Hey, Dude, it's heavy metal time

[Richard Long]

I think, that several of us are really suffering from the effects of chronic exposure to toxic environmental metals, like the Heavy Metal, lead (Pb)& a host of others....

Or exposure "kick started" what was later diagnosed as MS.

Gulf war vets, refinery workers, painters. ceramic glaze workers, old home renovators,the list is quite extensive.

http://brain.hastypastry.net/forums/showthread.php?t=57338

[agate]

Who knows what toxic substances everyone in the industrialized parts of the world might have been exposed to over time? Lead exposure may be just the tip of the iceberg.:(

[biogirl7]

I don't know if anyone else watches Family Guy....but I read the title of this post and thought to myself...

"It's Peanut Butter Jelly Time!!!!"


Sorry to interrupt the post... ;)

[renee]

Richard, I thought you discovered Metallica or Guns & Roses.
More power to you.

I'm happy that noone else in my family has this pestilence of a diss-ease.

[Annie1234]

My father was a machinist for 40 years... he smells of heavy oil and metal to this day, and the smell seeps into his clothing, bed sheets and even into the living room furniture. I have to wonder if his sperm were somehow affected when I was conceived or if his hugs or my sitting on the furniture contaminated me in some way. Yes, interesting.

[Matthew's Mom]

Or exposure "kick started" what was later diagnosed as MS

I grew up near a chemical plant and a dump. The fumes were awful especially in the summer. Cluster of cancer in my old neighborhood also, along with other illnesses.:(

I believe some of us are more susceptible to toxins, and like you said it kick starts something.

My main example is my son who exposed to lindane for headlice developed many brain abnormalities and Tourettes Syndrome.

I too thank God that it is me that has MS and not my brother or sisters.

Pam

[Abby2006]

I was tested back in the 90's and have all kinds of things lurking in my body

Abby

[Braindead]

There are two METALS that are a problem for MS folks.

ZINC and IRON

Some ZINC is good and necessary for good health however HIGH levels of ZINC is highly suspected of causing MS. Several "hot clusters" of MS have been found around locations where high levels of zinc were being released.

I do not think it would be wise for a person with MS to take ZINC supplements.

I think this may have something to to with MMP formation. All 27 types of MMPs have a zinc at the "business end" and use it to cut our Myelin into little pieces by breaking the hydrogen bonds. I think that the body may adapt to the high levels of ZINC by making LOTS of "very agressive" MMPs.

MMPs levels are elevated JUST BEFORE and DURING a MS attack.

Braindead
.
.
: J Neuroimmunol. 1997 Feb;72(2):155-61.

Matrix metalloproteinases, tumor necrosis factor and multiple sclerosis: an
overview.

Chandler S, Miller KM, Clements JM, Lury J, Corkill D, Anthony DC, Adams SE,
Gearing AJ.

British Biotech Pharmaceuticals Limited, Cowley, Oxford, UK.

The matrix metalloproteinases (MMPs) are a family of at least 14 zinc-dependent
enzymes which are known to degrade the protein components of extracellular
matrix. In addition, MMPs and related enzymes can also process a number of cell
surface cytokines, receptors, and other soluble proteins. In particular we have
shown that the release of the pro-inflammatory cytokine, tumor necrosis
factor-alpha, from its membrane-bound precursor is an MMP-dependent process.
MMPs are expressed by the inflammatory cells which are associated with CNS
lesions in animal models of multiple sclerosis (MS) and in tissue from patients
with the disease. MMP expression will contribute to the tissue destruction and
inflammation in MS. Drugs which inhibit MMP activity are effective in animal
models of MS and may prove to be useful therapies in the clinic.

Publication Types:
Review
Review, Tutorial

PMID: 9042108 [PubMed - indexed for MEDLINE]
.
.

1: Arch Environ Health. 2001 Sep-Oct;56(5):389-95.

Comment in:
Arch Environ Health. 2002 Jul-Aug;57(4):383; author reply 383.

A multiple sclerosis cluster associated with a small, north-central Illinois
community.

Schiffer RB, McDermott MP, Copley C.

Department of Neuropsychiatry, Texas Tech University Health Sciences Center,
Lubbock 79430, USA. psyrbs@ttuhsc.edu

The authors investigated a reported incidence cluster of multiple sclerosis (MS)
cases in a small, north-central Illinois community to determine validity and
statistical significance. DePue, Illinois--a small, north-central Illinois
community--has previously been the site of significant environmental heavy-metal
exposure from a zinc smelter. Significant contamination of soil and water with
zinc and other metals has been documented in this community during the time
period of interest. In the mid-1990s, several cases of MS were reported to the
Illinois Department of Public Health within the geographic limits of this
community. Available medical records from purported MS cases reported to the
Illinois Department of Public Health were reviewed, and living individuals were
seen and examined. Statistical analyses were conducted with clinically definite
MS cases; onset dates were determined by first symptom, and expected incidence
rates were determined from published epidemiologic studies. Nine new cases of
clinically definite MS occurred among residents of DePue, Illinois, during the
period between 1971 and 1990. Seven of the 8 living subjects included in the
final analyses were examined by one author (RS). The computed incidence rate
deriving from these cases within DePue Township, Illinois, represented a
statistically significant excess of new MS cases over expected. During the
period from 1971 through 1990, a significant excess of MS cases occurred within
the population of DePue, Illinois. Significant exposure of this population to
mitogenic trace metals, including zinc, was also documented during this time
period.

PMID: 11777019 [PubMed - indexed for MEDLINE]

[MomtoM]

What's bad about the iron? Just wondering because I've had 7 months of IV iron to bring my iron up and sometimes it seemed like the higher my Hg was, the more tired I felt.

Deb

[Braindead]

What's bad about the iron? Just wondering because I've had 7 months of IV iron to bring my iron up and sometimes it seemed like the higher my Hg was, the more tired I felt.

Deb

Iron deposite have been noticed in MS lesions for some time. It also has been noted that iron deposits can be toxic/damage neurons.

The deposits seem to be the results of abnormal cell death that leaves behind its Iron which because the cell deaths continue they (iron deposits)accumulates in rather large amounts.

So the iron deposits do not cause MS but cause additional cell/neuron deaths as they increase in size and number.

I did not post all this at the time I mentioned IRON as being a problem in MS because I was trying to find some GOOD recent abstracts that showed that they were present in MS folks and that they did measurable harm.

It appears that the ability to measure these deposits has matured but what they mean/do in MS is still speculative/unproven/unpublished.

I will post what I have found.

Braindead

: Med Hypotheses. 2008 Aug;71(2):293-7. Epub 2008 Apr 8.

Hypothetical molecular mechanisms by which local iron overload facilitates the development of venous leg ulcers and multiple sclerosis lesions.

Simka M, Rybak Z.
Department of Angiology, Wodzislawska 78, 43-200 Pszczyna, Poland.

This paper presents a hypothetical model of role for iron in the development of venous leg ulcers and multiple sclerosis.

Elevated concentrations of iron were found in the skin affected by venous hypertension and also in the areas of brain with multiple sclerosis lesions.

Individuals with hemochromatosis gene (HFE) mutations: C282Y and H63D, which result in a less efficient transport of iron by macrophages, are characterized by an increased risk for venous leg ulcer and multiple sclerosis.

Multiple sclerosis is a T cell-mediated disease, and T cells probably participate in the development of venous ulcers.

This deleterious role of ferric ions could be related to the regulation of T cell proliferation and apoptosis. Under normal conditions excessive accumulation of T cells cannot take place, because nitric oxide and interferon-gamma drive these cells toward apoptosis.

However, in tissues with a high concentration of iron, T lymphocytes proliferate instead of undergoing apoptosis. This is possible due to the internalization of the INF-gammaR2 chain of the interferon-gamma receptor, the downregulation of inducible nitric oxide synthase expression in macrophages and the inactivation of the active site of caspases.

Yet, it should be emphasized that this hypothesis does not claim for the increased concentration of iron as a direct causal factor for the development of venous ulcerations or multiple sclerosis, but rather, iron is a factor that modulates and exaggerates the autoimmune process.

Iron chelators, administered systemically or locally, should potentially exhibit therapeutic and prophylactic activity against venous leg ulcers and multiple sclerosis.

PMID: 18400414 [PubMed - indexed for MEDLINE

[Braindead]

I really hate to mention this BUT because so much damage is done by these iron deposits, some neuroligist talk about "Iron-related inflammation and neurogenerative disorders like Multiple Sclerosis" being helped by removing some of this Iron via chelation.

Green Tea's EGCG also does nice things to t-cells:

http://home.ix.netcom.com/~jdalton/egcg-neorond-ms.pdf

Braindead

for example:


1: J Alzheimers Dis. 2008 Oct;15(2):211-22.

Cell signaling pathways and iron chelation in the neurorestorative activity of green tea polyphenols: special reference to epigallocatechin gallate (EGCG).

Mandel SA, Amit T, Kalfon L, Reznichenko L, Weinreb O, Youdim MB.

Eve Topf Center for Neurodegenerative Diseases Research and Department of Pharmacology, Faculty of Medicine, Technion, Haifa, Israel.

Although much progress has been made in understanding the pathogenesis of Alzheimer's disease (AD), the current therapeutic approaches are merely symptomatic, intended for the treatment of cognitive symptoms, such as disturbances in memory and perception.

Novel promising strategies suggest the use of anti-inflammatory drugs, antioxidants including natural occurring plant flavonoids, iron-complexing molecules, neurotrophic factor delivery, inhibitors of the amyloid-beta protein precursor processing secretases, gamma and beta, that generate amyloid-beta peptides and the interference with lipid and cholesterol metabolism.

Human epidemiological and new animal data suggest that tea drinking may decrease the incidence of dementia, AD and Parkinson's disease.

In particular, its main catechin polyphenol constituent (-)-epigallocatechin-3-gallate (EGCG) has been shown to exert neuroprotective/neurorescue activities in a wide array of cellular and animal models of neurological disorders.

This review provides a detailed overview on the multimodal activities of green tea polyphenols with emphasis on their iron chelating, neurorescue/neuroregenerative and mitochondrial stabilization action.

PMID: 18953110 [PubMed - indexed for MEDLINE
.
.
1: J Immunol. 2004 Nov 1;173(9):5794-5800.

Green Tea Epigallocatechin-3-Gallate Mediates T Cellular NF-{kappa}B Inhibition
and Exerts Neuroprotection in Autoimmune Encephalomyelitis.

Aktas O, Prozorovski T, Smorodchenko A, Savaskan NE, Lauster R, Kloetzel PM,
Infante-Duarte C, Brocke S, Zipp F.

Institute of Neuroimmunology, Neuroscience Research Center, Charite, Berlin,
Germany;

Recent studies in multiple sclerosis and its animal model, experimental
autoimmune encephalomyelitis (EAE), point to the fact that even in the early
phase of inflammation, neuronal pathology plays a pivotal role in the sustained
disability of affected individuals.

We show that the major green tea constituent, (-)-epigallocatechin-3-gallate (EGCG), dramatically suppresses EAE induced by proteolipid protein 139-151.

EGCG reduced clinical severity when given at initiation or after the onset of EAE by both limiting brain inflammation and reducing neuronal damage. In orally treated mice, we found abrogated proliferation and TNF-alpha production of encephalitogenic T cells.

In human myelin-specific CD4(+) T cells, cell cycle arrest was induced,
down-regulating the cyclin-dependent kinase 4. Interference with both T cell
growth and effector function was mediated by blockade of the catalytic
activities of the 20S/26S proteasome complex, resulting in intracellular
accumulation of IkappaB-alpha and subsequent inhibition of NF-kappaB activation.

Because its structure implicates additional antioxidative properties, EGCG was
capable of protecting against neuronal injury in living brain tissue induced by
N-methyl-d-aspartate or TRAIL and of directly blocking the formation of
neurotoxic reactive oxygen species in neurons.

Thus, a natural green tea constituent may open up a new therapeutic avenue for young disabled adults with inflammatory brain disease by combining, on one hand, anti-inflammatory and, on
the other hand, neuroprotective capacities.

PMID: 15494532 [PubMed - as supplied by publisher]

[Mariel]

My ferritin level is now 7, very low. That measures iron storage. I had to have phlebotomies because of my Myeloproliferative disease. And I have Porphyria.

When I was young, however, I had anemia, hematocrit of 26. I tried to take iron, but I could not, because of the porphyria. I learned I could not take iron very young, and had a hysterectomy rather than trying to cure my anemia by taking iron.

Then later, I got too high hematocrit and platelets, so I get phlebs, but I haven't had to have one in months because I got my iron down to very low, so the hematocrit does not come up fast.

Sooner or later, more phlebs on my horizon.

It's good to know my low iron has something good in it, better for MS.

I too was given iron IV when young, the worst thing could have happened to me. I was the subject of a lot of experimentation, most of it bad. However, Mom to M, I don't criticize your iron IV if there's a good reason for it. You are not me!

[Mariel]

Oh, yes, on the general subject of this thread, I believe we are all heavily poisoned by our world, but most of us can more or less detox the poisons. Much more than lead, zinc, mercury. Benzine and other poisons in car exhaust. Solvents in cleaners. Additives in food. Junk in particle board. Formalin in new clothes. Really bad coatings in new carpet.
Pesticides, herbicides.

Some people eventually build up a load of this because they are less adept than others in detoxing.
I grew up in a world where there was only a small fraction of this stuff, so I was healthy and an athlete until
I went to college, where I got a blast of formaldehye, solvents, and herbicide. I was less able to detox it than
the dorm-mates. So I was told I was emotionally in trouble. All the while building up lesions in my brain. And later neuropathy.

That's where we are as a modern society, but of course many older societies also had poisoned environments.

[Braindead]

Iron deposite have been noticed in MS lesions for some time. It also has been noted that iron deposits can be toxic/damage neurons.

The deposits seem to be the results of abnormal cell death that leaves behind its Iron which because the cell deaths continue they (iron deposits)accumulates in rather large amounts.

So the iron deposits do not cause MS but cause additional cell/neuron deaths as they increase in size and number.

I did not post all this at the time I mentioned IRON as being a problem in MS because I was trying to find some GOOD recent abstracts that showed that they were present in MS folks and that they did measurable harm.

It appears that the ability to measure these deposits has matured but what they mean/do in MS is still speculative/unproven/unpublished.

I will post what I have found.

Braindead

: Med Hypotheses. 2008 Aug;71(2):293-7. Epub 2008 Apr 8.

Hypothetical molecular mechanisms by which local iron overload facilitates the development of venous leg ulcers and multiple sclerosis lesions.

Simka M, Rybak Z.
Department of Angiology, Wodzislawska 78, 43-200 Pszczyna, Poland.

This paper presents a hypothetical model of role for iron in the development of venous leg ulcers and multiple sclerosis.

Elevated concentrations of iron were found in the skin affected by venous hypertension and also in the areas of brain with multiple sclerosis lesions.

Individuals with hemochromatosis gene (HFE) mutations: C282Y and H63D, which result in a less efficient transport of iron by macrophages, are characterized by an increased risk for venous leg ulcer and multiple sclerosis.

Multiple sclerosis is a T cell-mediated disease, and T cells probably participate in the development of venous ulcers.

This deleterious role of ferric ions could be related to the regulation of T cell proliferation and apoptosis. Under normal conditions excessive accumulation of T cells cannot take place, because nitric oxide and interferon-gamma drive these cells toward apoptosis.

However, in tissues with a high concentration of iron, T lymphocytes proliferate instead of undergoing apoptosis. This is possible due to the internalization of the INF-gammaR2 chain of the interferon-gamma receptor, the downregulation of inducible nitric oxide synthase expression in macrophages and the inactivation of the active site of caspases.

Yet, it should be emphasized that this hypothesis does not claim for the increased concentration of iron as a direct causal factor for the development of venous ulcerations or multiple sclerosis, but rather, iron is a factor that modulates and exaggerates the autoimmune process.

Iron chelators, administered systemically or locally, should potentially exhibit therapeutic and prophylactic activity against venous leg ulcers and multiple sclerosis.

PMID: 18400414 [PubMed - indexed for MEDLINE

Green Tea is an Great IRON CHELATOR (removes excess iron).

"Metal-Chelating Activity
One cardinal feature of neurodegenerative diseases including
AD, PD, Huntington’s disease, ALS, Friedreich’s
ataxia, multiple sclerosis, and aceruloplasminemia is the
appearance of excessive iron at degenerative neuronal
sites [17] . The buildup of an iron gradient in conjunction
with ROS (superoxide, hydroxyl radical and nitric oxide)
are thought to constitute a major trigger in the demise in
all theses diseases. Therefore, the chelation of free cellular
ferric and ferrous ions by the different metal chelators
make them potential agents to combat iron-induced generation
of reactive oxygen radicals (by the Fenton and
Haber-Weiss reactions) and aggregation of alpha ( _ )-
synuclein and A _ in PD and AD, respectively."

"Conclusions
It is likely that syndromes such as AD and PD will require
multiple- drug therapy to address the varied pathological
aspects of the disease. Therefore, the use of compounds
with poly-pharmacological activities or cocktail
of drugs is a promising therapeutic approach for the treatment
of neurodegenerative diseases. Indeed, a wealth of
new data indicates that green tea catechins are being recognized
as multifunctional compounds for neuroprotection.
They act as radical scavengers, iron chelators and
modulators of pro-survival genes, and PKC signaling
pathway. The use of EGCG as a natural, non-toxic, lipophilic
brain permeable neuroprotective drug is advocated
for ‘ironing out iron’ from those brain areas where it preferentially
accumulates in neurodegenerative diseases
[106] . Thus, green tea catechins may have potential disease-
modifying action. Future efforts in the understanding
of the protective mechanism of action of these polyphenols
should concentrate on deciphering the cellular
targets affected by these compounds and other neuroprotectants."


Above extracted from below paper.

This paper talks about neuro protection by Green Tea (egcg).

Multifunctional Activities of Green Tea Catechins in Neuroprotection
Modulation of Cell Survival Genes, Iron-Dependent Oxidative Stress and PKC
Signaling Pathway

.
http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowPDF&ProduktNr=224154&Ausgabe=230907&ArtikelNr=85385&filename=85385.pdf

Braindead

p.s. I think I will stop soon .. pleaese someone stop me!!!