Thumb your nose at swine flu

Judging from what we know about vitamin D, it is highly probable that it confers substantial protection from viral infections, including swine flu.

Dr. John Cannell of the Vitamin D Council (www.vitamindcouncil.com) first connected the dots, identifying the possibility of an influence of vitamin D on incidence of flu.

In 2006, Dr. Cannell reports noticing that the patients in his psychiatric ward in northern California were completely spared from the influenza epidemic of that year, while plenty of patients in adjacent wards were coming down with flu. Dr. Cannell proposed that the apparent immunity to flu in his patients may have been due to the modest dose of 2000 units vitamin D per day he had prescribed that the patients in other wards had not been given. (Since the hospital was run by the state of California, Dr. Cannell apparently had only so much leeway with vitamin D dosing.) While it’s not proof, it’s nonetheless a fascinating and compelling observation.

A similar conclusion was reached in a recent analysis of the National Health and Nutrition Examination Survey demonstrating that the higher the vitamin D blood level, the less likely respiratory infections were.

Personally, I used to suffer through 2 or 3 episodes of a runny nose, sore throat, hacking cough, fevers and feeling crumby every winter. Over the last 3 years since I’ve supplemented vitamin D, I haven’t been sick even once. The past two years I didn’t bother with the flu vaccine, since I suspected that my immunity had been heightened: no flu either winter.

And so it has been with the majority of my patients. Since I began having patients supplement vitamin D to achieve normal blood levels (we aim for 60-70 ng/ml), viral and bacterial infections have become rare.

New research is uncovering myriad new ways that vitamin D enhances natural immune responses to numerous infections, including tuberculosis, bacteria such as those causing periodontal disease and lung infections, and viruses like the influenza virus. Enhanced immunity against cancer is also an intensive area of research on vitamin D.

Will vitamin D supplementation sufficient to achieve desirable blood levels confer sufficient immunity to swine flu should it come to your door? From what we know and what we’ve seen in the few years of vitamin D experience, I think it will in the majority. But I do believe that we should still heed public health warnings to avoid contact with others, minimize exposure to crowds, avoid travel to affected areas, etc.

Will the real LDL please stand up?

The results of the latest Heart Scan Blog poll are in.

The question: How has your LDL been measured? The 187 responses broke down as:


I have only had a conventional calculated value
108 (57%)

NMR LDL particle number
35 (18%)

Apoprotein B
21 (11%)

Direct LDL cholesterol
21 (11%)

Non-HDL cholesterol
8 (4%)

I don't know what you're talking about
23 (12%)


Remember the TV game show, To Tell the Truth? Celebrities would have to guess which of three guests represented the real person, such as the notorious con man, Frank Abagnale, Jr., or Mad Magazine publisher, William M. Gaines (who stumped celebrity Kitty Carlisle, heard to exclaim, "I never figured it was him. I mean look at the way he's dressed. I was looking for someone who ran a very successful magazine, so I thought it couldn't be him!")

The celebrities playing the game were permitted to ask the three guests a series of questions, hoping to discern who was the real person vs. the two impostors. At the end, each celebrity had to guess who was truly the person of interest. "Will the real Frank Abagnale, Jr. please stand up!"

If we were to act as the celebrities in our LDL game, we quickly discover some telling facts:

--Conventional LDL cholesterol (the only value 57% of our poll respondents have had) is calculated, not measured. LDL is calculated using the 40-year old Friedewald calculation.

--Directly measured LDL cholesterol (the value 11% of respondents had) is just that: directly measured. It eliminates some of the uncertainties of calculated LDL.

--Apoprotein B-Every LDL and VLDL particle produced by the liver contains one apoprotein B molecule. ApoB therefore provides a crude particle count measure of LDL and VLDL particles. Of course, it includes VLDL and is not completely the same as just an LDL measure. Some lipid authorities Like Dr. Peter Kwiterovich have advocated that apoB replace calculated LDL, and that calculated LDL essentially be discarded.

--Non-HDL cholesterol--I mention this more for completeness. Hardly anybody uses this crude value in practice--Indeed, only 4% of our poll respondents had this measure/calculation. Non-HDL is simply total cholesterol minus HDL cholesterol = Non-HDL cholesterol. It is thus a combination of cholesterol in LDL and VLDL (triglycerides), similar to apoprotein B. While, like apoB, it is a bit different in that it includes VLDL, it has proven a superior measure of risk.

--LDL particle number--In my view, this is the gold standard for LDL and risk measurement, obtained by only 18% of our poll respondents. LDL particle number is proving superior for discriminating who is truly at risk for a cardiovascular event, particularly when metabolic syndrome or diabetes is part of the picture, i.e., when HDL and triglycerides are considerably distorted, leading to substantial corruption of calculated LDL.


While 18% is a minority, it still represents growth in recognition that conventional calculated LDL cholesterol is an unreliable, inaccurate, and outdated value. If the real LDL were to stand up, I believe that it is LDL particle number that would spring to its feet.

Vitamin D and inflammation

We already know that vitamin D reduces inflammatory processes, since several markers, including c-reactive protein and IL-6 have previously been shown to drop substantially with vitamin D. Inflammation underlies coronary atherosclerotic plaque growth, as well as plaque rupture that triggers heart attack.

A German group has now shown that the important inflammatory marker, tumor necrosis factor (TNF), is also reduced by vitamin D supplementation. Many studies have implicated increased TNF levels in promoting cancer.

In this study, a modest vitamin D dose of 3320 units (83 micrograms) was given vs. placebo. The 25-hydroxy D level reached in the treated group was 34.2 ng/ml (85.5 nmol/L), which resulted in a 26.5% reduction in TNF compared with 18.7% reduction (?) in the placebo group.


Vitamin D supplementation enhances the beneficial effects of weight loss on cardiovascular disease risk markers.

Zitterman A, Frisch S et al.

BACKGROUND: High blood concentrations of parathyroid hormone and low concentrations of the vitamin D metabolites 25-hydroxyvitamin D [25(OH)D] and calcitriol are considered new cardiovascular disease risk markers. However, there is also evidence that calcitriol increases lipogenesis and decreases lipolysis.
OBJECTIVE: We investigated the effect of vitamin D on weight loss and traditional and nontraditional cardiovascular disease risk markers in overweight subjects.
DESIGN: Healthy overweight subjects (n = 200) with mean 25(OH)D concentrations of 30 nmol/L (12 ng/mL) received vitamin D (83 microg/d) or placebo in a double-blind manner for 12 mo while participating in a weight-reduction program.
RESULTS: Weight loss was not affected significantly by vitamin D supplementation (-5.7 +/- 5.8 kg) or placebo (-6.4 +/- 5.6 kg). However, mean 25(OH)D and calcitriol concentrations increased by 55.5 nmol/L and 40.0 pmol/L, respectively, in the vitamin D group but by only 11.8 nmol/L and 9.3 pmol/L, respectively, in the placebo group.


(Calcitriol = 1,25-dihydroxy vitamin D.)


Knowing your vitamin D blood level is crucial, as individual need for vitamin D varies widely from one person to the next. You can get your vitamin D tested at home by going to Grassroots Health or the Track Your Plaque Marketplace.

Even monkeys do it


It all started back in the 1960s, when ape-watching anthropologists, Drs. Jane Goodall and Richard Wrangham, observed chimps foraging for a specific variety of leaf, which they consumed whole while wrinkling their noses in presumed disgust. Subsequent study showed that the leaves contained a powerful anti-parasitic compound.

A similar observation followed in 1987 by Dr. Michael Huffman from the University of Kyoto. During his year of living in the jungles of Tanzania, he observed chimpanzees in their native habitat. On one unexpected morning, he observed a female chimp, Chausiku:

Chausiku goes directly to and sits down in front of a shrub and pulls down several new growth branches about the diameter of my little finger. She places them all on her lap and removes the bark and leaves of the first branch to expose the succulent inner pith. She then bites off small portions and chews on each for several seconds at a time. By doing this, she makes a conspicuous sucking sound as she extracts and swallows the juice, spitting out most of the remaining fiber. This continues for 17 minutes, with short breaks as she consumes the pith of each branch in the same manner.”

Dr. Michael Huffman’s description of Chausiku documents a fascinating example of animal self-medication what some call "zoopharmacognosy."
In this instance, the chimpanzee, weak, clutching her back in pain, and listless, was ingesting the leaves of the plant, Vernonia amygdalina, to purge an intestinal parasite. She recovered by the next morning.

Vernonia leaves have since been found to contain over a dozen potential anti-parasitic compounds. Chimps in this region commonly suffer infestations of parasites like Strongyloides fuelleborni (thread worm), Trichuris trichiura (whip worm), and Oesophagostomum stephanostomum (nodular worm). They have somehow stumbled onto a treatment that they administer themselves.

Chimpanzees have inhabited earth for over 6 million years. Who knows how long they and other primates have practiced some form of self-medication.

If chimpanzees can do it, I believe that we, as human primates, can also practice a similar form of self-directed health--homopharmacognosy?



Image courtesy Wikipedia

Cath lab energy costs

In honor of Earth Day, I thought I'd highlight the unexpectedly high carbon costs of activities in hospitals, specifically the cardiac catheterization laboratory.

A patient enters the cath lab. The groin is shaved using a plastic disposable razor, the site cleaned with a plastic sponge, then the site draped with an 8 ft by 5 ft composite paper and plastic material (to replace the old-fashioned, reusable cloth drapes). A multitude of plastic supplies are loaded onto the utility table, including plastic sheaths to insert into the femoral artery (which comes equipped with a plastic inner cannula and plastic stopcock), a multi-stopcock manifold that allows selective entry or removal of fluids through the sheath, a plastic syringe to inject x-ray dye, plastic tubing to connect all the devices (total of about 5 feet), and multiple plastic catheters (3 for a standard diagnostic catheterization, more if unusual arterial anatomy is encountered).

All these various pieces come packed in elaborate plastic (polyethylene terephthalate or other polymers) containers, which also come encased in cardboard packaging.

Should angioplasty, stenting, or similar procedure be undertaken, then more catheters are required, such as the plastic "guide" catheters that contain a larger internal lumen to allow passage of angioplasty equipment. An additional quantity of tubing is added to the manifold and stopcock apparatus, as well as a plastic Tuohy-Borst valve to permit rapid entry and exit of various devices into the sheath.

Several new packages of cardboard and plastic are opened which contain the angioplasty balloon, packaging which is usually about 4 feet in length. The stent likewise comes packaged in an 18-inch or so long package with its own elaborate cardboard and plastic housing.

At the conclusion of the procedure, another cardboard/plastic package is opened, this one containing the closure device consisting of several pieces of plastic tubes and tabs.

If the procedure is complicated, the number of catheters and devices used can quickly multiply several-fold.

By the conclusion of the procedure, there are usually two large, industrial-sized trash bins packed full of cardboard, plastic packaging, and discarded tubing and catheters. The trash is so plentiful that it is emptied following each and every procedure. None of it is recycled, given the contamination with human body fluids.

That's just one procedure. The amount of trash generated by these procedures is staggering, much of it plastic. I don't know how much of the U.S.'s annual plastic trash burden of 62 billion pounds (source: EPA) originates from the the cath lab, but I suspect it is a big number in total.

So if you are truly interested in reducing your carbon footprint and doing your part to be "green," avoid a trip (or many) to the cath lab.

Wag the Dog

What if the system to provide heart care has already gotten as big as it should be?

Worse (for hospitals), what if it’s already far larger than it needs to be? Can the system continue to increase revenues if they’ve already attained titanic proportions and outgrown demand? After all, darn it, there are only so many sick people around.

Hospital administrators might have to face an unpleasant choice: downsize to strip excess capacity and suffer the consequences in a competitive market, or . . . fabricate demand for their services.

Like the Dustin Hoffman and Robert DeNiro characters in the movie, Wag the Dog, about how two media-manipulators divert public attention away from a Presidential sex scandal by fabricating a war, spin is everything. It’s enough to sidetrack public attention from a scandal, obscure a truth, send us on a useless detour.

If healthcare for the heart isn’t driven by need, but many still desire to reap the benefits of the procedure-focused system, why not increase the perceived need?

That’s precisely the course that many hospital systems have chosen to follow. If the market you serve has been tapped to its full potential, then grow the market.

Imagine if a company like General Motors were to operate this way. In 2006, for instance, GM sold 9.1 million automobiles. If GM executives were to decide that they’d like to outstrip Toyota by boosting sales by 10% to 10 million, how would they do it? They would first have to determine whether it was feasible to grow demand for their product. If deemed possible, the company would need to ramp up manufacturing capacity to anticipate increased demand. If they miscalculate, GM could be stuck with a costly surplus and have to swallow the costs, maybe selling leftovers at a loss. (We don’t mean to pick specifically on GM; they’re a fine company as far as we’re concerned. This is just a hypothetical illustration.)

But what if a company could concoct some sort of scheme to persuade the car-buying public that they just had to have their cars or trucks? In other words, they could, in effect, create demand for their products.

As perverse as it sounds, that is exactly what occurs in healthcare for heart disease. The system long ago exceeded the necessary level of infrastructure to maintain a high-quality level of care accessible to most Americans. Instead, it continues to grow through a distortion of perception, delivering more services of increasing complexity to larger and larger numbers of people.

The size of the market is therefore a manipulable thing, something that can be massaged and cultivated. There are a variety of clever ways to exaggerate the need for heart procedures.

Why not raise the alarm for heart disease every chance you get? When a local sports figure survived a heart attack here in Milwaukee, St. _____ marketing department was right there, broadcasting the process in TV ads after his recovery. What could be more American than baseball, apple pie . . . and St. _____ Hospital? After his hospital discharge, the 57-year old local icon was shown on the sidelines with his team, back on the job, and at home with family, all beaming, just three months after a bypass operation. “I received only the very best care at St. _____ Hospital. They treated me like family. St. _____ doctors and nurses are the best!” Predictably, a two-month long spike in hospital testing followed filled with people worried whether they, too, might be in imminent danger. Several local cardiologists boasted of the many sports figures who came through the stress testing and heart catheterization labs, though virtually all checked out to be fine.

Though it can serve a legitimate purpose in some situations, stress tests are the ultimate example of a heart scam built on the perception of danger. Pull people in with promises of reassuring them whether or not they have heart disease, only to provide murky results that usually do no such thing. The pitfalls of the test are turned to advantage. The all too common equivocal or mildly abnormal result can be converted into a hospital procedure. (Imagine you could perform such alchemy on the uncertain calculations on your income taxes.)

With millions of stress tests performed every year and the push to perform more and more screening tests, the market has, in effect, been expanded—even though no increase in the disease itself has actually occurred.

Beware: As the scramble for heart patients intensifies, you are going to feel like you are being pulled closer and closer into the jaws of this hungry monster called the American cardiovascular healthcare machine.

Heart scan book



There are only two books on heart scans available.

One, of course, is Track Your Plaque.

The other is the basic book on heart scans, What Does My Heart Scan Show?

Lost in the navigation column to the left on this blog is the link to get the electronic version of the book. In case you didn't know, we make this available for free.

If you're interested, just go here. This book can provide many basic answers to the questions that often arise regarding heart scans, such as the expected rate of increase in score, how your score compares to other people, when should a stress test be considered. Many heart scan centers use this book for educational purposes to help patients understand the importance of their heart scan scores.

(The sign-up for the book requires that an e-mail address be entered.)

The hard copy of What Does My Heart Scan Show? is available from Amazon, also, for $12.99.

Lies, damned lies, and statistics

In the last Heart Scan Blog post, I discussed the question of whether statin drugs provide incremental benefit when excellent lipid values are already achieved without drugs.

But I admit that I was guilty of oversimplification.

One peculiar phenomenon is that, when plaque-causing small LDL particles are reduced or eliminated and leave relatively benign large LDL particles in their place, conventional calculated LDL overestimates true LDL.

In other words, eliminate wheat from your diet, lose 25 lbs. Small LDL is reduced as a result, leaving large LDL. Now the LDL cholesterol from your doctor's office overestimates the true value.

Anne raised this issue in her comment on the discussion:

I eliminated wheat - and all grains - from my diet nearly three years ago (I eat low carb Paleo). My fish oils give me a total of 1680 mg EPA and DHA per day, and my vitamin D levels since last year have varied between 50 ng/ml and 80 ng/ml. However, my lipid profile is not like either John's or Sam's:

LDL cholesterol 154 mg/dl
HDL cholesterol 93 mg/dl
Triglycerides 36 mg/dl
Total cholesterol 255 mg/dl

My cardiologist and endocrinologist are happy with my profile because they say the ratios are good, no one is asking me to take a statin. My calcium score is 0.



However, if we were to measure LDL, not just calculate it from the miserably inaccurate Friedewald equation, we would likely discover that her true LDL is far lower, certainly <100 mg/dl. (My preferred method is the bull's eye accurate NMR LDL particle number; alternatives include apoprotein B, the main apoprotein on LDL.)

So Anne, don't despair. You are yet another victim of the misleading inaccuracy of standard LDL cholesterol determination, a number that I believe should no longer be used at all, but eliminated. Unfortunately, it would further confuse your poor primary care doctor or cardiologist, who--still believe in the sanctity of LDL cholesterol.

By the way, the so-called "ratios" (i.e., total cholesterol to HDL and the like) are absurd notions of risk. Take weak statistical predictors, manipulate them, and try to squeeze better predictive value out of them. This is no better than suggesting that, since you've installed new brakes on your car, you no longer are at risk for a car accident. It may reduce risk, but there are too many other variables that have nothing to do with your new brakes. Likewise cholesterol ratios.

Aspirin, Lipitor, and a low-fat diet

Despite all the hoopla heart disease receives in the media, I continue to marvel at how many people I meet who still think that aspirin, Lipitor, and a low-fat diet constitute an effective heart attack prevention program.

It doesn't. No more than washing your hands prevents all human infections. It helps, but it is a sad substitute for a real prevention program.

Of course, aspirin, Lipitor, and a low-fat diet is the same recipe followed by the unfortunate Tim Russert and his doctors. You know how that turned out. Mr. Russert's experience is far from unique.

What is so magical about aspirin, Lipitor and a low-fat diet?

There is a simple rationale behind this approach. Aspirin doesn't reduce atherosclerotic plaque growth, but it inhibits the propagation of a blood clot on top of a coronary plaque that has "ruptured," thereby reducing likelihood of heart attack (which occurs when the clot fills the artery). So aspirin only provides benefit if and when a plaque ruptures.

Lipitor and other statin drugs reduce LDL cholesterol, promote a modest relaxation of constricted plaque-filled arteries (normalization of endothelial dysfunction), and exerts other effects, such as inflammation suppression.

A low-fat diet is intended to reduce saturated fat that triggers LDL cholesterol formation and to encourage intake of whole grains that reduce cardiovascular events and LDL cholesterol.

If that is the extent of your heart disease prevention program, you will have a heart attack, bypass surgery, or stent--period. It may not be tomorrow or next Friday, or even next month. Aspirin, Lipitor, and a low-fat diet may delay your heart attack or procedure for a few years, but it will not stop it.

Some flaws in the aspirin, Lipitor, low-fat program:

--Aspirin can only exert so much blood clot-blocking effect. It can be overwhelmed by many other factors, such as increased blood viscosity, increased fibrinogen (a blood clotting protein that also triggers plaque), and plaque inflammation.
--Lipitor reduces LDL, but does not discriminate between the relatively harmless large LDL and the truly plaque-triggering small LDL--it reduces all LDL, but small LDL can still persist, even at extravagant levels since neither aspirin nor Lipitor specifically reduces small LDL, while a low-fat diet increases small LDL.
--Low-fat diet--A diet reduced in fat and loaded with plenty of "healthy whole grains" will trigger increased small LDL (an enormous effect), c-reactive protein, high blood sugar, resistance to insulin, high blood pressure, and an expanding abdomen ("wheat belly").


Aspirin, Lipitor and a low-fat diet do not address:

--Vitamin D deficiency
--Omega-3 fatty acid deficiency and the eicosanoid path to inflammation
--High triglycerides
--Small LDL particles
--Distortions of HDL "architecture"
--Lipoprotein(a)--the worst coronary risk factor nobody's heard of
--Thyroid status

In other words, the simple-minded, though hugely financially successful, conventional model of heart disease prevention is woefully inadequate.

Don't fall for it.

Statin drugs for everybody?

Who is better off?

John takes Crestor, 40 mg per day:

LDL cholesterol 60 mg/dl
HDL cholesterol 60 mg/dl
Triglycerides 60 mg/dl
Total cholesterol 132 mg/dl




Or Sam:

LDL cholesterol 60 mg/dl
HDL cholesterol 60 mg/dl
Triglycerides 60 mg/dl
Total cholesterol 132 mg/dl


who obtained these values through vitamin D normalization (to increase HDL); wheat elimination (to reduce triglycerides and LDL); and omega-3 fatty acids (to reduce triglycerides).


Believe the drug industry (motto: If some statin is good, more statin is better!), then John is clearly better off: He has obtained all the "benefits" of statin drugs. They refer to the "pleiotropic" effects of statin drugs, the presumed benefits that extend outside of cholesterol reduction. The most recent example are the JUPITER data that demonstrated 55% reduction in cardiovascular events in people with increased c-reactive protein (CRP). Media reports now unashamedly gush at the benefits of Crestor to reduce inflammation.

However, on Sam's program, elimination of wheat and vitamin D both exert anti-inflammatory effects on CRP, typically yielding drops of 70-90%--consistently, rapidly, and durably.

So which approach is really better?

In my experience, there is no comparison: Sam is far better off. While John will reduce his cardiovascular risk with a statin drug, he fails to obtain all the other benefits of Sam's broader, more natural program. John will not enjoy the same cancer protection, osteoporosis and arthritis protection, relief from depression and winter "blues," and increased mental and physical performance that Sam will.

If our goal is dramatic correction of cholesterol patterns and reduction of cardiovascular risk, for many, many people statin drugs are simply not necessary.
What does "Success" mean in the Track Your Plaque program?

What does "Success" mean in the Track Your Plaque program?

Say you begin with a CT heart scan score of 400.

You correct your lipoprotein pattterns, take fish oil, correct 25-OH-vitamin D3 to 50 ng/ml, correct your other hidden patterns, follow a diet suited to your patterns.

One year later, you get another heart scan. What score would constitute "success"?

With all of our recent talk about record-setting reductions in heart scan scores, is it really necessary to drop your score that much to succeed?

For instance, is our latest record-setting 63% drop in score better than "only" a 10% drop in score? Both represent reversal of coronary plaque. Both signify huge reductions in risk for plaque rupture, or heart attack.

You can read about how we view the various forms of success in the program by reading our latest Track Your Plaque Special Report, Winning Your Personal War with Heart Disease: The Track Your Plaque 5 Stages of Success.

We are making the Report available to everyone. Just go to the www.cureality.com homepage.

Comments (11) -

  • WCCAguy

    10/2/2007 11:22:00 AM |

    Hi Dr. Davis,

    This post touches on a point I've been wondering about.

    You write that a drop in CT heart scan score signifies a "huge reduction in risk for plaque rupture, or heart attack."

    As I understand it, strictly speaking, the score indicates a reduction in the volume of calcium/plaque in the arteries.

    In your books and articles you provide references to the studies which document the statistical correlation between FIXED scores and rupture/heart attack.

    My question is this (and you may have answered this question already elsewhere):  Have there been studies that document a statistically significant relationship between a reduction in plaque volume (as opposed to a fixed value) and risk of a CAD event?

    A follow up question:  Is the actual reason for the risk reduction due to score reduction actually known?  I can imagine that one reason might be that because the arteries have plaque reduced, they are actually larger in terms of blood flow supported than they were before the plaque was reduced.

    My belief, however, is that there could be additional reasons for a reduced plaque over time = less risk correlation.

    Thoughts about this?

    Thanks.

  • Dr. Davis

    10/2/2007 12:13:00 PM |

    Great questions.

    We do know that, if plaque is permitted to grow (by several measures including angiographic studies, carotid ultrasound, as well as heart scan scores), the likelihood of events escalates along with it. This is known with absolute confidence.  

    We also know that reductions in plaque burden are also correlated with reductions in risk, also by just about any measure, though the magnitude of reduction varies, since each approach provides a different persective on plaque composition, all differ on incorporation of the Glagov phenomenon ("remodeling"). More data on event reductions are needed, however. But until recently, genuine bona fide reversal had been elusive.

    Lastly, actual examination of tissue that has regressed is very limited. As you can imagine, if someone asked you, having regressed, to allow a sample of artery tissue to be removed, you'd likely not be interested. Thus, the observations are indirect and come from animal studies and observations like intracoronary ultrasound.

    Actually, reductions in heart scan scores are a surrogate for inactivation of plaque, removal of inflammatory cells, removal of fat-laden tissue, etc. The reduction  in calcium is a parallel phenomenon that we can see. I also wonder, given the wonderful effects of vit D and possibly K2, whether the reduction in calcium provides benefits of its own, independent of the inactivating effects.

  • Anonymous

    10/3/2007 3:56:00 AM |

    While everyone agrees that reduction of atherosclerotic plaque is a good thing, there are several clinical studies that suggest that reduction of calcium in the plaque may not be good. For example, this study found that culprit stenoses in arteries of patients with stable angina had more calcium than those of patients with unstable angina, which had more calcium than those with acute myocardial infarction. This suggests that plaque accumulation in a specific location may actually be beneficial if it stabilizes the plaque and makes it less likely to rupture.

    There is not much data on calcium score reduction because it is so rarely seen. What is needed are long-term studies showing that calcium score reduction does reduce the number of adverse coronary events.

  • Dr. Davis

    10/3/2007 11:53:00 AM |

    I disagree.

    There is a commonly offered argument that calcium stabilizes plaque. I think this is nonsense. There are studies by Renu Virmani and others that demonstrate that the shear and tension forces at the edges of calcified plaque are, in fact, areas of greater stress and thereby risk for plaque rupture.

    While intracoronary ultrasound will sometimes show that a small segment of a recently ruptured plaque will involve a non-calcified segment, we are NOT using calcium in a lesion-specific fashion. We use it as an index of total plaque.

    I also believe that emerging concepts, such as the influence of vitamin D3 on gamma-carboxyglutamic acid Gla protein in vascular tissue are pointing towards the fact that vascular calcification is part of a regulated, active process that influences plaque activity and rupture potential. (See Johnson et al, Vascular calcification: pathobiological mechanisms and clinical implications. Circulation Research 2006 Nov 2006;99(10):1044-59.)

    Increasing calcium scores have been conclusively associated with dramatic increases in coronary events. Likewise, emerging data, including our own, show reducing calcium scores is associated with virtual elimination of events.

    Do you have something better?

  • Anonymous

    10/3/2007 1:53:00 PM |

    No, I don't have anything better - I don't argue that an increasing calcium score is good, only that we have nothing more than anecdotal evidence to show that calcium score reduction is beneficial. And, there are other experts in the field that do not agree that it is. The recent torcetrapib clinical trial shows that not all ways of increasing a generally beneficial lipid such as HDL are theraputic. Have you considered documenting the results of your practice, i.e., what percent of your patients show calcium score change in each of several percentage ranges including reductions, and what their follow-up results are in terms of hard cardiac events? That might stimulate interest in a controlled clinical trial to verify your results.

  • Dr. Davis

    10/3/2007 2:21:00 PM |

    What experts "agree" that a reduction in calcium score is not beneficial? Can you specify who? I know the literature on calcium scoring quite well, and I don't ever recall such a study.

  • WCCAguy

    10/3/2007 9:27:00 PM |

    Dr. Davis,

    The wizard, hmmm, I mean, Dr. Oz says on Oprah that "we'd rather focus on the plaque itself—because the calcium actually might help stabilize the plaque and reduce the chance of it rupturing."

    http://www2.oprah.com/health/yourbody/youdocs/youdocs_faqs_io_10.jhtml

    So, there's the proof you asked for.  It was on the Oprah show.

    And by the way, Oprah's doc says that Ornish has the answer here:

    http://www2.oprah.com/health/yourbody/youdocs/youdocs_faqs_io_11.jhtml

    Seriously, this question of the Calcium Score relationship to risk reduction is a key issue and I appreciate your sharing your knowledge about the question.

    It will be interesting to see if Anonymous gets back to you with expert reference list you've asked for.

  • Anonymous

    10/3/2007 11:05:00 PM |

    I don’t think there is a study that shows that because calcium reduction is so infrequently seen. I have discussed it with the Director of Preventive Cardiology at a State University Hospital who is of the opinion that calcium reduction may not be beneficial. I suspect that most experts would say that there isn’t enough data to conclude that reduction of calcium is either beneficial or detrimental because most have never seen it.

    My point is that several studies show that plaque rupture tends to happen in arteries that have “spotty,” but not extensive calcium, and that coalescence of small calcium deposits into larger deposits reduces the surface area in contact with softer plaque, thereby reducing the extent of the stress risers that can lead to plaque rupture. Quoting from some of these

    “…double helical computerized tomography demonstrates that extensive calcium characterizes the coronary arteries of patients with chronic stable angina, whereas a first AMI [acute myocardial infarction] most often occurs in mildly calcified or noncalcified culprit arteries.” Shemesh et. al., American Journal of Cardiology, 1998 Feb 1;81(3):271-5, Comparison of coronary calcium in stable angina pectoris and in first acute myocardial infarction utilizing double helical computerized tomography.

    “Acute coronary syndromes are associated with a relative lack of calcium in the culprit stenoses compared with stenoses of patients with stable angina.” Joshua A. Beckman et. al., Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:1618, Relationship of Clinical Presentation and Calcification of Culprit Coronary Artery Stenoses.

    “The relationship between calcification and clinical events likely relates to mechanical instability introduced by calcified plaque at its interface with softer, noncalcified plaque. In general, as calcification proceeds, interface surface area increases initially, but eventually decreases as plaques coalesce. This phenomenon may account for reports of less calcification in unstable plaque.” Moeen Abedin et. al.,  Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:1161, Vascular Calcification - Mechanisms and Clinical Ramifications.  

    “In AMI patients, the typical pattern was spotty calcification, associated with a fibrofatty plaque and positive remodeling. In ACS [acute coronary syndrome] patients showing negative remodeling, no calcification was the most frequent observation. Conversely, SAP [stable angina pectoris] patients had the highest frequency of extensive calcification…To the best of our knowledge, the present IVUS study is the first to demonstrate the relationship between calcification patterns, arterial remodeling, and the morphology of plaques within the culprit lesion segment. The major finding is that there is a significant difference in the pattern of coronary calcifications at the culprit lesion segment, particularly with respect to size, number, and length of the deposits, among patients with AMI, UAP [unstable angina pectoris], and SAP. Small calcium deposits were significantly more frequent in the culprit lesion segments in ACS than in SAP patients.” Shoichi Ehara, et. al., Circulation. 2004;110:3424-3429, Spotty Calcification Typifies the Culprit Plaque in Patients With Acute Myocardial Infarction.

    Also, there is an MRI study of  the carotid arteries of CAD patients who had been given niacin, lovastatin, and colestipol for 10 years. In comparison with matched, untreated patients, the carotid plaque of the treated patients showed much less lipid but much more calcium than the untreated patients. Xue-Qiao Zhao, Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:1623, Effects of Prolonged Intensive Lipid-Lowering Therapy on the Characteristics of Carotid Atherosclerotic Plaques In Vivo by MRI.

    It seems that reduction of the “spotty” calcium may reduce the likelihood of plaque rupture, but reduction of coalesced calcium such as is seen in stable angina patients may  increase the surface area of calcium (if the coalesced calcium reverts to spotty deposits) and therefore be detrimental. From the standpoint of evidence-based medicine, the only way to be sure of the effects of calcium reduction is to conduct a clinical trial of patients undergoing such reduction.

    In the meantime, Dr. Davis, since you are one of the few cardiologists whose patients are experiencing calcium score reduction, it would be of great benefit if you would document the results of your practice in a quantitative way.

  • Dr. Davis

    10/4/2007 12:30:00 AM |

    I believe that you are confusing two phenomena.  

    Tissue characterization of specific plaque locations that are prone to rupture (or have ruptured) examined by techniques such as intracoronary ultrasound, is distinct from the concept of using coronary calcium scoring as a surrogate measure of total plaque volume.

    I believe that lipid-laden, calcium-poor plaques do tend to identify sites more prone to rupture. I have witnessed this myself in many intracoronary ultrasound procedures personally performed.

    This is different from using calcium as an index of plaque. While we are uncertain of the relationship of calcium to total plaque in people who have experienced calcium score reduction, all circumstantial evidence points towards dramatic regression of lipid laden plaque, regression of inflammatory cell composition, replacement by fibrous tissue matrix, reduction of oxidative capacity, reduction of  matrix metalloproteinase content, in other words, all the factors that trigger plaque rupture.  

    Though just my suspicion, I believe that the initial relative composition of calcium to plaque of 20% is likely increased, meaning calcium occupies more of total plaque volume. In other words, my suspicion is that, if calcium regresses, total plaque volume has regressed even MORE.

    We plan to publish our data this spring. We had planned to publish our experience much sooner, but the addition of vitamin D to the program has boosted success so much that we decided to start over again around 2 years ago.

  • Anonymous

    12/13/2009 6:34:36 PM |

    hm... bookmarked style Smile)

  • Anonymous

    4/29/2010 4:00:38 AM |

    so great, your arteries are cleared up but you'll get cancer and die from all of those ct scans.
    lovely.

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