Synthroid, Armour Thyroid, and the battle for T3

In the last Heart Scan Blog post on thyroid issues, Is normal TSH too high?, the provocative findings of the the HUNT Study were discussed. The text of the study can be found at:

The association between TSH within the reference range and serum lipid concentrations in a population-based study. The HUNT Study

Hypothyroidism, or low thyroid that is signaled by high thyroid-stimulating hormone, TSH, is proving far more prevalent an issue than previously thought. While previous estimates put hypothyroidism as affecting only about 3% of younger populations, 10-20% of older populations (women more so), data like the HUNT Study suggest that, if lower and lower TSH levels (higher thyroid) are necessary for perfect heart health, then many more people stand to benefit than we used to think.

But another crucial issue in the world of hypothyroidism: Is T4 (thyroxine) enough? Or should we be supplementing T3 (triiodothyronine) along with T4?

Your friendly neighborhood primary care doctor or endocrinologist would likely argue vehemently that T4 (as Synthroid, Levoxyl, levothyroxine, and others) is adequate and not subject to the impurities and contaminants of natural thyroid extracts. They would also argue that T4 is effectively converted to T3 at the tissue level, and exogenous supplementation is unnecessary.

Others--most of all thyroid patients themselves, along with thyroid advocates like Mary Shomon and Janie Bowthorpe, along with some physicians--argue that supplementing T3 along with T4 can be very important. They argue that people feel better, have more physical energy, lose weight more effectively, and more completely resolve many of the phenomena of hypothryoidism with T3 added. There are also some data that argue the same.

Adding T3 to the mix may address the presumed poor conversion of T4 to T3 that is peculiar to some people. It may overcome the "reverse T3" phenomenon, the production of a useless look-alike T3 that occurs in some people. It may also (anecdotally) exert greater effects on some lipid/lipoprotein parameters, such as Lp(a).

My experiences adding T3 to T4 have been mixed: Some feel better, others do not. Some show objective improvements, others do not.

Nonetheless, hypothyroidism, or incompletely corrected hypothryoidism by way of inadequate T3, is an issue to consider in your plaque-control program.

More on this somewhat complex issue, along with practical solutions to consider, can be found on the Special Report to be released this week on the Track Your Plaque website.

Letter to New York Times

All right. I sent a Letter to the Editor to the New York Times. No word from them; it's no longer news.

So here is what I tried to convey.

While the authors overall did a credible job of talking to my colleagues and laying out the issues, they made the crucial and boneheaded mistake of confusing CT heart scans with CT coronary angiograms. Sadly, many people who may have been considering having a simple screening heart scan may be scared away by the confused authors, Alexn Berenson and Reed Abelson.

They do correctly point out that, while CT coronary angiograms are fascinating examples of technology and a way of visualizing coronary arteries, this test all too often is being subverted into the "let's make money from high-tech testing" medical model. It's also a test that frequently leads to the "real" test, heart catheterization, since the "time bomb" you have in your arteries might "need" a stent.

CT coronary angiograms are also virtually useless for purposes of tracking disease, since they are not longitudinally (along the length of the artery) quantitative, nor should anyone be exposed to this much radiation repeatedly.

A simple heart scan, on the hand, provides a longitudinal summation of coronary plaque volume. Radiation exposure is sufficiently low that repeated scanning can be performed for purposes of tracking . . .yes, track your plaque.

Poorly-informed reporters can do a lot of damage. As always, you and I must dig a little deeper for the truth.




Dear Editor,

Re: Weighing the Costs of a CT Scan’s Look Inside the Heart

The Times featured an article on June 29th that discussed rapidly expanding use of CT scans for the heart:
Weighing the Costs of a CT Scan’s Look Inside the Heart.

The authors, Alex Berenson and Reed Abelson, stated that CT heart scans “expose patients to large doses of radiation, equivalent to at least several hundred X-rays, creating a small but real cancer risk.”

I’d like to offer a clarification.

Though the authors discuss both CT heart scans and CT coronary angiograms, they confuse the two and use the terms interchangeably.

A heart scan is a simple screening test for coronary atherosclerotic plaque. It detects the presence of calcium in the heart’s arteries, provided as a “score.” (Because calcium occupies 20% of total plaque volume, knowing the amount of calcium tells you how much total coronary plaque is present by applying this simple proportion.) Just having a high score should not prompt heart procedures, since people undergoing simple screening heart scans are without symptoms. However, a stress test may yield some useful information.

On present-day CT devices, heart scans expose a patient to 0.4 mSv of radiation on an electron-beam, or EBT, device, and on up to 1.2 mSv on a 64-slice multi-detector, or MDCT, device, compared to 0.1 mSv during a standard chest x-ray. CT heart scans are therefore performed with about the same quantity of radiation as a mammogram done to screen women for breast cancer, or about the equivalent of four chest x-rays on an EBT scanner, up to 12 chest-xrays on a MDCT scanner.

CT coronary angiograms, while performed on the same devices as heart scans, require x-ray dye to fill the contours of the coronary arteries. It also requires up to several hundred times more radiation. While new engineering innovations are being introduced that promise to reduce this exposure, the current devices being used today do indeed require a radiation dose equivalent to 100 to 400 chest x-rays (usually in the range of 10-15 mSv), a value that equals or exceeds that obtained during a conventional heart catheterization.

While heart scans are most useful to detect and quantify plaque that can help determine the intensity of a heart disease prevention program, CT coronary angiograms are generally used as prelude to hospital procedures like catheterizations, stents and bypass surgery. That’s because they are performed to look for (or rule out) “severe” blockages.
CT heart scans and CT coronary angiography are therefore two different tests that yield two different kinds of information, and yield two entirely different levels of radiation exposure.

This confusion from a major and respected media outlet like the New York Times is unfortunate, because it could persuade millions of people who otherwise could benefit from simple heart scans to avoid them because of misleading information on radiation exposure of a different test.

Thank you.

William Davis, MD

Red yeast rice alert

While there have been some positive reports in the media lately about the cholesterol-reducing effects of red yeast rice, Consumer Lab has issued a very concerning report.

Because Consumer Lab is a subscription website (incidentally, the $20 per year membership fee is money well spent for insightful tests on many supplements, though new reports only come out a handful of times per year), I won't discuss the results of their red yeast rice in its entirety.

However, Consumer Lab testing uncovered several disturbing findings:

--The lovastatin content varied by a factor of 100, from 0.1 mg per tablet/capsule in one brand up to 10.6 mg in another brand. By FDA regulations, lovastatin is a drug and NO red yeast rice preparation is supposed to contain ANY lovastatin. Nonetheless, despite the marketing of supplement manufacturers, it is probably the lovastatin that is largely responsible for the LDL-reducing effect. The monacolins or mevinolins in red yeast rice add little, if any, further LDL-reducing effect.

--Several preparations contain a potential kidney toxin called citrinin. The Walgreen's product, specifically, contained substantial quantities of this toxin.



Interestingly, the FDA has taken repeated action against red yeast rice manufacturers and distributors because they continue to contain lovastatin. In the FDA's most recent action in August, 2007, for instance, Swanson's product and Sunburst Biorganics' Cholestrix, were both sent letters to stop selling their product because it contained lovastatin.

The Consumer Lab findings would explain the enormous variation in LDL-reducing effect of various red yeast rice products. In my experience, some work and reduce LDL 40 mg/dl or so, some fail to reduce LDL at all, others generate a modest effect, e.g., 5-10 mg/dl LDL reduction.

In effect, red yeast rice IS a statin drug, albeit a highly variable and weak one. Although readers of The Heart Scan Blog know that I am a big fan of nutritional supplements and self-empowerment in health, I am a bigger fan of truth. I despise B--- S---- of the sort that emits from some nutritional supplement manufacturers and drug companies.

I am puzzled by much of the public's readiness to embrace a statin drug if it comes from a supplement company while avoiding it if it comes from a drug manufacturer. Personally, I do not like the drug industry, their questionable (at best) ethics, their aggressive marketing tactics, their sleazy sales people.

But, in this instance, if a statin effect is desired, I'd reach for generic lovastatin before I purchased red yeast rice. The Consumer Lab report tells us that red yeast rice IS essentially a statin drug, an inconsistent one that often contains a potential toxin.

"Average amount of heart disease for age"

A 72-year old woman came to my office after a complicated hospital stay (unrelated to heart disease). She'd undergone a CT coronary angiogram and heart scan as part of a pre-operative evaluation prior to a surgery for a non-heart related condition.

The heart scan portion of the test (I was impressed they even did this) yielded a heart scan score of 212. The CT coronary angiogram portion of the test revealed a 50% blockage in one artery, a lesser blockage in one other artery.

The cardiologist consulting on the case advised her that the amount of coronary disease detected was insufficient to pose risk during her surgical procedure. He also advised her that she had "an average amount of disease for age." He thought that nothing further was necessary since she was "average."

Say what?  

What if I told you that you have an average amount of cancer for your age? After all, cancers become more common the older we get. Who would find that acceptable?

Then why should ANY amount of coronary atherosclerotic plaque be "acceptable for age"? Coronary plaque is a degenerative disease that poses risk for rupture. While it is indeed common, by no means should it be acceptable.

I would bet that this same cardiologist would be from the same school of thought that would be eager to advise heart catheterization, stent, and other procedures--revenue-generating procedures--should she have a heart attack appropriate for age.

I wish that I could tell you that this silly comment was provided by some peculiar, "everyone-knows-he's-crazy" doctor. But it was not. It was a solidly mainstream physician. He pooh-poohs nutrition, laughs when asked about nutritional supplements, thinks anyone complaining about symptoms less than a full-blown heart attack is a baby. He is respected by the primary care physicians, lectures on the advantages of prescription medications. In short, he is your typical conventional cardiologist.

This is the way they think. I know, because I was one of them. Thankfully, something banged me upside my head one day (my Mother's sudden cardiac death) and tipped me off to the painful irony of the conventional approach to heart disease.

There is NO amount of coronary disease appropriate for age. This notion is a remnant of the paternalistic, "I-know-better-than-you" attitude of the last century of medicine.

The 21st century promises a new age.

Quantum leaps

A reader of The Heart Scan Blog and member of the Track Your Plaque program posted this comment on The Heart.org:

*The facts speak for themselves.*

Dr. William Davis and Dr. William Blanchet, your patients thank you for the low cost PREVENTIVE care you prescribe. The published facts speak for themselves. It is indeed a sad state of affairs, that the larger cardiology community does not take the time to research the data and results you have been reporting. Unfortunately it is the patients who are the victims of the mainstream, inappropriate, treatment protocols, as evidenced with the ongoing high rate of CV death rate.

I am dumbfounded by the lack of open-minded inquisitive curiosity to thoroughly research your claims by many/most cardiologists. Understood, we are all busy, but that is no excuse to stick with practices that do not result in major breakthrough improvements in patient outcomes.

Then again, we are all humans, and when "we" are convinced that "our" approach is correct, "we" tend to conveniently ignore any evidence to the contrary. "We" like to believe "we" have been right all along.

A very insightful book, recently published, says it all in its title: "Mistakes were made (but not by me)."

From the intensity of the comments on this topic, it is clear that we are in the middle of a battlefield. It is to be hoped that the facts will become visible before too much smoke obscures the field, and before the patients are all dead.

George Orwell said it correctly, back in 1946:

“We are all capable of believing things which we know to be untrue, and then, when we are finally proved wrong, imprudently twisting the facts so as to show that we were right. Intellectually, it is possible to carry on this process for an indefinite time: the only check on it is that sooner or later a false belief bumps up against solid reality usually on a battlefield.”

And, after several posts that preventive care with EBT would be too costly.....

*Heroic*

Prevention is what matters, but it is not very heroic. A hospital that advertises the highest volumes in heart bypasses and other heart "repair" procedures, sounds to many like a go-to place when one gets into trouble with one's heart.

Cardiologists who perform impressive surgical procedures are heroes. Not unlike fire-fighters. We celebrate them (deservedly!) for rescues and life saving heroic actions.

We tend to not pay much attention to the folks that work hard to minimize risk of calamities in the first place.

Similarly, we recently learned that it is too costly to build schools that are earthquake resistant in China. Parents had to look at their children's bodies, crushed.

Is it too graphic to imagine 20,000 American bodies, who died of heart disease, piled up on a field?

What will it take before we make prevention our first priority?


AL, Ann Arbor, Michigan


The reader also tells me that, prompted by his father's death from heart attack while following conventional advice after heart catheterization, he has lost 50 lbs and corrected his lipid patterns on the Track Your Plaque program. The reader is currently struggling with full correction of his severe small LDL pattern and is following some of the advice we discussed on our webinar recently.

Another Heart Scan Blog reader, Stan the Heretic, posted this quote from scientist, Max Planck, in his comment:


"A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die and a new generation grows up that is familiar with it." - M. Planck

(Max Planck was a German physicist who developed quantum theory, a disruptive set of ideas that supplanted other explanations of energy mechanics of the day.)


I fear that may prove to be the case for heart disease. The revenue-generating formula for heart disease management that dominates practice in cardiovascular medicine today is so deeply ingrained into the thinking and revenue expectations of practicing cardiologists that a preventive or reversal approach just won't cut it--even if it is vastly superior.

That's why it is important for you to take control yourself. You will be the one who obtains and applies the information that saves your life or the lives of those around you. It is, in all likelihood, NOT your doctor who will save your life, but YOU.

Body count

Imagine the following headline:

War in Iraq a growing success: 20,000 Americans now dead!


If a newspaper ran that headline, we would all be outraged, and rightly so. Deaths in war are a tragedy. They are not something we celebrate.

Then why do we hear hospitals boasting about the number of bypass operations performed every year, number of heart catheterizations performed, number of heart attacks treated?


"_______ Hospital breaks 1000-heart bypass per year milestone"

"We treat more heart attacks than other other hospital in the state!"

"More people come to ________ Hospital than any other in the region!"




I hear this stuff on the radio, on TV, see it in newspapers and magazines, even on highway billboards every single day in Milwaukee.

Heart procedures, like deaths in war, are casualties of health.

They are not successes (though, of course, you can have a "successful" bypass). I see most procedures as a failure of prevention.

Death from heart attack is a failure of prevention. Tim Russert's death was a (unnecessary) failure of prevention. But so are bypass surgery, stents, and the like.

Such is the perverse state of affairs in hospitals and health: They celebrate illness. They glamorize it with ads displaying high-tech equipment, efficient staff in scrubs, "caring and friendly staff." But it is illness they are celebrating. Why? Because it has become a business necessity, a necessary strategy to remain competitive and profitable in the business called "healthcare" that makes money from treating people. The biggest return is from major procedures like bypass operations.

Every success in prevention denies the hospital an $80,000+ opportunity. You'll never hear that advertised.

Dr. Bill Blanchet: A ray of sunshine

Another heated discussion is ongoing at The Heart.org, this one about Tim Russert's untimely death: Media mulls Russert's death as cardiologists weigh in

Although I posted a couple of brief comments there, I quickly lost patience with the tone of many of the other respondents. Should you choose to read the comments, you will see that many still cling to old notions like heart attack is inevitable, defibrillators should be more widely available, "vulnerable" plaques cannot be identified before heart attacks, etc.

I quickly lose patience with this sort of outdated rhetoric. However, our good friend, Dr. Bill Blanchet of Boulder, Colorado, has a far stronger stomach for this than I do.

Here, a sample of his wonderfully persuasive comments:


Heart disease cannot be stopped but we can certainly do better!

Goals we must achieve if we hope to solve the Rube Goldberg of coronary disease:

1. Find something more reliable than Framingham risk factors to determine who is at risk. Framingham risk factors are wrong more often than they are right. If you are comfortable treating 40% of the patients destined to have heart attacks, continue to rely on “traditional” risk factors only.

2. Treat to new standards beyond NCEP/ATP-III. These accepted standards prevent at best 40% of heart attacks in patients treated. This is unacceptable, and arguably why Tim is dead today! Why prevention protocols emphasize LDL and more or less ignore HDL, triglycerides and underemphasize blood pressure eludes me.

3. Motivate patients to participate in coronary prevention. Saying “you need to get exercise and lose weight” is not adequate motivation, it hasn't worked to date and probably won't work tomorrow. If you are satisfied saying it is "the patient's fault for not listening to me" so be it, that excuse doesn't work for me!

Currently “good results” consist of being able to convince 50% of patients at risk by traditional risk factors to participate in prevention and hopefully 30% will be treated to goal. Of those treated to goal, 60% of the heart attacks will still happen anyway. Mathematically we can hope to prevent <10% of heart attacks with this approach!

I have personally found a solution to this dilemma. It goes like this:

1. EBT-CAC [electron-beam tomography coronary artery calcium] is the most reliable predictor of coronary events period, the end! Anyone who disagrees has not objectively read the literature. The only test more predictive than the initial calcium score is the follow up score 12 to 36 months later. EBT predicted Tim Russert’s event 10 years before it happened; passing his stress test gave him inappropriate reassurance 2 months before he died. If only Tim had the benefit of a second EBT sometime over the last 10 years he and his doctor would have known that what they were doing was insufficient and improvements could have been made.

2. I treat to the standard of stable calcified plaque by EBT (<15% annualized progression, preferably <1% annualized progression). This correlates with a very low incidence of coronary events. Even the ACC/AHA 2007 position paper agrees with this. This is accomplished with aspirin, omega-3 fatty acids, diet, exercise, weight control, smoking cessation, treatment of sleep apnea, stress reduction, control of HDL, triglycerides and LDL cholesterol and excellent control of BP and insulin resistance plus the recent addition of vit D-3. Meeting an LDL goal of 70 is easy but prevents only a minority of events, treating to the goal of stable CAC by EBT is a challenge but when achieved, the reward is near elimination of heart attacks and ischemic strokes. This has indeed been my personal experience!

3. A picture of plaque in the coronary artery is a monumental motivator for patients to get on board to make things better. The demonstration of progression of that plaque despite our initial therapies gets all but a few suicidal patients interested in doing a better job. I think that similar motivational results can be had with carotid imaging; the difference is that CAC by EBT is clinically validated as being a much stronger predictor of events with progression and non-events with stability than any ultrasound test including IVUS.



Wow! I couldn't have said it better.

Sadly, I doubt even Dr. Blanchet's persuasive words will do much to convince my colleagues on this forum. And the cardiologists on this forum are likely among the more inquisitive and open-minded. The ones stuck in the cath lab day and night, or implanting defibrillators, are even less inclined to entertain such conversations.

While I admire Dr. Blanchet's energy for continuing to argue with my colleagues, the lesson I take is: Take charge of health yourself. If you wait for your doctor to do it for you, you could be in the same situation as poor Tim Russert. This is an age when your physician should facilitate your success, not prevent it or leave you wallowing in ignorance.

The Russert Protocol at work

Without a concerted effort at prevention, heart scan scores (coronary calcium scores) grow like weeds. The average rate of growth is 30% per year.

Keith is an illustrative case. At age 39, Keith's heart scan score was 29, in the 99th percentile due to his young age. (In other words, young people before age 40 have no business having plaque. If they do, it's bad.)

True to conventional practice, Keith's doctor prescribed a cholesterol drug (Zocor), asked him to take a baby aspirin, and prescribed a blood pressure medicine. He asked Keith to cut the fat in his diet. His doctor even exceeded conventional (ATP-III) LDL cholesterol treatment targets.

Keith, an intelligent and motivated businessman, happily complied with his doctor's instructions. Eighteen months later, a 2nd heart scan showed a score of 68, representing an increase of 135%, or 76% per year.

This is the very same approach that the late Mr. Tim Russert's doctors employed: treat (calculated) LDL cholesterol with a statin drug, treat high blood pressure, reduce saturated fat, take aspirin. It was a miserable failure in Keith, whose plaque continued to grow at a frightening rate of 76% per year. It was also an obvious failure in poor Tim Russert.

Further investigation in Keith uncovered:

--Severe small LDL--80% of all LDL was small (despite a favorable HDL of 58 mg/dl)
--Measured LDL particle number (NMR) showed that "true" LDL was actually about 60 mg/dl higher than suggested by the crude calculated LDL
--An after-eating (postprandial) disorder (IDL)
--A pre-diabetic blood sugar and insulin
--Severe vitamin D deficiency
--Very low testosterone

All these patterns were present despite the steps Keith and his doctor had instituted. It's no wonder his plaque was undergoing explosive growth.

The conventional approach to coronary disease prevention is inadequate, more often than not a mindless adherence to one-size-fits-all template crafted to a great degree by drug industry interests and "experts" who often stand at arm's length from real live patients.

Keith's "residual" abnormalities are all readily correctable. He has since made dramatic improvements in all parameters. Among the strategies used is a wheat- and cornstarch-free diet that resulted in 12 lbs lost within the first few weeks of effort.

If you are on the "Russert Protocol," have a serious conversation with your doctor about the continued advisability of remaining on this half-assed approach to heart disease. Or, consider finding another doctor.

Petition to the National Institutes of Health

A petition to the National Institutes of Health (NIH) is being circulated in response to the mis-statement made in an NIH-sponsored study, ACCORD.

The ACCORD Trial included over 10,000 type II diabetics and compared an intensive, multiple-medication group to achieve a target HbA1c of <6.0%, with a less intensively treated group with a target HbA1c of 7-7.9%. (HBA1c is a long-term measure of glucose, averaging approximately the last 3 months glucose levels.) To the lead investigators' surprise, the intensively treated group experienced more death and heart attack than the less intensive group. The conclusion suggested that intensive management of diabetes may not be a desirable endpoint and may result in greater risk for adverse events.

The petitioners argue that the problem was not with intensive glucose control per se, but the use of multiple side-effect-generating medications. Unfortunately, the ACCORD conclusions give the impression that loose control over blood sugar may be desirable.

The petition originates from the Nutrition and Metabolism Society, a non-profit organization seeking to promote carbohydrate restriction.


The petition reads:

National Institute of Health re: the ACCORD Diabetes Study: "Intensively targeting blood sugar to near-normal levels ... increases risk of death. "

This statement is untrue. This study lowered blood glucose levels only by aggressive drug treatment.

Preventative measures and proven non-drug treatments are being ignored by the NIH, ADA and many other governing agencies.

There is abundant scientific evidence proving a carbohydrate restricted diet can be as effective as drugs in lowering blood glucose levels safely. Many times diet is more effective than medication in controlling diabetes - all without side effects or increased risk of death.

I ask that the NIH publicly retract the above statement. It is misleading the public.

I also request that the NIH acknowledge the existing science and fund more research by the experts who have experience with carbohydrate restriction as a means of treatment for diabetes.

For more info, or to help people with diabetes, please e-mail info@nmsociety.org .

Thank you.




I added my comment:

In my preventive cardiology practice, I have been employing strict carbohydrate restriction in both diabetics and non-diabetics. This results in dramatic improvement in lipids and lipoprotein abnormalities, substantial weight loss, and improved insulin sensitivity. This experience has been entirely different from the heart disease-causing and diabetes-causing low-fat diets that I used for years.

I have a substantial number of diabetics who have been to reduce their reliance on prescription medication for diabetes or even eliminate them. In my experience, the power of carbohydrate-restricted diets is profound.

However, better clinical data to further validate this approach is needed, particularly as diabetes and pre-diabetes is surging in prevalence. I ask that more funding to further explore and validate this research be made available if we are to have greater success on a broader basis.




If you are interested in adding your voice, you can also electronically sign the petition. It is optional, but you can also add your own comments regarding your own views or experiences.

Wheat withdrawal

It happens in the hospital every so often: A clean-cut, law-abiding person is hospitalized for, say, pneumonia, kidney stones, knee surgery, etc.

Everything's fine until . . . they're running down the hospital hallway stark naked, screaming about snakes on the wall, accusing nurses of trying to kill him, all while yanking out IV's and monitor patches.

It's called alcohol withdrawal. Alcohol withdrawal can range from tremulousness and sweatiness, all the way to delirium tremens, the full-blown form that leads to disorientation, seizures, fever, even death. Withdrawal can also be associated with a number of chronically used agents, such as sedatives/sleeping pills, pain medication/opiates, among others.

How about wheat?

I wouldn't have believed it, but after witnessing this effect countless times, I am convinced there is such a phenomenon: Wheat withdrawal.

You'll recognize it in someone who previously ate bread and other wheat flour-containing products freely, then eliminates them. This is followed by extreme cravings, usually for bread, cookies, or cake; profound fatigue; shakiness; mental fogginess; blue moods. The syndrome can last for up to one week.

Then, bam! Sufferers of wheat withdrawal report mental clarity superior to their wheat-crazed days, improved energy, decreased appetite and cravings, heightened mood, and, of course, fantastic drops in weight.

Why would removal of wheat from the diet trigger a withdrawal phenomenon? I can only speculate, but I believe that at least part of this response is due to a physical conversion from a glycogen (sugar)-burning metabolism to that of a fatty acid (fat mobilizing) metabolism. People who lived in the up-and-down cycle of craving and eating wheat constantly fed the sugar furnace for years and are enzymatically impaired in fat burning; they've been growing fat stores. Eliminating wheat deprives the body of this easy source of glycogen, forcing it to mobilize fatty acids in the fatty tissues. Sluggish at first, people feel fatigue, mental fogginess, etc. Once the enzymatic capacity for fat mobilization revs up, then these feelings dissipate.

Could it also relate to the opioid sequences apparently present in wheat? I wasn't even aware of this fact until a reader of The Heart Scan Blog, Anne, left this comment:

Wheat protein contains a number of opiod peptides which can be released during digestion. Some of these are thought to affect the central and peripheral nervous systems.

When I gave up gluten, I felt much worse for a few days. This is a very common reaction in those who stop eating gluten cold turkey.


Dr. BG provides a fascinating commentary on the addictive/opioid aspect of wheat addictions in her Animal Pharm Blog.

Whatever the mechanism, I believe it is a real phenomenon. It can, at times, be so overwhelming that about 20% of people who try to eliminate wheat find they are simply unable to do it without being incapacitated. Of course, that might be a lesson in itself: If withdrawal is so profound, it hints that there must be something very peculiar going on in the first place.
Life Extension article on vitamin D

Life Extension article on vitamin D


For anyone looking for a discussion about the emerging role of vitamin D as a cause for coronary disease, see my recent article, Vitamin D’s Crucial Role in Cardiovascular Protection, in Life Extension Magazine, now posted online at:

http://www.lef.org/magazine/mag2007/sep2007_report_vitamind_01.htm.




Vitamin D has assumed an absolutely critical role in the Track Your Plaque program for coronary plaque reversal and dropping CT heart scan scores. Since adding vitamin D and aiming for blood levels of 50-60 ng/ml, our success rate has skyrocketed. In fact, I wonder just how well our two most recent record holders--51% and 63% drops in heart scan scores--would have fared without it. (They probably would have dropped, but no where near as much.)

Also, a full-length booklet that contains just about everything you want to know about vitamin D (or at least a right-this-moment summary of what is known about it) will be available to Track Your Plaque Members for free before the end of the year.

If you haven't done so already, DO THE D!!

Comments (5) -

  • wccaguy

    9/14/2007 5:24:00 AM |

    Dr. Davis,

    I continue to be amazed at how much value you are providing all the time to those of us deeply concerned about heart disease.

    Whether it's at this blog, at LEF.org, at your TrackYourPlaque.com site, or in your Track Your Plaque book, your contribution is pretty astounding.

    I only found your work in the last 2-3 weeks and already it has made a deep impression on me and I'm getting clearer about what I need to do to combat heart disease in myself and in family members.

    Thanks for all you're doing!

  • Dr. Davis

    9/14/2007 12:14:00 PM |

    Wow!

    Thanks for the feedback. I'm glad it's helping you. It is wonderful to hear back about the impact the program is having.

  • Bix

    9/15/2007 9:45:00 AM |

    Excellent article!  I especially liked the tie-in to poor kidney function.

  • Rich

    9/17/2007 1:14:00 AM |

    Dr. Davis: In your excellent LEF article, I found your reference to a fascinating statement about statins and vitamin D by Dr. David Grimes of the UK. For those interested, here is the Lancet source article (reprinting for educational purposes):

    The Lancet 2006; 368:83-86
    DOI:10.1016/S0140-6736(06)68971-X

    Are statins analogues of vitamin D?
    David S Grimes MD, Blackburn Royal Infirmary, Blackburn, Lancashire BB6 8HE, UK

    Summary

    There are many reasons why the dietary-heart-cholesterol hypothesis should be questioned, and why statins might be acting in some other way to reduce the risk of coronary heart disease. Here, I propose that rather than being cholesterol-lowering drugs per se, statins act as vitamin D analogues, and explain why. This proposition is based on published observations that the unexpected and unexplained clinical benefits produced by statins have also been shown to be properties of vitamin D. It seems likely that statins activate vitamin D receptors.
    Back to top

    During the late 19th century, conventional wisdom held that masturbation was the cause of epilepsy, a more plausible explanation than the previous notion that epilepsy was the result of possession by the devil, and illness in general the result of divine interference. Since bromide was thought to reduce sexual desire, it became the logical treatment. Although reasonably successful, bromide worked for reasons that are different from the theory on which it was based. Can the same be said of statins for heart disease?

    The emergence of coronary heart disease (CHD) in the 20th century required an explanation. Some had noted that cholesterol accumulated in the walls of the arteries, and a process of accretion was hence described as the major mechanism. Cholesterol was assumed to originate from diet, and the diet-cholesterol-heart hypothesis was established. The logical treatment was to reduce dietary and serum cholesterol concentrations.

    Many inconsistencies in this hypothesis have emerged and been disregarded. In the London banking and transport study,1 for example, men with the highest dietary cholesterol intake had the lowest incidence of CHD. Furthermore, the results of the Framingham study2 showed that raised concentrations of serum cholesterol were predictive of CHD only in men younger than age 55 years. Findings of studies from Honolulu3 and Paris4 suggest a protective effect of high serum cholesterol concentrations, and the Leningrad paradox5 indicates that those exposed to famine subsequently have a high incidence of CHD, the opposite of what is expected. In Europe, populations that consume a large amount of dietary fat and cholesterol have a low incidence of CHD (the French paradox),6 and the lowest incidence of CHD is seen in European nations with the lowest consumption of wine and the most socioeconomic deprivation (the Albanian paradox).7

    Initial treatments to reduce serum cholesterol were not effective. When introduced, however, statins did greatly reduce serum cholesterol concentrations by interfering with its synthesis; the beneficial effects of statins in CHD have been assumed to be the result of cholesterol-lowering, an assumption that I believe is a serious mistake.

    Statins and the heart

    The first statin trial was the Scandinavian Simvastatin Survival Study (4S),8 and its findings indicated a significant clinical benefit from simvastatin. The results of the West of Scotland Coronary Prevention Study (WOSCOPS)9 also showed clinical benefit from statins (pravastatin) and of a greater magnitude than expected; the mortality reduction was about 35%, whereas the reduction in cholesterol concentrations predicted a mortality reduction of only 25%. WOSCOPS9 showed no association between cholesterol-lowering and clinical benefit,10 indicating that cholesterol-lowering was not the mechanism by which pravastatin reduced coronary events.

    In WOSCOPS, statins lowered serum cholesterol concentrations, but also raised concentrations of HDL cholesterol and lowered those of serum triglyceride, indicating that inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase was not the only metabolic action. The clinical experiment of cholesterol-lowering was thus intrinsically flawed, and what must be understood is that 4S and WOSCOPS were trials of statin therapy and not trials of cholesterol-lowering.

    Unexpected benefits of statins

    It is noteworthy that the participants treated with pravastatin in WOSCOPS had a reduced incidence of diabetes compared with controls.11 Additionally, when pravastatin was given to recipients of heart transplants in an attempt to reduce the likelihood of CHD, a reduction in the rate of rejection and an increase in overall survival was noted, irrespective of CHD status.12 The same pattern was seen in recipients of kidney transplants.13 Clinical benefits of statins have also been noted in a placebo-controlled trial14 of atorvastatin for rheumatoid arthritis. Furthermore, simvastatin has been used successfully to treat patients with multiple sclerosis.15 As with CHD, diabetes, rheumatoid arthritis, and transplant rejection, the benefit noted with respect to multiple sclerosis is independent of any effect on serum cholesterol.
    Statins also have an effect on bone, and women who take statins have a greater bone density than those who do not.16 Moreover, the findings of the 10-year follow-up study of participants in 4S17 indicate a significantly reduced risk of cancer, particularly colorectal, lung, and prostate cancer, in those who received simvastatin. Results of a population study from Israel18 also show a greatly reduced risk of colorectal cancer in those taking statins.

    In 1974,19 a group of illustrious diet-cholesterol-heart researchers studied the association between cholesterol and cancer. They noted that high serum cholesterol concentrations conferred protection against colon cancer. The effects of statins mentioned above hence present a major paradox: how can a drug that lowers serum cholesterol concentrations reduce the risk of colon cancer when high serum cholesterol concentrations are, in fact, protective?

    A drug can act as a poison by blocking normal metabolic processes, but to produce a beneficial effect (other than antibacterial) we should assume that it is switching on or enhancing a normal metabolic process. I therefore suggest that statins mimic many of the actions of vitamin D and can be considered analogues of vitamin D.

    Sunlight and vitamin D

    Heart disease

    In Europe, there is a higher rate of mortality from CHD in the northern than in the southern countries, with the lowest rates noted along the Mediterranean coast.20 This pattern suggests that susceptibility to CHD is affected by duration of exposure to sunlight. This notion is supported by findings from the USA21,22 that the higher the altitude of residence, and hence the greater the sunlight intensity, the lower the risk of heart disease.

    Furthermore, the only dietary change that consistently protects against CHD is an increase in consumption of oily fish and fish oil, which contain large amounts of vitamin D.23 In the Netherlands, mortality from CHD was more than 50% lower in men who consumed at least 30 g of fish per day than in those who did not eat fish.24 A similar result was reported in women from a 16-year follow-up study in the USA.25

    Multiple sclerosis

    Multiple sclerosis also shows a latitude gradient in Europe, with the world's highest incidence reported in Scotland.26 The risk of developing the disease is reduced by a third by regular supplementation with vitamin D.27

    Cancer

    The risk of breast cancer and colon cancer is high in northwest Europe and much lower in the Mediterranean countries.28 And, in the UK, people die more readily from cancer in the north than in the south of the country. After being diagnosed, 34% of men with cancer and resident in Oxfordshire survive for 5 years compared with 26% of those who live in the northwest and Yorkshire. Men with stomach cancer who live in London survive on average twice as long as those who live in the northwest of England; the same applies to bladder cancer.29 Patients with colon cancer also have a greater chance of survival if they live in the south of England rather than in the north.30 The benefits of sunshine and vitamin D would explain these associations.
    Results of a study31 done in 1941 in the USA and Canada showed that the cancer death rates among residents of the most northern cities were two and a half times those of the most southern cities. An extensive study32 of more than 5000 locations in the USA has shown that incidence rates of cancer are lowest where ultraviolet light exposure is greatest. Bladder, breast, colon, kidney, oesophageal, ovarian, prostate, rectal, stomach, and uterine cancers, and non-Hodgkin lymphoma are associated with low exposure to ultraviolet light.32

    In the USA, cancer of the prostate has an increasing incidence with distance from the equator, suggesting a protective effect of sunshine. The incidence is highest in the eastern states and lowest in the west.33 This is exactly the same as with CHD, and is probably the result of a high altitude being protective because of greater ultraviolet light exposure. The association between prostate cancer and insufficient access to ultraviolet light has also been noted in the UK,34 with men exposed to low levels of ultraviolet light developing cancer at a younger age than those exposed to high levels (median age 67•7 years vs 72•1 years).

    In a study35 of 456 people with early-stage lung cancer who had undergone surgery, those diagnosed and operated on in the summer, spring, or autumn had a significantly higher 5-year survival rate than those diagnosed and operated on in the winter. The survival rate was 29% in those who took no vitamin D supplements and had treatment in the winter compared with 72% in those who took vitamin D supplements and were treated in the summer.35


    Diabetes

    The international distribution of diabetes in children is very similar to that of CHD, with incidence increasing with distance from the equator,36 again suggesting a protective effect of sunlight and vitamin D. Furthermore, children of women who do, compared with those who do not, take cod liver oil during pregnancy have a reduced incidence of type 1 diabetes.37 The findings of a retrospective study,38 undertaken in Finland and involving 10 821 children born in 1966, indicate that the incidence of diabetes in adulthood is almost ten times higher in those who do not, compared with those who do, take vitamin D supplements in childhood. The benefit of vitamin D supplementation during infancy has been further strengthened by the findings of a large study undertaken in Norway.39

    Rhematoid arthritis

    Kröger and colleagues40 noted that 16% of 143 women with rheumatoid arthritis, compared with the general population, had very low concentrations of serum calcidiol. During the winter, 73% had levels of calcitriol below the seasonally adjusted normal range and the lowest levels were in patients with very active disease. In another study,41 of 19 patients with rheumatoid arthritis given vitamin D supplements, nine reported a complete remission of symptoms, and eight a satisfactory response. Inflammatory markers also improved: the mean erythrocyte sedimentation rate fell by 43% and the mean concentrations of C-reactive protein by 52%. This study is a small one but although far from conclusive the results conform to a pattern that should not be ignored.


    Testing of my hypothesis

    In view of the above, there is a striking similarity between the benefits of vitamin D and the benefits of statin therapy. I believe that the unexpected and unexplained beneficial effects of statin therapy might be mediated by activation of vitamin D receptors by this group of drugs. This hypothesis is, in theory, easy to test.
    A prospective study should be undertaken in cancer treatment and prevention, with a factorial design, so that patients receive statins, vitamin D, a combination of statins and vitamin D, or placebo. A similar outcome in the three treatment groups would lend support to the suggestion of statins acting via vitamin D receptors. If vitamin D and statins are activating the same receptors, then if both are given in sub-maximum doses, the two together would have a greater effect than each individually. Intervention studies should also be undertaken to look at the relapse rates of established illnesses, including CHD, multiple sclerosis, and rheumatoid arthritis, comparing statins and vitamin D.

    The difficulty in doing these studies is that we know only the minimum dose of vitamin D necessary to prevent and heal rickets: we do not know the dose necessary to increase to a maximum the other effects, especially those that enhance immune competence. The same applies to statins: their effect on serum cholesterol concentrations is easy to measure, but we do not know what to measure as a biochemical surrogate for the other effects, again probably those enhancing immune competence. As such, a range of treatment doses of vitamin D and statins need to be investigated. Additionally, clinical trials of established treatments—eg, statins for CHD—are difficult to design because of the ethics of not giving an established medication (a statin), but in place a trial medication (vitamin D). Comparisons with vitamin D supplements could be undertaken, but only once the optimum dose of vitamin D has been established.

    Colonic mucosa and colonic cancer cells contain vitamin D receptors,42 strengthening my suggestion that vitamin D is biologically active in these tissues. Furthermore, vitamin D has an inhibitory effect on colonic carcinoma cell lines.43 Do statins have a similar effect? In-vitro experiments are one way that the effects of statins on vitamin D receptors could be investigated directly.

    Conclusion

    Anomalous results, such as the unexpected benefits of statins detailed here, lead to the advancement of science. Such an opportunity for research should not be overlooked. Statins should be looked at objectively and the diet-cholesterol-heart hypothesis on which the treatment was based disregarded. Statins have been described as wonder drugs because of their unexpected benefits; my hypothesis gives an opportunity for new thinking. The explanation of statins as analogues of vitamin D, if correct, would be reassuring to the millions of people who take them every day. Finally, sunlight and vitamin D might at last be recognised for their widespread health benefits.

    Conflict of interest statement
    I declare that I have no conflict of interest.


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    Affiliations

    a. Blackburn Royal Infirmary, Blackburn, Lancashire BB6 8HE, UK

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