isolated from synovial fluid aspirated routinely from
the
joints . These cell types were stained for ferritin and transferrin
receptor
immunocytochemically. Nramp 1 and Nramp 2 were identified by reverse
transcriptase polymerase chain reaction.
A high iron content has been noted in synovial membraines in RA , but
the
uptake and storage of iron and its potential relation to imflammation
of the
joints has been unknown until now.

http://tinyurl.com/7axjx

Ann N Y Acad Sci. 2004 Mar;1012:252-266. Related Articles, Links


The Role of Iron in the Pathogenesis of Experimental Allergic
Encephalomyelitis
and Multiple Sclerosis

http://tinyurl.com/bx6kv

Apoferritin Attenuates Experimental Allergic Encephalomyelitis

http://tinyurl.com/9wfa2

New Pain Therapy Reverses Glial Activation

By medinews.com staff writers
Posted on 17 December 2003

Iron Reduction Therapy - inexpensive antioxidant treatment.

http://herbivore.7h.com/depriv.html

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DEAD PEOPLE WALKING
http://pages.ivillage.com/iron*justi...dpeoplewalking

ironjustice@aol.com wrote:
No shit, sherlock. I guess it's those micro bleeds (leakage) resulting
from chronic inflamation due to autoimmune attack (you know, that little
thing that actually causes rheumatoid arthritis which you haven't the
capacity to understand). Stop the inflamation, you stop the leakage, and
you don't end up with iron in the joints from blood. However, depriving
yourself of iron while on the medications to stop the inflamation is a
moronic thing to do, which I guess is why you suggest it. You see, these
medications not only retard the autoimmune attack they also suppress the
bone marrow, which can in some people lead to lower blood cell
production. The last thing they need is to further hinder their marrow
funciton by creating a state of iron deficiency anaemia. But you
wouldn't be able to understand any of this, because you have no idea
what you're talking about, you just cut and paste things you find on the
internet without having an inkling of what they mean or how they fit
into the larger picture of disease management. Now it's your turn to do
your Willam Shatner impression and start typing like Captain Kirk. Tell
me, have you been able to recruit another member to join you in your
cult yet, or are you still all alone?

Cheers!

Ari

--
spammage trappage: replace fishies_ with yahoo

I'm going to die rather sooner than I'd like. I tried to protect my
neighbours from crime, and became the victim of it. Complications in
hospital following this resulted in a serious illness. I now need a bone
marrow transplant. Many people around the world are waiting for a marrow
transplant, too. Please volunteer to be a marrow donor:
http://www.abmdr.org.au/
http://www.marrow.org/

So .. THAT .. is .. YOUR .. 'contribution' ..

Eh ..

You didn't even open your mouth .. WHEN .. the poster .. asked for
input ..

But .. when 'input' .. IS .. provided .. WITH .. medical studies .. YOU
... 'contribute' ..

Eh ..

Keep your 'contributions' .. to .. yourself ..

You 'know' .. something .. MORE .. than .. me ..

Do .. ya ..

You have 'some success' .. and THEN .. open your stupid fkg .. trap ..

UNTIL .. then ..

Just .. S-T-F-U ..

Do some .. oxy ..

Just .. stfu ..

leads to ..
IMPROVED .. anemia ..

So .. according to THIS article .. anemia .. does NOT .. necessarily ..
mean ..
iron deficiency ..


So since iron has been implicated IN the CAUSE of .. diabetes .. and
since
anemia is ONE of your .. problems .. then .. as I said before .. epogen
/
erythropoeitin is NOT .. necessarily .. your ONLY .. option ..


One might .. consider .. the effect of iron reduction .. as evidenced
... below
...


REDUCTION .. of .. anemia ..


GuyClin Exp Rheumatol. 1986
Jan-Mar;4(1):25-9. Related Articles, Links


Antianemic and potential anti-inflammatory activity of desferrioxamine:

possible usefulness in rheumatoid arthritis.


Giordano N, Sancasciani S, Borghi C, Fioravanti A, Marcolongo R.


In order to study the role of excessive synovial iron sequestration in
the
production of anemia in rheumatoid arthritis (RA), the antianemic
efficacy and
anti-inflammatory effect of desferrioxamine administered in a
short-term
treatment (14 days), were evaluated in 10 patients suffering from
classic or
definite RA and hyposideremic anemia. Treatment with desferrioxamine
showed an
elevated urinary iron excretion, a significant increase of serum iron,
UIBC and
hemoglobin, and a marked progressive decrease of serum ferritin. A
moderate
improvement of the pain intensity, morning stiffness and Ritchie's
index was
also observed. The results obtained suggest that excessive
reticuloendothelial
iron deposits occur in RA and that the iron uptake can be an important
factor
in the production of anemia. Desferrioxamine seems to be useful in the
treatment of patients suffering from RA and anemia, in order to release
iron
from synovial tissue, reduce the inflammatory process and improve
anemia,
changing an anemia which is typically resistant to the martial therapy
into an
iron-sensitive anemia.


Publication Types:
Clinical Trial


PMID: 3516495 [PubMed - indexed for MEDLINE]


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

------


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DEAD PEOPLE WALKING
http://pages.ivillage.com/iron*justi...dpeoplewalking <

..

Iron(III)-mediated intra-articular crystal deposition in arthritis: a
therapeutic role for iron chelators.


Naughton DP


School of Pharmacy and Biomolecular Sciences, University of
Brighton,
Cockcroft Building, Moulsecoomb, Brighton, UK.
D.P.Naugh...@bton.ac.uk


Crystal deposition in arthritic diseases has attracted much
interest.
Many reports have established the presence of calcium pyrophosphate
(CPPD), hydroxyapatite (HAP) and urate crystals throughout the range

of arthritic diseases. In particular, HAP crystals have been
detected
in 30-60% of synovial fluid (SF) samples from patients suffering
from
osteoarthritis (OA) and 33% of those suffering from rheumatoid
arthritis (RA). In OA, crystal deposition has been linked to greater

joint deterioration. The mechanism of intra-articular calcification
is
unknown. Nucleation is required to transform a 'metastable'
phosphate-
and calcium-rich biofluid into one that generates crystals. Ferric
ions have been demonstrated to induce crystallization of these
stable
supersaturated solutions via the process of nucleation.The inflamed
arthritic joint is prone to iron loading. Microbleeding from
compromised vasculature contributes to intra-articular iron loading
in
arthritic conditions. Low-molecular-mass redox-active iron complexes

have been detected in SF in inflammatory joint diseases. These
species
are credited with mediating oxidative stress via interaction with
peroxides and superoxide. In addition, adventitious
low-molecular-mass
iron complexes can cause nucleation leading to crystal growth within

the joint.Decorporating agents capable of removing this misplaced
iron
from the arthritic joint would have the joint benefit of relieving
oxidative stress and preventing crystal nucleation. Systemic side
effects could be overcome by the targeting suitable chelators using
bioreductive delivery systems that are activated in hypoxic inflamed

synovial tissue. Copyright 2001 Harcourt Publishers Ltd.


PMID: 11421639, UI: 21317021

______________________________*___________________ ___________*_____


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______________________________*___________________ ___________*_____


Rheumatol Int 1996;16(2):45-8


Effects of desferrioxamine therapy on chronic disease anemia associated
with
rheumatoid arthritis.


Salvarani C, Baricchi R, Lasagni D, Boiardi L, Piccinini R, Brunati
C,
Macchioni P, Portioli I


2Divisione di Medicina, Azienda Ospendaliera Arcispedale S. Maria
Nuova, Reggio Emilia, Italy.


OBJECTIVE: To investigate the effects of desferrioxamine (DFO)
infusion on chronic disease anemia (CDA) of rheumatoid arthritis
(RA)
by evaluating interleukin-6 (IL-6) and erythropoietin (EPO)
production. PATIENTS AND METHODS: Five patients with RA and CDA
(group
I) were treated with DFO, 500 mg daily, through a continuous 10-h
subcutaneous infusion 5 days a week for 4 weeks. One month after
withdrawal, DFO was resumed in all five group I patients (group II)
with an increase to 1 g daily following the previous treatment
schedule. Clinical and laboratory parameters were evaluated weekly
during the two study periods. Serum EPO was measured by
radioimmunoassay. IL-6 was detected by the enzyme-linked
immunoabsorbent assay method. RESULTS: No significant variations in
hematological parameters, IL-6 or EPO levels were observed in group
I
patients. After 1 week of DFO 1 g daily, reticulocyte counts and EPO

improved significantly. Hemoglobin and hematocrit rose significantly

after 3 weeks of 1 g daily DFO therapy. Four weeks after DFO
withdrawal, EPO, reticulocyte counts, hemoglobin and hematocrit
returned to baseline levels. A significant improvement in the
clinical
parameters of disease activity was observed, particularly in group
II
patients. CONCLUSION: DFO improves CDA in RA patients. The
beneficial
effects on erythropoiesis seem to be related to improved EPO
responsiveness to the anemia.


PMID: 8853224, UI: 97005925

______________________________*___________________ ___________*_____


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Tom


<

Investigation of the anti-inflammatory properties of
hydroxypyridinones.


Hewitt SD, Hider RC, Sarpong P, Morris CJ, Blake DR


Cancer Research Unit, University of York, Heslington.


Synovial iron deposition associated with rheumatoid disease may
result
in the production of highly reactive oxygen free radicals, leading
to
tissue damage. This chain of events can be interrupted by iron
chelation. Families of strong iron (III) chelators have been tested
for their iron scavenging properties in vitro and their effects
assessed in vivo using a rat model of inflammation. All the
chelators
competed successfully for iron with apotransferrin, and some removed

up to 34% of iron from ferritin. The best anti-inflammatory effects
were achieved with the most hydrophilic chelators and those which
chelated iron most avidly. Activity was dependent on dose. The route

of administration was also an important factor with lower affinity
chelators. This work introduces a range of simple bidentate iron
chelators, which under certain conditions exceed desferrioxamine in
their iron scavenging abilities, and some of which, in this simple
animal model, approach indomethacin in their anti-inflammatory
capabilities.


Comments:
* Comment in: Ann Rheum Dis 1990 Nov;49(11):956-7


PMID: 2730166, UI: 89272259

______________________________*___________________ ___________*_____


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DEAD PEOPLE WALKING
http://pages.ivillage.com/iron*justi...dpeoplewalking
<

Daily News


Vegan Diet Improves Rheumatoid Arthritis Symptoms
11/14/02 - Healthnotes Newswire—A strict vegetarian diet led to
improvement
in symptoms of rheumatoid arthritis (RA), according to a clinical trial

published in Rheumatology (2001;40:1175–9).
Thirty-eight people with rheumatoid arthritis were assigned to consume
a vegan
diet (a vegetarian diet that also excludes dairy products and eggs) and
also to
avoid gluten-containing grains (wheat, oats, barley, and rye) for one
year.
Twenty-eight other people with RA were assigned to eat a more typical
unrestricted diet, including meat (control group).


Only 22 of the 38 people assigned to eat the vegan diet completed at
least nine
months of the dietary intervention. Of those, 40% (nine people)
experienced
improvement in the symptoms of RA compared with only 4% (one person) in
the
group eating the standard diet.


RA is one of a group of conditions called autoimmune diseases. In
autoimmune
disease, the body’s immune system, which is designed to fight off
infectious
agents and other foreign substances, mistakenly attacks its own
tissues. In RA,
the autoimmune damage is to the joints, but other tissues and organs
are
frequently affected as well. Conventional therapy includes drugs that
reduce
inflammation or suppress the immune system. Surgery may also be
recommended, if
the joint damage is severe. While these treatments are often helpful,
many
individuals with RA continue to experience symptoms. Moreover, drugs
used to
treat RA can cause significant side effects, ranging from bleeding
peptic
ulcers to bone marrow damage. Any safe treatment that might help
relieve
symptoms of RA would, therefore, be welcomed.


There are several possible explanations for the improvements seen in
this
study. Meat is high in a specific fatty acid (arachidonic acid) that is

believed to promote inflammation in the body. Because vegetarian diets
contain
less arachidonic acid than omnivorous diets, consuming a vegetarian
diet might
produce an anti-inflammatory effect. Another possible explanation for
the
improvement is that plant-based diets are high in certain
anti-inflammatory
compounds such as essential fatty acids and enzymes. Finally, the
results may
be attributable in part to the avoidance of common food allergens, such
as
wheat and dairy products. Although the relationship between food
allergy and
arthritis remains controversial, a growing body of evidence suggests
that
allergy is a contributing factor, at least in a minority of individuals
with
RA.


Other natural treatments that have been reported to be helpful for
people with
RA include zinc, borage oil, black currant seed oil, and fish oil.
Individuals
with RA who wish to pursue the dietary or nutritional-supplement
approach
should consult a doctor knowledgeable in natural medicine.


—Matt Brignall, N.D.


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'true' workings of aspirin .. as a chelator of .. iron ..?


http://news.excite.com/news/r/*010928/18/health-iron


Iron Imbalance in Brain May Cause Migraine
Updated: Fri, Sep 28 6:22 PM EDT


By Will Boggs, MD


NEW YORK (Reuters Health) - Abnormalities in the way the brain's
pain
control center handles iron may lead to the development of migraine
attacks and headaches, according to a study by Kansas researchers.


During migraine, a portion of the brain known as the periaqueductal
gray matter (PAG) may fail to "switch on" to prevent pain, Dr. K.
Michael Welch of the University of Kansas Medical Center in Kansas
City told Reuters Health.


"In migraine, a trigger such as stress activates the PAG but it does

not switch on because it is dysfunctional," he explained, "or else
switches on an abnormal part."


The result? "Pain instead of no pain," according to Welch.


His team studied levels of iron in the PAG of patients with either
migraine headaches or recurrent, non-migraine headaches and compared

them to levels in people without headache or migraine.


Changes in iron levels can reflect changes in the way the cells of
the
PAG work, the authors pointed out.


According to the report, published in a recent issue of the journal
Headache, iron levels in the PAG were significantly increased in
patients with migraine and those with headache compared to the
headache-free group.


In fact, the researchers pointed out, the longer patients had
experienced headaches, the higher the iron levels in the PAG were,
though iron levels at the beginning of their illness were still
clearly higher than normal.


Increased iron levels may be both a cause of migraine attacks and a
result of repeated headaches, the investigators noted.


"Thus, we believe that the increased (iron levels) in our migraine
groups reflect impaired iron (balance), possibly associated with
(nerve) dysfunction or damage," the authors concluded.


"Perhaps the PAG abnormality is essential to the cause of the
headache
in migraine," Welch said. "The gradual deposition of iron increases
dysfunction, and headaches coalesce from episodic to continuous."


How, then, might one minimize the damage from increased iron stores?

Welch advised, "Treat episodes quickly and prevent (attacks)
whenever
possible."


SOURCE: Headache 2001;41:629-637.
Email this story | Printer-friendly version


Subject: chelate/aspirin


Med Hypotheses 1998 Mar;50(3):239-51


A chelate theory for the mechanism of action of aspirin-like drugs.


Wang X


Department of Pathology, Cornell University Medical College, New
York,
NY 10021, USA. x...@mail.med.cornell.edu


Two hundred years after the discovery of the pharmaceutical
usefulness
of aspirin, it and aspirin-like drugs, a family with an
ever-increasing number of members, are an indispensable part of
modern
life. However, the question as to how these drugs work in the body
has
remained unsettled. It is postulated here that this group of drugs
may
exert their therapeutic (and adverse) effects by chelating various
physiologically important metallic cations in the body. The chelate
theory is supported by the vast majority, if not all, of the
observations on these drugs made in the past.


Publication Types:
* Review
* Review, academic


PMID: 9578329, UI: 98237440

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<

MULTIPLE Sclerosis Tied to Iron in Brain
WebMD
Oct. 22, 2003 -- Iron deposits deep in the brain may cause multiple
sclerosis,
new imaging studies suggest. The findings come from ...
<http://my.webmd.com/content/ar*ticle/75/89853.htm?z=1728_0000*0_1000_nb_02>



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http://www.bufflink.org/NewsText/379426443981482.html

Multiple Sclerosis Tied to Iron in Brain

Studies Point to Cause, Location of MS Brain Damage

By Daniel DeNoon
WebMD Medical News

Reviewed By Brunilda Nazario, MD
on Wednesday, October 22, 2003

Oct. 22, 2003 -- Iron deposits deep in the brain may cause multiple
sclerosis, new imaging studies suggest.

The findings come from studies of computer-assisted brain scans using a
specialized magnetic resonance imaging (MRI) device. University at
Buffalo, N.Y., researchers Rohit Bakshi, MD, and colleagues are the
first to use this technique to study multiple sclerosis. Bakshi
reported the findings at this week's annual meeting of the American
Neurological Association in San Francisco.

Multiple sclerosis has been considered a disease of the white matter in
the brain and spinal cord -- the neural pathways that allow areas of
gray matter to communicate with one another. But the new findings link
iron deposits in the gray matter to movement and thinking impairments
in multiple sclerosis.

"If we're going to treat this disease, we have to know where the damage
is," Bakshi says in a news release. "Traditionally, we thought MS was
strictly a white-matter disease. ... We were able to visualize gray
matter structures deep in the brain of MS patients and found some to be
atrophied."

These areas of brain damage contained abnormally high levels of iron.
It's not yet clear that the iron is the cause of the brain damage. It
could be that dying brain cells leave a trail of iron behind.

Walking, Thinking, and Gray Matter

Bakshi's team put 41 multiple sclerosis patients through a walking
test. They also gave tests of learning, speed of information
processing, and memory to 28 MS patients.

The more unnatural darkness the brain scans saw in a patient's gray
matter, the worse the patient's MS symptoms. It was the only factor
studied that independently predicted impaired walking and thinking.

"We suspect that MS patients have defective blood-brain barriers, the
cell layer that prevents potentially toxic substances from entering the
brain," Bakshi says. "Excessive iron entering the brain may damage the
deep gray matter structures."

Possible Treatment

If iron is indeed the culprit, it seems possible to do something about
it. Bakshi's team is exploring two ideas. The first is simply to remove
excess iron from patients' bodies, and then to devise a way to prevent
future iron build-up.

If that is impractical, it may be possible to prevent iron from killing
brain cells. The excess iron may be causing free radicals -- extremely
reactive molecules that damage brain cells. Antioxidants -- such as
vitamins C and E, or even more powerful agents -- might mop up free
radicals before they do their dirty work.

Even if the iron deposits are the effect, rather than the cause, of
brain cell death, the study still offers a way to measure the severity
of MS and the efficacy of new treatments.

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

SOURCES: American Neurological Association 128th Annual Meeting, San
Francisco, Oct. 19-22, 2003. News release, University at Buffalo, N.Y.

© 2003 WebMD Inc. All rights reserved.



© 2002 BuffLink, Inc. All rights reserved.


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DEAD PEOPLE WALKING
http://pages.ivillage.com/iron*justi...dpeoplewalking

ironjustice@aol.com wrote:
And so begins the Shatner-esque rant we've all grown to know and giggle
over :-) You're a joke, Tom. Go back to therapy and take your
medication, when you're well enough you'll actually be able to
contribute to society (I would have finished that sentence with 'again',
but I'm not so sure it would have been accurate).

Cheers!

Ari

--
spammage trappage: replace fishies_ with yahoo

I'm going to die rather sooner than I'd like. I tried to protect my
neighbours from crime, and became the victim of it. Complications in
hospital following this resulted in a serious illness. I now need a bone
marrow transplant. Many people around the world are waiting for a marrow
transplant, too. Please volunteer to be a marrow donor:
http://www.abmdr.org.au/
http://www.marrow.org/

According to your sig line .. you don't pick your fights .. well ..

Learn from it ..

F-O ..

Dig .. ?
Comprendez .. ?
Unnerfkgstand .. ?

Who loves ya.
Tom
Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com
Man Is A Herbivore!
http://pages.ivillage.com/ironjustice/manisaherbivore
DEAD PEOPLE WALKING
http://pages.ivillage.com/ironjustice/deadpeoplewalking

ironjustice@aol.com wrote:
Unlike you Tommy, I actually put my money where my mouth is when it
comes to helping people. I guess a shut in (by choice) like yourself
wouldn't understand that (ignorance and cutting and pasting from what
other people have done doesn't really count, now does it, Tommy?). It's
nice to see that you're consistent, though: I wonder what we'd all do if
you ever learned how to speak in a way other than that of an old TV
sci-fi character. The results could be catastrophic!

Cheers!

Ari

--
spammage trappage: replace fishies_ with yahoo

I'm going to die rather sooner than I'd like. I tried to protect my
neighbours from crime, and became the victim of it. Complications in
hospital following this resulted in a serious illness. I now need a bone
marrow transplant. Many people around the world are waiting for a marrow
transplant, too. Please volunteer to be a marrow donor:
http://www.abmdr.org.au/
http://www.marrow.org/

THAT .. is .. it .. ?

THAT .. is .. your .. 'contribution' ..?

Attack the .. poster ..

Heh .. heh ..

You are some piece of work ..

EVERY .. isp in the world says .. sht the fk up ..

But ... youuuuuu ...

Don't have to ..

That must be because you are .. spodosaurus ..

read my lips you two bit little jrkff ..

You either begin to refute the medical studies .. supplied .. or ..
attempt to .. at least ACT .. like a fkg .. man ..

Who loves ya.
Tom
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Man Is A Herbivore!
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DEAD PEOPLE WALKING
http://pages.ivillage.com/ironjustice/deadpeoplewalking

"spodosaurus" <spodosaurus@_yahoo_.com> wrote in message :
People with diseases such as MS are not accepted as blood donors, bone
marrow donors, blood cell donors and probably organ donors in general. I
was given a letter of rejection as soon as I was diagnosed with MS.

Because not enough is known about the etiology of MS, those gathering blood
for use on others should not endanger the lives of seriously ill or surgical
patients by supplying blood which could lead to another illness.

--

"spodosaurus" <spodosaurus@_yahoo_.com> wrote in message
news:42adb61f$1@quokka.wn.com.au...

ironjustice@aol.com wrote:
Dear dear Tommy, you're getting spittle all over your 14" dusty old CRT!
My contributions are many, including original empirical research, but in
this case it's pointing out to those who may not know better (yet) that
you're a complete boob. I also clarified why you're a complete boob and
gave a brief explanation of your typical misunderstandings and invalid
assumptions. I understand the things you copy and paste as well as
understanding the interplay of factors involved. Unfortunately, you have
neither the grey matter nor the willpower to work through an education
in order to actually carry out any research, and this is why you copy
and paste things and proclaim 'look, studies!' when you haven't a clue
as to what these studies really mean, the populations to which they may
apply, or the various factors involved in the disease processes (nor do
you comprehend their interactions). All you do is type incorrectly
spelled obscenities in broken english with horrendous punctuation and
nothing original to offer: the rest is copy and paste from the people
who are really contributing empirical research. Unfortunately it seems
you'll have a hard time understanding what I've written, but that's your
choice, just like it's your choice to sit at home all day and do nothing
but try and recruit people to your lonely little cult without any chance
of success (and in this case it's not persistence on your part, it's
stupidity). You'll excuse me while I continue with my real work and try
to finish up a few projects that have been backlogged due to
hospitalisations (I'm sure you'll understand that much, having studied
my signature so intently). I await your next round of spew on the edge
of my seat, though I really shouldn't as it's inevitable: you haven't
the self control not to issue forth more vitriol from that murky
cesspool that resides within you and grows deeper by the day.

Cheers!

Ari

PS- I thought about paragraphing this post, but I decided against it as
it might prove too overwhelming for you. Best to try and get through to
you with a style you're more familiar with :-)


--
spammage trappage: replace fishies_ with yahoo

I'm going to die rather sooner than I'd like. I tried to protect my
neighbours from crime, and became the victim of it. Complications in
hospital following this resulted in a serious illness. I now need a bone
marrow transplant. Many people around the world are waiting for a marrow
transplant, too. Please volunteer to be a marrow donor:
http://www.abmdr.org.au/
http://www.marrow.org/

kamel wrote:
'Tis true, there are restrictions applied to who can be marrow donors
(covered in those sites I have listed in my signature - snipped in this
post to avoid redundancy). It would be unfortaunte to have a recipient
survive the dangers of a marrow transplant only to develop an auto
immune disease (beyond graft versus host disease) from the transplant
itself. There are also age restrictions on marrow donation, though these
may be waived in some special cases for specific recipients.

It's always exciting to watch new developments in MS (and other
illness) research but this has to be tempered with the knowledge that
often these discoveries are 5-10 years (minimum) from leading to an
implementation of a treatment.

I
was given a letter of rejection as soon as I was diagnosed with MS.

Because not enough is known about the etiology of MS, those gathering
blood
for use on others should not endanger the lives of seriously ill or
surgical
patients by supplying blood which could lead to another illness
<

It is a matter of convincing the doctor that a level of . NID / near
iron deficiency .. is NOT .. harmful .. and .. possibly is .. HELPFUL
...

Since there are researchers who believe oxidative stress IS .. involved
IN .. the pathogenesis OF .. both .. MS and arthritis .. then it would
take some articles .. such as the aspirin .. article .. to convince the
doctor elevated / unbound iron 'might' .. be .. involved.

And since there ARE researchers who believe a little anemia / iron
deficiency .. "never hurt nobody" .. then studies which SHOW pain
killers work BY .. binding of iron .. combined WITH studies which show
... iron .. TO BE .. 'there' .. might entice the / your doctor to
attempt a little 'heroic medical intervention' .. ?

As in the testing of .. NID / near iron deficiency ..

Throw in the .. "minocycline ..is an iron chelator" .. and .. ??

Who loves ya.
Tom
Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com
Man Is A Herbivore!
http://pages.ivillage.com/ironjustice/manisaherbivore
DEAD PEOPLE WALKING
http://pages.ivillage.com/ironjustice/deadpeoplewalking

Rheumatology (Oxford). 2003 Dec;42(12):1550-5. Epub 2003 Jun 27.
Related Articles, Links


Near-iron deficiency-induced remission of gouty arthritis.

Facchini FS.

Department of Medicine, San Francisco General Hospital and University
of California San Francisco, 94143, USA. fste2000@yahoo.com

OBJECTIVES: Previous evidence supports a role for iron in the
pathogenesis of gout. For example, iron, when added to media containing
urate crystals, stimulated oxidative stress with subsequent complement
and neutrophil activation. Conversely, iron removal inhibited these
responses as well as urate-crystal-induced foot pad inflammation in
rats in-vivo. The objective of the present study was to investigate
whether or not iron removal may improve the outcome of gouty arthritis
in humans as well. METHODS: Quantitative phlebotomy was used to remove
iron in 12 hyperuricaemic patients with gouty arthritis and maintain
their body iron at near-iron deficiency (NID) level (i.e. the lowest
body iron store compatible with normal erythropoiesis and therefore
absence of anaemia). RESULTS: During maintenance of NID for 28 months,
gouty attacks markedly diminished in every patient, from a cumulative
amount of 48 and 53 attacks per year before (year -2, -1), to 32, 11
and 7 during induction (year 0) and maintenance (year +1, +2) of NID,
respectively. During NID, attacks were also more often of milder
severity. CONCLUSIONS: During a 28-month follow-up, maintenance of NID
was found to be safe and beneficial in all patients, with effects
ranging from a complete remission to a marked reduction of incidence
and severity of gouty attacks.

Publication Types:
Clinical Trial

PMID: 12832712 [PubMed - indexed for MEDLINE]

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

Who loves ya.
Tom
Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com
Man Is A Herbivore!
http://pages.ivillage.com/ironjustice/manisaherbivore
DEAD PEOPLE WALKING
http://pages.ivillage.com/ironjustice/deadpeoplewalking