Roger's near-miss CT angiogram experience

Heart Scan Blog reader, Roger, described his near-miss experience with CT coronary angiograms.

Hoping to obtain just a simple CT heart scan, he was bullied to get a CT coronary angiogram instead. Roger held strong and just asked for the test that we all should be having, a CT heart scan.


I posted yesterday that I was about to have my first CT heart scan...well, it was an interesting experience for reasons I coudn't possibly have anticipated. Dr. Davis has commented in the past on the confusion in the media about the difference between a CT calcium score scan, and a CT angiography, the latter requiring a far higher dose of radiation. I assumed this was a source of confusion only among patients and lay folks, but, lo and behold, I discovered today that doctors--or at least their helpers--can be just as confused.

Here's my story:

After checking in, I asked the receptionist to see if she had any information on whether my medical insurance was covering the scan. She called someone, and I heard her say over the phone, "He's here for a CT angiogram." At that point my ears perked up. I explained I wasn't here for a CT angiogram, only a regular CT scan. "Well, do you want to call your doctor and talk about this?" she asked. No, I said, I would like to ask one of their folks to verify exactly what test my doctor had ordered. As luck would have it, the technician was walking by at that point. "Is this a CT angiogram?" the receptionist asked. "No, it's just a CT calcium score scan" was the reply. But apparently the technician had been unclear herself, and had called my doctor just to verify. In other words, the "default" procedure they were accustomed to doing at this august Houston vascular clinic was a CT angiogram.

In fact, my appointment was even listed on their calendar as a "CT angiogram." For all I know, my insurance will be billed for the same. Later, during the procedure, the technician acted surprised I wasn't doing the "full test." I explained I had minimal risk factors (actually only one, an HDL of 34 a couple of years ago, which has since been raised to 50 partly as a result of taking advice from this site), but that my doctor was progressive (he is an MD for the Houston Astros) and thought it was a good idea since there is heart disease in my immediate family. My doctor did indeed prescribe only a CT calcium score scan, but it seems to have been an order that this clinic, at least, wasn't all that used to seeing.

So, I guess the message is: we have a lot of educating to do. Had I not been a faithful reader of these pages, I certainly wouldn't have known what kind of test I was about to get, or what questions to ask!

As for the heart scan itself, a piece of cake. If you can hold your breath, you can take this test. Just be sure it is the right one!



Why the "push" towards CT coronary angiograms and not "just" a CT heart scan? Well, I know it's shocking but it's . . . money!

CT coronary angiograms yield around $1800-$4000 per test. CT heart scans yield somewhere around $200. Though the scan center support staff might not care too much about the money themselves, their administrators likely make the cost distinctions clear to them.

Another reason: Most scan center staff, ironically, don't understand what a heart scan means, nor do they understand how it might serve to launch a program of prevention. They do understand that severe blockage by CT angiogram "needs" to be stented or bypassed. So they push patients towards things they understand.

Nobody makes money from CT heart scans, just as nobody makes money from a mammogram. Heart scans also don't lead to heroic, "lifesaving" procedures. They just lead to this sleepy, unexciting, inexpensive thing called prevention.

The Myth of Prevention: Letter to the Wall Street Journal





The June 20-21, 2009 Wall Street Journal Weekend Journal featured a provocative front page article written by physician, Dr. Abraham Verghese:

The Myth of Prevention

While eloquently written, I took issue with a few crucial points. Here is the letter I sent to the Editor at Wall Street Journal:


Dear Wall Street Journal Editor,

Re: Dr. Abraham Verghese’s article, The Myth of Prevention in the June 20-21, 2009 Weekend Journal.


I believe a more suitable title for Dr. Verghese’s article would be: “The Myth of What Passes as Prevention.”

As a practicing cardiologist, I, too, have witnessed firsthand the systemic “corruption” described by Dr. Verghese, the doing things “to” people rather than “for” them. Heart care, in particular, is rife with this form of profit-driven health delivery.

There is a fundamental flaw in Dr. Verghese’s otherwise admirable analysis: He assumes that what is called “prevention” in mainstream medicine is truly preventive.

Dr. Verghese makes issue of the apparent minor differences between preventing a condition and just allowing a condition to run its course. Prostate cancer screening is one example: Men subjected to repeated screenings have little length-of-life advantage over men who just allow their prostate to suffer the expected course of disease.

What if, instead, “prevention” as practiced today is nothing more than a solution that has been adopted in mainstream practice to suit yet another doing “to” strategy than doing “for”? In the prostate cancer example, PSA and prostate exam screenings often serve as little more than a means of harvesting procedures for the local urologist.

That’s not prevention. It is a prototypical example of “prevention” being subverted into the cause of revenue-generating procedures.

I submit that Dr. Verghese has fallen victim to the very same system he criticizes. His views have unwittingly been corrupted by the corrupt profit-driven system he describes.

What if, instead, prevention were just that: prevention or elimination of the condition. What if “prevention” of prostate cancer eliminated prostate cancer? What if heart disease “prevention” prevented all heart disease? What if this all proceeded without regard for profit or revenue-generating procedures, but just on results?

Dr. Verghese specifically targets heart scans or coronary calcium scoring, a test he likens to “miracle glow-in-the-dark minnow lures,” calling them “moneymakers.” Yes, when subverted into a corrupt algorithm of stress test, heart catheterization, stent, or bypass, heart scans are indeed a test used wrongly to “prevent” heart disease.

But what if the risk insights provided by heart scans prompt the start of a benign yet effective “prevention” program that inexpensively, safely, and assuredly prevents--in the true sense of the word--or eliminates heart disease? Then I believe the differences in mortality, quality of life, and costs would be substantial. Such strategies exist, yet do not necessarily include prescription drugs and certainly do not include the aftermath of heart catheterization and bypass surgery. Yet such programs fail to seize the limelight of media attention with no new high-tech lifesaving headline nor a big marketing budget to broadcast its message.

The problem in medicine is not prevention and its failure to yield cost- and life-saving results. It is the pervasively profit-driven mindset that keeps true preventive strategies from entering mainstream conversation. It is a repeat of Dr. Ignaz Semmelweis’ late 19th-century pleads for physicians to wash their hands before delivering babies to reduce puerperal sepsis, ignominious advice that earned him life and death in an asylum. We are essentially continuing to deliver children with unwashed hands because there is no revenue-generating procedure to clean them.

No, Dr. Verghese, the economic and medical failings of preventive strategies are not at fault. The failure of the medical system, in which everyone is bent on seizing a piece of the financial action for himself, has resulted in the failure to support the propagation of true preventive strategies that could genuinely save money and lives.

President Obama’s goal of cultivating preventive practices in medicine can work, but only if the profit-motive for “prevention” does not serve as the primary determinant of practice. Results-driven practices that are applied without regard to profit have the potential to yield the sorts of cost-saving and life-saving results that can reduce healthcare costs.


William Davis, MD
Milwaukee, Wisconsin
Medical Director, The Track Your Plaque Program (www.cureality.com)
Blog: http://heartscanblog.blogspot.com

A victory for SHAPE, CT heart scans, and doing what is RIGHT

The efforts of Texas House of Representatives Rep. Rene Oliveira and the SHAPE Guidelines committee have paid off: The Texas legislature passed a bill that requires health insurers to cover CT heart scans.

(NOTE: Don't make the same mistake that the media often makes and confuse CT heart scans with CT coronary angiography: two different tests, two different results, two different levels of radiation exposure. The difference is discussed here.)

Track Your Plaque previously reported the release of the SHAPE Guidelines, an ambitious effort to open CT heart scanning to people who would benefit from a simple screening test for coronary disease. Rep. Rene Oliveira initially introduced the bill in 2006, after having a heart scan uncovered extensive coronary plaque that resulted in coronary bypass surgery.

The bill requires that health-benefit providers cover the cost of CT heart scans (and carotid ultrasound) in men between the ages of 45-76, women 55-76, as well as anyone with diabetes or at "intermediate-risk" or higher for coronary disease by Framingham risk score.

The usual panel of cardiology knuckleheads stepped to the media podium, expressing their incredulity that something as "unvalidated" as heart scans could gain the backing of legislative mandate. Heartwire carried this comment:

"Contacted by heartwire, Dr Amit Khera (University of Texas Southwestern Medical Center, Dallas) confirmed there are still no comprehensive, adequately powered studies showing that these screening tests lead to better outcomes. In a phone interview, Khera said he has major concerns about how physicians will use these tests, particularly primary-care physicians. "I gave a talk last week to primary-care doctors, and there were probably 250 people in the room, and when I asked how many people had ordered a calcium scan, just one person raised a hand. . . . Most people don't even know what to do with the Framingham risk score, so they're going to follow an algorithm that they don't know how to follow to order a test result that they don't know what to do with."

It's the same criticisms hurled at heart scans over the years despite literally thousands of studies validating their application.

Studies have conclusively shown that:

--Coronary calcium scores generated by a CT heart scan outperform any other risk measure for coronary disease, including LDL cholesterol, c-reactive protein, total cholesterol, HDL cholesterol, blood pressure.
--Coronary calcium scores yield a graded, trackable index of coronary risk. Scores that increase correlate with increased risk of cardiovascular events; scores that remain unchanged correlate with much reduced risk.
--A coronary calcium score of zero--no detectable calcium--correlates with extremely low 5-year risk for cardiovascular events.
--Coronary calcium scores correlate with other measures of coronary disease. Heart scans correlate with coronary angiography, quantitative coronary angiography, carotid ultrasound (intimal-medial thickness and plaque severity), ankle-brachial index, and stress tests, including radionuclide (nuclear) perfusion imaging.

The reluctance of my colleagues to embrace heart scans stems from two issues, for the most part:

1) No study has yet been performed showing that knowing what the score is vs. not knowing what the score is changes prognosis. That's true. But it is also true of the great majority of practices in medicine. While many wrongs don't make a right, the miserable and widespread failure of other coronary risk measures, like LDL cholesterol or c-reactive protein, to readily and reliably detect hidden coronary disease creates a gaping void for improved efforts at early detection. If your LDL cholesterol is 140 mg/dl, do you or don't you have coronary disease? If your doctor's response is "Just take a statin drug anyway" you've been done a great disservice. (If and when this sort of study gets done, its huge cost--outcome studies have to be large and last many years--it will likely be a statin study. It is unlikely it will include such Track Your Plaque strategies that help reduce heart scan scores, like vitamin D and correction of small LDL particles.)

2) Fears over overuse of hospital procedures triggered by heart scans. This is a legitimate concern--if the information provided by a heart scan is misused. Heart scans should never--NEVER--lead directly to heart catheterization, stents, bypass surgery. Heart scans do not change the indications for performing revascularization (angioplasty, stents, bypass). Just because 20% of my cardiology colleagues are more concerned with profit rather than patient welfare does not invalidate the value of the test. Just because the mechanic at the local garage gouged you by replacing a carburetor for $800 when all you need was a new spark plug does not mean that we should outlaw all auto mechanics. Abuse is the fault of the abuser, not of the tool used to exercise the abuse.


All in all, while I am not a fan of legislating behavior in healthcare, the blatant and extreme ignorance of this simple tool for uncovering hidden heart disease makes the Texas action a huge success for heart disease prevention. I hope that this success will raise awareness, not just in Texas, but in other states and cities in which similar systemic neglect is the rule.

Remember: CT heart scans are tools for prevention, not to uncover "need" for procedures. They serve as a starting point to decide whether or not an intensive program of prevention is in order, and I don't mean statin vs. no statin.

Though not a multi-million dollar statin drug study, I have NEVER seen a heart attack or "need" for procedure in any person who has stopped progression or reduced their heart scan score. A small cohort from my practice was reported:

Effect of a Combined Therapeutic Approach of Intensive Lipid Management, Omega-3 Fatty Acid Supplementation, and Increased Serum 25 (OH) Vitamin D on Coronary Calcium Scores in Asymptomatic Adults.

Davis W, Rockway S, Kwasny M.

The impact of intensive lipid management, omega-3 fatty acid, and vitamin D3 supplementation on atherosclerotic plaque was assessed through serial computed tomography coronary calcium scoring (CCS). Low-density lipoprotein cholesterol reduction with statin therapy has not been shown to reduce or slow progression of serial CCS in several recent studies, casting doubt on the usefulness of this approach for tracking atherosclerotic progression. In an open-label study, 45 male and female subjects with CCS of >/= 50 without symptoms of heart disease were treated with statin therapy, niacin, and omega-3 fatty acid supplementation to achieve low-density lipoprotein cholesterol and triglycerides /=60 mg/dL; and vitamin D3 supplementation to achieve serum levels of >/=50 ng/mL 25(OH) vitamin D, in addition to diet advice. Lipid profiles of subjects were significantly changed as follows: total cholesterol -24%, low-density lipoprotein -41%; triglycerides -42%, high-density lipoprotein +19%, and mean serum 25(OH) vitamin D levels +83%. After a mean of 18 months, 20 subjects experienced decrease in CCS with mean change of -14.5% (range 0% to -64%); 22 subjects experienced no change or slow annual rate of CCS increase of +12% (range 1%-29%). Only 3 subjects experienced annual CCS progression exceeding 29% (44%-71%). Despite wide variation in response, substantial reduction of CCS was achieved in 44% of subjects and slowed plaque growth in 49% of the subjects applying a broad treatment program.

Sleep: A to Zzzzzzzzzz

Take a look at the results from the Heart Scan Blog's most recent reader poll (399 respondents):

How many hours do you sleep per night (on average)?


9 or more hours per night
15 (3.7%)

8-9 hours per night
72 (18%)

7-8 hours per night
152 (38.1%)

6-7 hours per night
111 (27.8%)

5-6 hours per night
38 (9.5%)

Less than 5 hours per night
11 (2.8%)


Like many issues in health, too much or too little of a good thing can present undesirable consequences.

Too much sleep: While psychologists and sleep researchers advise us that at least 9 hours are required to fully eliminate sleep "debt" and achieve optimal vigilance and mental performance, epidemiologic studies have shown increased mortality with this quantity of sleep.

Too little sleep: Getting less than 7 hours habituallly increases blood sugar, appetite, inflammatory measures, and encourages weight gain. Mortality is also increased, just as with sleeping too much. It is also associated with increased likelihood of a positive heart scan score.

7-8 hours per night from a health viewpoint is that Goldlilocks "just right" value: just enough to not erode mental performance substantially, but not so little that inflammatory, insulin-disrupting, and appetite-increasing effects develop.

Of our 399 respondents in the poll, 56.1% (38% + 18%) slept what appears to be an optimal amount for health. While only 3.7% slept too much (9 hours or more), the remaining 40.1% slept too little.

Our informal poll confirms what most of us observe in everyday life: The majority of people shortchange sleep in order to meet the demands of their high-pressure, squeeze-as-much-as-possible-into-every-day lives. But not paying off your sleep "debt" is like not paying the mortgage for a couple of months. You wouldn't expect your friendly neighborhood bank to say, "Oh, you forgot to pay your mortgage? Forget about it. Just pay next month's." Sure, fat chance. But if you don't pay off your sleep "debt," you will pay it back with health.

Beating the Heart Association diet is child's play



In response to the Heart Scan Blog post, Post-Traumatic Grain Disorder, Anne commented:


While on the American Heart Association diet my lipids peaked in 2003. I even tried the Ornish diet for a short time, but found it impossible.

Total Cholesterol: 201
Triglycerides: 263
HDL: 62
LDL: 86

After I stopped eating gluten (I am very sensitive), my lipid panel improved slightly. This past year I started eating to keep my blood sugar under control by eliminating sugars and other grains. Now this is my most recent lab:

Total Cholesterol: 162
Triglycerides: 80
HDL: 71
LDL: 75


Isn't that great? This is precisely what I see in practice: Elimination of wheat and sugars yields dramatic effects on basic lipids, especially reductions in triglycerides of up to several hundred milligrams, increased HDL, reduced LDL.

Beneath the surface, the effects are even more dramatic: reductions or elimination of small LDL particles, reduction or elimination of triglyceride-containing lipoproteins, elimination of the marker for abnormal post-prandial (after-eating) lipoproteins, IDL, reduced c-reactive protein. Add weight loss from abdominal fat stores and reduced blood pressure.

In fact, I would go so far as to speculate that, if the entire nation were to follow Anne's lead and eliminate wheat and sugars, "need" for 30% of all prescription medications would disappear. The incidence of diabetes would be slashed, the U.S. would no longer lead the world in obesity.

Anne and I are not the first to make this observation. It has also been made in several studies, such as:

The Duke University study of low-carbohydrate diets in type II diabetics. In this study, 50% of low-carb participants became non-diabetic: They were cured.

One of the many studies conducted by University of Connecticut's Dr. Jeff Volek, demonstrating dramatic improvement in glucose, insulin (reduced 50%) and insulin responses, and lipids.

Dr. Ron Krauss' early studies that hinted at this effect, even though the "high-fat" diet wasn't really low-carbohydrate.

If wheat and sugar elimination has been shown to achieve all these fabulous benefits, why hasn't the American Heart Association spoken in favor of this dietary approach and other- low-carbohydrate diets ? Why does the American Heart Association maintain its "Check-Mark" stamp of approval on Cocoa Puffs and Count Chocula cereals?

Victim of Post-Traumatic Grain Disorder

Heart Scan Blog reader, Mike, shared his story with me. He was kind enough to allow me to reprint it here (edited slightly for brevity).



Dr. Davis,

I was much intrigued to stumble onto your blog. Heart disease, nutrition, and wellness are critically important to me, because I’m a type 2 diabetic. I’m 53 and was diagnosed as diabetic about 5 years ago, though I suspect I was either diabetic or pre-diabetic 5 years before that. Even in a metropolitan area it's next-to-impossible to find doctors sympathetic to any approach beyond the standard get-the-A1c-below 6.5, get LDL <100, get your weight and blood pressure normal, and take metformin and statins.

I’m about 5’10-and-a-half and when I was young I had to stuff myself to keep weight on; it was an effort to get to 150 pounds, and as a young man, 165 was the holy grail for me. I always felt I’d look better with an extra 10-15 pounds.
I ate whatever I wanted, mostly junk, I guess, in my younger years.

When I hit about age 35, I put on 30 pounds seemingly overnight. As I moved toward middle age I became concerned with the issue of heart health, and around that time Dr. Ornish came out with his stuff. I was impressed that he’d done a
study that supposedly showed measurable decrease in atherosclerotic plaque, and had published the results of his research in peer-reviewed journals. It looked to me as though he had the evidence; who could argue with that? I tried his plan on and off, but as so many people note, an almost-vegan diet is really tough. It was for me, and I could never do it for any length of time. But given that the “evidence” said that I should, I kept trying, and kept beating up on myself when I failed. And I kept gaining weight. I got to almost 200 pounds by the time I was 40 and have a strong suspicion that that’s what caused my blood sugar to go awry, but my doctor at the time never checked my blood sugar, and as a relatively young and healthy man, I never went in very often.

I’ve had bouts of PSVT [paroxysmal supraventricular tachycardia, a rapid heart rhythm] every now and again since I was 12 or so. I used to convert the rhythm with Valsalva, but as I moved into my forties, occasionally my blood pressure would be elevated and it made me nervous to do the procedure because it was my understanding that it spikes your blood pressure when you do it. So I began going to the ER to have the rhythm converted, which they do quite easily with adenosine. On one of my infrequent runs to the ER to get a bout of PSVT converted, they discovered my blood glucose was 500 mg/dL, and I’d never experienced any symptoms! They put me in the hospital and gave me a shot of insulin, got it town to 80 mg/dL easily,
diagnosed me as diabetic, and put me on 500 mg. metformin a day.

I was able to get my A1c down to 7, then down to 6.6, and about that time I read a number of Dr. Agatston’s books, and began following the diet, and pretty quickly got my A1c down to 6.2, and my weight down, easily, to 158. That was fine with my doctor; he acted as though I was in good shape with those numbers. Soon I ran into Dr. Bernstein’s material, and came face to face with a body of research that suggested I needed to get the A1c down to below 5! That was both discouraging and inspiring, and frankly it’s been difficult for me to eat as lo-carb as I appear to need to, so I swing back and forth between 6.2 and 6.6. I know I need to work harder, be more diligent in my carb control, and I see with my meter that if I eat low-carb I have great postprandial and fasting blood sugars, but since I don’t particularly get any support or encouragement from
either my doctor or my wife for being so “radical,” it’s hard to pass the carbs by.

One thing that always confused me was that though I saw on my meter that BG [blood glucose] readings were better with a lo-carb diet, and though I saw the preliminary research suggesting that lo-carb could be beneficial in controlling CVD, I didn’t understand why Ornish had peer-reviewed research demonstrating reversal of atherosclerosis on a very-lowfat diet. How could two opposing approaches both help? I wondered if it were possible that one diet is good for diabetes, and the
other good for heart health. That would mean diabetics are screwed, because they always seem to end up with heart disease.

From time to time I’d look for material that explained this seeming contradiction. I was determined to try to stay lo-carb, simply because I saw how much better my blood sugars are when I eat lo-carb; but it’s hard in the face of this or that website that tells you about all the dangers of a lo-carb diet and that touts the lo-fat approach. That tends to be the conventional wisdom anyway.

Finally in one of those searches I came across your material, and saw you offer what was at last an explanation of what Ornish had discovered--it wasn’t a reversal of atherosclerotic plaques he was seeing; it was that his diet was improving endothelial dysfunction in people who had had high fat intakes.

Odd as it may seem to you, that little factlet has been enough to allow me to discard entirely the lingering ghost of a suspicion that I ought to be eating very-lowfat. In fact, I was very excited to see your claim that your approach can reverse atherosclerotic plaque.

It would be nice to find a doctor who’d be supportive of your approach. My doctor isn’t much interested in diet or
nutrition. He just wants my weight in the acceptable range, my blood pressure good, and my LDL 100 or below (which I know isn’t low enough). He’s not particularly interested in getting a detailed lipid report. I hope I can talk him into ordering one so that it’s more likely I can get it covered by my insurance.

I very much appreciated the links you gave to Jenny’s diabetes websites, and I’ve resolved to get even better control of my BG by being more diligent with my diet. I’m planning on joining your site, reading your book, and following your advice. I just have this sort of deflating feeling that it would have been better if I’d stumbled upon this before I had diabetes. Still, it’s nice to have a site that offers to laypeople the best knowledge available concerning how to take care of their heart.



Mike is yet another "victim" of the "eat healthy whole grains" national insanity, the Post-Traumatic Grain Disorder, or PTGD. The low-fat dietary mistake has left many victims in its wake, having to deal with the aftermath of corrupt high-carbohydrate diets: diabetes, heart disease, and obesity.

We should all hope and pray that "low-fat, eat healthy whole grains" goes the way of Detroit gas guzzlers and sub-prime mortgages.

Drug industry "Deep Throat"

A Heart Scan Blog reader brought the following letter from a former pharmaceutical sales representative to congress to my attention.

Interesting excerpts:

As a former drug representative for Eli Lilly, I spent 20 months increasing the market share of my company’s drugs. I was recruited fresh from college with an eager desire to employ my degree in molecular biology and biochemistry. Shortly after my hiring, it became clearly apparent that a drug sale had much more to do with establishing personal relationships than it did with understanding the latest science. However, any doubts I held regarding the effectiveness of such methods were dispelled by the results of my persuasiveness and the financial rewards I received for my efforts. The latter also helped me rationalize the many ethically dubious situations I routinely encountered in my work. Upon my departure from the industry, I began working for the public’s health. Seven years later, as a result of my experiences and education I am more convinced than ever that the goals of the pharmaceutical industry often stand in direct conflict with the practice of ethical and responsible medicine. Nothing in my recent research causes me to believe that my experiences were anything but typical of the training and practice of the majority of drug reps plying their trade today.


“There’s a big bucket of money sitting in every [doctor’s] office.” – Michael Zubillaga, Astra Zeneca Regional Sales Director, Oncology


The majority of drug reps entering the work force today are young and attractive. The ranks of reps are replete with sexual icons: former cheerleaders, ex-military, models, athletes. Of course, as a sales job, the reps must be eloquent and convincing. Depending on the population, certain ethnicities are preferred either to make the rep distinct among other reps or to provide them with a cultural advantage in connecting with their clients. Noticeably lacking among most new reps is any significant scientific understanding. My personal case illustrates this point rather vividly: In my training class for Eli Lilly's elite neuroscience division, selling two products that constituted over 50% of the company's profits at the time, none of my 21 classmates nor our two trainers had any college level scientific education. In fact, that first day of training, I taught my class and my instructors the very basic but crucial process by which two nerve cells communicate with one another. It is very likely that the majority of my class couldn't explain the difference between a neuron and a neutron prior to sales school. While it's certainly a bonus to have a scientifically educated representative, it is far from a primary recruitment criterion. Youth is a much higher criterion for the sales position.

Sales representative trainers are almost always veteran sales representatives and consequently, much of the training they offer is implicit in the anecdotes they give. This informal training parallels the standard training offered by the industry and in many ways compliments it. It is tacitly accepted by management and perceived as the "real" training by many veteran sale representatives. Among the more dubious "unofficial" lessons a new rep learns are: how to manipulate an expense report to exceed the spending limit for important clients, how to use free samples to leverage sales, how to use friendship to foster an implied "quid pro quo" relationship, the importance of sexual tension, and how to maneuver yourself to becoming a necessity to an office or clinic.

The most troubling aspect of pharmaceutical sales is systematic befriending of our clients. In addition to the psychological profiling mentioned above, drug reps are taught to constantly be on the lookout for personal effects that will help us connect to our doctors. When entering an office for the first time, we nonchalantly survey it for clues to ingratiate ourselves with our client. Similarly, conversations are intentionally steered into the realm of personal details such as religion, family, or hobbies to acquire similar information. As a matter of training, we collect this data subtly. In the course of a conversation with clients, we may glean facts about their prescribing preferences, the dates of their children’s birthdays, where they were born, or what music they enjoy. Training encourages us to commit these details to memory just long enough to return to our cars and instantly type up a “call report” listing the details of our conversation. On a daily basis, we connect our computers to a central database that uploads the information we’ve acquired, allowing us to share it with our partner drug reps and company marketers. Subsequently, drug reps interweave pieces of conversation specifically tailored to appeal to their client drawn from personal information that wasn’t necessarily shared with them. For example, Dr. Jones will be nothing but grateful when I supply him with a cake celebrating his children’s birthday when, in fact, he told my partner (and not me) the birthdates several months prior in a personal conversation.


The writer's comments ring true: The relentless attention-grab of sales representatives, using clever tactics that include access to detailed records of physician prescribing habits, big smiles and eye-winking, are detailed perfectly.

There's nothing wrong with a business doing its job by marketing its products and services. What is so wrong about this picture is that one side is so well-equipped, heavily funded, with access to extraordinary resources that the other side (physicians) don't have. And the physicians aren't the victims--YOU are.

A middle-aged, receding hairline physician, faced with a 28-year old attractive woman asking all manner of ingratiating questions but knowing full well what she is doing, having strategized for weeks on how to manipulate the behavior of her "mark," is helpless.

Like the mortgage-backed security crisis, we've reached another phenomenon of crisis proportions. Direct-to-consumer drug advertising, drugs for non-conditions and well people, pinpoint marketing of drugs to physicians--it's all gone too far.

Personally, drug representatives are not welcome in my office. This generally prompts puzzled, followed by angry, looks from the representatives, often traveling with a district supervisor hoping to help polish their pitch. If patients didn't request free samples, the reps would not step foot in the office.

Triglyceride Buster-Update

In the last Heart Scan Blog post, I described Daniel's experience reducing his triglycerides from 3100 mg/dl to around 1100 mg/dl with use of omega-3 fatty acids from fish oil, along with modifications in his diet. This was accomplished in the space of around two weeks.

An update: Daniel has continued another 10 days on his fish oil, along with elimination of wheat, cornstarch, and sugars.

Repeat triglyceride: 202 mg/dl. That's 93.5% reduction in the space of three weeks--no drugs involved.

Daniel really did nothing extraordinary. He simply followed the simple advice I provided to take a moderate dose of EPA+DHA from over-the-counter fish oil supplements, along with elimination of the foods that are extravagant triggers of triglycerides.

He's got just a little further to go to achieve the biologically ideal level of less than 60 mg/dl. You can see that it is not really that difficult--provided someone didn't load you down with nonsense about "cutting your fat," or statin or fibrate drugs.

Triglyceride buster

Two weeks ago, Daniel started with a triglyceride level of 3100 mg/dl, a dangerous level that had potential to damage his pancreas. The inflammatory injury incurred could leave him with type I diabetes and inability to digest foods, since the insulin-producing capacity and the enzyme producing capacity of the pancreas are lost.

Daniel added 3600 mg of omega-3s per day. Within 10 days, his triglycerides dropped nearly 2000 mg to just over 1100 mg/dl--still too high, but an incredible start.

The power of omega-3 fatty acids from fish oil to reduce triglycerides is illustrated most graphically by people with a condition called "familial hypertriglyceridemia" that is responsible for triglyceride levels of 500, 1000, even several thousand milligrams. That's what Daniel has. Given appropriate doses of omega-3s, triglycerides drop hundreds, even thousands, of milligrams.

No question: Omega-3 fatty acids from fish oil are the best tool available for reduction of triglycerides. The effect is dose-dependent, i.e., the more you take, the greater the triglyceride reduction.

How omega-3s exerts this effect is unclear, though there is evidence to suggest that omega-3s suppress several nuclear receptors involved in triglyceride (VLDL) production and increase the expression or activity of the enzyme lipoprotein lipase, an enzyme that clears triglycerides from the blood.

I am continually surprised at the number of people with high triglycerides who are still treated with a fibrate drug, like Tricor, or a statin drug, when fish oil--widely available, essentially free of side-effects, with a proven cardiovascular risk-reducing track record--should clearly be the first choice by a long stretch.

Among its many benefits, omega-3 fatty acids from fish oil also:

Reduce matrix metalloproteinases (MMP)--Two fractions of MMPs, MMP-2 and MMP-9, are inflammatory enzymes present in atherosclerotic plaque that are suspected to trigger plaque "rupture." Omega-3s have been shown to reduce both forms of MMP.

Block uptake of lipids in the artery wall--Suggested by a study in mice.

Modify postprandial responses--In the first few hours after eating (the "postprandial" period), a flood of digestive byproducts of a meal are present in the bloodstream. While research exploring postprandial effects is still in its infancy, it is clear that omega-3 fatty acids have the capacity to favorably modify postprandial patterns. One common surrogate measure for postprandial abnormalities is intermediate-density lipoprotein, or IDL, that we obtain in fasting blood through lipoprotein panels like NMR and VAP. With sufficient omega-3s alone, IDL is completely eliminated.

Unfortunately, most of my colleagues, if they even think to use omega-3s, choose to use the prescription form, Lovaza. Indeed, several representatives from AstraZeneca, the pharmaceutical outfit now distributing this miserably overpriced product, frequently barge their way into my office poking fun at our use of nutritional supplements instead of the prescription Lovaza. "But insurance covers it in most cases!" they plead. "And your patients will know that they're getting the real product, not some fake. And they'll have to take fewer capsules!"

I never use Lovaza to reduce triglycerides, even in familial hypertriglyceridemia--the FDA-approved indication for Lovaza--and have not yet seen any failures, only successes.

Newsweek, Time, and other fronts for the drug industry

I used to believe that conventional print media--newspapers, magazines--were unbiased, untouchable flames of truth. Perhaps there was a time when this was true, when the young reporter, eager to change the world, uncovered the story that righted some huge wrong.

Those days are drawing to a close.

Today, the once powerful print media are collapsing due to the competition of the cheaper, broader reach of the internet.

The myth of mild coronary disease

I hear this comment from patients all the time:

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

That's one big lie.

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

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

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

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

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


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

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


Image courtesy Wikipedia.

Copyright 2008 William Davis, MD

Red flags for lipoprotein(a)



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

How do you know you have it?

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

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

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

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

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

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

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

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

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

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

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

The NY Times reporting of the story:

Drug Has No Benefit in Trial, Makers Say

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

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

(Vytorin is the combination of simvastatin and Zetia.)

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

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

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

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

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

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

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

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

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

Dr. Arthur Agatston in the news



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

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

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


• Maintain a healthy weight through diet.

• Undergo CT heart scans to check for arterial plaque.

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

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


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

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

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

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

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

Take this survey: I DOUBLE-DARE YOU

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

Here's what I said:

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

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

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

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

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

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

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


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

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

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

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

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

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

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



Copyright 2008 William Davis, MD

Michael Pollan on Nutritionism



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

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

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

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

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

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


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

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

Cholesterol follies

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

His basic cholesterol values:

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

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

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

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


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

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

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

Here they are (NMR; Liposcience):

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

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

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


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

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

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

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

Equal calories, different effects

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

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

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

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

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

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

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

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

Lipids differed between the two diets, however:


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

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

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

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

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


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

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

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

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

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


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

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


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

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

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

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

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

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

Is skinny necessary for reversal?

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



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

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

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

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

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

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

Then is it okay to be fat or overweight?

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

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

So, which is it, fat or skinny?

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

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


Image courtesy Wikipedia.

Copyright William Davis, MD 2008

MESA Study: Track Your Plaque-Lite?

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

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

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

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

1) What risk factors predict heart scan scores?

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

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

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

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

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

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

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


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

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

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



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


Copyright 2008 William Davis,MD