The Track Your Plaque “Rule of 60”

The Track Your Plaque recommended targets for conventional lipids (i.e., LDL, HDL, triglycerides) are LDL 60 mg/dl, HDL 60 mg/dl, and triglycerides 60 mg/dl: 60-60-60.

Not only is this set of values easy to remember—60-60-60—but is grounded in science and the results of clinical trials.

LDL 60 mg/dl
The LDL target is based on experiences such as that of the Reversal Trial, the PROVE-IT Trial, and the Asteroid Trial, all of which showed that LDL cholesterol values in the range of 60 mg/dl dramatically enhance the likelihood of stopping plaque growth or achieving regression, reducing risk of heart attack more than more lenient LDL targets.


HDL 60 mg/dl
Achieving HDL cholesterol of 60 mg/dl is not as well grounded as LDL targets, mostly because increasing HDL is more difficult. There’s also no tremendously profitable way to raise HDL, as there is for reducing LDL (statin drugs). But epidemiologic observations strongly suggest that HDL of 60 mg/dl provides maximum control over both coronary plaque growth, as well as slashing rates of heart attack. Numerous smaller trials have borne this phenomenon out.


Triglycerides 60 mg/dl
Triglycerides of 60 mg/dl is based principally on studies that have shown a virtual elimination of abnormal lipoproteins, especially small LDL, when this value is achieved. Reduction of triglycerides is an effective means to reduce hidden lipoproteins like small LDL and VLDL. Triglycerides in the conventionally acceptable range of 100-150 mg/dl can be associated with dramatic abnormalities of lipoproteins.


Thus, the Track Your Plaque “Rule of 60”. In our day to day experience of trying to stamp out plaque growth from its terrifyingly rapid 30% per year, or reversing it—-dropping your heart scan score—-the Rule of 60 has held up time and again. Getting your lipids to 60 mg/dl does not guarantee that plaque growth stops, but it appears to be a necessary requirement that tips the scales heavily in your favor.

Those of you who’ve discussed lipid targets with your doctor will quickly recognize that the Track Your Plaque targets appear laughably ambitious, perhaps unnecessary. Recall that your doctor likely has no idea of what coronary plaque regression means. He/she likely conforms to the lax targets set by the National Cholesterol Education Panel (NCEP). (These targets depend on a number of factors such as whether you’re diabetic, sex, risk factors, etc.) Based on trial experiences like the few mentioned above, as well as my experience with purposeful coronary plaque reversal, the lipid guidelines as advocated by NCEP guarantee heart disease. Let me emphasize that again: Follow the guidelines set by the NCEP for your doctor to follow, and progression of heart disease is a virtual certainty. At best, it may slow growth of plaque and delay your heart attack or bypass surgery, but it will not stop it.

Now, that point made, let me make another: Just knowing about the targets and even becoming a member of the Track Your Plaque program does not mean that your lipids with automatically go to 60-60-60. We’ve actually had an occasional person tell us that they were disappointed that, by becoming Members, why hadn’t their lipids gone to 60-60-60?

Knowing that the 60-60-60 targets provide real advantage is not the same as actually achieving them.

A little bit of fish oil


The British National Health Service (NHS) has announced that, in light of the substantial data documenting that omega-3 fatty acid intake from fish reduces likelihood of cardiovascular events by around 40%, that Brits discharged from hospital following a heart attack should be "prescribed" 1000 mg of prescription fish oil per day.

Hardly a revolutionary concept. Part of the timidity of the British NHS seems to relate to the potential cost to the government, since apparently much of the cost will be borne by the government-subsidized health system.

But prescription fish oil? Why prescription fish oil? Prescription Omacor, one capsule per day, costs around $70 (U.S.) per month. If I go to Sam's Club the same quantity of omega-3 fatty acids (in three capsules) will cost around $2.50. That's less than 5% of the cost of the prescription form.

Omacor is clearly more concentrated. But is the prescription form better--more effective, more purified, less contaminated, etc.? I have seen no independent verification of this. Of course, manufacturers make all sorts of claims. The only independent, unbiased testing I'm aware of comes from organizations like Consumer Reports and www.consumerlabs.com. Omacor has not been compared to non-prescription fish oil in any of their analyses. Head-to-head comparison of Omacor to nutritional supplement fish oil is unlikely to come from Solvay, the manufacturer of Omacor. Drug companies powerfully resist head-to-head comparisons, fearing it will not play out in their favor. Let the public remain ignorant and hope marketing conquers all.

Why would the NHS only recommend eating fish and prescription fish oil? I don't know, but it smells awfully fishy to me. As soon as an opportunity for profit is built into a treatment, all of a sudden it gains endorsement. Perhaps lobbying by those parties with potential for profit drove the process.

Nonetheless, despite the filthy politics and under-the-table dealings, some good comes out of the NHS's action: broader recognition of the power of fish oil. Perhaps when a British patient or an American patient gets discharged with a prescription for Omacor, the patient will take the initiative and go to the health food store instead and save him (or his insurer) $67.50 per month.

For your coronary plaque control program and control and/or reversal of your heart scan score, we start at 4000 mg per day of standard fish oil, providing 1200 mg per day of omega-3 oils. This amount as a nutritional supplement costs only a few dollars a month. And you have the satisfaction of not only taking a powerful step for your health, but also not enriching the overflowing pockets of drug companies.

AHA: Doctors don't have time for prevention

Doctors "don't have enough time to educate their patients and to stop and think about what measures the patient really needs," says Dr. Raymond Gibbons, new head of the American Heart Association.

Dr. Gibbons highlighted how the system reimburses generously for performing procedures, but reimburses relatively little (often just a few dollars) for providing preventive counseling. He claims to have several ideas for solutions.

Good for Dr. Gibbons. There's no doubt that the lack of truly effective preventive information and counseling is a systemic, built-in flaw in the current medical environment. It is especially true in heart disease.

Another problem: "If a doctor didn't say it, it must not be true." That's the attitude of many of my colleagues. Despite their broad and systematic failure to provide preventive counseling, most physicians (my colleagues the cardiologists especially) pooh-pooh information that comes from other sources. Yet, it's my prediction that much of healthcare will go the way of optometry--direct access to care, often delivered in non-healthcare settings like a store or mall. People are hungry for truly self-empowering health information. Too many physicians can't or won't provide it. You've got to turn elsewhere for it.

That's one of the main reasons I set up the Track Your Plaque program. It's direct access to self-empowering information. A flaw: You still require the assistance of a physician to obtain lab values, lipoproteins, and to monitor certain treatments (e.g., niacin at higher doses). If I knew of a way around this, I'd tell you. But right now I don't. We remain constrained by legal and moral obligations.

Nonetheless, phenomena like CT heart scanning and the Track Your Plaque program are just a taste of things to come.

Confusion about Lp(a)

Since the recent reader question about Lp(a), I've had several other instances of confusion over Lp(a).

To help you navigate through some of the often confusing issues behind this complex genetic abnormality, here are some common sense rules to follow. When you ask your doctor to draw a Lp(a), try to be certain that:

--the same laboratory is always used. Just going from lab to lab can account for huge variation in Lp(a). As standardization proceeds internationally, this will be become less important. But in 2006, it's still an issue.

--you and your doctor resist the temptation to check Lp(a) frequently. I saw a patient recently who was having Lp(a) levels nearly every month. This is pointless. Lp(a) changes very slowly. Checking it frequently will not allow any treatment to be fully reflected. All you'll observe is random variation that can be frustrating. We wait at least 6 months before re-checking after a new treatment is introduced.

If you have a choice, I would recommend you opt for the measure provided by Liposcience (NMR). The technique they use is a particle count measure, rather than a weight-based measure. This may be more accurate, particularly when Lp(a) is small.

Lp(a) remains among the more difficult patterns to understand and correct. Don't be surprised if you encounter a lot of confusion from your doctor, as well. You may end up providing much of his/her education.

Calculus of the cardiologist

I call this the "calculus of the cardiologist":

Heart procedures = big money

More procedures = more big money

You do the math. If you do more procedures, you get more money.
What if your patients don't need more procedures? That's easy. You lower the bar on reasons to do procedures. You scare the pants off people and lead them to think that all heart disease or questions about heart disease are potentially life-threatening. You could even appear to be doing the patient a big favor. "My Lord! This is potentially dangerous. We need to perform a procedure without delay!"

There are incentives beyond direct cash payment. A patient of mine today showed me a memo to employees in his company that showed why certain hospitals are targeted for care. The criteria for choosing centers was based on number of procedures performed. In other words, the more procedures performed at a hospital, the more procedures will be directed there. Of course, this makes sense at some level. More procedures can also mean greater skill.

But have we lost sight of the fact that the mission is not more procedures and more money, but to get rid of a disease? If the intensity of effort devoted to heart procedures were re-directed to early detection, prevention, and reversal of disease, we'd have half the hospitals we now have. We'd also chop a huge chunk out of the national healthcare budget.

Lipoprotein(a) treatment alternatives

A question from a reader:


Two years ago, my doctor recommended a comprehensive lipid screening because both of my parents had heart disease. My only blood component way out of line was LP (a) [lipoprotein(a)]. It was 130. According to the lab that conducted the screening, Berkeley Heart Lab, a level above 30 should be cause for concern. I was stunned that mine was more than quadruple the danger level.

I began taking two grams [2000 mg] of niacin a day in addition to the Lipitor I was already taking. The next reading, a few months later, was 87. Over a period of about 18 months, I had a total of four readings from Berkley Heart Lab. My LP (a) fluctuated in the 80-130 range – still way above normal. My doctor said there was little else I could do to control it.

That doctor has since retired. I now see another doctor who uses a different lab. My first LP (a) reading with him a few months ago was 17, which is normal. I am still taking the same amount of niacin and Lipitor and I can’t think of anything that would account for the huge discrepancy. I’m going to have another test again soon.

Is one of the labs giving erroneous readings? If so, how can I tell which? If Berkeley Heart Lab is correct, is there anything I can do about my increased coronary risk due to high LP (a)?

Tom D.

Tom's frustration on the variation of Lp(a) is due to the fact that laboratories run the Lp(a) test by several different techniques and will generate tremendous variation in values. The key is to stick to the same measure over and over from the same lab, else you'll be terribly confused and frustrated. Tom essentially should ignore the value obtained that was unexpectedly low.

Another issue: Lp(a) is a turtle. It responds very slowly. In fact, we rarely check it more than once or twice a year. Check it too soon after a treatment change and it won't fully reflect the effect. You've got to wait at least several months before re-checking.

How about treatment alternatives? They are:

--More niacin. Not my favorite choice, since niacin >2000 mg per day begins to generate more side-effects, but it is a choice. You can go to 4000-5000 per day, but only with your doctor's supervision due to liver effects.

--Testosterone for males. We use topical testosterone from Women's International Pharmacy in Madison, Wisconson. Prescription patches like Testim are also effective.

--Estrogen for females. This is less "clean" than testosterone, introducing questions about endometrial and breast cancer risk, but it is a choice.

--DHEA--A small effect but every little bit can help. We use 25-50 mg per day, depending on blood levels and only if you're 45 years old or older.

--l-carnitine--In my experience, a small effect. It requires 2000 mg per day, which is expensive. Sometimes, an expected large effect develops, so it's worth a try if it fits in your budget.

--Fibrates--These are the drugs Tricor and Lopid. I don't like these agents very much because I think they're weak, including the effect on Lp(a) reduction. But they are choices for you and your doctor.

Lastly, you can simply be guided by your heart scan score. For example, if Tom's initial heart scan score is 200, and he continues his current program and one year later his score is 300, then alternative treatments are worth considering. But what if Tom's score is 189--he's regressed his coronary plaque. Then, who cares what his Lp(a) is?

Another issue to keep in mind is that, in the presence of Lp(a), keeping LDL to very low numbers (e.g., 60 mg/dl) may added value in preventing coronary plaque growth.

Trapped in a low-fat world

If you would like to...

--Reduce (good) HDL

--Raise triglycerides, sometimes by hundreds of points

--Raise blood sugar into the pre-diabetic range

--Raise blood pressure

--Accelerate coronary plaque growth

then go on a low-fat diet like the one promoted by long-time super low-fat advocate, Dr. Dean Ornish. Every day I have to educate patients that a low-fat diet as advocated by Dr. Ornish is a destructive, counter-productive process that makes coronary plaque grow and increases your heart scan score.

If you want to gain control over coronary plaque, do not follow the Ornish program or anything resembling it. The Ornish program is a dead end.

Instead, the crucial components of a healthy diet for plaque control are:

--Low saturated and hydrogenated fat, but not low all fats.

--High monounsaturated and omega-3 fats

--Low glycemic index (i.e., slow sugar release)

--High fiber

That simple. An excellent program to put these limits to practical use is the South Beach Diet. Or, follow the more detailed guidelines on the Track Your Plaque website (open content section).

Blame the niacin

Despite the fact that niacin is:

1) A vitamin--vitamin B3

2) One of the oldest cholesterol-reducing agents around with a long-standing track record of effectiveness and safety

3) Available as a prescription drug as well as a variety of "nutritional supplements"

most physicians remains shockingly unaware of its benefits, effects, and side-effects. Most, in fact, are either ignorant or frightened of advising their patients on niacin use. As a result, I commonly have to tell my patients to resume the niacin that their primary care physician has (wrongly) stopped because of itchy feet, grumpiness, groin rash, urinary tract infections, nightmares, diarrhea, hair loss, runny nose, etc. All of these are REAL reasons doctors have advised patients to stop niacin (though none were actually due to niacin).

Is niacin really that troublesome? No, it's not. In fact, if used properly, it's among the most effective and safe tools available for correction of low HDL, small LDL and other triglyceride-containing lipoproteins, lipoprotein(a), and dramatic reduction of heart attack risk. If added to a statin agent, the heart attack risk reduction can approach 90%.

Statins are just too easy for doctors to prescribe. Niacin, on the other hand, requires a good 15-20 minutes to describe how to use it. It could generate an occasional phone call from a patient who struggles with the annoying but largely harmless and temporary "hot-flush" feeling, a lot like a hot blush. Given a choice, most doctors would simply choose not to be bothered. For this reason, I'll commonly see many, many people with uncorrected low HDLs and other patterns.

Have a serious discussion and press for confident answers if you find your doctor reflexively telling you that the wart on your thumb should be blamed on niacin.

Here are the steps we advise that really make taking niacin easy and tolerable:

1) Take with dinner.

2) Take with 2 extra glasses of water. If you experience the hot-flush later on, drink an additional 2 8-12 oz glasses of water i.e., a total of 16-24 oz). Extra hydration is extremely effective for blocking the hot-flush.

3) Take a 325 mg, uncoated aspirin. This is only necessary in the beginning or with any increase in dose, rarely chronically for any length of time.


This is not to say that there aren't occasional people who are truly and genuinely intolerant to niacin. It does happen. But those people are a small minority, less than 5% of people in my experience. Niacin is far more effective and safe than most physicians would have you believe.

Eat fish three times a day

Patients commonly ask, "Why can't I get vitamin D from food? I drink milk and eat fish."

They're absolutely right: both vitamin D and some oily fish contain vitamin D. However, it's a matter of quantity. An 8 oz. glass of milk contains 100 units of vitamin D (at least it's supposed to; this is not always true). A serving of oily fish like salmon or herring may contain up to 400 units. Thus, if you ate fish three times a day like the Eskimos or the Inuit, you might obtain sufficient vitamin D to prevent the broad and alarming spectrum of phenomena associated with deficiency.

I suspect that most people don't want to eat fish three times a day, nor drink the 20 to 50 glasses of milk per day that would be required to obtain a truly healthy quantity of vitamin D.

The vocal and outspoken Dr. John Cannell of the Vitamin D Council (www.vitamindcouncil.com) has written eloquently on the potential relationship between influenza and vitamin D deficiency. He and his co-authors on a recently published paper point out that the peculiar and unexplained seasonality of influenza corresponds to vitamin D levels. Read his eloquent discussion in Medical News Today at http://www.medicalnewstoday.com/medicalnews.php?newsid=51913.

In the article, Dr. Cannell explains:

"The vitamin D steroid hormone system has always had its origins in the skin, not in the mouth. Until quite recently, when dermatologists and governments began warning us about the dangers of sunlight, humans made enormous quantities of vitamin D where humans have always made it, where naked skin meets the ultraviolet B radiation of sunlight.
We just cannot get adequate amounts of vitamin D from our diet. If we don't expose ourselves to ultraviolet light, we must get vitamin D from dietary supplements...Today, most humans only make about a thousand units of vitamin D a day from sun exposure; many people, such as the elderly or African Americans, make much less than that. How much did humans normally make? A single, twenty-minute, full body exposure to summer sun will trigger the delivery of 20,000 units of vitamin D into the circulation of most people within 48 hours. Twenty thousand units, that's the single most important fact about vitamin D. Compare that to the 100 units you get from a glass of milk, or the several hundred daily units the U.S. government recommend as “Adequate Intake.” It's what we call an “order of magnitude” difference.

"Humans evolved naked in sub-equatorial Africa, where the sun shines directly overhead much of the year and where our species must have obtained tens of thousands of units of vitamin D every day, in spite of our skin developing heavy melanin concentrations (racial pigmentation) for protecting the deeper layers of the skin. Even after humans migrated to temperate latitudes, where our skin rapidly lightened to allow for more rapid vitamin D production, humans worked outdoors. However, in the last three hundred years, we began to work indoors; in the last one hundred years, we began to travel inside cars; in the last several decades, we began to lather on sunblock and consciously avoid sunlight. All of these things lower vitamin D blood levels. The inescapable conclusion is that vitamin D levels in modern humans are not just low - they are aberrantly low."


Like Dr. Cannell, I am absolutely convinced that vitamin D deficiency plays an important role in a number of illnesses, including coronary disease. The more we mind our patients/participants vitamin D status (blood levels of 25-OH-vitamin D3), the more easily we gain control over LDL cholesterol, pre-diabetic patterns, blood pressure, blood sugar, and coronary plaque. In fact, I am becoming rapidly convinced that vitamin D deficiency is an extremely important coronary risk factor.

Because I live in Wisconsin (bbrrrrr!) where seeing the sun is a cause for celebration and sun exposure is possible three months a year, I take 6000 units per day vitamin D. This is the amount necessary to raise my blood levels into the true, physiologic range of 50-70 ng/ml. My wife takes 2000 units per day, and each of my kids takes 1000 units per day, though I believe that my 14-year old son (my size now) should take more. We'll judge by blood levels.

If there is a little-known secret to reducing heart scan scores, vitamin D is that "secret".

To read more from Dr. Cannell or to subscribe to his free and very informative newsletter, go to Vitamin D Council

What if I had a cure for coronary disease?

If I had a cure for coronary disease, what would it look like? What would constitute cure? Would you recognize it if I showed it to you?

In the strictest sense, "cure" means an absolute elimination of any sign of coronary plaque, as well as elimination of any and all dangers associated with coronary disease. It would also mean elimination of the factors that created coronary atherosclerotic plaque in the first place.

In a more practical sense, you could argue that "cure" means a reduction of the amount of material that constitute coronary disease along with a dramatic reduction of the associated risks (i.e., heart attack).

You might call this second, more lax definition "regression" or "reversal".

Is "cure" in the strictest sense possible? No, not to my knowledge in 2006. Yes, there are many (kooks) who claim this is possible, but there's no objective evidence of this occurring.

Regression, or reversal, however, is indeed possible. In fact, I've seen it countless times following the participants in the Track Your Plaque program. If your heart scan score goes from 1000 (a bad score with high risk for heart attack) to 750, you've experienced a large reduction in the amount of atherosclerotic plaque that is behind coronary disease. You've also reduced your risk of an "event" like heart attack to near zero (provided you remain on the program that achieved regression in the first place).

Unfortunately, with present technology regression or reversal does not mean that the original causes of coornary plaque are eliminated. They're just controlled. Fish oil, for example, powerfully reduces triglyceride-containing lipoproteins that trigger coronary plaque growth. But if you stop fish oil, the evil lipoproteins come right back and start injuring your coronaries, causing more plaque growth.

The Track Your Plaque program is the closest thing I know of to a "cure" for coronary disease, that is, "cure" in the sense of regression or reversal. Perhaps in future we'll have a "cure" in the strict sense. Until now, this program is the best there is.

The battle for natural hormones

The battle for preservation of availability of compounded natural hormones goes on.

It started with pharmaceutical manufacturer, Wyeth, who petitioned the FDA to disallow the mixing of pharmaceuticals, especially natural human hormones, by specially trained pharmacists at what are called "compounding pharmacies." These are pharmacies that have special equipment and where trained pharmacists can mix up specific preparations for dispensing. These are available by prescription.

For instance, I have been prescribing natural human testosterone and progesterone for nearly 10 years. I have found service to be excellent, with lots of learning materials provided to patients by the pharmacy. The pharmacists I've spoken to have been courteous and knowledgeable. Compounded hormones are also shockingly less expensive. While a testosterone patch from a pharmaceutical company costs around $4.00 per day, the same quantity of testosterone cream formulated by a compouding pharmacy costs around $0.50 per day--87.5% less.

Wyeth hides behind a smoke screen of concern over quality. But the price differences tells the entire story: they want to eliminate the inexpensive competition and hold us all hostage to the far more expensive, often inferior products that they produce. They'd sooner force a woman to use horse-derived Premarin than to allow her access to human estrogens and progesterone.

To me, this is an outrageous affront to our freedom of choice, both as consumers as well as a physician. If you feel as strongly as I do about opposing the unfair and bullying ways of Wyeth Pharmaceuticals and the FDA, the P2C2 association of compounding pharmacists makes writing a letter to your Senator easy by going to

http://iacprx.convio.net/site/PageServer?pagename=P2C2

Just enter your info and personalize the comments, and the e-mails will be generated for you.

Lipitor and memory

At first, I was skeptical. A book from a nutty author and physician named Duane Graveline kept on coming up in conversations with patients. His book, Lipitor: Thief of Memory , details his personal experience with dramatic changes in memory and thought while taking Lipitor.



Now this is a drug that I've seen used thousands of times. But I've now seen about a dozen people who have had distinct struggles with memory and clarity of thinking while taking Lipitor. Most took doses of 40 mg per day or more, though an occasional person takes as little as 10 mg. The association seems to be undeniable, since it improves after two weeks off the drug, recurs when resumed. Just today, I saw two people where this effect may be an issue.

Curiously, I've not seen it with any other statin agent. Unfortunately, uncovering any scientific data on the issue is a hopeless quest. Either it's very uncommon or, worse, the data has been suppressed.

Any way, I believe that Dr. Graveline was right: Lipitor, in a small number of people, does indeed seem to exert real detrimental effects on the mind.

If you take Lipitor, should you stop it in fear of long-term effects on your mental capacity? I think it's premature to toss the drug out based on this relatively uncommon relationship. This particular effect is likely to be idiosyncratic, i.e., peculiar to an occasional person but does not seem to apply to the majority, probably by some quirk of metabolism or penetrability of the barrier between the blood and nervous system tissue.

If, however, you feel that your thinking and memory have deteriorated on the drug, please speak to your doctor.

EKG's and heart disease


How helpful are EKG's for detecting hidden heart disease?

I pose this question because several patients asked this question just this week. It's also a frequent point of confusion and misperception.

Your EKG is nothing more than an expression of the surface electrical activity emitted by heart muscle activity. Multiple (12) leads are attached to the body simply to provide various "views" of this electical activity. EKG, or sometimes "ECG", is short for "electrocardiogram".

What modifies this surface electrical activity? Anything that modifies the electrical activity within the heart itself, or interferes with the detection of the activity. An old heart attack modifies the patterns of electrical conduction in the heart and that can change your EKG. An ongoing heart heart attack likewise. High blood pressure commonly creates changes in the EKG, as does lung disease. A bellyache can change your EKG, as can a stroke. (These non-heart-related phenomena probably are often due to changes in autonomic, or "automatic," nervous system activity.) The heart generates electrical activity in a predictable sequence that generates the heart beat, or "rhythm". EKG's are useful for monitoring heart rhythm, also.

Does having plaque in your coronary arteries have any effect on the EKG? None whatsoever, unless plaque rupture caused heart attack or is about to cause heart attack. So, you can have a horrendous CT heart scan score of, say, 3000, yet maintain a perfectly normal EKG, as long as the heart muscle is normal.

Then why bother with these iffy tests? They are indeed useful to diagnose the cause of active symptoms. For instance, go to the ER with chest pain and an EKG could show changes suggesting that the chest pain is a heart attack. EKG's are also useful for future comparison. Any change in EKG can suggest certain things, like new heart rhythm disturbances unrelated to coronary plaque.

Think of your EKG as just like buying a used car. Say I'm trying to sell you my 1999 Buick Century. It looks pretty good from the outside and I tell you that it has 70,000 miles and runs well. You ask to open the hood, look in the interior and take it out for a drive. I tell you no, you can't do that.

Would you buy the car? Of course you wouldn't. You were permitted only a very superficial examination of the car. You have no idea what's going on inside. Just because the paint job looks brand new doesn't mean the engine and transmission are good.

The same with your EKG: It's a superficial look at one aspect of this used car called your heart. If the EKG is normal, that's good, just like a good exterior on the Buick. But you cannot assume that the heart is otherwise normal.

View the EKG as a simple, superficial test that can only provide minimal reassurance, no matter how often you have it done.

A new Track Your Plaque record

Neal, a 40-year old school principal, and his young wife were terrified on learning of his CT heart scan score of 339, a concerningly high score for any age, particularly age 40.

To make matters worse, all of Neal's plaque was located in the critical left mainstem coronary artery, the shared stem of two of the three coronary arteries. A heart attack in this location is instantly fatal.

So, it was especially gratifying that Neal has set the Track Your Plaque record for largest magnitude of plaque reversal: 51% in his first year.

Studies that show a reduction in heart attack make the news. They talk about 1, 2, up to 6% regression, all achieved with high doses of statin drugs. Yet we are seeing huge, extraordinary quantities of heart disease reversal that haven't yet made headlines, amounts that far exceed those featured in the news. We should be encouraged by experiences like Neal's.

Watch for the upcoming Track Your Plaque newsletter for more details on Neal's story--how he came to the program, how he accomplished this huge effect, and why his experience was such a success. If you haven't yet subscribed, go to the www.cureality.com homepage and click on the upper right hand corner.

The Plavix Scam

Periodically, I'll see a flurry of TV ads for Plavix. It comes with a polished computer-animated cartoon that shows how platelets clump and form a blood clot, causing heart attack.

Imagine there's a pile of oil-soaked rags in a corner of your garage. I come by and tell you to get a good fire extinguisher to keep next to the rag pile in case they spontaneously ignite.

Does that make sense to you?

Wouldn't it be better to get rid of the oily rags and forget about the fire extinguisher?

Plavix is the fire extinguisher. The oil rags are your coronary plaque. The solution is to gain control over plaque behavior. Unfortunately, the TV ads (intentionally, I suspect) give the impression that blood clots just form out of the blue for no reason. Of course that's not true. It requires active, growing, inflamed atheroslcerotic plaque that ruptures, uncovering the "angry" and platelet-adhering material underneath the thin covering or endothelial lining.

Urging everybody to take Plavix is absurd. The TV ads urge many people who have no business taking the drug to take it. There are, without a doubt, groups of people who are better off taking Plavix and aspirin: people who are in the midst of heart attack, people who have unstable plaque, people with recent stents or bypass. Perhaps people at high risk for plaque rupture, e.g., extensive coronary plaque that has continued to grow.

These tactics are consistent with the experiences I've had with the sales representatives from the company (when I used to actually talk to sales reps; my office is now barred from them). The reps very aggressively would urge me to consider having everyone take Plavix. No kidding.


For us, i.e., for people who just have a heart scan score but interested in engaging in a powerful program of prevention and reversal, Plavix rarely provides any advantage. The answer is, just like our oily rag analogy, control the plaque, not put out the fire.

Lipoprotein(a) and small LDL

You won't find a lot of scientific validation for this, but it is my firm impression that small LDL, by some crazy means, has the capacity to "turn on" or "turn off" lipoprotein(a), Lp(a).

Recall that Lp(a) is a specific genetic trait, passed to us (if you have it) by mother or father. It falsely elevates LDL cholesterol and escalates heart disease risk more than just about any other known abnormality.

A frequent hint that Lp(a) might be present is a comment I hear often from patients: "My doctor said statin cholesterol drugs don't work for me. I tried them all and my cholesterol won't go down." Or, the result was substantially less than expected. That's because, when Lp(a) is lurking in your cholesterol value, it is unaffected by the statins.

It's been my in-the-trenches observation that, the more fully expressed the small LDL pattern becomes, the worse the Lp(a) behaves. In other words, if small LDL is suppressed effectively, Lp(a) doesn't seem to carry the same dangers as in someone who has plenty of small LDL. I don't know why this is. (I expect that the answer will come from someone like Dr. Marcovina at Stanford, who is at the forefront of Lp(a) structural research. Lp(a) is a complex molecule with several components. How and why it interacts with other particles remains a mystery.)

There are a little bit of data to confirm this. The Quebec Cardiovascular Study has presented some data to this effect, that the combination of small LDL particles and Lp(a) are a particularly lethal combination. We are trying to correlate our data from a CT heart score perspective to discern any statistical relationships.

This raises a very important therapeutic issue if you have Lp(a): the worst thing you can do if you have Lp(a) is become overweight. Excess abdominal fat is a huge trigger to create small LDL particles. Even though being overweight itself has no effect on the measured level of Lp(a), it activates small LDL which, in turn, throws gasoline on the Lp(a) fire.

If you have Lp(a), stay skinny.

Optimal medical therapy

I was re-reading some of the details behind the recently announced COURAGE Trial comparing angioplasty/stent in 1100 people compared to "optimal" medical therapy in another 1100. You'll recall that no difference was found.

In particular, over approximately 5 years, 20% of participants in each group died, experienced heart attacks, or strokes. Of those treated with "timal" medical therapy, 32% ended up getting a procedure like stents or bypass anyway due to deteriorating symptoms.

What is "optimal" medical therapy? I bring this up again because the study investigators in COURAGE, as well as in similar trials, say this with a straight face. Optimal medical therapy means aspirin and/or Plavix (the anti-platelet, aspirin-like blood thinner); "aggressive" statin drug therapy to reduce LDL cholesterol to 60-85 mg/dl; and "anti-ischemic" therapy (that reduces angina and the phenomena of poor coronary blood flow) using nitroglycerin preparations, beta blockers, and other drugs.

I do give credit to the investigators for having the courage to perform this trial in a world hell bent on doing procedures and still reporting the neutral outcome. But the notion of "optimal" medical therapy begs for comment.

Indeed, this is regarded as optimal by most practitioners. Some would even argue excessive, based on the low LDL target achieved. Would you be satisfied with a 20% likelihood of heart attack, stroke, or death or 5 years, a 1 in 5 roll of the dice? I would not. Recall that we aim for near-total elimination of risk.

What could have been further "optimized"? Plenty. For instance:

--What is the real LDL, not the fabricated, calculated LDL? The two can be commonly 100 mg/dl different.

--How about raising HDL to 60 mgd/?

--What about reducing the proportion of small LDL particles? After all, small LDL is the number one cause of heart disease in the U.S., not high LDL.

--What is Lp(a)? If you treat LDL with a statin drug, Lp(a) is unaffected and continues to trigger huge plaque growth. You will fail if this is not identified and corrected.

--What is vitamin D3? One of the most powerful facilitators of plaque reversal I know of.

--What are triglycerides? Triglycerides create hidden particles in the blood like intermediate-density lipoprotein, potent triggers for coronary plaque growth. Speaking of intermediate-density lipoprotein, that's another very important pattern to identify, the after-eating persistence of dietary fats.

--Why aren't they taking fish oil? With a 28% reduction in heart attack and 45% reduction in sudden death from heart attack, this alone would have halved the number of "events" in the "optimal" medical treatment group.

Of course, there's more. But the idea that aspirin, statins, and anti-ischemic therapy is somehow optimal is silly and sad at the same time. But that's the bias. The COURAGE Trial does represent a step forward, a step away from the "stent everyone and everything" mentality that motivates my colleagues, aided and abetted by their co-conspirators, the hospitals. But you and I know better. "Optimal" medical therapy, in truth, can mean a far better approach that can dramatically reduce, perhaps eliminate, risks for events like heart attack. The conventional "optimal" medical therapy will suffice only if you're content with a 20% likelihood of heart attack, death or stroke, or a 32% likelihood of an urgent procedure in your future.

Niacin, postprandial patterns

For a detailed report on the very important postprandial (after eating) patterns that contribute hugely to heart disease risk, read my recent article in Life Extension Magazine, available (no cost) at:

Uncovering a Hidden Source of Cardiovascular Disease Risk
at http://www.lef.org/magazine/mag2007/mar2007_report_heart_01.htm


For a report on using niacin to reduce risk of heart disease, see another report in the same issue of Life Extension:

Ask the Doctor: Using Niacin to Improve Cardiovascular Health
at
http://www.lef.org/magazine/mag2007/mar2007_atd_01.htm.

Also, keep your eyes open for a lengthy report focused exclusively on the Track Your Plaque program in an upcoming issue of Life Extension. I'll provide links in this Blog when it comes out.

What's better than fish oil?

One of the recent questions on our Track Your Plaque Forum related to what to do about a triglyceride level of 101 mg/dl while on fish oil.

Recall that, contary to conventional thinking like that articulated in the ATP-III cholesterol treatment guidelines, we aim to reduce triglycerides to 60 mg/dl or less. This is important to suppress the formation of abnormal triglyceride-containing lipoprotein particles, especially small LDL, reduced HDL, lack of healthy large HDL, VLDL. ATP-III advises a level of 150 mg/dl or less. Unfortunately, triglyceride levels this high guarantee appearance of all these undesirable particles and an increasing heart scan score.

What's better than 4000 mg of fish oil for its 1200 mg of EPA and DHA (omega-3 fatty acids)? More fish oil. In other words, the 4000 mg fish oil providing 1200 mg EPA + DHA is our minimum. A simple increase to 6000 mg to provide 1800 mg EPA + DHA is usually all that is necessary to reduce triglycerides and put a halt to the cascade of abnormal lipoprotein particles that trigger plaque growth. Occasionally, a somewhat higher dose may be required. Doses are best divided into two, with meals (e.g., three capsules twice a day).

Another important issue: An over-reliance on wheat products can also increase triglycerides. This includes any flour product like breads (regardless of whether it's white, whole wheat, or whole grain--they all raise triglycerides), pretzels, bagels, breakfast cereals, and pasta. A dramatic reduction in wheat-containing products will reduce triglycerides substantially, help you reduce your abdominal fat, reduce blood pressure, raise HDL and reduce small LDL, clear your mind, provide more energy, avoid afternoon "fogginess" . . . Huge benefits.

Valve disease and vitamin D

There are two common forms of heart valve disease: aortic valve stenosis (stiffness) and insufficiency (leakiness), and mitral anular calcification.

Both valve issues are regarded as evidence of senescence, or aging--the older you are, the more likely you will have one or both. Both conditions involve progressive calcium deposition and, to some degree, cholesterol deposition. They might be regarded as phenomena of "wear and tear" just like hip arthritis.

There are no known therapies to stall or stop the development of mitral anular calcification. However, several attempts have been made over the years to identify treatments that can slow or stop the progression of aortic valve disease, which is becoming increasingly common and is addressed by surgical valve replacement when severe. The most recent trials have examined whether high-dose Lipitor (80 mg) has any effect (it did not) and high dose Crestor (40 mg), which slowed but did not stop the deterioration of stiff valves.

It's been my suspicion that vitamins D and K2 may play a crucial factor in valve health. After all, vitamin D is the master controller of calcium deposition. Preliminary data also suggest that people who are intentionally made vitamin K deficient with the drug, Coumadin, develop twice the calcium deposition on aortic valves that non-Coumadin takers develop.

I saw a patient Friday, Marianne. In addition to a moderate heart scan score of 379 at age 71, Marianne had a leaky (insufficient) aortic valve. By an echocardiogram 18 months ago, the valve was moderately leaky. I put Marianne on vitamin D, 4000 units, to raise her blood level to 50 ng/ml.

Last week, I asked Marianne to have another echocardiogram. This time, no leakiness whatsoever--none. I have never seen this happen before. Although Marianne is only one example and we don't want to extrapolate too far from the experience of one person, it's hard not to attribute this phenomenal response to vitamin D supplementation.

I wonder what would have happened if we had added vitamin K2, as well?

Anyway, just another potential wonderful effect of vitamin D restoration.