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Old 06-09-2009, 06:02 PM
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jackD jackD is offline
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Join Date: Jan 2008
Location: Maryland outside WASH DC
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15 yr Member
jackD jackD is offline
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Join Date: Jan 2008
Location: Maryland outside WASH DC
Posts: 258
15 yr Member
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"A concern of mine is whether we should take calcium supplements due to this murderous effect described in your post. What channel blocker are you taking? I have also been on BP meds for several years." gonnamakeit

I would say you should take vit D3, magnesium AND calcium supplements as they work well together and help the MS condition.

It is HOW the cells USE Calcium that needs regulating.

I take Nifedia CC which a timed release form of Nitrendipine mentioned below. I am still researching this.

jackD


"Document title
Calcium channel blockers ameliorate disease in a mouse model of multiple sclerosis

Author(s)
BRAND-SCHIEBER Elimor (1) ; WERNER Peter (1 2) ;
Author(s) Affiliation(s)
(1) Department of Neurology, Albert Einstein College of Medicine, Bronx, NY 10461,
(2) Department of Pathology (Neuropathology), Albert Einstein College of Medicine, Bronx, NY 10461


Abstract
Multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), an animal model of MS, are inflammatory demyelinating diseases of the central nervous system. The inflammatory attacks lead to glial dysfunction and death, axonal damage, and neurological deficits.

Numerous studies in rat suggest that extracellular calcium influx, via voltage-gated calcium channels (VGCC), contributes to white matter damage in acute spinal cord injury and stroke. Our immunohistochemical finding that mouse spinal cord axons display subunits of L-type VGCC also supports this hypothesis.

Furthermore, we hypothesized that VGCC also play a role in EAE, and possibly, MS.

In our study, administration of the calcium channel blockers (CCB) bepridil and nitrendipine significantly ameliorated EAE in mice, compared with vehicle-treated controls.

Spinal cord samples showed reduced inflammation and axonal pathology in bepridil-treated animals.

Our data support the hypothesis that calcium influx via VGCC plays a significant role in the development of neurological disability and white matter damage in EAE and MS."
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Kitty (06-10-2009), SallyC (06-09-2009)