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Old 06-20-2008, 07:18 PM #21
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Yeah not sure I would exceed 1000 iu a day. Slow and steady is the way I am building mine back up.
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Old 06-20-2008, 09:05 PM #22
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This is the most comprehensive information about Vitamin D I have yet to find. As you get towards the bottom ( long) it explains why doses are being given above 2000 IU a day.

It is very interesting because it cites how steroids affect calcium and Vitamin D, and how other medications alter absorption.

http://ods.od.nih.gov/factsheets/vitamind.asp

For more info google: vitamin + D + absorption

Thanks for the article from the Journal of Clinical Nutrition!
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Old 06-21-2008, 07:22 AM #23
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I cant keep my Vit D level up. I have taken lots of different over the counter stuff too. I was recently placed on Rx stuff. I hope that helps. I already feel better after just a couple of weeks on it.
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Old 06-21-2008, 12:22 PM #24
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Default D2 vs. D3

Kristi, I'm quite surprised you were prescribed D2 as opposed to D3 (aka Cholecalciferol). D3 is the equivalent to the "sunshine" factor and is processed in the body as a hormone -- it's specifically that form that's been the hot topic.

I started reading a lot about D3 after I was dxed and have been taking a little over 3,000 IUs daily for at least 9 months. (I ADD UP the D in my calcium and mult-vitamin and then supplement with two 1,000 capsules made by Jarrow.) Vitamin D can build up in the body and can be toxic so your levels should be monitored, as well as your liver function. I don't know if my levels were low before I started supplementing but my endocrinologist tested me a few months ago and even with the amount I'm taking, I was still within normal range (and my liver function was fine). However, I will continue to be monitored, having these tests repeated in future blood work. My endo explained to me that for some reason, they're finding that those high 50,000 IU doses weekly do not seem to present the same problems as high doses building up over time.

The RDA UL for "healthy" people has been raised to 600 IUs. There have been several studies about vitamin D (D3 specifically) possibly being helpful with various neurological disorders, not only MS (and not only in terms of prevention). I know many people with MS in the U.S. whose doctors have been recommending (if not prescribing) vitamin D3 to their patients even if their levels are not low. Most of the things I've read about using this supplement like a "drug" recommend up to 4,000 IUs daily but to reduce intake in the summer or if you live in a sunny climate year round. Again, do be careful though -- do your own research, speak to your doctors and if you DO take it, have your D levels and liver function tested periodically.
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Old 06-21-2008, 12:41 PM #25
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Default The dark side & Vit K1 &K2

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.

Last edited by jackD; 06-21-2008 at 04:25 PM.
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Old 06-21-2008, 12:47 PM #26
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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.
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Old 06-21-2008, 01:12 PM #27
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Default Vinpocetine & MS

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]

Last edited by jackD; 06-21-2008 at 03:27 PM.
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Old 06-21-2008, 04:15 PM #28
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Quote:
Originally Posted by lady_express_44 View Post
The best way to source Vitamin D naturally is by getting 5-30 minutes of DIRECT sun exposure between 10 AM and 3 PM, at least twice a week. This exposure can be to (NOTE: EITHER) the face, arms, legs, or back.
Cherie
When I got diagnosed 10 months ago I was told I had an extremely low Vitamin D level. To be perfectly honest I was shocked since I had lived in San Diego for 10 years (sun all the time) and moved to sunny/hot Texas and have been here the past 4 years. Thus, I'm not sure everyone's bodies can get the Vitamin D they need from the sun -- clearly that wasn't the case for me over the past 14 years and I spend a lot of time outdoors.

I took the 50,000 IU pills once a week for 9 weeks. It bumped my level up into low normal range. I am now taking 1,000 IU a day.

The MS specialist I saw at the Mayo Clinic in MN. said that I should be taking Vitamin D supplements every day. The MS specialist I saw in my own city 2 weeks ago said that Vitamin D deficiency is a risk factor for MS (apparently I hit the MS jackpot and as she put it "the stars lined up" because I had 4 risk factors: 1) Vitamin D deficiency 2) grew up in Mass. until age 22 3) mother just diagnosed with MS last year right before me 4) wicked mono/epstein barr infection the year before my diagnosis).
Lucky me! <heavy sarcasm>

Anyhow, nothing proves that taking Vitamin D after the fact will slow the disease down but why not take the supplement? There does appear to be a correlation of some sort.
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Old 06-21-2008, 08:05 PM #29
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Quote:
Originally Posted by Bearygood View Post
Kristi, I'm quite surprised you were prescribed D2 as opposed to D3 (aka Cholecalciferol). D3 is the equivalent to the "sunshine" factor and is processed in the body as a hormone -- it's specifically that form that's been the hot topic.

I started reading a lot about D3 after I was dxed and have been taking a little over 3,000 IUs daily for at least 9 months. (I ADD UP the D in my calcium and mult-vitamin and then supplement with two 1,000 capsules made by Jarrow.) Vitamin D can build up in the body and can be toxic so your levels should be monitored, as well as your liver function. I don't know if my levels were low before I started supplementing but my endocrinologist tested me a few months ago and even with the amount I'm taking, I was still within normal range (and my liver function was fine). However, I will continue to be monitored, having these tests repeated in future blood work. My endo explained to me that for some reason, they're finding that those high 50,000 IU doses weekly do not seem to present the same problems as high doses building up over time.

The RDA UL for "healthy" people has been raised to 600 IUs. There have been several studies about vitamin D (D3 specifically) possibly being helpful with various neurological disorders, not only MS (and not only in terms of prevention). I know many people with MS in the U.S. whose doctors have been recommending (if not prescribing) vitamin D3 to their patients even if their levels are not low. Most of the things I've read about using this supplement like a "drug" recommend up to 4,000 IUs daily but to reduce intake in the summer or if you live in a sunny climate year round. Again, do be careful though -- do your own research, speak to your doctors and if you DO take it, have your D levels and liver function tested periodically.
Hi,Bearygood

I don't know why my neuro prescribed vit D2,heck I didn't know there was a
D2 and D3, I just thought there was just Vit D period. I'm glad I started this thread,I've found out alot of good information from alot people here.
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Old 06-23-2008, 08:45 PM #30
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Default Nerve Growth Factor -good Stuff

Most folks do not know much about this but NGF Nerve Growth Factor is great stuff to have in sufficient quantity to take care of those small? brain repair jobs common to MS folks.

If you are LOW in Vitamin D then you are probably LOW in NGF Nerve Growth Factor also.

I probably should start a new thread to elaborate on this topic.(Nerve Growth/Repair)

Suffice it to say that Vitamin D makes the body make NGF as stated in the below abstract.

http://www.copewithcytokines.de/cope.cgi?key=NGF (a GREAT sources of my info)

This is why I take 4000 IUs of Vit D3 supplement each day. The excess is GOOD for MS folks because our NEED is greater.

jackD

http://www.ncbi.nlm.nih.gov/pubmed/9...ubmed_RVDocSum

Quote:
1: Nippon Yakurigaku Zasshi. 1997 Oct;110 Suppl 1:39P-43P.

[Novel pharmacological activity of a vitamin (novel pharmacological action of vitamin D)][Article in Japanese]


Fukuoka M, Ohta T, Kiyoki M.
Teijin Institute for Bio-Medical Research, Tokyo, Japan.

The endocrine system to maintain calcium homeostasis involves the active vitamin D, as well as parathyloid hormone (PTH). Based on this 'classical' calcium-regulatory function, 1,25-(OH)2D3 and 1 alpha OHD3 was developed as the drug for vitamin D resistant rickets, renal dystrophy, and osteoporosis. Psoriasis is a chronic skin disease which is characterized by hyperproliferation and abnormal differentiation of epidermis. As an anti-psoriatic drug, 1,24R-(OH)2D3 has been on clinical use. The efficacy for psoriasis is explainable by the differentiation-inducing activity of this compound. 1,25-(OH)2D3 was also reported to suppress proliferation and induce differentiation of tumor cells including breast cancer, colon cancer and so forth, suggesting the possible therapy of malignant tumors.

In immune system, active vitamin D3 exerts various effects; 1,25-(OH)2D3 suppresses proliferation and cytokine production in T cells and antibody production in B cells. Animal models of autoimmune diseases and skin-graft suggest active vitamin D becomes a novel immuno suppressant.

Since 1,25-(OH)2D3 induces the synthesis of nerve growth factor (NGF), it will be a new therapy for the treatment of neuronal degenerative diseases.

PMID: 9503403 [PubMed - indexed for MEDLINE]

Last edited by jackD; 06-24-2008 at 03:05 PM.
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