In my opinion the reason MS folks have lower zinc levels is that their sick mutant bodies
are extracting it from their tissue in order to make many more MMP-9s to help eat their brain.
Biometals. 2012 Feb 19. [Epub ahead of print]
Zinc aspartate suppresses T cell activation in vitro and relapsing experimental autoimmune encephalomyelitis in SJL/J mice.
Stoye D, Schubert C, Goihl A, Guttek K, Reinhold A, Brocke S, Grüngreiff K, Reinhold D.
Institute of Molecular and Clinical Immunology, Otto-von-Guericke-University, Leipziger Str. 44, 39120, Magdeburg, Germany.
Zinc is an essential trace element with a critical role in normal growth and development and in immune homeostasis. Zinc deficiency impairs both the innate and the adaptive immune system and can be normalized by zinc supplementation. On the other end of the spectrum, high dosages of zinc diminish immune cell functions similar to zinc deficiency. Here, we investigated the influence of zinc aspartate on proliferation and cytokine production of stimulated human T cells and mouse splenocytes in vitro. Furthermore, the effect of zinc aspartate was examined in mice with experimental autoimmune encephalomyelitis (EAE), an animal model of Multiple Sclerosis (MS) with a Th1/Th17 T cell-mediated immunopathogenesis. Zinc aspartate suppressed proliferation as well as IL-2, IL-10 and IL-17 production in stimulated human T cells and mouse splenocytes. Importantly, administration of a medium range dose of 30 μg/day zinc aspartate [1.5 mg/kg body weight (BW)] in a therapeutic manner led to a significant reduction of the clinical severity of the EAE during the first relapse of the disease. A lower zinc aspartate dose (6 μg/day, 0.3 mg/kg BW) had no significant therapeutic effect on the severity of the EAE, while administration of higher zinc aspartate amounts (120 μg/day, 6 mg/kg BW) led to more severe disease.
Taken together, our data suggest that zinc aspartate can modulate activation, proliferation and cytokine production of effector T cells in vitro and in vivo and that activated autoreactive T cells may be potential therapeutic targets of tightly controlled zinc supplementation in autoimmune diseases like MS.
PMID: 22350510 [PubMed - as supplied by publisher]
Arch Environ Health. 2002 Jul-Aug;57(4):383; author reply 383.
A multiple sclerosis cluster associated with a small, north-central Illinois
Schiffer RB, McDermott MP, Copley C.
Department of Neuropsychiatry, Texas Tech University Health Sciences Center,
Lubbock 79430, USA. firstname.lastname@example.orgThe 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
PMID: 11777019 [PubMed - indexed for MEDLINE]
1: 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.
PMID: 9042108 [PubMed - indexed for MEDLINE]I have posted thingies that can lower MMP-9s ...
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