Can I stop my Coumadin?

Here I go again.

While I will try to keep this blog on topic, i.e., coronary heart disease prevention and reversal using nutritional and other natural strategies, I believe that a "critical mass" of frequently asked, though off topic, questions keep cropping up.

One such question revolves around Coumadin, or warfarin.

Somehow, my Nattokinase scam blog post draws traffic about Coumadin. I tried to make the point that a conventional blood thinning agent like Coumadin that undoubtedly has undesirable side-effects cannot be replaced by an agent that has an uncertain track record. In the case of nattokinase, no track record.

To illustrate how far wrong the "nattokinase as replacement for Coumadin" idea can go, here is a question from Anna:


I came across your blog while perusing.

I am a bit bummed because I have been on Coumadin (warfarin) for around 22 years since I was 6 years old. I have a mechanical heart valve (St. Jude's), as I have heart-related issues, including hypertrophic obstructive cardiomyopathy.

Well, it is just that the warfarin seems to interact with nearly everything. I feel like I can not get the nutrients my body requires. I desire to consume more raw foods and vegan foods, though I do not want anything to damage my heart valve or risk a stroke/heart attack or internal bleeding.

I have been underweight the majority of my life, malnourished , currently am still somewhat underweight, though enjoying food again, as I had what mimicked Crohn's Disease for several years (horrendous pain), from which I am in remission now. I was diagnosed with osteoporosis, which may or may not be caused from consuming warfarin.

Is it possible to get off of warfarin and effectively keep my blood thinned ? I currently take 1.5 mg to 2 mg dosage. Does the warfarin destroy Vitamin K and if so does that mean while on warfarin I never get the Vitamin K nutrients even if I did consume foods with it in it?

Thank you
Anna


No, sorry, Anna. Stopping Coumadin with your unique issues, i.e., a prosthetic mechanical heart valve (likely mitral, judging by your history of hypertrophic obstructive cardiomyopathy, in which the patterns of blood flow ejected from the heart disrupt the natural mitral valve function) and cardiomyopathy, can be fatal. Without blood thinning, the mechanical heart valve can trigger blood clot formation, since it is a foreign object implanted into the bloodstream.

There are no natural alternatives available with track records confident enough to bet your life on. Aspirin nor Plavix are blood thinners, but platelet inhibitors. These two agents, while they work for other forms of arterial (but not venous) blood clot inhibition, will not work for your unique situation.

Likewise, a purported oral lytic agent like nattokinase should not be substituted for Coumadin. Even if there was plausible science behind it, you should demand substantial evidence that it provides at least blood thinning equivalent to Coumadin. Should a blood clot, even a small one, form in or around the prosthetic valve, the valve can stop working within seconds. This can lead to death within minutes.

I believe it would be foolhardy to bet your life based on the marketing--let me repeat: MARKETING--of a "nutritional supplement" by supplement manufacturers eager to make a buck.

Nor are there any other nutritional supplements that can safely replace the Coumadin. I wish that were NOT true, as I am no stranger to the long-term dangers of Coumadin and I am a big believer, in general, in nutritional supplements. I am a BIGGER believer, however, in the truth. Weighing the options available to us today, there really is no rational choice but to remain on Coumadin.

By the way, I tell my patients to eat a substantial amount of green vegetables while they take Coumadin. I know that conventional advice is to reduce or eliminate green vegetables due to their content of Coumadin-antagonizing vitamin K. I think this is wrong, also. Green vegetables are the best foods on earth. They reduce risk for cancer, diabetes, bone disease, and coronary heart disease.

To obtain the benefits of green vegetables without mucking up your blood thinning (your "protime" or International Normalized Ratio, INR), I advise my patients who take Coumadin to eat green vegetables--but do so every day in relatively consistent quantities, so that the protime or INR is not disrupted and remains reasonably constant. It may mean that your total dose of Coumadin may be somewhat higher, e.g., 3 or 4 mg instead of 2 mg, but the dose is immaterial outside of blood thinning. That way, you obtain all the wonderful health benefits of green vegetables while maintaining fairly consistent blood thinning/protime/INR. Coumadin does not block all the health benefits of vegetables, only those related to vitamins K1 and K2.

With regards to protecting yourself from the osteoporosis promoting effects of Coumadin, I would be sure to follow a program of natural bone health, such as the one I discussed in Homegrown osteoporosis prevention and reversal. You will have to be extra careful, however, with the vitamin K2. Ideally, you have a doctor knowledgeable about vitamin K2 who can assist you in managing K2 intake while on Coumadin. This is something you can definitely NOT manage on your own. (I am a big believer in self-managed care, but this is way beyond the limit.)

Lastly, it is my belief that anyone with an inflammatory bowel condition, such as Crohn's disease or ulcerative colitis, should absolutely, positively, and meticulously AVOID WHEAT and all other gluten sources (such as rye, barley, and oats). Even if you test negative for celiac markers (e.g., anti-gliadin antibodies, emdomysium and transglutaminase antibodies), the enhanced intestinal permeability will allow wheat proteins, such as gluten, to gain ready entry into the bloodstream. Not to mention that wheat should have no place in the human diet anyway, in my view.

Comments (20) -

  • Myron

    9/5/2010 7:09:35 AM |

    Coumadin is considered a Natural Medicine having been derived from mold acting on Sweet Clover.

    Most Pharmaceutical Drugs have a Natural Basis.

  • Anonymous

    9/5/2010 8:32:30 AM |

    What about using heparin derivatives as a replacement of Marevan / Coumarin?

  • Anonymous

    9/5/2010 8:38:52 AM |

    As mentioned in Wikipedia, low molecular weight heparin (LMWH) is used in pregnancy. It should be possible to change Marevan / Coumarin with LMWH.
    http://en.wikipedia.org/wiki/Marevan#Pregnancy

    Heparin can not be taken orally, so you have to get injections if you decide to change medication.

  • Dr. William Davis

    9/5/2010 9:54:16 AM |

    Yes, indeed.

    But anyone who has taken low-molecular weight heparin injections will tell you it's no picnic. The injections can be painful and leave a bruise. After a few weeks, you can feel like a pincushion and be riddled with bruises. Not a happy alternative.

  • Chris Masterjohn

    9/5/2010 4:56:00 PM |

    Hi Dr. Davis,

    Great, although somewhat depressing, post.

    What is the point of taking the K2 when K2 interferes with the therapy (as Vermeer's group showed) and the dose will have to be adjusted?  The drug interferes with the recycling of vitamin K so it should affect both forms equally.  Are you hoping it may shift the balance of residual vitamin K activity towards the bones and blood vessels?  That seems to make some sense if there is substantial residual vitamin K activity.

    Chris

  • Anonymous

    9/5/2010 6:13:38 PM |

    Chris, I think you are going down the right path with your thinking.  Some K2 survives warfarin therapy as evidenced here:


    "In conclusion, our study indicates that in a rat model
    arterial media calcification is prevented by a high dose of
    MK-4."

    http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowPDF&ProduktNr=224160&Ausgabe=229786&ArtikelNr=75344

    The question then becomes how high a dose is therapeutic in humans and can you get it from diet alone?

    I'm a prisoner of life long warfarin therapy and have consciously shifted my K intake to K2 by eating lots of eggs, cheese and grass fed/finished beef instead of green leafy vegetables because of the way warfarin hammers conversion of K1 to K2.  Sure green leafy vegetables have health properties but they won't help with warfarin driven arterial calcification and osteoporosis.  So far I have avoided taking a K2 supplement and adjusting warfarin dosage because I don't have confidence in the consistency of the K2 in a supplement form.  It becomes another wildcard.  But the bottom line is I really don't know if there is enough K2 to make a difference from food alone.

  • Anonymous

    9/5/2010 6:19:24 PM |

    Dr. Davis, do you have any thoughts on arginine supplementation as a driver of nitric oxide production for the purpose of blood vessel dilation?  I am showing signs of venous insufficiency from a blood clot in my leg suffered over a decade ago.  You mention aspirin and Plavix as platelet inhibitors that don't impact venous clotting.  Arginine also affects platelet activity and I can't find anything definitive about whether or not that is an issue with warfarin.  Arginine is also associated with mitigating atherosclerosis which would seem to make it a good choice for people on warfarin.

  • Anonymous

    9/5/2010 8:04:38 PM |

    Dr davis

    after reading your blog two things have stuck in my mind. one about the role of vaccines in development of disease. and two role of GM foods in destroying health.

    kindly shed light on it. im splitting my hair over it

    Smile

  • Anonymous

    9/5/2010 8:37:04 PM |

    This topic has to be of great interest to the many people on Warfarin for atrial fibrillation,  particularly the issue of warfarin-induced calcification and osteoporosis.  This article http://bloodjournal.hematologylibrary.org/cgi/content/full/109/8/3607 suggests that levels of 45mcg of K2 supplementation would be safe, but what is a therapeutic dose and how does it work with Warfarin? (One of the authors has ties with Natto Pharma, seller of K2; they also suggest it is a safe dose.) Until specific studies are done, we will not know how it works.

    Will one of the newer anticoagulants in the pipeline, such as Dabigatran, which I understand is not a vitamin K agonist, be approved soon and will it be effective?

  • Anonymous

    9/6/2010 3:16:19 PM |

    Dear Dr. Davis:

    This topic is really distressing.  My father has been on Warfarin for 10 years due to atrial fib. I can't help but wonder if his increasingly worsening calcium scores were due in part to Warfarin. It seems to be an extremely nasty - but necessary - drug.

    Over the past year he has been increasingly tired and two months ago had a triple bypass. He has been on a low carb diet, lost 25lbs and started taking fish oil and 5,000 i.u Vitamin D3. He is not taking any K2, but he does eat green vegetables every day. He recently started taking 10,000 i.u. of D3.  Should anyone taking larger D3 doses who is also on Warfarin be worried about arterial calcification? How does one find a doctor in Milw. or elsewhere who has knowledge about K2 and Warfarin? What else can Warfarin users do about their heart disease?

  • Dr. William Davis

    9/7/2010 1:45:50 AM |

    Sadly, there are no data--none, zero, zip--that address the end result of taking vit K2 in any dose or any form while on warfarin.

    No doubt: It will drive INR down, driving warfarin need up. But there are no data on what effects will result at the bone or artery level.

    I wish that weren't true, but we cannot invent data where it doesn't exist. It also cannot be extrapolated from existing data or experiences without incurring substantial risk.

    Sometimes, we just need the data.

  • Anand Srivastava

    9/7/2010 7:14:21 AM |

    How does Omega3 supplementation help?
    I have read that Omega6 is one of the agents that triggers blood clotting.
    Also I read that coumadin actually works by inhibiting action of K1/K2.
    So adding K1/K2 will actually be against the coumadin therapy.

    But since Omega6 is required for the signalling that causes blood clots. If you reduce the Omega6 and increase the Omega3 then the blood clots should not happen naturally.
    It will be like the Inuits.
    Their arteries are in a bad shape but they never get a heart problem, because they do not get blood clots in their blood.
    The only problem is that they don't get blood clots while bleeding also.
    So if you use excess Omega3 with very little Omega6 you will be doing the same. But the side effect is that you have to be careful about bleeds.
    I would think that the same problem will be there for coumadin

  • Anonymous

    9/7/2010 5:20:15 PM |

    Dear Dr. Davis:

    The FDA Advisory Council is meeting regarding Dabigatran on September 20th and word is that its approval is expected by the end of the year or early 2011. I have even seen Boehringer-Ingelheim ads on the online JACC to the effect of "Coming Soon - Pradaxa" (the brand name).

    Will this be the paradigm-shifting Warfarin alternative for AF patients?  As Dabigatran is not a Vitamin K agonist, will its users be able to also use food and supplemental sources of Vitamin K2?

    Apart from the supposed reduction in bleeding risk, will Dabigatran be a preferable anticoagulant for long-term Warfarin users?

  • Chris Masterjohn

    9/8/2010 7:07:28 PM |

    Dear Dr. Davis,

    Did you mean that there are no data on whether K2 will protect against the heart valve calcification that occurs on these drugs, or that there are no data showing its effect on INR?

    Vermeer's group compared vitamin K2 as MK-7 to K1 and showed that it is much more potent at driving down the INR value:

    http://bloodjournal.hematologylibrary.org/cgi/content/full/109/8/3279

    By the way, since you are a fan of K2, if you haven't already seen it, you might enjoy the large review I wrote on it back in 2007, which argued that it was the "Activator X" discovered by Weston Price:

    http://www.westonaprice.org/abcs-of-nutrition/175-x-factor-is-vitamin-k2.html

    Love your blog!

    Chris

  • Chris Masterjohn

    9/8/2010 7:12:27 PM |

    Anonymous, I have seen that study but I don't think it shows how much residual activity of K2 there is, or to what extent it can protect against calcification for someone on warfarin.

    The reason is that K2 potently interferes with these drugs.  In the study, they used a massive dose without cranking up the warfarin proportionately.  However, if you take K2 and you actually need to be on these drugs, your doctor will have to adjust the dose of the drug according to the dose of K2 you are taking.  So it is not very apparent that it is actually possible to obtain the beneficial effects of K2 while taking these drugs.

    (As a side point, the massive dose of K2 could provide enough K2 in these studies to allow each molecule to act once and then get converted to the epoxide form without being recycled, and actually exert a meaningful effect.  Off memory, I don't remember whether they did calculations to show whether there was residual reductase activity (i.e. activity of the enzyme that recycles vitamin K, which is the target of warfarin), but the principle that high dose K2 protects against calcification does not show that the dose of warfarin used allowed residual activity of the enzyme, necessariliy.)

    Chris

  • Anonymous

    9/8/2010 9:03:01 PM |

    Sounds as if AF patients should ask their physicians to change them to Dabigatran as soon as it comes out. Less bleeding risk, no constant monitoring and, importantly, the ability to avail oneself of good nutrition without worrying about INR's. The British Heart Foundation is campaigning for the drug to replace Warfarin.  

    Used widely to get rid of rat infestations in post-Katrina New Orleans, maybe Warfarin will soon be relegated to only killing rats.

  • Chris Masterjohn

    9/8/2010 10:10:20 PM |

    Anonymous,

    Good points -- warfarin was actually developed specifically as a rat poison, so if it came back into fashion post-Katrina, that's nothing new.

    Chris

  • Lacie

    9/10/2010 10:21:24 PM |

    I spent 18 unhappy months on Warfarin after a DVT/pulmonary embolism episode due to oral contraceptive use (I have Factor V leiden).  Happily, my physician took me off blood thinners last year after a doppler scan to confirm all of my clots were gone.

    If you really need a blood thinner (artificial heart valve, active blood clot, severe prolonged a-fib, homozygous Factor V leiden), there's just no good alternative to Warfarin at the moment.  Several alternatives have been tested and rejected due to severe side effects.

    A lower-risk propensity to blood clotting (hterozygous Factor V leiden, mild, short-duration a-fib, etc.) might respond to vitamin E.  I started taking it while on Warfarin and my INR readings shot up from 2 to 4.5.  See study by Harvard researcher Robert Glynn, published in September 25, 2007, issue of Circulation journal

  • Holistic health Blog

    6/29/2011 1:07:21 PM |

    Surely the answer is to take the nattokinase, keep a close watch on the INR & if it goes up significantly titrate the warfarin down.

  • Sal P

    5/15/2013 6:40:08 PM |

    Hello Doc,

    I have the same conflict as many here. I take Coumadin for my mechanical heart valve but I do eat green veggies such as broccoli, spinach, or a small salad everyday. I also take Omega 3 daily. My PT INR is usually around the required goal of 2.0. As long as I have this consistent INR reading, is it safe to continue to to have all the above mentioned in my body? I am hoping that my Coumadin dosage can be lowered with the same INR results.

    Please Advise

Loading
Sleep: A to Zzzzzzzzzz

Sleep: A to Zzzzzzzzzz

Take a look at the results from the Heart Scan Blog's most recent reader poll (399 respondents):

How many hours do you sleep per night (on average)?


9 or more hours per night
15 (3.7%)

8-9 hours per night
72 (18%)

7-8 hours per night
152 (38.1%)

6-7 hours per night
111 (27.8%)

5-6 hours per night
38 (9.5%)

Less than 5 hours per night
11 (2.8%)


Like many issues in health, too much or too little of a good thing can present undesirable consequences.

Too much sleep: While psychologists and sleep researchers advise us that at least 9 hours are required to fully eliminate sleep "debt" and achieve optimal vigilance and mental performance, epidemiologic studies have shown increased mortality with this quantity of sleep.

Too little sleep: Getting less than 7 hours habituallly increases blood sugar, appetite, inflammatory measures, and encourages weight gain. Mortality is also increased, just as with sleeping too much. It is also associated with increased likelihood of a positive heart scan score.

7-8 hours per night from a health viewpoint is that Goldlilocks "just right" value: just enough to not erode mental performance substantially, but not so little that inflammatory, insulin-disrupting, and appetite-increasing effects develop.

Of our 399 respondents in the poll, 56.1% (38% + 18%) slept what appears to be an optimal amount for health. While only 3.7% slept too much (9 hours or more), the remaining 40.1% slept too little.

Our informal poll confirms what most of us observe in everyday life: The majority of people shortchange sleep in order to meet the demands of their high-pressure, squeeze-as-much-as-possible-into-every-day lives. But not paying off your sleep "debt" is like not paying the mortgage for a couple of months. You wouldn't expect your friendly neighborhood bank to say, "Oh, you forgot to pay your mortgage? Forget about it. Just pay next month's." Sure, fat chance. But if you don't pay off your sleep "debt," you will pay it back with health.

Comments (5) -

  • Anonymous

    6/23/2009 7:30:43 PM |

    Some thoughts I have about the causality vs. correlation. Those studies that show correlation with increased mortality /disease with sleep times longer than 9 hours per day could suggest that people with deseases sleep longer because of the disease?  Not that longer sleep periods them selfs are the cause of the disease and early death but a sign of troubles in health which need more time for the body to trying to recuperate?

    I personally sleep between  7 - 9 hour per day if I can rest up to my taste, but if I'm stressed I sleep less and if I'm sick I sleep more.

    (Sorry for possible spelling mistakes, I'm not native english speaker.)

    WBR:
    JVAS

  • Dr. William Davis

    6/23/2009 7:40:51 PM |

    Anon--

    Excellent point.

    In fact, I wonder if greater sleep need is, for many, a red flag for hypothyroidism, in addition to other conditions.

  • kris

    6/24/2009 2:04:35 PM |

    Brain study shows differences in night owls, early risers
    Last Updated: Tuesday, June 23, 2009 | 5:36 PM MT  
    CBC News  

    Scientists at the University of Alberta have found there are significant differences in the way our brains function, depending on whether we are early risers or night owls.

    Using magnetic resonance imaging-guided brain stimulation, neuroscientists tested muscle torque and the excitability of pathways through the spinal cord and brain.

    "We found that the brains of morning people are more excitable in the morning and evening people are completely opposite," neurophysiology researcher David Collins said Tuesday.

    "The evening people ... it's almost a perfect storm of excitability in the central nervous system, where the brain is maximal in the evening and the spinal cord is maximal in the evening.... They generate the most force in the evenings," he said.

    David Collins, neurophysiology researcher at the University of Alberta (CBC) "Morning people ... their brains are most excitable in the morning, but their spinal cords are most excitable in the evening," Collins said.  

    The results may suggest that morning people are performing below their maximum possible level at all times of the day because of this, he said.
    Morning person may be steadier

    If you could change morning people into evening people, maybe their performance would be best in the evening, he suggested. This doesn't mean it's necessarily better to be an evening person, he said.

    "A morning person may be a more consistent, steady plodder over the course of the day," Collins said.

    Kaitlin Cleveley, a sports performance researcher at the U of A, likes to begin work around 10 p.m. and go until 3 a.m.

    "Anything that starts in the morning is absolutely brutal for me to try and get up and try and function," she said. This study brings new perspective to training, she said.

    "It's about trying to peak the athlete.... It can help to set up a sleep program, and it can help to reduce jet lag and sort of help you to determine you know 'When should I book the flight?, When should I get there?'" Cleveley said.

    The research has lots of applications, including understanding mental and physical peaks and how people can maximize performance, she said.

    Initially the research was to determine if brain function changes over the day, Collins said.

    The study evolved with some early findings around two subjects in the study. One proved to be an extreme morning person, the other an extreme evening person, he said.

  • Anonymous

    6/27/2009 12:15:28 AM |

    How does napping fit into this?  Does napping count in the "hours per night" or is it separate?  Any statistics on mortality and napping?

    A lot of cultures have an afternoon siesta but Americans tend to frown on napping.

  • Anna

    6/29/2009 6:43:05 PM |

    A close family member just underwent double bypass surgery in the past few weeks (doing well now, though it took a blood transfusion to get over a 2 day slump while in the hospital), after more than a year of symptoms with exertion,  poor stress test results, a lot of career stress recently, etc.  None of us were told though until just before the recent angiogram.   I always viewed this situation as a "when", not an "if", because I had a different view than the AHA's, but it's always "too soon", even if expected.

    The angiogram revealed multiple sites of stenosis in locations not suitable for stents, so double bypass was performed.

    Aside from family history (her father died of CVD at age 50), there were other risk factors, so she faithfully followed most of the AHA guidelines since at least the 80s - regular chol panels (high results), statins, HRT, low fat/high chol, reduced saturated fat, reduced fat dairy, lean meats, lots o' carbs (even lots of whole grains), etc.  

    But obviously, this didn't work (I think it's a recipe for a bypass), because  CVD happened anyway despite all this adherence to  "prevention" (I use that word loosely in this context).  

    Other risk factors include tendency toward "apple" shape, "strong explosive" personality (sort of Type A), and as I suspected, diabetes (though that was concealed from the family until just before the surgery).  On top of that ...(drum roll)...

    and pertinent to this post - 25+ years of working the third shift as a nurse in L & D.  She was *chronically* and noticeably sleep-deficient (very often apparent, even over the phone), not to mention also Vitamin D deficient (her calcium supplement only added a tiny amount).  The coronary calcium scan wasn't done until last year, when there was marked plaque and shortness of breath & fatigue symptoms.  Of course no program such as Track Your Plaque was suggested or undertaken.  It was fate, right? - the family history - nothing could be done to override that, right? Note: if you are reading this with a sarcastic tone, that's about right Wink.

    Talk about an AHA failure to prevent. Everything I've  I shared about about the AHA's misguided approach to prevention, low carb and grain restriction to manage BG and diabetes, and all the other ways to prevent CVD fell on deaf ears.  Still does.  Still keeping my fingers crossed that the bypass arteries don't clog up.

Loading