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.

Alex had lipoprotein(a), Lp(a), at a high level. With a heart scan score of 541 at age 53, treatment of this pattern would be crucial to his success.

Part of Alex's treatment program was niacin. However, Alex complained about the niacin "flush" to his primary care physician. So, his doctor told him to stop the niacin and replace it with a statin drug (Vytorin in this case).

Is this a satisfactory replacement? Do statin drugs reduce Lp(a)?

No, they do not. In fact, that's how I often meet people who have Lp(a): Their doctor will prescribe a statin drug for a high LDL cholesterol that results in a poor response. The patient will be told that statin drugs don't work for them. In reality, they have Lp(a) concealed in the LDL that makes the LDL resistant to treatment.

Lp(a) responds to a limited number of treatments, like niacin, testosterone, estrogen, and DHEA. But not to statin drugs.

Now, statin drugs may still pose a benefit through LDL reduction. But they do virtually nothing for the Lp(a) itself. Unfortunately, most practicing physicians rarely go any farther than Lipitor, Zocor, Vytorin, and the like.

If your doctor tries to shove a statin drug on you as a treatment for Lp(a), put up a fight. Voice your objections that statins do not reduce Lp(a).

(Image courtesy of Brandon Blinkenberg and Wikipedia.)

What do breakfast cereals and toilet paper have in common?

You guessed it: They both belong in the toilet.

If you would like some insight into why your friends and neighbors have protruding bellies that conceal any glimpse of their toes, have to conduct that peculiar side-to-side gait that now characterizes many Americans' walking style, and are pre-diabetic or diabetic, look no further than your supermarket cereal aisle.

The Fanatic Cook has some particularly biting comments about this strangely American phenomenon at http://fanaticcook.blogspot.com.

Breakfast cereals range in quality from awful to bad. I don't know of any that fit into the Track Your Plaque program that aims to eliminate the risk of heart disease.

A number of our Track Your Plaque Members have encountered unexpected difficulty obtaining the 2nd page of their NMR Lipoprofile lipoprotein results when their blood was drawn in a LabCorp laboratory. This is the page that displays the lipoprotein subclasses in graphic format: VLDL, IDL, LDL, and HDL subclasses.

If you are unable to view page 2, you're stuck with the averaged values displayed on page 1. In my view, page 1 is is a drastically "watered down" version that sacrifices some crucial information, particularly if you use NMR lipoprotein analysis in a serial fashion, comparing one study to the next over time.

Why would LabCorp do this? The response I received from a Mr. Theo McCormick, Director of Marketing at LabCorp, was some corporate-speak about . . . Actually, I'm not sure what he was saying. (Members can read the complete Track Your Plaque conversation in the Forum.)

In my view, withholding this information is none of their business. If you or your insurance company paid for the test, then the information is yours to view. This would be like saying that "Sure you paid for the blood test, but we decided that you really won't know what to do with it, so we're keeping it from you."

Please send your objections to the contact info below. Several of the Members who have participated in the Track Your Plaque Forum conversation have already done so. It can only help to add to the growing objections to this silly and unfair practice.

Alternatively, just boycott any laboratory associated with LabCorp. If they are capable of such ridiculous withholding of information, who knows what else these people do?

Contact info:

Theo McCormick, Director of Marketing
Laboratory Corporation of America
1904 Alexander Drive
Research Triangle Park, NC 27709
Phone 919-572-7454 (Direct)
919-361-7700 Main
Fax 919-361-7149
theo_mccormick@labcorp.com

Until we hear about some real action from them, please DO NOT USE ANY LABCORP LABORATORY.

I hope I'm not getting my hopes up prematurely, but I believe that I've seen it once again: Dramatic reversal of aortic valve disease.

This 64-year old man came to me because of a heart scan score of 212. Jack proved to have small LDL, lipoprotein(a), and pre-diabetes. But there was a wrench in the works: Because of a new murmur, we obtain an echocardiogram that revealed a mildly stiff ("stenotic") aortic valve, one of the heart valves within the heart that can develop abnormal stiffness with time.

You can think of aortic valve disease as something like arthritis--a phenomenon of "wear and tear" that progresses over time, but doesn't just go away. In fact, the usual history is that, once detected, we expect it to get worse over the next few years. The stiff aortic valve eventually causes symptoms like chest pains, breathlessness, lightheadedness, and in very severe cases, passing out. For this reason, when symptoms appear, most cardiologists recommend surgical aortic valve replacement with a mechanical or a bio-prosthetic ("pig") valve.

Now, Jack's first aortic valve area (the parameter we follow by echocardiogram representing the effective area of the valve opening when viewed end on) was 1.6 cm2. A year later: 1.4 cm2. One year later again: 1.1 cm2.

In other words, progressive deterioration and a shrinking valve area. Most people begin to develop symptoms when they drop below 1.0 cm2.

Resigned to a new valve sometime in the next year or two, Jack underwent yet another echocardiogram: Valve area 1.8 cm2.

Is this for real? I had Jack come into the office. Lo and behold, to my shock and amazement, the prominent heart murmur he had all along was now barely audible.

I'm quite excited. However, it remains too early to get carried away. I've now seen this in a handful of people, all with aortic valve disease.

Aortic valve stenosis is generally regarded as a progressive disease that must eventually be corrected with surgery--period. The only other strategy that has proven to be of any benefit is Crestor 40 mg per day, an intolerable dose in my experience.

If the vitamin D effect on aortic valve disease proves consistent in future, even in a percentage of people, then hallelujah! We will be tracking this experience in future.

I asked one of the CT technologists at Milwaukee Heart Scan what quesetions are often asked by people undergoing their first CT heart scan.

"That's easy," she said. " 'How often do you call an ambulance?' "

She went on. "People are very scared when they have their heart scan. In fact, some people don't even want to see their heart scan images and don't want to know their score--even after they paid $200 for the scan!"

I think she's right. People often remember the headlines that some heart scan centers have used: "Heart scan saved so and so's life!," when a high score led to a heart catheterization, stents, or bypass surgery. It's the sort of headline that gives people the impression that ambulances pull up to the scan center whenever a score is high.

So, how often is an ambulance called to the scan center? Never. Not once. A CT heart scan score is NEVER an emergency.

Emergencies occur in other places when people can't breathe, or are having pain in their chest, or pass out, emergencies that should not take anyone to a heart scan center. When heart scans are used properly, it is the person without symptoms who undergoes a scan to look for hidden heart disease. This cannot lead to an emergency.

Of course, that doesn't mean that a high score shouldn't prompt quick action in the next few days or weeks, like seeing your doctor to discuss the results, undergoing a stress test, discussing how to stop the score from progressing.

But call an ambulance? Forget about it.

If you are contemplating a scan but are scared that it could lead to a 911 call, don't let that stop you. But, in the event that you go to an unscrupulous center or get bad information, be sure to be armed with the best information possible. One good start would be to take look at our free downloadable book, What does my heart scan show? available for free on the www.cureality.com website.

Here's a fascinating 2002 study by Dr. Brenda Davy and colleagues at Colorado State University that examined the NMR lipoprotein differences between a diet enriched in oats and one enriched with wheat. (Davy BM, Davy KP, Ho RC et al. High-fiber oat cereal compared with wheat cereal consumption favorably alters LDL-cholesterol subclass and particle numbers in middle-aged and older men. Am J Clin Nutr 2002; 76:351-358.)

36 sedentary, overweight men (average BMI around 30--obese), aged 50-75 years, were given a diet enriched with either oat bran (as oatmeal and oat bran, providing 5.5 grams of beta-glucan) or wheat (as a hot cereal or Frosted Mini-Wheats), with equivalent calories in each group. All underwent baseline NMR lipoprotein analysis.

Three months later, there were no differences in "anthropometrics" like weight, waist size, or BMI (though there was a trend towards larger waistlines in the wheat group). The NMR lipoprotein analysis was repeated.

Comparison of the lipoprotein changes revealed:

--LDL cholesterol: Down 2.5% with oats, up 8.0% with wheat.

--LDL particle number: Down 5% with oats, up 14.2% with wheat.

--Small LDL: Down 17.3% with oats, up 60.4% with wheat.

--Triglycerides: Down 7.6% with oats, up 22.0% with wheat.

The across-the-board differences between the wheat and oat effects were astounding. In particular, note the extraordinary effect on small LDL particles: wheat triggered a 60% increase.

Similar studies yielding similar results have been conducted elsewhere, including Dr. Ronald Krauss' group at University of California-Berkeley.

Now, this was a study conducted under the somewhat artificial circumstances of a study. But imagine this sort of habitual intake continues, not for just three months, but for years. After all, wheat has expanded and metastasized to all three meals, snacks, every day, 7 days a week in most Americans' diet.

What a wonderfully graphic representation of the undesirable effects of wheat products. When you see Mini-Wheats, Shredded Wheat, whole grain bread, whole wheat bread, whole wheat crackers, Raisin Bran, and the thousands of other wheat-containing products that promise health, run the other way. Grab some oat bran on the way out.

This has nothing to do with coronary plaque reversal, nor directly with the Track Your Plaque program, but I found Dr. John Cannell's discussion about the possible relationship between vitamin D and autism so compelling that I thought I just had to pass it on.

So, below are Dr. Cannell's latest thoughts. He takes some criticisms along with praise. I think we owe him a lot for continuing to doggedly promote the benefits of vitamin D.

Vitamin D Newsletter

August, 2007

Dear Dr. Cannell:

I saw an article from a Toronto newspaper about autism and vitamin D. I am currently searching for a vitamin D specialist in the Washington D.C. area to perform a medical work up on my daughter to look for vitamin D-related disorders. The reason I am in search of a vitamin D specialist is that I believe I have stumbled upon a complex relationship in my daughter involving her foot pain, vitamin D, and her autism.

In April 2006, a few weeks after my 3-year-old profoundly autistic daughter began refusing her daily PediaSure drink, she began having excruciating foot spasms lasting from 10-30 minutes at a time, several times a week. She would throw herself on the floor, curl her toes, slam her heels against the floor, and rub the tops of her feet against the carpet, all while screaming the entire time. These were horrible for her to endure, and horrible for my wife and myself to watch. This went on for a year.

From what I read, the symptom was perhaps like foot spasms associated with carpopedal syndrome or tetany. But her blood work did not support that at all. Calcium level was normal (10.2 mg/dL); 25-Hydroxy-vitamin D low (23.5 ng/ml); 1,25 dihydroxy-vitamin D normal (24.7). Despite some vitamin D deficiency, I was assured by medical professionals that nothing supported a vitamin D cause of these particular spasms, so vitamin D was dismissed. Because her calcium level was normal, they told me she did not have tetany, and vitamin D could not be the cause of the pain.

All medical consultants were stymied. I made another research effort and found a 2003 article on WebMD that stated vitamin D has been found to have some link to basic, unexplained muscle and bone pain. By chance, vitamin D was the next supplement we had at home to begin giving my daughter to treat her autism. So, in April 2007 we began giving my 4 year-old profoundly autistic daughter Vitamin D supplements. Her foot spasms which had plagued her for a year diminished within days and disappeared within three weeks. She has not had a spasm in over two months.

In addition, we noted clear improvements in her autistic condition which appear to be from the vitamin D supplements. Eye contact went from zero to fantastic. Her vocalizations increased markedly (still only babbling; she remains completely nonverbal). She appears even happier than previously (she has always been a somewhat happy child). (Please note that my wife and I have tried many dietary supplements over the past 1.5 years guided by a doctor and dietician who both specialize in autism. We honestly state that this is the only thing that has ever had a positive effect on my daughter. We have seen nothing else work.)

My daughter and vitamin D have a complicated relationship. By all counts, looking at her lab work and general condition, vitamin D should have played no role in those excruciating foot fits. And yet it is apparently exactly what is involved in them. And, my wife and I believe at the same time her autistic condition has improved from the vitamin D. The foot fits and her autism appear linked; it was not just a coincidence that this autistic child has those mysterious foot spasms, and the link appears to be vitamin D.

And so I wonder if this is just the tip of the iceberg, if perhaps there is more to know about my child's relationship with vitamin D and what that might mean for her autism. Does she have a specific vitamin D-related disorder? If so, might direct treatment of it also improve her autism further? These are the questions I would like to pose to a vitamin D specialist who could perform a medical work up on my daughter. Please let me know if you know of anyone in the Northern Virginia/Washington DC area. Also, where is the best place to get vitamin D? Thank you for your time.

Sincerely,
Paul, Washington, D.C.

Dear Paul:

I know of no such specialist in the Washington area, indeed no vitamin D/autism expert exists in the world. As far as a specific "vitamin D disorder," linking her spasms, autism, and vitamin D, the world's English language medical literature contains no description of such a disorder. From your daughter's case, it sounds as if PediaSure was her only regular source of vitamin D. If so, her spasms began two weeks after stopping the small amount of vitamin D contained in PediaSure. The spasms continued for a year, ending a few days after you started giving her vitamin D again, this time in the form of a supplement. Several weeks after restarting vitamin D, both you and your wife noticed an improvement in her autism. To my knowledge, this "case report" - your daughter's - is the first ever published.

As no medical literature has ever been published on any of this, all you can do is give her enough vitamin D to get her 25-hydroxy-vitamin D, known as 25(OH)D, into high normal ranges and then wait and hope. Vitamin D's extraordinary mass-action pharmacology implies that simply providing more substrate ([25(OH)D] will help children with low enzyme activity produce more activated vitamin D (calcitriol) in their brains. The vitamin D theory of autism is not simply that vitamin D deficiency in gestation or early childhood causes the disorder. Instead, the theory holds that a quantitative or qualitative abnormality exists in the enzyme system that activates vitamin D.

It could as simple as the normal variation in the enzyme, an enzyme whose activity would vary in a normal or Gaussian distribution, much like height. Some people are tall, some are short, most are in the middle. The same may be true of the enzyme that forms activated vitamin D (calcitriol), some children have a lot of enzyme and some only a little; most are in the middle. As the substrate [25(OH)D] the enzyme metabolizes fell over the last 20 years with sun-avoidance, more and more children on the low end of the enzyme curve are effected by marginally low 25(OH)D levels, explaining both its genetic basis and exploding incidence.

At this point, all your daughter needs is a physician willing to periodically measure her 25(OH)D. Then you can safely supplement your daughter with doses higher than the current Upper Limit for children (2,000 IU/day). You did not tell me your daughter's weight but, assuming she weighs about 30 pounds, even without 25(OH)D blood tests, you can safely give her 50 mcg/day which is 2,000 IU per day. In fact, the U.S. government says this dose is safe for children over the age of one. Life Extension Foundation sells 250 of the 1,000 IU capsules for about ten bucks with powdered vitamin D inside. The powder is tasteless and dissolves easily in juice. Bio Tech Pharmacal, of Fayetteville, Arkansas, told me they were going to be making a 1,000 IU capsule. Or you can get 1,000 IU capsules in a pharmacy or at Costco and crush them. A Canadian firm is now making vitamin D liquid, called Ddrops, with 1,000 IU per drop, but their mail order web site is not yet easily accessed. Beware of cod liver oil; do not use it because vitamin A inhibits the actions of activated vitamin D, and due to the potential for low-grade vitamin A toxicity.

Remember, more and more researchers now believe autism is a progressive, inflammatory, disorder. That is, the inflammation probably progressively destroys brain tissue as the child ages. As I said in my recent paper, I think there is a chance that vitamin D may have a treatment effect in young autistic children if given in adequate doses, due to its anti-inflammatory properties, and its ability to upregulate glutathione, the master antioxidant that also chelates (binds) and then helps excrete heavy metals like mercury. Unfortunately, I see no way, even if the vitamin D/autism theory turns out to be true, that vitamin D can regenerate brain tissue. However, if it stops the inflammation, and cell death, the brain could then begin to develop and learn. These are big ifs. However, you have nothing to lose by trying, the worst that will happen is that it will not help and vitamin D will be added to the long list of false-hope treatments.

Actually, there is a worse possibility. Say the parents of a three-year-old autistic child decide today that vitamin D is nonsense, another false hope, and that I'm a quack. They decide not to give vitamin D supplement their autistic child, who is probably - like your child - vitamin D deficient. Then, it turns out five years from now that scientific evidence shows vitamin D does indeed help. By that time, the child will be eight and will have suffered additional, irreparable, brain damage. In my mind, that is more tragic than another false hope.

Dear Dr. Cannell:

After that article appeared in the Toronto paper, I started my four-year-old son on 1,000 IU of vitamin D two weeks ago. So far the only thing I noticed is that after about ten days, he didn't seem so miserable. The thing that has always broken my heart is that look of sadness and suffering on his face. After about two weeks of vitamin D, I noticed he seemed less miserable. I wouldn't say he looks happy now but that look of misery seems to be gone. Will it come back? I'm not sure I can take it if it comes back. What else might happen? Also, last summer we noticed he seemed to get better, but then he got worse in the fall. We never thought about it until we read about vitamin D.

Susan, Toronto, Canada

Dear Susan:

I don't know. I think all parents have had their heart pierced by that look at one time or another. I would advise increasing the dose to 2,000 IU per day, making sure it is cholecalciferol and not ergocalciferol, and having your doctor order a 25(OH)D every two months to see if he needs higher doses. You want to get his blood level up to between 50 ng/ml and 80 ng/ml (In many countries outside of the USA, that would be reported as between 125 and 200 nmol/L.) and keep it there, summer and winter, and that may take more than 2,000 IU/day in the winter. If vitamin D has a treatment effect, it will take many months to see its full effect. As you noted, if the theory is correct, autistic children who spend time outdoors in the summer should show some seasonal improvements - if they don't wear sunblock and they expose enough of their skin to generate significant amounts of vitamin D.

Dear Dr. Cannell:

I resent you calling autism a tragedy. My son is not a tragedy and I'm glad he was born and is in our lives. He is our joy. Autism is not a tragedy.

Emma, London, England.

Dear Emma:

I'm glad he is your joy and I believe you. I'm new to the autism field and was not aware how much thought and speech control exists in the discussion of the disease. Nevertheless, I have a few politically incorrect questions. If autism is a joy, I assume you would like other parents to have an autistic child? If autism is such a joy, why is there a huge industry forming to prevent and treat it? At the risk of sounding insensitive - apparently one of the most serious charges leveled in the autism debate - autism is a tragedy. As I pointed out in my paper, research shows that having an autistic child, puts the family under more emotional stress than having a child with a fatal illness.

Dear Dr. Cannell:

Who are you to write an article on autism? You didn't even publish it in a medical journal. You are not with a university. You have not published very much. You have no expertise on autism. No autism experts support your theory. There is no evidence to support the theory. Shouldn't you leave this to experts before you give parents more false hopes?

Mary, Trenton, New Jersey.

Dear Mary:

You are right, I am a nobody; just ask my ex-wife. In the Toronto Globe, I explained why I have not yet submitted the paper. As far as giving false hopes, I've thought about that charge. Right now, regardless of what advocacy groups say, autism is rather hopeless. That is, no treatment, including vitamin D, has been shown to materially affect the clinical course of autism. As a psychiatrist, my observation is that people would rather live with a false hope than with no hope.

Furthermore, if autistic children began taking vitamin D, the worse that can happen is that a period of false hope will followed by dashed hopes and then parents will be back to hopelessness. In the meantime, they will have made their child vitamin D sufficient. Vitamin D deficiency is a serious problem in childhood.
Postgrad Med J. 2007 Apr;83(978):230-5.

The Telegraph, Why is Vitamin D So Vital?

As far as the theory having no support from experts, Dr. Richard Mills, research director of the National Autistic Society in England, was quoted in the Telegraph article on the autism/vitamin D theory: "There has been speculation in the past about autism being more common in high-latitude countries that get less sunlight and a tie-up with rickets has been suggested - observations which support the theory."

Finally, you said there is no evidence to support the theory. I assume you meant there is no proof. The first statement is absolutely false, the second absolutely true. As I detailed in my paper, there is a lot of evidence to support the theory. In fact, if anyone can come up with an autism fact, that the theory cannot explain, I'd like to know about it. Even the announcement of a link between television viewing and autism supports the theory. Furthermore, the TV/autism link is actually evidence of a treatment effect. That is, if autistic children who play outside in the sunshine more - watching less TV - have less severe illness, it may be due to the Sun-God, who bestows her precious gift of calcitriol into the brains of children playing outside in her sunlight but not into the brains of children watching TV inside in the darkness.
Natl Bur Econ Res Bull Aging Health. 2007 Winter;(18):2-3.

As far as proof the theory is true, there is, of course, none. In medicine, proof means randomized controlled human trials, the gold standard for proof. However, proof is the last step, not the first. First comes evidence, then comes a theory, then comes researchers disproving those theories. It works that way. Sometimes we never get to the last step, proof. For example, please point me to a single randomized controlled human trial proving cigarette smoking is dangerous? Instead, the convincing evidence of smoking's dangerousness lies in epidemiological studies, not randomized controlled trials. Proof, or disproof, of the autism vitamin D theory will take years, years during which young autistic brains will continue to suffer irreparable damage. Perhaps vitamin D' powerful anti-inflammatory actions will help prevent that damage, perhaps not.

It's something of a Pascal's wager, betting on vitamin D instead of the existence of God, risking your child's brain instead of eternal damnation. "If you believe vitamin D helps autism and turn out to be incorrect, you have lost nothing -- but if you don't believe in vitamin D and turn out to be incorrect, your child will suffer irreparable brain damage."

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

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. This newsletter is not copyrighted. Please reproduce it and post it on Internet sites. Remember, we are a non-profit and rely on donations to publish our newsletter and maintain our website.

I just found this great podcast of an April, 2006 National Public Radio (NPR) interview with Omnivore's Dilemma author, Michael Pollan:

Author Michael Pollan: 'The Omnivore's Dilemma'

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

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

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

Try a little experiment:

Side by side, try a yogurt made with fructose or high fructose corn syrup as one of the first ingredients on the label along with a yogurt made without fructose.

Yoplait and Dannon brands, for instance, fit the bill for fructose. Several brands do not use fructose products. Many of these are the unflavored or unsweetened versions. You may therefore have to add some blueberries, strawberries, or some other fruit for some flavor. ( I doubt that you would add high fructose corn syrup.) Add nuts, seeds, flaxseed, or oat bran to either.

Many people who do this will notice a peculiar effect: The fructose or high fructose corn syrup containing product is, to most, delicious. It also triggers a desire for more. You can't have just one--you've got to have another, or you've got to eat something else.

The non-fructose containing product is more likely to generate satiety, a feeling that you've had enough.

If you experience this effect, the solution is simple: avoid fructose and high fructose corn syrup. I believe that the most worrisome health effect of fructose is this hunger-increasing aspect, difficult to document, perhaps impossible to measure, but a great boon to the food industry who practice an "eat more" philosophy to increase revenues year after year.

Perhaps you will also see weight drop (since you will be more satisfied), see triglycerides drop (since fructose raises triglycerides), and maybe obtain all the downstream benefits of reduced triglycerides (higher HDL, less small LDL, less VLDL, more rapid clearance of post-prandial lipoproteins).

Most people who follow this idea gain better control over appetite, lose weight, and do better in health, including in their Track Your Plaque program.

Clinical studies can be designed in a number of ways. The ease and cost of these studies differ dramatically, as does the confidence of the findings.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Do statin drugs reduce lipoprotein(a)?

Breakfast cereals and toilet paper

Another lipoprotein hurdle

More on aortic valve disease and vitamin D

"How often do you call an ambulance?"

Oat vs. wheat

Vitamin D and autism

Michael Pollan Podcast

Are you addicted to fructose?

Chicken Little