All posts by william-davis

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.

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.

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.

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.

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.

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.

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).

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.

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

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.

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

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

Vitamin D Newsletter

August, 2007

Dear Dr. Cannell:

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

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

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

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

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

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

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

Sincerely,
Paul, Washington, D.C.

Dear Paul:

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

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

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

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

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

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

Dear Dr. Cannell:

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

Susan, Toronto, Canada

Dear Susan:

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

Dear Dr. Cannell:

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

Emma, London, England.

Dear Emma:

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

Dear Dr. Cannell:

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

Mary, Trenton, New Jersey.

Dear Mary:

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

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

The Telegraph, Why is Vitamin D So Vital?

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

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

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

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

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

This is a periodic newsletter from the Vitamin D Council, a non-profit trying to end the epidemic of vitamin D deficiency. If you don't want to get the newsletter, please hit reply and let us know. This newsletter is not copyrighted. Please reproduce it and post it on Internet sites. Remember, we are a non-profit and rely on donations to publish our newsletter and maintain our website.

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

Author Michael Pollan: 'The Omnivore's Dilemma'

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

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

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

Try a little experiment:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Some of the math-savvy will have noticed that we often report drops in CT heart scan scores on a percentage basis. Unfortunately, it this were a competition (which, of course, it is not), this would be unfair.

A score of 50, for instance, that drops "only" 25 points would represent a 50% drop in score.

But someone with a score of 1050 who drops his or her score the same quantity, or 25, will have dropped their score less than 5%.

In other words, the magnitude of your starting score determines how large a percentage drop you achieve, even when the absolute, or real, quantity of plaque reversal is the same as someone who begins with a lower score.

I qualify this discussion in this vein because of Grady's story. Grady, a soon-to-retire attorney, started with a heart scan score of 1151. On the Track Your Plaque program, he saw his score drop nearly 200 points--200 points!

But, if we gauged Grady's success just on a percentage basis, he dropped his score only a measly 17% or so. (Imagine the headlines if this program were sponsored by a drug manufacturer. The Track Your Plaque program proudly has nothing to do with the drug industry.)

Of course, the Track Your Plaque program is not a competition. It is an effort to help everyone possible, the more the better. Even if Grady failed to set a new Track Your Plaque record gauged on a percentage basis, he will have achieved an extraordinary advantage in health: the virtual elimination of the dangers of heart disease.

With this drop in score, Grady's risk for heart attack plummets from a spine-chilling 25% per year to nearly zero. (I know of NO other program that can claim such a track record.)

Grady's full story will be reported in the August, 2007 Track Your Plaque newsletter. To subscribe or to just view when it is posted, go to www.cureality.com website, click on the upper right hand corner What Does My Heart Scan Show? graphic, which then takes you to the page to view the newsletter. Or, Track Your Plaque Members can just go to the Library and click on newsletter archives.

One of the basic requirements that stack the odds in your favor of stopping or dropping your CT heart scan score is to achieve basic lipid targets of 60-60-60.

In other words, we generally see best results when LDL is reduced to 60 mg/dl, HDL raised to 60 mg/dl, triglycerides reduced to 60 mg/dl. Now, these are not absolute requirements. Someone can have a spectacular drop in heart scan score even with an HDL of 56, LDL of 71. But the "Rule of 60" provides a useful target that is easy to remember, packs real power, and is clearly beyond that achieved with conventional approaches.

People often ask, "Just how tough is it to get to these targets?"

It's really not that tough. Interestingly, whenever I tell my cardiologist or primary care colleagues that I advocate these 60-60-60 targets, they declare that it's tough, perhaps impossible, except for the most highly motivated.

I agree that it requires motivation. A cigarette-smoking, TV-addicted, 70-lb overweight, chip- and pretzel-eating couch potato is not going to achieve them.

On the other hand, you don't have to be a marathon running vegetarian to do it, either.

Most people, in fact, engaged in the Track Your Plaque program achieve the 60-60-60 targets---or exceed them. It's not uncommon, for instance, for HDL to skyrocket to 80 or 90 mg/dl with many of our strategies. (Of course, if your starting HDL is 20 or 25 mg/dl, 80 or 90 is not possible with current technology.)

But it certainly does require more than the "Take Lipitor and stick to your low-fat diet" approach that is the mantra repeated in the vast majority of medical offices across the U.S. For instance, reducing LDL to 60 mg/dl when starting at 170 mg/dl will require addition of oat bran and other soluble or viscous fibers; raw almonds and walnuts; perhaps the use of Benecol butter substitute; reduction or elimination of wheat products if small LDL comprises a substantial proportion of LDL particles. Reducing triglycerides requires the generous use of omega-3 fatty acids from fish oil. Attention to vitamin D must be a part of the effort.

So, yes, it is not as simple as the conventional approach. But the results are far superior in reducing or eliminating heart attack and in dropping your heart scan score.

But it can be done. We do it every day.

It happened yet again.

Mel came to the office. CT heart scan score: 799--quite high, enough to pose a real threat very soon. Thus, no time to lose in instituting an effective prevention program.

We do the usual--identify the six causes of coronary plaque; begin fish oil, show him how to correct his plaque causes. You've heard it before.

Vitamin D blood level in March: 17 ng/ml--severe deficiency.

Vitamin D replacement needs to be a part of his coronary plaque control program. So I suggested 6000 units per day of an oil-based preparation of vitamin D3 (cholecalciferol). Conveniently, there is a Vitamin Shoppe outlet across the street from my office. I just point and tell people to go across the street.

Mel did just that. However, he also informed his primary care physician about his vitamin D deficiency. His primary physician promptly told him he needed to take a prescription form of vitamin D and not to bother with just a supplement.

So Mel stopped his vitamin D capsules and started taking vitamin D prescription "medication." Mel figured, naturally, that if it requires a prescription, it must be better. Unfortunately, Mel and his doctor failed to pass the change in strategy onto us.

So, four months later, Mel got repeat vitamin D blood level: 19 ng/ml.

I've seen this too many times. The prescription form of vitamin D is nonsense. There's hardly any effect on blood levels of vitamin D3 at all. The body's conversion of this non-human form of D is extremely inefficient and therefore virtually useless. While it raises the blood level of vitamin D2 (ergocalciferol) and thereby total D (D3 + D2), there is negligible effect on the real human and active form, D3.

How and why this preparation got through the FDA process to obtain approval as a drug is beyond me, though I am not a defender of FDA practices and politics.

This notion that "if it's a prescription, it must be better" is a fiction perpetuated by the drug industry. The same principle gets tossed around with fish oil, hormones like estrogens and testosterone, and others. Often, the principal difference between prescription and non-prescription is patent protection. Patent protection provides profit protection. Selling a product without patent protection can be risky business. It's certainly less profitable.

As always, getting at the truth is sometimes the most difficult job of all. Prescription vitamin D belongs in the garbage. Vitamin D capsules (gelcaps) do the job and do it well, over and over, with reliable, consistent and substantial rises in blood levels of 25-OH-vitamin D3. I take 6000 units per day (3 2000 unit capsules) that cost me $5.99 for a bottle of 120 capsules, or about $4.50 a month.

And nobody--nobody--pays me to say this. I say it because I believe it's true.

What does angioplasty have over the Track Your Plaque program?

Well, first of all, the Track Your Plaque program has a lot to boast about. What other approach can claim to have reduced heart disease 30, 40, 51, and now 63%? That's as close to a cure that's ever--EVER--been achieved. Statin drug manufacturers can talk about an occasional 1, 2, or 5% reversal. We're talking 10 times more.

The Track Your Plaque program also uses as little prescription medication as necessary. Fish oil, vitamin D, coenzyme Q10, niacin--some of the frequent tools used for plaque reversal in our program. Yes, we do use prescription medications, but only when there is truly a benefit and nutritional strategies have failed to achieve the goals we're seeking. We do not endorse shotgun prescription approaches conceived of by some marketing department at a pharmaceutical company.

So what possible advantage can coronary angioplasty have? Why don't more people embrace a program like Track Your Plaque that has already proven itself enormously effective?

Because angioplasty is easy. There's little worrying ahead of time. Just wait for the symptoms or other problem to appear, go to the hospital and get your procedure. You can live the free and easy life beforehand--no exercise, no diet efforts, no nutritional supplements. Just be sure to go to the hospital when suspicious symptoms strike. (Of course, you gamble that you survive the appearance of symptoms, a process 30-50% of people fail to survive.)

That means you can eat all you want, drink all you want, save the money you otherwise might have thrown away on supplements, pocket the monthly costs of an exercise club membership, etc. Go to the hospital when you experience the sensation of an anvil on your chest or of suffocation, let the emergency room do their thing, meet your cardiologist, go to the catheterization laboratory, get two or three stents, go home the next day!

Why bother with a prevention program, especially one that requires involvement, learning, and effort like Track Your Plaque?

Because it's your way to stack the odds enormously in your favor of 1) surviving the appearance of symptoms, 2) avoiding the prospect of heart procedures, which are not as clean and easy as they often seem, 3) have a longer lasting durability than a stent which could buy you a couple of years before your next procedure or heart catastrophe, and 4) it's the right thing to do for the sake of the huge societal cost of heart disease.

Many of you have the equivalent of a cure for heart disease at your fingertips. Unless you have a soft spot in your heart for hospitals, cardiologists, or the pharmaceutical or medical device industry, there isn't a choice.

In case anyone missed this in the June, 2007 Track Your Plaque Newsletter, I'm again posting how we calculate the annual rate of score increase, should it occur.

For instance, say your score in January, 2005, is 100. In November, 2006, you undergo another scan and the score is 140. Obviously, your score has increased an undesirable 40%. But what is the annual rate of score increase, the amount of increase per year?

In this example, the annual rate of score increase is 19%--not anywhere near as bad as the 40% that can scare the heck out of you.

Obviously, the best rate of heart scan score increase is a negative number, i.e., a drop in score from, say 100, to 60. You might even eliminate the need for this calculation altogether if you drop your score.

Nonetheless, whenever there is a score increase over an uneven period of time, a fraction of year(s), this is the method we use to annualize the calculation. The equation we use is a modified form of the annual compound interest equation using continuous compounding, since that’s how coronary atherosclerotic plaque grows--just like money. The difference is, of course, is that while you might want more money, you certainly don't want more plaque.

You will need a calculator for this calculation, one with an exponential “y to the power x” function. For ease, calculate "1/t first, then use it as the “x” exponent on your y^x function and "(score 2 / score 1)" as the "y".

Annual rate of plaque growth (APG) = ( score 2 / score 1 ) ^1/t - 1

Multiply the result by 100 to yield a percent.

“Score 1” is your 1st heart scan score, “score 2” is your 2nd (or any subsequent heart scan score); “t” is the amount of time between the two scans expressed in years in decimal form. Time between scans should be expressed in years or fractions of years. To obtain the time interval in fractions of years, simply divide the number of months between scans by 12 (e.g., 18 months / 12 = 1.5 years ; 22 months / 12 = 1.83 years).

It’s not as tricky as it looks. For example, if your first heart scan score is 300 and your next scan 16 months later (or 16/12 = 1.33 years) is 372, then:

Annual rate of plaque growth (APG) = ( 372 / 300 ) ^1/1.33 - 1 = 0.175

Multiply 0.175 x 100 = 17.5% annual rate of plaque growth

Some scan centers will do the calculation for you as part of a repeat scan. However, the equation can be used if you're left on your own, or if you go to a different scan center. If this is too much effort, perhaps it's just another reason to add to the list of reasons to drop your heart scan score!

In The Track Your Plaque program, we advocate decreasing triglycerides to 60 mg/dl or less.

That's the level of triglycerides that minimize the presence of triglyceride-containing undesirable lipoproteins causing plaque, such as small LDL, VLDL, and the after-eating persistence of IDL (intermediate-density lipoprotein, a bad player). (The enzyme, cholesteryl-ester transfer protein, or CETP, is responsible for exchanging one triglyceride molecule for one cholesterol molecule between HDL and other lipoprotein particles. Thus, an excess of triglyceride availability permits CETP to operate unrestrained, creating more undesirable lipoproteins. This was the basis for Pfizer's now defunct CETP inhibitor, torcetrapib.)

Of course, this triglyceride target is far below that of the conventional guidelines. The Adult Treatment Panel-III of the National Cholesterol Education Panel suggests a triglyceride level of 150 mg/dl is okay.

In my view, a level of 150 mg/dl is highly abnormal, permitting the persistence of multiple lipoprotein particles and virtually guarantees plaque growth. In short, triglycerides of 150 are awful.

Curious thing: Successful participants in our program, i.e., people who achieve desirable weight, reduce processed carbohydrate junk foods and saturated fat sources, and aim for the 60-60-60 targets for conventional lipids, commonly end up with triglyceride levels of 25-50 mg/dl.

We have seen many people drop their heart scan scores just by achieving a triglyceride level of 60 mg/dl or less. So achieving a lower level below 60 is not necessarily a requirement for coronary plaque regression.

But it makes me wonder if a triglycere level of 30s or 40s is the level for perfect health. These are levels ordinarily regarded as impossibly low. When colleagues see the numbers we readily and routinely achieve, they declare that the numbers are spurious, temporary, or just flukes. "No way you can do that all the time!"

This level also seems to, in virtually all cases, eliminate the triglyceride-containing undesirable lipoproteins small LDL, IDL, etc., and allow full conversion of HDL into the healthy, large fraction.

Should we move the Track Your Plaque triglyceride target to below 45 mg/dl or even lower? I don't think so, but it makes me wonder.

The Track Your Plaque “Rule of 60”

A little bit of fish oil

AHA: Doctors don't have time for prevention

Confusion about Lp(a)

Calculus of the cardiologist

Lipoprotein(a) treatment alternatives

Trapped in a low-fat world

Blame the niacin

Eat fish three times a day

What if I had a cure for coronary disease?

Vitamin D and autism

Michael Pollan Podcast

Are you addicted to fructose?

Chicken Little

200 point drop in heart scan score

How tough is the Track Your Plaque 60-60-60 target?

Vitamin D2 belongs in the garbage

Angioplasty vs. Track Your Plaque

Plaque is like money

Triglycerides: What is normal?