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.

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

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.

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.

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.

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.

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.

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.

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.

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.

Although Dr. John Cannell's most recent Vitamin D Newsletter concerns the connection between autism and vitamin D, and has nothing to do with coronary plaque reversal, this fascinating discussion between a mother of an autistic boy and Dr. Cannell is so enlightening that I thought that it was still worth passing on.

I also feel very deeply for parents with autistic children, who I see struggle with the developmental difficulties their children encounter. (I even have several patients who are parents of 2 or 3 autistic children.)

As always, Dr. Cannell is at the cutting-edge of converting hard scientific information into practical use. You will note several points or questions raised:

1) Dr. Cannell advocates a powdered capsule form of vitamin D. In my experience, most powdered or tablet forms do not work. But some do. He apparently has success with the brand he specifies.

2) Are there vitamin D-receptor (VDR) genotypes that respond differently? Should there be different 25 (OH) vitamin D blood level targets for different VDR genotypes? Nobody knows yet, but it will be an important question to explore in the future.

3) Is heavy metal toxicity, at least in its milder forms, a surrogate for vitamin D deficiency? (Are chelationists unwittingly treating vitamin D deficiency?)

4) If this is a genuine association, and vitamin D replenishment exerts profound neurologic effects in autistic children, does a similar, though less marked effect, hold in non-autistic children? Will children perform better, learn more effectively, etc. with vitamin D supplementation to normal levels?

5) Vitamin A--Is vitamin A with vitamin D good or bad? This one I do not have an answer to. Reading the literature Dr. Cannell cites didn't help much. (Dr. BG--Any comments? Dr. BG is a vitamin A advocate.)

Perhaps, should the association between autism and vitamin D hold, it raises more questions than it settles. But, true to my experience with vitamin D, every day I stumble on some unique, fascinating effect, all beneficial. We continue to learn new lessons about vitamin D and Dr. Cannell's insights as a practicing psychiatrist deeply concerned with vitamin D issues have helped enormously.

(Sorry, but I did not copy the links to the literature Dr. Cannell cites. To obtain the links, go to the original Vitamin D Newsletter.)

The Vitamin D Newsletter
June 2008

This month we feature a remarkable series of letters from a mother of an autistic son who treated her child with vitamin D. It is the first case report in the medical literature suggesting vitamin D has a treatment effect in autism.

First, a brief case report and then a more detailed exchange of emails between the mother and me.

Case Report:

John is a seven-year old boy living in the northeastern U.S. with a long-standing diagnosis of autism. Symptoms include temper tantrums, repetitive self-stimulatory behavior, impaired language, mood swings, fear of being alone, toileting problems, dysbacteriosis, and impaired muscle strength. John spends a lot of time outdoors starting in the spring and his mother noticed a distinct seasonal variation in his symptoms in that he improved in the summer and regressed in the winter. A 25-hydroxy-vitamin D in April of 2008 was 25 ng/ml and obtained after John had begun to play outside. Due to the seasonality of John's symptoms the mother consulted me. I advised the mother to stop all products containing vitamin A including cod liver oil and begin John on 5,000 IU of vitamin D3 per day for two weeks followed by 2,000 IU per day in the form of powdered vitamin D dissolved in juice. Within a week of starting the vitamin D, John's language began to return and he was no longer as fearful of being alone. At the end of two weeks his language showed further improvement, he began to toilet himself, counted to 10 and knew the spelling of his name. After three weeks language continued to improve and some improvements were noted in his dysbacteriosis. After four weeks of vitamin D treatment, the mother noted improvements in muscle strength as well as continued improvements in language. A repeat 25-hydroxy-vitamin D is pending while John continues taking 2,000 IU of vitamin D per day.

Before you read the series of emails between the mother and me, I'd like to caution that this is only a case report of sorts and does not prove a treatment effect. Spontaneous remissions, while rare in autism, have been reported, thus the supplemental vitamin D may have had nothing to do with his improvement. If the response is due to vitamin D, there is no assurance it will prove lasting. I think it unlikely that older autistic children or individuals with severe autism will show these sorts of apparent improvements. Furthermore, autism is a multifactorial disease with strong genetic roots and it is highly unlikely that treatment of vitamin D deficiency in all autistic children will result in similar improvements. Finally, I did not examine this child, and I am relying on the child's mother to report both his condition and his apparent response to vitamin D treatment. However, the mother agreed to speak with the press about her son and allow for independent confirmation of the apparent treatment response.

Below are the emails, edited for brevity, clarity, and confidentiality.

Dear Dr. Cannell:

I am writing because I believe my son John is strongly affected by vitamin D and I need some advice. John is seven and autistic and weighs 50 pounds. We live in the northeastern part of the United States . He starts spending lots of time outside in May and continues until September. Every year, like clockwork, he has the same patterns of behavior and ability. After about six weeks of sun exposure, every July, he begins feeling much better, seems to be comfortable in his skin, does not have as much self-stimulatory behavior, can eat a variety of foods and has language. This past summer, he was using 14-word sentences. By the end of November, he can't even ask you for a cup of juice. He becomes more exclusive, has emotional highs and lows, has tantrums and is easily frustrated.

His 25(OH)D level on April 15th was 25 ng/ml but he had already been going out in the sun so his level must have been lower in the winter. I have had his genetics tested (Nutrigenomic) and he has mutations in his vitamin D receptors:

VDR Bsm/Taq ++
VDR Fok --
VDR Taq ++

My first question, does it sound like the changes in his behaviors and abilities could be caused by lack of vitamin D? Could you elaborate on the time it would take to get adequate amounts of vitamin D to start seeing positive results? For example, even if he starts going out in the sun in May, it's usually not until July that I see positive changes. Then would it take a month or two to go back to being deficient, thus explaining his 'regression' by the time November comes around. Secondly, I am looking at different forms of vitamin D therapy: a vitamin D lamp, vitamin D3 cream, or oral vitamin D. Can you tell me what might be the best form during the winter months?

Thank you very much for your time and attention.

Jane, Boston MA

Dear Jane:

Yes, it is possible your son's autism is related to vitamin D. Such seasonality has been reported before in autism, both in an individual and in autistic children at a summer camp. Although suggestive, such seasonality does not prove a vitamin D connection. Sun exposure, unless it is full body, takes several months to get vitamin D levels up. If sunblock or clothes are worn sun exposure will not get 25(OH)D levels much above 30 ng/ml. As far as the "mutations" you list, they are actually vitamin D receptor (VDR) polymorphisms and not referred to as mutations although all such changes occurred through mutations at some time in the past. VDR polymorphisms are simply the different structures of the vitamin D receptor that different people have and they are widely distributed. A pilot study of actual VDR receptor mutations did not detect VDR mutations in 24 autistic individuals but they did not assess for VDR polymorphisms. However, a highly significant association exists between one VDR polymorphism and larger head size. Mean head circumference is larger in autism.

Yan J, et al. Vitamin D receptor variants in 192 patients with schizophrenia and other psychiatric diseases. Neurosci Lett 2005;380(1-2):37-41.

Handoko HY, et al. Polymorphisms in the vitamin D receptor and their associations with risk of schizophrenia and selected anthropometric measures. Am J Hum Biol 2006;18(3):415-7.

Lainhart JE, et al. Head circumference and height in autism: a study by the Collaborative Program of Excellence in Autism. Am J Med Genet A 2006;140(21):2257-74.

Lainhart JE, et al. Macrocephaly in children and adults with autism. J Am Acad Child Adolesc Psychiatry 1997;36(2):282-90.

I emailed the world's foremost expert on VDR polymorphisms asking him about your son's polymorphisms and his reply, quite technical, is below.

Dear John:

I apologize for the delay in getting back to you regarding VDR polymorphisms. Initial studies by Eisman and coworkers many years ago suggested that several of the polymorphs identified above in the VDR gene (Bsm/Tag) correlated strongly with osteoporosis. Despite the hoopla, subsequent analyses by many different investigators did not really confirm these results, i.e. only a very modest (3%) correlation. This spawned multiple studies searching for correlations between VDR polymorph's and cancer, autoimmune disease and so forth. It is fair to say from all of these studies that the correlation is at best weak, and in most cases non-existent. Part of this may be due to the fact that the Bsm and Taq polymorphs are located in VDR gene introns and as a first approximation cannot affect the VDR protein's function. This is not an absolute statement, however, as our work is now showing that regulatory regions that control the VDR's expression are located within introns as well as upstream. Therefore the possibility exists that these polymorphs could affect expression, although we have not found these regions to contain enhancers yet. This is clearly where gene and disease studies are going. The only polymorph that could affect function is the Fok1 site, which we identified many years ago following our initial cloning and structural analysis of the human VDR gene. The presence of this site leads to the expression of a shorter VDR protein (424 aa) that is purported to have a slight increase in transcriptional activity (10%?) vs the large protein (427 aa). The above analysis suggests that this polymorph is absent, leading to production of the larger perhaps less active protein. On a single patient basis, it is really difficult to conclude anything regarding this finding. Indeed, despite large numbers of patients, the VDR polymorph have not really revealed any significant insight. Given the summer correlations, it is probably more likely that the individual is low in vitamin D3 in winter.

Sincerely,

Professor John Doe

Thus, one of your son's polymorphisms may have less functionality but that should be easily overcome by higher vitamin D levels. The first thing to do is stop all vitamin A, multivitamins containing vitamin A, or cod liver oil and start vitamin D. As you will see below, vitamin A antagonizes the action of vitamin D and he should have plenty of vitamin A if he eats colorful vegetables, colorful fruit, eggs and fortified oatmeal. As far as vitamin D, I think the easiest way to give vitamin D is powdered capsules, not a cream. You can open the capsule and put the powder in about anything, such as juice. To buy the capsules, go toBio Tech Pharmacal and buy both a bottle of the 5,000 and the 1,000 IU capsules. He should take one 5,000 IU capsule a day for two weeks then take 2,000 IU per day. After a month, go to the doctor and have another 25-hydroxy-vitamin D blood test. Do not let your doctor order a 1,25-dihydroxy-vitamin D as it will give you and your doctor false information about your son's vitamin D status. The other option is buying a Sperti vitamin D light. Daily use of the light on both sides of his trunk will raise levels fairly quickly but he should still have a 25(OH)D blood test every month to assure his levels rise to the mid level of normal ranges, about 70 ng/ml. Vitamin D is very safe. Your son would have to take more than 10,000 IU a day for more than a year to have any risk of toxicity. If he improves and his level is 50 ng/ml, the next question is would he improve even more if his level was 70 ng/ml? Some lifeguards have levels of 80-100 ng/ml; normal ranges in the labs in the USA are 30 -100 ng/ml (ideal ranges are 50 -100 ng/ml.) If you have any more questions, let me know. I certainly want to know how he is doing.

Sincerely,

John Cannell

Dear Dr. Cannell:

It has been one week on 5,000 IUs of vitamin D3 daily and already we're getting some language back! We haven't had original language since probably around the end of November. The only language we have had in the past five months has been verbal scripting. Today John has already told me "turn off the TV" and "clean up the water". This is all very exciting. Will it last? I will continue to keep you updated on progress and change in behavior. One more thing, all winter long he was afraid to be by himself anywhere. Now he is starting to be able to be in another room or outside by himself.

Thanks so much,

Jane

Dear Jane:

I can't tell you how happy I am for you. I suspect John will continue to improve. Do you have any parent rating scales or does his treating pediatrician have any objective rating scales? If you have before and after rating scales or his treating doctor does then it becomes important to track his progress on an objective measure. Jane, if you are a member of any autism discussion groups, you should post about this, including doses used. If your son's case is typical, then hundreds of thousands of autistic children may be helped with vitamin D.

John Cannell

Dear Dr. Cannell:

It has been two weeks on 5,000 IU per day and I want to inform you that we are having continued success with language. Continued in the sense that it is consistent, it wasn't just a one day fluke. In addition, he is taking himself to the bathroom; this is another thing that goes away in winter months. I usually have to catch him holding it in and then suggest he go, but now he is going completely by himself. In therapy last week, he started drawing again. He drew a bee and then ran around the room buzzing. His toileting is consistent with his therapists, not just mommy. Last night, I asked him to count to 10 for me and he did - quite enthusiastically. Then I said what does J-O-H-N spell? It took him a bit but then he said "John."

Unfortunately, the last scale taken was when he was 3 when he had his first developmental evaluation. But we do track behavior and language on a weekly basis. The forms we fill out give a good indication as to how he is doing.

I belong to a parent forum. It was created by a doctor named Amy Yasko. She's a PhD, a researcher, not a medical doctor. It was through her that I got John's genetics tested. She advocates vitamin D as being very crucial. I will post something on her forum for the parents there. However, if the parents on the forum are following her recommendations, they should be taking it already - 2000 IUs in winter and 1000 IUs in summer is her recommendation. I will post something on the forum to really emphasize how important vitamin D is.

Jane

Dear Jane:

I'm glad the improvements are continuing. I see Dr. Yasko recommends 10,000 IU of vitamin A/day as well as cod liver oil. I strongly disagree. Make sure your son is taking neither vitamin A nor cod liver oil. Rather, make sure he eats colored fruits and vegetables as well as fortified oatmeal. Vitamin A interferes with vitamin D's function, especially at the doses Dr. Yasko recommends.

Vitamin A antagonizes the action of vitamin D. In humans, even the vitamin A in a single serving of liver impairs vitamin D’s rapid intestinal calcium response. Furthermore, the consumption of preformed retinols, even in amounts consumed by many Americans in both multivitamins and cod liver oil appears to be causing low-grade, but widespread, bone toxicity, perhaps through its antagonism of vitamin D. In a recent dietary intake study, Kyungwon et al found high retinol intake completely thwarted vitamin D’s otherwise protective effect on distal colorectal adenoma and they found a clear relationship between vitamin D and vitamin A intakes as the women in the highest quintile of vitamin D intake also ingested almost 10,000 IU of retinols/day. As early as 1933, Hess et al warned about vitamin A consumption, concluding, “as to a requirement of thousands of units of vitamin A daily, the unquestionable answer is that this constitutes therapeutic absurdity, which, happily, will prove to be only a passing fad.”

Rohde CM, Deluca HF. All-trans retinoic acid antagonizes the action of calciferol and its active metabolite, 1,25-dihydroxycholecalciferol, in rats. J Nutr. 2005;135(7):1647-1652.

Johansson S, Melhus H. Vitamin A antagonizes calcium response to vitamin D in man. J Bone Miner Res. 2001;16(10):1899-1905.

Penniston KL, Tanumihardjo SA. The acute and chronic toxic effects of vitamin A. Am J Clin Nutr. 2006;83(2):191-201.

Oh K, Willett WC, Wu K, Fuchs CS, Giovannucci EL. Calcium and vitamin D intakes in relation to risk of distal colorectal adenoma in women. Am J Epidemiol. 2007;165(10):1178-1186.

Hess AF, Lewis JM, Barenberg LH. Does our dietary require vitamin A supplement? JAMA. 1933;101:657-663.

Unfortunately, Hess’s prophecy of a passing fad proved premature and many Americans continue to consume “absurd” and dangerous quantities of vitamin A. For example, multivitamins, until recently, had small amounts of vitamin D (200 to 400 IU) but high amounts of preformed retinols (5,000 to 10,000 IU). This pales in comparison to a tablespoon of modern cod liver oil, which contains sub-physiological amounts of vitamin D (400 to 1200 IU) but supra-physiological amounts of completely preformed retinols (5,000 to 15,000 IU or in some cases 30,000 IU).

John Cannell

Dear Dr. Cannell:

It has been three weeks and he went from 5,000 IU of vitamin D per day to 2,000 IU per day a week ago. His language is increasing. He's now back to saying the things he wants with some prompting. He also has gut dysbiosis and I'm sure the D is helping with microbes in his gut. He has a lot of problems with his immune system and bacteria and viruses. Also, doesn't vitamin D aid in the production of glutathione? I feel that could be a big part of his increased language.

Jane

Dear Jane:

Yes, abnormal immune responses are associated with both autism and vitamin D deficiency. For example, autistic individuals have immune abnormalities that show a striking similarity to the immune functions affected by vitamin D. Animal evidence indicates some vitamin D deficiency induced brain damage may be malleable, that is, vitamin D may partially reverse the brain damage, if given early enough. These studies offer hope that sunlight or oral vitamin D, especially in young autistic children, may have a treatment effect.

Ashwood P, et al. The immune response in autism: a new frontier for autism research. J Leukoc Biol 2006;80(1):1-15.

Cantorna MT, et al. Vitamin D status, 1,25-dihydroxyvitamin D3, and the immune system. Am J Clin Nutr 2004;80(6 Suppl):1717S-20S.

Burne TH, et al. Combined prenatal and chronic postnatal vitamin D deficiency in rats impairs prepulse inhibition of acoustic startle. Physiol Behav 2004;81(4):651-5.

Both the brain and the blood of autistic individuals show evidence of ongoing chronic inflammation and oxidative stress. That is, the disease process is probably increasingly destructive. Further hope for a treatment effect rests in activated vitamin D's powerful anti-inflammatory properties. Its administration reduces production of inflammatory cytokines in the brain, which have consistently been associated with cognitive impairment. Furthermore, activated vitamin D is remarkably neuroprotective by stimulating neurotropin release, reducing toxic cellular calcium levels in the brain, inhibiting the production of nitrous oxide, and by its immunomodulating properties, especially in reducing inflammatory cytokines and by increasing brain glutathione.

Moore ME, Piazza A, McCartney Y, Lynch MA. Evidence that vitamin D3 reverses age-related inflammatory changes in the rat hippocampus. Biochem Soc Trans 2005;33(Pt 4):573-7.

Cohen-Lahav M, Shany S, Tobvin D, Chaimovitz C, Douvdevani A. Vitamin D decreases NFkappaB activity by increasing IkappaBalpha levels. Nephrol Dial Transplant 2006;21(4):889-97

Kalueff AV, Eremin KO, Tuohimaa P. Mechanisms of neuroprotective action of vitamin d(3). Biochemistry (Mosc) 2004;69(7):738-41.

This last function of vitamin D, increasing cellular levels of glutathione, may explain the purported link between heavy metals, oxidative stress, and autism. For example, activated vitamin D reduces iron-induced and zinc-induced oxidative injuries in rat brain. The primary route for the neurotoxicity of most heavy metals is through depletion of glutathione and subsequent generation of reactive oxygen and nitrogen species. Besides its function as a master antioxidant, glutathione acts as a chelating (binding) agent to remove heavy metals. Several studies indicate autistic individuals have difficulty excreting heavy metals, especially mercury. If vitamin D deficient brains are unable to utilize glutathione properly, and thus unable to remove heavy metals, they may be oxidatively damaged by heavy metal loads normal children easily excrete. The amount of activated vitamin D in the brain directly depends on how much vitamin D is made in the skin or put in the mouth.

Garcion E, Wion-Barbot N, Montero-Menei CN, Berger F, Wion D. New clues about vitamin D functions in the nervous system. Trends Endocrinol Metab 2002;13(3):100-5.

Chen KB, Lin AM, Chiu TH. Systemic vitamin D3 attenuated oxidative injuries in the locus coeruleus of rat brain. Ann N Y Acad Sci 2003;993:313-24.

Lin AM, Chen KB, Chao PL. Antioxidative effect of vitamin D3 on zinc-induced oxidative stress in CNS. Ann N Y Acad Sci 2005;1053:319-29.

Valko M, Morris H, Cronin MT. Metals, toxicity and oxidative stress. Curr Med Chem 2005;12(10):1161-208

Kern JK, Jones AM. Evidence of toxicity, oxidative stress, and neuronal insult in autism. J Toxicol Environ Health B Crit Rev 2006;9(6):485-99.

Sincerely,

John Cannell

Dear Dr. Cannell:

It has been a month now and John's Improvements are continuing. In the last week, he has been using his muscles more, he goes on the swing outside and lifts his legs and bends in ways that take core muscle strength. This is yet another skill or interest that left and is returning. I will report more next week.
Jane

Conclusion:

It is too early to say vitamin D has a treatment effect in autism. However, a simple risk/benefit analysis suggests that autistic children should be diagnosed and aggressively treated for vitamin D deficiency. If readers want to learn more about vitamin D and autism, they can obtain the entire paper on the link below. Unfortunately, Elsevier charges $31.50 to download it. You can read a similar document for free on the website, where we first published the theory a year ago.

Cannell JJ. Autism and vitamin D. Med Hypotheses. 2008;70(4):750-9.

http://vitamindcouncil.org/newsletter/2007-may.shtml

In summation, autistic children should be given enough vitamin D to get their 25(OH)D levels up to the mid to high range of normals, that is, 70 ng/ml (175 nmol/L in countries that use the metric system). In the absence of sun exposure, this usually requires long-term administration of about 1,000 IU/day per 20 pounds of body weight with a loading dose of 2,000 IU of vitamin D/day for every 20 pounds of body weight for the first two weeks. As individual variation in response is very high, they should have 25(OH)D blood tests every month until their level has stabilized around 70 ng/ml. They should stop all products containing preformed retinols (vitamin A), especially cod liver oil.

John Cannell, MD
The Vitamin D Council

This is a periodic newsletter from the Vitamin D Council, a non-profit trying to end the epidemic of vitamin D deficiency. If you don't want to get the newsletter, please hit reply and let us know. As we are a 501(3)(c) non-profit corporation, dedicated to ending vitamin D deficiency and not making money, the Vitamin D Council does not copyright this newsletter. Please reproduce it and post it on Internet sites. If this newsletter proves useful to a child you know with autism, the Vitamin D Council asks for a donation as we have not been able to secure a grant and our bank account balance is again below $5,000. Send your tax-deductible contributions to:

The Vitamin D Council
9100 San Gregorio Road
Atascadero, CA 93422

Rather than the headline New Study Could Change Heart Disease Diagnosis And Treatment being run in Utah TV and newspapers, instead it should read:

Make big money fast with CT scans!

Is your bottom line shrinking? Have you fallen on hard economic times? Is competition from other hospitals and providers threatening your financial health?

Then we have a solution: Do a CT coronary angiogram on everybody! Look for disease in people with no symptoms, scare the heck out of them, and voila! Instant need for bypass surgery!

Ka-ching!! That'll be $100,000, please.

Do it again, and again, and again, and your hospital will be quickly in the black in no time!

And, for the savvy marketer, tell the newspapers that you're going to conduct a study to see if this approach works--even before the study gets started! Even if the study pans, you'll come out a winner because you did it in the name of "research"!

Apparently a group of cardiologists at the Intermountain Medical Center and LDS Hospital in Salt Lake City, with the financial assistance of Siemens, a manufacturer of CT scanners, is funding a 1000-patient study of diabetics, all without symptoms of heart disease, half of whom will undergo "screening" CT coronary angiograms (not heart scans) followed by bypass surgery, if "needed". The other half will receive conventional, "aggressive" medical therapy. "Aggressive" means cholesterol treatment, blood pressure control, and blood sugar control (no kidding).

The outcomes of the two groups will be compared after two years.

To understand the absurdity of this study, note that they are proposing what amounts to "prophylactic" bypass surgery, since the participants are without symptoms. Since there are no stress tests, a measurement of flow or functional capacity (exercise tolerance) cannot be factored in. Decisions will be made on the basis of severity of "blockages" in asymptomatic people, a hazardous notion that has never been shown to provide benefit. No doubt: Some diabetics with extensive disease may obtain benefit from screening, but many more will undergo what amounts to unnecessary bypass that provides no benefit. We already know from studies dating back over 20 years to the days of the original CASS (Coronary Artery Surgery Study) that putting asymptomatic people through bypass surgery willy-nilly does not reduce mortality.

Of course, the "aggressive" preventive treatment they propose is more like the least common denominator level of treatment. In fact, I would characterize the "aggressive" preventive treatment as ridiculous. Doing less would be malpractice. Much more could be done, but doing a lot more would pose a real challenge to the bypass arm of the trial.

But the smell of money drives such efforts: More CT angiograms, more hospitalization for bypass surgery. The payoff to the hospitals from this effort is likely to exceed $5 to $10 million, all money that they might not have otherwise seen. The ill-informed people in the local media gush with enthusiasm, the hospital acts like they are at the cutting edge of medical technology, the doctors pose as saviors.

All this time, real preventive efforts go unmentioned. No fish oil (28% reduction in heart attack, 45% reduction in sudden death from heart attack), no genuine diet efforts (i.e., not the diabetes-promoting American Diabetes Association diet), no effort to identify sources of coronary risk beyond LDL cholesterol (low HDL,small LDL,and postprandial or after-eating abnormalities, for instance, are prominent sources of risk in diabetics), no vitamin D. In my view, the preventive arm of the study amounts to doing virtually nothing beyond prescribing statin drugs.

Don't fall for it.

The Fountain of Youth, Louis Cranach the Younger (1546)

In the Track Your Plaque program, we sometimes use the adrenal hormone, DHEA. It is a fascinating and--surprisingly--an over-the-counter hormone that can be useful and safe when used properly.

DHEA can be useful for:

--Reduction of Lp(a)--Though more effective in females, it can also be useful in males. In the women, DHEA often reduces Lp(a) 15-18%, somewhat less in males. The lower the starting DHEA, the greater the Lp(a) reduction.

--Improved libido--in both men and women. The effect is modest. It's magnified when used with other strategies. Although this is not specifically a goal in the program, it sure helps to get side-benefits like this, rather than unwanted side-effects.

--Increased energy and mood--The boost in mood is, for many, the most perceptible effect: More ambition, more stamina, greater staying power in work and exercise.

--Reduction in abdominal (visceral) fat--A modest effect, but one that, over a long period of use (>6 months) can yield improved insulin responses.

Most commonly, I will suggest DHEA supplementation when blood levels allow. Some people, however, Google "DHEA" and come back horrified that I would suggest such a dangerous supplement.

"I read that it makes women grow mustaches and makes their voices deeper!"

And it does--if you take a lot.

10-15 years ago, when the benefits of DHEA became apparent, some people wanted to believe that DHEA was the fountain of youth. People interested in the anti-aging potential for DHEA figured that, if 50 mg per day made you feel energized and vigorous, what would be the effect of 1000 mg, 2000 mg, or 3000 mg per day? A number of clinical trials were conducted using these doses and, interestingly, depression can lift, men and women increase muscle mass, there is a slight increase in bone density, even pain symptoms from rheumatoid arthritis and lupus may improve. But . . . women grow mustaches, become sexually aggressive, and develop deep voices. Men can become hyperaggressive or overly emotional.

No wonder: Any hormone taken in extraordinary, supraphysiologic doses will exert wacky effects. Imagine taking testosterone or estrogen at 50 times the usual dose.

The doses we use for the above benefits, including Lp(a) reduction, range from 25-100 mg per day; most people do fine with 50 mg. We also adjust doses to starting blood levels. In this dose range, I have never seen any of the above side-effects.

The only side-effects I see at these doses are 1) excessive assertiveness or crabbiness, and 2) insomnia if taken at bedtime.

In my experience, DHEA is a benign hormone, provided it is taken in limited doses and not abused. An occasional female younger than 55 years old will be able to tolerate only 10-20 mg per day before developing the edgy side-effects, but I've never witnessed masculinizing side-effects at these low doses, nor have I ever seen excessive increases in testosterone in men or women. (Women can raise testosterone levels slightly, but almost never enough to exert much effect beyond modestly increased libido.)

Copyright 2008 William Davis, MD

Here is detailed comment from a reader who figured out the wheat (and dairy) issue on her own with impressive results.

Though it seems an unpardonable over-simplification of diet, this concept of eliminating wheat-based products (along with obvious unhealthy foods like candy and soda) yields unexpectedly large results, as our reader relates.

Hi Dr. Davis,

Several years ago, chronic untreated asthma infections hospitalized me. I thought it was recurring bronchitis as I'd never had asthma in my life. Killed much of the alveoli... took awhile to de-crap the lungs and regrow the alveoli. Got assigned a cardiologist sort-of by accident while in the hospital for that (couple days of constant heated steroid, stress, a pain + situation combined, elevated my heart rate to 298 for a brief time). When I went to see him, he wrote me a prescription for the Eades' PPLP [Protein Power LifePlan] book.

It's taken awhile, since it's required radical gradual changes in most aspects of my overly Type-A life, but I'm now about 140 lbs lighter, and hopefully much more in the future.

Miraculously, after 10 days on a hard meat-eggs-cheese-veggie-berry approach (which I sadly confess was mostly pepperoni & mozz nuked... I was busy! ;-)), all my medical symptoms disappeared too. Acid reflux, acne, brain-fog, rashes, 'severe asthma', allergies, etc. etc. By trial and error I realized I wrongly attributed that to lowcarbing when it was getting off gluten that actually did it for me. Which since I'm lowcarb also means all the crap my celiac boyfriend can eat, I can't. Lowcarb does many great things for me (just dropping all the bloating and increasing the energy level are awesome), but getting off wheat was critical.

I've since found that a single tablespoon of "milk" in the morning, or something with wheat (say a tortilla), will make me ravenous *specifically for milk and wheat* all day. Conversely, I can be eating lowcarb and then eat total junk--but something without gluten--and not have it bother me much at all. But one pumpernickel slice at Outback and I am DOOMED. It doesn't always happen that instant; will-power has some sway; but the odds of my making a 'poor decision that leads to cascade failure and totally abandoning my eating plan' in the next 48 hours is astronomically higher if milk or wheat were involved. Oddly, cheese does not seem to affect me this way.

When I was younger (I'm 42 now) I had to stop drinking milk. If I drank some I wanted more. If I drank more I needed more. If I drank more, that was it: I'd be stumbling to the kitchen in the dark at 3am, drinking out of the carton, falling gasping against the refrigerator after several long gulps, like a heroin addict who just got a fix. I finally realized that since I'd lived on a ton of milk my whole life, maybe this was a milk problem; so I usually stayed away from it. So then it turned out wheat/gluten were an issue too. Which made me realize how much of my life was filled with not-eating most of the time (very busy, workaholic, but very sedentary), but when I did eat, ingesting amazing amounts of wheat products. I'm astounded that my whole life I mostly ate things I am apparently intolerant to "or something." Sometimes I wonder how much different even my brain would be if it'd been different.

This might contribute to my ending up weighing 500# at one point. The only amazing thing is that I didn't get a disease. (Well I did--obesity--but I mean any others.) I'm from a family of people who are mostly fat, mostly alcoholic, and mostly dead of cancer. I'm just fat, worse than the others but otherwise seemingly ok. Now I'm starting to think that maybe my whole family may have some 'issue' with the primary foods of our culture.

I tell friends that my horrible chronic acid reflux was solved merely by getting off gluten. They nearly all say, "I could never give up bread!" (Isn't it funny, you never hear people say, "Oh man, I could never give up broccoli!") I tried to convince one young friend to try it; her doctor told her eating more protein and fat was unhealthy, and gave her a prescription (this is lifetime--it doesn't cure it, merely treats the symptom) to a drug to help with acid reflux. I said you're kidding me, you think taking a drug the rest of your life is healthier than trading your pasta for a steak?? Go figure.

I still haven't figured out the milk connection (or why I seem ok with cheese for some reason; maybe there is a dosage-difference, or the sugar combined with it has some effect), but I think it's pretty clear that dropping milk and wheat has very radically changed my life for the better. I may actually live, which being a single mom to an awesome 11 year old girl, is a good thing.

Best,
P.

Given the confusion over what constitutes the "ideal" diet, a discussion that has been hotly debated for decades, some people become very angry that we still don't agree on what is truly healthy.

"Why should I even try if the experts don't agree? They say something is bad one day, then say it's okay the next!"

But that's a short-sighted half-truth born of frustration. We have certainly zigzagged in our understanding of diet over the years. The grand national experiment in low-fat eating, for instance, clearly failed to improve our health. In fact, the opposite occurred: The largest epidemic of obesity and diabetes in world history. You could get angry from this failed experiment . . . or you could learn from it, take what lessons we can and improve on it.

Step back for a moment and consider: In what other age could we even have this discussion?

If we lived in a world where you were hungry, your children were hungry, and you didn't know where the day's food was to be found, we would have no need whatsoever for this conversation: You would take whatever you could find, kill, or steal.

Say you woke up this morning and your cabinets and refrigerator were empty. The stores were far away or non-existent. You and your family would have to improvise, to forage or hunt your day's food. It would require hours. You wouldn't fuss about glycemic index, or saturated fat, or whether or not sugar or wheat was present. You would just eat whatever you could get your hands on. When caloric deprivation threatens, we take what is available.

But we live in a world of plenty--of enormous excess--that allows us choices. It is a world that encourages eating more than is required for existence, a world tailored more to indulgence than to simple satiety or sustenance. That's when distinctions among food types and quality make a difference. But it is a dilemma born of riches.

Starvation and caloric deprivation would settle the argument for us very quickly. It doesn't mean that we shouldn't continue to debate the finer points of diet. But don't do it with anger or frustration. Do it GRATEFULLY, recognizing that we are lucky to be able to have such a conversation in the first place.

Image courtesy Food and Agriculture Organization of the United Nations.

I frequently peruse conventional health websites to keep track of their message. One painfully conventional (read "drug company-supported") website that echoes the standard advice on heart disease and heart health is Everyday Health .

Since I subscribe to the newsletters for many conventional sites, I received an e-mail that took me to this Q & A about HDL cholesterol:

Q: I'm 36 years old and my good cholesterol is too low. What can I do?
– Nilsa, Florida

Dr. Lori Mosca of New York-Presbyterian Hospital responds:

A: A woman's HDL goal should be greater than 50 mg/dL (greater than 40 mg/dL in men). You can raise your HDL levels by eating a diet low in saturated fat and trans fat but high in monounsaturated fats. Lose weight if you need to and get at least 30 minutes of moderate-intensity exercise on a minimum of four days per week. If you smoke, quit. Despite positive lifestyle changes, though, some individuals may still be candidates for HDL-raising drug therapy because they are at increased risk for cardiovascular disease. Discuss your options with your health care provider.

Are you satisified with that answer? I certainly am not.

First of all, is this something you've never heard before? "Eat right, exercise, cut your unhealthy fats." Then why do people who follow this sort of conventional advice often still fail? Is the next step always medication?

Here's the part that Dr. Mosca and other conventional, drug-minded "authorities" have left out:

To raise HDL powerfully--not to 40 mg/dl for males or 50 mg/dl for females, but to 60, 70 or 80 mg/dl--think about the following strategies:

--Eliminate wheat and cornstarch products. I have droned on endlessly about this concept, but it is enormously effective. While the weight loss that inevitably follows elimination of these foods adds to the HDL-raising effect, there is also an independent effect, as well.

--Fish oil--The omega-3 fatty acids in fish oil reduce triglycerides. Triglycerides accelerate the destruction of HDL. Remove triglycerides, HDL goes up. (Though krill oil may share, even surpass this effect, we need more data than the single manufacturer-sponsored study.) Of course, this requires real doses, not the namby-pamby doses you often read about.

--Vitamin D--Achieving normal levels of 25(OH) vitamin D raises HDL with power I have never witnessed from any other strategy before, barring weight loss of 30+ lbs. Readers of the Heart Scan Blog know that just taking vitamin D is not enough. Verification with blood levels is an absolute necessity, particularly if raising HDL maximally is among your goals.

--Adding back saturated fat. I say "adding back" since most of us (including myself) went too far down the "saturated fat is bad" path over the past few years. While I do not advocate a carte blanche approach to saturated fat, I believe that adding back eggs (preferably free-range and/or omega-3 rich), lean meats, and hard cheeses is a good idea. The saturated fat in these foods raise HDL 5 or more mg/dl.

--Dark chocolate--Or other cocoa prepartions. What a cool way to raise HDL! Reach for the lowest-sugar, highest cocoa preparations.

--Alcoholic beverages--I am partial to the red wine/flavonoid-rich concept, being a wine drinker. Although all alcoholic beverages raise HDL due to the ethanol content, for benefits beyond alcohol (as well as to avoid wheat-based drinks like beer), I do believe that the bulk of data argue for flavonoid-rich red wines from southern France, Italy, and California.

--Achieve ideal weight--The toughest of all. But eliminating wheat and cornstarch makes it far easier.

Follow the conventional advice of those like Dr. Lori Mosca, and the majority of people will fail. ("It just so happens that I have a prescription drug just for that purpose!")

Buck the conventional advice, adopt strategies that won't be found in the drug ads, nor be provided by the conventionally-thinking, and you can succeed to heights you never thought possible.

Copyright 2008 William Davis, MD

Let me tell you a story, a tale of a woman who gained 30 lbs by eating one cracker.

At age 50, Claire's health was a disaster. Her initial lipoprotein patterns were a mess, including HDL 36 mg/dl, triglycerides 297 mg/dl, blood sugar 122 mg/dl (pre-diabetic range), blood pressure 155/99. Small LDL comprised over 90% of all LDL particles.

At 5 feet 3 inches, she weighed 210 lbs--90 lbs over her ideal weight. Her face was flushed and red, her eyes swollen and weighted down with bags, her eyes dull. While interested in hearing about how to improve her health, I would hardly call her enthusiastic.

We talked about how removing wheat products entirely from her diet could result in weight loss--enormous weight loss--yet with reduced appetite, increased energy, less daytime sleepiness and fogginess, improved sleep quality. Removing wheat would also allow substantial correction of her lipoprotein patterns with minimal medication.

At first, she seemed confused by this advice. After all, it ran directly opposite to what she'd been told by her family doctor, not to mention the advice from TV, food ads, and food packages.

To my surprise, Claire did it. She didn't return to the office for another 5 months. But she came in, a big beaming smile on her face.

Even at 167 lbs--still overweight--Claire looked great. She glowed. She'd already dropped nearly 2 1/2 inches from her waist. She felt lighter on her feet, discovered energy she thought she'd lost 10 years earlier. Her blood results matched, with dramatic shifts in each and every pattern.

I quizzed Claire on her diet, and she had indeed made substantial changes. In addition to eliminating all foods made of wheat flour, she also eliminated foods made with cornstarch, rice flour, snacks, and other sweets. She ate her fill of vegetables, fruits, raw nuts, lean meats, and healthy oils. She was less hungry while eating less. Even her husband, skeptical at first, joined Claire after the first two months and her initial 20 lbs of weight loss. He, too, was well on his way to dropping to ideal weight.

But a dinner party invitation came. In the few that Claire and her husband had gone to over the few months, she had religiously stuck to her program, choosing cheese, pickles, olives, vegetables that she dipped, but avoided the pretzels, breads, Doritos, potato chips, and others.

This time, a tray of whole wheat crackers was laid on the buffet table, covered with some sort of sweetened cheese. She had just one. She savored the taste that she'd missed. "Maybe one more. I'll be extra good this weekend,'" she told herself.

Now Claire was hungry. The bruschetta covered with tomatoes and mozzarella looked awfully good. "It's got some good things on it, too!" she thought. She had three.

The floodgates opened. I saw Claire three months later, weighing just shy of 200 lbs. "I almost cancelled this appointment," she whispered quietly, tears at the corner of her eyes. "I don't know what happened. I just lost control. After losing all that weight and feeling so good, I blew it!"

I've seen it before: Fabulous success eliminating the foods that created the situation--the insatiable appetite, the endless cycle of hunger, brief satiety, the rolling, rumbling hunger--followed by temptation, then disaster. The weight lost comes right back.

It's experiences like Claire's that have absolutely, positively convinced me: Wheat products are addictive. It's not true for everybody, but it's true for many people, certainly most people who have weight struggles. It triggers some sort of appetite button, a signal to eat more . . . and more, and more. Keep it up long enough, and you have drops in HDL, increases in triglycerides, upward jumps in blood sugar and blood pressure, diabetes, etc. It doesn't matter if it's whole grain, 7-grain, or 12-grain. Yes, the whole grains contain more fiber and more B vitamins. But they all share one characteristic: They trigger a desire for more.

So that's the story of how one whole wheat cracker caused one woman to gain 30 lbs.

Next week's story:

California woman claims: My children are aliens!

Just kidding.

Copyright 2008 William Davis, MD

Eliminate wheat from your diet and wonderful things happen:

--Lose 15-20 lbs, sometimes in the first 1-3 months. (More or less, depending on your prior dietary habits, weight, age, etc.)
--HDL cholesterol goes up, triglycerides go down
--Blood sugar drops
--Small LDL is reduced
--C-reactive protein is reduced
--Pre-diabetics often convert to non-diabetics
--Diabetics gain far better control over blood glucose. Some even become non-diabetic (as long as they maintain the wheat-free, low-glycemic index diet and weight control).
--You feel better: Less mental fogginess, more energy, better sleep.
--Appetite shrinks dramatically.

(Many diet programs makes lots of money promising similar results. Prescription medications like the pre-diabetes drugs, Actos and Avandia, and the fibrates, Tricor and Lopid, nearly--nearly--reproduce the effects of eliminating wheat. Of course, these medications do not lead to weight loss or make you feel better. In fact, Actos and Avandia usually trigger a weight gain of 8 lbs in the first year of use.)

All of these wonderful effects develop with elimination of wheat. . . unless you confuse wheat-free with gluten-free. There's a difference.

Remove wheat from your diet, but discover the world of gluten-free products made for people with celiac disease, or gluten enteropathy, and you can regain the weight and recreate many of the phenomena associated with wheat. I've talked about this in past, but it trips up so many people that it's worth talking about again.

The concept that I am advocating is really low-glycemic index (or low glycemic load, actually). Foods that trigger a substantial rise in blood sugar, whether immediate (like whole wheat crackers) or delayed (like whole wheat pasta) are the culprits. The same effects develop with candy, cookies, fruit drinks, pizza, chips, table sugar, and other junk foods.

However, I pick on wheat specifically because it so dominates the American diet. It has grown to fill so many processed food products. It is also a food ingredient that is falsely advertised as healthy. In reality, pretzels, whole wheat crackers, whole grain bread, high-fiber cereals, etc. exert the same effect on blood sugar as candy or white table sugar. They also generate all the "downstream" phenomena listed above.

But wheat is hardly the only food that makes us fat, diabetic, and unhealthy. This is true for foods made with cornstarch (taco shells, cornbread, tortillas, chips, breakfast cereals); rice flour, puffed rice, and polished rice; and potatoes, particularly pulverized potato starch (potato chips). There are others.

These are the gluten-free products that are marketed to the gluten enteropathy (celiac disease) market. Yes, you can make muffins with cornstarch and no wheat gluten, but is it good for you?

No. It is nearly as bad as wheat. It can still skyrocket blood sugar, drop HDL, raise triglycerides, create small LDL, heighten inflammation, etc.

Ground flaxseed, oat bran, barley, quinoa, are some of the alternatives that do not create these effects. But not the majority of gluten-free products on the market.

Ingredients: Potato starch, rice flour, modified corn starch, olive oil, yeast, vegetable protein(lupine), corn syrup, sugar, salt, hydroxypropyl methylcellulose, sodium bicarbonate, ammonium bicarbonate, diacetyltataric acid esters of mono- and diglycerides of edible fats, natural flavor.

". . . only naturally gluten-free and wheat-free ingredients and adhere to the strictest quality processes, testing every batch for gluten using the ELISA assay."

NUTRITION FACTS
Serving Size 7 bread sticks (31g)
Servings per container 5

Calories 120 Calories from fat 25
Amount per serving
Total Fat 2.5g
Saturated Fat 0.5g
Trans Fat 0g
Cholesterol 0mg
Sodium 310mg
Total Carb 24g
Dietary Fiber 1g
Sugars less than 1g
Protein less than 1g

Does chelation work?

It's a question I get asked fairly frequently. Although I have never performed chelation, IV or oral, and therefore have no direct experience, my concerns for this purported therapy have included:

1) The concept of extracting calcium from atherosclerotic plaque by removing it first from the blood is absurd. Early chelationists believed that this was the means by which EDTA might reverse coronary atherosclerosis. However, removing calcium from blood would more likely lead to osteoporosis or calcium extraction from bone, since bone is a more ready repository for calcium. Blood calcium levels are also tightly and narrowly controlled; any significant reduction in calcium ("hypocalcemia") can be life-threatening. And, indeed, there have been deaths from hypocalcemia in people receiving chelation.

More recently, chelationists have argued that removal of heavy metals like lead and mercury are responsible for the purported benefits of chelation. And, indeed, blood levels of these heavy metals can be reduced by chelation. That alone may be a benefit. But to then make the leap to say that it also regresses atherosclerotic plaque by the same mechanism has no basis in science.

2) Practitioners associated with chelation tend to be shady. I have seen homeopathic therapies (among THE most ridiculous of concepts), "energy balance" therapies, desiccated organ extracts ("applied kinesiology"), and a variety of other fringe treatments offered by practitioners offering chelation. This doesn't necessarily mean, of course, that chelation is also fringe or suspect, but it tends to be offered by practitioners who engage in generally unscientific, unfounded practices.

The few people I've seen go through multiple courses of chelation (usually 30 or so infusions) have shown no impact on heart scan scores or any other measure of heart disease.

In response to the many questions I receive on chelation, I had been answering that, if we would simply wait for the publication of the NIH-sponsored trial of IV chelation therapy, perhaps we'd know once and for all.

However, in a lengthy criticism, four expert authors argue that the TACT trial to assess chelation study is doomed to failure for an entire list of reasons and should therefore be abandoned. The discussion is available on Medscape Cardiology. (Free sign-in required.)

Why the NIH Trial to Assess Chelation Therapy (TACT) Should Be Abandoned
We investigated the social and the scientific histories of chelation therapy beginning in the 1950s. We examined TACT protocols and consent forms, which, in response to Freedom of Information Act (FOIA) requests, the NIH provided to us with curious redactions. We examined the existing RCTs and the numerous case series cited by the TACT protocols. We examined evidence for risks, including information that is not in the standard medical literature. We examined various hypotheses that advocates have offered to explain how chelation "works."

We present our findings in 4 parts. First, we provide a brief history of the use of disodium EDTA as a treatment for CAD. Next, we describe the origin and nature of the TACT. Next, we discuss the evidence for chelation as a treatment for CAD and for atherosclerosis in general, and place it in the context of other proposed treatments that have been ineffective after an initial period of enthusiasm. Finally, we discuss the risks. For each topic, we contrast our findings with relevant statements in the TACT literature, to the extent that such statements exist.

Among the highlights:

--Since the mid-1970s, court documents and newspapers have reported at least 30 deaths associated with IV disodium EDTA, most of it administered by ACAM members.

--Early chelation investigators had chosen the disodium salt of EDTA, reasoning that if it could remove calcium from atherosclerotic plaques, it might shrink them. That notion was soon demonstrated to be invalid. It has largely been replaced by a "toxic heavy metals" antioxidant hypothesis, which is based on the potential for metal ions to produce free radical damage. Chelationists now cite "removing heavy metals" as the basis for their claim that chelation is effective for approximately 70 conditions, ranging from schizophrenia and autism to cancer. This provides them with numerous reasons to ignore any trial that finds chelation ineffective for CAD.

--Biochemical literature, either not cited or misrepresented in the TACT protocols, has demonstrated that the heavy metals hypothesis is implausible. Antithetically, it also demonstrates that the chelation mixture used in the TACT has pro-oxidant effects in vitro.

--In our opinion, TACT literature -- including 2 versions of the protocol, the consent form, information posted on the NCCAM Web site, and 2 editorials co-authored by the PI -- has misrepresented chelation, its risks, and the facts of the study. It has exaggerated the value of supportive case series, not only by ignoring evidence of bias and incompetence, but by misrepresenting citations and reporting erroneous data. It has minimized the dangers, both by understatements and by omissions of specific, published complications. It has not acknowledged the deaths mentioned above. It has repeatedly conflated disodium EDTA and a different drug, calcium-sodium EDTA.

--The TACT includes nearly 100 "chelation site" co-investigators who, in our opinion, are unsuitable to care for human subjects or to report trial data. Most espouse implausible health claims while denigrating proven methods; several have been disciplined, for substandard practices, by state medical boards; several have been involved in insurance fraud; at least 3 are convicted felons. Several were members of the ACAM or GLACM IRBs mentioned above. Few appear to have real expertise, required by TACT literature, in treating patients with CAD or in conducting clinical trials. Most continue to promote chelation while the TACT is in progress, contrary to good science, to human studies ethics, and to US Federal Code.

While the criticism itself does not prove the point one way or another, as a clinical trial should, anyone contemplating chelation therapy would be well-advised to read the document first. Another reference: EDTA chelation therapy for cardiovascular disease: a systematic review.

The authors of the exhaustive discussion are:
Kimball C. Atwood IV, MD, Anesthesiologist, Newton-Wellesley Hospital, Newton, Massachusetts; Assistant Clinical Professor, Tufts University School of Medicine, Boston, Massachusetts; Associate Editor, Scientific Review of Alternative Medicine
Author's email: katwood@partners.org

Elizabeth Woeckner, AB, MA, President, CIRCARE (Citizens for Responsible Care and Research), Columbia, Maryland

Robert S. Baratz, MD, DDS, PhD, Medical Director, South Shore Health Center, Inc., Braintree, Massachusetts; Assistant Clinical Professor of Medicine, Boston University School of Medicine, Boston, Massachusetts; President, National Council Against Health Fraud, Inc.

Wallace I. Sampson, MD, Clinical Professor of Medicine (Emeritus), Stanford University, Stanford, California; Senior Attending Physician and formerly Chief of Medical Oncology, Santa Clara Valley Medical Center, San Jose, California; Editor-in-Chief, Scientific Review of Alternative Medicine

The authors provided the following disclosures:

Disclosure: Kimball C. Atwood IV, MD, has disclosed no relevant financial relationships in addition to his employment.

Disclosure: Elizabeth Woeckner, AB, MA, has disclosed that she has received compensation for consulting in civil litigation and professional disciplinary actions.

Disclosure: Robert S. Baratz, MD, DDS, PhD, has disclosed that he has been retained by state licensing boards, the Office of the US Attorney, and plaintiff counsel as an expert in disciplinary proceedings and litigation with regard to chelation therapy and associated matters. He is compensated only for his time and has no commercial interest in the outcome of the proceedings or litigation.

Disclosure: Wallace I. Sampson, MD, has disclosed no relevant financial relationships in addition to his employment.

These are actual quotes from the American Diabetes Association website:

Myth #2 (from list of Diabetes Myths): People with diabetes can't eat sweets or chocolate.
If eaten as part of a healthy meal plan, or combined with exercise, sweets and desserts can be eaten by people with diabetes. They are no more “off limits” to people with diabetes, than they are to people without diabetes.

Myth #5: If you have diabetes, you should only eat small amounts of starchy foods, such as bread, potatoes and pasta.
Starchy foods are part of a healthy meal plan. What is important is the portion size. Whole grain breads, cereals, pasta, rice and starchy vegetables like potatoes, yams, peas and corn can be included in your meals and snacks. The key is portions. For most people with diabetes, having 3-4 servings of carbohydrate-containing foods is about right. Whole grain starchy foods are also a good source of fiber, which helps keep your gut healthy.

How can I have sweets and still keep my blood glucose on target?
The key to keeping your blood glucose on target is to substitute small portions of sweets for other carb-containing foods in your meals and snacks. Carb-containing foods include bread, tortillas, rice, crackers, cereal, fruit, juice, milk, yogurt, potatoes, corn, and peas. For many people, having about 45 to 60 grams at meals is about right. Serving sizes make a difference. To include sweets in your meal, you can cut back on the other carb foods at the same meal.

For example, you’d like to have cookies with your lunch. Your lunch is a turkey sandwich with two slices of bread. Your first step is to identify the carb foods in your meal. Bread is a carb. You decide to swap two slices of bread for two slices of low-calorie bread and have the cookies -- it’s an even trade. Your total amount of carbohydrate remains the same for the meal.

Can I eat foods with sugar in them?
For almost every person with diabetes, the answer is yes! Eating a piece of cake made with sugar will raise your blood glucose level. So will eating corn on the cob, a tomato sandwich, or lima beans. The truth is that sugar has gotten a bad reputation. People with diabetes can and do eat sugar. In your body, it becomes glucose, but so do the other foods mentioned above. With sugary foods, the rule is moderation. Eat too much, and 1) you'll send your blood glucose level up higher than you expected; 2) you'll fill up but without the nutrients that come with vegetables and grains; and 3) you'll gain weight. So, don't pass up a slice of birthday cake. Instead, eat a little less bread or potato, and replace it with the cake. Taking a brisk walk to burn some calories is also always helpful.

Or take a look at the recipes for breads, muffins, cakes, pies, cookies, and pizza.

My point? As I often say, while the "official" organizations like the American Diabetes Association, the American heart Association, and the USDA dominate the message provided to mainstream Americans, to those of us who know better, they have become irrelevant. You can see how obviously boneheaded their advice is. I'd go so far as to say that, if you want diabetes, follow the American Diabetes Association diet. If you have diabetes, and you'd like to accelerate complications like kidney disease, heart disease, and neuropathy, then follow the American Diabetes Association diet.

I'm going to bet that American Diabetes Association sponsors like Lilly, Novo Nordisk, Merck, Pfizer, Abbott ($1 million or more annual contributions) and Cadbury Schweppes (3-year, multi-million dollar support for Weight Loss Matters program) will continue to charge full-speed ahead to maintain the status quo. Cadbury Schweppes are the proud makers of Dr. Pepper, Hawaiian Punch, Snapple, Motts' Apple Juice, and Hires Root Beer--you know, the foods and drinks that you can have as long as you adjust your insulin dose or talk to your doctor about adjusting your diabetes medications. And if you gain, say, 30 or 40 lbs eating these foods. . . well, we've got a treatment for that. Merck's Januvia , for instance, can help you out for only about $200 a month!

Looking at the facts this way, and it seems like some cheap conspiracy theory: They're all out to get us. Dispense information that virtually guarantees propagation of the disease, and all your friends and cronies profit. I don't know if it is or it isn't, but it sure smells like it sometimes.

Synthroid, Armour Thyroid, and the battle for T3

Letter to New York Times

Red yeast rice alert

"Average amount of heart disease for age"

Quantum leaps

Body count

Dr. Bill Blanchet: A ray of sunshine

The Russert Protocol at work

Petition to the National Institutes of Health

Wheat withdrawal

Vitamin D Newsletter-Autism and Vitamin D

"Make big money fast with CT scans"

Is DHEA dangerous?

Wheat addiction: 140 lbs lost

Diet: Don't be angry, be GRATEFUL

HDL for Dummies

"I gained 30 lbs from one cracker"

Wheat-free is not gluten-free

Death to chelation?

American Diabetes Association