Vitamin D and MS ?

jackD · 06-21-2008, 12:41 PM

I have recently added Vit K to my supplement list because I found in the
MPEG of my body CT Scan noticeable Calcium deposits around my heart aorta
and some considerable Calcification in my right Femoral Artery.

One of the causes of this is Vitamin D supplementation!!!

Note --- there are different kinds of vit K

K1 (phylloquinone) is present naturally in plants.
K2 (menaquinone) is made by bacteria in the intestinal tract of humans and
animals
K3 (menadione) is man made.
K4 (menadiol) is man made. It can be used by intestinal bacteria to make K2.
Unlike the fat-soluble compounds K1, K2 and K3, K4 is water-soluble

I have discovered that Vit K supplements will stop and help remove this
excess calcium. I also believe that Vinpocetine may have a similar action(at
least in rabbit tests). I am taking the LEF(life Extension Foundation)
"SUPER K with K2" supplement which has 9 mg of Vit K1 and 1 mg of Vit K2

http://www.lef.org/newshop/items/ite...ced-K2-Complex

jackD

Quote:

1: Z Kardiol. 2001;90 Suppl 3:57-63.Links
Role of vitamin K and vitamin K-dependent proteins in vascular calcification.Schurgers LJ, Dissel PE, Spronk HM, Soute BA, Dhore CR, Cleutjens JP, Vermeer C.
Department of Biochemistry, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands.

OBJECTIVES: To provide a rational basis for recommended daily allowances (RDA) of dietary phylloquinone (vitamin K1) and menaquinone (vitamin K2) intake that adequately supply extrahepatic (notably vascular) tissue requirements.

BACKGROUND: Vitamin K has a key function in the synthesis of at least two proteins involved in calcium and bone metabolism, namely osteocalcin and matrix Gla-protein (MGP). MGP was shown to be a strong inhibitor of vascular calcification. Present RDA values for vitamin K are based on the hepatic phylloquinone requirement for coagulation factor synthesis. Accumulating data suggest that extrahepatic tissues such as bone and vessel wall require higher dietary intakes and have a preference for menaquinone rather than for phylloquinone.

METHODS: Tissue-specific vitamin K consumption under controlled intake was determined in warfarin-treated rats using the vitamin K-quinone/epoxide ratio as a measure for vitamin K consumption. Immunohistochemical analysis of human vascular material was performed using a monoclonal antibody against MGP. The same antibody was used for quantification of MGP levels in serum.

RESULTS: At least some extrahepatic tissues including the arterial vessel wall have a high preference for accumulating and using menaquinone rather than phylloquinone. Both intima and media sclerosis are associated with high tissue concentrations of MGP, with the most prominent accumulation at the interface between vascular tissue and calcified material. This was consistent with increased concentrations of circulating MGP in subjects with atherosclerosis and diabetes mellitus.

CONCLUSIONS: This is the first report demonstrating the association between MGP and vascular calcification. The hypothesis is put forward that undercarboxylation of MGP is a risk factor for vascular calcification and that the present RDA values are too low to ensure full carboxylation of MGP.

PMID: 11374034 [PubMed - indexed for MEDLINE]

Quote:

1: J Neurosci. 2003 Jul 2;23(13):5816-26. Links
Novel role of vitamin k in preventing oxidative injury to developing oligodendrocytes and neurons.Li J, Lin JC, Wang H, Peterson JW, Furie BC, Furie B, Booth SL, Volpe JJ, Rosenberg PA.
Department of Neurology, Division of Neuroscience, Children's Hospital, Boston, MA 02115, USA.

Oxidative stress is believed to be the cause of cell death in multiple disorders of the brain, including perinatal hypoxia/ischemia. Glutamate, cystine deprivation, homocysteic acid, and the glutathione synthesis inhibitor buthionine sulfoximine all cause oxidative injury to immature neurons and oligodendrocytes by depleting intracellular glutathione.

Although vitamin K is not a classical antioxidant, we report here the novel finding that vitamin K1 and K2 (menaquinone-4) potently inhibit glutathione depletion-mediated oxidative cell death in primary cultures of oligodendrocyte precursors and immature fetal cortical neurons with EC50 values of 30 nm and 2 nm, respectively. The mechanism by which vitamin K blocks oxidative injury is independent of its only known biological function as a cofactor for gamma-glutamylcarboxylase, an enzyme responsible for posttranslational modification of specific proteins. Neither oligodendrocytes nor neurons possess significant vitamin K-dependent carboxylase or epoxidase activity. Furthermore, the vitamin K antagonists warfarin and dicoumarol and the direct carboxylase inhibitor 2-chloro-vitamin K1 have no effect on the protective function of vitamin K against oxidative injury.

Vitamin K does not prevent the depletion of intracellular glutathione caused by cystine deprivation but completely blocks free radical accumulation and cell death. The protective and potent efficacy of this naturally occurring vitamin, with no established clinical side effects, suggests a potential therapeutic application in preventing oxidative damage to undifferentiated oligodendrocytes in perinatal hypoxic/ischemic brain injury.

PMID: 12843286 [PubMed - indexed for MEDLINE]

Arterial calcification is characterized as a buildup of calcium in the
arterial walls. It is a process that can begin as early as the second decade
of life and continue throughout adulthood. Although calcium is an essential
nutrient in maintaining human bone integrity, the trick is to keep it out of
the arteries. Studies have revealed that adequate levels of vitamin K may
help in keeping calcium in bones and out of arterial walls.

Caution
Those taking anticoagulant drugs such as Coumadin or heparin should avoid
vitamin K supplements.

Bearygood · 06-21-2008, 12:47 PM

Thanks, Jack. I'd heard about this in regard to calcium supplementation and have been meaning to look to research it more thoroughly. I'm definitely going to mention it to my endocrinologist when I see him in September.

jackD · 06-21-2008, 01:12 PM

Here is the rabbit thing plus the Bladder thingie. I take 10mg of Vinpocetine twice a day.

jackD

p.s. It is also the BEST cure for MS(58% reduction in lesion activity) and fixes my bladder problems. There is some considerable hyperboyle in the preceding statement but that is what the study showed.

Quote:

1: J Int Med Res. 1990 Mar-Apr;18(2):142-52.

Calcium, phosphorus and aluminium concentrations in the central nervous system, liver and kidney of rabbits with experimental atherosclerosis: preventive effects of vinpocetine on the deposition of these elements.

Yasui M, Yano I, Ota K, Oshima A.

Division of Neurological Diseases, Wakayama Medical College, Japan.

Calcium, phosphorus and aluminium concentrations in the central nervous system, liver and kidneys were determined in 16 rabbits with atherosclerosis experimentally induced by a cholesterol-rich diet and the protective effect of 3 or 10 mg/kg.day vinpocetine (14-ethoxycarbonyl-(3 alpha,16 alpha-ethyl)-14,15-eburnamenine) given orally on the deposition of these elements was assessed.

Rabbits fed a cholesterol-rich diet developed atherosclerosis after 3 months and these rabbits possessed high concentrations of calcium, phosphorus and aluminium in the central nervous system, determined by neutron activation analysis.

In atherosclerotic rabbits fed a vinpocetine supplement, there was a decrease in concentrations of these elements in tissues.

It is suggested that calcium, phosphorus and aluminium may be implicated in the aetiology of atherosclerosis and that vinpocetine may have a preventive action on the deposition of these elements in central nervous tissue, liver and kidney.

PMID: 2340946 [PubMed - indexed for MEDLINE]

Quote:

1: Mult Scler. 2000 Feb;6(1):56-8.

Drop in relapse rate of MS by combination therapy of three different phosphodiesterase inhibitors.

Suzumura A, Nakamuro T, Tamaru T, Takayanagi T.
Department of Neurology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-0813, Japan.

Phosphodiesterase inhibitors (PDEIs), when used in combination, synergistically suppress TNFalpha production by various cells and also suppress experimental demyelination at very low concentrations.

We conducted a pilot study to determine whether the combination of three PDEIs suppresses the relapse of MS at the usual therapeutic doses. Of the 12 relapsing remitting MS, the mean relapse rate/year dropped remarkably (from 3.08+/-3.32 to 0.92+/-1.86) after PDEI treatment. Seven out of 12 (58.3%) were relapse-free in the follow up period (499+/-142 days).

The combination of three PDEIs can be safe and useful strategy for the future treatment of MS. - 58

PMID: 10694847 [PubMed - indexed for MEDLINE]

Bladder - thingie

Quote:

1: World J Urol. 2000 Dec;18(6):439-43.

Initial clinical experience with the selective phosphodiesterase-I isoenzyme inhibitor vinpocetine in the treatment of urge incontinence and low compliance bladder.

Truss MC, Stief CG, Uckert S, Becker AJ, Schultheiss D, Machtens S, Jonas U.
Department of Urology, Medizinische Hochschule Hannover, Germany. truss.michael@mh-hannover.de

Current pharmacological treatment modalities for urge incontinence and low compliance bladder are limited by a low clinical efficacy and the significant side effects of the standard drugs available. Previous in vitro studies indicated a possible functional relevance of the intracellular phosphodiesterase (PDE)-1 isoenzyme in the regulation of human detrusor smooth muscle contractility.

We therefore investigated the effect of the PDE-1 inhibitor vinpocetine in nonresponders to standard pharmacological therapy. In 11/19 patients (57.9%) clinical symptoms and/or urodynamic parameters were improved. Although these initial data are preliminary, they represent the first evidence that isoenzyme-selective PDE inhibition may be a novel approach to the treatment of lower urinary tract disorders.

PMID: 11204266 [PubMed - indexed for MEDLINE]

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