Unexpected effects of a wheat-free diet

Wheat elimination continues to yield explosive and unexpected health benefits.

I initially asked patients in the office to eliminate wheat because I wanted to help them reduce blood sugar and pre-diabetic tendencies.

A patient would come to the office, for example, with a blood sugar of 118 mg/dl (in the pre-diabetic range) and the other phenomena of pre-diabetes or metabolic syndrome (high blood pressure, high inflammation/c-reactive protein, low HDL, high triglycerides, small LDL), and the characteristic wheat belly. Eliminate wheat and, within three months, they lose 30 lbs, blood sugar drops to normal, blood pressure drops, triglycerides drop by several hundred milligrams, HDL goes up, small LDL plummets, c-reactive protein drops.

People also felt better, with flat tummies and more energy. But they also developed benefits I did not anticipate:

--Improved rheumatoid arthritis--I have seen this time and time again. Eliminate wheat and the painful thumbs, fingers, and other joints clear up dramatically. Many former rheumatoid sufferers people tell me that one cracker or pretzel will trigger a painful throbbing reminder that lasts a couple of hours.

--Improved ulcerative colitis--People incapacitated with pain, cramping, and diarrhea of ulcerative colitis (who are negative for the antibodies for celiac disease) can experience marked improvement. I've seen people be able to stop all their nasty colitis medications just by eliminating wheat.

--Reduction or elimination of irritable bowel syndrome

--Reduction or elimination of gastroesophageal reflux

--Better mood--Eliminating wheat makes you happier and experience more stable moods. Just as wheat is responsible for a subset of schizophrenia and bipolar illness (this is fact), and wheat elimination generates dramatic improvement, when you or I eliminate wheat, we also experience a "smoothing" of mood swings.

--Better libido--I'm not sure whether this is a consequence of losing a belly the size of a watermelon or improvement in sex hormones (esp. testosterone) or endothelial responses, but more interest in sex typically develops.

--Better complexion--I'm not entirely sure why, but various rashes will often dissipate, bags under the eyes are reduced, itching in funny places stops.


It's also peculiar how, after someone eliminates wheat for several months, re-exposure of an errant cracker or sandwich results in cramping and diarrhea in about 30% of people.

Obviously, people with celiac disease, who can even die of exposure to wheat, are even worse. What other common food do you know of that makes us sick so often, even occasionally with fatal outcome?

Is Lp(a) part of your legacy to your children?

If you have lipoprotein(a), Lp(a)--the most aggressive known cause of heart disease that no one has heard of--then you need to tell your children.

Lp(a) is a "cleanly" inherited genetic pattern: If either parent has it, there's a 50% chance that you have it. If you have it, then there's a 50% likelihood that each of your children has it. (Note that each child experiences a likelihood of 50%, not 50% of your children. This is because each child is conceived as an independent statistical event. So much for romance!)

The atherogenicity (plaque-causing potential) of Lp(a) also tends to get transmitted. In other words, if your Dad had a heart attack at age 50 due to Lp(a) and you share Lp(a), then you likely share a similar magnitude of risk as your Dad. If your Mom had Lp(a), though passed quietly at age 89 without any overt evidence of heart disease, then you are likely to share the relatively benign form of Lp(a).

For most of us with Lp(a), however, it is best to assume that it has at least some potential for causing heart disease, being the most aggressive cause known. (That is, until we have the ability in everyday clinical practice to characterize Lp(a) by assessing such factors as the size of the apoprotein(a) molecule, the number of kringle "repeats" on the tail, etc. Until then, we need to rely on the crude, though helpful, observation of family history.)

At what age should you inform your children? There's no hard-and-fast rule. However, I generally suggest to patients that they talk about Lp(a) with their children when they reach their 20s or 30s, old enough to begin to understand the implications and begin to think about adopting healthier lifestyles. Is treatment required at, say, age 35? That depends on the pattern of Lp(a)-related heart disease in the family: With exceptionally aggressive forms, it might be reasonable to begin treatment at this relatively early age.

Do "Heart Healthy" sterols cause heart disease?

The sterol question continues to pop up.

Sterols are an ingredient widely added by food manufacturers that allows a "heart healthy" claim, since sterols have been shown to reduce LDL cholesterol (at least transiently). HOWEVER, sterols have also been implicated in possibly increasing risk for heart disease. After all, people with the genetic condition called sitosterolemia absorb sterols into the blood and develop coronary heart disease in their teens and twenties. Those of us without sitosterolemia who increase sterol intake with sterol-enriched foods increase blood levels of sterols several-fold. Is this healthy, or does it contribute to coronary plaque as it does in people with sitosterolemia?

Below, I've reprinted a previous Heart Scan Blog post on sterols.


Sterols should be outlawed

While sterols occur naturally in small quantities in food (nuts, vegetables, oils), food manufacturers are adding them to processed foods in order to earn a "heart healthy" claim.

The FDA approved a cholesterol-reducing indication for sterols , the American Heart Association recommends 200 mg per day as part of its Therapeutic Lifestyle Change diet, and WebMD gushes about the LDL-reducing benefits of sterols added to foods.


Sterols--the same substance that, when absorbed to high levels into the blood in a genetic disorder called "sitosterolemia"--causes extravagant atherosclerosis in young people.

The case against sterols, studies documenting its coronary disease- and valve disease-promoting effects, is building:

Higher blood levels of sterols increase cardiovascular events:
Plasma sitosterol elevations are associated with an increased incidence of coronary events in men: results of a nested case-control analysis of the Prospective Cardiovascular Münster (PROCAM) study.

Sterols can be recovered from diseased aortic valves:
Accumulation of cholesterol precursors and plant sterols in human stenotic aortic valves.

Sterols are incorporated into carotid atherosclerotic plaque:
Plant sterols in serum and in atherosclerotic plaques of patients undergoing carotid endarterectomy.




Though the data are mixed:

Moderately elevated plant sterol levels are associated with reduced cardiovascular risk--the LASA study.

No association between plasma levels of plant sterols and atherosclerosis in mice and men.




The food industry has vigorously pursued the sterol-as-heart-healthy strategy, based on studies conclusively demonstrating LDL-reducing effects. But do sterols that gain entry into the blood increase atherosclerosis regardless of LDL reduction? That's the huge unanswered question.

Despite the uncertainties, the list of sterol-supplemented foods is expanding rapidly:




Each Nature Valley Healthy Heart Bar contains 400 mg sterols.












HeartWise orange juice contains 1000 mg sterols per 8 oz serving.













Promise SuperShots contains 400 mg sterols per container.














Corozonas has an entire line of chips that contain added sterols, 400 mg per 1 oz serving.














MonaVie Acai juice, "Pulse," contains 400 mg sterols per 2 oz serving.














Kardea olive oil has 500 mg sterols per 14 gram serving.










WebMD has a table that they say can help you choose "foods" that are sterol-rich.

In my view, sterols should not have been approved without more extensive safety data. Just as Vioxx's potential for increasing heart attack did not become apparent until after FDA approval and widespread use, I fear the same may be ahead for sterols: dissemination throughout the processed food supply, people using large, unnatural quantities from multiple products, eventually . . . increased heart attacks, strokes, aortic valve disease.

Until there is clarification on this issue, I would urge everyone to avoid sterol-added "heart healthy" products.


Some more info on sterols in a previous Heart Scan Blog post: Are sterols the new trans fat? .

Why obese people can't fast

Why do obese people claim it is impossible to fast?

Most overweight people are terrified at the prospect of facing any period of time without ready access to food. Persuading them to begin a program of intermittent fasting is a hopeless cause. They just refuse.

Contrary to popular opinion, this is not just glutonny at work. It is the effect of what I call "the cycle of hunger," the 2-hour up and down cycle of rising sugar and insulin, followed by their inevitable fall. The precipitous fall of sugar and insulin triggers mental fogginess, fatigue, and insatiable hunger. (By the way, this is the same phenomenon underlying the silly notion of "grazing.")

According to an LA Times article, fasting may be difficult to impossible for some people:

"Ruth Frechman, a registered dietitian in Burbank and spokeswoman for the American Dietetic Assn., says she frequently sees such extreme strategies backfire. 'You're hungry, fatigued, irritable. Fasting is not very comfortable. People try to cut back one day and the next day they're starving and they overeat.'"
(Not surprising, coming from the American Diatetic Assn. They, along with such agencies as the American Diabetes Association, are vocal proponents of low-fat, high-carbohydrate, "healthy whole grain" diets--you know, the diets that make us fat and diabetic.)

Ms. Frechman is correct: Having someone engage in a period of fasting, no matter how brief, when the diet leading up to the fast is filled with "healthy whole grains" and other carbohydrates will result in painful hunger that eventually overcomes any effort. A period of overeating typically follows the aborted attempt.

Fasting cannot work as long as the 2-hour cycle of hunger continues. The first step: Eliminate the 2-hour cycle of hunger by dramatically reducing or eliminating carbohydrates. Our preferred method is to eliminate wheat, cornstarch, and sugars. (Just be aware of wheat withdrawal, the fatigue that develops in the first 5 days after wheat elimination that affects up to 30% of people.)

Once wheat, cornstarch, and sugars are eliminated, hunger reverts to that of physiologic need--appetite will be smaller and less intense, since it is driven by your body's needs, not by abnormal stimulation from wheat, cornstarch, and sugar. The fear of not having food dissolves, the 2-hour cycle of mental fogginess, fatigue, and hunger will be gone.

Intermittent fasting is a wonderful strategy for reducing weight; gaining control over lipids, lipoproteins, and coronary plaque; regaining appreciation for food; reducing appetite. But it's not even worth trying unless you've already eliminated the unnatural appetite triggers that will booby-trap any fasting effort.

Test your own thyroid

134 people responded to the latest Heart Scan Blog poll:


When I ask my doctor to test my thyroid, he/she:

Accommodates me without question 45 (33%)

Questions why, but orders the tests 49 (36%)

Refuses because you seem "healthy" 20 (14%)

Refuses without explanation 4 (2%)

Ridicules your request 16 (11%)



That's better than I anticipated: 69% of physicians complied with this small request. After all, you're not asking for major surgery. You're just asking for a very basic test, as basic as a blood count or electrolytes. 36% of respondents said that their doctor asked why, but still complied; this is simply practicing good medicine--If there is a problem, your doctor would like to know about it.

However, the remainder--31%--were refused in one way or another. Incredibly, 11% were ridiculed.

Although this was not asked in the poll, I believe that it is a safe assumption that you asked with good reason: you're abnormally fatigued, you have been gaining weight for no apparent reason or can't lose weight despite substantial effort, or you feel cold at inappropriate times.

Let's say you're tired. Ever since last summer, you've suffered a gradual decline in energy.

So you ask your doctor to assess your thyroid. He refuses. "You're just fine! There's nothing wrong with you."

You disagree. In fact, you are quite convinced that there is something physically wrong. What do you do?

You could:

--Drink more coffee
--Exercise more in the hopes that it will snap you out of your lethargy
--Sleep more
--Take stimulants of various sorts

Or, you could get your thyroid assessed and settle the issue. But how can you get this done when your doctor won't accommodate you, even though you have perfectly fine health insurance and are simply interested in feeling better and preserving your health?

You could test your thyroid yourself. This is why we're making self-testing kits available. Test kits are available here.

This is yet another facet of the powerful revolution that is emerging: Self-directed health.

Trains, planes, and heart scans

A Heart Scan Blog reader posted the following question:

It is not clear to me why getting a cardiac scan is the necessary first step, if in fact the next step would be to bring down small LDL particles which is revealed on a NMR lipoprofile or VAP test. Why isn't the NMR or VAP test the first thing?

Good question. Think of it this way:

Lipoproteins, as measured via VAP (Vertical Auto Profile) or NMR (Nuclear Magnetic Resonance), provide a snapshot of risk from a metabolic viewpoint at that moment. Lipoproteins shift with the tides of age, menopause, weight changes, even what you ate last evening for dinner (especially small LDL). There are also other factors that cause coronary plaque, as well, not revealed through lipoprotein testing, such as vitamin D deficiency, smoking, high blood pressure, phosopholipase A2, lipoprotein(a), inflammatory factors, thyroid dysfunction, omega-3 fatty acid deficiency, etc.

A heart scan, providing a coronary calcium score, provides an indirect measure of coronary plaque that is the sum total of lipoprotein and other plaque-causing factors that have accumulated up to the time of your scan--regardless of the cause.

It means that two females, each 60 years old, with 70% small LDL, HDL 42 mg/dl, triglycerides 150 mg/dl, and mild hypertension, have identical markers for potential coronary risk, but can have widely different heart scan scores. One might have a score of zero, while the other might have a score of 300.

Why would the same panel of causes measured at one moment yield wildly different quantities of plaque? Several reasons:

1) The lifestyles, eating habits, and weight of each woman differed during their earlier years, not currently reflected in this moment's lipid or lipoprotein patterns. Perhpaps one experienced several years of extraordinary stress from a failed marriage, or suffered through two years of depression that caused her to smoke and overeat.

2) There are hidden factors that affect coronary plaque growth that we are presently not able to detect, e.g., vitamin D receptor genotype, cholesteryl-ester transfer protein variants, variation in inflammatory factors. If we can't measure it, we won't know whether it might influence coronary plaque risk.


With all the changes that occur over a person's life, with the uncertainties of yet-to-be-identified causes for coronary plaque, how can you possible know what your risk for heart disease truly is? Yup--a heart scan. Do it and you will know.

D2 and D3 are two different things

Helena posted this instructive comment in response to the Heart Scan Blog post, Weight loss and vitamin D. It illustrates the confusion common among physicians and pharmacists on the differences between D2 and D3.

(Edited slightly for clarity.)

Not many weeks ago a colleague of mine (let’s call him Eric) asked me if I knew the difference between D2 and D3 and I told Eric that D2 comes from irradiated mushrooms and D3 comes from wool. In other words, D3 is the same kind of vitamin as humans get from the sun. Humans just don’t get enough and we can’t produce it on our own, like the sheep can. (D3 is natural for humans, D2 is not.)

After telling Eric this, he asked me how he would know what he is taking and I gave him the medical definitions of them both (D2 = Ergocalciferol; D3 = Cholecaliciferol). Since I was aware that he had gotten his Vitamin D by prescription, I told him “I am 99.9% sure that you are taking D2, but I would be thrilled to find out I am wrong.”

Eric called his pharmacy right away and got the answer I was expecting: ergocalciferol. On confronting the person Eric was talking to, the answer he got back was that Ergocalciferol is the only Vitamin D they are giving out.

A week later, Eric had a new appointment with his doctor and decided to ask him about the D2/D3 issue. The doctor said he knew that there was a difference in them both, but could not say what, not even the basic facts I mentioned above. But the doctor stamped a post-it with what he had sent to the pharmacy just to show Eric. “Vitamin D3; 50,000IU tab” is what the stamp said.

Eric, off course, got confused and was starting to believe that the pharmacy had made a mistake by giving him Ergocalciferol (D2) since the doctor had given him D3, or at least that is what was stamped on the little note he had.

Today, after getting a refill of his Vitamin D he also got and kept all his paperwork that came along with it. Still believing that stamp the doctor had given Eric earlier, he asked me to double and triple check that my definition of D2 and D3 was correct. I did, just for my own sanity, and I was still right.

One of the sheets Eric brought me today was the “Patient Education Monograph” sheet stating the drugs and how to use it and so on. The thing that jumped out the most to me was this:

Generic Name: Vitamin D – Oral
Common Brand name(s): Drisdol, Maximum D3
Identification: PA140 Green Oval Capsule

This is the Drug Eric was given: Vitamin D 1.25 MG softgel; Generic name: Ergocalciferol

My researching mind went into high concentration mood and I started to dig. And this is what I found:

The brand name Drisdol is Ergocalciferol (D2), not D3. The Brand name Maximum D3 seems to be hard to find out there in cyber space as a brand name. But the ones I found that were called Maximum D3 seems to be the real stuff, however none of them required a prescription.

When trying to find out through the identification number on the pills (PA140) I now know for sure that Eric is taking Vitamin D2 and not the preferred Vitamin D3. The brand name, Drisdol, had the identification W on one side and D92 on the other, but it is still Ergocalciferol.

The only conclusion I can draw from all this is that the medical industry does not know or care about the difference in D2 and D3 – it is all same to them. And as long as the pharmacies only give out D2 it does not matter what the doctor prescribe anyway.

I know that people are most likely to be prescribed a D2 pill than to be told to buy over-the-counter D3. But it was almost heart breaking to see the letter D and number 3 right next to the drug Drisdol, as we know is a D2 vitamin. It just didn’t make sense to me that they can be labeled as the same type of medication, when we know it is not!



Incredible.

Why prescribe plant form D2 when you can get perfectly reliable, safe, effective D3--the human form, at the health food store for about $6?

Once again, it's the peculiar false bias of physicians and pharmacists: If it's prescription, it must be good; if it comes from a health food store, it must be bogus.

Humans need human vitamin D. Plain and simple.

For more on the D2 vs. D3 issue, see the Heart Scan Post, The case against vitamin D2.

Weight loss: Different causes, different solutions

Heart Scan Blog reader, Kris, related this enlightening story of weight loss (slightly edited for clarity).

Kris learned that excess weight is gained through multiple causes. The solutions are therefore multiple, not just one change in diet or two.


I started studying about my thyroid issue much earlier and did lose some weight. But ever since I started following Dr. Davis’s blog, it has given me confidence that I was on the right track. I did have my thyroid and iodine figured out from other sources, but Dr. Davis helped me to understand the issues with not only the thyroid but vitamin D3, fructose, fish oil, niacin, wheat etc. I have lost 43lb in last 14 months.

It seems to me that there are certain percentages of weight connected with different issues. For example, after I gave up alcohol and sugar, I lost about 14lbs from total weight of 243lbs, weight came down to about 229lb. Then it stopped at 229lb, even though I was in the gym almost 5 to 6 days a week with full workouts.

After I changed my thyroid medication to natural thyroid hormones (took synthetic T4 for over 10 years), the weight dropped down further 13lbs or so in matter of few days, shape of the face changed from moon shape/double chin to ordinary long face. Then it kind of stopped at around 213-216 lbs.

After giving up wheat, reducing carbs, increasing protein intake (whey protein, chicken etc. no soya, no fructose) the weight came down another 14lbs. Now it is around 200-202lbs and I am over 6.2 tall with heavy set of bones.

I feel better than I have ever in my life. More stamina, more clarity/no fog, more confidence and 99% of the time relaxed and being able to see the situation from multiple angles.

I use to be able to drink a liter or more jack denial without a problem in one evening but now can’t stand half a can of beer (I miss JD). Drinking alcohol makes me sick. I sleep well and if I wake up in the middle of the night, I have no problem going back to sleep. No more out of breath stair climbing at all.

One other thing: I used to be the most attractive meal to the mosquitoes, but not anymore. This year I haven’t been bitten once. I take my dog to the park everyday and I do not use any mosquito repellent, what a relief. I don’t know if it is because of thyroid, iodine, wheat or something else. Skin texture has changed dramatically. I do not use full soap or shampoo, 20% borax, 10 percent of my soap or shampoo for scent and rest water, mixed in a 500ml bottle. No more dandruff, dry skin, pimples for me.

Dr. Davis I am thankful to people like you who have the ability to see beyond what you have been taught and have the guts to say the way it is. Most of us work to make living on daily basis but some make their living while spreading their knowledge to save lives. Dr Davis you are one of those few people. Please keep it going.

Calling all losers!

I'd like to invite anyone who has followed the Track Your Plaque Break the Weight Barrier program to consider posting their stories and photos on the Heart Scan Blog.

Because our focus is prevention and reversal of coronary heart disease, we have not made an effort to catalog the weight loss experience that people have while on the program. For many, weight loss has been substantial. (Several people this week alone have reported weight loss of 9 to 46 lbs in the past 6 months.)

It would be helpful to hear and see these results.

For those of you who don't mind having a story and photo on this Blog, please come back in future to post your results. You will find this post by entering "weight loss" into the site-specific search bar at the top of the page.

Weight loss and vitamin D

At the start of her program, Penny's 25-hydroxy vitamin D blood level showed the usual deficiency at 22 ng/ml.

She supplemented with 8000 units of vitamin D. Another 25-hydroxy vitamin D blood level several months later showed a level of 67.8 ng/ml, right on target.

But Penny also began our diet, including the elimination of wheat, cornstarch, and sugars, and, over 6 months, lost 34 lbs.

Now a much trimmer 146 lbs (still more to go!), another vitamin D blood level: 111 ng/ml.

Penny's weight loss means that the vitamin D is distributed in a smaller total volume, particularly a lower volume of fat.

This is a common phenomenon with substantial weight loss: lose weight and the need for vitamin D is reduced. The reduction in dose is roughly proportion to the weight lost. Vitamin D should therefore be reassessed with any substantial change in weight of, say, 10 lbs or more, either up or down, because of the influence of fat on vitamin D blood levels.

Some references on this effect:

Men and women over age 65:
Adiposity in relation to vitamin D status and parathyroid hormone levels: a population-based study in older men and women.

Obese women:
Low 25-hydroxyvitamin D concentrations in obese women: their clinical significance and relationship with anthropometric and body composition variables

Obese children:
Hypovitaminosis D in obese children and adolescents: relationship with adiposity, insulin sensitivity, ethnicity, and season.

African-Americans:
Relationship of vitamin D and parathyroid hormone to obesity and body composition in African Americans.

Although the bulk of the effect is most likely due to sequestration by fatty tissue, perhaps less sun exposure in obese people also contributes:
Body mass index determines sunbathing habits: implications on vitamin D levels.
All posts by william-davis

More Vitamin D and HDL

I’m seeing more and more of it and I am convinced that there is a relationship: significant boosts in HDL cholesterol from vitamin D supplementation.

To my knowledge this remains an undescribed and uncharacterized phenomenon. There have been several observers over the last two decades who have noticed that total cholesterol shows a seasonal fluctuation: cholesterol goes up in fall and winter, down in spring and summer; year in, year out. This phenomenon was unexplained but makes perfect sense if you factor in vitamin D fluctuations from sun exposure.

I have come across no other substantiating evidence about fluctuations of HDL. But I am convinced that I am seeing it. Replace vitamin D to a blood level of 50 ng/ml, and HDL goes up if it is low to begin with. If HDL is high to begin with, say, 63 mg/dl, it doesn’t seem to change.

But, say, starting HDL is 36 mg/dl. You take niacin, 1000 mg; reduce high-glycemic index foods like breakfast cereals, breads, cookies, bagels, and other processed carbohydrate foods; exercise four days a week; add a glass of red wine a day; even add 2 oz of dark chocolate. You shed 15 lbs towards your ideal weight. After 6 months, HDL: 46 mg/dl. Better but hardly great.

Add vitamin D at a dose of, say, 4000-6000 units per day (oil-based gelcap, of course!), and re-check HDL two or three months later: 65 mg/dl.

I’ve seen it happen over and over. It doens't occur in everybody but occurs with such frequency that it’s hard to ignore or attribute to something else. What I’m not clear about is whether this effect only occurs in the presence of the other strategies we use to raise HDL, a “facilitating” effect, or whether this is an independent benefit of HDL that would occur regardless of whatever else you do. Time will help clarify.

We are tracking our experience to see if it holds up, how, and to what degree on a more formal basis. Until then, a rising HDL is yet another reason—-among many!-—to be absolutely certain your 25-OH-vitamin D3 level is at 50 ng/ml or greater.

How high is an ideal vitamin D blood level? If 50 ng is good, is 60 or 70 ng even better? Probably not, but there are no data. We have to wait and see. Unlike a drug that enjoys plentiful “dose-response” data, there are no such observations for vitamin D into this higher, though still “physiologic,” range.

Thin ice

How long can an industry built on ignorance and deception continue its practices in the new Information Age?

I don’t think it can for long. I talk to hospital administrators who believe that their source of competition is the hospital across town, battling for the same patients. I speak to my colleagues, the cardiologists, who believe that the current model is sustainable—take every willing body to the catheterization laboratory or operating room for heart procedures, the revenue-generating engine of income and expanding heart programs.

I speak to primary care physicians, who are dumbfounded and perplexed and have no idea which way things are going. They are trapped in a peculiar position: most have signed contracts and are employees of the hospital. They are legally bound to support the cardiologists who take anybody possible to the catheterization laboratory or direct patients to other profit-making procedures.

Much of this system depends on the willingness of the participant, meaning you and the health care seeking public. What happens when the truth comes out and disseminates widely through the thinking populace? What happens to hospitals and physicians and the vast structures they’ve built when the bottom drops out for 50% of their “market?

The proverbial cow manure will hit the fan. Upheavals in the medical industry will rival the changes that the automobile or telephone brought early in the last century. Cardiologists, immense hospital heart programs, and the vast economic infrastructure they spawned will go the way of stage coach manufacturers and the telegraph.

What form will the broad exposure of detailed information in health take? I’m not sure, but it will certainly come. The collaborative efforts that created the Linux operating system and have challenged the monopoly of Microsoft Windows, or the emergence of the extraordinary Wikipedia as a repository of human knowledge that dwarfs the venerated Encylopedia Brittanica, will eventually overtake the American medical system, the heart disease industry in particular.

If you base your future on the welfare of your local hospital or the manufacturers of stents, operating room equipment for heart bypass, or similar industries, watch out. The ice is thin. And as the spring warms the air around you, it gets thinner.

The Track Your Plaque program is our first step in broadcasting the message of self-empowerment in heart health care and an attempt to wrestle control away from the profit-seeking forces that dominate. As we grow, we not only hope to broadcast the message more widely, but expand the message to other areas of health. I predict that the collaborative, let’s-all-pitch-in-and-help spirit of the Information Age, “version 2.0,” will spark the change.

Vitamin D and cancer

Although this is a Blog about heart scans and heart disease, I came across a helpful video from Dr. Joseph Mercola about vitamin D and cancer that's worth viewing. Though I do not agree with many of Dr. Mercola's on-the-edge views, he does come up with some good thoughts and, in this instance, a useful educational tool about vitamin D.

You can view his video (which he claims crashed his server, due to the excessive demand for downloads) by cutting and pasting the address into your URL bar (above):

http://v.mercola.com/blogs/public_blog/How-to-Reduce-Your-Risk-of-Cancer-By-50--8790.aspx

Also, for my many patients who I've directed to look in my Blog for Dr. Reinhold Vieth's webcast presentation on vitamin D, here's the address:

http://tinyurl.com/f93vl

Perhaps I carry on too much about vitamin D. But I've come to respect this "nutrient" as among the most powerful strategies I've seen for dramatically improving control over coronary plaque growth as well as other aspects of health, as Drs. Mercola and Vieth eloquently detail.

Lipoprotein(a), menopause, and andropause

Lipoprotein(a) is a curious lipoprotein. Not only is it a genetic pattern with numerous variations, it is also one that shows a predictable age-dependent rise.

Women in particular are prone to this effect, men to a lesser degree. As we age, many hormones recede, particularly growth hormone, testosterone, the estrogens (estradiol, estriol, estrone), progesterone, and DHEA, among others. This is not a disease but the process of senescence, or aging.

When we're young, estrogens, testosterone, and DHEA all exert suppressive effects to keep lipoprotein(a), Lp(a), at bay. But as a woman proceeds through her pre-menopausal and menopausal years, and as a male passes through his fourth decade, there is an accelerated decline of these hormones. As a result, Lp(a) crawls out of its cave and starts to sniff around.

Typically, a woman might have a Lp(a) of 75 nmol/l (approximately 30 mg/dl) at age 38. Ten years later, at age 48, her Lp(a) might be 125 nmol/l (app. 50 mg/dl), all due to the decline of estrogens and DHEA. A parallel situation develops in males due to the drop in testosterone. For this reason, it may be necessary to re-check Lp(a) once after the fourth decade of life if you've had a level checked in your younger years.

This opens up some interesting therapeutic possibilities. If receding hormones are responsible for unleashing Lp(a), hormones can be replenished to reduce it. In males, this is relatively straightforward: supplement human testosterone and Lp(a) drops about 25%.

In women, however, it's a bit murkier, thanks to the negative experince reported using horse estrogens (AKA Premarin) in the HERS Trial and Women's Health Initiative. You'll recall that women who take horse estrogens and progestins (synthetic progesterone) do not experience less heart attack and develop a slightly increased risk of endometrial and breast cancer. There was, however, a poorly-publicized sub-study that showed that women with Lp(a) experience up to 50% fewer heart attacks on the horse/synthetic combination.

Wouldn't it be nice to have a large trial examining the safety/advisability of human estrogens and progesterone? To my knowledge, no such confident study in a significant number of women exists, since there's so little money to be made with human hormonal preparations.

For these reasons, we use lots of DHEA, generally at doses of 25 to 50 mg per day. It makes most people feel good, boosts energy modestly, increases muscle, and reduces Lp(a) up to 18% in women, a lesser quantity in men.

"I have never seen regression"

At a presentation at the American College of Cardiology meetings in New Orleans yesterday (March 27, 2007), Dr. Arthur Agatston declared "I have been doing CT for many years, and I have never seen regression."

Whooooaaaa. Wait a minute here. I have great respect for the work Dr. Agatston has done over the years. He is, after the originator of the scoring algorithm that allows us to score CT heart scans (though a more accurate measure, the volumetric score, is the one we often use behind closed doors because of modestly increased accuracy and reproducibility). His diet program, the South Beach Diet, has achieved enormous success and is indeed an effective approach for both weight loss and correction of many weight-related causes of heart disease.

But he has never seen regression? Why would this be when we see it all the time? When we see heart scan scores drop 30%, it's hard to believe that with some savvy he has never seen regression (drop in score).

I can only attribute the difference to the more intensive endpoints we advocate (e.g., 60-60-60 for lipid values); the incorporation of adjuncts like fish oil, vitamin D, l-arginine; attention to non-cholesterol issues and intensified treatments for each. I doubt that the populations we see differ substantially.

As much as I admire Dr. Agatston's accomplishments, I believe that he is behind the times on this issue. No regression is so starkly different from the Track Your Plaque experience. I believe that relying only on statin drugs and diet will slow but will not stop plaque growth. It will also rarely, if ever, drop your score.

Attention to detail and a little insight into better preventive strategies really pays off. While not everyone in the Track Your Plaque experience will drop their score, a substantial number do. Many more slow plaque growth dramatically. And, as time goes on, our track record gets stronger and stronger.

COURAGE to do better

The results of the long-awaited COURAGE Trial were announced today at the American College of Cardiology meetings in New Orleans.

In this trial, 2200 participants with stable coronary disease (i.e., not unstable, in which heart attack or death is imminent) were randomly assigned ("randomized") to either angioplassty/stent or "maximal medical therapy." Medical therapy means such things as aspirin, beta blocker drugs, and statin cholesterol drugs. There was virtually no difference between the groups in rate of heart attack and death from heart disease over a period of up to 7 years.

These results have caused a stir in the media and my colleagues, trying to sort out of the implications. However, I think there's one observation in particular worth making for those of us who tend to scoff at the conventional approach to coronary disease. That is, 1 of 5 people had a heart attack or died from heart disease in both groups. That's a lot. Even more ended up with a procedure (angioplasty, stent, or bypass). In other words, the "maximal medical therapy" instituted in participants was hardly a success. Though angioplasty and stenting failed to prove superiority, both really stunk. Both permitted a lot of catastrophes to occur.

"Maximal medical therapy," in other words, is a laughable concept. It doesn't include raising HDL, suppressing small LDL, reducing Lipoprotein(a), addressing inflammatory issues. It does not include omega-3 fatty acids from fish oil, nor does it address the severe degrees of vitamin D deficiency that are proving, in the Track Your Plaque experience, to be among the most potent causes of atherosclerotic plaque known. It includes a sad attempt at diet, as advocated by the American Heart Association, a diet that, in my view, causes heart disease and is distorted by the powerful political and financial influence of food manufacturers.

If the trial were to be done again, I'd like to see the "maximal medical therapy" arm be represented by a more effective program like the Track Your Plaque approach.

Value of a zero heart scan score

Margaret is 73. She's a very good 73. She loves children and works full-time in a daycare. She manages her own household, goes to dinner at least once each week with one or more of her adult children. She is slender and has never been in the hospital--until she developed an abnormal heart rhythm called atrial fibrillation.

Most people who develop atrial fibrillation do so with no immediate identifiable cause. However, Margaret has been a widow since her husband died 15 years ago of a heart attack. She was therefore especially frightened of any heart issues in her own health. Her doctor also raised the question of whether atrial fibrillation might represent the first hint of future heart attack.

So we advised a CT heart scan. Score: zero, or no detectable plaque whatsoever. This put Margaret's risk for heart attack as close to zero as humanly possible. (Nobody is truly at zero risk for heart attack for a number of reasons. One reason is that people do irrational things like take cocaine or amphetamines, or they take too much decongestant medication, all of which can trigger heart attack.)

The heart scan settled it. Margaret has the sort of atrial fibrillation which likely simply develops as a result of "wear and tear" on the heart's electrical impulse conducting system and it has nothing to do with coronary heart disease or heart attack.

As that MasterCard commercial goes: Cost of a heart scan: About $200. Peace of mind: priceless.

You're at the cutting edge

If you're a participant in the Track Your Plaque program for atherosclerotic plaque regression, you are at the cutting edge of health.

Few physicians give this issue any thought. Chances are, for instance, that if you were to bring up the subject of reversal of heart disease to your primary care physician, you'd get a dismissive "it's not possible," or " Yeah, it's possible but it's rare."

Ask a cardiologist and you might make a little more progress. He/she might tell you that Lipitor 80 mg per day or Crestor 40 mg per day might achieve a halt in plaque growth or a modest reduction of up to 5-6%. If they've tried this strategy, they would likely also tell you that hardly anybody can tolerate these doses for long due to muscle aches. I'd estimate that 1 of 10 of my colleagues would even be aware of these studies.

Both groups are, however, reasonably adept at diagnosing chest pain, an everyday occurrence in hospitals and offices. Chest pain, for them, is a whole lot more interesting. It holds the promise of acute catastrophe and all its excitement. It also holds the key to lots of hospital revenues. Did you know that 80% of all internal medicine physicians are now employees of hospitals? They're also commonly paid on an incentive basis. More revenues, more money.

Ask Drs. Dean Ornish or Caldwell Esselstyn about reversal of heart disease and they will tell you that a very low-fat diet (<10% of calories)can do it. That's true if you use a flawed test of coronary disease like heart catheterization (angiograms) or nuclear stress tests (Ornish calls them "SPECT"). It would be like judging the health of the plumbing in your house by the volume of water flowing out the spigot. It flows even when the pipes are loaded with rust.

In the Track Your Plaque experience, extreme low-fat diets (i.e., high wheat, corn, and rice diets) grotesquely exagerrate the small LDL particle size pattern, among the most potent triggers for coronary plaque growth. This approach also makes your abdomen get fatter and fatter and inches you closer to diabetes. Triglycerides go up, inflammation increases.

If you were able to measure the rust in the pipes, that would be a superior test. You can measure the "rust" in your "pipes," the atherosclerotic plaque in your coronary arteries, using two methods: CT heart scans or intracoronary ultrasound. Take your pick. I'd choose a heart scan. It's safe, accurate, inexpensive. I've performed many intracoronary ultrasounds for people in the midst of heart attacks or some other reason to go to the catheterization laboratory. But for well people, without symptoms, who are interested in identifying and tracking plaque? That's the place for heart scans.

In our program, 18-30% reductions in heart scan scores are common.

A stent--just in case

Burt came to me last week. He'd received a stent a few months earlier. He'd been feeling fine except for some fatigue. A nuclear stress test proved equivocal, with the question of an abnormal area of blood flow in the bottom (inferior wall) of the heart.

"The doctor said I had a 50% blockage. Even though it wasn't really severe, he said I'd be better off with a stent, just in case."

Just in case what? What justification could there be for implanting a stent "just in case"? (The artery that was stented did not correspond to the area of questionable poor blood flow on the nuclear stress test.)

Just in case of heart attack? If that's the case, what about the several 20 and 30% blockages Burt showed in other arteries? The cardiologist was apparently trying to prevent the plaque "rupture" that results in heart attack by covering it with a stent. Why stent just one when there were at least 7 other plaques with potential for rupture?

That's the problem. And that's why stents do not prevent heart attack (unless the stent is implanted in the midst of heart attack, when the rupturing plaque declares itself.) Of course, when no plaque is in the midst of rupturing, as with Burt, there's no way to predict which plaque will do so in future. Since only one plaque was stented, there is a 7 out of 8 chance (87.5%) that the wrong plaque was chosen. And that's assuming that there aren't plaques not detected by catheterization angiogram; there commonly are. The odds that the right plaque was chosen would be even lower.

In other words, stenting one blockage that is slightly more "severely blocked" in the hopes of preventing heart attack is folly. If it's not resulting in symptoms and blood flow is not clearly reduced, a stent can not be used to prevent plaque rupture. A stent is not a device to be used prophylactically. It is especially silly when an approach like ours is followed, since plague progession is a stoppable process.

Note: This issue is distinct from the one in which symptoms and/or an abnormal stress test show clearly reduced blood flow and flow is restored by implantation of a stent. While some controversies exist here, as well, a stent implanted under these circumstances may indeed provide some benefit.

How will you know your score dropped?

This issue came up twice this week.

Bill is a busy accountant. Two years ago, just after the tumult of the 2005 tax season was over, he got a CT heart scan. His score: 398. At age 53, this was a significant score. His internist did the usual: prescribed a statin (Zocor), told him to cut the fat in his diet, and be sure to exercise. (Yawn.)

Since then, Bill quit preparing tax returns and migrated to a less harried job in corporate accounting. It took two years since his heart scan for Bill to start thinking that perhaps his doctor's advice wasn't enough. If it was, he realized, everyone on a statin drug who made these minimal lifestyle changes would be cured of heart attack risk. Clearly not the case.

So Bill enrolled in the Track Your Plaque program. Our first step: Get another heart scan.

Bill was surprised. "Why another scan? I already had one!"

I explained to Bill that atherosclerotic plaque is like money: it grows in percentages, just like money in a bank account or in a mutual fund. If, for instance, you deposit $500 in a mutual fund and it yields 5% return, then after one year you will have $550. One year later, you will have 5% x $550, or $605. Another year: $665. In other words, growth is not 10% of the original amount you deposited. Growth is compounded, year over year. That's why money, when compounded, can grow so quickly.

Atherosclerotic plaque and your CT heart scan score do the same thing: they grow by a percentage of the current plaque quantity. In fact, we use the compound interest equation to calculate the annualized rate of plaque growth. But plaque grows at the extraordinary rate of 30% per year, on average. Imagine that was the rate of return on your money. You'd be the richest man or woman on earth.

Back to Bill. Now Bill, in his defense, was on a statin drug and did make modest efforts towards a (mis-guided) low-fat diet and walking four days per week. If, on a second CT heart scan, his score was:

398--No change. That's a success, since the expected rate of increase of 30% has been stopped. However, on his current program, this is highly unlikely. (I've seen it happen just once ever out of about 2000 people.)

250--Pop the cork on your champagne, because Bill needs to celebrate. He has substantially reversed his plaque. Highly unlikely on the current effort.

525 --The score is higher by 30%, so it has slowed, but it surely hasn't stopped. This is the most typical result on the sort of program Bill is following.

The message: Don't delay after your first heart scan score. It plaque grows like money with a huge return, there's no time like the present to take the steps to regain control.