Dr. Joseph Prendergast and l-arginine

In response to a discussion started by Track Your Plaque Member, Rich, on the Member Forum, I tracked down Dr. Joseph Prendergast, who had posted a video on his unique experiences, both personal and professional, with l-arginine.

Dr. Prendergast describes some of this in a brief webcast. Here, I quote Rich:

“This 90-second video by a Palo Alto physician (internal/endocrine, diabetes specialist) will totally blow your mind.

http://enews.endocrinemetabolic.com/2007/08/16-12-years.html

You will see in the link below that he reversed his personal atherosclerotic disease, diagnosed in abdominal aorta at age 37—completely reversed. He's now much older."

http://www.endocrinemetabolic.com/about/press/larginine.pdf



I contacted Dr. Prendergast to find out more.

Dr. Joseph Predergast is founder of the Endocrine Metabolic Medical Center in Palo Alto, California, focused on providing care for people with diabetes. In addition to the website, he provides Blogs and newsletters, though most of his conversation is about diabetes issues. Dr. Predergast’s website is located at http://www.endocrinemetabolic.com.

I asked Dr. Prendergast several questions about his l-arginine experience. His brief answers are below.



1) What dose of l-arginine have you employed in your patients and why this dose?

The dose is 3 - 6 grams as suggested by the Stanford Cardiovascular Research Department Chairman John Cooke. http://med.stanford.edu/profiles/John_Cooke/

2) I gather that you have preference for specific preparations of l-arginine. Can you say why some preparations seem superior to others in your experience?

I started with pharmaceutical l-arginine from the pharmacy. I gradually began to add components that would augment the power of the l-arginine and have gone through 12–15 different products. I have completely reversed my own very severe atherosclerosis discovered at age 37 and there has been less than 0.05% cardiovascular disease in my endocrine practice in almost 17 years. Both my exams were evaluated with CT technology. I am now using ProArgi9 Plus that includes several anti-aging components and will likely never switch. http://www.synergyworldwide.com/synergycorp/home.aspx

3) Are you employing any other unique practices in your patients to reduce cardiovascular events?

Withdrawing as many prescription drugs as possible.




Interesting. Of course, I also advocate l-arginine as a facilitator of atherosclerotic plaque regression, though I am not as ebullient about its use as Dr. Prendergast.

Instead, I see l-arginine as a method that yields forced normalization of “endothelial dysfunction,” the abnormal constriction and other effects that develop when abnormal lipoproteins and unhealthy food by-products are present in the circulation. Endothelial dysfunction is an inevitable accompaniment of plaque.

However, unlike Dr. Predergast’s experience, despite our use of doses higher than he uses, I have never seen plaque regression just using l-arginine alone. Nonetheless, it’s good to hear that others are seeing at least some positive effects.

By the way, we have also had some positive posts on our Forum about the ProArgi9 product he uses.

Dr. Dwight Lundell on omega-3s and CLA



An interview with Dr. Dwight Lundell, cardiac surgeon and author of the new book, "The Cure for Heart Disease."


Dr. Lundell comes to us with a unique pedigree. He is a cardiothoracic surgeon practicing in the Phoenix, Arizona, area. Despite having performed thousands of coronary bypass operations, including numerous "off-pump" procedures earning him a place in the Beating Heart Hall of Fame and a listing in Phoenix Magazine’s Top Doctors for 10 years, more recently Dr. Lundell has turned his attentions away from traditional surgical treatment and towards prevention of heart disease and.

In particular, Dr. Lundell is a vocal advocate for omega-3 fatty acids from fish oil and conjugated linoleic acid, or CLA.

When I heard about Dr. Lundell’s unique perspectives, I asked him if he’d like to tell us a little more about his ideas. Here follows a brief interview with Dr. Lundell.



You’re a vocal advocate of the role of omega-3 fatty acids from fish oil in heart disease prevention. Can you tell us how you use it?

In my book, I recommend 3 g of fish oil daily. This would normally yield about 1000 mg of EPA and DHA depending on the concentration of the supplement. This is approximately the dose that reduced sudden cardiac death by 50%, and all cause death, by 25% in patients with previous heart attack.

In patients with signs of chronic inflammation such as heart disease, obesity, arthritis, metabolic syndrome or depression or in those patients with elevation of CRP, I would recommend higher doses, 2000 to 3000 mg per day of EPA and DHA. The FDA has approved up to 3400 mg for treating patients with severely elevated triglycerides.

I personally take a 2000 mg EPA and DHA per day because I have calcium in my coronary arteries.




Of course, in the Track Your Plaque program we track coronary calcium scores. Do you track any measures of atherosclerosis in your patients to chart progression or regression?

Carotid ultrasound with measurement of IMT [intimal-medial thickness] has been shown to be a good surrogate marker for coronary disease, as has vascular reactivity in the arm. CT scanning with calcium scoring is a direct marker of coronary disease. CT does not differentiate between stable or unstable plaque but there is no good noninvasive way of doing this.

The dramatic value of CT scan calcium scoring is to demonstrate to people that they actually do have coronary disease and to motivate them to make the necessary lifestyle and nutritional changes to reduce it. CT scan with calcium scoring is a direct way to measure the progression or regression of coronary artery disease. If there is a choice between a direct measurement and indirect measurement, always choose the direct method.

Every patient treated with CLA in my clinic, experienced significant reductions in C-reactive protein. These patients were also on a weight-loss program, so I can't prove whether it was the CLA or the weight-loss that improved their inflammatory markers. In the animal model for arteriosclerosis, CLA has a dramatic effect of reducing and preventing plaque. This has not yet been proven in humans.

Normally, when people lose weight 20% or more of the loss is lean body mass (muscle) this lowers the metabolic rate and frustrates further weight-loss. My patient, from teenagers to retirees, lost no lean body mass and continued to have satisfactory weight-loss when CLA was used as part of the plan.



In reading your book, your use of conjugated linoleic acid (CLA) as a principal ingredient struck me. Can you elaborate on why you choose to have your patients take CLA?

My enthusiasm for CLA is based on:

1) Safety?this is of paramount importance. Animal toxicity studies have been done, as well as multiple parameters measured in human studies, both of these are well reviewed recently in the American Journal of Clinical Nutrition (2004:79(suppl)1132s). CLA, a naturally-occurring substance, is not toxic or harmful to animals or humans. The only negative report is by Riserus in Circulation (2002), where he found an elevated c- reactive protein; however, he used a preparation that is not commercially available and not found in nature as a single isomer.

2) Effectiveness?also critically important. A recent meta-analysis [a reanalysis of compiled data] in the American Journal of Clinical Nutrition (2007; 85:1203-1211) demonstrated the effectiveness of CLA in causing loss of body fat in humans. The study also reconfirmed the safety of CLA.

Since we now know that atherosclerosis is an inflammatory disorder, any strategy that reduces low-grade inflammation without significant side effects would seem to be beneficial in the treatment and prevention of atherosclerosis. CLA not only has antioxidant properties, but it modulates inflammatory cascade at multiple points. CLA reduces PGE2 (in much the same way as omega-3) CLA also has been shown to reduce IL-2, tumor necrosis factor-alpha and Cox–2. It reduces platelet deposition and macrophage accumulation in plaques. It also has some beneficial effect in the PPAR [peroxisome proliferator-activated receptors, important for lipid and inflammatory-mediator metabolism] area.

Part of the effect of CLA may be because it reduces fat mass and thus the amount of pro-inflammatory cytokines produced by fat cells.

I reiterate and fully admit that CLA has not been shown to have any effect on atherosclerosis in human beings. However, the results in the standard animal models for atherosclerosis (rabbits, hamsters,APO-E knockout mice) are very dramatic.

From all I know, it appears that the effective dose for weight loss and the animal studies in atherosclerosis would be equal to about 3 g of CLA per day. The anti-inflammatory properties of CLA seem to work better in the presence of adequate blood levels of omega-3.



I’m curious how and why a busy cardiothoracic surgeon would transform his practice so dramatically. Was there a specific event that triggered your change?

The transition from a very busy surgical practice to writing and speaking about the prevention of coronary disease has not been particularly easy, but it has been very interesting. I can't really point to any specific epiphany, it was a general feeling of frustration that we were not making any progress in curing heart disease, which is what I thought I was doing when I began my medical career.

Of course, I enjoyed the technical advances, the dramatic life-saving things that you do and I did on a daily basis. American medicine is spectacularly good at managing crises and spectacularly horrible at preventing those crises.

The lipid hypothesis is old and tired, even the most aggressive statin therapy reduces risk of heart attack by about 30% in a relatively small subset of people. It's interesting that we're now looking at statins as an anti-inflammatory agent.


Thanks, Dr. Lundell. We look forward to future conversations as your experience with CLA and heart disease prevention and reversal develops!


More about Dr. Lundell's book, The Cure for Heart Disease can be found at http://www.thecureforheartdisease.net.


Note: We are planning a full Special Report on CLA for the Track Your Plaque website in future.

High-tech heart attack proofing


I was reminiscing the other day about what I was taught about heart disease in medical school some 20 years ago.

In the 1980s, the world was still (and remains) fascinated with this (then) novel "solution" to heart disease called coronary bypass surgery. As medical students, we all fought for a chance to watch a bypass operation being performed. And there was lots of opportunity. I was a medical student at St. Louis University School of Medicine, a center that boasted of a busy thoracic surgery service, performing up to 10 bypass operations every day.

Back then, coronary angioplasty was just a twinkle in Andreas Gruentzig's eye, still contemplating whether it was possible to put an inflatable device in the blockages of coronary arteries to re-establish blood flow. Risk detection for heart disease consisted of EKGs, screening for symptoms, detection of heart failure, and tests that are long forgotten in the dust bin of medical curiosities, tests like systolic-time intervals, phonocardiography (using amplified sound to detect abnormal heart sounds), and detailed physical examination. Treatment for heart attack involved nitroglycerin and extended bedrest. Bypass surgery would come after you recovered.

In other words, NONE of the tools we now use in the Track Your Plaque program for heart disease control and reversal were available just twenty years ago. There was no lipoprotein testing, no CT heart scans. Nobody recognized the power of omega-3 fatty acids (although epidemiologic observations were just beginning to suggest that eating fish might be the source of reduced risk for heart attack and cardiovascular death). Vitamin D? Why, that's in your milk so your babies don't get rickets.

So much of what we do today was not available then, nor were they even in the crystal ball of forward-looking people. I certainly had no idea whatsoever that I'd be talking and obsessing today about reversal of heart disease based on what I saw and learned back then.

Things have certainly come a long way and all for the better. The problem is that much of the world is stuck in 1985 and haven't yet heard that coronary disease is a manageable and reversible process. They've been sidetracked by the fiction propagated by the likes of Dr. Dean Ornish, the nonsense of low-fat diets aided and abetted by the food manufacturing industry and the USDA, the extravagant claims of some practitioners and the supplement industry. They haven't yet stumbled on the real-life experiences that are chronicled here in this Blog and the accompanying Track Your Plaque website.

Our program has been criticized for being too "high-tech," involving too many sophisticated measures like small LDL, lipoprotein(a) treatment, vitamin D blood levels. But when you see a woman reduce her heart scan score 63%, or a school principal's score plummet 51%, then that's reward in itself.

It's all about plaque

Just to keep my finger on the pulse of what is being said in the world of heart disease by the media, I subscribe to many publications.

Conversations abound about cholesterol, low-fat diets, now low-carb diets, not smoking, inflammation, etc. No doubt, these all have some importance in the conversation.

But the great majority of discussions fail to identify the one truly crucial factor to identify and track: coronary atherosclerotic plaque.

Sugar for breakfast

We were reviewing Stuart's diet because of his persistent small LDL, low HDL, modestly elevated triglycerides, and blood sugar of 107 mg/dl.

"I've changed my diet, doc. No kidding. We never fry our foods. No butter, no goodies. I don't know what else I can possibly do."

"Okay. Let's review your diet. What did you have for breakfast?"

"Orange juice, a big glass. Gotta get my potassium. Then cereal like Cheerios or Shredded Wheat, sometimes Kashi or Raisin Bran, always in skim milk. Gotta have my one slice of toast, no butter. I'll put some fruit preserves on it. You know, real fruit. Only whole wheat bread, never white. On Sundays, we always go out for pancakes, but now we order only whole wheat."

Many of us have gotten into a peculiar habit: Having what amounts to pure sugar for breakfast. Perhaps there's a little fiber thrown in with it, but many people indulge in breakfasts that are sugar and plenty of it. That's precisely what Stuart is doing: A breakfast that, while it doesn't contain a huge amount of sugar outside of the orange juice, is promptly converted to sugar. If we were to check his blood sugar just after his standard breakfast, it would rise substantially.

This pattern has become deeply ingrained into the American psyche. Some people will act like I've suggested we overthrow the government when I suggest that breakfast cereals need to be eliminated from their lives. We all share memories of Tony the Tiger, the leprechaun on Lucky Charms ("They're magically delicious!), reading the brightly colored boxes often including games and prizes. Breakfast cereals seem as American as apple pie. But the wheat and corn content ensures a big rise in blood sugar, the sort that create small LDL, low HDL, etc.--all the patterns Stuart is showing--and make us fat.

Orange juice? Too much sugar all at once. Get your potassium from whole vegetables and fruits, not from orange juice. (Bananas are another problem source of potassium for similar reasons despite being a whole fruit.)

Toast? Any diabetic who monitors their blood sugar after meals will tell you: Even one slice of bread, ANY bread, skyrockets blood sugar. Add the fruit preserves made with sugar syrup and it's doubly worse.

Pancakes? Even if made with plenty of fiber, blood sugars go absolutely berserk after a meal like this, especially if maple syrup is added.

In other words, the seemingly healthy breakfast Stuart eats guarantees that he fails to control all his patterns that contribute to his coronary plaque growth.

After I pointed out Stuart's dietary faux pas, he asked, "Then what the heck can I eat?"

"There's actually lots of good choices: Eggs (preferably free-range, if available, or the 'omega-3' enriched) or Egg Beaters; oat products, but true oat products like slow-cooked oatmeal, or the best of all, oat bran, used as a hot cereal; ground flaxseed as a hot cereal with added fruit, berries, nuts; a handful of raw almonds, walnuts, pecans; some cheese, preferably traditional fermented cheese and not processed; low-fat cottage cheese; low-fat yogurt that you flavor yourself with berries and nuts; raw seeds like sunflower and pumpkin.

"Try and save some of your dinner foods for breakfast. For instance, save some green peppers and onions from your salad and put it in your scrambled eggs along with some olive oil. Save some of the chicken and add it to your breakfast. Save some of the cooked vegetables and have them as they are. You'll be surprised how filling dinner foods can be when eaten for breakfast."

It's not that tough. But Stuart and many other people need to break the hold that the food manufacturers have created. If you're hoping to seize hold of your heart scan score, get rid of the sugar foods in your morning, even the ones cleverly disguised as healthy.

The Low-Carb Man

If ever there was an enthusiastic disciple of deceased Dr. Robert Atkins of Atkins' Diet fame, it's Mr. Jimmy Moore.








Jimmy tells the story of how he was transformed by the Atkins' approach, losing 180 lbs in the course of one year. He continues to develop this conversation, in many ways elaborating on the conversation in more sophisticated ways than even Atkins did in his lifetime.

Though we've agreed to disagree on some points of nutrition, Jimmy and I had a recent discussion about heart disease, the mis-guided ways of conventional cardiac care,and the evils of processed carbohydrates. We do differ on the role of saturated fat in heart disease and health, but beyond that difference I was impressed (reading his Blog and listening to his many webcasts) with his level of understanding of the issues. Jimmy is not some over-enthusiastic dieter. He has a grasp of the issues that exceeds that of 99% of my colleagues.

If you are interested in reading our discussion or just perusing a really fun, informative Blog/website, go to LivinLaVidaLowCarb.com. The interview is posted at:

http://livinlavidalocarb.blogspot.com/2007/08/davis-wanna-cut-plaque-in-your-arteries.html


See Jimmy Moore's before and after pictures at http://livinlavidalocarb.blogspot.com/2005/07/my-before-pictures.html. He's quite an entertaining read.

Why average cholesterol values can be so bad

Jack had been told again and again that there was absolutely nothing wrong with his cholesterol panel. His numbers:

Total cholesterol 198 mg/dl

LDL cholesterol 119 mg/dl--actually below the national average (131 mg/dl).

HDL 48 mg/dl--actually above the average HDL for a male (42 mg/dl).

Triglycerides 153 ng/dl--right at the average.


So his primary care physician was totally stumped when Jack's heart scan revealed a score of 410.


Lipoprotein analysis (NMR) told an entirely different story:

LDL particle number 1880 nmol/l (take off the last digit to generate an approximate real LDL, i.e., 188 mg/dl).

Small LDL 95% of all LDL particles, a very severe pattern.

A severe excess of intermediate-density lipoprotein (218 nmol/l), suggesting that dietary fats are not cleared for 24 hours or so after a meal.

And those were just the major points. In other words, where conventional cholesterol values, or lipids, failed miserably, lipoprotein analysis can shine. The causes for Jack's high heart scan score become immediately apparent, even obvious. Jack's abnormalities are relatively easy to correct--but you have to know if they're present before they can be corrected. A shotgun statin drug approach could only hope to correct a portion of this pattern, but would unquestionably fail to fully correct the pattern.

As I've said before, standard cholesterol testing is a fool's game. You can squeeze a little bit of information out of them, but there's so much more information that can be easily obtained through lipoprotein testing like Jack had.

Cholesterol trumps heart scan?

Lela's heart scan score: 449--very high for a 49-year old, peri-menopausal woman. Her score placed her flat in the 99th percentile, or the worst 1% of women her age.

Lela first consulted her primary care physician. Her doctor looked at the result puzzled. "Now wait a minute. Your cholesterol numbers have been great." After a pause, her doctor (a woman) declared the heart scan wrong. "Tests aren't perfect. The heart scan is simply wrong. I'm going to believe the cholesterol numbers and there's no way you have heart disease."

Is that right? Can cholesterol numbers trump your heart scan score? Can the heart scan simply be wrong?

The answer is simple: NO.

The heart scan is not wrong. The heart scan is right. What is wrong with this picture is that standard cholesterol testing commonly and frequently fails to identify people at risk for heart disease.

What if this woman smoked? That wouldn't be revealed in her cholesterol panel. Or had high blood pressure, increased inflammatory responses like C-reactive protein, had increased small LDL or lipoprotein(a), was severely deficient in vitamin D? None of that would be revealed by cholesterol numbers.

So, no, the heart scan is not wrong. The cholesterol numbers are not wrong. The doctor's interpretation of the data is wrong.

Please do not allow false reassurances offered by those who do not understand the technology steer you wrong.

This woman proved to have an entire panel of hidden causes of her coronary plaque uncovered. No surprise.

Boycott LabCorp

Track Your Plaque Members have been following this conversation on the Track Your Plaque Forum.

A good number of people have had their blood drawn for NMR lipoprotein analysis through laboratories operated by the Laboratory Corporation of American, or LabCorp. When the results were returned, the very important page 2 of the report was withheld. Many of us have communicated with the company, only to be given some corporate-speak about internal policy.

I have personally expressed my dissatisfaction, my outrage, at this silly policy. Why would laboratory results that you or your insurance paid for be denied to you? It is my understanding that, on request, you are legally entitled to the information. The page 2 information is provided by the laboratory (Liposcience, Inc.) that actually performs the testing. LabCorp does nothing more than draw the blood, prepare the specimen, then convey and dilute the results that Liposcience reports to them.

My personal suspicion is that the LabCorp people do this to 1) make the results appear that they actually performed the tests and not farmed to an outside laboratory (Liposcience), and 2) not further confuse and befuddle the bungling primary care physician who barely understands cholesterol issues to begin with. "LDL, HDL, triglycerides . . . What now--a bunch of new information, bars even!?

To me, this LabCorp policy is criminal. In fact, I wonder if this has the substance to justify a class action lawsuit against LabCorp. I believe that we can easily make a case that crucial health information is being systematically denied to people.

If this has affected you, or if you share in the frustration of many people who have had watered down lipoprotein results provided, write to:


Ken Younts, VP of Sales at LabCorp. Yountsk@labcorp.com


Or, write to:

Tom MacMahon
Chairman of the Board

David P. King
President and Chief Executive Officer

Laboratory Corporation of America Holdings
358 South Main Street
Burlington, NC 27215



Thanks to the Track Your Plaque Members who have already participated in this campaign and written to the LabCorp people. And thanks to our Members who uncovered the contact information.

Until then, please BOYCOTT LABCORP LABORATORIES. Please do not use LabCorp Laboratories if you can avoid it. Simply ask the laboratory staff who operates the lab and they should tell you. It is your right to know.

Useless low-fat diets

If you would like to read an ironic testimonial to the futility of conventional low-fat diets, read:

Cutting Cholesterol, an Uphill Battle on the New York Times website at http://www.nytimes.com/2007/08/21/health/21brod.html?_r=2&adxnnl=1&oref=slogin&ref=health&adxnnlx=1187928650-f0mfyzGTFdsLmtInHcGPUw

In this story, author and columnist Jane Brody recounts her struggles with her cholesterol levels. She describes how she followed an increasingly strict low-saturated fat diet, hoping to reduce LDL cholesterol. But she saw the opposite occur: LDL climbed from an initial 134 to 171, a level that caused her doctor to prescribe a statin drug.

Yet she states that "About 85 percent of the cholesterol in your blood is made in your body. The remaining 15 percent comes from food. But by reducing dietary sources of saturated fats and cholesterol and increasing consumption of cholesterol-fighting foods and drink, you can usually lower the amount of harmful cholesterol in your blood."

Had Ms. Brody and her doctor been just a bit better informed and performed lipoprotein analysis instead, they would have seen some obvious phenomena:

--All the increase in LDL was in the fraction of small particles, the sort highly likely to cause heart attack.

--The conventional LDL that she quotes is a calculated value that miserably misrepresents the real LDL when actually measured. Her calculated LDL of 171 mg/dl, in fact, was probably more like 220 to 250 mg/dl--much higher than they think.


Of course, Ms. Brody turns to her conventionally-thinking physician who then predictably prescribes a statin drug.

Ms. Brody's well-articulated story achieves the ironic, unintended result of proving the idiocy of the conventional low-fat diet. The low-fat diet, as currently practiced by most people, raises LDL cholesterol and escalates risk for heart disease. In fact, Ms. Brody probably increased her risk far more than suggested by a 30 mg increase in LDL.

One of my favorite blogs, the Fanatic Cook, has a tremendously insightful post on Ms. Brody's misadventures.

If all she did was eliminate all wheat flour containing products and reduce the overall glycemic index of her diet, she would witness an enormous drop in LDL cholesterol, both calculated and measured.

I hope that Ms. Brody survives her diet mistakes and her doctor's ignorance.

Overweight, hungry, diabetic, and fat-free

Let me tell you about my low-fat experience from 20 years ago.

At the time, I was living in Cleveland, Ohio, and served on the faculty at a large metropolitan university-affiliated hospital, supervising fellows-in-training and developing high-tech cath lab procedures like directional athererectomy and excimer laser coronary angioplasty. (Yes, another life.)

I was concerned about personal heart disease risk, though I knew next to nothing about lipids and coronary risk prediction outside of the little I learned in training and what the drug industry promoted.

I heard Dr. Dean Ornish talk while attending the American College of Cardiology meetings in Atlanta. Dr. Ornish spoke persuasively about the dangers of fat in the diet and how he "reversed" coronary disease using a low-fat, no added oils, no meat, vegetarian diet that included plenty of whole grains. So I thought I'd give it a try.

I eliminated all oils; I removed all meat, eggs, and fish from my diet. I shunned all nuts. I ate only low-fat products like low-fat yogurt and cottage cheese; and focused on vegetables, fruit, and whole grains. Beans and brown or wild rice were a frequent staple. I loved oatmeal cookies--low-fat, of course!

After one year of this low-fat program, I had gained a total of 31 lbs, going from 155 lbs to 186 lbs. I reassessed some basic labs:

HDL 28 mg/dl
Triglycerides 336 mg/dl
Blood sugar 151 mg/dl (fasting)


I became a diabetic. All through this time, I was also jogging. I ran on the beautiful paths along the Chagrin River in suburban Cleveland for miles north and south. I ran 5 miles per day most days of the week.

It was diabetes that hit me alongside the head: I was eating low-fat meticulously, exercising more than 90% of the population, yet I got fat and diabetic!

I have since changed course in diet. Last time I checked, my lipid values on NO statin agent:

HDL 67 mg/dl
Triglycerides 57 mg/dl
Blood sugar 91 mg/dl

That was my lesson that fat restriction is a destructive, misguided notion. The data since then have confirmed that restricting total fat is unnecessary, even undesirable, when fat calories are replaced by carbohydrate calories.

This is your brain on wheat

Here's just a smattering of the studies performed over the past 30 years on the psychological effects of wheat consumption.

Oddly, this never makes the popular press. But wheat underlies schizophrenia, bipolar illness, behavioral outbursts in autism, Huntington's disease, and attention deficit hyperactivity disorder (ADHD).

The relationship is especially compelling with schizophrenia:

Opioid peptides derived from food proteins: The exorphins.
Zioudrou C et al 1979
"Wheat gluten has been implicated by Dohan and his colleagues in the etiology of schizophrenia and supporting evidence has been provided by others. Our experiments provide a plausible biochemical mechanism for such a role, in the demonstration of the conversion of gluten into peptides with potential central nerovus system actions."


Wheat gluten as a pathogenic factor in schizophrenia
Singh MM et al 1976
"Schizophrenics maintained on a cereal grain-free and milk-free diet and receiving optimal treatment with neuropleptics showed an interruption or reversal of their therapeutic progress during a period of "blind" wheat gluten challenge. The exacerbation of the disease process was not due to variations in neuroleptic doses. After termination of the gluten challenge, the course of improvement was reinstated. The observed effects seemed to be due to a primary schizophrenia-promoting effect of wheat gluten."


Demonstration of high opioid-like activity in isolated peptides from wheat gluten hydrolysates
Huebner FR et al 1984


Is schizophrenia rare if grain is rare?
Dohan FC et al 1984
"Epidemiologic studies demonstrated a strong, dose-dependent relationship between grain intake and the occurrence of schizophrenia."

Small LDL: Perfect index of carbohydrate intake

Measuring the number of small LDL particles is the best index of carbohydrate intake I know of, better than even blood sugar and triglycerides.

In other words, increase carbohydrate intake and small LDL particles increase. Decrease carbohydrates and small LDL particles decrease.

Why?

Carbohydrates increase small LDL via a multistep process:

First step: Increased fatty acid and apoprotein B production in the liver, which leads to increased VLDL production. (Apoprotein B is the principal protein of VLDL and LDL)

Second step: Greater VLDL availability causes triglyceride-rich VLDL to interact with other particles, namely LDL and HDL, enriching them in triglycerides (via the action of cholesteryl-ester transfer protein, or CETP). Much VLDL is converted to LDL.

Third step: Triglyceride-rich LDL is "remodeled" by enzymes like hepatic lipase, which create small LDL.


Carbohydrates, especially if they contain fructose, also prolong the period of time that triglyceride-rich VLDL particles persist in the blood, allowing more time for VLDL to interact with LDL.

Many people are confused by this. "You mean to tell me that reducing carbohydrates reduces LDL cholesterol?" Yes, absolutely. While the world talks about cutting saturated fats and taking statin drugs, cutting carbohydrates, especially wheat (the most offensive of all), cornstarch, and sugars, is the real key to dropping LDL.

However, the effect will not be fully evident if you just look at the crude conventional calculated (Friedewald) LDL cholesterol. This is because restricting carbohydrates not only reduces small LDL, it also increases LDL particle size. This make the calculated Friedewald go up, or it blunts its decrease. Conventional calculated LDL will therefore either underestimate or even conceal the real LDL-reducing effect.

The reduction in LDL is readily apparent if you look at the superior measures, LDL particle number (by NMR) or apoprotein B. Dramatic reductions will be apparent with a reduction in carbohydrates.

Small LDL therefore serves as a sensitive index of carbohydrate intake, one that responds literally within hours of a change in food choices. Anyone following the crude Friedewald calculated LDL will likely not see this. This includes the thousands of clinical studies that rely on this unreliable measure and come to the conclusion that a low-fat diet reduces LDL cholesterol.

Fat "conditioning"

Here's a great study from the prolific laboratory of Dr. Jeff Volek from the University of Connecticut. (Full text here.)


http://jn.nutrition.org/cgi/content/full/134/4/880

Video Teleconference with Dr. William Davis


Dr. Davis is available for personal
one-on-one video teleconferencing

to discuss your heart health issues.


You can obtain Dr. Davis' expertise on issues important to your health, including:

Lipoprotein assessment

Heart scans and coronary calcium scores

Diet and nutrition

Weight loss

Vitamin D supplementation for optimal health

Proper use of omega-3 fatty acids/fish oil



Each personalized session is 30 minutes long and by appointment only. To arrange for a Video Teleconference, go to our Contact Page and specify Video Teleconference in your e-mail. We will contact you as soon as possible on how to arrange the teleconference.


The cost for each 30-minute session is $375, payable in advance. 30-minute follow-up sessions are $275.

(Track Your Plaque Members: Our Member cost is $300 for a 30-minute session; 30-minute follow-up sessions are $200.)

After the completion of your Video Teleconference session, a summary of the important issues discussed will be sent to you.

The Video Teleconference is not meant to replace the opinion of your doctor, nor diagnose or treat any condition. It is simply meant to provide additional discussion about your health issues that should be discussed further with your healthcare provider. Prescriptions cannot be provided.

Note: For an optimal experience, you will need a computer equipped with a microphone and video camera. (Video camera is optional; you will be able to see Dr. Davis, but he will not be able to see you if you lack a camera.)

We use Skype for video teleconferencing. If you do not have Skype or are unfamiliar with this service, our staff will walk you through the few steps required.

Track Your Plaque challenges

Of all the various factors we correct in the Track Your Plaque program in the name of achieving reversal of coronary plaque, there are two factors that are proving to be our greatest challenges:

1) Genetic small LDL

2) Lipoprotein(a)

More and more people are enjoying at least marked slowing, if not zero change or reduction, in heart scan scores following the Track Your Plaque program. We achieve this by correcting a number of factors. Some factors, like vitamin D deficiency, are easily corrected to perfection--supplement sufficient vitamin D to achieve a blood level of 25-hydroxy vitamin D of 60-70 ng/ml. Correcting standard lipid values--LDL cholesterol, HDL cholesterol, and triglycerides--child's play, even to our strict targets of 60-60-60.

However, what I call "genetic small LDL" and a subset of lipoprotein(a) are proving to be the most resistant of all.

Let's first consider genetic small LDL. Small LDL is generally the pattern of the carbohydrate-ingesting, overweight person. It has exploded in severity over the past decade due to overconsumption of carbohydrates due to the ridiculous low-fat notion. Reduce or eliminate carbohydrates, especially wheat, which permits weight loss, and small LDL drops like a stone. But there is a unique subset of people who express the small LDL pattern who start at or near ideal weight. Take Chad, for instance. At 6' 2" and 152 lbs and BMI of 19.6, there's no way excess weight could be triggering his small LDL. Yet he starts with 100% small LDL particles. All efforts to reduce small LDL, such as wheat, cornstarch, and sugar elimination; niacin; vitamin D normalization; thyroid normalization; and several supplements that yield variable effects, such as phosphatidylcholine, all leave Chad with more than 90% small LDL.

Lipoprotein(a) is a bit different. Over the past 5 years, our choices in ways to reduce Lp(a) expression have improved dramatically. Beyond niacin, we now have high-dose EPA + DHA, thyroid normalization that includes use of T3, and hormonal manipulation. In the Track Your Plaque experience, approximately 70% of people with Lp(a) respond with a reduction in Lp(a). (In fact, the 4 out of the 5 record holders for reduction of heart scan scores have Lp(a) that was successfully treated.) But about 30% of people with Lp(a) prove resistant to all these treatments--they begin with a Lp(a) of, say, 260 nmol/L and, despite niacin, high-dose EPA + DHA, and various hormones, stay at 260 nmol/L. It can be frustrating and frightening.

So these are the two true problem areas for the Track Your Plaque program, genetic small LDL and a subset of Lp(a).

We are actively searching for better options for these two problem areas. Given the collective exploration and wisdom that develops from such collaborative efforts as the Track Your Plaque Forum, I am optimistic that we will have better answers for these two stumbling blocks to plaque reversal in the future.

I'll supply the tar if you supply the feathers

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


DIRECT-TO-CONSUMER PHARMACEUTICAL ADVERTISING HAS:

Increased public awareness of medical conditions and their treatment
19 (11%)

Has had little overall effect on health and healthcare
29 (18%)

Needlessly increased healthcare costs
81 (50%)

Further empowered the revenue-obsessed pharmaceutical industry
130 (81%)


Clearly, there's a lot of negative sentiment against direct-to-consumer (DTC) drug advertising.

It looks as if a small minority believe that good has come from DTC advertising, judging by the meager 11% who voted for increased awareness. In fact, the poll results are heavily weighed towards the negative: 50% voted for "needlessly increased healthcare costs," while an astounding 81% voted for "empowered the revenue-obsessed pharmaceutical industry."

It is, indeed, an odd situation: Pharmaceutical agents available only by prescription being hyped directly to the consumer.

Personally, I would vote for choices 1,3, and 4. While awareness has increased, it has come with a hefty price, not all of it well spent. I believe the pharmaceutical industry still adheres to the rule that, for every $1 spent on advertising, $4 is made in revenue. They are, in effect, printing money.

What goes up can't come down

According to conventional wisdom, heart scan scores cannot be reduced.

In other words, say you begin with a heart scan score of 300. Conventional wisdom says you should take aspirin and a statin drug, eat a low-fat "heart healthy" diet, and take high blood pressure medications, if necessary.

If your heart scan score goes up in a year or two, especially at an annual rate of 20% or more, then you are at very high risk for heart attack. If the heart scan score stays the same, then your risk is much reduced. These observations are well-established.

But more than 99% of physicians will tell you that reducing your heart scan score is impossible. Don't even try: Heart scan scores can go up, but they can't go down.

Baloney. Heart scan scores can indeed go down. And they can go down dramatically.

It is true that, following conventional advice like taking a statin drug, following a low-fat diet, and taking aspirin will fail to reduce your heart scan score. A more rational approach that 1) identifies all causes of coronary plaque, 2) corrects all causes while including crucial strategies like omega-3 fatty acid supplementation, vitamin D supplementation, and thyroid function normalization, is far more likely to yield a halt or reduction in score.

While not everybody who undertakes the Track Your Plaque program will succeed in reducing their heart scan score, a growing number are enjoying success.

A small portion of our experience was documented this past summer. (I collected and analyzed the data with the help of Rush University nutrition scientist, Dr. Susie Rockway, and statistician, Dr. Mary Kwasny.)


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 > or = 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 < or = 60 mg/dL; high-density lipoprotein > or = 60 mg/dL; and vitamin D3 supplementation to achieve serum levels of > or = 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.

Gretchen's postprandial diet experiment

Gretchen sent me the results of a little experiment she ran on herself. She measured blood glucose and triglycerides after 1) a low-fat diet and 2) a low-carb diet.









Gretchen describes her experience:

Several years ago I received a windfall of triglyceride strips that would expire in a week or so. I hated to waste them, so I decided to use them to test my triglyceride and BG responses to two different diets: low carb and low fat.

The first day I followed a low-fat diet. For breakfast I ate a lot of carbohydrate, including 1 oz of spaghetti cooked al dente and ¾ cup of white rice. For the rest of the day I ate less carbohydrate but continued to eat low fat.

The second day I followed a low-carb diet. For breakfast I ate a lot of fat, including a sausage, mushrooms fried in butter, 2 slices of bacon, and ¼ cup of the creamy topping of whole-milk yogurt. For the rest of the day I ate less fat, especially less saturated fat, but continued to eat low carb.

Both days I measured both BG and triglyceride levels every hour until I went to bed. On the low-carb day I had 3 meals. On the low-fat day, I was constantly hungry, had 4 meals, and kept snacking.

You can see the results in Figure 1. On the low-fat diet, after a “healthy” low-fat breakfast of low-glycemic pasta with low-fat sauce, my BG levels shot up to over 200 mg/dL and took more than 6 hours to come down. My triglycerides, however, remained low, and at first I thought perhaps the low-fat diet might be better overall. However, after about 6 hours, the triglyceride levels started to increase steadily, and by the next morning, they were higher than they had been the day before.
On the low-carb diet, my BG levels stayed low all day. However, after meals, the triglyceride levels skyrocketed. After meals they came down, and by the next morning they were lower than they had been the day before.

As I interpret these results, the high triglyceride levels after eating the high-fat meals represent chylomicrons, the lipoproteins that transport fat from your meals to the cells of your body. The high triglyceride levels the morning after eating the low-fat meals represent very low density lipoprotein, which takes the cholesterol your liver synthesizes when your intake of dietary cholesterol is low and distributes it to cells that need it, or again, to the fat for storage.

There are several interesting factors to consider here. First, when you have a lipid test done at the lab, it’s usually done fasting, which means first thing in the morning after not eating for 8 to 12 hours. It tells you nothing about what your triglyceride levels were all day.

Second, the low-carb diet resulted in lower fasting triglyceride levels, but much higher postprandial triglyceride levels. Which are more dangerous? I’m afraid I don’t know. You should also note that the high-fat, low-carb breakfast was extremely high in fat, including saturated fat. I don’t normally eat that much fat but wanted to test extremes.

Third, although the low-fat diet didn’t produce the very high postprandial triglyceride levels that the high-fat diet did, it produced extremely high BG levels that persisted for 6 hours. Some people think that it’s oxidized and glycated lipids that are the dangerous ones, so high BG levels and normal triglyceride levels might be more dangerous than very high triglyceride levels and normal BG levels. Note that high BG levels also contribute to oxidation rates.

Fourth, this shows the results of an experiment with a sample size of one. My physiology might not be typical. If you want to know how your own body’s lipids respond to different types of diets, you should get a lipid meter and test yourself. Unfortunately, your insurance is unlikely to want to pay for this, so it will be an expensive experiment.

The main point of this is that the results of different diets are complex. We have to eat. And what we eat can affect many different systems in our bodies. Finding the ideal diet that matches our own physiology and results in the best lipid levels as well as BG levels is a real challenge.



This was a lot of effort for one person. Thanks to Gretchen for sharing her interesting experience.

Gretchen makes a crucial point: Some of the effects of diet changes evolve over time, much as triglyceride levels changed substantially for her on the day following her experiment. Wouldn't it be interesting to see how postprandial patterns develop over time if levels were observed sequentially, day after day?

The stark contrast in blood sugars is impressive--Low-carb clearly has the advantage here. Are there manipulations in diet composition in low-carb meals that we can make to blunt the early (3-6 hour) postprandial lipoprotein (triglyceride) peak? That's a topic we will consider in future.

More of Gretchen's thoughts can be found at:

http://wildlyfluctuating.blogspot.com
http://www.healthcentral.com/diabetes/c/5068

After-eating effects: Carbohydrates vs. fats

In the ongoing debate over whether it's fat or carbohydrate restriction that leads to weight loss and health, here's another study from the Oxford group examining the postprandial (after-eating) effects of a low-fat vs. low-carbohydrate diet. (Roberts R et al, 2008; full-text here.)

High-carbohydrate was defined as 15% protein; 10% fat; 75% carbohydrate (by calories), with starch:sugar 70:30.

High-fat was defined as 15% protein; 40% fat; 45% carbohydrate, with starch:sugar 70:30. (Yes, I know. By our standards, the "high-fat" diet was moderate-fat, moderate-carbohydrate--too high in carbohydrates.)

Blood was drawn over 6 hours following the test meal.




Roberts R et al. Am J Clin Nutr 2008

The upper left graph is the one of interest. Note that, after the high-carbohydrate diet (solid circles), triglyceride levels are twice that occurring after the high-fat diet (open circles). Triglycerides are a surrogate for chylomicron and VLDL postprandial lipoproteins; thus, after the high-carbohydrate diet, postprandial particles are present at much higher levels than after the high-fat diet. (It would have been interesting to have seen a true low-carbohydrate diet for comparison.) Also note that, not only are triglyceride levels higher after high-carbohydrate intake, but they remain sustained at the 6-hour mark, unlike the sharper decline after high-fat.

It's counterintuitive: Postprandial lipoproteins, you'd think, would be plentiful after ingesting a large quantity of fat, since fat must be absorbed via chylomicrons into the bloodstream. But it's carbohydrates (and obesity, a huge effect; more on that in future) that figure most prominently in determining the pattern and magnitude of postprandial triglycerides and lipoproteins. Much of this effect develops by way of de novo lipogenesis, the generation of new lipoproteins like VLDL after carbohydrate ingestion.

We also see this in our Track Your Plaque experience. Rather than formal postprandial meal-testing, we use intermediate-density lipoprotein (IDL) as our surrogate for postprandial measures. A low-carbohydrate diet reduces IDL dramatically, as do omega-3 fatty acids from fish oil.
All posts by william-davis

Excessive Heart Procedures Makes New York Times Headline


One example of flagrant cardiac procedure excess has made New York Times headlines:


Heart Procedure Is Off the Charts in an Ohio City
The number of angioplasties performed in Elyria is so high that Medicare is starting to ask questions.

(The full article can be accessed through the New York Times website at http://www.nytimes.com/2006/08/18/business/18stent.html?pagewanted=2&ei=5094&en=b81be5f43f98a99b&hp&ex=1155960000&partner=homepage)



Cardiologists in little Elyria, Ohio, about a 30-minute drive west of Cleveland, do more coronary angioplasties and insert more stents than any other location in the U.S.--four times more than the national average, three times more than the Cleveland average. They perform even more than the recently-indicted cardiologist in Louisiana, who performed twice the national average of procedures.


The Times article, part of a series about financial incentives in medical care, provides a responsible and incredibly balanced report on the situation in Elyria. I have to give them credit, because from the eyes of a colleague (myself), this looks like blatant and extreme profiteering: "cathing for dollars".

I find it outrageous that this group of cardiologists claims that they have some special insight into heart care that justifies this extraordinary reliance on heart procedures. There's bound to be variation in practice patterns, but this is so outside the norm that I believe criminal behavior will be exposed. In fact, I believe that even the "norm", or average, rate of procedures is also excessive.

This is symptomatic of the perverse equation in heart disease care. If there's money to be made in major heart procedures, who wants to bother with prevention? Programs like the Track Your Plaque program present real potential to stop coronary heart disease in its tracks for many, if not most, participants--but don't expect to hear about it from your cardiologist. Don't expect to hear about it from the increasingly hospital-employed primary care physician.

Hopefully, media exposure like that in the New York Times is just the beginning of a public re-analysis of not only what's wrong with medicine today, but recognition of the tremendous power in preventive strategies when everyone stops being so enamored with hospital-based procedures. CT-based heart scanning that ignites your heart disease prevention program is your way to dodge the mainstream obsession with procedures.

More on "Bio-identical hormones" and Wyeth Pharmaceuticals

In October 2005, Wyeth petitioned the FDA, requesting that it completely ban the bioidentical alternatives that women have been using in ever-increasing numbers to achieve optimal hormone balance. With bioidentical replacement therapy clearly reducing its market share, Wyeth asked the FDA to outlaw all compounded bioidentical hormone formulations that compete with its own discredited drugs. If Wyeth is successful, then menopausal women will have no choice other than to take potentially life-threatening hormone drugs or to forgo hormone replacement therapy altogether, thus enduring the physically and emotionally debilitating effects of menopause-induced hormone depletion.

Dave Tuttle
Life Extension Magazine
August, 2006



For more commentary on Wyeth Pharmaceutical's outrageous and brazen petition to the FDA to bar prescription "bio-identical" hormones, i.e., hormones that are identical to natural human forms, read Life Extension's article, Health Freedom Under Attack!
Drugmaker Seeks to Deny Access to Bioidentical Hormones





This well-researched article is in the August, 2006 issue of Life Extension Magazine. The article can also be accessed online at http://www.lef.org/magazine/mag2006/aug2006_cover_attack_01.htm

or go to www.lef.org and click on the August, 2006 issue.

The author, Dave Tuttle, details the baseless arguments raised by Wyeth, a pathetic and amazingly selfish act in the name of protecting profits for Premarin, their prescription agent. It's bad enough to be selling this worthless drug. It's even worse--criminal, in my mind--to try to stamp out our right to have a physician write a prescription for a pharmacy to mix up hormones identical to that humans produce, individualized to our needs.

If you are as angry about this as I am, please go to the Life Extension online reprint that provides access to the International Academy of Compounding Pharmacists website to send the FDA an e-mail describing your opinion, or go to www.iacprx.org.

How accurate is LDL cholesterol?

Watch TV and you'd get the impression that the world revolves around LDL cholesterol: Commercials for Lipitor, Zetia, Vytorin, etc., all drugs to reduce cholesterol (total and LDL). Your doctor looks first and often only at LDL cholesterol.

If there's so much attention paid to LDL, how accurate is it? 100%? 90%? 80%?

Well, it varies widely. Occasionally, it's truly accurate, but most of the time it's miserably inaccurate . Every single day, I see people with LDL cholesterols that underestimates true (measured) LDL by 40%, 50%, and even over 100%. In other words, LDL cholesterol might be 120 mg/dl by the conventional method, but the genuine measured value might be 160 mg/dl, or even 240 mg/dl. It can be that far off--and it's not rare.

The converse can occasionally be true, though rarely in my experience: that conventional LDL overestimates true LDL. I saw someone in the office today like this, with a conventional LDL of 142 mg/dl but a true measured LDL of 115 mg/dl. I may see one or two more people like this the rest of this year.




Why is LDL so inaccurate? Several reasons:

--LDL in most labs is calculated, not measured. The "Friedewald calculation" derives LDL by substracting HDL and triglycerides (divided by 5) from total cholesterol. The higher triglycerides are, especially above 150 mg/dl, the more inaccurate the calculation becomes. As HDL drops below 50 mg/dl, this also introduces greater and greater inaccuracy.

--LDL particles vary in size. A more accurate representation and measure of LDL's dangers are therefore found in measures of LDL particle number , rather than a weight-based measure or calculation. LDL particle number can be measure as just that, LDL particle number (NMR), or as apoprotein B, the protein in LDL that occurs one apoB per LDL.

I liken conventionally calculated LDL cholesterol to a broken speedometer. You simply won't have an accurate measure of how fast you're going, though you may have a ballpark sense. But try telling that to the state patrol.

Or, as a cardiologist colleague said to me in a similar conversation about LDL: "Well, it's better than nothing!"

The lesson: If you're interested in plaque control, and control or reduction of heart scan score, you need a measured LDL, preferably LDL particle number by NMR or an apoprotein B. Another option is "direct" LDL.

Green tea: friend or faux?

The www.HealthCastle.com website is a helpful website on healthy eating that sends out a free newsletter. The content is all produced by licensed dietitions and nutritionists. Although I don't agree with everything said on the site, there's still some good information.

I'm a fan of green tea. Although I believe the effects are relatively modest (weight reduction, cholesterol reduction, anti-oxidation, etc., with theaflavin and/or green tea as a beverage,) they alerted me to the fact that the Lipton Green Tea product is one you should steer clear of. Here are their comments:



"More like Soft drink than Green Tea!With 200 calories, 13 teaspoons of added sugar and a long list of artificial ingredients, Lipton Iced Green Tea is more like a bottle of soft drink than tea, in our opinion."


The Lipton website lists the ingredients:

Water, high fructose corn syrup, citric acid, green tea, sodium hexametaphosphate, ascorbic acid (to protect flavor), honey, natural flavors, phosphoric acid, sodium benzoate (preserves freshness), potassium sorbate (preserves freshness), calcium disodium edta (to protect flavor), caramel color, tallow 5, blue1.

An 8 oz serving yields 21 grams of sugar. If you drink the full 20 oz. bottle (not hard to do!), that yields 52.5 grams of sugar! You will also notice that the second ingredient listed after water is high fructose corn syrup. This ingredient, you may recall, causes triglycerides to skyrocket, causes an insatiable sweet tooth, and is a probable contributor to obesity and diabetes.

In their defense, the Lipton people do also offer a sugar-free alternative without the excessive sweeteners and empty calories.

Do the Lipton products offer the same kind of benefits from green tea catechins (flavonoids) offered by freshly brewed teas? This product has not been formally tested by an independent lab to my knowledge, though, in general, commercially prepared and bottled teas tend to have dramatically less catechin/flavonoid content compared to brewed. (The USDA website provides access to an extraordinary collection of flavonoid food content at their USDA Database for the Flavonoid Content of Selected Foods - 2003. You'll find it at http://www.ars.usda.gov/Services/docs.htm?docid=6231.)

I think the HealthCastle people got it right: Brew your own, making sure to steep for at least 3 minutes. Alternatively, a green tea or theaflavin supplement provides many of the benefits. (Theaflavin has been used in trials at doses of 375 to 900 mg per day.) An in-depth report on green tea will be coming in a future Special Report on the www.cureality.com Membership website.

The Track Your Plaque guide to getting grotesquely overweight

If you'd like to gain huge quantities of weight, here's a number of helpful tips:

1) Follow the advice of food manufacturers and eat the products they label "healthy", or "heart healthy", or "part of a nutritious breakfast" etc., like Shredded Wheat cereal, pretzels ("a low-fat snack"!), low- or non-fat salad dressings.

2) Cut your morning calorie intake by skipping breakfast.

3) Hang around with other heavy people. They will confirm that it's okay to be overweight.

4) Call walking your dog "exercise".

5) Get a sedentary desk job. Use your swivel desk chair to scoot about whenever possible, rather than getting up to do things.

6) Say "I've worked hard all week long. Weekends are for relaxing, not for physical activities. I deserve a rest."

7) Eat foods without thinking about it: Eat chips while watching football, eat while on the phone, daydream over the sink.

8) Eat to provide comfort when stressed.

9) Eat foods that have sentimental value, whether or not they're good for you: Freshly-baked cakes that remind you of Mom, Pop Tarts that you used to carry in your lunchbox when you were a kid, hot dogs just like Dad would buy at the baseball stadium.

10) Cut back on sleep and generate insatiable starch cravings.

11) Stack your shelves at home with great variety. That way, you'll always have something to suit your mood.

12) Say to your spouse: "It's none of your damn business what I eat! I'm a grown man/woman!" Prove it by over-indulging in obviously unhealthy foods.

13) Tell yourself that you're just too busy to pay attention to food choices. Just grab whatever you can out of a convenience store or vending machine.

See, it's easy! And that just a start.

Of course, I don't really want you to do any of these things. But if you see yourself in any of the above, and you're struggling with weight, you should seriously rethink your approach.

Your heart scan is just a "false positive"

I've seen this happen many times. Despite the great media exposure and the growing acceptance of my colleagues, heart scans still trigger wrong advice. I had another example in the office today.

Henry got a CT heart scan in 2004. His score: 574. In his mid-50s, this placed him in the 90th percentile, with a heart attack risk of 4% per year. Henry was advised to see a cardiologist.

The cardiologist advised Henry, "Oh, that's just a 'false positive'. It's not true. You don't have any heart disease. Sometimes calcium just accumulates on the outside of the arteries and gives you these misleading tests. I wish they'd stop doing them." He then proceeded to advise Henry that he needed a nuclear stress test every two years ($4000 each time, by the way). No attempt was made to question why his heart scan score was high, since the entire process was outright dismissed as nonsense.

I'm still shocked when I hear this, despite having heard these inane responses for the past decade. Of course, Henry's heart scan was not a false positive, it was a completely true positive. I'm grateful that nothing bad happened to Henry through two years of negligence, though his heart scan score is likely around 970, given the expected, untreated rate of increase of 30%.

The cardiologist did a grave disservice to Henry: He misled him due to his ignorance and lack of understanding. I wish Henry had asked the cardiologist whether he had read any of the thousands of studies now available validating CT heart scans. I doubt he's bothered to read more than the title. The cardiologist is lucky (as is Henry) that nothing bad happened in those two years.

Do false positives occur as the cardiologist suggested? They do, but they're very rare. There's a rare phenomenon of "medial calcification" that occurs in smokers and others, but it is quite unusual. >99% of the time, coronary calcium means you have coronary plaque--even if the doctor is too poorly informed to recognize it.

What's better than a heart scan?


Do you know what's better than a heart scan?

Two heart scans. No other method can provide better feedback on the results of your program.

Say you've made efforts to correct high LDL; lost weight to raise HDL and reduce small LDL; added soluble fibers, nuts, and dramatically reduced wheat products; take fish oil, vitamin D, and follow a flavonoid-rich diet. Has it worked?

After a year or so of your program, that's when another heart scan can give you invaluable feedback on whether it's been successful. I tell my patients that it's relatively easy to correct lipid and lipoprotein abnormalities. The difficult part is to know when it's good enough. Is your LDL of 67 mg/dl and HDL of 50 mg/dl good enough? Another heart scan score is the best way I know of to find out.

Variation in plaque growth differs hugely from one person to another, even at equivalent lipoprotein values. Why? Lots of reasons. Humans are inconsistent day to day. Lipoproteins, being a snapshot in time and not a cumulative value, change somewhat from day to day. There's also the possibility of unmeasured, unrecognized factors that influence coronary plaque growth. We may not be smart enough to identify these hidden factors yet. But your heart scan score will incorporate the effects of these hidden factors.

Ideally, we aim for zero growth in plaque (no change in score) or a reduction. But, particularly in the first year, 10% or less plaque growth is still a good result that predicts much reduced risk of heart attack. More than 20% per year and your program needs more work--or else you know what's ahead.

Lipids are snapshots in time; heart scans are cumulative

Let me paint a picture. It's fictional, though a very real portrait of how things truly happen in life.

Michael is an unsuspecting 40-year old man. He hasn't undergone any testing: no heart scan, no lipids or lipoproteins. But we have x-ray vision, and we can see what's going on inside of him. (We can't, of course, but we're just pretending.) Average build, average lifestyle habits, nothing extraordinary about him. His lipids/lipoproteins at age 40:

--LDL cholesterol 150 mg/dl
--HDL cholesterol 38 mg/dl
--Triglycerides 160 mg/dl
--Small LDL 70% of all LDL

At age 40, with this panel, his heart scan score is 100. That's high for a 40-year old male.

Fast forward 10 years. Michael is now 50 years old. Michael prides himself on the fact that, over the past 10 years, he's felt fine, hasn't gained a single pound, and remains as active at 50 as he did in 40. In other words, nothing has changed except that he's 10 years older. His lipids and lipoproteins:

--LDL cholesterol 150 mg/dl
--HDL cholesterol 38 mg/dl
--Triglycerides 160 mg/dl
--Small LDL 70% of all LDL

Some of you might correctly point out that just simple aging can cause some deterioration in lipids and lipoproteins, but we're going to ignore these relatively modest issues for now.)

Lipids and lipoproteins are, therefore, unchanged. Michael's heart scan score: 1380, or an approximate 30% annual increase in score. (Since Michael didn't know about his score, he took no corrective/preventive action.)

My point: If we were to make our judgment about Michael's heart disease risk by looking at lipids or lipoproteins, they would'nt tell us where he stood with regards to heart disease risk. His lipids and lipoproteins were, in fact, the same at age 50 as they were at age 40. That's because measures of risk like this are snapshots in time.

In contrast, the heart scan score reflects the cumulative effects of life and lipids/lipoproteins up until the day you got your scan.

Which measure do you think is a better gauge of heart attack risk? I think the answer's obvious.

The recognition of the metabolic syndrome as a distinct collection of factors that raise heart disease risk has been a great step forward in helping us understand many of the causes behind heart disease.

Curiously, there's not complete agreement on precisely how to define metabolic syndrome. The American Heart Association and the National Heart, Lung, and Blood Institute issued a concensus statement in 2005 that "defined" metabolic syndrome as anyone having any 3 of the 5 following signs:





Waist size 40 inches or greater in men; 35 inches or greater in women

Triglycerides 150 mg/dL or greater (or treatment for high triglycerides)

HDL-C <40 mg/dL in men; <50 mg/dL in women (or treatment for reduced HDL-C)

Blood Pressure >130 mmHg systolic; or >85 mmHg diastolic (or drug treatment for hypertension)

Glucose (fasting) >100 mg/dL (or drug treatment for elevated glucose)


Using this definition, it has become clear that meeting these criteria triple your risk of heart attack.

But can you have the risk of metabolic syndrome even without meeting the criteria? What if your waste size (male) is, 36 inches, not the 40 inches required to meet that criterion; and your triglycerides are 160, but you meet none of the other requirements?

In our experience, you certainly can carry the same risk. Why? The crude criteria developed for the primary practitioner tries to employ pedestrian, everyday measures.

We see people every day who do not meet the criteria of the metabolic syndrome yet have hidden factors that still confer the same risk. This includes small LDL; a lack of healthy large HDL despite a normal total HDL; postprandial IDL; exercise-induced high blood pressure; and inflammation. These are all associated with the metabolic syndrome, too, but they are not part of the standard definition.

I take issue in particular with the waist requirement. This one measure has, in fact, gotten lots of press lately. Some people have even claimed that waist size is the only requirement necessary to diagnose metabolic syndrome.

Our experience is that features of the metabolic syndrome can occur at any waist size, though it increases in likelihood and severity the larger the waist size. I have seen hundreds of instances in which waist size was 32-38 inches in a male, far less than 35 inches in a female, yet small LDL is wildly out of control, IDL is sky high, and C-reactive protein is markedly increased. These people obtain substantial risk from these patterns, though they don't meet the standard definition.

To me, having to meet the waist requirement for recogition of metabolic syndrome is like finally accepting that you have breast cancer when you feel the two-inch mass in your breast--it's too late.

Recognize that the standard definition when you seen it is a crude tool meant for broad consumption. You and I can do far better.

What role DHEA?




DHEA, the adrenal gland hormone, has suffered its share of ups and downs over the years.

Initially, DHEA was held up as the fountain of youth with hopes of turning back the clock 20 years. Such extravagant dreams have not held up. But DHEA can still be helpful for your program.

All of us had oodles of DHEA in our bodies when we were in our 20s and 30s. Gradually diminishing levels usually reach nearly blood levels of around zero by age 70.



In our heart disease prevention program, of course, we aim to stop or reduce your CT heart scan score. Does DHEA reduce your score? No, it most certainly does not. But it can be helpful for gaining control over some of the causes behind coronary plaque.

For instance, DHEA can:

--Help reduce abdominal fat and increase muscle mass (slightly)
--Provide more physical stamina.
--Boost mood.
--It may modestly reduce some of the phenomena associated with the metabolic syndrome (high blood pressure, high blood sugar, high insulin, low HDL, small LDL, etc.)

In my experience, people who feel better do better on their overall program. If you're always tired and run down and run out of steam by 3 pm, I won't see you riding your bicycle outdoors or at the aerobics class. But if you're bursting with energy until you put your head on the pillow, you're more inclined to walk, bike, dance, play with the kids, dance, take Tai Chi, etc.

Some downsides to DHEA: Some people experience aggression. Backing off on the dose usually relieves it. Also, sleeplessness. Taking your DHEA in the morning usually fixes it.



The dose is best tailored to your age and blood levels. People less than 40 years old should not take DHEA. The older you are, the higher the dose, though we rarely ever have to exceed 50 mg per day. If you've never had a blood level and your doctor refuses to obtain one, 25 mg per day is a reasonable dose (10-15 mg in women 40-50 years old). It's always best to discuss your supplement use, particularly agents like DHEA, with your doctor.

Track Your Plaque Members: Stay tuned to the www.cureality.com website for a Special Report more completely detailing the hows and whys behind DHEA.
All posts by william-davis

Goodbye, Dr. Jarvik

HeartWire, the news service of www.theheart.org, posted the following report:

Pfizer pulls Lipitor ads featuring Dr Robert Jarvik in HeartWire

New York, NY - After a series of questions and attacks over its choice of Dr Robert Jarvik to endorse Lipitor in a series of TV commercials, Pfizer has announced that it is withdrawing the ads. As previously reported by heartwire, Jarvik invented the first artificial heart, but he is not a cardiologist, nor does he hold a medical license—factors that drew criticism from detractors and made him and Pfizer a target of a US House Committee on Energy and Commerce investigation into celebrity endorsements in direct-to-consumer advertisements.

In a January 2008 statement, committee chair Rep John D Dingell (D-MI) observed: "Dr Jarvik's appearance in the ads could influence consumers into taking the medical advice of someone who may not be licensed to practice medicine in the United States. Americans with heart disease should make medical decisions based on consultations with their doctors, not on paid advertisements during a commercial break."

Complaints about Jarvik went up a notch this month when the latest ad in the series depicted the inventor rowing a racing scull across a lake, despite the fact that Jarvik himself does not row and the commercial used a body double.


This is typical pharmaceutical industry sleight-of-hand, now you see it, now you don't, that has come to define their policies. And this is just the stuff that comes to light because of some obvious blunders. We can only begin to imagine what sorts of other shenanigans have been swept under the rug, especially adverse effects of drugs that never made it to the light of publication.

Is this just another example of how direct-to-consumer advertising has backfired? I now have patient after patient tell me that they have been so overwhelmed and fed up with TV and magazine ads for drugs that they



Other media outlets have reported that Jarvik was guaranteed $1.35 million for the ads and that Pfizer spent $258 million on Lipitor advertisements between January 2006 and September 2007.

Hammers and nails

I'm sure you've heard the old saying that,

To a man with a hammer, everything looks like a nail.


It couldn't be truer than in heart procedures (the man with the hammer) and heart disease (the nail).

What does it take in 2008 to become an interventional cardiologist trained in all the techniques of angioplasty, stenting, intracoronary ultrasound, etc.? Start with your undergraduate degree (4 years), then medical school (another 4 years), then training in internal medicine (3 years), then general cardiology taining (3 years), then an additional year in interventional cardiology. Each step along the way also involves competing for these spaces, a process that requires much time, money, and sweat.

The total time investment is 15 years after high school. Many if not most college students graduate with debt. Pile on the substantial cost of medical school. Training after medical school pays a modest salary, enough for a single person. Many trainees by then have spouses and a family, would like to buy a house, have bills to pay. (I managed to buy my first house for $69,000 in Columbus, Ohio and paid my mortgage by sleeping only every other night and moonlighting on my off nights.)

By the time the interventional cardiologist-in-training finishes his/her 15 years, they are hungry for a hefty increase in income. After such a time and money investment, I do believe that there is at least some justification for generous income for the years of work involved.

Back to our hammer and nail metaphor. Not only do we now have a man or woman with a hammer, but a really expensive hammer that required a substantial amount of effort to obtain. Now, our hapless hammer-bearer is desperate to see everything in sight as a nail.

You're seen in consultation by this fresh interventional cardiologist in practice for only a few years. Guess what he/she advises? Go straight to the catheterization laboratory, of course. Throw in the fact that insurance reimbursement is most generous for heart procedures, far more than for consulting in the office, doing a stress test, or other simpler, non-invasive tests, and the incentives are clear.

The system, you see, is set up to follow such a path. The path to the cath lab is heavily incentivized, paths in the other direction discouraged, disparaged, or just ignored.

My message: Don't get nailed.

What is abnormal?

What is abnormal?

You'd think that the answer would be easy and straightforward.

However, consider these instances of medical findings that I have witnessed fall repeatedly into the "normal" category:

Diameter of the thoracic aorta: 4.5 cm

Mild coronary plaque by heart catheterization

Carotid plaque of 30-50%


Why isn't a thoracic aorta (the big artery in your chest) of 4.5 cm normal? Because it can be expected to increase in diameter by about 2.5 mm (0.25 cm) per year. Even at its current diameter, it means that stroke risk is greater, since enlarged aortas are diseased aortas that commonly accumulate atherosclerotic plaque with potential to fragment and shower debris to the brain. It means that high blood pressure and/or cholesterol/lipoprotein abnormalities have been uncorrected for years that have allowed the aorta to enlarge.

How about "mild coronary plaque"? Followers of the Track Your Plaque program already know the answer to this one. Mild plaque does not mean mild risk. In fact, most plaques that cause heart attack are mild plaques, not severe blockages. While severe blockages can provide symptom warning and are detected by stress tests, it's the mild blockages that rupture without symptom warning and cause heart attack. So "mild coronary plaque" is no less dangerous than severe coronary plaque.

Likewise, carotid plaque of 30-50%, while it doesn't justify surgery, can grow within just a few years to a severity that allows it to fragment and shower debris to the brain, i.e., a stroke. As with the enlarged aorta, it means that multiple causes of carotid plaque are likely active, including high blood pressure and cholesterol or lipoprotein abnormalities.

Then why would any of these findings be labeled "normal"?

Simple. In the minds of many physicians, if a condition doesn't pose immediate risk, or if it doesn't qualify for surgical "correction," then it is labeled "normal" or "mild."

Thus, an aorta of 4.5 cm cannot justify surgical replacement until it achieves a diameter of 5.5 cm. It is therefore labeled "normal."

"Mild coronary plaque" does not justify insertion of stents or performance of bypass surgery. It must therefore be "normal."

Carotid plaque over 70% is surgically removed, but not 30-50%. 30-50% is therefore "normal."

The tragedy is that many "normal" or "mild" findings, if cast in the proper light, could lead to corrective strategies that could prevent danger long-term or keep surgery from becoming necessary.

The enlarged aorta, for instance, could be stopped and an aneurysm (defined as 5.5 cm or greater) could be prevented, along with dramatically reducing risk for stroke. Carotid plaque, more so than coronary plaque, is a controllable and manipulable condition that should trigger a program of prevention and reversal. Instead, it usually generates advice to have another ultrasound in a year to see if it has yet achieved severity sufficient to justify surgery.

Of course, "mild coronary plaque" is the reason for the Track Your Plaque approach, a chance to seize control over this disease years or decades before procedures are necessary and reduce danger now, not years from now.


Copyright 2008 William Davis, MD

Niacin and hydration

Many people know about niacin's curious effect of the "hot flush," a feeling of warmth that covers the chest and neck, occasionally the entire body.

However, many people are unaware of the fact that hydration can block this effect. In fact, many people who were not advised of this will come to the office describing miserable experiences with niacin--hot flushes that last for hours, intolerable itching, etc.--only to experience little or none of these effects with generous hydration.

The vast majority of the time, two 8-12 oz glasses of water when the hot flush occurs will eliminate the flush within a few minutes.

Sometimes, the hot flush will occur many hours after taking niacin. Nine times out of ten, this delayed effect is also due to poor hydration. For instance, you might be engrossed in your work and forget to keep up with fluid demands. Or, it may be warm and you've lost fluids through sweating. That's when you begin to feel the hot flush creep up on you.

The cure: Lots of water. In this situation, in which you have allowed dehydration to develop, it may require more than two big glasses. Relief from the flush may also take more time, but it still works nearly every time.

On those rare occasions when water by itself is insufficient, then an adult (325 mg), uncoated aspirin or 200 mg ibuprofen can also be used to accelerate relief.

Why go to some much bother? Well, niacin remains the best agent we have for reduction of small LDL, raising HDL (although vitamin D is proving to be a powerful competitor in this arena), and reducing lipoprotein(a). How much do statin drugs contribute to these effects? Very little, if at all.

Several drug manufacturers are also working on "antidotes" to the hot flush effect of niacin that will be packaged within the niacin tablet. Naturally, it will also boost the cost up many times higher.

In the meantime, if or when you experience the niacin hot flush, just think: Put out the "fire" with plenty of water.

Let me float an idea

I'd like to float an idea.

The Track Your Plaque program is a fee-for-membership website. We chose this method of covering our costs--website development, graphics, software coding, etc.--since we do not accept advertising. I do believe that not having any advertising on our website has kept us impartial and unbiased--we mean what we say and not because we are selling something.

But there's a downside to assessing a membership fee: It limits the number of people who are willing or able to access the information. It also limits the dissemination of these concepts, due to such phenomena as limited content exposure to internet search engines.

Actos, Avandia, and vitamin D

Up until a few years ago, if a patient showed signs of the metabolic syndrome/pre-diabetes, or early diabetes, I would often prescribe one of the drugs, Actos (pioglitazone) or Avandia (rosiglitazone), known as the thiazolidinediones, or TZD's for short. Although I do not manage diabetes, I was witnessing a flood of patients with pre-diabetic patterns that inhibited correction of lipoprotein patterns. So I saw the TZD's as a means of potentially assisting with correction of these abnormalities.

My rationale back then was that many people with metabolic syndrome struggled to raise HDL cholesterol, reduce triglycerides, reduce small LDL, reduce the inflammatory measure c-reactive protein (CRP), as well as reduce blood sugars towards the normal range. The TZD's partially corrected these phenomena.

But over the last 2 1/2 years, I haven't written a single prescription for these agents since I've added vitamin D to the regimen.

Vitamin D in my experience in the Track Your Plaque approach:

--Raises HDL--far more than the TZD's ever did.

--Reduces small LDL

--Reduces triglycerides

--Reduces c-reactive protein

--Reduces blood pressure

--Reduces blood sugar

In other words, vitamin D appears to not only reproduce many of the effects of the TZD's, but exceeds the effects. The effects are often so wonderful that I've taken many people off their TZD's.

Vitamin D, of course, also provides numerous benefits for bone health, reduction of cancer risk, and other health benefits that the TZD's simply cannot compete with. Vitamin D also lacks the quite substantial side-effects of TZD's: water retention and weight gain (around 8 lbs in the first year of treatment), possible increase in risk for heart attack (Avandia), definite increased likelihood of congestive heart failure in those prone to it.

How about cost? Actos goes for about $2 per pill (30 mg tablet). Vitamin D in the gelcap form (the only form we use) costs around $0.05 per capsule--5 cents. That's a 40-fold difference in price for what I would regard as an inferior--substantially inferior--product.

Throw into the mix a dramatic reduction or elimination of wheat products and other high-glycemic index foods, and all the phenomena of the metabolic syndrome and its associated lipoprotein patterns show even more improvement or full reversal.

In fact, with this approach we are seeing record-setting magnitudes of correction of these parameters every day. Getting HDL, for instance, into the 60 mg/dl or 70 mg/dl range has never been so easy.

What if heart scans become obsolete?

What will we do if or when CT heart scans become outdated and something better comes along?

Heart scans are, after all, our principal tool for detection and precise quantification of coronary atherosclerotic plaque. They provide the basis for the Track Your Plaque program: serial heart scans to track progression or regression of coronary plaque.

So what the heck will we do if heart scans become obsolete, if some other technology proves superior for precise lengthwise quantification of coronary plaque?

Simple: Then we will convert to that measure.

Say, for instance, that in 5 years, MRI advances to the point where it is quick and precise, despite the rapid motion of the heart that has, in past, caused this technology to stumble for plaque quantification. Instead of obtaining a heart scan score of, say, 350, instead an MRI might yield information like:

Calcium volume: 350 cubic mm
Soft plaque elements: 200 cubic mm
Fibrous tissue: 700 cubic mm

In other words, while a CT heart scan provides a calcium score that serves as a surrogate measure of total plaque volume, perhaps the next wave of technology will directly measure total plaque volume.

Don't CT coronary angiograms already measure total plaque volume?

No, they definitely do not. At present, the best they can do is visualize the non-calcific elements and suggest the diameter reduction created by plaque at a specific point. Thus, results like "50% blockage in the mid-left anterior descending." What they do not provide is a lengthwise total volume of plaque and all its elements. Perhaps some software manipulation in future will yield such information (and I think it will, though I personally have been unable to accomplish it).

So neither the Track Your Plaque program nor the Heart Scan Blog are necessarily bound to heart scans. But heart scans, in 2008, remain the number one best tool for plaque quantification that is easy, precise, available, and inexpensive. For those reasons, CT heart scans continue to serve as the basis for these programs, and not CT angiograms, MRI, or other non-quantitative technology.

Scare tactics

Does the media engage in scare tactics?

Read the headlines in local newspapers, and you'd believe that your friends and neighbors are dropping like flies, all victims of heart attacks.

I occasionally peruse the headlines run in newspapers and magazines around the U.S. by subscribing to a feed service through Google. For the phrase, "heart attack," you can get a sample of what is being said around the country about people having heart attacks.

What continues to impress me is just how far off a truly constructive and helpful message the media provides every day. Not only are they guilty of delivering a flawed message, they also favor headlines and stories that scare the heck out of people. "This could happen to you!"

Is it just the quest for headlines that grab readers' attentions? Is there some complicity with the medical systems that pay significant advertising revenues for their heart disease programs and hospitals?

I doubt such complicity exists to any substantial degree. But the fact remains: Every day across the U.S., the media does an effective job of scaring the heck out of the public--enough for you to run to your doctor or hospital to find out if you, too, could fall victim to heart disease. A stress test, perhaps heart catheterization, three stents or bypass often results.

In effect, these headlines make great hospital PR, an inducement that flushes out the patient highly motivated to pursue further costly heart testing--whether or not it's needed.

A sampling:

Stress test could help prevent sudden heart attack

DAWN ZERA Times Leader Correspondent

Bob Schultz, 67, was feeling a persistent pain in his back, which he was pretty sure was caused by working on a deck for his son’s home.

But after the deck was finished, the pain was still there.

“It was nagging, but not enough to hurt,” Schultz said.

He visited his primary care physician, thinking maybe some muscle relaxants would be prescribed. The doctor sent him to a clinic in Tunkhannock to do a complete body CAT scan, and then had Schultz do a stress test. The on-site cardiac stress testing at a Geisinger Medical Group office in Tunkhannock showed that things did not look good: Schultz had a blockage. He was scheduled for a cardiac catheterization.

It was a surprise; a heart problem had not even crossed Schultz’s mind as a possible cause of his back pain.

“I had good cholesterol, have been the same weight for years, and had excellent blood pressure,” Schultz said.

He went for the catheterization at Geisinger Wyoming Valley, and there doctors discovered Schultz’s condition was even more serious. He had three blockages – 99 percent, 95 percent and between 80 and 90 percent.

“It shocked the living daylights out of everyone. It was surreal,” Schultz said.

The catheterization turned into open heart surgery that very same day.

The surgery was on a Tuesday, and he was home by Sunday. He never even had time to fully think about having the operation. And he had never experienced the typical warning signs of a heart problem, such as chest pain or shortness of breath.

“The doctors said I had the worst alarm system they’d ever seen,” Schultz said. “They probably saved my life, with me not knowing I had a problem.”

It also made him think about his brother, who had had been in good health but suddenly died in his 40s of a suspected heart attack.

“We never had any heart problems in our family, so we never believed it. But now I think, geez, it probably was true,” Schultz said.

His experience has served as a cautionary tale for friends and family. Just this past month, a friend specifically requested a stress test for himself.

“It sets off alarms in your circle. People think ‘if it can happen to him, it could happen to me,’ ” Schultz said. “It triggered people to think about what could happen to them.”



Firefighter Saves Heart-Attack Victim on D.C. Court

ABC News

A 30-year-old man suffered a heart attack while playing basketball on a D.C. court.

That's when a Brian Long's firefighter training kicked into action. The 25-year-old D.C. firefighter's team had just finished their pick-up league game Friday evening at Lafayette Elementary School's basketball court when the man stumble to the ground.

"He ran a few feet and collapsed again so I turned him over and I looked at him his eyes rolled back and he just stopped breathing," Long said.

Long began performing chest compressions and soon he was joined by Anthony Gadson, a pharmaceutical sales representative, who learned CPR years ago and starting assisting with mouth to mouth resuscitation.

"If that were me, somebody would've done the same thing for me, so I feel like I did what I was supposed to do," Gadson explained.

While Long and Gadson worked to keep the victim's heart going, all the players and spectators, including teammate and league commissioner Bob Johnson, gathered around the lifesaving effort.

"We gathered in a circle and one of the wives of one of the players just led us in this huge prayer," said Johnson.

"It makes me feel great," Long told ABC 7/NewsChannel 8. "I am just glad that I am a D.C. Firefighter."



Free Drugs After Heart Attack Would Save Money, Lengthen Lives
More patients would take recommended medications, study says


By Ed Edelson

MONDAY, Feb. 18 (HealthDay News) -- Eliminating the cost of medications for people who have heart attacks would lead to longer lives and lower overall medical costs, new research suggests.

"These are highly effective medications that are relatively inexpensive, and the events they are designed to prevent are extremely expensive," said study author Dr. Niteesh K. Choudhry, a researcher in the division of pharmacoepidemiology and pharmacoeconomics at Brigham and Women's Hospital in Boston and an assistant professor at Harvard Medical School. His report is published in the Feb. 19 issue of Circulation.

The study covered four drugs commonly prescribed after heart attacks -- aspirin, beta blockers, ACE inhibitors or angiotensin receptor blockers (ARBs), and statins. Use of those drugs is relatively low under the current system, in which people share the cost with Medicare or other health insurance plans, Choudhry said. For example, only 46 percent of people take beta blockers after heart attacks, and only 50 percent take cholesterol-lowering statins. Less than 20 percent of heart patients used all four of the medications, according to the study.

The model set up by Choudhry and his colleagues doesn't assume a major increase in compliance with prescriptions, because "cost is just one reason why patients do not take medications," he said, adding that relying on previous studies of drug cost and use, the model assumes an increase of about 14 percent, with perhaps 64 percent of people taking the medicines if they were free.

The result would be an increase in average survival after a heart attack, from the present 8.21 quality-adjusted life years to 8.56 years. "That is small in an absolute sense, but in an aggregate sense, it is very large," Choudhry said.

And medical costs over a lifetime would go down, from the current $114,000 to $111,600, the study added.

"This study adds to a growing body of research showing how important it is to reduce or eliminate patient co-payment for drugs," said Robert M. Hayes, president of the Medicare Rights Center in New York. "Medicare should take the lead in forging the creation of drug coverage that allows patients to get the medications their doctors consider vital."

"It certainly makes sense from the medical point of view," said Dr. Richard A. Stein, a professor of medicine at New York University. "Studies have shown that giving even middle-income people free drugs improves outcome. The greatest benefit will go to people in the lower socioeconomic and immigrant population."

But the study is theoretical, Stein noted. "One would like to see some real-world trial to determine whether this works in fact, whether providing free drugs without co-payment would make a difference, he said.

Such a study has begun at Harvard, Choudhry noted. His group is working with a major health insurer, not Medicare, in a trial that assigns some people to get medications without cost, while others will get the standard co-payment.

"It will take several years for us to get answers," Choudhry said. But similar investigations are being started by other medical insurers and corporations, he added.

The idea is potentially applicable to some other chronic conditions, such as congestive heart failure and diabetes, Choudhry noted. And, if the use of recommended medications after a heart attack goes up more than predicted by the model, "the cost savings would be phenomenal," he said.

More information

To learn about how to stay on your statins, consult the National Heart, Lung, and Blood Institute.




Heart Attack Threatens Young, Old

BAKERSFIELD, Calif. -- Nearly 1.2 million men and women suffer a heart attack every year in the United States, according to the American Heart Association. However, not all of the victims are old.

Brian Connell considers himself a lucky guy. At the age of 39, he's physically active, he has a high-level job, and he is also a heart attack survivor. "I know I was overweight and obviously had some other risk factors against me," said Connell. "I wish I did more to prevent it, certainly."

Connell is doing plenty of things now. He met with a nutritionist and changed his diet. He gets regular exercise and takes medication to control his cholesterol. He also gets regular checkups.
Click here to find out more!

Cardiologist Jeffrey Popma said it's not unusual to see younger heart attack patients. "We have dozens of patients in our system every year who have been under 40 years old who have suffered a major heart attack," said Dr. Popma.

Popma said getting medical help quickly is the key to survival. Connell said that is what made all the difference for him. And when people ask him if that was his first heart attack, Connell said he is quick to tell them it was his last heart attack.

Copyright 2008 by TurnTo23.com. The Associated Press contributed to this report. All rights reserved.


The messages I take from such stories:

1) Get yourself to a hospital ASAP for any symptoms even vaguely suspicious of heart disease, because they will know what to do. You'll be doomed if you don't.

2) Hospitals and doctors are expert at saving you from the brink of disaster. The process, once you enter, is rapid and smooth and you will be eternally grateful.

3) Medicines save lives. You're going to die if you don't take medication.


As I've often said, one of the toughest battles of all in health and heart disease is sorting out fact from fiction. Unfortunately, the media continues to propagate the scare tactics that support the status quo of procedural heart care. Wittingly or unwittingly, they serve a $400 billion dollar a year gargantuan industry that remains hungry for growth.

Lost in the headlines are the messages that could have been included, like:

Heart disease detectable decades before disaster

Or:

"Heart disease preventable, reversible, and--curable?"



Copyright 2008 William Davis, MD

Which statin is best?

The statin drugs can indeed play a role in a program of coronary plaque control and regression.

However, thanks to the overwhelming marketing (and lobbying and legislative) clout of the drug manufacturing industry, they play an undeserved, oversized role. I get reminded of this whenever I'm pressed to answer the question: "Which statin drug is best?"

In trying to answer this question, we encounter several difficulties:

1) The data nearly all use statins drugs by themselves, as so-called monotherapy. Other than the standard diet--you know, the American Heart Association diet, the one that causes heart disease--it is a statin drug alone that has been studied in the dozens of major trials "validating" statin drug use. The repeated failure of statin drugs to eliminate heart disease and associated events like heart attack keeps being answered by the "lower is better" argument, i.e., if 70% of heart attacks destined to occur still take place, then reduce LDL even further. This is an absurd argument that inevitably encounters a wall of limited effects.

2) The great bulk of clinical data examining both the incidence of cardiovascular events as well as plaque progression or regression have all been sponsored by the drug's manufacturer. It has been well-documnted that, when a drug manufacturer sponsors a trial, the outcome is highly likely to be in favor of that drug. Imagine Ford sponsors a $30 million study to prove that their cars are more reliable and safer. What is the likelihood that the outcome will be in favor of the competition? Very unlikely. Such is human nature.

If we were to accept the clinical trial data at face value and ignore the above issues, then I would come to the conclusion that we should be using Crestor at a dose of 40 mg per day, since that was the regimen used in the ASTEROID Trial that achieved modest reversal of coronary atherosclerotic plaque by intravascular ultrasound.

But I do not advocate such an ASTEROID-like approach for several reasons:

1) In my experience, nobody can tolerate 40 mg of Crestor for more than few weeks, a few months at most. Show me someone who can survive and tolerate Crestor 40 mg per day and I'll show you somebody who survived a 40 foot fall off his roof--sure, it happens, but it's a fluke.

2) The notion that only one drug is necessary to regress this disease is, in my view, absurd. It ignores issues like hypertension, metabolic syndrome, inflammatory phenomena, lipoprotein(a), post-prandial (after-eating) phenomena, LDL particle size, triglycerides, etc. You mean that Crestor 40 mg per day, or other high-intensity statin monotherapy should be enough to overcome all of these patterns and provide maximal potential for coronary plaque reversal? No way.

3) Plaque reversal can occur without a statin agent. While statin drugs may provide some advantage in the reduction of LDL, much of the benefit ends there. All of the other dozens of causes of coronary atherosclerotic plaque need to be addressed.

So which statin is best? This question is evidence of the brainwashing that has seized the public and my colleagues. The question is not which statin is best. The question should be: What steps do I take to maximize my chances of reversing coronary atherosclerotic plaque?

The answer may or may not involve a statin drug, regardless of the subtle differences among them.


Copyright 2008 William Davis, MD

Lipoprotein(a)--neglected and unappreciated


Lipoprotein(a), or just Lp(a) to its close friends and neighbors, is among the most underappreciated and neglected of causes of coronary plaque. It's the Rodney Dangerfield of lipoproteins.

Lp(a) rarely gets diagnosed before people come to my office. They've often been through the ringer: doctors have thrown their hands up in frustration because of poor response to "standard" treatment (AKA statin drugs); the patient doesn't understand why they might be thin and active yet have the high blood pressure of someone 70 lbs heavier; they have heart disease despite wonderful cholesterol values.

One blood test and the answer becomes clear: They have Lp(a). It explains all these phenomena.

They why don't more physicians order this simple test? Why don't we hear more about this prevalent (1 in 5 people with coronary plaque have it) genetic pattern that accelerates risk for heart disease?

There are a number of reasons. But I believe the most powerful reason is simply that there is no big revenue-generating drug to treat it. Statins reduce LDL cholesterol to the tune of $27 billion dollars a year (2007 revenue). There's no such blockbuster for Lp(a). Of course, Niaspan represents the relatively anemic attempt to commercialize a pharmaceutical treatment for Lp(a), but side-effects and the lack of FDA trials for the Lp(a)-reducing indication have stalled its commercial success. (Efforts to block the flush with various products, by the way, may re-invigorate niacin as a pharmaceutical agent. The drug companies smell money here.)

Another reason for Lp(a)'s unpopularity: Though there are mounds of data that document--without question--that Lp(a) is an important risk for coronary disease and other forms of atherosclerotic disease, we lack treatment trials. For instance, niacin vs. placebo for 5 years, then count the number of heart attacks and deaths. We have numerous, repetitive, overlapping, redundant trials with statins adhering to this design. We have none for niacin and the treatment of Lp(a).

Niacin is also a pain in the neck for your doctor. He/she rapidly tires of the calls about the crazy and disconcerting flushing with niacin. Most are unaware that proper hydration reduces or eliminates the flush for the majority of people. It takes too much time and energy to educate people. (By the way, prescription Niaspan makes no mention of purposeful hydration. They only suggest the nonsensical "Take with a low-fat snack," i.e., snacks that actually counter the therpaeutic effects of niacin. What they should be saying is "take with a high-fat snack" like raw almonds, foods that facilatate the benefits of niacin.)

Should someone concoct a successful pharmaceutical treatment for Lp(a), it will make the news, headlines in health magazines and health sections of the newspaper will blare about how important Lp(a) is. Yet it has been there all along, frustrating people and their physicians.

In the Track Your Plaque experience, Lp(a) clearly 1) correlates with heart scan scores, 2) correlates with progression of heart scan scores without treatment, and 3) poses special challenges for treatment. Interestingly, some of our biggest failures have been with Lp(a), as well as some of our biggest successes. (Our current record holder for the largest percentage reduction in heart scan score has Lp(a).)

If you have coronary plaque, or if there is family risk of heart disease, then Lp(a), in my view, is an absolutely essential factor to test for. Yes, treatment poses challenges. But once you know who your enemy is, then you can focus your efforts on it. Not knowing whether or not you have it leaves your efforts unfocused and generally flawed.

Track Your Plaque Members, be sure to read our in-depth Special Report, Unique Treatments for Lipoprotein(a) Reduction.



Copyright 2008 William Davvis, MD