Wheat five times a day

20. April 2007 William Davis (3)
Terri couldn't understand why her weight wouldn't drop.

At 5'3", 208 lbs., she had the typical mid-abdominal excess weight that went with small LDL, low HDL, high triglycerides, a post-prandial (after-eating) fat clearance disorder, high blood sugar, increased c-reactive protein, and high blood pressure.

She claimed to have tried every diet and all had failed. So we reviewed her current "strict" diet:

"For breakfast, I had Shredded Wheat cereal in skim milk. No sugar, just some cinnamon and a little Splenda. For lunch, I had low-fat turkey breast sandwich--no mayonnaise--on whole wheat bread. For snacks, I had pretzels between breakfast and lunch, and a whole wheat bagel with nothing on it before dinner. For dinner, we had whole wheat pasta with tomato sauce and a salad. While we watched TV, I did have a couple of whole wheat crackers.

"I don't get it. I didn't butter anything, I didn't sneak any sweets, cakes, I didn't even touch cookies. And I love cookies!"

Did you see the pattern? I pointed out to Terri that what she was doing, in effect, was eating sugar 5 or more times a day. Many of her meals, of course, contained no sugar. All were low fat. But the excessive wheat content yielded quick conversion to sugar--glucose--immediately after ingestion.

Repeated surges of blood sugar like this trigger the excessive insulin response that yields low HDL, higher triglycerides, small LDL, etc., everything that Terri had.

Terri was skeptical when I suggested that she attempt an "experiment": Try a four week period of being entirely wheat-free. This meant more raw nuts and seeds, more lean proteins like low-fat yogurt and cottage cheese, chicken, fish, lean red meats, more vegetables and fruits.

After only two weeks, Terri dropped 5 1/2 lbs. She also reported that the mood swings she had suffered, afternoon sleepiness, and uncontrollable hunger pangs had all disappeared. The mental cloudiness that she had experienced chronically for years had lifted.

What happened was that the load of sugar from wheat products, followed by an insulin surge then a precipitous drop in sugar, and finally fogginess, irritability, and cravings for food all disappeared. With it, the entire panel of downstream phenomena (small LDL, CRP, etc.) all faded.

Though she started out intending to complete a four week trial, I believe that, having seen the light, she will continue to be wheat-free, or nearly so, for a lifetime.
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Comments (3) -

  • Anonymous

    4/27/2007 9:20:00 PM |

    This description fits me to a 'tee' - including the unsuccessful attempts at dieting.

    I was a low-fat vegetarian with a wheat-heavy diet for 12 years.  I was convinced of the healthiness of my eating plan, despite the slow weight gain, ever-higher blood pressure, tryglicerides and cholosterol numbers.  It wasn't until my doctor shocked me with a diagnosis of Type 2 Diabetes that I realized the problem was how I was eating.

    After 9 months of a wheat-free and starch-free diet, a re-introduction of animal proteins from free-range poultry and wild seafoods, and much organic produce and nuts and seeds, I have shed 60 pounds - almost effortlessly.  My waist circumference is back to normal as are all my 'numbers'.  Without any medication.

    But no one could have convinced me prior to the diagnosis shock:  I was that successfully brainwashed by the conventional low-fat wisdom.

  • Dr. Davis

    4/28/2007 2:22:00 AM |

    Eloquently said.

    I fear that there's an entire nation that would concur, if they were aware. Sound the alarm!

  • Jonathan Byron

    4/22/2009 1:41:00 PM |

    You have repeatedly mentioned wheat and corn starch as culprits in a wide variety of disease factors. How much of this is specifically those two foods, and how much is the carb content (and the fact that these are so widely consumed in the west)? Our household is wheat-free (hashimoto's disease in one member), but we eat corn chips, corn tortillas and and corn noodles. Would switching from corn to rice be a logical next step, or would a low-carb diet with fewer grains of all types be better??

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Chicken Little

Chicken Little

11. August 2007 William Davis (1)
Clinical studies can be designed in a number of ways. The ease and cost of these studies differ dramatically, as does the confidence of the findings.

The most confident way to design a clinical study is to tell neither the participants nor the investigator(s) what treatment is being offered, then to administer treatment or placebo. Neither the people doing the research nor the participants know what they are receiving. Of course, there needs to be some way to find out what was given at the end of the study in order to analyze the outcome.

This is called a “double-blind, placebo-controlled” clinical study. While not perfect since it tends to examine a treatment phenomenon in isolation (e.g., the effects of a single drug in a select group of people), it is the best sort of study design that is most likely to yield confident results, both negative and positive. This sort of design is followed, for instance, for most prescription drugs.

There are pitfalls in such studies, of course, and some have made headlines lately. For instance, beyond tending to examine single conditions in a select group of participants, a double-blind, placebo-controlled study can also fail to uncover rare effects. If a study contains 5000 participants, for instance, but a rare complication develops in 1 person out of 20,000, then it’s unlikely such an ill-effect will be observed until larger numbers of people are exposed to the agent.

Another pitfall (though not so much of study design, but of human greed) is that study outcomes that are not favorable can be suppressed by simply failing to publish the results. This has undoubtedly happened numerous times over the years. For this reason, a registry has been created for all human clinical trials as a means to enforce publication of outcomes, both favorable and unfavorable.

Despite its weaknesses, the double-blind, placebo-controlled study design remains the most confident way to show whether or not some treatment does indeed yield some effect. It is less prone to bias from either the participant or the investigator. Human nature being what it is, we tend to influence results just to suit our particular agenda or interests. An investigator who knows what you are given, drug or placebo, but owns lots of stock in the company, or is hoping for special favors from the pharmaceutical company sponsor, for instance, is likely to perceive events in a light favorable to the outcome of the study.

Now, most studies are not double-blind, placebo-controlled studies. These are notoriously difficult studies to engineer; raise lots of ethical questions (can you not treat a person with an aggressive cancer, for instance, and administer a placebo?); often require substantial numbers of participants (thousands), many of whom may insist on payment for devoting their time, bodies, and perhaps even encountering some risk; and are tremendously expensive, costing many tens of millions of dollars.

For this reason, many other study designs are often followed. They are cheaper, quicker, may not even require the active knowledge or participation of the group being studied. That’s not to say that the participants are being tricked. It may simply be something like trying to determine if there are more heart attacks in people who live in cities compared to rural areas by comparing death rates from heart attack from public records and population demographic data. Or, a nutritional study could be performed by asking people how many eggs they eat each week and then contacting them every month for 5 years to see if they’ve had a heart attack or other heart event. No treatment is introduced, no danger is added to a person’s established habits. Many epidemiologic studies are performed this way.

The problem is that these other sorts of study designs, because they generate less confident results, are not generally regarded as proof of anything. They can only suggest the possibility of an association, an hypothesis. For real proof to occur, a double-blind, placebo-controlled may need to follow. Alternatively, if an association suggested by a study of lesser design might, by reasons of a very powerful effect, be sufficient. But this is rare. Thalidomide and catastrophic birth defects are an example of an association between a drug and fetal limb malformation that was so clear-cut that no further investigation was required to establish a causative association. Of course, no one in their right mind would even suggest a blinded study.

Where am I going with this tedious rambling? Lately, the media has been making a big to-do about several studies, none of which are double-blind, placebo-controlled, but were cross-sectional sorts of observations, the sorts of studies which can only suggest an effect. This happened with Dr. Steve Nissen’s study of Avandia (rosiglitazone) for pre-diabetes and risk for heart attack and the recent study suggesting that cancer incidence is increased when LDL cholesterol is low. Both were observations that suggested such associations.

Now, those of you following the Heart Scan Blog or the www.cureality.com website know that we do not defend drug companies nor their drugs. In fact, we’ve openly and repeatedly criticized the drug industry for many of its practices. Drugs are, in my opinion, miserably overused and abused.

But, as always, I am in the pursuit of truth. Neither of these studies, in my view, justified the sort of media attention they received. They are hypothesis-generating efforts—that’s it. You might argue that the questions raised are so crucial that any incremental risk of a drug is simply not worth it.

Despite the over-reaction to these studies, good will come of the fuss. I do believe that heightened scrutiny of the drug industry will result. Many people will seek to avoid prescription drugs and opt for healthy changes in lifestyle, thus reducing exposure to costs and side-effects.

But beware of the media, acting as our Chicken Little, reporting on studies that prove nothing but only raise questions.
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Comments (1) -

  • jpatti

    9/11/2007 10:26:00 AM |

    There's another issue with double-blind studies, for things other than drugs or supplements, they're impossible.  

    Your example of the number of eggs in a person's diet is a good example; there's no "placebo" for eggs.  Similarly, if I increase my level of exercise, I notice that - it can't be blinded.  For diet and other lifestyle changes, we will never be able to gain the amount of evidence as for drug trials.

    I think this is why many doctors don't think so much about prescribing these types of things, except for a cursory instruction to "eat better, lose weight and exercise," they're just not as strongly convinced of the benefit of these changes because they can't be proven as strongly.  But... not being able to prove something doesn't mean it's not important to health!  

    As a diabetic, I measure my bg multiple times a day and make changes to my food intake, exercise and medication dosage to hit established bg goals.  While I think tightly-controlling bg is probably the number one thing I can do for my heart health, it can never be proven in a double-blind study.

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How old are you?

How old are you?

17. October 2009 William Davis (21)
George walks into my office. I ask him his age.

"I'm 21 years old," he declares.

Yet I look at George. He's got gray thinning hair, his posture is slumped forward rather than erect, the flesh on his upper arms hangs loosely, he's got wrinkles on his hands and face, brown spots on the back of his hands and arms. He looks more like 70 years old to me. "I don't think you're 21 years old. I think you're 70."

"Prove it," he says.

Okay. What now? Minus any formal identification like a driver's license, how do I prove that George is really 70-something and not 20-something? Not an easy thing, when you think about it. If George were a tree, I'd cut him down and count his rings. Is there such a phenomenon in humans?

This is actually a fascinating area of research, looking for reliable biomarkers of aging.

Among the most quantitative markers of aging is telomere length. Telomeres were once dismissed as nonsense sequences in DNA. However, more recent thought among geneticists is that telomeres shorten with aging and provide the body's cells a timeline of aging. This way, George's cells act like they are 70, not 13, and don't start producing gobs of growth hormone and testosterone in preparation for puberty.

What can slow or stall the shortening of telomere length? There are two I'm aware of:

1) Caloric deprivation--i.e., taking in fewer calories. This was among the theories explored by Dr. Roy Walford during his Biosphere2 experience, based on his work in mice that showed that caloric deprivation nearly doubled lifespan.

2) Vitamin D--Richards et al (2007) found that, the higher the vitamin D, the longer the telomere length. The highest vitamin D levels conferred a 5-year effective difference in telomere length.

So, if I could look inside George's cells and count his telomeres, I could judge with confidence whether he was 21 or 70. Or, he could take vitamin D sufficient to increase blood levels to a healthy range and be more like 65.
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Comments (21) -

  • Ellen

    10/17/2009 11:20:26 AM |

    "gobs"


    Hahaha... I can so tell you are from Milwaukee. That is such a Wisconsin expression.  Laughing

  • LeonRover

    10/17/2009 9:44:35 PM |

    Another take on the Greek philosophical question: what is time? Even tho' they could count days and years, their answer was: "time is the measure of change". But perhaps that should be reversed to: "change is the measure of time".

    Doc, it seems to me the burden of proof was on the guy. You simply say: you only left high school three years ago? Gosh, there are no reports that any male has undergone the developmental changes I can see, in such a short time!
    Another point, the number of telomeres at the end of cells has to be calibrated against other measures, such as the sun going round the earth. All any particular individual has to claim is: my telomeres are lost 10 times faster than any one else's, now YOU prove otherwise.

    Y'all have a good day, now.

  • Anonymous

    10/17/2009 11:22:20 PM |

    "If George were a tree, I'd cut him down and count his rings"
    Too funny, Dr Davis.

    George's telomere's....reduced to T-stumps.

    Ellie

  • Telephone Triage

    10/18/2009 7:57:18 AM |

    Lovely blog...it is scary the way we are being attacked by the diseases at very early ages also.

  • Tim

    10/18/2009 9:26:05 AM |

    Al Sears says that high homocystein levels shortens telemores three times faster.

  • Peter

    10/18/2009 2:19:57 PM |

    I take vitamin D and I want to live longer.  I believe it will help because you said so,and I believe everything you say, including when you say you're not sure.

  • Peter

    10/18/2009 2:27:49 PM |

    Regarding "gobs", this is a popular expression in Oregon, too, and I'm not sure how you tell where an expression originated.

  • Dr. B G

    10/18/2009 6:41:26 PM |

    Very cool post, Dr. D!!!

    I've been into telomeres for awhile!!  Mag-deficiency is associated with reduced telomeres in vivo in rats(and reduced glutathione). HERE

    NAC can ameliorate some of the Mag-deficiency oxidative stress in vitro. NAC is the precursor for one of the most potent antioxidants, glutathione. HERE

    Glutathione peroxidases which generate more protective glutathione are selenium-containing enzymes. Selenium was correlated to longer telomeres and lower BP. Selenium.

    Glutathione strongly and positively affects telomere lengthening and telomerase activity. Role of nuclear glutathione as a key regulator of cell proliferation

    Curiously, (?via epigenetics and X-related telomere genetics?) maternal diet can shorten telomeres in rats. Epigenetics: maternal diet shortens aortic telomeres.

    Precursors of glutathione are:
    --NAC (sulfur proteins)
    --undenatured whey protein (sulfur proteins, like glutamine, arginine, taurine)
    --SAMe

    (PO suppl w/ GSH apparently doesn't work well)

    Of course there are many other ways to increase glutathione... Like the TYP program -- flavonoids, fish oil, alpha lipoic acid, MELATONIN, silymarin (WCCA's fave), selenium, magnesium, zinc, etc.

    I believe the omega-6:3 index is one of the best biomarkers for aging, at least until we can count our 'tree rings'! In post-MI rats, n-3 PUFAS increased glutathione and was incredibly protective. HERE

    The traditional 1960s rural Cretans shared the same low CAD rate as Japan with a high fat diet. To me,  the Cretan diet is  associated with high glutathione, selenium, low n-6, high high  n-3 ALA EPA DHA, 41% fat (like TYP Diet 3), intermittent fasting (Greek Orthodox practice), pastured-raised eggs, chicken, goat, mutton, wild seafood/snails, and very fatty sheep/goat yogurt and cheeses (rich in taurine and saturated fatty acids). HERE and HERE. And Simopoulus.

    -G

  • Dr. B G

    10/18/2009 6:41:26 PM |

    Very cool post, Dr. D!!!

    I've been into telomeres for awhile!!  Mag-deficiency is associated with reduced telomeres in vivo in rats(and reduced glutathione). HERE

    NAC can ameliorate some of the Mag-deficiency oxidative stress in vitro. NAC is the precursor for one of the most potent antioxidants, glutathione. HERE

    Glutathione peroxidases which generate more protective glutathione are selenium-containing enzymes. Selenium was correlated to longer telomeres and lower BP. Selenium.

    Glutathione strongly and positively affects telomere lengthening and telomerase activity. Role of nuclear glutathione as a key regulator of cell proliferation

    Curiously, (?via epigenetics and X-related telomere genetics?) maternal diet can shorten telomeres in rats. Epigenetics: maternal diet shortens aortic telomeres.

    Precursors of glutathione are:
    --NAC (sulfur proteins)
    --undenatured whey protein (sulfur proteins, like glutamine, arginine, taurine)
    --SAMe

    (PO suppl w/ GSH apparently doesn't work well)

    Of course there are many other ways to increase glutathione... Like the TYP program -- flavonoids, fish oil, alpha lipoic acid, MELATONIN, silymarin (WCCA's fave), selenium, magnesium, zinc, etc.

    I believe the omega-6:3 index is one of the best biomarkers for aging, at least until we can count our 'tree rings'! In post-MI rats, n-3 PUFAS increased glutathione and was incredibly protective. HERE

    The traditional 1960s rural Cretans shared the same low CAD rate as Japan with a high fat diet. To me,  the Cretan diet is  associated with high glutathione, selenium, low n-6, high high  n-3 ALA EPA DHA, 41% fat (like TYP Diet 3), intermittent fasting (Greek Orthodox practice), pastured-raised eggs, chicken, goat, mutton, wild seafood/snails, and very fatty sheep/goat yogurt and cheeses (rich in taurine and saturated fatty acids). HERE and HERE. And Simopoulus.

    -G

  • Matthew

    10/19/2009 12:54:33 AM |

    Dr. Davis,

    Have you heard about ELC (earlobe crease) as a possible key sign of aging? It seems that tons of studies show a very strong positive connection between younger people with an earlobe crease and CVD. What do you think?

  • David Throop

    10/19/2009 3:07:30 PM |

    Doc Davis,

    Last week, the U.S. Preventive Services Task Force came out with a review and with recommendations about using emerging risk factors for predicting and managing heart disease.  I think there's a lot in there that you'll agree with.  But they were negative about calcium scoring.

    Sandy Swarz, whose scholarship is pretty sharp, gives a summary.

    I'd really like to see your response to all this.

  • Michelle

    10/19/2009 7:54:03 PM |

    It is scary how many young people are getting elderly diseases. I know someone who died of a massive MI at the age of 26. I am also proof of that. I have CAD, hypothyriodism, Low Vitamin D, Low B12, gastritis, and valve disease and I am only 35. I am looking forward to being able to reverse some of these diseases naturally.

    Michelle

  • Dr. William Davis

    10/19/2009 9:58:42 PM |

    Hi, Matthew--

    I believe there's some evidence that ear lobe creases are associated with increased coronary risk, but I don't know of any data relating them in younger people specifically.

    I have one myself, and it's been there for as long as I can remember and does indeed correlate with my family's aggressive heart disease pattern.

  • Dr. William Davis

    10/19/2009 10:00:02 PM |

    Hi, G--

    As always, you are full of unique observations.


    Hi, Ellen--

    Perhaps I should have said "oodles."

  • rezzrovv

    10/20/2009 4:21:27 PM |

    Dr. Davis,

    See David Throop's comment above.  I actually came looking to see if you might have commented on this yet.  Curious your take.

    Scott Pierce

  • Anonymous

    10/22/2009 5:19:03 AM |

    Hi Dr. Davis,

    Have you observed a correlation between earlobe creases and coronary calcification among your patients?

    Thanks,

    David

  • Stan (Heretic)

    10/24/2009 5:06:47 PM |

    Hi Dr. B G,

    Interesting.  Magnesium deficiency vs telomeres length could also be explained as a secondary effect caused by the excessive metabolism of carbohydrates as the primary factor.  High magnesium intake is required for glucose metabolism, see for example Implications of oxidative stress in high sucrose low magnesium diet fed rats

    Similar situation may exist with glutathione, high glutatione may be a secondary marker for a diet high in dairy and (thus automatically) lower in carbohydrates.  This paper you linked Maternal diet influences DNA damage, aortic telomere length, oxidative stress, and antioxidant defense capacity in rats seems to be pointing to a high carb diet as one of the factors that may cause accelerated growth of low birth weight babies (the paper discusses human studies as well), which then is correlated with higher CVD risk, shorter telomeres and worsens other markers (bones abnormality etc).

       In contrast to this, high fat low carb nutrition seems to slow down babies and infants growth and slows the onset of puberty, which according to the logic presented by the papers discussed above, ought to reduce oxidative stress, slow down the shortnening of telomeres and reduce the CVD risk later in life.
    Regards,
    Stan

  • Dr. B G

    10/26/2009 4:44:49 PM |

    Hi Stan,

    Yes -- there are many implications to such data and other epi-genetic data. Low protein maternal  diets increase Met Syn for 2 generations in rat pups.

    Low Sat Fat maternal diets?  High carb, low protein, allergenic wheat maternal diets?  I believe we are epi-genetically affecting many future generations and their metabolism, growth hormone, thyroid hormone, leptin/ adiponectin and perhaps even vitamin D hormone pathways... This may explain why right now CAD and diabetes is rampant compared to just 1-2 generations ago. I have 80-90s year old patients how are 20x more healthier than my 30-40 year olds! Have we genetically predisposed ourselves to the 'over summer' mode that Dr. T at Nephropal has talked about by our mother's diets and her lack of sunlight, rich fatty foods, omega-3, and excess omega-6 in utero??

    I believe so.

    -G

  • Dr. B G

    10/26/2009 4:44:49 PM |

    Hi Stan,

    Yes -- there are many implications to such data and other epi-genetic data. Low protein maternal  diets increase Met Syn for 2 generations in rat pups.

    Low Sat Fat maternal diets?  High carb, low protein, allergenic wheat maternal diets?  I believe we are epi-genetically affecting many future generations and their metabolism, growth hormone, thyroid hormone, leptin/ adiponectin and perhaps even vitamin D hormone pathways... This may explain why right now CAD and diabetes is rampant compared to just 1-2 generations ago. I have 80-90s year old patients how are 20x more healthier than my 30-40 year olds! Have we genetically predisposed ourselves to the 'over summer' mode that Dr. T at Nephropal has talked about by our mother's diets and her lack of sunlight, rich fatty foods, omega-3, and excess omega-6 in utero??

    I believe so.

    -G

  • buy jeans

    11/3/2010 2:24:30 PM |

    However, more recent thought among geneticists is that telomeres shorten with aging and provide the body's cells a timeline of aging. This way, George's cells act like they are 70, not 13, and don't start producing gobs of growth hormone and testosterone in preparation for puberty.

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Michael Pollan Podcast

Michael Pollan Podcast

15. August 2007 William Davis (3)
I just found this great podcast of an April, 2006 National Public Radio (NPR) interview with Omnivore's Dilemma author, Michael Pollan:

Author Michael Pollan: 'The Omnivore's Dilemma'

available at http://www.npr.org/templates/story/story.php?storyId=5342514

The Science Friday segment is a great encapsulation of all the fascinating spins this wonderfully insightful author has on human eating habits and the developing distortions of food choices, much magnified by the food manufacturing industry.

One of my favorite comments from Pollan: "The USDA should be called "The Department of Corn," referring to the ubiquitous dissemination of corn products into livestock and human foods that has increasingly led to the enormous health problems we're all facing in 2007.
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Comments (3) -

  • Bix

    8/16/2007 6:12:00 PM |

    Oh man, I really enjoyed that.  Thanks for posting it.  Pollan is a nicely engaging speaker, easy to listen to.  I loved the story about the farm ecosystem ... carting in the chicken coop to eat the grubs in the cow manure.  And of course the USDA Dept of Corn.  Great listen.

  • Jen

    7/23/2008 5:12:00 AM |

    A little late on this post --- but I am currently reading In Defense of Food and I love it.  I am waiting patiently for my library copy of The Omnivore's Dilemma.  Thanks for the link to the podcast.  I heard the more recent interview a couple of weeks ago.  Glad to hear this one as well.

  • buy jeans

    11/2/2010 8:26:18 PM |

    The Science Friday segment is a great encapsulation of all the fascinating spins this wonderfully insightful author has on human eating habits and the developing distortions of food choices, much magnified by the food manufacturing industry.

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Warfarin is scary stuff

Warfarin is scary stuff

19. April 2008 William Davis (16)
Gilbert is a 58-year old high school science teacher.

When I first met Gil, he'd been having bouts of atrial fibrillation and had required various medications to suppress recurrences of the rhythm. However, because his rhythm proved somewhat difficult to control, his electrophysiologist (heart rhythm specialist) prescribed warfarin to reduce the risk of stroke. With atrial fibrillation, because of blood stagnation (in the left atrial appendage) in the heart, there is a stroke risk of approximately 8% per year. Warfarin reduces this risk substantially, to about 2%.

I met Gil because he had a cholesterol disorder. In my practice, the first step in gauging the implications of a lipid or lipoprotein disorder is to obtain a heart scan. If the heart scan score is zero, great. It means that we have plenty of time to treat the disorder since risk for cardiovascular events is near zero also; it means less intensive efforts less intensive efforts are necessary. But if the heart scan score is, say, 1200, then an aggressive approach in short order is required, since the risk for heart attack may as high as 20-25% per year, even in the absence of symptoms.

Gil's heart scan score: 787--high and posing a risk for heart attack of about 5-10% per year without preventive efforts. Gil did indeed prove to have a complex lipoprotein disorder, as well as high blood pressure, vitamin D deficiency, and several other potential contributors to coronary plaque.

Gil did just about everything right: He exercised, followed the recommended diet, achieved better than the Track Your Plaque 60-60-60, lost 18 lbs of abdominal fat.

Gil's rhythm stabilized for several months, only to have atrial fibrillation break through again. So Gil's electrophysiologist re-prescribed warfarin.

18 months later, Gil's 2nd heart scan score: 1410--a near doubling. Unsettling to Gil and to us, to say the least.

How can this happen in the face of perfect lipids/lipoproteins, correction of hidden causes like lipoprotein(a) and inflammation, along with a vigorous lifestyle effort?

I fear that the culprit might be warfarin.

Warfarin, better known by its brand name, Coumadin, may have some effects that intersect with the Track Your Plaque mission of reducing coronary plaque.

It is no secret that, beyond the obvious risk of bleeding from blood thinning, warfarin also may:

--Accelerate aortic valve calcification
--Accelerate calcification of the framework of the mitral valve (the mitral "anulus")
--Accelerate osteoporosis
--Induce an artificial situation of vitamins K1 and K2 deficiency.

The vitamin K1 deficiency is the route by which blood thinning is achieved. However, the K2 deficiency may have undesirable consequences, among which are the above list of various pathologic calcifications.

I therefore wonder if warfarin dramatically accelerated the coronary calcium that we track to gauge the progression of coronary atherosclerosis. One experience is hardly sufficient reason to sound the alarm. It is also difficult to pinpoint the cause of the explosive growth in Gil's coronary calcium specifically on warfarin.

That all said, I am quite certain it was the warfarin.

Unfortunately, some people are unavoidably committed to warfarin, such as those with specific genetic blood clotting disorders, prosthetic valves, prior deep vein thromboses and pulmonary emboli, etc.--serious reasons. Until an alternative emerges, warfarin remains a necessity for some people. (No, nattokinase is NOT an alternative, at least not one that would permit survival.)

My personal policy is that warfarin be used only when absolutely necessary and the gains markedly outweight the risks--including that of possible accelerated calcification of multiple sites.

Whether we will be able to get Gil off warfarin and potentially gain control over his coronary disease/plaque/calcium remains to be seen. I sure hope so.




Caraballo PJ, Heit JA, Atkinson EJ et al. Long-term use of oral anticoagulants and the risk of fracture. Arch Intern Med 1999; 159 (15): 1750–6. PMID 10448778.

Pilon D, Castilloux AM, Dorais M, LeLorier J. Oral anticoagulants and the risk of osteoporotic fractures among elderly. Pharmacoepidemiol Drug Saf 2004;13(5): 289–294.PMID 15133779.

Gage BF, Birman-Deych E, Radford MJ, Nilasena DS, Binder EF. Risk of osteoporotic fracture in elderly patients taking warfarin: results from the National Registry of Atrial Fibrillation 2. Arch Intern Med 2004; 166(2):241–246.PMID 16432096.



Copyright 2008 William Davis, MD
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Comments (16) -

  • Anonymous

    4/19/2008 1:59:00 AM |

    Interesting--a good friend of mine had an angiogram 10 years ago to check a heart irregularity. Turned out he need a valve. the angiogram showed no stenosis or detatectable CAD. He had a mechanical valve put in and went on Comudin. Five years ago he had a heart attack with significant blockages. He has since had another heart attack. Your article would explain what happened.

  • Harry35

    4/20/2008 4:28:00 AM |

    There are other references that substantiate the negative effects of warfarin on the arteries. The effect of warfarin on coronary calcium score was investigated by Koos, et. al. in a study published in the American Journal of Cardiology, Vol 96, Issue 6, page 747 entitled "Relation of Oral Anticoagulation to Cardiac Valvular and Coronary Calcium Assessed by Multislice Spiral Computed Tomography," 15 Sept 2005. They found that the coronary artery calcium Agatston score of warfarin-treated patients with calcific aortic disease was about twice as high as that of similar patients not on warfarin (1561 vs 738). They concluded that "The results of our study have demonstrated that oral anticoagulation may be associated with increased valvular and coronary calcium in patients with aortic valve disease, presumably due to decreased activation of the matrix Gla protein."

    Also, there is a study by Price et. al. in Arteriosclerosis, Thrombosis, and Vascular Biology, 1998;18 pages 1400-1407,"Warfarin Causes Rapid Calcification of the Elastic Lamellae in Rat Arteries and Heart Valves." These rats were given Vitamin K to counteract the anticoagulant effects of warfarin, but they still experienced extensive calcification.

    Hopefully some of the new anticoagulants that don't interfere with warfarin, like Rivaroxaban, will be approved soon so that people in need of long-term anticoagulation won't have to rely on warfarin.

  • Anonymous

    4/20/2008 11:07:00 AM |

    I'm glad to see you are sometimes posting references at the bottom of your blog.  It doesn't help me so much, but it might be helping  doctors become believers.  

    Two former medical doctors, one is now a salesman, the other a researcher, have not shown  interest in TYP until last week for some reason.  One is from Germany, and when he was in town on  business i talked with him in person. he only had criticism for  TYP ideas.  The other from China didn't criticize but seemed to believe the supplements recommended were to similar to Chinese herbalist.  He would tell me that he wants western drugs not vitamin supplements for heart care.

    I don't know why but both doctors seem to have changed their mind on TYP last week.  The German doctor did not talk with me, he talked with a friend about buying the right kind of vitamin D to take for the TYP program.  Same change of heart happened with the Chinese salesman, as he contacted me wanting basic information on TYP.
    The Chinese friend will hopefully read this blog posting on vitamin K, and Warfarin, which I forwarded to him. I believe this is one of the medicines he takes.        

    The two do not know each other.    I don't know what happened to cause this turn around, but something did.

  • Mike

    4/20/2008 1:37:00 PM |

    Don't aspirin and Fish oil (omega-3s) also help thin the blood?

  • Anonymous

    4/24/2008 1:27:00 AM |

    I had a-fib until it was successfully treated at the Mayo Clinic by Dr Brady. Based on my experience I'd suggest Gil see an EP at one of the large centers with lots of experience ablating a-fib. You want an operator with +500 a-fib procedures under their belt.

    Three months after treatment, I was off warfarin.

  • Dr. B G

    4/26/2008 2:38:00 AM |

    EP fails most of the time (unfortunately). However, there appear to be many theories abounding that afib is a consequence of inflammation.... (ummm... just like CAD and heart disease).

    And guess what causes inflammation?

    Excessive carbs, insulin and diabetes/metabolic syndrome!

    http://www.ncbi.nlm.nih.gov/pubmed/15240964
    Sata N et al. C-reactive protein and atrial fibrillation. Is inflammation a consequence or a cause of atrial fibrillation?
    Jpn Heart J. 2004 May;45(3):441-5.
    PMID: 15240964

    Boos CJ, Lip GY.  Inflammation and atrial fibrillation: cause or effect? Heart. 2008 Feb;94(2):133-4. No abstract available.  PMID: 18195117

    Watson T, Kakar P, Lip GY. Cardioversion for atrial fibrillation: does inflammation matter? Am J Cardiol. 2007 Jun 1;99(11):1617-8. Epub 2007 Apr 17. No abstract available.

  • Dr. B G

    4/26/2008 2:38:00 AM |

    EP fails most of the time (unfortunately). However, there appear to be many theories abounding that afib is a consequence of inflammation.... (ummm... just like CAD and heart disease).

    And guess what causes inflammation?

    Excessive carbs, insulin and diabetes/metabolic syndrome!

    http://www.ncbi.nlm.nih.gov/pubmed/15240964
    Sata N et al. C-reactive protein and atrial fibrillation. Is inflammation a consequence or a cause of atrial fibrillation?
    Jpn Heart J. 2004 May;45(3):441-5.
    PMID: 15240964

    Boos CJ, Lip GY.  Inflammation and atrial fibrillation: cause or effect? Heart. 2008 Feb;94(2):133-4. No abstract available.  PMID: 18195117

    Watson T, Kakar P, Lip GY. Cardioversion for atrial fibrillation: does inflammation matter? Am J Cardiol. 2007 Jun 1;99(11):1617-8. Epub 2007 Apr 17. No abstract available.

  • Dr. B G

    4/27/2008 5:48:00 AM |

    Dear Anonymous,

    I hope your physician friends become as enamored with TYP as you are Smile  
    This is the 'trickle up' effect!

    Thanks for your endorsements and support!

  • Dr. B G

    4/27/2008 5:48:00 AM |

    Dear Anonymous,

    I hope your physician friends become as enamored with TYP as you are Smile  
    This is the 'trickle up' effect!

    Thanks for your endorsements and support!

  • Anonymous

    7/24/2008 12:07:00 AM |

    What if Gil abstained from consuming all (plant source) vitamin K1 rich foods and supplimented with vitamin K2 at a dose that would make his INR managable?  Would that at least help stop his calcium score from going up further?

    Also, with a better than 60/60/60 lipid profile, won't the more dangerous soft "unstable" plaques and small LDL particles still remain minimized?  And if that's true, would that make Gil, and people like him, be a rare exception to the "heart scan score" being the "golden standard" to predict future heart attack risk?

  • phuli cohan

    2/20/2009 9:22:00 PM |

    Vitamin K2 deficiency can be safely corrected while on warfarin, there is an excellent article about how to do this safely ( Pharmacotherapy 2005;25:1746-1751).  There are also specialty labs that measure K2.  All cardiac patients should maintain normal levels of K2

  • buy jeans

    11/3/2010 3:46:34 PM |

    Gil's heart scan score: 787--high and posing a risk for heart attack of about 5-10% per year without preventive efforts. Gil did indeed prove to have a complex lipoprotein disorder, as well as high blood pressure, vitamin D deficiency, and several other potential contributors to coronary plaque.

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  • Jeorjette

    6/12/2011 1:48:54 PM |

    I had open heart surgery 14 months ago to repair the mitral valve of a infection that had attached itself as a vegetation. I ended up having AF and now on warfarin. I was told you can't have this and can't have that. Rubbish. For over a year I have self medicated myself with 40mg of Vitamin K in the form of stem enhance followed with superabsorable CoQ10, gamma E, and many other high quality vitamins, lots of anti-oxidents and growth hormone releasing agents in the form of amino acids. Also L-Arginine and nician. I am doing extremely well.
    Not only that. I also mix raw cabbage, sweet potato, beetroot, celery, broc ,tumeric, carrot and more
    I am taking warfarin but the trick is balancing and consistancy and you can do extremely well regardless of the set back. Don't say no. Don't sit and die. Think beyond the square

  • Jeorjette

    6/12/2011 11:26:10 PM |

    Secondly, warfarin does do damage. Use natural products to counterbalance these. Using amino acid stacks you can also trigger your own growth hormone, not only to counterbalance the damage warfarin does but it also excel the rest of the body. Anti-oxidents should also be taken in a wide spectrum like Acai Berry, Vit C, CoQ10,gamma E, Nanoresveratrol, Calcium complex, Omega 3. Whey powder, colstrum, Stem cell enhance
    most products  www.life-enhancement.com  and www.lef.com  also look at pituiatry support to start growth hormone release

  • Hal

    4/19/2012 4:01:44 PM |

    How does Pradaxa fair in this tail?  I have AFib and recently switched from warfarin to Pradaxa.  Well on Warfarin I did (and on Pradaxa will continue to) supplement with K2 but it appears that this was at lower levels than recommended here.  I plan on increasing my K2 intake.

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