My life is easy

In the old days (the 1980s and 1990s), practicing cardiology was very physically and emotionally demanding. Since procedures dominated the practice and preventive strategies were limited, heart attacks were painfully common. It wasn't unusual to have to go to the hospital for a patient having a heart attack at 3 am several times a week.

Those were the old days. Nowadays, my life is easy. Heart attacks, for the most part, are a thing of the past in the group of people who follow the Track Your Plaque principles. I can't remember the last time I had a coronary emergency for someone following the program.

But I am reminded of what life used to be like for me when I occasionally have to live up to my hospital responsibilities and/or cover the practices of my colleagues. (Though I voice my views on prevention to my colleagues, the most I get is a odd look. When a colleague recently covered my practice for a weekend while I visited family out of town, he commented to me how quiet my practice was. I responded, "That's because my patients are essentially cured." "Oh, sure they are." He laughed. No registration that he had witnessed something that was genuine and different from his experience of day-to-day catastrophe among his own patients. None.)

I recently had to provide coverage for a colleague for a week while he took his family to Florida. During the 7 days, his patients experienced 4 heart attacks. That is, 4 heart attacks among patients under the care of a cardiologist.

If you want some proof of the power of prevention, watch your results and compare them to the "control" group of people around you: neighbors, colleagues, etc. Unfortunately, the word on prevention, particularly one as powerful as Track Your Plaque, is simply not as widespread as it should be. Instead, it's drowned out in the relentless flood of hospital marketing for glitzy hospital heart programs, the "ask your doctor about" ads for drugs like Plavix, which is little better than spit in preventing heart attacks (except in stented patients), and the media's fascinating with high-tech laser, transplant, robotic surgery, etc.

Prevention? That's not news. But it sure can make the slow but sure difference between life and death, having a heart attack or never having a heart attack.

My bread contains 900 mg omega-3

Phyllis is the survivor of a large heart attack (an "anterior" myocardial infarction involving the crucial front of the heart) several years ago. Excessive fatigue prompted a stress test, which showed poor blood flow in areas outside the heart attack zone. This prompted a heart catheterization, then a bypass operation one year ago.

FINALLY, Phyllis began to understand that her unhealthy lifestyle played a role in causing her heart disease. But lifestyle alone wasn't to blame. Along with being 70 lbs overweight and overindulging in unhealthy sweets every day, she also had lipoprotein(a), small LDL particles, and high triglycerides. The high triglycerides were also associated with its evil "friends," VLDL and IDL (post-prandial, or after-eating, particles).

When I met her, Phyllis' triglycerides typically ranged from 200-300 mg/dl . Fish oil was the first solution, since it is marvelously effective for reducing triglycerides, as well as VLDL and IDL. Her dose: 6000 mg of a standard 1000 mg capsule (6 capsules) to provide 1800 mg EPA + DHA, the effective omega-3 fatty acids.

But Phyllis is not terribly good at following advice. She likes to wander off and follow her own path. She noticed that the healthy bread sold at the grocery store and containing flaxseed boasted "900 mg of omega-3s per slice!". So she ate two slices of the flaxseed-containing bread per day and dropped the fish oil.

Guess what? Triglycerides promptly rebounded to 290 mg/dl, along with oodles of VLDL and IDL.

A more obvious example occurs in people with a disorder called "familial hypertriglyceridemia," or the inherited inability to clear triglycerides from the blood. These people have triglycerides of 800 mg/dl, 2000 mg/dl, or higher. Fish oil yields dramatic drops of hundreds, or even thousands of mg. Fish oil likely achieves this effect by activating the enzyme, lipoprotein lipase, that is responsible for clearing blood triglycerides. Flaxseed oil and other linolenic acid sources yield . . .nothing.

Don't get me wrong. Flaxseed is a great food. As the ground seed, it reduces LDL cholesterol, reduces blood sugar, provides fiber for colon health, and may even yield anti-cancer benefits. Flaxseed oil is a wonderful oil, rich in monounsaturates, low in saturates, and rich in linolenic acid, an oil fraction that may provides heart benefits a la Mediterranean diet.

But linolenic acid from flaxseed is not the same as EPA + DHA from fish oil. This is most graphically proven by the lack of any triglyceride-reducing effects of flaxseed preparations.

Enjoy your flaxseed oil and ground flaxseed--but don't stop your fish oil because of it. Heart disease and coronary plaque are serious business. You need serious tools to combat and control them. Fish oil is serious business for triglycerides. Flaxseed is not.

More Omnivore's Dilemma

Another irresistible quote from Michael Pollan’s book, The Omnivore’s Dilemma:

“In many ways breakfast cereal is the prototypical processed food: four cents’ worth of commodity corn (or some other equally cheap grain) transformed into four dollars’ worth of processed food. What an alchemy! Yet it is performed straightforwardly enough: by taking several of the output streams issuing from a wet mill (corn meal, corn starch, corn sweetener, as well as a handful of tinier chemical fractions) and then assembling them into an attractively novel form. Further value is added in the form of color and taste, then branding and packaging. Oh yes, and vitamins and minerals, which are added to give the product a sheen of healthfulness and to replace the nutrients that are lost whenever whole foods are processed. On the strength of this alchemy the cereals group generates higher profits for General Mills than any other division. Since the raw materials in processed foods are so abundant and cheap (ADM and Cargill will gladly sell them to all comers) protecting whatever is special about the value you add to them is imperative.”

A food manufacturer’s nightmare is when you and your family shop in the produce aisle in the grocery store. Produce is unmodified (aside from the pesticide and genetic-engineering issues), not added to, and therefore of no interest to the food manufacturer, since no additional profit can be squeezed out of it. If you pay 45 cents for a cucumber, there’s no room for a processor to multiply it’s return.

Vegetables and fruits have imperfections, no doubt, particularly pesticide residues and the “dumbing-down” of some foods to increase their desirability (e.g., green grapes, what I call “grape candy”). But vegetables and fruits are the closest you can get to foods that are essentially unmodified by a food manufacturer. Due to the absence of processing, they are not calorie-dense like a bag of chips; they include all the naturally-occurring healthy factors like flavonoids that food scientists have, thus far, struggled and failed to identify, quantify, and control; and they lack all the unhealthy additives that processed foods require for extended shelf life, palatability, and reconstitution (anti-separating agents, emulsifiers, sweeteners, etc.)

Vegetables, in particular, should be the cornerstone of your plaque control program. Not breakfast cereals, breads, bacon, sausage, mayonnaise, fruit drinks and soda, all the foods that worsen the causes of coronary plaque and raise your heart scan score.

If you would like to understand how the current perverted state of affairs in food have come about, Pollan’s book is must reading.

Pollan's The Omnivore's Dilemma


‘You are what you eat’ is a truism hard to argue with, and yet it is, as a visit to a feedlot suggests, incomplete, for you are what what you eat eats, too. And what we are, or have become, is not just meat but number 2 corn and oil.”

Author Michael Pollan offers unique, enlightening, and entertaining insights into the food we eat in his new book, The Omnivore’s Dilemma: A natural history of four meals.

Pollan draws parallels between the dilemma of the primitive human living in the wild, having to stumble through the choices of animals and plants that could nourish or kill, and the ironically modern return of this phenomenon in present-day supermarkets. While the dangers of food choices aren’t as immediate as in the wild (eat the wrong mushroom or herb, for instance, and you die), they can nonetheless be life-threatening, or at least health-threatening. Hydrogenated oils, high-fructose corn syrup, carageenan, guar gum. . .“What is all this stuff anyway, and where in the world did it come from?”

Among the issues Pollan discusses is that of modern cattle raising practices: the rush to fatten a cow from an 80 lb calf to a 1200-pound, bloated cow over a period of 14 months. Nature created this animal to mature over a 4 to 5 year period through grazing, thus it’s beautifully “engineered” ruminant system that allows it to digest cellulose in grasses, a process that humans and other mammals are incapable of. The pressures to bring greater quantities of beef to market at a reduced price and make more money have resulted in a farming industry that encourages the incorporation of unnatural, often inhumane practices like corn feeding (rather than grass grazing), refeeding of bovine body parts (thus “mad cow disease”), and widespread and chronic administration of hormones and antibiotics.

(I can't help but think that the rapid and perverse fattening of cattle by industrial "farming" is paralleled by the fattening of the eating American. After all, we are the hapless recipients of this flood of cheap, unhealthy, plasticized food.)

The industrialization of food has de-personalized the act of eating. You no longer have any connection with the green pepper in your salad (unless you grew it yourself), nor do you have any appreciation for the suffering of the cow in your hamburger. Worse, the distortion of livestock raising practices has modified the food composition of meat. Range-fed animals, leaner and richer in omega-3 fatty acids, have been replaced by the marbled, saturated fat-rich modern grocery bought meats.

This is a theme that Pollan reiterates time and again: how food processing adds value to the manufacturer, often starting with a healthy ingredient but modifying it, adding ingredients, taking out others, until it’s something decidedly unhealthy. Yet the manufacturer will trumpet the fact that a healthy ingredient is included. Breakfast cereals are the most blatant example of this. What the heck are Cheerios but an over-processed attempt to make more money out of the simple oat?

Pollan’s eloquent and unique insights into food are definitely worth reading.

As always, per our Track Your Plaque policy, I recommend Mr. Pollan’s book strictly on its merits. We obtain no “cut”, commission, or other financial gain by recommending his book. Track Your Plaque members pay their modest membership fee for truth. They do not pay for us to advertise something that provides hidden advantage to us. We do not advertise, editorialize to steer you towards a specific product or service. What we say, we truly believe.

The most frequently asked question of all

The most frequently asked question on the Track Your Plaque website:

"Can you recommend a doctor in my area who can help me follow the Track Your Plaque program?"

This is a problem. Unfortunately, I wish I could tell everyone that we have hundreds or thousands of physicians nationwide who have been thoroughly educated and adhere to the principles I believe are crucial in heart disease:

1) Identify and quantify the amount of coronary atherosclerotic plaque present. In 2007, the best technique remains CT heart scans.

2) Identify all hidden causes of plaque. This includes Lp(a), post-prandial disorders, small LDL, and vitamin D deficiency.

3) Correct all patterns.


But we don't.

You'd think that this simple formula, as straightforward and rational as it sounds, would be easily followed by many if not most physicians. But Track Your Plaque followers know that it simply is not true. My colleagues, the cardiologists, are hell-bent on implanting the next new device, providing a lot more excitement to them as well as considerably more revenue.

The primary care physician is already swamped in a sea of new information, going from osteoporosis drugs, to arthritis, to gynecologic issues, to skin rashes and flu. Heart disease prevention? Oh yeah, that too. They can only dabble in heart disease prevention a la prescription for Lipitor. That's quick and easy.

Nonetheless, I believe we should work towards identifying the occasional physician who is indeed willing to help people follow a program like Track Your Plaque. As we grow, we will need to identify some mechanism of professional education and we will maintain a record of these practitioners. But right now, we're simply already stretched to the limit just doing what we are doing.

If you come across a physician who practices in this fashion and you've had a positive relationship, we'd like to hear about it.

Do stents kill?

There's apparently a lively conversation going on at the HeartHawk Blog (www.hearthawk.blogspot.com). Among the hot topics raised was just how bad it is to have a stent.

I think that my comments some time back may have started this controversy. I've lately noticed that having a stent screws up your heart scan scoring in the vicinity of the stent. I was referring to the fact that I've now seen several people in the Track Your Plaque program do everything right and then show what I call "regional reversal": unstented arteries show dramatic drops in score of 18-30%, but the artery with a stent shows significant increase in score.

This is consistent with what we observe in the world outside Track Your Plaque when stents are inserted. Someone will get a stent, for instance, in the left anterior descending artery. A year later, there will be a "new" plaque at the mouth of the stent or just beyond the far end. This is generally treated by inserting another stent. Use of a drug-coated stent seems to have no effect on this issue.

Now, my smart friends in the Track Your Plaque program would immediately ask, "Does this mean you continually end up chasing these plaques that arise as a result of stents? Do you create an endless loop of procedures?"

Thankfully, the majority of times you do not. Rarely, this does happen and can lead to need for bypass surgery to circumvent the response. But it is unusual. The tissue that grows above and below stents does seem to be unusually impervious to the preventive efforts we institute.

Perhaps there's some new supplement, medication, or other strategy that will address this curious new brand of plaque growth. Until then, you and I can only take advantage of what is known. If it's any consolation, the plaque that seems to grow because of a previously inserted stent seems to lack the plaque "rupture" capacity of "naturally-occuring" plaque. It is, indeed, somehow different. It is more benign, less likely to cause heart attack. It's always been my feeling that this tissue behaves more like the "scar" tissue that grows within stents, causing "re-stenosis", a more benign, less rupture-prone kind of tissue.

Dr. Reinhold Vieth on vitamin D

A Track Your Plaque member brough the following webcast to our attention:

Prospects for Vitamin D Nutrition
which can be found at http://tinyurl.com/f93vl

Despite the painfully dull title, the webcast is the best summary of data on the health benefits on vitamin D that I've seen. The presenter is Dr. Reinhold Vieth, who is among the handful of worldwide authorities on vitamin D. In 1999, Dr. Vieth authored the first review to concisely and persuasively argue that vitamin D nutrition was woefully neglected and that its potential for health was enormous.
(See Vieth R, Am J Clin Nutr 1999 May;69(5):842-856 at http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=10232622&query_hl=1&itool=pubmed_DocSum.)

I predict that, after viewing Dr. Vieth's hour-long discussion, you will be as convinced as I am that vitamin D is crucial for health. Unfortunately, Dr. Vieth doesn't delve into the conversation about the potential effects on heart disease, since his audience was primary interested in multiple sclerosis, a disease for which vitamin D replacement promises to have enormous possibilities. Even in 2007, the data suggesting that vitamin D has heart benefits is circumstantial. Nonetheless, from our experience, I am thoroughly convinced that, with replacement to blood levels of vitamin D to 50 ng/ml, heart scan scores drop more readily and faster.

If you view Dr. Vieth's wonderful webcast, keep in mind that when he discusses vitamin D blood levels, he's using units of nmol/l, rather than ng/ml. To convert nmol/l to ng/ml, divided by 2.5. For example, 125 nmol/l is the same as 50 ng/ml (125/2.5 = 50).

Vitamin D on Good Morning America


Positive comments about vitamin D made it to a discussion on Good Morning America today about the new and exciting developments in nutrition and "functional foods".

I'm thrilled that the media is conducting these conversations. It sure is making my job easier, not having to persuade patients that taking vitamin D is truly and hugely beneficial for health. I still have to struggle with my colleagues, who tell patients to stop the "poisonous" doses we use.

But I worry that many of the details behind vitamin D don't quite make it to the media conversation. These are crucial, make-it-or-break-it issues, such as:

--Vitamin D must be vitamin D3 or cholecalciferol, not D2 or ergocalciferol. D2 is virtually worthless. Little or none is converted to the active D3, despite the fact that D2 is the form often added to some foods.

--Vitamin D3 supplements must be oil-based capsules, or gelcaps. Tablets are so poorly or erratically absorbed that it's simply not worth the effort. (We get ours from the Vitamin Shoppe.)

--The dose should be sufficient to eliminate the phenemena of deficiency, which is around 50 ng/ml. I take 6000 units per day. Dr. John Cannell of www.vitamindcouncil.com takes 5000 units per day. I give my wife 2000 units per day (she's not as deficient as I was), each of my kids 1000 units per day, except for my 180 lb. 15 year old who takes 2000 units.

I fear that, when people hear that vitamin D packs fabulous effects for health, they will take a 400 unit tablet--nothing will happen. They will not obtain the benefits such as reduction of blood pressure and blood sugar; increased bone density, reduction of arthritis, dramatic reduction in risk for fractures; reduction in risk for colon, prostate, and breast cancer; reduction in risk for multiple sclerosis; reduction in inflammatory processes such as those evidenced by C-reactive protein; and facilitation of reduction of heart scan score.

Would you bet your life on chelation?


Hugh's heart scan score was 1751, an awful score. Recall that, at this level of scoring, Hugh's heart attack and death risk is 25% per year.

Obviously, serious efforts need to be taken. In this situation, much as I despise drug companies and what they represent and their heavy-handed ways, I'm more inclined to resort directly to prescription agents, as well as our nutritional supplements and other strategies. The price of dilly-dallying could be his death.

Hugh and his wife asked about chelation. Now, there are five studies I'm aware of that have tried to examine the value of chelation. None showed any measurable benefit, though all were rather weak in design and small in number of participants. One study, for instance, looked at whether anginal chest pains were provoked any later after chelation. Another looked at whether calf claudication, or calf cramping while walking due to artery blockages in the leg arteries, was delayed on treadmill testing after chelation. No benefit was observed: no delay in provocation of angina, no delay in provocation of claudication.

However, the adherents of chelation have been vehement enough that the NIH has funded a large, multi-center study to settle the question once and for all. Best I can tell, the study has not been contaminated by any drug company involvement. It is meant to be an unbiased, objective study of whether chelation has any value.

My personal experience in patients who underwent chelation is that, despite spending hundreds or thousands of dollars, plaque grew at the expected rate--no effect at all.

None of this constitutes proof of efficacy nor proof of lack of efficacy. We will need to await the NIH trial to have better information.

Should Hugh bet his life on chelation? I advised him strongly against it. At this point, the only reason I can see to pursue chelation would be faith--that is, expectation based not on fact, but on hope.

The powerful forces preserving the status quo


An interesting quote from the book, Critical Condition: How health care in American became big business--and bad medicine:


Politics and Profits

To protect its interests and expand its influence, the health care industrial complex has done what all successful special interests do: It's become a big donor and a high-powered lobby in Washington. In the last fifteen years, HMOs, insurers, pharmacuetical companies, hospital corporations, physicians, and other segments of the industry contributed $479 million to political campaigns--more than the energy industry ($315 million), commercial banks ($133 million), and big tobacco ($52 million). More telling is how much the health care industry spends on lobbying. It invests more than any other industry except one, according to the nonpartiisan Center for Responsive Politics. From 1997 to 2000, the most recent year for which complete data is available, the industry spent $734 million lobbying Congress and the executive branch. Only the finance, insurance, and real estate lobby exceeded that amount in the same period, with a ttoal of $823 million. In contrast, the defense industry spent $211 million--less than one-third of the health care expenditure.


These telling statistics indicate just how vigorously profit-seeking forces in heart care are trying to preserve the status quo. Hospitals want to protect their valuable procedure-driven enterprise, the pharmaceutical industry wants to protect its enormous though little-known niche of procedure-based medications (like $1200 a dose ReoPro), and the medical device industry wants to maintain the multi-billion dollar-generating machine aided and abetted by the FDA's 501k rule (that makes entry to market a breeze).

The current procedure based formula for heart disease profits so many and they are desperate to preserve it. Resistance to the deep-pocketed efforts of industry and hospitals will come from people like you and me, trying to propagate a better way.

Remember: hospital procedures for coronary disease represent the failure of prevention. They are not--any longer--successes in and of themselves.

Read a scathing insight into some of these practices by reading investigative journalists' Donald Barlett and James Steele's book, Critical Condition. I found their descriptions painfully accurate. (But don't get too angry! Remember: only optimists reverse their plaque! We need to turn the conversation in a positive direction, not just in this Blog or the Track Your Plaque website, but nationwide.)

One of the new missions for the www.cureality.com website is to help you understand just how powerful, insidious, shrewd, and pervasive the efforts to maintain the current system truly are.

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