Getting the blood thinned to the theraputic level

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Postby Arcee » Fri Aug 07, 2009 9:20 am

Not sure if this comment will help in any way, but the approach my PCP and I have been taking is that there is not a "no-no" list, that I can eat whatever I typically do as long as I don't binge on anything. So, I do eat blueberries and greens every day and we have settled, for now, on .75 of coumadin (1 and 1/2 pills) five days a week and 1.0 (2 pills) two days a week.
I totally get that a focus on diet with exclusions and inclusions can affect the numbers, and that may be the right route for some people. I just wanted to express this other strategy so people coming onto the blood thinners are aware of different approaches.
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Postby jimmylegs » Fri Aug 07, 2009 10:20 am

arcee, most of this thread is about the pharmaceutical approach, with a couple of posts on alternatives. your approach is probably by far the status quo treatment for the majority of patients dealing with stents.
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Postby skydog » Fri Aug 07, 2009 2:01 pm

Thanks JL for the sunflower oil info. I use maybe a TBSP per day of sunflower seed butter on either celery sticks or apple slices for a in between meal snack. I never used the oil for cooking or for making a salad dressing. I like a fresh salad from the garden undressed or with just a squeeze of lemon juice. Marie I thought blueberries were low in vitamin k and ok on a coumadin diet. It seems that there is always conflicting info out there when it comes to food. I guess just maintain a steady diet of your choice and adjust the coumadin to get the INR right. This for me is a difficult task as my diet changes with the season. Now the pumpkin season is just around the corner and it would be nice not to have to worry about the seeds as that is the best part. We make a awesome tasting pumpkin smoothie with the inside scrapings seeds and all blended high speed with a little pumpkin spice. Just like drinking pumpkin pie. Now I dont even want to know how off the chart vitamin k they are. Hope my daily double dose will do it. Really can hardly wait to say adios to couaidin. Peace, Mark
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Postby jimmylegs » Sat Aug 08, 2009 6:37 am

eeeewwwww drinking pumpkin pie :S lol!
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Postby catfreak » Sat Aug 08, 2009 7:19 am

My niece is growing some pumpkins. I'll have to get HER to try that one first!!!. :oops: :oops:

In case I missed it, has anyone posted a list of foods to eat or not to eat while on the blood thinners?

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Postby peekaboo » Sat Aug 08, 2009 7:30 am

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Postby catfreak » Sat Aug 08, 2009 8:17 am

Thank you Holly!!

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Postby jimmylegs » Sat Aug 08, 2009 9:35 am

cf, check out page 2 of this topic also maybe...
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Postby Loobie » Wed Aug 12, 2009 5:44 am

I found this article rather perplexing after deciding not to go on this drug for cost reasons:

http://online.wsj.com/article/SB125003545637224263.html
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Postby skydog » Wed Aug 12, 2009 8:33 am

I really hope we can get the Doc's to accept a combination approach. A little med with a sup or two that works together. Costs will be less for both the body and the pocket book. Heading down to see Dr. D for a follow up the first of September with lots of questions. Cheers, Mark
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Postby jimmylegs » Fri Aug 14, 2009 9:35 am

was just reading that calcium promotes blood clotting, if i had seen that before it didn't sink in at the time!

...the effect of calcium on the three distinguishable phases of clot formation, (1) proteolysis of fibrinogen, (2) fibrinogen-fibrin monomer complex formation, and (3) fibrin monomer polymerization, were investigated. ...there was a marked increase in the rate of fibrin monomer polymerization in the presence of calcium ions. These data show that calcium decreases the time required for fibrin formation from fibrinogen by markedly accelerating the phase of fibrin monomer polymerization.


so, if warfarin is doing something about calcium and not just vit K...

The present studies demonstrate that growth and vitamin D treatment enhance the extent of artery calcification in rats given sufficient doses of Warfarin to inhibit {gamma}-carboxylation of matrix Gla protein, a calcification inhibitor known to be expressed by smooth muscle cells and macrophages in the artery wall.


there's something called 'osteoprotegerin' that can help mitigate the arterial calcification effects of warfarin. sounds like backing off on the d3 while on warfarin might also be wise. even though d3 also can deplete k too?? anyway, something to know about at least.
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Postby skydog » Thu Aug 20, 2009 8:39 am

Now I am beginning to wonder if there might be something my body is doing to keep the INR right around normal. I have tweaked my diet a little by avoiding or cutting way back on the highest vitamin k foods. Salads are nearly a thing of the past, Blueberries are in the freeze, strawberries are dehydrated, saving them for winter use and Christmas gifts. The last couple of weeks my diet has included daily fresh salmon in which I eat the oiliest parts which have always been my favorite anyway, have not missed a day without adding a tsp of sunflower seed butter and increased the raw nut consumption. Drinking water like a fish and getting plenty of exercise. Now the last blood test my INR dropped from 1.4 to 1.1 and that was after doubling the warfrin dose to 10 mg. I still bleed very little and have yet to bruise more than slightly which disappears overnight. I wonder if there might be a connection to an ongoing infection like CPN or EBV and of the more known mechanisms the microbes use to create anergy thus hyper coagulation. The microbes tend to live in your endothelium where the food is most abundant. There they trigger the coagulation mechanism to lay down a layer of fibrin on top of them to evade recognition by your immune system. Now does someone want to tackle this connection to the blood thinning issues? Marie, help this gets way beyond my current knowledge base and would hate to lead anyone astray with wrong thinking. Cheers, Mark
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Postby jimmylegs » Thu Aug 20, 2009 11:23 am

well this is weird... i was reading about hypercoagulation and genetic protein c deficiency, predisposition to venous thrombosis etc, and then i googled protein c and MS together.
i imagine some of you have already seen/discussed this one?
Nature. 2008 Feb 28;451(7182):1076-81. Epub 2008 Feb 17.
Proteomic analysis of active multiple sclerosis lesions reveals therapeutic targets.
Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA.

Understanding the neuropathology of multiple sclerosis (MS) is essential for improved therapies. Therefore, identification of targets specific to pathological types of MS may have therapeutic benefits. Here we identify, by laser-capture microdissection and proteomics, proteins unique to three major types of MS lesions: acute plaque, chronic active plaque and chronic plaque. Comparative proteomic profiles identified tissue factor and protein C inhibitor within chronic active plaque samples, suggesting dysregulation of molecules associated with coagulation. In vivo administration of hirudin or recombinant activated protein C reduced disease severity in experimental autoimmune encephalomyelitis and suppressed Th1 and Th17 cytokines in astrocytes and immune cells. Administration of mutant forms of recombinant activated protein C showed that both its anticoagulant and its signalling functions were essential for optimal amelioration of experimental autoimmune encephalomyelitis. A proteomic approach illuminated potential therapeutic targets selective for specific pathological stages of MS and implicated participation of the coagulation cascade.
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Postby mrhodes40 » Thu Aug 20, 2009 11:41 am

I wonder if there might be a connection to an ongoing infection like CPN or EBV and of the more known mechanisms the microbes use to create anergy thus hyper coagulation. The microbes tend to live in your endothelium where the food is most abundant. There they trigger the coagulation mechanism to lay down a layer of fibrin on top of them to evade recognition by your immune system


Well this is the way my primary care doctor thinks and I have been tested and treated for hyper-coagulable blood for some years as well as being on antibiotics. This theory is a little "out there" as afar as chronic infections go, the general medical community does not subscribe tot he idea of cryptic CPn hanging around causing coagulation...

That having been said they DO know that:
a person with toxic shock has a bacteria caused hyper-coagulable state,
that CPn is a germ that can be cryptic and that it lives in blood vessels,
that atherosclerotic plaques always have CPn in them (though no one knows if it starts the plaque or is secondary)

I have had high thrombin antithrombin complexes and high fibrin for some years and have periodically had a d-dimer that was 4 where negative or at least less than 1 is normal. A high d dimer can mean a clot is dissolving somewhere and the body is actively needing to do that, along with the high coagulation factors it suggests there is some coagulation happening and dismantling in my body in an ongoing way.

I do not know what my d dimer is like after being off the coumadin. It was normal all the time I was on coumadin and it had been 4 just 3 days before going to stanford.

Maybe you could focus on the natural antibiotic/antiviral foods for now? Grarlic anyone? Gilroy is pretty close is it not?
I'm not offering medical advice, I am just a patient too! Talk to your doctor about what is best for you...
http://www.thisisms.com/ftopic-7318-0.html This is my regimen thread
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Postby questor » Thu Aug 20, 2009 4:47 pm

A question for those of you who have completed the CCSVI procedure with Dr. Dake: How long after surgery did you wait before meeting with your GP to start monitoring INR?

I'd like to know so that I can schedule the first appointment with my GP in advance.

It sounds like most of you were being tested at least once a week unless there were problems, right? With an ideal INR level of between 2.5 and 2.8?

Thanks in advance,

--Tracy
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