America: The world’s diet laboratory

Low-fat, low-carb, high-protein, Pritikin, Ornish, Atkins, South Beach, Sonoma, Sugar-Busters, Weight Watchers, vegetarian . . . Have Americans tried them all?

We’ve witnessed the relative success of diet habits in selected regions world-wide: the longevity of the Japanese on a spare soy and fish-based diet; the reduced heart disease incidence of the French despite an indulgent food-centered culture; the extreme heart disease-free lives of the Cretan Greeks.

Contrast this with the startling failure of the American diet experiment: We’re all (speaking for the collective whole) fat, diabetic, and miserably mired in the diseases of obesity. We’ve experimented with every possible iteration of diet from grapefruit or cabbage only, to calorie deprivation (a al Weight Watchers), to restricting this or that element of diet. The “official” organizations have made their contributions, as well: the American Heart Association’s Therapeutic Lifestyle Changes (formerly Step I and II diets), a program eerily similar to what Americans are already eating and resulting in failure; the American Diabetes Association diet, incomprehensibly embracing carbohydrates when they are the root of the nutrition-habit-gone-wrong that caused the disease in the first place; the USDA and their Food Pyramid, encompassing a design that contains the germ of wisdom but is so heavily overweighted in grains that it is a sure-fire way to increase weight and heart disease were you to follow their recommendations.

What have we learned from our grand experiment, our nationwide misadventure in nutrition?

I believe that we’ve learned how not to eat: Processed snack foods, meals delivered in a fast-food setting with the offer to “super-size” your order, make-believe food ingested in your car eaten for the sake of staving off the inevitable hunger pangs. Few would argue that these are certain paths to obesity and poor health.

Certainly, if we’ve learned how not to eat, can we extrapolate just how to eat? And not just for weight loss, since most diets focus just on that, but on health, particularly heart health?

If Americans have so far failed to learn the lessons of the nutritional world, we certainly have not failed at talking about it. From books to blogs, websites, information gurus to infomercials, we certainly celebrate the capacity to share our experiences, our grief over our nutritional “misfortune,” despite a world of plenty.

Yet we swim in a sea of information. Can we sift through the chaff to discover the essential truth?

Let me articulate an extreme (extreme meaning closer to the truth, I hope) interpretation of nutritional wisdom:

--If it requires a label or nutritional analysis, reject it. The wondrous green pepper, or bottle of olive oil, for instance, require no such qualifications. Some exceptions: milk, yogurt, cottage cheese (unless, of course, you purchase straight from a local producer). I am always impressed with the contortions and frustrations people experience trying to decipher labels. Ironically, the healthiest foods don’t even require labels.

--If it is ingested in a rush, it’s likely to add to poor health. True food is meant to be consumed at leisure, not in haste to satisfy some irrational, unthinking impulse.

--Search for natural, whole foods. Natural, whole foods require no marketing. You pay a premium for a company to adorn a product with glitz, glamour, and appeal. Repackage Cocoa Puffs as chocolate flavored, round overly-processed wheat flour, sans marketing spin, and what is left? Processed foods are?intentionally?addictive. They are added to, modified, high-fructose corn syruped, etc. to increase desirability, but also create addiction. Eliminate them just as a smoker eliminates cigarettes.

--A corollary to the above issue: purchase foods that appear as if you had grown it or raised it yourself. If you were to grow corn in your backyard garden, you would eat it on the cob or some similar way. You would not grind it, pulverize, process it, nor serve it as cornstarch and add to a pile of chemicals to make breakfast cereal. Eat foods in their natural state, not the highly processed food-product that requires a colorful package and advertising to sell.

--Don’t keep bags of chips, boxes of breakfast cereal and crackers, frozen dinners, all “just in case.” Don’t allow yourself that opportunity because you will more than likely seize it. An alcoholic who keeps a secret bottle of gin hidden in the cabinet is well aware that it’s there and will eventually give in to impulse.

--When you eat meat, try to find free-range, organic products. Even better, purchase from a local producer who you trust.

--For anyone with patterns like low HDL, small LDL, high triglycerides, and blood sugar >100 mg/dl, following a diet that is as free of wheat products as possible will yield enormous benefits. Wheat is a part of all breads, virtually all breakfast cereals, pretzels, crackers, bagels, cookies, cupcakes, pancakes, waffles, etc. Going wheat-free is also a surprisingly effective weight loss strategy.

That’s just a few thoughts. The approach we use in the Track Your Plaque program helps achieve weight loss, but also helps correct lipoprotein patterns, often dramatically.

Many diets have failed to keep pace with the changing nutritional habits of Americans. In 1960, we ingested close to zero high-fructose corn syrup. We’re now approaching 80 lbs per year per American. Breakfast cereal in 1950 consisted of a handful of products, eaten intermittently; today, it is a staple with enough products to fill a modern supermarket’s entire aisle. Meats have changed, thanks to the factory farm phenomenon feeding its animals corn in inhumanely restricted conditions, a dietary shift for livestock that has modified the fat composition to something far different than 50 years ago, not to mention the antibiotics and other chemicals used to accelerate growth and fight off infection from the artificial, overcrowded conditions.

The American nutritional shift, along with rampant obesity, have also caused a relatively new cause of coronary heart disease to explode: small LDL particles. The contribution of small LDL has been enormously underestimated, since most physicians don’t know what it is, don’t know how to check for it, and don’t know what to do with it. Yet it has emerged as the number one cause for heart attack and heart disease nationwide.

Stay tuned for our rewritten New Track Your Plaque diet to be released as a Special Report on the www.cureality.com website in future.

Dr. Jarvik, is niacin as bad as it sounds?

A popular health newsletter, Everyday Health, carried this headline:

A Cholesterol-Busting Vitamin?

Did you know that niacin, one of the B vitamins, is also a potent cholesterol fighter?
Find out how niacin can help reduce choleseterol.


At doses way above the Recommended Dietary Allowance — say 1,000–2,500 mg a day (1–2.5 grams) — crystalline nicotinic acid acts as a drug instead of a vitamin. It can reduce total cholesterol levels by up to 25%, lowering LDL and raising HDL levels, and can rapidly lower the blood level of triglycerides. It does so by reducing the liver’s production of VLDL, which is ordinarily converted into LDL.


I'd agree with that, except that it is rare to require doses higher than 1000-1500 mg per day unless you are treating lipoprotein(a) and using niacin as a tool for dramatic drops in LDL. But for just raising HDL, shifting HDL into the healthy large class, reducing small LDL, and for reduction of heart attack risk, 1000-1500 mg is usually sufficient; taking more yields little or no further effect.

But after that positive comment comes this:

Niacin is safe — except in people with chronic liver disease or certain other conditions, including diabetes and peptic ulcer. . . However, it has numerous side effects. It can cause rashes and aggravate gout, diabetes, or peptic ulcers. Early in therapy, it can cause facial flushing for several minutes soon after a dose, although this response often stops after about two weeks of therapy and can be reduced by taking aspirin or ibuprofen half an hour before taking the niacin. A sustained-release preparation of niacin (Niaspan) appears to have fewer side effects, but may cause more liver function abnormalities, especially when combined with a statin.


Strange. After a headline clearly designed to pull readers in, clearly stating niacin's benefits, the article then proceeds to scare the pants off you with side-effects.

But look to the side and above the text: Ah . . . two prominent advertisements for Lipitor, complete with Dr. Robert Jarvik's photo. "I've studied the human heart for a lifetime. I trust Lipitor to keep my heart healthy."

Niacin bad. Lipitor good. Even celebrity doc says so. Sounds like bait and switch to me. "You could try niacin--if you dare. But you could also try Lipitor."

Who is Dr. Jarvik, anyway, that he serves as spokesman (or at least figurehead) for this $13 billion dollar a year drug? Of course, he is the 1982 inventor of the Jarvik artificial heart, surely an admirable accomplishment. But does that qualify him to speak about heart disease prevention and cholesterol drugs?

Jarvik has never--never--actually prescribed Lipitor, since he never completed any formal medical training beyond obtaining his Medical Doctor degree, nor has he ever had a license to practice medicine. He does, however, continue in his effort to provide artificial heart devices, principally for implantation as a "bridge" to transplantation, i.e., to sustain a patient temporarily who is dying of end-stage heart failure.

So where does his expertise in heart disease prevention come from? It's beyond me. Perhaps it was the thousands of dollars likely paid to him. That will make an "expert" out of just about anybody.

Robert Bazell, science reporter, for CNBC, made this report on the Jarvik-Lipitor connection in his March, 2007 report, Is this celebrity doctor's TV ad right for you?

Mr. Bazell writes:

On May 16, 1988, an editorial in the New York Times dubbed the artificial heart experiments, “The Dracula of Medical Technology.”

“The crude machines,” it continued, “with their noisy pumps, simply wore out the human body and spirit.”

Since then, in a series of start-up companies, Jarvik has continued his quest to make an artificial heart — as have several other firms. One competitor recently won FDA approval to sell its device for implantation in extreme emergencies.

Perhaps Jarvik’s chances of success with another artificial heart account for his willingness to serve as pitchman for Pfizer. I inquired, without success, to find the going rate for a semi- celebrity like Jarvik to appear in such ads. Thomaselli of Advertising Age said whatever it is, it is “infinitesimal” compared to Pfizer’s expenditures of $11 billion a year on advertising, much of it for Lipitor.

Why spend so much marketing Lipitor?

Because Lipitor is only one of six drugs in the class called statins that lower cholesterol. Many cardiologists say that for the vast majority of people any one of these drugs works just as well as the other. Two of them, Mevacor and Zocor, have already lost their patent protection so they cost pennies a day compared to $3 or more a day for Lipitor.

In 2010, when Lipitor loses its patent protection, it, too, will cost pennies a day, and Pfizer will no longer need Dr. Robert Jarvik.



So, is niacin so bad after all? Or is this Everyday Health report just another clever piece of advertising for Pfizer?

Is niacin as bad as it sounds?

A popular health newsletter, Everyday Health, carried this headline:

A Cholesterol-Busting Vitamin?

Did you know that niacin, one of the B vitamins, is also a potent cholesterol fighter?
Find out how niacin can help reduce choleseterol.


At doses way above the Recommended Dietary Allowance — say 1,000–2,500 mg a day (1–2.5 grams) — crystalline nicotinic acid acts as a drug instead of a vitamin. It can reduce total cholesterol levels by up to 25%, lowering LDL and raising HDL levels, and can rapidly lower the blood level of triglycerides. It does so by reducing the liver’s production of VLDL, which is ordinarily converted into LDL.


I'd agree with that, except that it is rare to require doses higher than 1000-1500 mg per day unless you are treating lipoprotein(a) and using niacin as a tool for dramatic drops in LDL. But for just raising HDL, shifting HDL into the healthy large class, reducing small LDL, and for reduction of heart attack risk, 1000-1500 mg is usually sufficient; taking more yields little or no further effect.

But after that positive comment comes this:

Niacin is safe — except in people with chronic liver disease or certain other conditions, including diabetes and peptic ulcer. . . However, it has numerous side effects. It can cause rashes and aggravate gout, diabetes, or peptic ulcers. Early in therapy, it can cause facial flushing for several minutes soon after a dose, although this response often stops after about two weeks of therapy and can be reduced by taking aspirin or ibuprofen half an hour before taking the niacin. A sustained-release preparation of niacin (Niaspan) appears to have fewer side effects, but may cause more liver function abnormalities, especially when combined with a statin.


Strange. After a headline clearly designed to pull readers in, clearly stating niacin's benefits, the article then proceeds to share the pants off you with side-effects.

But look to the side and above the text: Ah . . . two prominent advertisements for Lipitor, complete with Dr. Robert Jarvik's photo. "I've studied the human heart for a lifetime. I trust Lipitor to keep my heart healthy."

Sounds like bait and switch to me. "You could try niacin--if you dare. But you could also try Lipitor."

Who is Dr. Jarvik, anyway, that he stands as the spokesman (or at least figurehead) for this $13 billion dollar a year drug. Of course, he is the 1982 inventor of the Jarvik artificial heart, surely an admirable accomplishment. But does that qualify him to speak about heart disease prevention and cholesterol drugs? Jarvik has, never actually prescribed Lipitor, since he never completed any formal medical training beyond obtaining his Medical Doctor degree, nor has he ever had a license to practice medicine. He does, however, continue in his effort to provide artificial heart devices, principally for implantation as a "bridge" to transplantation, i.e., to sustain a patient temporarily who is dying of end-stage heart failure.

So where does his expertise in heart disease prevention come from?

Omega-3 fatty acids: Frequency vs. quantity

I believe I have been observing an unexpected phenomenon: When it comes to fish oil and omega-3 fatty acids, the frequency of dosing may be as important, perhaps more important, than the actual dose.

First of all, why advocate omega-3 fatty acids from fish oil? There’s a list of lipid/lipoprotein reasons, including reduction of triglycerides and triglyceride-containing particles (VLDL, intermediate-density lipoproteins), reduction of small LDL, and increase in HDL. There’s also solid benefit in reduction of heart attack risk, reduction in death from heart attack, and reduction in stroke. There are also anti-inflammatory benefits and improvements in mood, reduction in depression.

Fish oil is a crucial ingredient in the Track Your Plaque program. I am honestly uncertain of just how much success we would give up if fish oil were NOT a part of the program, but I am unwilling to find out. The data are simply too compelling to not include omega-3 fatty acids from fish oil. Of course, supplementation of omega-3 fatty acids assumes greater importance in a modern world in which your food has become terribly depleted of the omega-3 fraction of oils. (Cultures that rely heavily on fish or wild game probably would not benefit to the same extent, since these foods contain omega-3 fatty acids.)

But I believe I have observed a curious effect over the past year or two. With the proliferation of many different preparations of fish oil that provide seemingly endless choices—low-potency fish oil, high-potency fish oil, paste forms of fish oil like Coromega, liquids such as Carlson’s, etc.¾I’ve observed that frequency of dosing may exert as much of an effect as the dose.

For example, someone might take the basic, low-potency preparation like Sam’s Club that contains 180 mg EPA and 120 mg DHA per capsule, four capsules per day. That yields a total of 1200 mg EPA and DHA per day. This is our minimum dose that provides the basic heart attack-reducing effect, though with modest effect on triglycerides and associated patterns.

Say someone switches to a high-potency preparation of 360 mg EPA and 240 mg DHA, providing a total of 600 mg omega-3 fatty acids per capsule, or twice the dose of the low-potency preparation. Would you expect double the effect?

Curiously, no. What I have observed, however, is that more frequent dosing may provide a larger effect. The least effective dosing is once per day; twice per day is far more effective. Three times per day¾though cumbersome¾provides even greater effect.

So, which is more important: dose or frequency?

I can’t say for certain, since my observations are informal and have not been obtained by a formal statistical analysis of our data. That will come with time.

For the present, suffice it to say that, if you are struggling with suppression of patterns like increased triglycerides, IDL, or low HDL, then at least twice- or three-times-per-day dosing might be worth considering, even before you increase the dose further.

Best: Greater dose, or higher-potency preparation, combined with higher frequency.

Lipoprotein testing

This is an update of a post I made about a year ago. However, I'm reposting it since the question comes up so often.


How can I get my lipoproteins tested?
This question came up on our recent online chat session and comes up frequently phone calls and e-mails.

If lipoprotein testing is the best way to uncover hidden causes of coronary heart disease, but your doctor is unable, unknowledgeable, or unwilling to help you, then what can you do?

There are several options:

1) Get the names of physicians who will obtain and interpret the test for you. That’s the best way. However, it is also the most difficult. Lipoprotein testing, despite over a decade of considerable scientific exploration and validation in thousands of research publications, still remains a sophisticated tool that only specialists in lipids will use. But this provides you with the best information on you’re your lipoproteins mean.
2) If you don’t have a doctor who can provide lipoprotein testing and interpretation, go to the websites for the three labs that actually perform the lipoprotein tests: www.liposcience.com (NMR); www.berkeleyheartlab.com (electropheresis or GGE); www.atherotech.com (ultracentrifugation). None of them will provide you with the names of actual physicians. They can provide you with the name of a local representative who will know (should know) which doctors in your area are well-acquainted with their technology. I prefer this route to just having a representative identify a laboratory in your area where the blood sample can be drawn, because you will still need a physician to interpret the results¾this is crucial. The test is of no use to you unless someone interprets it intelligently and understands the range of treatment possibilities available. Don’t be persuaded by your doctor if he/she agrees to have the blood drawn but has never seen the test before. This will be a waste of your time. That’s like hoping the kid next door can fix your car just because he says he fixed his Mom’s car once. Interpretation of lipoproteins takes time, education, and experience.

3) Seek out a lipidologist. Lipidologists are the new breed of physician who has sought out additional training and certification in lipid and lipoprotein disorders. Sometimes they’re listed in the yellow pages, or you can search online in your area. One drawback: Most lipidologists have been heavily brainwashed by the statin industry and tend to be heavy drug users.

4) Contact us. I frankly don’t like doing this because I feel that I can only provide limited information through this method and, frankly, it is very time consuming. I provide a written discussion of the implications and choices for treatment with the caveat to discuss them with your doctor, since I can’t provide medical advice without a formal medical relationship. We also charge $75 for the interpretation. But it’s better than nothing.

5) Make do with basic testing. Basic lipids along with a lipoprotein(a), C-reactive protein, fibrinogen, and homocysteine would provide a reasonable facsimile of lipoprotein testing. You’ll still lack small LDL and postprandial (after-eating) information, but you can still do reasonably well if you try to achieve the Track Your Plaque targets of 60-60-60. It’s sometimes a necessary compromise.

Our discussions on the Track Your Plaque Forum have impressed me with the difficulty many people encounter in getting lipoproteins drawn and interpreted. Some of our Members have been very resourceful identifying blood draw laboratories around the country, such as Lab Safe, that will at least provide the blood draw service.

I wish it was easier and we are working on some ideas to facilitate this nationwide. It will take time.

In 20 years, this will be a lot easier when doctors more commonly use lipoprotein testing. But for now, you can still obtain reasonably good results choosing one of the above alternatives.

Is it exercise or diet?

Wayne, a 61-year old retired school superintendent, had been an exercise fanatic all his adult life. If not running long distances and occasional marathons, he'd bike up to 70 miles a day. He did this year-round. In cold weather, he set his bicycle up on an indoor device and also ran on a treadmill and added weight training.

That's why it was kind of surprising that he sported a large belly. At 5 ft 8 inch and 190 lbs, that put his Body Mass Index (BMI) also high at 28.8 (desirable <25). You'd think that vigorous, almost extreme, exercise like this would guarantee a slender build.

Wayne also had lipoproteins to match: triglycerides 205 mg/dl, LDL 176 mg/dl but LDL particle number much higher at 2403 nmol/l (an effective LDL of 240 mg/dl); 75% of LDL particles were small.

I asked Wayne about his diet. "I eat healthy. Cheerios for breakfast usually. Some days I'll skip breakfast. Lunch is almost always a sandwich: tuna, turkey, something like that on whole wheat bread or a whole wheat bagel. Chips, too, but I guess that's not too healthy. Dinners vary and we eat pretty healthy. Almost never pizza or junk like that."

"Pasta?" I asked.

"Oh. sure. Two or three tiems a week. Always whole wheat. With a salad."

Wayne was well aware of the conventional advice for whole grains and, indeed, had been trying to increase his intake, particularly since his basic cholesterol numbers had been high in past. To his surprise, the more he tried at diet, the more LDL seemed to go up, as did triglycerides.

I see this situation every day: The obsession with processed carbohydrate foods, worsened by the message perpetuated by the American Heart Association, the USDA Food Pyramid, Kraft, Kelloggs, Post, etc. Eat more fiber, eat whole grains.

NY Times columnist, Jane Brody, chronicles her (embarassing) mis-adventure following the same mis-guided advice in Cutting Cholesterol, an Uphill Battle.

According to the USDA Food Pyramid, Wayne is not getting enough grains and whole grains, particularly since he is highly physically active. Consistent with the message given by the food industry: "Eat more!"

The food industry-supported Whole Grain Council advises:

Whole Grains at Every Meal
The US Dietary Guidelines recommend meeting the daily requirement by eating three "ounce-equivalents" of breads, rolls, cereals or other grain foods made with 100% whole grains. A slice of bread or a serving of breakfast cereal usually weighs about an ounce.

Want an easier way to think about it? Just look at your plate at each meal, and make sure you've included some source of whole grains. That's why our slogan is "Whole Grains at Every Meal."



By this scheme, if you are overweight, it's because you lack fiber and you're too inactive. "Get up and go!" It's not the diet, they say, it's you!

See through this for what it is: Nonsense. Wayne was overweight, packing 20 extra pounds in his abdomen from his over-dependence on processsed carbohydrates--"whole grains"--not from inactivity.

Instant heart disease reversal


What if reversal of heart disease--regression of coronary atherosclerotic plaque--were achievable instantly? Just add water and--voila!!

To my knowledge, it is not--yet. But I sometimes play with this idea in my head. I could imagine that such a program would consist of a few essential elements:

--A fast or semi-fast, or at least a very spare diet, over a period like 10 days to promote net catabolism. It is also supremely anti-inflammatory to restrict calories.

--High-dose vitamin D, e.g., 20,000 units per day of D3 to fully replenish depleted stores and achieve all the metabolism-correcting effects of D3 restoration.

--EPA + DHA at a higher than usual dose with frequent throughout-the-day dosing to encourage replacement of cellular lipid constituents with the more stable omega-3 fraction of fatty acids.

Beyond this, I'm uncertain. What role l-arginine, statins, niacin . . . conjugated linoleic acid? ApoA1 Milano infusions?

This is simply whimsical at this point. I don't know if such an approach would work. But if it did, you might imagine that it would offer an opportunity--for the properly motivated--as an alternative treatment for angina, advanced coronary disease, a means to pull someone back from the brink.

With the insights gained from our slow-but-powerful Track Your Plaque approach, perhaps we will also gain insights into how to accelerate such a process of reversal so that it is achievable in days, rather than months or years.

The small LDL epidemic

Ten years ago, small LDL was fairly common, affecting approximately 50% of the patients I'd see. For instance, an LDL particle number of 1800 nmol/l would be 40-50% small LDL in about half the people.

But in the last few years, I've witnessed an explosion in the proportion of people with small LDL, which now exceeds 80-90% of people. The people who show small LDL also show more severe patterns. 80-90% small LDL is not uncommon.

Why the surge in the small LDL pattern? Two reasons: 1) The extraordinary surge in excess weight and obesity, both of which favor formation of small LDL particles, and 2) over-reliance on processed carbohydrates, especially wheat-based convenience foods.

The constant media din that parrots such nonsense as the report on CNN Health website, Healthful Breakfast Tips to Keep You Fueled All Day, helps perpetuate this misguided advice. The dietitian they quote states:

"If you don't like what you're eating, you won't stick with it. If your choices aren't the most nutritious, small tweaks can make them more healthful. For example, if you have a sweet tooth in the morning, try a piece of nutty whole-grain bread spread with a tablespoon each of almond butter (it's slightly sweeter than peanut butter) and fruit preserves instead of eating foods that offer sweetness but little nutritional benefit, like doughnuts or muffins. If you enjoy egg dishes but don't have time to prepare your favorite before work, try microwaving an egg while toasting two slices whole wheat or rye (whole-grain) bread. Add a slice of low-fat cheese for a healthful breakfast sandwich that's ready in minutes. And don't overlook leftovers. If you feel like cold pizza (which contains antioxidant-filled tomato sauce, calcium-rich cheese, and lots of veggies), have it. It's a good breakfast that's better than no breakfast at all."

It sure sounds healthy, but it's same worn advice that has resulted in a nation drowning in obesity. The food choices advocated by this dietitian keep us fat. It also perpetuates this epidemic of small LDL particles.

If you have small LDL and its good friend, low HDL, it's time for elimination of wheat products, not some politically-correct silliness about increasing fiber by eating whole grains. Whole grains create small LDL! Or, I should say, what passes as whole grains on the supermarket shelves.

For some helpful commentary on this issue, see Fanatic Cook's latest post, Playing with Grains.

Mini-dose CTA?

I caught this little news report in the online edition of Canyon News , an LA paper, under the title Cedars-Sinai Develops Test to Prevent Heart Attacks .

They report that Dr. Daniel S. Berman M.D., chief of Cardiac Imaging and Nuclear Cardiology at Cedars-Sinai, reports that a new method of performing CT coronary angiography, "mini-dose CTA," has been developed that allows both coronary calcium scoring as well as CT coronary angiography (CTA) at a dose as low as 10% of standard dose. No technical details were provided.

Now, that may be worth knowing more about. If this is true, then CTA may indeed be useful as a "screening" procedure. However, we are going to need to know more: What devices are capable of doing this, what settings on the devices were used, etc. It does indeed come from a reputable source in Dr. Dan Berman, who is well known in nuclear cardiology circles.

We will try and dig for info. Stay tuned.

The myth of mild coronary disease

I hear this comment from patients all the time:

"They told me that I had only mild blockages and so I had nothing to worry about."

That's one big lie.

I guess I shouldn't call it a lie. Is it a lie when it comes from ignorance, arrogance, laziness, or greed?

"Mild coronary disease" is usually a label applied to coronary atherosclerotic plaque that is insufficient to block flow. Thus, having a few 20%, 30%, or 40% blockages would be labeled "mild." No stents are (usually) implanted, no bypass surgery performed, and symptoms should not be attributable to the blockages. Thus, "mild."

The problem is that "mild" blockages are no less likely to rupture, the eruptive process that resembles a little volcano spewing lava. Except it's not lava, but the internal contents of atherosclerotic plaque. When these internal contents of plaque gain contact with blood, the coagulation process is set in motion and the artery both clots and constricts. Chest pains and heart attack result.

So, the essential point is not necessarily the amount of blood flow through the artery, but the presence of coronary atherosclerotic plaque. Just having plaque--any amount of plaque--sets the stage to permit plaque rupture.

One thing is clear: The more plaque you have, the greater the risk for rupture. But the quantity of plaque cannot be measured by the "percent blockage." It is measured by the lengthwise extent of plaque, as well as the depth of plaque within the wall. Neither of these risk features for plaque rupture can be gauged by percent blockage.


Coronary atherosclerosis is a diffuse process that involves much of the length of the artery. It is therefore folly to believe that a 15 mm long stent has addressed the disease. This is no more a solution than to replace the faucet in your kitchen in a house with rotting pipes from the basement up.

The message: ANY amount of coronary plaque is reason to engage in a program of prevention--prevention of plaque rupture, prevention of further plaque growth, perhaps even regression (reversal). It is NOT a reason to be complacent and buy into the myth of "mild" coronary disease, the misguided notion that arises from ill-conceived procedural heart disease solutions.


Image courtesy Wikipedia.

Copyright 2008 William Davis, MD

Red flags for lipoprotein(a)



Lipoprotein(a), Lp(a), is an important cause for heart disease, heart attack, and coronary atherosclerotic plaque.

How do you know you have it?

Of course, it could be as simple as checking a blood level. But there are also a number of red flags for the presence of Lp(a), tell-tale signs that suggest it is present and contributing to the growth of coronary plaque.

I've seen so much of this pattern over the years that it's gotten so that I can pretty much pick out most of the people with Lp(a) just by either looking at them or by hearing their story. I do this simply by knowing what hints to look for.

Some of the red flags for Lp(a) include:

--High blood pressure in a slender person. Overweight is the overwhelmingly common reason for high blood pressure. However, inappropriate high blood pressure in a slender person can serve to tip you off that Lp(a) is present.

--HIgh LDL cholesterol poorly responsive to statin drugs. For instance, someone's LDL cholesterol of 190 mg/dl will be treated with Lipitor 40 mg, but drops to only 165 mg/dl, a very poor response. This can sometimes point towards Lp(a).

--Family clustering of heart disease in people before age 60. For instance, father with heart attack age 53, uncle with heart attack at age 55, aunt with heart attack age 59, etc. This clustering of risk, more often than not, signals Lp(a).

--Coronary disease or high heart scan score in the presence of relatively bland appearing lipids. For instance, LDL cholesterol 130 mg/dl, HDL 55 mg/dl, triglycerides 70 mg/dl on no medications or other efforts--figures ordinarily not associated with high likelihood of heart disease--yet heart disease is indeed present. This can mean that Lp(a) is the concealed culprit behind coronary atherosclerosis.

These red flags are not perfect. If you lack any of them, it doesn't necessarily rule out the possbility of having Lp(a). They simply serve as signs to suggest that Lp(a) may be lurking.

Once Lp(a) is identified, then the battle begins to gain control over this somewhat troublesome genetic pattern. Resourcesfulness and some ingenuity may be required. However, knowing that you have it shows you where to concentrate your efforts.

Vytorin study explodes--But what's the real story?

The makers of Vytorin, Merck/Schering-Plough Pharmaceuticals, issued a press release about the the Enhance Study yesterday. The news has triggered a media frenzy.

The NY Times reporting of the story:

Drug Has No Benefit in Trial, Makers Say

The 700 participants in the trial all had a condition called "heterozygous hypercholesterolemia," a genetic disorder that permits very high LDL cholesterols. The average LDL at the start was 318 mg/dl.

The Times reported that, while Vytorin cut "LDL levels by 58 percent, compared to a 41 percent reduction with simvastatin alone," but "the average thickness of the carotid artery plaque increased by 0.0111 of a millimeter in patients taking Vytorin, compared to an increase of 0.0058 of a millimeter in those taking only simvastatin." There was no difference in heart attacks or other "events" between the two groups.

(Vytorin is the combination of simvastatin and Zetia.)

In other words, the participants taking Vytorin had 53 ten-thousands of a millimeter more plaque growth than the group taking just simvastatin.

I am always uncomfortable when put in the position of defending a drug or drug company. However, it is patently absurd that this study has generated such attention. I suspect the public and media are waiting for another Vioxx-like debacle, with memories of concealed or suppressed data that suggested heightened heart attack risk that was dismisssed by the drug manufacturer. (That's not to say that the company hasn't been trying to delay or modify the outcome of the study, which they apparently have, much to the objections of the FDA.)

However, at this point, there is no reason to believe that this question possesses any parallels to the Vioxx fiasco.

If we accept the data as reported, however, we might say it calls the entire "Lipid Hypothesis" into question: If LDL cholesterol is significantly reduced but is not correlated with reduction in plaque, is LDL the means by which atherosclerotic plaque progresses? This trial does not answer that question, but does serve to raise some doubt.

Another issue: Heterozygous hypercholesterolemia, and thereby LDL cholesterol, may not be the overwhelming driver of plaque growth in this population. It is probably the number of small LDL particles, a factor which is not revealed by LDL cholesterol. For this reason, heterozygous hypercholesterolemia by itself is insufficient to cause heart disease. Some other factor(s) needs to be present. I would propose that it is the size of the LDL particle: When small, heart disease develops; when large, heart disease is less likely to develop. This issue was not addressed by this study. Readers of The Heart Scan Blog know that conventional LDL cholesterol, the number used in this study, is a virtually worthless number for truly gauging plaque behavior because of its flagrant inaccuracy.

So, there are substantial uncertainties, contrary to the absolute certainty expressed by people like Dr. Steve Nissen (who, by the way, has no expertise in lipoprotein disorders). It is premature to reach any firm conclusions from this study. The only conclusions that I personally come to are 1) Is this yet another reason to question the entire Lipid Hypothesis as it stands? and 2) What would the results have been had LDL particle number and LDL particle size been examined, not just LDL?

I would not automatically conclude that Zetia causes carotid plaque. This is absurd. And I am definitely not one to come to the rescue of a drug or drug manufacturer. I am simply after understanding and truth.

As an interesting aside, Dr. Howard Hodis of the University of Southern California and an expert in carotid scanning for heart disease prevention research, made a comment relevant to us in the Track Your Plaque program:

"Clearly, progression of atherosclerosis is the only way you get events,” Dr. Hodis said. “If you don’t treat progression, then you get events."

Dr. Arthur Agatston in the news



The Miami Herald has a new report on Dr. Arthur Agagtston (of South Beach Diet fame) to announce his new book, The South Beach Heart Health Revolution:
The South Beach Diet doctor takes on cardio care

Agatston, the granddaddy of CT heart scanning, is always at least worth listening to. Although his diet may not be perfect, it clearly has jumped light years ahead of conventional diets like the inane American Heart Association diet. The South Beach Diet focuses on healthy oils, nuts, lean meats, vegetables, and fruits, while slashing grains (except in the often disastrous phase III).

The article lists Dr. Agatston's advice to achieve a "heart healthy" lifestyle:


• Maintain a healthy weight through diet.

• Undergo CT heart scans to check for arterial plaque.

• Do aerobic exercise, along with stretching and strengthening workouts.

• Ask your doctor about taking statins and other cholesterol-lowering drugs.


We wouldn't have CT heart scan scoring (at least in its present form) without Dr. Agatston, who developed the algorithm for scoring years ago in the early days of heart scanning. We also need to credit him with putting together a rational diet despite the counter-information emanating from the Heart Association, the USDA (a la Food Pyramid, the one that makes Americans fat and diabetic), and the American Diabetes Association, among others.

But "Ask your doctor about taking statins and other cholesterol-lowering drugs"? This is where Dr. Agatston begins to falter. While he is putting his enormous notoriety to use, his message is bland and ineffective. "Do aerobic exercise"? We don't need Dr. Agatston to tell us this.

As much as Art Agatston has added to the national conversation on heart disease and diet, he has failed to deliver the message of true heart disease prevention. His approach lacks just a few crucial ingredients like lipoprotein testing, diagnosis of hidden causes of heart disease (like Lp(a)), and vitamin D. (Two years ago I had a patient I saw for an opinion after he'd showed Dr. Agatston his lipoprotein panel. The patient said Dr. Agatston looked at the report and didn't know what to do with it and handed it back to him without comment. He then asked if he wanted his autograph.)

Anyway, the rising tide raises all boats. Agatston's repeated public endorsements of heart scans will help deliver the message that heart disease is detectable in its early stages and should trigger action to follow a heart disease prevention program.

That alone is an accomplishment in a world hell-bent on dragging us into the hospital for procedures.

Take this survey: I DOUBLE-DARE YOU

In a previous post I entitled Heart disease reversal a big "No No", I posed a challenge--a dare--to readers to ask their doctors if coronary heart could be reversed.

Here's what I said:

I dare you: Ask your doctor whether coronary heart disease can be reversed.

My prediction is that the answer will be a flat "NO." Or, something like "rarely, in extraordinary cases," kind of like spontaneous cure of cancer.

There are indeed discussions that have developed over the years in the conventional scientific and medical literature about reversal of heart disease, like Dean Ornish's Lifestyle Heart Trial, the REVERSAL Trial of atorvastatin (Lipitor) and the ASTEROID Trial of rosuvastatin (Crestor). Reversal of atherosclerotic plaque in these trials tends to be small in scale and sporadic.

The concept of reversal of heart disease has simply not gained a foothold in the lexicon nor in the thinking of practicing physicians. Heart disease is a relentlessly, unavoidably, and helplessly progressive disease in their way of thinking. Perhaps we can reduce the likelihood of cardiovascular events like heart attack and death with statin drugs and beta blockers. But reverse heart disease? In your dreams!

We need to change this mentality. Heart disease is a reversible phenomenon. Atherosclerosis in other territories like the carotid arteries is also a reversible pheneomenon. Rather than throwing medicines and (ineffective) diets at you (like the ridiculous American Heart Association program), what if your doctor set out from the start not just to reduce events, but to purposefully reduce your heart's plaque? While it might not succeed in everyone, it would certainly change the focus dramatically.

After all, isn't this the theme followed in cancer treatment? If you had a tumor, isn't cure the goal? Would we accept an oncologist's advice to simply reduce the likelihood of death from cancer but ignore the idea of ridding yourself completely of the disease? I don't think so.

Then why accept "event reduction" as a goal in heart disease? We shouldn't have to. Heart disease reversal--elimination--should be the goal.


I know of one person who actually followed through on this challenge and asked his cardiologist whether his heart disease could be reduced or reversed. As predicted, the answer was no. No explanation followed.

But allow me to reiterate: Heart disease is 1) detectable, 2) quantifiable, 3) controllable, and, in many cases 4) reversible.

What if there was a big payoff to your doctor if heart disease was reversed, say $100,000? That's enough to dwarf the payoff from procedures. Guess what? You'd have doctors fighting for your business, a chance to reverse your disease, ads to that effect, champions of reversal emerging. No new tools would be necessary. They could use the tools already available. Then why hasn't this happened? Is the technology unavailable? Are the treatments ineffective?

No, heart disease is a controllable and reversible process with tools that are available today. But there is, of course, no big payoff for doing it. So the financial incentive remains to do procedures, not to reverse the disease.

But I'd like to re-pose this challenge. Ask your doctor if heart disease can be reversed, or at least reduced. I've even posted a Survey at the top left for anyone who tries.

Again, my prediction: Nobody will try it and nobody will post survey results. Why? Despite my rantings (and those of a few others) about the concept of heart disease being a reversible process, in the public's consciousness it remains a death sentence and the only solution is hospital procedures. My colleagues continue to cultivate this attitude and it serves them well financially.

I'll be disappointed if I prove to be right. I hope that I am wrong. But I don't think that I am.



Copyright 2008 William Davis, MD

Michael Pollan on Nutritionism



The wonderfully articulate Michael Pollan has written another book. Although he presents little new to anyone who read his previous book, The Omnivore's Dilemma: A natural history of four meals, he is such a wonderful writer, with such clever ways of seeing the world, that I couldn't resist this new, less ambitious book.

The new book is In Defense of Food: An eater's manifesto.

As in Omnivore's Dilemma, Pollan reminds us that we've lost contact with real food, foods that our great grandmother would recognize, not the just-add-water, dried, pulverized, sweetened, high-fructose, hydrogenated, shrink-wrapped, artificially-colored products that pass as foods in the grocery store.

In particular, Pollan attacks what he calls the ideology of Nutritionism. "The widely shared but unexamined assumption is that the key to understanding food is indeed the nutrient. Put another way: Foods are essentially the sum of their nutrient parts." He calls this "Nutritionism."

In the section called "Nutritionism comes to market," he uses margarine as the prototypical product of this philosophy:

"No idea could be more sympathetic to manufacturers of processed foods, which surely explains why they have been so happy to jump on the nutritionism bandwagon. Indeed, nutritionism supplies the ultimate justification for processing food by implying that with a judicious application of food science, fake foods can be made even more nutritious than the real thing. This of course is the story of margarine, the first important synthetic food to slip into our diet. Margarine started out in the nineteenth century as a cheap and inferior sustitute for butter, but with the emergence of the lipid hypothesis in the 1950s, manufacturers quickly figured out that their product, with some tinkering, could be marketed as better--smarter!--than butter: butter with the bad nutrients removed (cholesterol and saturated fats) and replaced with good nutrients (polyunsaturated fats and then vitamins). Every time margarine was found wanting, the wanted nutrient could simply be added (Vitamin D? Got it now. Vitamin A? Sure, no problem. But of course margarine, being the product not of nature but of human ingenuity, could never be any smarter than the nutritionists dictating its recipe, and the nutritionists turned out to be not nearly as smart as they thought. The food scientists' ingenious method for making healthy vegetable oil solid at room temperature--by blasting it with hydrogen--turned out to produce unhealthy trans fats, fats that we now know are more dangerous than the saturated fats they were designed to replace. Yet the beauty of a processed food like margarine is that it can be endlessly reengineererd to overcome even the most embarrassing about-face in nutritional thinking--including the real wincer that its main ingredient might cause heart attacks and cancer. So now the trans fats are gone, and margarine marches on, unfazed and apparently unkillable. Too bad the same cannot be said of an unknown number of margarine eaters."


Anyone who reads and thinks a lot about nutrition will find little new here. But nobody says it better than Pollan. While Gary Taubes (Good Calories, Bad Calories) is the real thinker of our age about nutrition, Michael Pollan is the true writer about it.

With books like these making the bestsellers list, I believe that we are gradually seeing rationality return to eating. It makes people skeptical of the glitzy ads that run on TV around the clock. I hope that Pollan's new book will make more and more people leery of the latest health claim that adorn some product. "More omega-3!" "A low-fat snack." "Heart Healthy!" "High in healthy fiber!"

Cholesterol follies

Rudy is a 59-year old man. He's had three heart catheterizations, two of which resulted in stent implantations. Obviously, Rudy should be the beneciary of a prevention program.

His basic cholesterol values:

Total cholesterol 164 mg/dl--pretty good, it seems.

LDL cholesterol 111 mg/dl--Wow! Not too bad.

HDL cholesterol 23 mg/dl--Uh oh, that's not too good.

Triglycerides 148 mg/dl--By national (NCEP ATP-III) guidelines, triglycerides of 150 mg/dl and below fall within the desirable range.


So we're left with an apparently isolated low HDL cholesterol, nothing more. On the surface, it doesn't seem all that bad.

Of course, we need to keep in mind that this pattern landed Rudy in the hospital on several occasions and prompted several procedures.

Should we rely on these results? How about Rudy's lipoproteins?

Here they are (NMR; Liposcience):

LDL particle number 2139 nmol/l--Representing an effective LDL of 213--over 100 mg higher than the standard value (above) suggests.

Small LDL particles 2139 nmol/l--In other words, 100% of all Rudy's LDL particles are small. (Thus, weight-based measures of LDL cholesterol fail to tell us that he has too many small particles.)

Large HDL 0 (zero) mg/dl--Rudy has virtually no functional HDL particles.


If we had relied only on Rudy's standard cholesterol values, we would have focused on raising HDL. However, lipoprotein analysis uncovered a smorgasbord of additional severe patterns. The high LDL particle number comprised 100% of small particles is especially concerning.

Truly, conventional cholesterol testing is a fool's game, one that time and again fails to fully uncover or predict risk for heart disease. One look at Rudy's lipoproteins and it becomes immediately obvious: This man is at high risk for heart disease and the causes are clear.

Of course, many physicians and insurance companies argue that the added information provided by this portion of the lipoprotein test added around $70 more to the expense.

When you see results like this, is there even a choice?

Equal calories, different effects

A great study was just published in the Journal of the American College of Cardiology:

Metabolic effects of weight loss on a very-low-carbohydrate diet compared with an isocaloric high-carbohydrate diet in abdominally obese subjects.

88 obese adults with metabolic syndrome were placed on either of two diets:

1) A very low-carbohydrate, high-fat diet (VLCHF): 4% calories from carbohydrates (truly low-carb); 35% protein; 61% fat, of which 20% were saturated. In the first 8 weeks, carbohydrate intake was severely limited to <20 grams per day, then <40 grams per day thereafter.

2) A high-carbohydrate, low-fat diet (HCLF): 46% calories from carbohydrates; 24% protein; 30% total fat, of which <8% were saturated.

Both diets were equal in calories (around 1400 calories per day--rather restrictive) and participants were maintained on the program for six months.

At the end of the six month period, participants on the VLCHF diet lost 26.4 lb, those on the HCLF diet 22.2 lbs (though the difference did not reach statistical significance). Thus, both approaches were spectacularly successful at weight loss.

Surprisingly, blood pressure, blood sugar, insulin and insulin sensitivity (a measure called HOMA) were all improved with both diets equally. Thus, these measures seemed to respond more to weight loss and less to the food composition.

Lipids differed between the two diets, however:


VLCHF:
Total cholesterol: initial 208.4 mg/dl final 207.7 mg/dl

LDL: initial 125 mg/dl final 123 mg/dl

HDL: initial 55 mg/dl final 64.5 mg/dl

Triglycerides: initial 144 mg/dl final 74 mg/dl

Apoprotein B: initial 98 mg/dl final 96 mg/dl


HCLF
Total cholesterol: initial 208.4 mg/dl final 187.5 mg/dl

LDL: initial 126 mg/dl final 108 mg/dl

HDL: initial 51 mg/dl final 54.5 mg/dl

Triglycerides: initial 157.6 mg/dl final 111 mg/dl

Apoprotein B: initial 100 mg/dl final 95 mg/dl


Some interesting differences became apparent:
--The VLCHF diet more effectively reduced triglycerides and raised HDL.
--The HCLF diet more effectively reduced total and LDL.
--There was no difference in Apo B (no statistical difference).

The investigators also made the observation that individual responsiveness to the diets differed substantially. They concluded that both diets appeared to exert no adverse effect on any of the parameters measured, both were approximately equally effective in weight loss with slight advantage with the carbohydrate restricted diet, and that lipid effects were indeed somewhat different.


What lessons can we learn from this study? I would propose/extrapolate several:

When calories are severely restricted, the composition of diet may be less important. However, when calories are not so severely restricted, then composition may assume a larger role. When calories are unrestricted, I would propose that the carbohydrate restriction approach may yield larger effects on weight loss and on lipids when compared to a low-fat diet.

The changes in total cholesterol are virtually meaningless. Part of the reason that it didn't drop with the VLCHF diet is that HDL cholesterol increased. In other words, total cholesterol = LDL + HDL + trig/5. A rise in HDL raises total cholesterol.

Despite no change in Apo B, if NMR lipoprotein analysis had been performed (or other assessment of LDL particle size made), then there would almost certainly have seen a dramatic shift from undesirable small LDL to less harmful large LDL particles on the VLCHF diet, less change on the HCLF diet.

The lack of restriction of saturated fat in the VLCHF that failed to yield adverse effects is interesting. It would be conssistent with the re-analysis of saturated fat as not-the-villain-we thought-it-was put forward by people like Gary Taubes (Good Calories, Bad Calories).

In the Track Your Plaque experience, small LDL is among the most important measures of all for coronary plaque reversal and control. Unfortunately, although this study was well designed and does add to the developing scientific exploration of diet, it doesn't add to our insight into small LDL effects. But if I had to make a choice, I'd choose the low-carbohydrate, high-fat approach for overall benefit.

Is skinny necessary for reversal?

Nothing we do in the Track Your Plaque program guarantees that coronary atherosclerotic plaque or your heart scan score is reduced or reversed.



But everything we do weighs the odds in your favor of successfully achieving reversal: correction of lipoprotein patterns, uncovering hidden patterns like Lp(a), vitamin D, being optimistic--it all tips the scales in your favor.

But how necessary is it to be skinny, meaning somewhere near your ideal weight?

It is important, but not as important as it used to be. Let me explain.

I used to tell people that plaque would not regress unless ideal weight was achieved and all the parameters of abdominal obesity and metabolic syndrome were corrected. This includes blood pressure, blood sugar, low HDL, small LDL, high triglycerides, and high c-reactive protein. Curiously, though, as we've gotten better and better at reducing coronary calcium scores, I've been finding that complete correction of all parameters, including achieving ideal weight, don't seem to be as necessary to achieve plaque reversal.

I almost hate to say this, but I've even witnessed significant drops in heart scan scores in people with body mass indexes (BMI) of 30--obese.

The necessary change doesn't seem to be weight, per se, but the consequences of weight. In other words, if you remain overweight, but blood sugar, HDL, small LDL, etc. have shown substantial improvement, then reversal is still achievable.

Then is it okay to be fat or overweight?

Reducing weight to ideal weight does indeed tip the scales in your favor, since it represents an observable, perceptible measure of all associated patterns. Dropping weight can also minimize the need for efforts to correct the consequences of overweight--you might need less niacin, fish oil, exercise, blood pressure medication, etc. to succeed at plaque reversal. Achieving ideal weight may also provide benefits like reduced risk of cancers and degenerative diseases of the hips and knees. But, to my recent surprise over the last two years, achieving ideal weight is not an absolute requirement to achieve reversal.

This is contrary to what some others say. For instance, in an upcoming interview with Dr. Joel Fuhrman on the Track Your Plaque website, Dr. Fuhrman argues that 10% body fat for males, 22% body fat for females, accelerates plaque and symptom reversal. Dr. Fuhrman is author of Fasting and Eating for Health, Eat to Live, and a new upcoming 2-part book, Eat for Health, and proponent of high-nutrient vegetarian diets and fasting. Dr. Fuhrman has been helpful in teaching us some important lessons on how to apply periodic fasting to accelerate plaque reversal.

So, which is it, fat or skinny?

If given a choice (which everyone has), I'd choose skinny. But, provided all the parameters associated with overweight are corrected, then remaining overweight doesn't necessarily mean that you can't still succeed at plaque reversal.

If you are interested in knowing what your ideal weight is, there are a number of software calculators and tables available, including the HealthCentral.com calculator and the National Heart, Lung, and Blood Institute BMI Calculator.


Image courtesy Wikipedia.

Copyright William Davis, MD 2008

MESA Study: Track Your Plaque-Lite?

The long-awaited data analyses from the Multi-Ethnic Study of Atherosclerosis (MESA) are finally making it to press.

The MESA Study is an enormously ambitious and important study of 6800 people, 45 to 84 years old, that includes white, black, Hispanic, and Chinese participants from six communities around the U.S. (Forsyth County, NC; Northern Manhattan and the Bronx, NY; Baltimore and Baltimore County, Md; St Paul, Minn; Chicago, Ill; and Los Angeles County, California.) Participants had no history of heart disease at enrollment. All underwent a heart scan (either EBT or multi-detector heart scans) at the start. It is therefore the largest prospective study involving heart scans ever performed. It is, not unexpectedly, yielding some fascinating observations relevant to the Track Your Plaque program. The MESA study is, incidentally, funded by the non-commercial, publicly-funded National Heart, Lung, and Blood Institute and is therefore presumably free of commercial bias.

Among the most recent publications is Risk factors for the progression of coronary artery calcification in asymptomatic subjects: Results from the Multi-Ethnic Study of Atherosclerosis (MESA) In this analysis of 5700 of the MESA participants, a repeat heart scan was obtained an average of 2.4 years after the first. Conventional risk factors for heart disease were obtained at the start (see below for details under Measurement of Covariates.)

After analyzing the data and risk factors assessed, such as age, sex, race, blood pressure, body mass index (BMI), presence of diabetes, blood sugar, and family history of heart disease, two questions were asked:

1) What risk factors predict heart scan scores?

2) What risk factors predict progression (i.e., increase) in heart scan scores?

(The second question is particularly relevant to us and the Track Your Plaque experience.)

The MESA analysis showed that essentially all the risk factors assessed correlated with both the initial heart scan score, as well as the rate of progression. No surprises here.

But the most eye-opening finding was that the conventional risk factors assessed explained only 12% of the variation and progression in heart scan scores (coefficient of determination, or R squared, = 0.12.) In other words:

--Conventional risk factors like LDL cholesterol, diabetes, and excess weight explain only a tiny fraction of why someone develops coronary atherosclerotic plaque as represented by a heart scan score.

--The great majority of risk for a high heart scan score remains unexplained by conventional risk factors.

--The great majority of risk for progressive increase in heart scan scores also remains unexplained by conventional risk factors.


In light of the MESA analysis, it's no surprise that strategies like reducing LDL cholesterol with statin drugs fails to prevent most heart attacks. It's no surprise that conventional prevention programs that talk about "knowing your numbers," eating a "balanced" or low-fat diet, etc., fail miserably to prevent the vast majority of heart attacks and heart procedures.

MESA confirms what we've been saying these past few years: If you want control over coronary heart disease, you won't find it in Lipitor, a low-fat diet, and other limited conventional notions of risk. Correction of conventional risk factors like cholesterol and blood pressure are, in a word, a failure. I wouldn't even call the conventional approach Track Your Plaque-Lite. They don't even come close.

If conventional risk factors can explain only 12% of the reason behind heart disease, we've got to look elsewhere to understand why you and I develop this process.



Measurement of Covariates
Information on demographics, smoking, medical conditions, and family history was collected by questionnaire at the initial examination. Height and weight were also measured at the baseline examination, and blood was drawn for measurements, including lipids, inflammation, fasting glucose, fibrinogen, and creatinine. Resting blood pressure was measured 3 times in the seated position, and the average of the last 2 measurements was used in the analysis. Medication use was determined by questionnaire. Additionally, the participant was asked to bring to the clinic containers for all medications used during the 2 weeks before the visit. The interviewer then recorded the name of each medication, the prescribed dose, and frequency of administration from the containers.


Copyright 2008 William Davis,MD