I don't care about hard plaque!

I ran into a cardiology colleague this weekend. He was aware of my interest in CT heart scanning and plaque reversal.

Out of the blue, he declared "I don't care about hard plaque! I only care about soft plaque." He then proceeded to describe to me how everyone--EVERYONE--needs a CT coronary angiogram to identify "soft plaque".

Is there any truth to this view? Are we only identifying "hard plaques" by focusing on calcium and calcium scores on simple CT heart scans?

Several issues deserve clarification. First of all, CT heart scans don't identify hard plaque. They identify total plaque. Because calcium is a component of the majority of atherosclerotic plaque, comprising approximately 20% of its volume, a calcium "score" can be used to indirectly quantify total plaque, both "hard" and "soft".

Anyone cardiologist who performs a lot of the procedure, intracoronary ultrasound, knows that most human plaque is also not purely soft or hard, it is mixture of both. (I've been performing this procedure since 1995.) Quantifying only soft or only hard plaque is therefore only possible in theory, not in practice.

I believe my colleague does have a valid point in one regard, however. There is indeed a small percentage of people, probably around 5% of all people who have CT heart scans, who have scores of zero yet have a modest quantity of pure "soft" plaque. These people may be misled by having a zero score. How can these people benefit from better information?

Several ways. First, people like this tend to have very high LDL cholesterols, generally 180 mg/dl or greater. They may have a very worrisome family history, e.g., father with heart attack in his 30s or 40s. This small proportion of people with zero heart scan scores may benefit from receiving X-ray dye with their heart scan, i.e., a CT coronary angiogram. Keep in mind that we're assuming everyone is without symptoms, also. If symptoms are part of the picture, everything changes.

But should everybody get a CT coronary angiogram? I don't believe so. A CT coronary angiogram involves far more radiation exposure, greater expense (usually $1800 to $4000), and, with present day technology, does not yield quantitative (measurable) information that is useful for longitudinal use for repeated scans. You don't want to undergo yearly CT coronary angiograms, for instance.

Stay tuned for more on this issue. In the meantime, I continue to try and inform my colleagues about what is right, what is wrong, what is preferable for patient safety and yields truly empowering information, and try to impress on them that the practice of cardiology is not just about enriching their retirement accounts.

Try an experiment in a wheat-free diet

Years back, I'd heard some people argue that wheat-based products were detrimental to health. At the time, I thought they were nuts. After all, wheat is the principal ingredient in a huge number of American staples like breakfast cereals and bread.

What changed my mind was the low-fat movement of the 1980s and 1990s. Proponents of low-fat diets claim that heart disease is caused by excess fat in the diet. A diet that is severely restricted in fat therefore might cure or reverse heart disease.

But low-fat diets evolve into high-carbohydrate diets. This nearly always means an over-reliance on wheat products. People will say to me "I had a healthy breakfast: shredded wheat cereal in skim milk and two slices of whole wheat toast." Yes, it is low-fat, but is it healthy?

Absolutely not. Followers of the Track Your Plaque program know that low-fat diets ignite the formation of small LDL particles (a VERY potent trigger of coronary plaque growth), drops HDL, raises triglycerides, causes resistance to insulin and thereby diabetes, raises blood pressure. They also make you fat, with preferential accumulation of abdominal visceral (intestinal lining) fat.

Look at people with gluten enteropathy, a marked intolerance to wheat products that results in violent bowel problems, arthritis, etc. if unrecognized. These people, if the diagnosis is made early, are strikingly slender and commonly unusually healthy otherwise. There's a message here.

If you need convincing, try an experiment. Eliminate--not reduce, but eliminate wheat products from your diet, whether or not the fancy label on the package says it's healthy, high in fiber, a "healthy low-fat snack", etc. This means no bread, pasta, crackers, cookies, breads, chips, breading on chicken, rolls, bagels, cakes, breakfast cereal...Whew!

You won't be hungry if you replace the lost calories with plentiful raw almonds, walnuts, pecans, sunflower and pumpkin seeds; more liberal use of healthy olive oil, canola oil and flaxseed oil; adding ground flaxseed and oat bran to yogurt, cottage cheese, etc.; and more lean proteins like lean beef, chicken, turkey, and fish.

I predict that, not only will you lose weight, sometimes dramatically, but you will feel better: more energy, more alertness, sleep better, less moody. Time and again, people who try this will tell me that the daytime grogginess they've suffered and lived with for years, and would treat with loads of caffeine, is suddenly gone. They cruise through their day with extra energy.

Success at this can yield great advantage for your heart scan score control and reversal efforts. It will give you greater control over small LDL and pre-diabetic patterns, in particular.

Bigger, faster plaque reversal

Perhaps it's too early to tell whether it's true, but believe that we're seeing coronary plaque reversal--i.e., reduction of CT heart scan score--that is BIGGER and FASTER than ever before. We are now witnessing 20-30% reductions in score, even in the first year.

Early in our experience, I was thrilled with a slowing of plaque growth. Recall that coronary plaque grows at the rate of 30% per year. We would often seen slowing to 10-15% per year in the first year, then a levelling off to little or no increase in the 2nd or 3rd year. Regression, or reduction of score, was less common.

Now, with some further tweaking of our program, we are seeing these large magnitudes of coronary plaque reversal routinely. Not in everybody, of course. There are exceptions that mostly includes people who are less motivated and occasional people with more difficult to control lipoprotein patterns.

I believe that part, or perhaps most, of our recent success is from normalizing blood levels of 25-OH-vitamin D3 levels to 50-70 ng/ml. I'm unable to tell you why this occurs, but I am convinced that it has added huge advantage. Raising blood vitamin D levels to normal carries enormous implication: reduction of colon and prostate cancer risk, reduction of blood pressure, sensitization to insulin, prevention of arthritis and multiple sclerosis, and--I believe--control over coronary plaque calcification and growth.


Watch for a profile of one of our latest success stories, a physician who was experiencing 20% per year plaque growth three years in a row until he followed the Track Your Plaque approach and promptly experienced an 18% reduction in heart scan score. You'll find it in our next newsletter. To subscribe, go to the www.cureality.com homepage and click on the free book download.

I need to do more procedures!

I sat next to a cardiology colleague of mine last evening at a dinner. He was lamenting the fact that, because of changes in hospital affiliations of his several-member cardiology group, he'd seen a drop in the volume of heart catheterizations he was performing.

"I'm used to doing 5 cases a day! Now I'm down to 3 or 4 a day." He went on to tell me how he's working to increase his volume. "I'm branching out into doing carotid stents and anything I can find in the legs." He also described how he was cultivating referring physicians to send him more procedural patients.

Now, this colleague, I believe, is a hard-working, conscientious physician. But his attitude reflects the perverse logic of many physicians: I need to do more procedures, not because it benefits patients, but because that's what I want to do--to be busy, make more money, acquire more experience, build my ego, etc.

Doing more procedures has nothing to do with an altruistic goal of doing more good for society. It is purely for selfish reasons. Beware of this shockingly common, pervasive attitude. There's a proper time and place for heart procedures, or any procedure, for that matter. But feeding your doctor's ambitions is not a good reason.

Fast food and quick plaques

Such was the title of Dr. William Roberts' editorial back in 1987 discussing the health effects of fast foods.

If you need a graphic illustration of the extraordinarily damaging health effects of fast foods, take a look at trends in mainland China. A recent editorial in the American Journal of Cardiology written by Dr. Tsung Cheng of George Washington University makes several points:

--The popularity of fast food in China is booming, with Chinese now more likely than Americans to eat in a fast food restaurant. Each week, 41% of Chinese eat in a fast food restaurant at least once, compared to 35% in the U.S.

--Average total cholesterol levels have skyrocketed from 150 mg/dl in 1958 to 230 mg/dl in 2003.

--50% of Chinese with normal blood pressure in 1992 are now hypertensive.

--Hospitalization for heart disease rose from the 5th most common diagnosis to #1, now constituting nearly 50% of all hospital admissions.

McDonald's and KFC dominate the fast food landscape in China, but up and coming competitors are growing at exponential rates. A media conversation that will surely be reported in the near future is the boom in obesity and diabetes in China as these trends express themselves in weight gain, as it has in the U.S.


I hope you've all seen the entertaining but frightening documentary, Supersize Me chronicling the travails of 30-something Morgan Spurlock as he eats all his meals for one month at McDonald's restaurants in 20 cities. Though focusing on McDonald's, the movie is about a lot more than that. It paints a picture of how fast food as well as food manufacturers in general have changed--distorted--our eating habits.

If you haven't yet seen it, I would urge you to do so and watch it with the rest of the family. My kids (ages 8, 12, and 14) were shocked (and entertained) and they haven't set food in a fast food restaurant since.

But fish oil is too drastic!

Ted is a 74-year old physician, still conducting a busy practice. He came to me because of some vague fatigue and breathlessness. He also got himself a CT heart scan. His score: 1277.

When he came to my office, he clearly became breathless with just minimal effort. A stress test confirmed an area of much reduced blood flow to the front of his heart muscle. A heart catheterization identified a severe blockage of 95% in the left anterior descending artery and a stent was inserted. This resulted in relief of Ted's symptoms.

When Ted returned to the office after his discharge from the hospital, I advised him that some major changes in his prevention program were overdue. "After all, Ted, you were lucky this time. You were provided some warning. It doesn't always work that way." So I advised Ted to make a number of changes in his diet (he was following an old-fashioned, and quite self-destructive, low-fat diet), have lipoproteins assessed to identify hidden causes of coronary plaque, and take fish oil.

"Fish oil? I don't think so. That's pretty drastic!" he exclaimed. He felt that all the nutrition he needed was contained in the food he ate. Even after several lipoprotein abnormalities were uncovered like small LDL and excessive after-eating (post-prandial) patterns, he still resisted any changes. "I'm going to just wait and see how I feel. But I will take aspirin."

Such is the state of mind of the older physician: procedures are okay, low-fat diets prevent heart disease, and the Beatles are touring America. But fish oil? No way!

Unfortunately, Ted's attitude encapsulates the attitudes of many of my medical colleagues who don't share the excuse of age. They still practice the woefully outdated ways of physicians like Ted, clinging to notions of "balanced diets", nitroglycerin representing a rational treatment for coronary disease, and adequate rest being curative for heart conditions.

The world is changing. We're entering an exciting age of self-empowerment. The ridiculous notions of health practiced in the last half of the 20th century are withering and dying. Poor Ted. He must view the current healthcare landscape as increasingly incomprehensible to a guy who started out delivering babies at home. Perhaps, in some respects his world was better. But, in coronary disease prevention, attitudes like this need to go the way of steam engines and racial segregation--good riddens!

A curious case of coronary plaque regression and progression

John received a coronary stent in 2003 following a small heart attack. The artery causing the heart attack was a diagonal artery, a branch of the important left anterior descending coronary artery (in the front of the heart). His cardiologist at the time advised him, "Take Lipitor and we'll do stress tests every year. Come back if you have any more chest pain." That was the full extent of John's preventive care.

He came to me for a second opinion and, naturally, we enrolled him in our program. We began by obtaining a CT heart scan score, though we had to exclude the stented diagonal artery. His score: 471. At age 51 and physically active, John had 7 additional abnormal lipoprotein patterns identified. We counseled John on better approaches to food choices, his weight target, fish oil, and correction of all lipoprotein patterns.

Two years later, John's repeat heart scan score: 511 . John was initially disappointed with the increase. But a closer look yielded something entirely different: the right coronary artery and circumflex (no stents) showed 20-30% reduction in their scores. The increase in total score was entirely due to substantial increase in score just outside the stent, in the left anterior descending artery. In other words, all of the increase in score was due to growth of a plaque at the mouth of the stent in the diagonal artery.

This is curious: profound regression of plaque with a big drop in score in the "un-instrumented" arteries, but tremendous growth of plaque and an increase in score in the "instrumented", or stented, artery, all in the same person's heart.

I don't know how controllable this specific situation in the left anterior descending and stented diagonal will be, and I'm unaware of any specific strategies to impact on this situation. The whole world of tissue growth within or around stents is littered with high hopes followed by failures. The drug-coated stents have been the only partial solution to this problem, though that's precisely the sort of stent John received.

Is there a message here? The message I take from this is that you and I should work like mad to keep from receiving a stent. Once they're implanted, we have less control over our coronary future. We can indeed regress ("reverse") coronary plaque. But we may not be able to regress the sort of tissue that grows in response to a stent implantation.

When is a heart scan score of 400 better than 200?

Imagine two people.

Tom is a 50-year old man. Tom's initial heart scan score is 500--a bad score that carries a 5% or more risk for heart attack per year.

Harry is also 50 years old. His heart scan score is 100--also a concerning score but not with the same dangers of Tom's much higher score.

Tom follows a powerful heart disease prevention program like the Track Your Plaque program. He achieves the 60:60:60 lipid targets; chooses healthy foods; takes fish oil; raises his blood vitamin D level to >50 ng/ml, etc. One year later, Tom's heart scan score is 400, a 20% reduction from his starting score.

Harry, on the other hand, doesn't understand the implications of his score. Neither does his doctor. He's casually provided a prescription for a cholesterol drug by his doctor but nothing else. One year later, Harry's heart scan score is 200, a doubling (100% increase) of the original score.

At this point, we're left with Tom having a score of 400, Harry with a score of 200. That is, Tom has twice the score, or 200 points higher, compared to Harry. Who's better off?

Tom is better off. Even though he has a significantly higher score, Tom's plaque is regressing. It is therefore quiescent with its components being extracted, inflammation subsiding, the artery is in a more relaxed state, etc.

Harry's plaque, in contrast, is active and growing: inflammatory cells are abundant and producing enzymes that degrade supportive tissue, excessive constrictive factors are constantly causing the artery to pinch partially closed, fatty materials are accumulating and triggering a cascade of abnormal responses.

This is therefore a peculiar situation in which a higher score is actually better than a lower score. It reflects the power of adhering to a preventive program. It also demonstrates how two scans are better than one because they show the rate of increase given a particular preventive approach.

Warning: Your cardiologist may be dangerous to your health!

Warren had a moderately high LDL cholesterol for years and took a statin drug sporadically over the past 7 years. Finally retired from a successful real estate investment business, he had a CT heart scan to assess his heart disease status.

Warren's score: 49. At age 59, this put him in the lowest 25%, with an estimated heart attack risk of 1% per year or less--a relatively low risk. At this heart scan score, the likelihood of an abnormal stress test was less than 3%, or a 97% likelihood of a normal stress test. Most would argue that a stress test would be unproductive, given its low probability of yielding useful information. In other words, there would be a 97% probability of normal blood flow through Warren's coronary plaque, and less than 3% likelihood that a stent or bypass surgery would be necessary.

Warren was also without symptoms. He hiked and biked without any chest discomfort or breathlessness. A prevention program like Track Your Plaque to gain control over future coronary plaque growth was all that was necessary and Warren had high hopes for a life free of heart attack and major heart procedures.

Then why did he go through a heart catheterization?

Warren did indeed undergo a heart catheterization on the advice of his cardiologist. When I met Warren for another opinion, it became immediately obvious that the heart catheterization was completely unnecessary. Then why was this invasive procedure done? There can only be a few reasons:

--The cardiologist didn't truly understand the meaning of the heart scan score. "We need to do a 'real' test."

--The cardiologist was terrified of malpractice risk for underdiagnosing or undertreating any condition, no matter how mild.

--The cardiologist wanted to make more money. Talking about heart disease prevention is a money-saving, not a money-making, approach.

Regardless of which of the three motivations was at work here, they're all inexcusable. A disservice was done to this man: he had an unnecessary procedure, incurred some risk of complication in the process, and gained nothing.

An ignorant or profit-seeking cardiologist is worse than the unscrupulous car mechanic who, when presented with an unknowing car repair customer, proceeds to replace the carburetor and rebuild the engine when a simple 5-minute adjustment would have taken care of the problem.

I estimate that no more than 10% of my colleagues follow such practices, but it's often hard to know who is in that 10%. Ask pointed questions: Why is the catheterization necessary? What is the likelihood of finding information useful to my health? What are the alternatives? (By the way, the emerging CT coronary angiograms can be a useful alternative in some situations like this.)

Track Your Plaque is your source for credible information. Be well armed.

I don’t have high blood pressure!

Art undeniably had high blood pressure.

At age 53, he had all the “footprints” of high blood pressure that’d been present for at least several years: abnormal patterns by EKG, abnormally thick heart muscle, and an enlarged aorta by an echocardiogram. These sorts of changes require many years to develop. Art’s blood pressure was 140/85 sitting quietly in the office.

“That’s about what my primary care doc gets, too. Whenever it’s high, he takes it again after a few minutes and it always comes down.”

Art tried to persuade me that his blood pressure was high today only because of the traffic on the way into the office. When I dismissed this as a cause, he insisted that stress he’d been suffering because of his teenage son was the cause. “I just know I don’t have high blood pressure!”




Who’s right here? Well, Art is not here to defend himself. But one fact is crystal clear: you cannot develop complications of high blood pressure unless you truly have high blood pressure!

In other words, Art’s abnormal changes in heart structure (thickened heart muscle and enlarged aorta) are serious changes that develop only with years and years of sustained blood pressure at least as high as the one in the office. His blood pressure almost certainly ranged much higher at other times, particularly during stressful situations like waiting in the check-out line at the grocery store, watching a suspenseful TV show, petty irritations at his job, and on and on.

Blood pressure does not have to be high all the time to generate complications of high blood pressure. It can be sporadic, variable, even occasional. Clearly, sustained high blood pressure is the worst situation that creates adverse consequences more quickly. But blood pressure that wavers from low to high only some of the time can still, given sufficient time, cause the very same unwanted effects.

Control of blood pressure is crucial to your coronary plaque control program. Blood pressure may be boring: not as exotic, say, as lipoproteins, and not as fun as talking about nutritional supplements. But neglect blood pressure issues and you will not gain full control over coronary plaque growth—-your heart scan score will increase.

Watch for an upcoming Special Report on the Track Your Plaque Membership website, a full detailed discussion of how to recognize when blood pressure is an important issue, along with a full discussion of nutritional methods to reduce it, often sufficient to minimize or eliminate the need for medication.
All posts by william-davis

China fiction?

Dr. Colin Campbell caused a stir with publication of his 2005 book, The China Study. Dr. Campbell, after extensive animal and epidemiologic research conducted in China over 20 years, concluded that a diet high in animal protein, especially casein, was associated with increased cancer, osteoporosis, and heart disease risk.

Richard Nikoley of Free the Animal and Stephan Guyenet of Whole Health Source have been talking about an analysis of the China Study raw data performed by a young woman named Denise Minger.

Denise's analysis is nothing short of brilliant, absolutely "must" reading for anyone interested in nutrition.

Her comments on the relationship of wheat to heart disease:

Why does Campbell indict animal foods in cardiovascular disease (correlation of +1 for animal protein and -11 for fish protein), yet fail to mention that wheat flour has a correlation of +67 with heart attacks and coronary heart disease, and plant protein correlates at +25 with these conditions?

Speaking of wheat, why doesn’t Campbell also note the astronomical correlations wheat flour has with various diseases: +46 with cervix cancer, +54 with hypertensive heart disease, +47 with stroke, +41 with diseases of the blood and blood-forming organs, and the aforementioned +67 with myocardial infarction and coronary heart disease?

Carbohydrate-LDL double whammy

Carbohydrates in the diet trigger formation of small LDL particles. Because carbohydrates, such as products made from wheat, increase triglycerides and triglyceride-containing lipoproteins (chylomicrons, chylomicron remnants, VLDL, and IDL), LDL particles (NOT LDL cholesterol) become triglyceride-enriched. Triglyceride-enriched LDL particles are "remodeled" by the enzyme, hepatic lipase, into triglyceride-depleted, small LDL particles.

The list of reasons why small LDL particles are more atherogenic, i.e., plaque-causing, is long:

--Small LDL particles, being smaller, more readily penetrate the endothelial barrier of the arterial wall.
--Small LDL particles are more adherent to glycosaminoglycans in the artery wall.
--Small LDL particles are poorly taken up by the liver LDL receptor, but enthusiastically taken up by macrophage receptors of the sort in your artery walls.
--Because of their poor liver clearance, small LDL persists in the bloodstream far longer than large LDL.
--Small LDL particles are more oxidation-prone. Oxidized LDL are more likely to trigger inflammatory phenomena and be taken up by macrophages in the artery wall.

Let me add another reason why small LDL particles are more likely to cause plaque: They are more likely to undergo glycation. (More on glycation here.)

Glycation occurs when glucose (sugar) molecules in the blood or tissue modify proteins, usually irreversibly. Small LDL particles are uniquely glycation-prone. (This is likely due to a conformational change of the apoprotein B in the small LDL particle, exposing lysine residues along apo B that become glycated.)

Here's a great demonstration of this phenomenon by Younis et al:


"LDL3" is the small type. Note that small LDL particles are 4-5 times more glycated than large LDL. That's a big difference.

Once glycated, small LDL is especially resistant to being taken up by the liver. Like annoying in-laws, they hang around and hang around and . . . The longer they hang around, they more opportunity they have to contribute to plaque formation.

So, carbohydrates trigger formation of small LDL particles. Once formed, small LDL particles are glycated when blood sugar increases. While LDL can be glycated even when blood sugars are in the normal range (90 mg/dl or less), glycation goes berserk when blood sugars go higher, such as a blood sugar of 155 mg/dl after a bowl of steel-cut oatmeal.

To lose weight, prick your finger

We know that foods that trigger insulin lead to fat storage. Putting a stop to this process allows you to mobilize fat and lose weight. If you're starting out from scratch, rapid and dramatic weight loss can be experienced, as much as one pound per day.

So how can you stop triggering insulin?

The easiest way is to eliminate, or at least minimize, carbohydrates. My favorite method to restrict carbohydrates is to eliminate wheat and minimize exposure to other carbohydrates, such as oats, cornstarch, and sugars. All these foods, wheat products worst of all, cause blood sugar and insulin to skyrocket.

Another way is to check your blood sugar one hour after completing a meal and keep your after-eating, or "postprandial," blood sugar 100 mg/dl or less. Let's say you are going to eat stone ground oatmeal, for example. Blood sugar prior to eating is, say, 90 mg/dl. One hour after oatmeal it's 168 mg/dl--you know that this is going to trigger insulin and make you fat. Oatmeal should therefore be eliminated.

Keeping blood sugar to 100 mg/dl or less after eating teaches you how to avoid provocation of insulin. A shrinking tummy will follow.

To do this, you will need:

1) A glucose meter--My favorite is the One Touch Ultra Mini ($13.42 at Walmart). It's exceptionally easy to use and requires just a dot of blood. Drawback: Test strips are about $1 each. Accuchek Aviva is another good device. (We've had a lot of problems with Walgreen's brand device.)
2) Test strips--This is the costly part of the proposition. Purchased 25 or 50 at a time, they can cost from $0.50 to $1.00 a piece.
3) Lancets--These are the pins for the fingerstick device that comes with the glucose meter. A box should be just a few dollars.

No prescription is necessary, nor will insurance pay for your costs unless you're diabetic. To conserve test strips, use them only when a new, untested food or food combination is going to be consumed. If you had two scrambled eggs with green peppers, sundried tomatoes, and olive oil yesterday and had a one hour postprandial glucose of 97 mg/dl, no need to check blood sugar again if you are having the same meal again today.

Iodine update

As the iodine experience grows, I've made several unique observations.

Up to several times per day, I see people who are responding in some positive way to iodine supplementation. (See previous Heart Scan Blog posts about iodine: Iodine deficiency is REAL and The healthiest people are the most iodine deficient.)

Among the phenomena I've observed:

1) A free T4 thyroid hormone at the low end of normal, or even in the below normal range, along with a highish TSH (usually >1.5 mIU/L) are the most frequent patterns that signal iodine deficiency. Occasionally, a low free T3 value will also increase, though this is the least frequent development.

2) At a dose of 500 to 1000 mcg iodine per day, it requires anywhere from 3 to 6 months to obtain normalization of thyroid measures.

3) Reversal of small goiters also occurs over about 6 months.

4) Iodine intolerance is uncommon. If it occurs, using a low starting dose, e.g., 100-200 mcg per day, usually works. The dose can be increased gradually over the ensuing months.

5) Perceptible benefits of iodine occur only occasionally. The most common perceptible effects are increased energy and increased warmth, especially of the hands and feet.

6) Some people who have taken thyroid hormones for years will develop reduced need for their medication with iodine supplementation. In other words, their physician was inadvertently treating iodine deficiency with thyroid hormone replacement. Anyone already on any thyroid preparation(s), e.g., Synthroid, levothyroxine, Armour thyroid, Naturethroid, etc., should watch for signs of hyperthyroidism when iodine is added. But having your own thyroid gland make its own thyroid hormones is better and healthier than relying on the prescription agents. Just be sure to monitor your thyroid measures.

7) Iodine toxicity can occur--Two people in my clinic population developed iodine toxicity by taking 6000 mcg iodine per day for 6 or more months. (Both patients did it on their own based on something they read). Iodine toxicity is evidenced by shutting down your thyroid, i.e., marked increase in TSH, e.g., 15 mIU/L.


Most of the people in my clinic obtain their iodine from kelp tablets. Some use potassium iodine (KI) drops. A handful have used the high-potency Iodoral (12.5 mg or 12,500 mcg iodine per tablet); this was also the form that generated the toxic effects in the two females.

All in all, iodine deficiency is actually far more common than I ever suspected. Not everybody is iodine deficient. But a substantial minority of the Midwest population I see certainly are.

Why haven't you heard about lipoprotein(a)?

Lipoprotein(a), or Lp(a), is the combined product of a low-density lipoprotein (LDL) particle joined with the liver-produced protein, apoprotein(a).

Apoprotein(a)'s characteristics are genetically-determined: If your Mom gave the gene to you, you will have the same type of apoprotein(a) as she did. You will also share her risk for heart disease and stroke.

When apoprotein(a) joins with LDL, the combined Lp(a) particle is among the most aggressive known causes for coronary and carotid plaque. If apoprotein(a) joins with a small LDL, the Lp(a) particle that results is especially aggressive. This is the pattern I see, for instance, in people who have heart attacks or have high heart scan scores in their 40s or 50s.

Lp(a) is not rare. Estimates of incidence vary from population to population. In the population I see, who often come to me because they have positive heart scan scores or existing coronary disease (in other words, a "skewed" or "selected" population), approximately 30% express substantial blood levels of Lp(a).

Then why haven't you heard about Lp(a)? If it is an aggressive, perhaps the MOST aggressive known cause for heart disease and stroke, why isn't Lp(a)featured in news reports, Oprah, or The Health Channel?

Easy: Because the treatments are nutritional and inexpensive.

The expression of Lp(a), despite being a genetically-programmed characteristic, can be modified; it can be reduced. In fact, of the five people who have reduced their coronary calcium (heart scan) score the most in the Track Your Plaque program, four have Lp(a). While sometimes difficult to gain control over, people with Lp(a) represent some of the biggest success stories in the Track Your Plaque program.

Treatments for Lp(a) include (in order of my current preference):

1) High-dose fish oil--We currently use 6000 mg EPA + DHA per day
2) Niacin
3) DHEA
4) Thyroid normalization--especially T3

Hormonal strategies beyond DHEA can exert a small Lp(a)-reducing effect: testosterone for men, estrogens (human, no horse!) for women.

In other words, there is no high-ticket pharmaceutical treatment for Lp(a). All the treatments are either nutritional, like high-dose fish oil, or low-cost generic drugs, like liothyronine (T3) or Armour thyroid.

That is the sad state of affairs in healthcare today: If there is no money to be made by the pharmaceutical industry, then there are no sexy sales representatives to promote a new drug to the gullible practicing physician. Because most education for physicians is provided by the drug industry today, no drug marketing means no awareness of this aggressive cause for heart disease and stroke called Lp(a). (When a drug manufacturer finally releases a prescription agent effective for reducing Lp(a), such as eprotirome, then you'll see TV ads, magazine stories, and TV talk show discussions about the importance of Lp(a). That's how the world works.)

Now you know better.

How to have a heart attack in 10 easy steps

If you would like to plan a heart attack in your future, here are some easy-to-follow steps to get you there in just a few short months or years:


1) Follow a low-fat diet.

2) Replace fat calories with "healthy whole grains" like whole wheat bread.

3) Eat "heart healthy" foods like heart healthy yogurt and breakfast cereals from the grocery store.

4) Use cholesterol-reducing plant sterols.

5) Take a multivitamin to obtain all the "necessary" nutrients.

6) Take the advice of your doctor who declares your heart "in great shape" based on your cholesterol values.

7) Take the advice of your cardiologist who declares your heart "like that of a 30-year old" based on a stress test.

8) Take a statin drug to reduce LDL and c-reactive protein while maintaining your low-fat diet.

9) Neglect sun exposure and vitamin D restoration.

10) Limit your salt intake while not supplementing iodine.



There you have it: An easy, 10-step process to do your part to help your local hospital add on its next $40 million heart care center.

If you would instead like to prevent a heart attack in your future, then you should consider not doing any of the above.

Kick inflammation in the butt

C-reactive protein, or CRP, is a protein produced by the liver in response to inflammatory signals its receives. Thus, CRP has emerged as a popular measure to gauge the underlying inflammatory status of your body. Higher CRP levels (e.g., 3.0 mg/L or greater) are associated with increased risk of heart attack and other cardiovascular events.

The drug cartel have jumped on this with the assistance of Harvard cardiologist, Dr. Paul Ridker. Most physicians now regard increased CRP as a mandate to institute statin therapy, preferably at high doses based on such studies as The JUPITER Trial, in which rosuvastatin (Crestor), 20 mg per day, reduced CRP 37%.

I see this differently. Two strategies drop CRP dramatically, nearly to zero with rare exception: Vitamin D restoration and wheat elimination. Not 37%, but something close to 100%.

Yes, I know it sounds wacky. But it works almost without fail, provided the rest of your life is conducted in reasonably healthy fashion, i.e., you don't live on Coca Cola, weigh 80 lbs over ideal weight, and smoke.

How can something so easily reduced like CRP mean you "need" medication? Easy: Increased CRP means there are fundamental deficiencies and/or inflammation provoking foods in your diet. Correct neither and there is an apparent benefit to taking a statin drug.

Why not just correct the underlying causes?

Life without Lipitor

One of the most common reasons people come to my office is to correct high cholesterol values without Lipitor. (Substitute "Lipitor" with Crestor, simvastatin, Vytorin, or any of the other cholesterol drugs; it's much the same.)

In the world of conventional healthcare, in which you are instructed to follow a diet that increases risk for heart disease and not advised to correct nutrient deficiencies like vitamin D and omega-3 fatty acids, then a drug like Lipitor may indeed provide benefit.

But when you are provided genuinely effective information on diet, along with correction of nutrient deficiencies, then the "need" and apparent benefits of Lipitor largely dissolve. While there are occasional genetic anomalies that can improve with use of Lipitor and other statins, many, perhaps most, people taking these drugs really would not have to if they were just provided the right information.

Anyone following the discussions on these pages knows that wheat elimination is probably one of the most powerful overall health strategies available. Wheat elimination reduces real measured LDL quite dramatically. Provided you limit other carbohydrates, such as those from fruits, as well, LDL can drop like a stone. That's not what your doctor tells you. This approach works because elimination of wheat and limiting other carbohydrates reduces small LDL. Small LDL particles are triggered by carbohydrates, especially wheat; reducing carbohydrates reduces small LDL. Conventional LDL of the sort obtained in your doctor's office will not show this, since it is a calculated value that appears to increase with reduced carbohydrates, a misleading result.

Throw vitamin D normalization and iodine + thyroid normalization into the mix (both are exceptionally common), and you have two additional potent means to reduce (measured) LDL. Not restricting fat but increasing healthy fat intake, such as the fats in lots of raw nuts, olive oil, and flaxseed oil reduce LDL.

While I still prescribe statins now and then, a growing number of people are succeeding without them.

(Note that by "measured" LDL I am referring to the "gold standard," LDL particle number by NMR provided by Liposcience. A second best is measured Apoprotein B available through most conventional labs.)

In search of wheat: Emmer

While einkorn is a 14-chromosome ancient wheat (containing the so-called "A" genome), emmer is a 28-chromosome wheat (containing the "A" and "B" genomes, the "B" likely contributed by goat grass 9000 years ago).

Both einkorn and emmer originally grew wild in the Fertile Crescent, allowing Neolithic Natufians to harvest the wild grasses with stone sickles and grind the seeds into porridge.

Having tested einkorn with only a modest rise in blood sugar but without the gastrointestinal or neurological effects I experienced with conventional whole wheat bread, I next tested bread made with emmer grain.

The emmer grain was ground just like the other two grains, cardiac dietitian Margaret Pfeiffer doing all the work of grinding and baking. Margaret added nothing but water, yeast, and a little salt. The emmer rose a little more than einkorn, but not to the degree of conventional whole wheat.

I tested my blood sugar beforehand: 89 mg/dl. I then ate 4 oz of the emmer bread. It tasted very similar to conventional whole wheat, but not as nutty as einkorn. Also not as heavy as einkorn, only slightly heavier than conventional whole wheat.

One hour later, blood sugar: 147 mg/dl. I felt slightly queasy for about 2-3 hours, but that was the end of it. No abdominal cramps, no sleep disturbance or crazy dreams, no nausea, no change in ability to concentrate.

I asked four other wheat-sensitive people to try the emmer bread. Likewise, nobody reacted negatively (though nobody tested blood sugar).

So it seems to me, based on this small, unscientific experience, that ancient einkorn (A) and emmer (AB) wheat seem to act like carbohydrates, similar to, say, rice or quinoa, but lack many of the other adverse effects induced by conventional wheat.

Modern wheat , Triticum aestivum, contains variations on the "A," "B," and "D" genomes, the "D" contributed by hybridization with Triticum tauschii at about the same time that emmer wheat hybridization occurred. It is likely that proteins coded by the "D" genome are the source of most of the problems with wheat products: immune, neurologic, gastrointestinal destruction, airway inflammation (asthma), increase in appetite, etc. This is consistent with observations made in studies that attempt to pinpoint the gliadin proteins that trigger celiac, the area in which much of this research originates.

If I ever would like an indulgence of cookies or cupcakes, I think that I will order some more einkorn grain from Eli Rogosa.

In search of wheat: Another einkorn experience

Lisa is a trained dietitian. Unlike many of her colleagues, she has "seen the light" and realized that the conventional advice that most dietitians are forced to dispense through hospitals, clinics, and other facilities is just plain wrong. 

I know Lisa personally and we've had some great conversations on diet and nutritional supplements. I told Lisa about my einkorn experience and how I witnessed a dramatic difference between bread made from einkorn wheat and that made from conventional whole wheat. So she decided to give it a try herself. 

Here's Lisa's experience:


This past Friday, June 18th, I conducted my "Einkorn Wheat Experiment".

7 am 
FBG [fasting blood glucose] 97 mg/dl

8 am-9 am 
1 hour high-intensity aerobic workout

10:05 am 
BG 99

10:05 am 
I embarked upon the journey of choking down, I mean enjoying, the hefty piece of Einkorn bread. Wow, was that bread dense!  It was a lot of work chewing. 

10:50 am 
(45 minutes after consumption, wanted to see what BG did a bit before the 1 hr mark)  BG 153

11:05 am 
1hr PP 120

11:35 am 
90 mins PP [postprandial] 113

12:05 pm 
2 hours PP  114 ... at this time I ate an egg & veggie omelet for lunch.

12:50 pm 
BG 100

Before dinner 5:10 pm 
BG 88

I was surprised with the BG of 153. However, it was good to see my insulin response is reactive and decreased BG 33 points in 15 minutes to end up with a BG of 120 1 hr after the bread.  

So, it appears my response is similar. A slight elevation of BG at the 1 hour mark, but not to the degree of conventional whole grain wheat bread.  

Of note, also, was the fact that I cannot remember the last time I ate a piece of wheat bread of this magnitude that did not make me bloated... not at all: No cramps, no brain fog, no headache and, did I mention not bloated?  

I believe you are on to something with tolerance of Einkorn wheat for those of us with wheat sensitivities, in addition to its apparent lower glycemic response.

Along with Lisa, I asked four other people with various acute intolerances (all gastrointestinal) to conventional wheat, i.e., people who experience undesirable effects from wheat within minutes to several hours, to eat the einkorn bread. None experienced their usual reactions.

Obviously, this does not constitute a clinical trial. Nonetheless, I find this a compelling observation: People like myself who generally experience distinct undesirable reactions to wheat did not experience these reactions with einkorn.

Note, however, that einkorn behaves like a carbohydrate. No different, say, from brown rice or quinoa. However, unlike modern whole wheat flour from Triticum aestivum,  in this little experience there were no immune reactions, no neurologic phenomena, no gastrointestinal distress--just the blood sugar consequences.

While this may not be true for all people consuming einkorn, it suggests that primordial einkorn wheat is quite different from modern conventional wheat for most people.
Calcium chaos

Calcium chaos


Imagine that I'm planning to build a wall of bricks. I start by throwing cement at a pile of bricks, hoping that it forms a nice, orderly brick wall.

Fat chance, you say.

I believe that is what appears to be emerging as the situation with calcium supplementation.

A recent study from New Zealand reported an experience with 1,471 postmenopausal women, mean age of 74 years, who were randomized to treatment with either calcium supplements or placebo. Calcium was supplied as calcium citrate (Citrical) to provide 1000 mg of (elemental) calcium per day (400 mg morning, 600 mg evening).

(Bolland MJ, Barber PA, Doughty RN et al. Vascular events in healthy older women receiving calcium supplementation: randomised controlled trial. Brit Med J BMJ, doi:10.1136/bmj.39440.525752.BE; published 15 January 2008)

Over 5 years, women taking calcium had twice the risk of having a heart attack compared with women taking the placebo; women taking calcium had a 47 percent higher risk of having any one of three "events" (heart attack, stroke or sudden death) than women in the placebo group.

The findings of this study run counter to what we've been telling people all these years: Calcium supplementation, usually taken to halt deteriorating bone health and osteoporosis, modestly reduces blood pressure, reduces LDL and raises HDL cholesterol. At first blush, we might thereby presume that it also reduces cardiovascular events.

This study suggests that calcium supplementation does not result in reduction of cardiovascular events, perhaps even increases risk.

Certainly, this new finding will serve to confuse the public even more than it is already, particularly when it comes to strategies that modify risk for heart attack. However, this may make more sense once we stop and think for a moment.

Calcium supplementation inarguably slows, occasionally halts, calcium resorption from bone (through suppression of parathyroid hormone). Calcium also accumulates as part of atherosclerotic plaque in coronary and other arteries.

How does oral calcium know where to go--bones, not arteries or kidneys, in addition to serving all its other crucial functions?

Keep in mind that, in many roles, calcium is passive, something that responds to control exerted by some other factor. Vitamin D is that factor. Vitamin D controls the absorption of calcium in the intestinal tract (calcium aborption quadruples when vitamin D is restored to normal), it controls whether calcium is deposited in bone or extracted from arteries. It is the master control over the fate of calcium. Calcium just goes along for the ride.

Bone and arterial health do indeed intersect via calcium, but not through calcium supplementation. Instead, the control exerted by vitamin D (and vitamin K2, another conversation) connects the seemingly unrelated processes.

At what calcium dose threshold do the benefits stop and the adverse effects begin? That remains unanswered, particularly in light of this new study. However, this study calls into serious question the wisdom of supplementing calcium at a dose of 1000 mg, particularly when taken without normalization of vitamin D.

Calcium is therefore emerging as an important player in artery health. But just taking calcium makes no more sense than our brick wall and cement analogy. You might regard vitamin D as the mason that skillfully lays down both brick and cement in a neat, orderly way.

Comments (30) -

  • Anne

    1/23/2008 7:47:00 AM |

    Dear Dr Davis,

    Sometimes I think I must be living in the Matrix - I thought this article so interesting as I have been prescribed calcium supplements for osteoporosis, but just a few weeks ago I had to stop taking them because I discovered they were the cause of severe diarrhoea I had been having for nearly a year. Stopping the calcium supplements halted the diarrhoea straight away, trying it again, even a different make, brought it back even on low dose. Anyway, it was just then that I read a lot about vitamin D3 on your blog and Dr Eades, just at that very time, so I upped my D3 intake to 5,000iu in the hopes it will help me absorb as much of my dietary calcium as possible. I cannot take dairy products so I get my calcium from leafy green veggies, nuts, seeds and fish. And now you wrote on your blog to look at vitamin D3 for aortic valves (I'm the one with bicuspid aortic valve) too. The Matrix ! Or I've found the best doctors on the internet Smile

    all the best,
    Anne

  • Anonymous

    1/23/2008 5:23:00 PM |

    I'm taking Vit D3 in gel form for my bones, heart, and to help prevent cancer, until it warms up here so I can get some sun. I'll be getting plenty of direct sun while gardening and bike riding, but the rest of the time outside, I'll sit in the the shade so I won't get too much UVA, since my family had a few skin cancers (caught early).

    I'm going to look for natto when I finally make it to the Asian store. I've heard it tastes pretty bad for people that have never eaten it, so I'll have to try to mix it in with something else probably. I've also read that some people compare it to blue cheese, so maybe I'll start with blue cheese recipes to try to mellow the natto taste.

    S

  • Red Sphynx

    1/23/2008 6:50:00 PM |

    Granted, calcium supplements leave a lot to be desired.

    But this article didn't cast any light on the problem.  Read Sandy Szwarc' excellent Fisking of this study over at JunkFoodScience.

    Adam Becker Sr

  • Anonymous

    1/23/2008 8:53:00 PM |

    Doesn't calcium compete with magnesium for absorption from the gut?  In which case, supplemental magnesium in addition to the calcium would be indicated

  • Anonymous

    1/24/2008 12:49:00 AM |

    I am so confused about this whole chotesterol/ heart attack risk argument. I've been reading your blog for months now and follow everything you say because it sounds like it all makes great sense. So whats the problem? We keep hearing more and more that total cholesterol, as was once thought, is not a very good indcator of impending heart attack. So how come Dr.William Castelli, the one time director of the famous Framingham Study says in over 60 years following thousands of people, they have NEVER had a heart attack in ANYONE with a total cholesterol below 150 regardless of what the HDL may be? If that doesn't indicate that total cholesterol CAN be a strong indicator I don't know what can. I understand if your cholesterol is higher than 150 this may not tell you anything, but for those of us below doesn't it? Or does no heart attacks in a 60 year period with thousands of people tell us nothing?

  • Dr. Davis

    1/24/2008 2:44:00 AM |

    I do not agree with Dr. Castelli's observation. I have seen MANY heart attacks with total cholesterols <150 mg/dl. I do not understand the discrepancy.

    For instance, an HDL of 23 mg/dl--very high risk--can easily be concealed within a low total cholesterol, as can smoking, diabetes, and Lp(a).

  • Peter

    1/24/2008 9:05:00 AM |

    Anonymous, even the most cursory glance at any of the aggressive LDL-C lowering trials will give you the information about the accuracy of Dr Castelli's statement. Let's not be too explicit.

    Peter

  • donnyrosart

    1/24/2008 1:33:00 PM |

    It looks like going into the study, the authors suspected the opposite (calcium prevents heart disease) was true. They mention speculation that calcium supplementation might be heart healthy by increasing malabsorption of fat, and quote a study where calcium supplementation doubled fecal fat and bile. Personally, I try to eat things I'd like to absorb.
    The first study they reference to (I think it's their own study) showed calcium supplementation increased Hdl, and decreased ldl, but had no effect on triglycerides. If ldl decreases, but triglycerides remain the same, does that suggest anything about ldl particle size?
    Really like your blog.

  • Dr. Davis

    1/24/2008 4:19:00 PM |

    Good question.

    I've not looked specifically for a LDL size effect from calcium, nor am I aware of any specific literature to this effect. However, I do believe that many of us are trending towards less and less calcium supplementation, particularly in light of vit D supplementation.

  • Anonymous

    1/24/2008 7:59:00 PM |

    I apologise maybe I worded my question incorrectly. Dr. Castelli doesn't claim that if you have a total cholesterol under 150 you will not have a heart attack, he says in The Framingham study ( involving 3 generations and over 10,000 people ) there has never been one. I suppose we could blow this off and claim he's lying ( I doubt it ) or try to learn something from it. Thats a VERY large long lasting study and once again he has said "under 150 REGARDLESS of HDL score" there HAS to be a reason for this, I was just wondering if anyone had a guess.

  • brittany lady

    1/24/2008 10:59:00 PM |

    This now has me totally confused.  My doctor recommended I take 1,000 mg. of Calcium in supplement form every day, and to make sure I get 800 mg. of Vitamin D.  I have done so faithfully plus drinking about 10 oz. of calcium added Lactaid fat free milk. I also learned after an x-ray, stress test and heart imaging that I have calcification at the base of my aorta, but my heart is not enlarged.  This has happened since 1999, and I have only been taking Vitamin D for the past year and a half. Now I wonder if large doses of Calcium before having my vitamin D levels tested might have caused this. On another note, I had very high triglycerides and started taking 2000 mg. of fish oil capsules daily.  My triglycerides dropped from 375 to 160 in 6 months.  That might be a solution to someone with these concerns.

  • Anne

    1/25/2008 8:23:00 AM |

    Since being diagnosed with osteoporosis last year I have done a lot of research on it and on various therapies. I am, btw, only 54 so it was a big shock. Anyway, looking at things logically, there is no way that someone my age would have got osteoporosis from lack of calcium, so why do they prescribe it ? It seems based on research done on elderly ladies in nursing homes. I've got osteoporosis because of health issues when I was younger yet, I was still told the usual to take 1000mg calcium and 800iu vitamin D. I refused bisphosphonates and have been prescribed Strontium Ranelate instead. I hope Strontium doesn't cause calcification, I don't think they know enough about it so I feel rather a guinea pig. Now that I can't tolerate calcium and have stopped taking it and upped the Vitamin D3 to 5000iu I feel more confident that this will help not only my bones but also my heart health. I also take 2,000mg of fish oil.....my triglycerides are currently 0.6 (53).

    Anne

  • Anne

    1/25/2008 1:39:00 PM |

    Something else to make one realise that calcium may not be as important as we have been told - if you look at countries in Africa where some people have sub-optimal diets and low in calcium, you usually don't often find osteoporosis ! I would hazard a guess that the reason they don't get osteoporosis is because they have plenty of Vitamin D from the sunshine and they probably do a lot of physical work.

    Anne

  • Dr. Davis

    1/25/2008 1:51:00 PM |

    Great thought.

    I am impressed that many of the "holes" in our thinking about health and nutrients is filling in with greater understanding of the role of vitamin D.

  • Rick

    1/25/2008 5:19:00 PM |

    Dr. Castelli also made the following observation:

    "For example, in Framingham, Mass, the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower the person’s serum cholesterol."

    For Dr. Eades's typically insightful take on the issue, go here:

    http://tinyurl.com/2d7bzw

    and here:

    http://tinyurl.com/24uqj2

  • Dr. Davis

    1/26/2008 5:05:00 AM |

    I couldn't agree more.

    Cholesterol (total and LDL) are lousy predictors of heart disease. They are, indeed, factors. But in the long list of factors causing heart disease, cholesterol is way down.

    But cholesterol is, no doubt, the most profitable. Revenues for statin drugs topped $27 billion last year.

  • Anonymous

    1/26/2008 3:05:00 PM |

    Great articles Rick, read them both and found them quite interesting however a little disappointed neither had anything to do with why after 60 years and following over 10,000 people NOT ONE of them with a total cholesterol under 150 ever had a heart attack. I eat low carb, loved Taubes book explaining the myths about eating fat, big proponent of Track your plaque and think Dr. Davis is brilliant and well ahead of his time. And yet either we think Dr. Castelli is a liar or anybody with ANY interest in preventive cardiology would want to know why no heart attacks in anyone with tot cholesterol under 150 in over 60 years in such a large group of people. My god we hear all the time about the stunning results of the HATS Trial which included a grand total of 161 people.

  • MAC

    1/26/2008 5:38:00 PM |

    Dr. Davis,
        Found this study while perusing Science daily today. Not sure how or if this intersects at all with the good results you get with Vit D.

    Vitamin D Deficiency May be a Sympton of Disease: Supplementations may make it worse:

    http://www.sciencedaily.com/releases
    /2008/01/080125223302.htm

    "Low blood levels of vitamin D have long been associated with disease, and the assumption has been that vitamin D supplements may protect against disease. However, this new research demonstrates that ingested vitamin D is immunosuppressive and that low blood levels of vitamin D may be actually a result of the disease process. Supplementation may make the disease worse."

  • Dr. Davis

    1/27/2008 2:18:00 AM |

    It refers to the so-called "Marshall Protocol." Having read his arguments, he mixes science with conjecture and enormous leaps of speculation, all with zero experience in real, live humans. (He's a "bench" researcher with experience that doesn't extend beyond mice and cell cultures.)

    It reminds me an awful lot of the pseudo-scientific tangent that misled Linus Pauling and Mathias Rath.

  • Rick

    1/27/2008 7:40:00 AM |

    Anonymous,

    No need to be disappointed.  Here's the relevance.  Dr. Eades quoted Dr. Kannel, who preceded Castelli as director of the Framinham study as saying:

    "...it is not possible to select a critical lipid value that separates potential CHD candidates from the rest of the population."

    That appears to contradict the implications of Castelli's quote.

    Dr. Eades also made the case that sometimes the pronouncement of the researchers is not supported by the evidence.

    What percent of the population had cholesterol lower than 150?  What was their age distribution?  These would be important things to know.

    In looking at a graph of the distribution, it appears that less than 5% of the population were in that category.  

    BTW, can you you provide a citation for your quote of Dr. Castelli?  Thanks.

  • Stan

    1/27/2008 3:32:00 PM |

    anonymous,

    Castelli said that there was no heart attack at all in the sub-population below 150mg/dl of cholesterol, and he said also
    that, quote:

    "For example, in Framingham, Mass, the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower the person’s serum cholesterol."

    This is a speculation but one possible explanation behind those two seemingly contradictory informations is that the
    subpopulation of people who had naturally low cholesterol in Framingham, were all young and/or  were all eating more animal fat and less carbohydrates than the other groups!  Younger people are more active and eat more calories too. Both factors (young age and a higher animal fat lower carbohydrate nutrition) tend to associate with low cholesterol
    and are simultanously cardioprotective.

    Is it improbable? I dont' think so. Dr. Davis's own results on vitamin D3 and essential fatty acids supplementation (naturally present in animal food, dairy, eggs, meat and fish!) also seem to point in the same direction.

    It would also fit another observation: I remember some published data on Masai population who also have or had very low total cholesterol (I think about 160 mg/dl on average), follow a high fat low carbohydrate nutrition and have very little heart disease!

    Stan (Heretic)

  • Anonymous

    1/28/2008 3:38:00 PM |

    http://tinyurl.com/24uqj2, Rick try this one but any search on google brings many citataions.

  • Anonymous

    1/28/2008 3:41:00 PM |

    Rick heres another better one.http://findarticles.com/p/articles/mi_qa3987/is_20070409/ai_n19031299/pg_2

  • Rick

    1/29/2008 12:32:00 AM |

    Anon,

    Thanks for the links, but the first one is the link I gave you, and the second is truncated.  

    If it's the article by the chiropracter, I've already seen that, but was hoping for  a primary source so I could read the context.  I've done a fair amount of googling but haven't been able to find it.

    Your quote speaks of 60 years of research, yet the artcle you cite (at least I think it's the same artcle) speaks of 40 years and the Framingham website is proudly celebrating 50 years of research.

    This is not to nitpick but it does make me wonder if this isn't one of those internet quotes that takes on a life of its own.

    I agree with you that it is confusing because so much of what I have read, along with my own experience renders his observation, whether true or not, meaningless.

  • Anonymous

    1/29/2008 12:51:00 AM |

    http://findarticles.com/p/articles/mi_qa3987/is_20070409/ai_n19031299/pg_2
    This article explains Dr. Castelli's position well.

  • Anonymous

    1/29/2008 12:55:00 AM |

    http://findarticles.com/p/articles/mi_qa3987/is_20070409/ai_n19031299
    Read this one Rick.

  • Anonymous

    1/30/2008 3:07:00 PM |

    The Framingham Study was begun in 1948. That seems to be the one point that is a fact.

  • Rick

    1/30/2008 7:14:00 PM |

    Thanks for the link.  That is one of the articles I'd already seen. ( Not to put too fine a point on it, but he does refer to 40 years, not 60 as in your quote.)

    The data I've seen confirms his statement.  People whose TC was below 150 didn't evidence CHD.  But, as I mentioned above, the number of those people was extremely small, less than 5% of the population. It may be true the nobody who's run a sub 2:10 marathon has suffered a heart attack, but so what?

    For the vast majority of the population in the study, those between 150 and 370, some did have CHD, some didn't.  The correlation was not strong except on the edges.  

    So what can we take away from this?  Get your TC below 150 and you're immune from CHD?  The same research shows correlation with low levels of TC and all cause mortality.  So choose your poison.

    And if, despite your best efforts, your numbers creep up above 150, are all bets off?  My TC over the years, has ranged from 140 to 180, most recently 160, yet my plaque burden put me in the 50th percentile for my peer group.  So the importance of Dr. Castelli's observation is lost on me.

    As pointed out by Dr. Davis, and many others, total cholesterol alone is not a very useful indicator. Check out the post on the Vytorin study. Those whose cholesterol dropped the most experienced a greater increase in plaque.

    So, while Castelli's statement is based in fact, there is a lot of room for interpretation.  And most of the rest of what is attributed to him in that article is speculation.

    Yes, Framingham was begun in 1948, but I doubt the data is available instantaneously.

  • Anonymous

    6/4/2008 1:31:00 PM |

    My sister and I got in argument at a picnic about whether calcium supplements are a good idea.  Afterward she sent me an article in favor, and I sent her one against.  Then I realized you wrote both articles!

  • ccruby

    8/17/2008 1:30:00 AM |

    Mayo Clinic diagnosed me with fluid around my heart.  I could feel it sloshing around.  Stopped calcium/mag and estrogen supplements and I could no longer feel it; I also kept telling it to go away.  Went back a couple of months later for MRI--Mayo said I had fat around my heart.  I know the original diagnosis was correct.

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Cureality | Real People Seeking Real Cures

Conventional therapy vs. alternative therapy

Rose is a 75-year old woman, mother of four, grandmother of many more.

Rose's story started after a heart attack 18 months ago that resulted in two stents. She was advised to follow an American Heart Association diet and take Lipitor. However, some months later, after her fourth stent, she became disilluioned in the conventional approach to heart disease and sought alternative therapies to help reduce or reverse her heart disease.

She found an alternative health practitioner who advised chelation, antioxidant vitamins for "excessive oxidation," and several homeopathic preparations.

Nothing was said about diet or exercise. Nothing was said about the baked flour products and pastries that occupied at least two meals every day. Nothing was said about the candies she indulged in several times per day, nor the soft drinks. Nothing was said about the wildly fluctuating blood sugars, poorly controlled by an oral diabetes agent. Thirty pounds of weight gain over the past 5 years with no exercise or physical activity? No comment here, too.

In short, Rose was the "graduate" of the conventional approach, as typically offered nationwide thousands of times a week. She was also the recipient of the insight of at least one alternative health practitioner, eager to reject conventional notions of how to achieve heart health.

So I then met her. She was experiencing chest pains every day, several times per day. Blood pressure over 200. At 5 ft, 3 inches, weight: 186 lbs.

Initial laboratory results:

HDL cholesterol 42 mg/dl
LDL 132 mg/dl
Triglycerides 263 mg/dl
Blood sugar 173 mg/dl


You can fill in the rest. In short, Rose was a disaster. Despite the attentions of several professionals from both the conventional as well as alternative camps, she was careening rapidly towards failure. She'd been given various crutches, Band-Aids, and salves, none of which resulted in any possibility of long-term relief from her aggressive disease.

My point: As I've said previously, all we want is truth. We want effective, rational approaches that yield real benefit. A stent? All that provides is temporary restoration of blood flow. Statin agents? They do indeed reduce LDL cholesterol. But what if Rose has 8, 9, or 10 other causes of heart disease unaffected by the statin drug? It will do little or nothing.

Nobody had addressed many of the root causes of Rose's disease: insulin resistance, high triglycerides, inactivity, obesity, hypertension (and identifying the reasons why her blood pressure was so high), vitamin D deficiency (virtually guarantted to be severe), junk foods including the ones known as "whole grains."

My message: Success in heart disease, as well as all aspects of health for that matter, doesn't necessarily have to come from an "alternative" approach, nor a "conventional" approach. It comes from applying what is truly effective, regardless of what label someone applied to it.

I would no sooner trust my health and life to an alternative health practitioner hawking unusual herbs and remedies than I would submit to a heart catheterization, three stents, followed by a statin drug. There's small benefit in both approaches, but none are the best. You've got to look elsewhere for that.


Copyright 2008 William Davis, MD

The JELIS Trial

The Japan eicosapentaenoic acid (EPA) Lipid Intervention Study (JELIS) is a clinical trial that all Track Your Plaquers should know about.

This enormous trial followed a simple design:

Japanese men, between 40-75 years, and Japanese postmenopausal women aged <75 years with total cholesterol 250 mg/dl or greater were enrolled. A total of 18,645 subjects (mean age, 61 years; 31% male) participated: 36% had hypertension, 15% had diabetes, and 20% had coronary disease (history of heart attack or heart procedure). Average starting total cholesterol 275 mg/dl; LDL 180 mg/dl. All participants were treated with pravastatin 10 mg/day or simvastatin 5 mg/day; approximately half also received the omega-3, EPA, 1800 mg/day, in addition to one of the statin drugs.

Treatment resulted in an average LDL reduction of 26% in all participants; the group taking EPA experienced an additional 10% reduction in triglycerides. All major cardiovascular events were tracked and tabulated, including sudden cardiac death, fatal or nonfatal myocardial infarction (MI), unstable angina pectoris, coronary artery bypass surgery, and coronary angioplasty.

After nearly five years, 3.5% of statin-only participants experienced an event; 2.8% of statin + EPA experienced an event. The (often misleading and frequently abused value) "relative reduction" was therefore 19%.

There are several features that make the JELIS trial interesting:

--There were an unusually low number of cardiovascular events in the entire group, lower than nearly all American and European trials of similar design. This likely points to the greater burden of atherosclerotic heart disease in the U.S. compared to Japan. Rates in comparable U.S.-based trials usually range from 6-14%, sometimes more.

--Both the participants without identified heart disease at enrollment and those with heart disease at enrollment obtained a similar magnitude of beneficial reduction in cardiovascular events.

--There was an unusual preponderance of women--69%--unlike most other trials of cardiovascular events. We might therefore argue that JELIS most conclusively showed that benefits of EPA are most confidently demonstrated for females.

--A fish oil preparation containing only EPA was used, rather than the usual EPA + DHA. There are discussions from some corners that argue that DHA is more important than EPA, e.g., algae sources. However, JELIS would argue that EPA does play a role. Is EPA with DHA better, worse, or no different? Unfortunately, there are insufficient data--large, randomized data like JELIS--to help us. Recall that GISSI Prevenzione used a combination of EPA and DHA, as have virtually all other trials examining the effects of fish oil. Also, keep in mind that the epidemiologic observations of the cardiovascular benefits of eating fish suggest that the naturally-sourced omega-3s--a combination of EPA and DHA--are associated with benefit.

--It's surprising that any difference at all was demonstrated, given the high intake of fish in the Japanese. In fact, blood levels of EPA in participants before taking EPA was five-fold higher than in western populations.


One potential difficulty: The study was funded by the manufacturer of the EPA preparation used, Mochida Pharmaceutical Company. We all know what that can do to results.

Nonetheless, the JELIS trial is a study that adds to the emerging wisdom in fish oil.


Copyright 2008 William Davis, MD

Omega-3 MUST be from fish oil

Despite my rants in this blog and elsewhere, at least once a day I'll have a patient say, "I cut back (or eliminated) my fish oil because I get my omega-3s from _______ (insert your choice of flaxseed oil, walnuts, yogurt, mayonnaise, bread, etc.)."

(See prior Heart Scan Blog post: Everything has omega-3.)

When I point out to them that the "omega-3s" in these products are not the same as the EPA and DHA from fish oil, they invariably declare, "But it says so here on the label: 'Contains 200 mg of omega-3 fatty acids'!"

Apparently, some of my colleagues have even endorsed this concept of replacing the omega-3s from fish oil with these "alternatives."

It's simply not true. The linolenic acid that is being labeled as omega-3, while it may indeed provide health benefits of its own, cannot replace the EPA and DHA that fish oil provides.

The most graphic example of the differences between the two classes of oils is in people with a condition called familial hypertriglyceridemia. People with this condition have triglyceride levels of 400, 600, even thousands of mg/dl--very high. Fish oil, usually providing EPA and DHA doses of 1800 mg per day and higher, reduce triglycerides dramatically. A person with a starting triglyceride level of, say, 900 mg/dl, may take 2400 mg of EPA and DHA from fish oil and triglycerides plummet to 150 mg/dl. This person then decides to replace fish oil with a linolenic acid source like flaxseed oil. Triglycerides? 900 mg/dl--no effect whatsoever.

Familial hypertriglyceridemia represents an exagerrated example of the differences between the two oils. Even if you don't have this genetic condition, the differences between the oils still apply.

EPA and DHA are activators of the enzyme, lipoprotein lipase, that accelerates clearance of triglycerides from the blood. Linolenic acid from flaxseed oil, walnuts, and other food sources does not. EPA and DHA block after-eating (post-prandial) accumulation of food by-products that can contribute to coronary and carotid plaque. Linolenic acid does not. EPA and DHA block platelets, reduce fibrinogen, and exert other healthy blood clot-inhibiting effects. Linolenic does not.

The 11,000-participant GISSI-Prevenzione Trial that showed 28% reduction in heart attack, 45% reduction in cardiovascular death with omega-3s used . . . fish oil.

The 18,000 participant JELIS trial that showed 19% reduction in cardiovascular events when omega-3s were added to statin therapy used . . . fish oil. (Actually, in JELIS, they used only EPA wtihout DHA.)

Linolenic acid is not a waste, however. It may exert anti-inflammatory benefits of its own, for instance. But it exerts none of the triglyceride-modifying effects of EPA or DHA.

EPA and DHA from fish oil and linolenic acid from foods each provide benefits in their own way. Ideally, you include both forms of oils--fish oil and linolenic acid sources--in your daily diet and obtain full benefit from each separate class. But they are not interchangeable.


Copyright 2008 William Davis, MD

Osteoporosis and coronary calcium

Several studies over the years have demonstrated a curious paradox:

People with more osteoporosis (thin bones) tend to be more likely to have coronary disease (heart attacks). They also tend to have higher heart scan scores (more coronary calcification as an index of atherosclerotic plaque).

People with more coronary disease and higher heart scan scores tend to have more osteoporosis.



In other words, regardless of which way you tackle the question--osteoporosis first or heart disease first--it leads to the same conclusion: Both conditions are somehow related.

I realize I harp an awful lot on this whole vitamin D issue. But, even after correcting the vitamin D blood levels of many hundreds of people, I remain enthusiastic as ever about the untapped potential of this fascinating factor.

So I couldn't resist showing this amazing comparison of how the long-term effect can be quite graphic.

The first scan is from a 46-year old man and shows normal coronary arteries without calcium and normal density of the vertebra (a common and reliable place to measure bone density).

























The second image is from a 79-year old man with both severe coronary calcification (and therefore severe coronary disease) and severe osteoporosis.
























It makes you wonder if the disordered metabolism of calcium through vitamin D deficiency allows transport of calcium away from bone and into coronaries. This has, however, been shown to not be the case. Instead, they are separate processes, each under local control, but sharing a common pathophysiology (causative factors).

An intriguing question: Would the 79-year old still look like the 46-year old had he begun increasing his vitamin D intake at, say, age 30?

About comment responses and moderation

Just a brief word about my responses to reader comments:

I appreciate the many often insightful and interesting reader comments I receive to the Heart Scan Blog. However, managing them and responding to them has simply become impossible, due to time demands.

I'm afraid that I am unable to answer questions seeking medical advice; this is for your doctor, who knows you and can diagnose and prescribe. I cannot.

I'm also unable to engage in lengthy debates; I've had commenters become very angry when I was unable to engage in lengthy conversations on some topic. Nor am I able to do Google or literature searches for commenters, or review studies, papers, or other materials.

I would urge any readers who wish to engage in in-depth discussions about these issues, talk about lipoproteins, heart disease reversal, etc. to do so on the Track Your Plaque Forums. Yes, it is a fee-for-membership website, a model that has become necessary to pay for the services we provide (not pay me).

I wish that I could answer all the concerns and questions that come my way, but it's simply physically impossible doing so while maintaining a full-time very busy cardiology practice, developing the Track Your Plaque website (which is becoming an enormous responsibility), publishing scientific data, maintaining hospital responsibilities, and spending time with my wife and family. We're all busy and I'm no different. I'm afraid that it's my responses to blog comments that I will have to sacrifice.

I invite commenters to continue to comment on these posts, as I've learned many new things by reading them and find them helpful feedback. And I do read them. Should an especially helpful comment be made, I will feature it in a new blog post, rather than respond directly.

"Flying in the fog"

I received this wonderful response to The Heart Scan Blog post Hammers and Nails:

I am 65 years old. I had a stent inserted in the "widow-maker" artery (80% blockage) a year ago. I had passed out a couple of times (heart rate dangerously low - 30s). I rode to the hospital in an ambulance. Tests revealed short LBBB episodes; mild mitral regurgitation, mild tricuspid regurgitation. Catherization showed 3 vessel CAD. I was told that a medicated stent was absolutely necessary given the situation; regardless, I have to accept that. A pacemaker was installed to prevent bradycardia and keeps heart rate from dropping below 60. I have 20% L distal main blockage and 90% lesion of the high first obtuse marginal at the takeoff. The right coronary had 60% posterior lateral branch stenosis.

Since then I have reduced TG from 360 to 60, LDL from 89 to 82 (although a few months ago it was in the mid-70s), and increased HDL from 30 to 46. I went from 265lbs to 190lbs and hope to eventually get to 180lb this Spring. I did it by progressing from walking to trotting (slow run) and dietstyle changes (low-GI veggies, fruits, etc.) .













On a recent visit the cardiologist said the the LDL needs to be 70 or below to "freeze" the 90% blockage and gave me a prescription for Lipitor. I asked if there were alternatives, like diet, supplements, etc. He admitted that he did not know about those alternative but did know Lipitor. When the only tool you have is a hammer then everything is a nail. I understand that the 90% blockage is important but will not take the Lipitor to achieve the 12 points reduction. Seems like an overkill.

I asked him if there was a way to evaluate my current condition. I was told there was no way. Basically, if I have no symptoms, good. If I have symptoms then it will have to be evaluated. Death could be the only symptom. I swear he was about to say bypass surgery ($$$$$$!) was inevitable. Something is wrong with this "fly-in-the-fog-and-hope-you-don't- hit-a-mountain" approach. Hope is not a strategy!

I am confident that I can reduce LDL to below 70 based on eliminating wheat-products in my diet plus increasing oat bran in my diet. I also take fish oil daily (EPA/DHA-2g). I am looking for a new cardiologist. I just recently purchased your book and find it very instructive. In the meantime I have an appointment with my primary care physician to discuss implementing the Track Your Plaque program. I realize that the one stent will skew the scan numbers but can be used as a baseline number.



Phenomenal weight loss! That alone has likely cut this man's risk in half. But is that it? Is the cardiologist correct--take Lipitor and hope for the best?

Of course not. There are many additional strategies to employ. Eliminating wheat from the diet is an excellent idea: HDL will skyrocket, triglycerides drop even further, small LDL will drop like a stone, blood sugar and blood pressure will drop. He will have more energy, get rid of afternoon energy slumps, sleep better.

He has already added fish oil. If his cardiologist did not mention this, I would say he was guilty of malpractice. The data supporting the addition of fish oil to the treatment program of anyone with heart disease is overhwelming. GISSI Prevenzione: 11,000 participants--28% reduction in heart attack, 45% reduction in death from heart attack. The Japanese JELIS trial of 18,645 participants--19% reduction in dangerous heart events. It's also clear that omega-3 fatty acids from fish oil also compound the benefits of statin agents, should this man choose to begin Lipitor.

Vitamin D brought to normal blood levels is his next "secret weapon" that will further boost his lipids and lipoproteins further into not just "normal" territory, but beyond belief. Even though we aim for 60-60-60 for LDL-HDL-triglycerides in the Track Your Plaque program, adding vitamin D can yield numbers you've never seen before. It's not uncommon, for instance, to see a 10 or 20 mg/dl jump in HDL.

Identify all other hidden causes of coronary plaque. If all the causes have not been fully identified, how can anyone hope to gain full control over coronary plaque growth?

Re: LDL cholesterol of 89 mg/dl at the start. Of course, this is a calculated value, not measured. Because HDL was low and triglycerides high at the start of his program, this means that true LDL--if actually measured--was probably more like 180 to 250 mg/dl, and it was probably nearly all small. So his cardiologist might have advised a helpful treatment, though for the wrong reasons.

Our reader has gone a long way on his own in creating his own prevention program. But there's yet more to do, particularly if the goal is reversal. It is shocking to me that a man like our reader, clearly articulate and motivated, gets virtually no advice beyond "take Lipitor" after all the procedural benefits have been reaped.

Even though one artery can no longer be "scored" due to the presence of the metallic stent, a heart scan would still be invaluable for long-term tracking purposes, just as we advocate in the Track Your Plaque program.



Copyright 2008 William Davis, MD

Goodbye, Dr. Jarvik

HeartWire, the news service of www.theheart.org, posted the following report:

Pfizer pulls Lipitor ads featuring Dr Robert Jarvik in HeartWire

New York, NY - After a series of questions and attacks over its choice of Dr Robert Jarvik to endorse Lipitor in a series of TV commercials, Pfizer has announced that it is withdrawing the ads. As previously reported by heartwire, Jarvik invented the first artificial heart, but he is not a cardiologist, nor does he hold a medical license—factors that drew criticism from detractors and made him and Pfizer a target of a US House Committee on Energy and Commerce investigation into celebrity endorsements in direct-to-consumer advertisements.

In a January 2008 statement, committee chair Rep John D Dingell (D-MI) observed: "Dr Jarvik's appearance in the ads could influence consumers into taking the medical advice of someone who may not be licensed to practice medicine in the United States. Americans with heart disease should make medical decisions based on consultations with their doctors, not on paid advertisements during a commercial break."

Complaints about Jarvik went up a notch this month when the latest ad in the series depicted the inventor rowing a racing scull across a lake, despite the fact that Jarvik himself does not row and the commercial used a body double.


This is typical pharmaceutical industry sleight-of-hand, now you see it, now you don't, that has come to define their policies. And this is just the stuff that comes to light because of some obvious blunders. We can only begin to imagine what sorts of other shenanigans have been swept under the rug, especially adverse effects of drugs that never made it to the light of publication.

Is this just another example of how direct-to-consumer advertising has backfired? I now have patient after patient tell me that they have been so overwhelmed and fed up with TV and magazine ads for drugs that they



Other media outlets have reported that Jarvik was guaranteed $1.35 million for the ads and that Pfizer spent $258 million on Lipitor advertisements between January 2006 and September 2007.

Hammers and nails

I'm sure you've heard the old saying that,

To a man with a hammer, everything looks like a nail.


It couldn't be truer than in heart procedures (the man with the hammer) and heart disease (the nail).

What does it take in 2008 to become an interventional cardiologist trained in all the techniques of angioplasty, stenting, intracoronary ultrasound, etc.? Start with your undergraduate degree (4 years), then medical school (another 4 years), then training in internal medicine (3 years), then general cardiology taining (3 years), then an additional year in interventional cardiology. Each step along the way also involves competing for these spaces, a process that requires much time, money, and sweat.

The total time investment is 15 years after high school. Many if not most college students graduate with debt. Pile on the substantial cost of medical school. Training after medical school pays a modest salary, enough for a single person. Many trainees by then have spouses and a family, would like to buy a house, have bills to pay. (I managed to buy my first house for $69,000 in Columbus, Ohio and paid my mortgage by sleeping only every other night and moonlighting on my off nights.)

By the time the interventional cardiologist-in-training finishes his/her 15 years, they are hungry for a hefty increase in income. After such a time and money investment, I do believe that there is at least some justification for generous income for the years of work involved.

Back to our hammer and nail metaphor. Not only do we now have a man or woman with a hammer, but a really expensive hammer that required a substantial amount of effort to obtain. Now, our hapless hammer-bearer is desperate to see everything in sight as a nail.

You're seen in consultation by this fresh interventional cardiologist in practice for only a few years. Guess what he/she advises? Go straight to the catheterization laboratory, of course. Throw in the fact that insurance reimbursement is most generous for heart procedures, far more than for consulting in the office, doing a stress test, or other simpler, non-invasive tests, and the incentives are clear.

The system, you see, is set up to follow such a path. The path to the cath lab is heavily incentivized, paths in the other direction discouraged, disparaged, or just ignored.

My message: Don't get nailed.

What is abnormal?

What is abnormal?

You'd think that the answer would be easy and straightforward.

However, consider these instances of medical findings that I have witnessed fall repeatedly into the "normal" category:

Diameter of the thoracic aorta: 4.5 cm

Mild coronary plaque by heart catheterization

Carotid plaque of 30-50%


Why isn't a thoracic aorta (the big artery in your chest) of 4.5 cm normal? Because it can be expected to increase in diameter by about 2.5 mm (0.25 cm) per year. Even at its current diameter, it means that stroke risk is greater, since enlarged aortas are diseased aortas that commonly accumulate atherosclerotic plaque with potential to fragment and shower debris to the brain. It means that high blood pressure and/or cholesterol/lipoprotein abnormalities have been uncorrected for years that have allowed the aorta to enlarge.

How about "mild coronary plaque"? Followers of the Track Your Plaque program already know the answer to this one. Mild plaque does not mean mild risk. In fact, most plaques that cause heart attack are mild plaques, not severe blockages. While severe blockages can provide symptom warning and are detected by stress tests, it's the mild blockages that rupture without symptom warning and cause heart attack. So "mild coronary plaque" is no less dangerous than severe coronary plaque.

Likewise, carotid plaque of 30-50%, while it doesn't justify surgery, can grow within just a few years to a severity that allows it to fragment and shower debris to the brain, i.e., a stroke. As with the enlarged aorta, it means that multiple causes of carotid plaque are likely active, including high blood pressure and cholesterol or lipoprotein abnormalities.

Then why would any of these findings be labeled "normal"?

Simple. In the minds of many physicians, if a condition doesn't pose immediate risk, or if it doesn't qualify for surgical "correction," then it is labeled "normal" or "mild."

Thus, an aorta of 4.5 cm cannot justify surgical replacement until it achieves a diameter of 5.5 cm. It is therefore labeled "normal."

"Mild coronary plaque" does not justify insertion of stents or performance of bypass surgery. It must therefore be "normal."

Carotid plaque over 70% is surgically removed, but not 30-50%. 30-50% is therefore "normal."

The tragedy is that many "normal" or "mild" findings, if cast in the proper light, could lead to corrective strategies that could prevent danger long-term or keep surgery from becoming necessary.

The enlarged aorta, for instance, could be stopped and an aneurysm (defined as 5.5 cm or greater) could be prevented, along with dramatically reducing risk for stroke. Carotid plaque, more so than coronary plaque, is a controllable and manipulable condition that should trigger a program of prevention and reversal. Instead, it usually generates advice to have another ultrasound in a year to see if it has yet achieved severity sufficient to justify surgery.

Of course, "mild coronary plaque" is the reason for the Track Your Plaque approach, a chance to seize control over this disease years or decades before procedures are necessary and reduce danger now, not years from now.


Copyright 2008 William Davis, MD

Niacin and hydration

Many people know about niacin's curious effect of the "hot flush," a feeling of warmth that covers the chest and neck, occasionally the entire body.

However, many people are unaware of the fact that hydration can block this effect. In fact, many people who were not advised of this will come to the office describing miserable experiences with niacin--hot flushes that last for hours, intolerable itching, etc.--only to experience little or none of these effects with generous hydration.

The vast majority of the time, two 8-12 oz glasses of water when the hot flush occurs will eliminate the flush within a few minutes.

Sometimes, the hot flush will occur many hours after taking niacin. Nine times out of ten, this delayed effect is also due to poor hydration. For instance, you might be engrossed in your work and forget to keep up with fluid demands. Or, it may be warm and you've lost fluids through sweating. That's when you begin to feel the hot flush creep up on you.

The cure: Lots of water. In this situation, in which you have allowed dehydration to develop, it may require more than two big glasses. Relief from the flush may also take more time, but it still works nearly every time.

On those rare occasions when water by itself is insufficient, then an adult (325 mg), uncoated aspirin or 200 mg ibuprofen can also be used to accelerate relief.

Why go to some much bother? Well, niacin remains the best agent we have for reduction of small LDL, raising HDL (although vitamin D is proving to be a powerful competitor in this arena), and reducing lipoprotein(a). How much do statin drugs contribute to these effects? Very little, if at all.

Several drug manufacturers are also working on "antidotes" to the hot flush effect of niacin that will be packaged within the niacin tablet. Naturally, it will also boost the cost up many times higher.

In the meantime, if or when you experience the niacin hot flush, just think: Put out the "fire" with plenty of water.