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oh INTERESTING i hadn't realized that was the angle cure was on.
i thought it was more along the lines of vitamin k helping with d status, not d depleting k. never read before that vit a would protect against d-related k depletion either. neat.
will be interesting to see how d intake and k status might correlate in human studies.

Well, I've been taking for the last 4 days a vitamin k supplement from Life extension which is 2,100micrograms of vitamin k activity and includes 100mcg of vit k2 as menaquinone-7, 1000mcg of vit k2 as menaquinone -4 and 1000mcg of vitamin k1. It is definitely doing something to my MS. I take the pill at night with 2020mg of salvia miltiorrhiza as I'm worried about too much coagulation! I have had 3 nights of no toilet going! I have had 3 nights of virtually no spasms. BUT in the morning my leg is a bit stiffer than they have been on salvia alone. However when I take my disgusting Chinese tea which now contains both ginkgo and salvia within an hour my leg feels a bit better to walk on....

mmm! I'm now going to increase a bit the salvia as I had, since my Christmas relapse, decided on really taking only 1020mg of salvia at night but now I think I can add a bit more back in.

more vitamin k stuff:

1: Cell Biochem Funct. 2007 Sep-Oct;25(5):485-90. Links
Effects of vitamin K1 supplementation on vascular responsiveness and oxidative stress in a rat femoral osteotomy model.Tasatargil A, Cadir B, Dalaklioglu S, Yurdakonar E, Caglar S, Turkay C.
Department of Pharmacology, Medical Faculty, Akdeniz University, Antalya, Turkey. ardatas@akdeniz.edu.tr

The main function of vitamin K1 is to act a co-factor for gamma-glutamyl carboxylase. However, it has also been shown to lessen oxidative stress. This study was aimed to evaluate the effect of vitamin K1 supplementation on vascular responsiveness and oxidative status in rats that underwent femoral osteotomy. Twenty-four male rats were divided into three groups to serve as sham, osteotomy and vitamin K1 groups. Indices of oxidative stress (catalase), and oxidative damage (malondialdehyde) were analysed in erythrocytes. In order to evaluate vascular reactivity, concentration-response curves to phenylephrine, angiotensin II, 5-hydroxytryptamine, bradykinin and histamine were constructed. The findings of this study clearly show that oxidative stress clearly increases after femoral osteotomy in rats. Also, this operation causes a significant depression in vascular responsiveness to contracting agents and endothelium-dependent vasodilators. However, vitamin K1 supplementation prevents vascular hyporeactivity by reducing oxidative stress and may represent a novel approach during osteotomy healing.

PMID: 16929463 [PubMed - indexed for MEDLINE

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not sure I like the look of this, gulp!

1: Toxicol Appl Pharmacol. 2006 May 15;213(1):10-7. Epub 2005 Oct 26. Links
Vitamin K1 (phylloquinone) induces vascular endothelial dysfunction: role of oxidative stress.Tirapelli CR, De Andrade CR, Lieberman M, Laurindo FR, De Souza HP, de Oliveira AM.
Department of Pharmacology, Faculty of Medicine of Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brazil.

We aimed to investigate the mechanisms underlying the vascular effects induced by phylloquinone (Vitamin K1; VK1). Vascular reactivity experiments, using standard muscle bath procedures, showed that VK1 (5 and 50 microM) enhances the contractile response of endothelium-intact, but not denuded, rat carotid rings to phenylephrine. Similarly, maximal contraction induced by phenylephrine was enhanced in the presence of the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME). The combination of L-NAME and VK1 did not produce any further additional effect. Pre-incubation of intact-rings with VK1 reduced both acetylcholine- and bradykinin-induced relaxation. VK1 induced an increment in tension on carotid rings submaximally pre-contracted with phenylephrine. VK1-induced increment in tension was completely abolished by endothelial removal or incubation of intact rings with L-NAME and L-NNA. Conversely, 7-nitroindazole, 1400 W, or indomethacin did not affect VK1-induced contraction. Moreover, VK1 reduced L-arginine-induced relaxation in endothelium-intact rings. Lucigenin-amplified chemiluminescence assays showed that VK1 induced an increase in the level of superoxide anions in endothelium-intact but not denuded rings. Measurement of nitrite and nitrate generation showed that VK1 did not alter nitrate formation but strongly inhibited the generation of nitrite. Finally, the superoxide anions scavenger tiron prevented the endothelial vasomotor dysfunction caused by VK1 on phenyleprine-induced contraction and acetylcholine or bradykinin-induced relaxation. In conclusion, our data show that VK1 disrupts the vasomotor function of rat carotid. Our results suggest that VK1-induced oxidative stress through production of superoxide anion is interfering with the NO pathway, which in turn is responsible for the altered vascular reactivity induced by VK1.

PMID: 16256160 [PubMed - indexed for MEDLINE

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there are lots of different forms of vitamin k. I'm taking some of this:

1: J Nutr Sci Vitaminol (Tokyo). 1999 Dec;45(6):711-23.Links
Vitamin K2 (menatetrenone) induces iNOS in bovine vascular smooth muscle cells: no relationship between nitric oxide production and gamma-carboxylation.Sano M, Fujita H, Morita I, Uematsu H, Murota S.
Department of Physiological Chemistry, Graduate School, Tokyo Medical and Dental University, Japan.

It has been recently reported that vitamin K2 (menaquinone-4: menatetrenone, VK2) has an anti-atherogenic effect as well as the ability to produce clotting factors and improve osteoporosis. However, the mechanism by which VK2 acts on atherosclerosis is still unclear. In this paper, we investigated the effects of vitamin K and its side chain on NO production as an anti-atherogenic substance in a cultured vascular system. Treatment of bovine vascular smooth muscle cells (SMC) with VK2 (30 microM) caused a time-dependent (24-72 h) increase in the nitrite (NO2) level in the conditioned medium, but not in bovine vascular endothelial cells. Classical NOS inhibitor (L-nitro arginine) and iNOS-specific inhibitors completely blocked the increased nitrite level induced by VK2 treatment, but D-nitro arginine could not it. Immunostaining and Western blotting analysis showed that VK2 induced iNOS protein in the SMC. VK2 has a naphtoquinone nucleus, which is identical in menadione (VK3), and an unsaturated side chain, which is called geranylgeraniol (GGO). To determine whether the structure of VK2 was related to an increasing nitrite level, we investigated the nitrite level in conditioned medium treated with VK3 or GGO. Neither VK3 nor GGO treatment of SMC increased the nitrite level. In addition, warfarin, an inhibitor of VK2-dependent gamma-carboxylation, did not affect the increased nitrite level induced by VK2 in SMC. In conclusion, VK2 caused NO production through iNOS induction in bovine SMC, that was not related to the structure of VK2, naphtoquinone nucleus or its side chain, independently of gamma-carboxylation.

PMID: 10737225 [PubMed - indexed for MEDLINE]

Related ArticlesCytotoxic effect through fas/APO-1 expression due to vitamin K in human glioma cells. [J Neurooncol. 2000] An anti-ulcer drug, geranylgeranylacetone, suppresses inducible nitric oxide synthase in cultured vascular smooth muscle cells. [J Hypertens. 2005] Amlodipine increases nitric oxide synthesis in cytokine-stimulated cultured vascualar smooth muscle cells. [J Hypertens. 2000] Review[Coagulation disorders caused by cephalosporins containing methylthiotetrazole side chains] [Acta Clin Belg. 1990] ReviewThe mechanism of action of vitamin K. [Annu Rev Nutr. 1995] » See Reviews... | » See All... Patient Drug Information
Warfarin (Coumadin®) Warfarin is used to prevent blood clots from forming or growing larger in your blood and blood vessels. It is prescribed for people with certain types of irregular heartbeat, people with prosthetic (replacement or mechan... » read more ...

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I did over a week on the vitamin K but by the end my walking had become much harder. I have now not been taking it for about 5 days and my walking is considerably better. However I am now back to going to the toilet at night and having occasional spasms. Mmm. I think getting the blood and vasculature to its optimum size and consistency is a highly variable affair. I can't wait for a zamboni liberation procedure.

In view of Dr. Terry Wahls' emphasis on dark green leafy vegetables in the diet, her dramatic improvement on such a diet, and her current clinical trial underway using that diet, I am resurrecting this thread for its WEALTH of information on vitamin K (found especially in dark green leafy vegetables, such as kale).

I think the information here is vital! Thank you, thank you to everyone who contributed.

drat it my earlier post got dumped. just wanted to add, for those who are concerned about vit K and clotting post CCSVI treatment, that there are many dark leafy greens which while high in K, are also high in vit E, a vitamin K antagonist.

warfarin effects on PIVKA II http://www.ncbi.nlm.nih.gov/pubmed/2381266
vitamin e effects on PIVKA II http://www.ajcn.org/content/80/1/143.full

"PIVKA II is an abbreviation for the underactive form of prothrombin produced in the presence of either vitamin K deficiency due to dietary or endogenous production defects, or to the presence of a vitamin K antagonist such as Coumadin (warfarin)" (JL: or vitamin E)

somewhat echoing posts from earlier, important functions of vitamin K that are not involved in clotting (from whfoods.com) include:
# Help protect your bones from fracture
# Help prevent postmenopausal bone loss
# Help prevent calcification of your arteries
# Provide possible protection against liver and prostate cancer

and from wikipedia:

Vitamin K is involved in "three physiological processes:
* Blood coagulation: (prothrombin (factor II), factors VII, IX, X, protein C, protein S, and protein Z).
* Bone metabolism: osteocalcin, also called bone Gla-protein (BGP), matrix gla protein (MGP)[6], and periostin.
* Vascular biology: growth arrest-specific protein 6 (Gas6)"

on the vascular point:

http://www.ncbi.nlm.nih.gov/pubmed/17064312
Gas6 and protein S. Vitamin K-dependent ligands for the Axl receptor tyrosine kinase subfamily.
"studies have shown the Gas6-Axl system to regulate cell survival, proliferation, migration, adhesion and phagocytosis... altered activity/expression of its components has been detected in a variety of pathologies such as cancer and vascular, autoimmune and kidney disorders"

http://www.ncbi.nlm.nih.gov/pubmed/11094334
The Gas6/Axl system: a novel regulator of vascular cell function
"Gas6/Axl signaling may impact on the response of blood vessels to injury, thereby contributing to the development of atherosclerosis and/or restenosis."

foods highest in both vit K AND vit E include parsley, kale/chard/collards (all cruciferous), and dandelion greens (as per www.nutritiondata.com nutrient search tool).

just got home from a shop actually, which included spring onions, parsley, dill and spinach for a spinakopita, plus kale and chard for sides with dinner the next couple of days (fish tonight, chicken tomorrow).

yum!

All this dandelion and kale talk is making me hungry. I used to make the greatest smoothie -- combine a handful of dandelions, a bunch of kale, and a mango with some ice cubes and water... it was magnificent, if I do say so myself. It was a bit rough to digest and (pardon the imagery) used to plug me up real good, but I definitely felt better after a few weeks of drinking it.

Neurosci. 2003 Jul 2;23(13):5816-26.

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.

Abstract
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]Free Article


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

JackD

I know this is last bit of info below is a waste of my time and yours, but here it is...

VINPOCETINE can help remove Calcium from soft tissues where it does NOT belong.

http://www.ncbi.nlm.nih.gov/pubmed/2340946

http://www.ncbi.nlm.nih.gov/pubmed/2390364

ViNPOCETINE can help lessen MS activity by up to 48%. Almost ALL Phosphodiesterase inhibitors lower MS activity but the side-effects SUCK. This is not the case for VINPOCETINE.

http://www.ncbi.nlm.nih.gov/pubmed/10694847

http://www.ncbi.nlm.nih.gov/pubmed/20448200

VINPOCETINE can help with some limited urine flow problems with the bladder.

http://www.ncbi.nlm.nih.gov/pubmed/11760783

Taking 30 mg (10 mg 3 times a day) could also make you smart like me.

VINPOCETINE is a Phosphodiesterase inhibitor (TYPE I) PDE1 and causes relaxation of the internal anal sphincter. This loss of sphincter control is a serious problem and really agrivates the constipation problem for many MS folks.

Dis Colon Rectum. 2002 Apr;45(4):530-6.

Phosphodiesterase inhibitors cause relaxation of the internal anal sphincter in vitro.

Jones OM, Brading AF, McC Mortensen NJ.

University Department of Pharmacology, John Radcliffe Hospital, Oxford, United Kingdom.

Abstract
PURPOSE: Pharmacologic treatments are gaining widespread acceptance as first-line therapy for anal fissure. However, existing treatments have limited clinical usefulness because of side effects and incomplete healing rates.

METHODS: Fresh human surgical resection specimens containing internal anal sphincter and rectal circular muscle were collected. Strips of smooth muscle were cut from each muscle group and mounted in a superfusion organ bath. The effects of increasing concentrations of phosphodiesterase inhibitors were evaluated.

RESULTS: All phosphodiesterase inhibitors tested caused a dose-dependent reduction in the tone of the internal anal sphincter, with potencies as follows: vinpocentine (phosphodiesterase-1 inhibitor; 50 percent maximum inhibition concentration = 0.87 +/- 0.10 microM), erythro-9-(2-hydroxy-3-nonyl) adenine hydrochloride (phosphodiesterase-2 inhibitor; 32 +/- 4.8 microM), trequinsin (phosphodiesterase-3 inhibitor; 0.28 +/- 0.041 microM), rolipram (phosphodiesterase-4 inhibitor; 63 +/- 9 microM), zaprinast (phosphodiesterase-1,5,6,9,11 inhibitor; 3 +/- 0.69 microM), and dipyridamole (phosphodiesterase-5,6,8,10,11 inhibitor; 5.5 +/- 2 microM). Although all inhibitors were also effective on rectal circular muscle strips, erythro-9-(2-hydroxy-3-nonyl) adenine hydrochloride, trequinsin, and rolipram were at least an order of magnitude more potent in this tissue than in the internal anal sphincter.

CONCLUSIONS: There are several functionally important phosphodiesterases in the internal anal sphincter and rectal circular muscle. Both adenosine 3', 5'-cyclic monophosphate and guanosine 3',5'-cyclic monophosphate appear to be important in the myogenic tone of the internal anal sphincter, and this study provides further evidence of the sphincteric specialization of this tissue. Phosphodiesterase inhibitors might represent a new therapy for the treatment of anal fissure.

PMID: 12006938 [PubMed - indexed for MEDLINE]