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.
I Wish I Had Lipoprotein(a)!

I Wish I Had Lipoprotein(a)!

Why would I say such a thing? Well, a number of reasons. People with lipoprotein(a), or Lp(a), are, with only occasional exceptions:

--Very intelligent. I know many people with this genetic pattern with IQs of 130, 140, even 160+.
--Good at math--This is true more for the male expression of the pattern, only occasionally female. It means that men with Lp(a) gravitate towards careers in math, accounting, financial analysis, physics, and engineering.
--Athletic--Many are marathon runners, triathletes, long-distance bicyclists, and other endurance athletes. I tell my patients that, if they want to meet other people with Lp(a), go to a triathlon.
--Poor at hydrating. People with Lp(a) have a defective thirst mechanism and often go for many hours without drinking water. This is why many Lp(a) people experience the pain of kidney stones: Prolonged and repeated dehydration causes crystals to form in the kidneys, leading to stone formation over time.
--Tolerant to dehydration--Related to the previous item, people with Lp(a) can go for extended periods without even thinking about water.
--Tolerant to periods of food deprivation or starvation--More so than other people, those with Lp(a) are uncommonly tolerant to days without food, as would occur in a wild setting.


In short, people with Lp(a) are intelligent, athletic, with many other favorable characteristics that provide a survival advantage . . . in a primitive world.

So when did Lp(a) become a problem? When an individual with Lp(a) is exposed to carbohydrates, especially those from grains. When an evolutionarily-advantaged Lp(a) individual is exposed to carbohydrates, more than other people they develop:

--Excess quantities of small LDL particles--Recall that Lp(a) is a two-part molecule. One part: an apo(a) made by the liver. 2nd part: an LDL particle. When the LDL particle within the Lp(a) molecule is small, its overall behavior is worse or more atherogenic (plaque-causing).
--Hyperglycemia/hyperinsulinemia--which then leads to diabetes. Unlike non-Lp(a) people, these phenomena can develop with far less visceral fat. A Lp(a) male, for instance, standing 5 ft 10 inches tall and weighing 150 pounds, can have as much insulin resistance/hyperglycemia as a non-Lp(a) male of similar height weighing 50+ pounds more.

Key to gaining control over Lp(a) is strict carbohydrate limitation. Another way to look at this is to say that Lp(a) people do best with unlimited fat and protein intake.

Comments (33) -

  • Bill Davis

    8/8/2012 1:17:58 PM |

    I have Lp(a) and am working on reducing it.
    Have been off wheat for several years now and on a low-carb diet. Hope I find that diet as well as fish oil, thyroid treatment, niacin and DHEA will bring it down.
    Thanks for making me feel special with this article! I have cross posted it. Scan coming up next month to give me a look at how I'm doing.
    The other Bill Davis

  • Joe

    8/8/2012 5:05:52 PM |

    I know this is probably a stupid question: but who doesn't have Lp(a)? My last VAP said that I have a Lp(a) of 7.0 and that <10.0 is preferred. Do some people actually have zero Lp(a)?

    Thanks!

  • randallbb

    8/9/2012 3:01:37 PM |

    I too am high Lp(a) and fit largely the profile Dr. Davis has outlined.  Am working on the Lp(a) with all guns blazing!  My new TYP lifestyle along with high amounts of fish oil and Niacin have brought it down markedly in just six months (from 61mg to 46mg on the NMR profile).  Am eating lots of cheese, nuts, etc, so am glad to hear that fats are a good thing!  Dr. Davis' post here reminds me to keep limited my carb intake!

  • Holly

    8/9/2012 10:44:08 PM |

    Any ideas why these traits would correlate with Lp(a)?

  • aerobic1

    8/11/2012 2:28:01 PM |

    Joe:

    Yes, some people do have "zero" Lp(a).  It is partly determined by your genetics which you have no control over.  But, as Dr. Davis suggests you gain gain control over your Lp(a) with dietary interventions such as elimination of wheat and other refined carbs, along with taking a few targeted supplements.  His interventions do not involve pharmaceutical drugs as there are no drugs that effectively treat Lp(a).

    Three years ago my first VAP test revealed a Lp(a) level of 22.  Three years of following Dr. Davi's advice my level is now 3.  For more information go to http://www.trackyourplaque.com/default.aspx.

  • Joe

    8/11/2012 4:59:41 PM |

    Thanks for the feedback!
    On the other hand, aren't you on the way to having no Lp(a)?  From 22 to 3?
    I'm still not sure why having "high" Lp(a) is a good thing. I'm still confused. Frown

  • jpatti

    8/11/2012 9:08:51 PM |

    We're also good-looking.  And very sexy.  And surprisingly modest!  ;)

    So why the heck would the thirst thing be going on?  I don't get it.  

    I have this issue; I have to carry drinks all the time or I completely forget about drinking.  I never go anywhere without carrying drinks cause I don't remember until I've got a killer headache.  I've got a giant mug of coffee and a liter of ice water flavored with lime shrub sitting next to me right now.  

    It's not that I'm not thirsty, if you ask me, I become aware of thirst.  It's just that "thirsty" is not something I am aware of at all.  I don't notice it unless I ASK myself if I'm thirsty.  

    I'm also ridiculously picky, I can have a drink sitting next to me, but if the ice has melted, I don't "want" it no matter how thirsty I am.  

    I don't understand why I'm like this.

  • aerobic1

    8/12/2012 2:48:06 AM |

    Joe:  
    There is nothing good whatsoever about having any measurable level of Lp(a).  Zero Lp(a) level should be your goal.  The personality characteristics Dr. Davis pointed out are just some typical observations of Lp(a)er's but do not assume the higher your Lp(a) is that the more intelligent, better at math or athletics, etc. you will become.  Lp(a) offers no advantage in that regard.

    There is plenty of good reading and advice from Dr. Davis on this subject on this blog on what Lp(a) is and how to self-manage it.  http://blog.trackyourplaque.com/category/lipoproteina.  Most all doctors are not well informed on this subject and therefore do not know how to treat it.

  • aerobic1

    8/12/2012 4:52:33 AM |

    jpatti:

    The sensation of thirst is governed by the Hypothalamus and Limbic System of the brain.  I do not have an understanding of why people with Lp(a) demonstrate this unusual thirst pattern that Dr. Davis has observed in people with Lp(a).  Here is a good explanation of how the typical thirst mechanism works.  http://www.enotes.com/thirst-reference/thirst.  

    Perhaps the normal brain hormone driven thirst mechanism in people with Lp(a) "malfunctions" and may not be producing enough arginine vasopressin to enhance thirst.  The relationship of renin, angiotensin II, and aldosterone also control water retension and thirst and may play a role too.

  • Joe

    8/12/2012 6:36:30 PM |

    Aerobic:
    Thanks again. I followed that link and it reiterated Dr. Davis' protocol, of: " i.e., wheat elimination followed by elimination of cornstarch, oats, and sugars; high-dose fish oil (total daily EPA + DHA of 6000 mg/day); vitamin D supplementation sufficient to achieve a 25-hydroxy vitamin D level of 60-70 ng/ml; iodine supplementation; and thyroid normalization which, in Ted’s case, required supplementation with the T3 thyroid hormone, liothyronine, at a small dose. "

    And I follow that protocol pretty closely (I don't take quite that much fish-oil).  My thyroid is fine. I have Pattern "A" LDL. Vitamin D of 90ng/ml. My TC is "high" but I have great trig and HDL numbers and ratios. My Lp(a) again is 7, which is well under the "reference range" of  <10 (according to VAP). But I'm unable to find anything anywhere that explains why having a zero Lp(a) is best, or what the mechanism is that makes it best. I'll keep looking around. Thanks for the help!

  • Joanna

    8/13/2012 8:16:28 PM |

    So we requested our doctor order an Lp(a) test along with several other blood tests that were being done - and later find out that our insurance company (Humana) will not cover the cost of the test, they gave some reason like it wasn't scientifically proven to be useful!!!  It's $65 so not sure if it would be worth fighting them on this one since they have been pretty good about covering most things.

  • Mark

    8/14/2012 2:59:56 AM |

    Hi Dr. Davis,
    I’m 47 yrs old. I’ve had migraines since I was a teen and I developed Athsma this past January (hate it). During the process of discovery the drs found I have a 50% blockage in one of the 5, non critical, arteries running along the back of my heart. Scared me, to say the least. I’ve always eaten quite healthfully (for what I knew), am thin @ 6′ 1″/155lbs (was 175lbs in Jan.). Had:
    Total Cholesterol of 200
    LDL of 146
    HDL of 50

    Drs wanted me to do Lipitor. Researched and said, “No, thanks.” Started exercising 5-6 days/wk (lifting + walk/run), taking red yeast rice, fish oils, fish, no meat, no dairy, no eggs, lots of veggies/fruit, etc., but still eat beans, oats (every AM), occasional wraps. After 6 wks my blood work (VAP) was as follows:
    LDL=86
    HDL=43
    VLDL=17
    TOT. CHOL=146
    Trigycerides=66
    Non-HDL (LDL+VLDL)=103.

    Seemed GREAT to me! The dr wasn’t impressed. Said my ‘particle size’ was small: LDL1(a)=8.1, LDL2(a)=0, LDL3(b)=39.5, LDL4(b)=24.9. Density Pattern=B.

    I’ve continued but don’t know how to elevate my HDL and reduce the particle size/change the pattern to the more favorable ‘A’. Getting down about this. Working hard but, seems like I can’t find answers that work, anywhere! What might you would work in my situation? Also, Is niacin ANDRed Yeast Rice a bad idea?
    I’ll hang up and listen. Thank you,
    Mark

  • Will

    8/14/2012 3:03:09 PM |

    Dr. Davis,

    Do you have any comments or response to the study released yesterday at the University of Western Ontario, comparing the risk of regular consumption of egg yolks to smoking on the increase of arterial plaque?

  • JoAnne

    8/15/2012 1:08:25 AM |

    Dr Davis, I recently had had a NMR LipoProfile done, but I don’t understand the numbers. I think it’s saying my LDL particle size is pattern A (good), but the total LDL-P number of 1985 nmoI/L is bad. And the HDL at 79 mg is good, but the TC at 307 is bad…. I’m so confused. Can you please summarize? I’ve been looking at the TYP website and I’m ready to join.

    LDL-P    1985 nmoI/L  (LDL Particle number)

    LDL-C    212 mg/dL  (calculated)
    HDL-C  79 mg/dL
    Triglycerides  82 mg/dL
    Total Cholesterol  307 mg/dL

    LDL & HDL Particles
    HDL-P   40.8 μmoI/L  (total)
    Small LDL-P  106 nmoI/L
    LDL size  22.1 nm

    Lipoprotein markers assoc with insulin resistance & diabetes risk
    Large VLDL-P  0.7 nmoI/L
    Small LDL-P    106 nmoI/L
    Large HDL-P  15.8 μmoI/L
    VLDL size    32.9 nm
    LDL size    22.1 nm
    HDL size    9.9 nm

    Insulin resistance score  0-100
    LP-IR score    5

  • kimsuoil

    8/15/2012 2:15:14 AM |

    Dr. Davis, I have Lp(a) and all of the traits above. Don't really know my IQ, but I am a Petroleum Geologist, been a runner for over 32 years,  can go many hours without water (ran a marathon in 3 hrs and 3 minutes when I was 24 in New Orleans and only had a small cup of water at the halfway point).  I have no problem eliminating foods and have high willpower to food.

    Before joining your Track Your Plaque program 3 years ago, I was on the "low fat"  high carb Am. Heart Assoc. recommended diet for many years.  At 48 I discovered that I had massive heart disease and received 6 stents.
    I now have to limit my carbs to very low to keep my small LDL particles somewhat low.

    Good news is now at 53 years old my carotids are getting better flow since on the TYP diet when I got my last carotid echo.

  • Gene K

    8/15/2012 5:59:29 PM |

    @Joanna
    We have coverage thru Blue Cross Blue Shield, and they require extensive review of why I would need an NMR or an Lp(a) test, after which they will decide whether to cover or not. I decided it was too much of a pain, so I order these tests thru privatemdlabs, and use their receipt to get reimbursed from my flexible spending account. If you have an FSA, you could do that, too.

  • Joanna

    8/15/2012 8:18:23 PM |

    Nope, no FSA account so that's not an option and they already have extensive records of why it would be warranted (if they even looked at medical expenses for the past year it would be obvious!)  Thanks for the tip though.

  • Dr. Davis

    8/17/2012 2:36:21 AM |

    Hey, Kim!

    Yes, we have to reverse this incredibly stupid tidal wave of low-fat that is enormously destructive.

    The proof is in the (carotid) pudding!

  • Dr. Davis

    8/17/2012 2:40:41 AM |

    There are a number of possibilities to explain this pattern, JoAnne.

    Among them:

    --Hypothyroidism
    --Apo E4 genetic type
    --Other genetic patterns

    Unfortunately, this is a pattern that may be difficult to correct with diet. You might also consider an HDL Labs sterol absorption panel to decide what role diet plays.

  • Dr. Davis

    8/17/2012 2:43:50 AM |

    This is a pattern that is highly responsive to diet, such as the diet used in the Track Your Plaque program, the diet discussed in these pages, and the diet I articulate in my book, Wheat Belly.

    By the way, you are currently on a diet that makes this pattern worse. Your diet of avoiding meats and eggs with lots of fruits causes the small LDL pattern and heart disease. And it sounds like you have an intellectually challenged doctor who wants to prescribe drugs but doesn't understand that your diet is contributing or outright causing your pattern.

  • Dr. Davis

    8/17/2012 2:45:54 AM |

    Nobody does.

    It is likely that the gene for the apo(a) protein of Lp(a) is somehow linked to a gene for thirst triggering and nothing more.

    More of a curiosity than anything else.

  • steve

    8/19/2012 1:36:11 AM |

    Hi Dr. Davis:
    Can LDL-P level ever be to low? I have heard lower is better, but when you get below 500, most of that can be small LDL-P.
    Thanks

  • Dr. Davis

    8/23/2012 2:00:59 PM |

    Yes, it can.

    But it should be mostly, if not all, large particles if you are following the diet advised here.

  • steve

    8/26/2012 8:39:17 PM |

    i do follow the diet, but unfortunately generate much in the way of small LDL-P
    I eat no wheat, small amounts of rice and potatoes, no other grains or sugars.  TRGS  were 26 which i thought  is an indication of carb intake.  Am guessing it is just genetics.
    How low is low for LDL-P and do you have any studies you can point that indite small particles?  All research I have seen indite LDL-P and say size does not matter.  Would be interested in seeing studies that show otherwise
    Thanks

  • jpatti

    8/28/2012 7:46:26 PM |

    Yes, I knew the hypothalamus was involved with thirst and the adrenals involved with electrolyte balance.

    Except... just last week, I had a board-certified endocrinologist tell me that ONLY the heart, liver and kidneys are involved in fluid/electrolyte balance:  
    http://gapsfort2.blogspot.com/2012/08/i-am-just-so-freaking-angry.html

  • Susan

    10/4/2012 9:59:33 PM |

    My pattern is very similar and I have had the sterol absorption panel, though I don't know what it means. Campesterol is optimal at 2.22, Campesterol ratio is Hypo at 63, Sitosterol is Hyper at 3.23, Sitosterol ratio is optimal at 88, Cholestanol is Hyper at 5.89 and Cholestanol ratio is Optimal at 172. What does this tell us?

  • Kindred

    10/31/2012 4:53:42 PM |

    My LP(a) was 167.  I got it down, in three months, to 22 using the strict vegan, Forks Over Knives approach coupled with 1500 mg of niacin before going to bed.  My math skills are deplorable as I have severe discalculia (the math version of dyslexia which I also have.)  I'm not competitive at all so, although very coordinated and active, I'm not athletic.  I drink lemon water or dandelion/chicory coffee frequently and frequently get up in the middle of the night for a glass of lemon water. I'm not diabetic and am tested for this annually.   I graze between  meals on celery sticks.   Also, I'm 1/8 Native American Indian. We are suppose to have low levels of LP(a.)

    I lightened up on the vegan diet using olive oil for cooking and my LP(a) rose in 3 months to 67 so it's back to Forks Over Knives again.

  • darin

    12/29/2012 5:47:33 PM |

    Confused, would this be the same thing as Lp(a) mass (mg/dl) i had on a recent Health diagnostics test?
    Mine is showing 44 and its supposed to be less than 30.

    There was also a Lp (a) cholesterol (mg/dl) and mine was 8- supposed to be <3

    Thanks

  • Fred Rutherford

    6/17/2013 5:00:36 AM |

    I have a lipid disorder. My doctor checks lpa once a month. Says thou I have minimal body fat I have to take cholesterol meds. Because my lpa is 14 times higher than what is considered high risk. This putting me at risk of blood clots. I under go quarterly ulta sounds of vascular system as well as annual Hart caths. A high price for being smarter than the average bear. Don't ya think?

  • Dr. Davis

    6/18/2013 1:29:29 AM |

    No, you have been misled.

    What you need are new doctors, plain and simple.

  • Mathieu Gagné

    6/18/2013 5:17:58 PM |

    That is very interesting! I never heard of this before, but it seems to fit to me pretty well. I have high IQ, I'm a physicist, don't drink enough water and would be fairly athletic if it wasn't for my crohn disease. The impact of giving up grains was huge on my health! A quick search and I've found this link between high Lipoprotein(a) and crohn disease:
    http://www.ncbi.nlm.nih.gov/pubmed/11742189

    It would be interesting to ask my doctor about it!

  • Mary Ann Joyce

    2/15/2014 8:07:55 PM |

    I've the Berkley tests three or four times, and my Lp(a) was 217 in 2007; the latest test shows 80Lp(a).
    I have been on Crestor for a very long time, and now realize it does noting to lower the Lp(a).  On the latest test, my small particle was 21.2 and the large was 11.4.  What does this mean?
    I want to get off the Crestor and onto the niacin, etc., including pomegranate juice which, I understand, has properties that will lower the Lp(a).  I am aiming to cut carbohydrates out completely as well as reduce sugar to near zero.  Do any of you have suggestions for me?  Even though I am 70 years old, I am not ready for a stroke nor MI.  Thanks!

  • Sandra Tremulis- Founder Lipoprotein(a) Foundation

    5/7/2014 6:12:44 PM |

    For those of you interested there is now a foundation for high Lipoprotein(a)  www.lipoproteinafoundation.org

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My letter to the Wall Street Journal: It's NOT just about gluten

My letter to the Wall Street Journal: It's NOT just about gluten

The Wall Street Journal carried this report of a new proposed classification of the various forms of gluten sensitivity: New Guide to Who Really Shouldn't Eat Gluten

This represents progress. Progress in understanding of wheat-related illnesses, as well as progress in spreading the word that there is a lot more to wheat-intolerance than celiac disease. But, as I mention in the letter, it falls desperately short on several crucial issues.

Ms. Beck--

Thank you for writing the wonderful article on gluten sensitivity.

I'd like to bring several issues to your attention, as they are often neglected
in discussions of "gluten sensitivity":

1) The gliadin protein of wheat has been modified by geneticists through their
work to increase yield. This work, performed mostly in the 1970s, yielded a form
of gliadin that is several amino acids different, but increased the
appetite-stimulating properties of wheat. Modern wheat, a high-yield, semi-dwarf
strain (not the 4 1/2-foot tall "amber waves of grain" everyone thinks of) is
now, in effect, an appetite-stimulant that increases calorie intake 400 calories
per day. This form of gliadin is also the likely explanation for the surge in
behavioral struggles in children with autism and ADHD.
2) The amylopectin A of wheat is the underlying explanation for why two slices
of whole wheat bread raise blood sugar higher than 6 teaspoons of table sugar or
many candy bars. It is unique and highly digestible by the enzyme amylase.
Incredibly, the high glycemic index of whole wheat is simply ignored, despite
being listed at the top of all tables of glycemic index.
3) The lectins of wheat may underlie the increase in multiple autoimmune and
inflammatory diseases in Americans, especially rheumatoid arthritis and
inflammatory bowel diseases (ulcerative colitis, Crohn's).

In other words, if someone is not gluten-sensitive, they may still remain
sensitive to the many non-gluten aspects of modern high-yield semi-dwarf wheat,
such as appetite-stimulation and mental "fog," joint pains in the hands, leg
edema, or the many rashes and skin disorders. This represents one of the most
important examples of the widespread unintended effects of modern agricultural
genetics and agribusiness.

William Davis, MD
Author: Wheat Belly: Lose the wheat, lose the weight and find your path back to health

Comments (7) -

  • HS4

    2/7/2012 11:08:16 PM |

    Fantastic, Dr Davis!  I read the article earlier today and was thinking of sending in my own response but yours is ever so much better and comes with greater credibility which is important.   I hope they publish your letter.

  • Dr. William Davis

    2/8/2012 3:02:38 AM |

    Thanks, HS4!

    But don''t hesitate to add your voice. The more they hear this message, the more likely others hear it, too.

  • Scott Hamilton

    2/10/2012 4:01:24 PM |

    There were some comments in past postings regarding ancient vartieties of wheat, such as Emmer and Einkorn. Although these types still pose problems from a total health perspective I was thinking perhaps an original form of barley might also provide better health benefits with less metabolic damage than the newer varieties.

    There are recipes where the addition of grains in relatively small amounts can improve texture and flavor and I have used barley for this purpose extensively in the past.


    Are ther sources of information or supply of older or alternative forms of barley?

  • Ronnie

    2/11/2012 6:53:52 PM |

    Go Doc!

  • farida

    8/7/2012 7:23:42 PM |

    I would like to know if Dr Davis would be interested in doing a 30 min tele lunch and learn workshop, we own a wellness company with 000's  of users on our health portal.  It would be a great way to promote his books/blogs.

  • Magnesium citrate versus glycinate

    8/15/2012 8:12:45 PM |

    [...] wheat from your diet. Give it a try for 2 or 3 weeks and see how you feel.    Here's why:  My letter to the Wall Street Journal: It’s NOT just about gluten | Track Your Plaque Blog  "1) The gliadin protein of wheat has been modified by geneticists through their work to [...]

  • [...] I'm suggesting.   What about WHEAT?  Wheat has been a Frankenfood for the last 40 years, bcfromfl:  My letter to the Wall Street Journal: It’s NOT just about gluten | Track Your Plaque Blog  "1) The gliadin protein of wheat has been modified by geneticists through their work to [...]

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