Heart disease reversal a big "No No"

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.

Of course, the medical literature is swamped with studies that have nothing to do with reversal, like what stent is best, what platelet-inhibiting intravenous drug is best, when should angioplasty or stents be used and when, do implantable defibrillators save lives, improvements in coronary bypass techniques, etc. There are tens of thousands of these studies for every study that focuses on the question of atherosclerotic plaque reversal.

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.

Demystification

Once upon a time, remember how medical information was mysterious, hospitals were places where frightening, inscrutable things happened, diseases were strange maladies that struck without reason, and obtaining information about health was like hunting for buried treasure? The full extent of many peoples' understanding of health came through relatively anemic sources like Readers' Digest. (Remember "I am Joe's Colon"?)

Compare this to what we have now. If I wanted to obtain information about ankylosing spondylitis (a rare genetic disease of the spine), a Google search yields 1.46 million citations. Not all the information, of course, is helpful or relevant, but there's certain to be a bounty of information that far exceeds what you could have uncovered 40 years ago.




Suppose you enter the search phrase "antithrombin III" into your Google search. Citations: over 900,000. (The number of search citations, in fact, exceeds the number of Americans with a deficiency of this blood clotting protein!)

The same is true with heart disease. There was a time, not more than 30-40 years ago, when information about the heart and heart disease was hard to come by. The most you would find were superficial discussions about heart attacks, what chest pain means, descriptions of bypass surgery. Ask your doctor, you'd likely receive a brief, cursory response about how you probably shouldn't worry it.

Even during medical school in the 1980s, I remember struggling to get answers to my questions from faculty during medical school and medical training. It was as if providing too much information would eliminate the advantage superiors wielded over trainees.

The same selfish sentiment, the "I know something you don't know" mentality reminiscent of a schoolboy's "naa na na naa naa!" unfortunately persists. But it is rapidly disintegrating. Soon it will join the junk heap of medical mis-information accumulated over the years (a big pile, to be sure). The internet and, I'll admit (grudgingly), the media, have been responsible for demystifying the formerly mysterious and indecipherable world of health.

You now have, at a moment's disposal, access to an extraordinary array and breadth of health information that was inconceivable just a few years ago.

Times are changing. Doctors no longer hold the monopoly over health information. The public--YOU--are rapidly becoming the arbiters of health, the informed consumers of a soon-to-be retail product called health care, and the increasingly savvy judges of what should join the mainstream path of health. It is all part of this wave of change that I've been advocating: the emerging concept of self-empowerment in healthcare.

Added to the junk heap of health-mistakes-of-years-past will be medical protectionism over health information, heart procedures, drug industry excesses, nutritional mis-information, among others. The demystification of health information will open the floodgates of individual insight into health. It delivers control over your own health destiny straight into your own lap.

Everything has omega-3

Walking the supermarket aisles, you may have lately noticed that numerous new products are appearing sporting "omega-3s" on the label.

Some products simply contain alpha-linolenic acid, a tiny amount of which is converted to the biologically active omega-3s, EPA and DHA. Natural Ovens' Brainy Bagel, for instance, carries a claim of "620 omega-3."



I find this confusing and misleading, since people will often interpret such a claim to mean that it contains 620 of EPA and DHA, similar to two capsules of standard fish oil (1000 mg capsules). Of course, it does NOT. I find this especially troublesome when people will actually stop or reduce their fish oil, since they've been misled into thinking that products like this bread contain active omega-3 fatty acids that yield all the benefits of the "real stuff."


Other products actually contain the omega-3, DHA, though usually in small quantities. Breyer's Smart with DHA is an example, with 32 mg DHA per container.


I find products with actual DHA (from algae) a more credible claim. However, the Center for Science in the Public Interest (CSPI) has looked at the actual contents of DHA in some of these products and found some discrepancies, including amounts of DHA less than the labeled amount and claims of omega-3 wihtout specifying DHA vs. linolenic acid. (It's probably linolenic acid, if it's not specified.)

All in all, the addition of DHA to food products is a nice way to boost your intake of this healthy omega-3. However, keep in mind that these are processed, often highly processed, foods and you will likely pay a premium for the little boost. For now, stick to fish oil, the real thing.

For a brief summary of the CSPI report and a link to the Nutrition Action Newsletter, see Omega-3 Madness: Fish Oil or Snake Oil.

Are cardiologists the enemy?

I'm sitting at dinner with two colleagues. One is a cardiology colleague, another an internist who, in addition to practicing general internal medicine, also takes heart disease prevention very seriously. He has, in fact, participated in the Track Your Plaque program and dropped his heart scan score substantially.

"Why don't we see you in the cath lab much?" my cardiology colleague asked me. He was puzzled, since he knew my background in cath lab work from years before, spending day and night doing procedure after procedure. He spends virtually all his days there.

"Well, my patients simply don't have events any more. Heart attacks and angina among people in my program are just about non-existent. They don't have symptoms and they don't have to go to the hospital. I can't remember the last time that I was woken up in the middle of the night for an urgent procedure for one of my patients."

The internist across the table smiled and expressed his agreement. "That's the same thing I'm seeing: No heart attacks, very few if any referrals to cardiologists for procedures. I remember when it was a several times a week thing. Now, almost never. "

Looking at my cardiology colleague, I saw the usual cardiologist reaction: Eyes searching left and right and behind us for something more interesting. Certainly, talking about a virtual cure for coronary heart disease was just too damn dull.

Such is the attitude of 98% of my colleagues: If it doesn't generate a revenue-producing procedure, why bother? Prevention is for general practitioners, the line of thinking goes. "And anyway, I'm too busy doing procedures! I don't ahve time to talk about prevention and health!" Of course, the poor general practitioner is already overloaded with caring for arthritis, flu, diabetes and all the new drugs for diabetes, headaches, vaccinations, diarrhea, and . . .oh, yes, heart disease prevention.

Are cardiologists the enemy? No, of course they are are not. But they often act like they are. Talking to cardiologists is like going to the car dealer with your checkbook out, pen in hand. The salesman gets to write the check himself and you just sign it. Talk to a cardiologist and more often than not you will end up with a heart procedure--whether or not you need it.

Unfortunately--tragically--they often forget what they are supposed to be doing: Taking care of a disease by preventing it. Putting in a defibrillator is not preventing a disease. Putting in three stents, laser angioplasty, and thrombectomy are not ways of preventing a disease.

I'm thankful for my internist friend who sees the light. Coronary heart disease is a an easily measurable, quantifiable, preventable, and REVERSIBLE process for many, if not most, people when provided the right tools. But don't ask your neighborhood cardiologists to give you those tools.

Are CETP inhibitors kaput?

Was torcetrapib’s crash and burn fatal for this class of drug?

At the 2007 American Heart Association meetings in Orlando, Florida, Dr. Philip Barter of Sydney, Australia, presented an update of the ILLUMINATE drug trial for the once-promising drug, torcetrapib, the billion-dollar bet that Pfizer made on its first entry into the new drug class.

You may recall that the crash and burn of Pfizer’s torcetrapib in December 2006 made headlines and prompted enormous disappointment for many patients and doctors who had hoped for a new drug choice to raise HDL cholesterol. Pfizer executives (heads flew!) and investors were also disappointed, anticipating release of a drug that might have become the number one biggest selling drug in the world—ever, surpassing even Lipitor's® $13 billion annual sales.

Torcetrapib is the first among the “cholesteryl-ester transfer protein inhibitors,” or CETP-inhibitors, drugs that block the exchange of cholesterol and triglycerides between HDL and VLDL particles and prevent formation of the unwanted small LDL particles. Preliminary efforts suggested that effects were positively enormous.

However, the 15,000-participant trial was abruptly terminated after 550 days when an excess of deaths were identified among the group taking the experimental drug: 59 deaths in control group; 93 deaths in the torcetrapib group.

In addition, cardiovascular events were 24% greater in the torcetrapib group, numbering 373 compared to 464 in the no-torcetrapib group, including a substantially greater number of heart attacks and hospitalizations. Another surprise came in the way of cause of death among some of the torcetrapib patients, with an excess of deaths due to cancers (twice as many in the torcetrapib group), strokes, and infections.

Why the divergence: enormous improvements in cholesterol values, yet increase in adverse effects including more heart attack? Deeper digging by the principal investigators uncovered unexpected distortions of electrolytes like sodium and potassium. They then re-analyzed blood samples from participants on both sides of the trial and discovered that participants taking torcetrapib experienced significant rise in the blood pressure hormone, aldosterone. This, they surmised, also likely accounted for the 4 mmHg average rise in blood pressure among those taking the experimental drug. (This is the same pathway blocked by blood pressure drugs like ACE inhibitors lisinopril and enalapril, ARBs like losartan.)

Simultaneously (what a coincidence!) with the torcetrapib data, investigators at competing drug manufacturer, Merck, reported encouraging data with their version of CETP inhibitor, anacetrapib. In a phase II FDA trial of 589 patients, anacetrapib reduced LDL-C levels by up to 40% and increased HDL-C up to 139%.


Spokesman Daniel Bloomfield, M.D., of Merck Research Laboratories reported that "The favorable lipid effects seen in this study with multiple doses of anacetrapib were significant, and confirm the continued evaluation of the clinical benefits of CETP inhibitors in the treatment of dyslipidemia." Quick to distinguish this drug from torcetrapib’s track record of dangerous effects on blood pressure, he added that "the decreased LDL-C concentrations, increased HDL-C concentrations and no demonstrable increase in blood pressure seen with anacetrapib are particularly encouraging results of this study."

However, the data reported only an 8 week expereince. Given the experience with torcetrapib, longer term data will obviously be required to assess safety. After Pfizer spent over $1 billion and sacrificed lives to obtain this experience, Merck will need to tread carefully.

It will clearly be many years before we have a confident answer on whether the CETP-inhibitor class of drugs will be a safe choice for correction of cholesterol abnormalities, especially low HDL. Are we helpless until then?

Though CETP inhibitors offer the potential for a one-stop opportunity to raise HDL substantially, there are still many strategies available to raise HDL.

Strategies that raise HDL and are available today include:
• Weight loss—to your ideal weight. A very effective strategy.
• Reduction in processed carbohydrates—like breads, pasta, cookies, pretzels, etc. Note that very low-fat diets reduce HDL. Often a huge effect.
• Fish oil—A small effect, more dramatic when triglycerides are high.
• Niacin—Vitamin B3, the best we have at present. Doses of 500-1500 mg per day raise HDL 20–50%; work with your doctor if you are contemplating niacin. We use this agent everyday and have had great success; good hydration is key to minimize the annoying “hot-flush” effect.
• Dark chocolate—40 grams, or about 2 inches square, a delicious way to squeeze out a little rise in HDL.
• Alcoholic beverages—Red wines are almost certainly the preferred route, rich in flavonoids.
• Exercise—HDL-raising effects vary, but can sometimes be as much as 10–20 mg.
• Other drugs—Though not commonly used for this effect, drugs like pioglitazone (for diabetes and pre-diabetes); fibrates (Tricor® or fenofibrate; Lopid® or gemfibrozil); and Pletal® or cilostazol are occasionally prescribed.
• Vitamin D—You won’t find validation of this effect in any scientific study, but our emerging experience in our heart disease reversal program is suggesting that this neglected nutrient can exert powerful HDL-raising effects. In fact, supplementing vitamin D has made my life much easier.


And, last I checked, none of these HDL-raising strategies are ever fatal.

Roto Rooter for plaque




Joe, a machinist, was frightened and frustrated.

With a heart scan score of 1644 at age 61, his eyes bulged when I advised him that, if preventive efforts weren't instituted right away, his risk for heart attack was a high as 25% per year. Joe had "passed" a stress test, thus suggesting that, while coronary plaque was present--oodles of it, in fact--coronary blood flow was normal. Thus, there would be no benefit to inserting three stents, say, or a bypass operation.


(Illustration courtesy Wikipedia)

"I don't get it, doc. Why can't you just take it out? You know, like Roto-Rooter it out? Or give me something to dissolve it!"

Of course, if there were such a thing, I'd give it to him. But, of course, there is not. It doesn't mean that there haven't been efforts in this direction over the years. Among the various attempts made to "Roto-Rooter" atherosclerotic plaque have included:

Coronary endarterectomy
This is a drastic procedure rarely performed anymore but enjoyed some popularity in the 1980s and 1990s. Coronary endarterectomy was performed during coronary bypass surgery, but few thoracic surgeons performed it. Milwaukee's Dr. Dudley Johnson was the foremost practitioner of this procedure (retired a few years ago after his own bypass operation) with a mortality in excess of 25%. A very dangerous procedure, indeed. The technical hurdle, beyond the tedium and length of time required to remove plaque that had a tendency to fragment, was blood clot formation after tissue was exposed upon plaque removal. I saw many lengthy hospital stays and deaths following this procedure.

Coronary atherectomy
This is an angioplasty-type procedure that has gone through several variations over the years.

In the early 1990s, transluminal extraction atherectomy (TEC) was a technique involving low-rpm drill bits with a suction apparatus that was used to clear soft debris, usually from large coronary arteries or, more commonly, bypass grafts. Then came direction atherectomy, in which a steel housing contained a sharp drill bit that captured atherosclerotic plaque in an aperture along the housing length and stuffed it into a nosecone, retrieved once the device was removed.

Then came high-speed rotational atherectomy in which a diamond-tipped drill bit rotated up to 200,000 rpm and essentially pulverized plaque to flow downstream and, presumably, eventually captured by the liver for disposal. Rotational atherectomy is still in use on occasion. Laser angioplasty, usually using the excimer wavelength, vaporizes plaque. I did plenty of all of these back in the early and mid-1990s.

While all atherectomy procedures sound clever, they are all plagued by the same problem: vigorous return of plaque. Remove plaque, it grows back. There are few instances today in which atherectomy is still performed.

Chelation
This involves a metal-binding, or "chelating," agent like EDTA normally used in conventional practice for lead poisoning. Usually administered IV, some have also advocated oral use. People who use chelation also tend to believe in faith healing and other practices based on faith, not science. There is an international trial that is nearing completion that should provide the final word on whether there is any role to intravenous chelation.

There are numerous other oral treatments that claim a Roto-Rooter-like effect. Nattokinase, for example--an outright, unadulterated, and unqualified scam.

Unfortunately, the helpless, ignorant, and gullible are many. When frightened by the specter of heart disease, there are plenty of people who will willingly pay for the hope provided by clever ads, fast-talking salespeople, and unscrupulous practitioners.

So, Joe, there is no Roto-Rooter for coronary atherosclerotic plaque, at least one that is safe, doesn't involve a life-threatening effort, provides results that endure beyond a few months, and truly works.

The Track Your Plaque program may not be easy. There are obvious common hurdles to adhering to these concepts: obtaining lipoprotein testing, getting intelligent interepretation of the results, persuading your doctor to measure vitamin D blood levels, battling the onslaught of prevailing food propaganda that confuses and misleads. The Track Your Plaque program also requires time, at least a year.

But it's the best program there is. Do you know of anything better?

"Beware nutritional supplements"



In our effort to expand the reach for the nationwide conversation on heart disease reversal, I'd like to welcome the newest contributor to the Track Your Plaque family, a new Member blogger, Heart Cipher.

We first came to appreciate the insights of Heart Cipher on our Member Forum. His curiousity and ability to cut through the bull--- have won over our hearts and minds. I think you will appreciate his unique perspective as someone who has experienced first hand the inadequacies of the present procedure-focused, drug-obsessed standard of medical care that dominates, yet has the intelligence and worldliness to recognize that there are better ways.

Read his post about meeting a new cardiologist for the first time and the reaction he receives when he describes the Track Your Plaque program here.

http://www.heartcipher.com/

The rules of reversal


For the last few years, most practicing physicians have followed a rough blueprint for cholesterol management provided by the Adult Treatment Panel-III “consensus” guidelines, or ATP-III, a lengthy document last released in 2001, updated in 2004.

For instance, ATP-III suggests reducing LDL cholesterol to 100 mg/dl or less for those deemed to be at high risk for future heart disease, arbitrarily defined as a risk of 20% over a 10-year period. It also suggests that a desirable triglyceride level is no more than 150 mg/dl. The ATP-III guidelines have been the topic of discussion in thousands of medical meetings, editorials, and reports. They have served as the basis for many dinners at nice restaurants, weeks in Vegas or Honolulu, many, many lunches catered by pharmaceutical representatives. For most internists, family doctors, cardiologists, and lipid clinics, ATP-III is the Bible for cholesterol management.

AT-III has also become the de facto standard that could conceivably held up as the prevailing "standard of care" in a court of law in cases of presumed negligence to treat cholesterol values. “Doctor, would you agree that the consensus guidelines issued by the National Institutes of Health and endorsed by the American Heart Association state that LDL cholesterol should be reduced to 100? You do? Then why was Mr. Jones’ LDL not addressed according to these guidelines?”

Who was on the ATP-III panel and on what scientific evidence were the guidelines based? Several problems:

1) Of the 9 physician members of the panel, 8 had ties to industry, some of them quite intimate.

2) The studies upon which the guidelines were based and figure prominently, such as the Heart Protection Study, PROVE IT, and 4S, were all funded by the pharmaceutical industry. Of course, it would be unreasonable to expect anyone other than the pharmaceutical industry to fund drug studies. But prominently neglected or understated in the guidelines are all the other insights and treatments for coronary atherosclerotic risk available that were NOT funded by industry.

Of course, there’s money to be made in reducing LDL cholesterol. Lots of it--$23 billion last year alone, in fact. Just keeping that fact in mind makes the ATP-III guidelines make far better sense.

ATP-III is really not a blueprint for heart disease prevention. It is a blueprint--by industry, for industry--on how and when to treat LDL cholesterol.


But what if ATP-III had been a map for navigating coronary plaque reversal instead? What if it were not obsessed with just reducing LDL cholesterol, but was focused on providing the corner internist, family doctor, or cardiologist a roadmap for navigating the highways and byways of reversal?

That would be interesting. Mainstream reversal. Imagine that.

Among the difficulties is that the path to reversal is not lined with deep pockets. Treat LDL and who gains? That's easy. Reverse heart disease and who gains? Beyond LDL reduction, very few (beyond you and me, of course).

That’s why the call for a new Age of Self-Empowerment in healthcare is necessary now more than ever. In my view, in the foreseeable future, we will not have an ATP-III-like blueprint for heart disease control or reversal, nor will we witness a boom of nationwide appreciation that coronary atherosclerosis is a reversible process.

It’s time to take the control back and put it in our own hands. Don't expect the American Heart Association to do it. Don't expect the pharmaceutical industry to do it. If there's anyone who's going to do it, it's YOU.

Incurable wheataholics

Greg slumped back in his chair.

"I'm sorry, doc. I feel like the world's biggest schlump!"

He was referring to the fact that he had gone wheat-free for two months--eliminated all breads, bagels, donuts, pasta, breakfast cereals, crackers, pretzels--and promptly lost 30 lbs. He felt great, discovered new levels of energy he thought he'd lost long ago.

Then some friends convinced him to have some cheeseburgers at a fast food restaurant.

"After that, it was downhill. I couldn't get enough. My wife made chile and I had to have four slices of bread with it. Then I'd have two more. I just couldn't stop."

Now, having regained the 30 lbs in the space of another two months, Greg was expressing his disgust.

And it's not the first time. Greg has struggled with his wheat-alholism for as long as I've known him. I've tried motivating him by showing him the flagrant lipoprotein patterns that his wheat habit and excess weight caused: markedly elevated LDL particle number, severe small LDL, low HDL, high triglycerides, high C-reactive protein, high blood sugar, high blood pressure. Greg has received a total of 7 stents over the past 5 years. His next stop is the operating room for a bypass if he can't bring his patterns and impulses under control.

But for some reason, Greg seems to always return to the wheat trough, gorging on breads, pretzels, cake, often in great quantities.

I'm not entirely sure what to do with someone with Greg's severe degree of wheat-aholism. I view wheat-aholism as similar to alcoholism. For some, it can be as addictive.

The only strategy that I know can work is to make a clean break and drop wheat products altogether. Just as an alcoholic cannot just satisfy him/herself with a drink or two a day, so a wheataholic can't be satified with just a couple of wheat crackers. It inevitably leads to the avalanche of wheat indulgences.

Perhaps we should form a new group: Wheataholics Anonymous. "Hi. My name is Greg and I'm a wheataholic."

The battle for asymptomatic disease

The heart disease revenue pie is shrinking. So is the "serving size" being shared by competing hospitals.

In other words, as more hospitals open heart programs, there is more competition for the same heart patient. Throw into the mix the drop in "acute" presentations of disease, probably due to the now widespread prescribing of statin drugs. When I first started cardiology practice 15 years ago, for instance, days and nights spent taking care of heart attacks coming through the emergency room was a common event. It still happens, but far less frequently. (I don't mean to suggest that the actual prevalence of coronary heart disease has decreased, just the acute, catastrophic version of it.)

Throw into this mix the results of the COURAGE Trial that has put a damper on the value of stents and angioplasty vs. "optimal" medical therapy in people with stable anginal symptoms, since there was little advantage of procedures. Though it has not stopped the practice, it has reduced the enthusiasm for procedures. Though data are hard to come by, I've heard talk of 10% or greater drops in total procedural volume over the past year.

It's not uncommon for hospitals to have overbuilt heart facilities in anticipation of continued growth of this--until recently--growth industry called heart disease. However, factors are converging that may provide a new profit opportunity for hospitals.

One such opportunity is CT coronary angiography. The usual scenario: Man or woman without symptoms is persuaded somehow--an ad, primary care physician, next door neighbor with a scary event, Dr. Mehmet Oz gushing about this sexy new technology on yet another Oprah episode--to undergo a CT coronary angiogram. A "severe" blockage is found, despite the lack of symptoms, and voila! A stent patient or bypass patient is created out of nothing! Do this repeatedly and systematically, and a hospital can regain its former high-procedural volume glory.

Heart scans, though I believe deeply in them and they are the basis for the Track Your Plaque prevention and reversal program, can also be used and abused this way. Asymptomatic person has a score 150. Concerned, they go to their physician who orders a nuclear stress test. An "inferior perfusion defect" is seen, presumably representing poor flow through the right coronary artery (but often just means that the diaphragm overlaps the heart muscle and yields this apparition, a "false positive" or misleading result). "But--wink--we've got to find out if there's a severe blockage, don't we? You don't want to end up in an early grave!"

Thus, the battle for new patients with asymptomatic disease is getting underway in earnest. The scramble for cardiologists to learn how to use CT coronary angiograms is proceeding at breakneck speed, with new training courses being offered nationwide several times and places every month. CT coronary angiography is a useful test, but it is also subject to enormous abuse. It also provides the ticket for the unscrupulous physician and the revenue-hungry hospital eager to expand its patient volume.

Many people believe that this cannot happen commonly in 2007, given scrutiny of practices, litigiousness, and the expectation of a moral sense in medicine. However, I've witnessed such incidents several times this month alone. If you need graphic proof of just how far this can go before action is taken, read Coronary, Stephen Klaidman's chilling tale of a cardiologist and cardiothoracic surgeon in small-town northern California who built an enormous heart center based on fabricated heart disease diagnoses. You'll also find their story in Shannon Brownlee's recently released Overtreated: Why Too Much Medicine Is Making Us Sicker and Poorer.





Of course, the Track Your Plaque program is meant principally for people without symptoms, also. But we are advocating that asymptomatic disease is a reason for prevention, not procedures. There's a difference.

By the way, the two practitioners who engineered the escapade detailed in these books, cardiologist Chae Hyun Moon and cardiac surgeon Fidel Realyvasquez, walked away with a monetary fine and suspension of their California medical licenses. It is likely that many people died because of their abusive practices, but the state struggled to make a sufficiently persuasive case for reasons that I still don't understand.

Pre-diabetes: An explanation for explosive coronary plaque growth

Art's first CT heart scan in March, 2006 yielded a concerning score of 1336. He felt fine--no chest discomfort, no breathlessness, etc.

Art agreed to take the statin cholesterol drug his primary care doctor prescribed. He also agreed to take the fish oil, niacin, and some of the nutritional supplements that we advised. But Art just couldn't bring himself to make the commitment to lose weight.

At the start of his program, Art--at 5 ft. 8 inches--was 40 lbs overweight (212 lb). This was important since his blood sugar wavered in the pre-diabetic range, going as high as 130 mg. (The American Diabetes Assn. defines diabetes as a blood glucose of 126 mg or greater.)

One year later, Art's lipid and lipoprotein values were corrected to perfection. But he still weighed in at a hefty 209 lbs--essentially no change. His blood sugar likewise hovered in the 120's.

I felt Art need to be prodded, so I asked him to undergo another heart scan. His score: 1935--a 600 point increase, or 45%!

Only now has Art begun to comprehend to power of diabetes and pre-diabetes to fan the flames of plaque growth. Recent published data, in fact, show that the majority of recently diagnosed diabetics already have well-established coronary artery disease.

Don't let this happen to you. Do not dismiss diabetic patterns as they will catch up to you. If Art can lose the 30-40 lbs in the abdominal weight that is creating the diabetic pattern, he will likely succeed in stopping plaque growth. Otherwise, it's just a matter of time before his heart attack, stent, or bypass.

Who cares if you're pre-diabetic?

Marta is a smart lady. She's worked in hospital laboratories for the last 23 years and knows many of the ins and outs of lab tests and their implications.

After years of being told that her cholesterol was acceptable, she needed to undergo urgent bypass surgery after experiencing severe breathlessness that proved to be a small warning heart attack at age 57. But this made Marta skeptical of relying on cholesterol to identify heart disease risk.

I met Marta two years after her bypass surgery when she was seeking better answers. And, indeed, she proved to have several concealed sources of heart disease: small LDL particles, Lipoprotein(a), intermediate-density lipoprotein (IDL--a very important abnormality that means she is unable to clear dietary fats from her blood), among others. But she was also mildly diabetic with a blood sugar of 131 mg (normal < or = 100 mg). This had not been previously recognized.

As I'm a cardiologist and our program focuses on reversal and control of coronary plaque, I asked Marta to return to her primary care doctor to continue the conversation about diabetes. She was a bit frightened but followed through.

"Well, you're not urinating excessively. And your long-term measure of blood sugar, hemoglobin A1C, is still normal. I wouldn't worry about it. We'll just watch it."

I guess I should know better. What the poor primary care doctor doesn't know is that pre-diabetes and mild diabetes are potent risks for heart disease. In fact, some of the most explosive rates of plaque growth occur when these patterns are present. It's well established that risk for heart attack in a diabetic is the same as that of someone who's already suffered a prior heart attack--very high risk, in other words.

Marta's primary care doctor's advice would be like inquiring about cancer and the doctor says "Let's just wait until it's metastatic--then we'll start to worry." Of course, this is insane.

Pre-diabetes and mild diabetes should not be ignored or just "watched". Even though the blood sugar itself may not be high enough to endanger you, the hidden patterns underlying your body's unresponsiveness to insulin creates a torrent of hidden coronary risk.

For better answers, Track Your Plaque members can read "Shutting Off Metabolic Syndrome" at http://www.cureality.com/library/fl_dp001metabolic.asp on the www.cureality.com website. ("Metabolic syndrome" is the name commonly given to the constellation of abnormalities associated with pre-diabetes and diabetes.)

Don't get smug!

It may sound silly, but after someone succeeds in stopping their heart scan score from increasing or reduces their score, I warn them to not get smug. Let me explain.

I'll tell you about Jack. I met Jack a few years ago after he had a heart scan at age 39. His score: 1441! A score this high at his age obviously puts him in the 99th percentile. Also recall that a score >1000 carries a 25% annual risk for heart attack.

This captured Jack's attention. At the start, his lipoproteins were disastrous with numerous abnormal patterns. Jack committed to the program. After one year, his lipoproteins were around 80-90% corrected towards perfection. He'd lost 27 lbs, was exercising six days a week, and felt great.

Jack's repeat score one year later: 1107--over a 300 point drop! A huge success. He was ecstatic.

Unfortunately, work and life in general distracted him. Jack allowed himself to drift back to old habits, indulging in fast food 2 or 3 times a week, slacking on exercise such that it became sporadic, half-hearted efforts, and regained 15 lbs. He even failed to show up for appointments and we lost contact for two years.

One day, Jack simply decided to see where he stood, so he got himself another heart scan. The score: 2473--over a doubling from his reduced score.

The message: Long-term consistency is key, even after you've achieved control over your score. Stick with your program--and don't get smug!

Holidays are dangerous!

If you're on holiday from work today, make sure you're not on holiday from your health, too.

Too often, people come back to the office telling me that the holidays simply got out of hand--cookouts, picnics, family gatherings, etc.--and they simply couldn't avoid overeating, overdrinking, sitting around--and gaining 3-5 lbs in a weekend. (Our record is 10 lbs in a weekend!)

I don't want to harp on this issue and ruin your holiday, but I can't stress how important it is that you don't allow this to happen to you. Weight gained in a brief space of time has exceptionally destructive effects. Ever see the movie "Super Size Me"? It's an entertaining and well-done yet graphic portrayal of the damaging effects of rapid weight gain.

Enjoy your time off. Relax, enjoy your family and friends--but continue to pay attention to choosing the right foods, don't overeat, take time out to do something (or several things) physical. It'll pay off hugely in the long run.

More on carotid plaque...

Although not a perfect test, carotid ultrasound is an exceptionally easy and accessible test. Using high-frequency sound, clear images are available for most people.

I say it's not perfect because the way it's done in 2006 makes it a non-quantitative test. It is a qualitative test. In other words, you may find out that there's a 30% blockage ("stenosis"), at the far end of the common carotid artery on the right side. Unfortunately, this gives you an isolated measure of diameter of the plaque compared to the artery. What it does not tell you is what the volume of the entire plaque is. That's a far more accurate measure (and one that is incorporated into your heart scan score, by the way).

Nonetheless, carotid ultrasound is easy, very safe, and available in most hospitals and many clinics. One difficulty: most insurance companies will not allow you to go through a carotid ultrasound scan as a "screening" procedure, i.e., a test just to see if you have a carotid plaque. They will generally pay if you're having symptoms of a stroke or "mini-stroke" (transient ischemic attack, or "TIA"), have an abnormal sound in your carotid ultrasound detected by your doctor (a carotid "bruit"), or some other unusual indications. Sometimes, a resourceful physician will muster up a diagnosis based on something in your history (e.g., left arm numbness, a common and often benign complaint that can also signal stroke).

Another option are the mobile scanners or some hospital services that offer carotid screening, usually for a very modest price. Drawback: Sporadic availability, difficulty in obtaining serial scans, and imprecise reporting since it's viewed as a screening test. But it's better than nothing.

My hope is that, as screening services using safe imaging techniques like ultrasound propagate and increase in direct availability to the public, you'll be able to circumvent the obstacles imposed by your insurance company and even, sometimes, your doctor. But try your doctor first.

Carotid plaque can be shrunk

Rose, a 64-year old woman, just had a 70% carotid blockage identified by a screening ultrasound. When the result was given to her doctor, he prescribed Lipitor and told Rose that an ultrasound would be required every year. She would need carotid surgery, an "endarterectomy", if the blockage worsened.

"Can't I reduce the amount of blockage I have?" asked Rose.

"No. Once you've got it, it doesn't get any better."


Is this true? Once you've got carotid plaque, you can only expect it to get worse and it can't be reduced?

This is absolutely not true. In fact, compared to coronary plaque, carotid plaque is easier to reduce!

Of course, the Track Your Plaque program is designed to help you control or reduce coronary plaque. But, in our experience, people who have both coronary and carotid plaque will show far greater and faster reduction of carotid plaque. Dramatic reductions are sometimes seen. I've personally seen 50-70% blockages reduced to <30% on many occasions.

The requirements to achieve reduction of carotid plaque are very similar to the approach we use to reduce coronary plaque. One difference is that hypertension may play a more important role with carotid plaque and needs to be reduced confidently to the normal range before carotid plaque is controlled.

I find it shocking that the attitude like the one provided by this physician continue to prevail. Unlike coronary plaque, which has a relatively small body of scientific literature documenting how it can be reduced, carotid plaque actually enjoys a substantial clinical literature. Part of the reason is that the carotids are more easily imaged using ultrasound. (Heart structures can be seen with ultrasound, but not the coronary arteries.)

Numerous agents have been shown to contribute to reduction of carotid plaque: statin drugs, niacin, fish oil, the anti-diabetic "TZD" drugs (Actos, Avandia), several anti-hypertensive drugs, vitamin E, pomegranate juice, and several others.

It outrages me to hear stories like this. Rose is not the only one.

Don't accept the flip dismissals or the over-enthusiastic referral for carotid procedures. Insist on a conversation about plaque regression.


Note: Although I am a vigorous advocate of atherosclerotic plaque regression, this does not mean that if you have a severe (70% blockage or greater), or if there are symptoms from your carotid disease, that you should engage in a program of reversal. You must always take the advice of your doctor if your safety is in question.

Vitamin D--A coronary risk factor

Look up "coronary risk factors" in any text and you'll find high cholesterol, smoking, diabetes, and high blood pressure listed. You won't find deficiency of vitamin D listed.

Ask 99% of physicians if a deficiency of vitamin D is a coronary risk factor and you'll get rolling eyes and a sigh.

Yet, in the Track Your Plaque experience, vitamin D is emerging as a very important factor in coronary plaque development. We have observed that there are a substantial number of people whose lipids and lipoproteins are not abnormal enough to fully explain their heart scan score. In other words, there seems to be something else necessary to satisfactorily explain the magnitude of coronary plaque.

I believe that severe vitamin D deficiency is at least one of the most important factors. We've seen many people with blood levels of vitamin in the range of severe deficiency (<20 ng/ml of 25-OH-Vitamin D3) yet bland lipids and lipoproteins.

Correcting vitamin D blood levels to 50 ng/ml also seems to be among the required factors in stopping coronary plaque growth, or stopping your heart scan score from increasing.

Keep your eye on this extremely important and exciting issue. Sadly, it won't be propelled into the media like the conversation about cholesterol or high-tech procedures, since no company stands to profit from it. But you and I don't have to play that game.

Cholesterol is dead!

I saw a patient in the office yesterday. He came to me for an opinion regarding his high heart scan score of 525, putting him in the 90th percentile (5% annual risk of heart attack).

His doctor had been puzzled because his LDL cholesterols had ranged from 110 to 131 mg--actually below average. (The average LDL for the U.S. is 132 mg.) Likewise, HDL was a favorable 63 mg.

Lipoprotein analysis told the story loud and clear. His LDL particle number, a far more precise measure of LDL, was 2448 nmol/l. This means that his true LDL was more like 240-250 mg! (You can get a sense for what the true LDL is from LDL particle number by dropping the last digit: 2448 becomes 244.) Conventional LDL was therefore inaccurate by over 100 mg.

He also had a severe small LDL particle pattern. The cause of his coronary plaque was a large excess of small LDL particles. LDL cholesterol (and total cholesterol, likewise) didn't even hint at this pattern. Nor did his favorable HDL.

Think of LDL particle number as an actual count of LDL particles per volume, e.g., number of particles per cc of blood. This makes it easier to conceptualize. LDL particle number is the measure you get when you have an NMR lipoprotein profile, our preferred method of lipoprotein testing. If this is unavailable to you, apoprotein B is a reasonable second choice, though not as accurate in my view. More info on NMR is available at their website, www.lipoprofile.com.

How to make a $1 million in cardiology

Want to make a $1,000,000 as a cardiologist in the next year? It's easy. All you have to do is:

1) Perform heart catheterizations or other procedures on anybody you can, even if it's not necessary. Perform them even if the patient has no symptoms and the stress test is normal.

2) Perform heart catheterizations if the patient is too timid or ill-informed to object.

3) Insert coronary stents in blockages, even when they're minor and it's not necessary.

4) Turn every heart procedure into a revenue-producing stream by looking for other profit opportunties, such as minor kidney artery blockages.

5) Heart disease is frightening. Scare the heck out of patients by exagerrating the dangers so they'll go through testing and procedures gratefully.


Sound absurd? Well, it would be if these weren't all true.

These are real examples, as awful as it sounds. I've witnessed all these behaviors. Not just occasionally, but with regularity.

Just today, I encountered a colleague who performs heart catheterizations routinely (up to several per day) when any symptom is present and the stress test is entirely normal. This is grossly inappropriate.

Your protection is being better-informed and avoid being sucked into the vast and frightening cardiovascular machine of revenue-yielding procedures. Part of your protection is to get a CT heart scan, then engage in a program of heart disease prevention.

Doctor, do I have lipoprotein (a)?

I met Joyce today for a 2nd opinion. She told me about this conversation she'd had with her cardiologist:

"Doctor, do you think I could have lipoprotein (a)? I read about how it can cause heart attacks even when cholesterol is controlled."

"What does it matter? Even if you have it, there's nothing we can do about it. There's no treatment for it."

Joyce was understandably groping for some means to prevent her coronary disease from causing more danger. At 56, she'd already survived a heart attack that resulted in two stents to her left anterior descending. Around 9 months later, she received a 3rd stent to another artery.

Her doctor had put her on Pravachol and said that was enough. "We know that cholesterol causes heart disease and the Pravachol reduces it. Why do we need to know anything more?"

So Joyce came to me for another view. I explained to her that there are, in fact, several ways to deal with lipoprotein(a). It is, without a doubt, among the more difficult patterns to manage--but not impossible. In fact, we have a growing list of participants in the Track Your Plaque program who have stopped or reduced their heart scan scores.

I continue to be horrified at the level of ignorance that prevails among my colleagues, the cardiologists, and the primary care community. If your doctor gives you advice like this, get a new doctor.