concepts), "energy balance" therapies, desiccated organ extracts ("applied kinesiology"), and a variety of other fringe treatments offered by practitioners offering chelation. This doesn't necessarily mean, of course, that chelation is also fringe or suspect, but it tends to be offered by practitioners who engage in generally unscientific, unfounded practices.


The few people I've seen go through multiple courses of chelation (usually 30 or so infusions) have shown no impact on heart scan scores or any other measure of heart disease.

In response to the many questions I receive on chelation, I had been answering that, if we would simply wait for the publication of the NIH-sponsored trial of IV chelation therapy, perhaps we'd know once and for all.

However, in a lengthy criticism, four expert authors argue that the TACT trial to assess chelation study is doomed to failure for an entire list of reasons and should therefore be abandoned. The discussion is available on Medscape Cardiology. (Free sign-in required.)



Why the NIH Trial to Assess Chelation Therapy (TACT) Should Be Abandoned
We investigated the social and the scientific histories of chelation therapy beginning in the 1950s. We examined TACT protocols and consent forms, which, in response to Freedom of Information Act (FOIA) requests, the NIH provided to us with curious redactions. We examined the existing RCTs and the numerous case series cited by the TACT protocols. We examined evidence for risks, including information that is not in the standard medical literature. We examined various hypotheses that advocates have offered to explain how chelation "works."

We present our findings in 4 parts. First, we provide a brief history of the use of disodium EDTA as a treatment for CAD. Next, we describe the origin and nature of the TACT. Next, we discuss the evidence for chelation as a treatment for CAD and for atherosclerosis in general, and place it in the context of other proposed treatments that have been ineffective after an initial period of enthusiasm. Finally, we discuss the risks. For each topic, we contrast our findings with relevant statements in the TACT literature, to the extent that such statements exist.



Among the highlights:

--Since the mid-1970s, court documents and newspapers have reported at least 30 deaths associated with IV disodium EDTA, most of it administered by ACAM members.

--Early chelation investigators had chosen the disodium salt of EDTA, reasoning that if it could remove calcium from atherosclerotic plaques, it might shrink them. That notion was soon demonstrated to be invalid. It has largely been replaced by a "toxic heavy metals" antioxidant hypothesis, which is based on the potential for metal ions to produce free radical damage. Chelationists now cite "removing heavy metals" as the basis for their claim that chelation is effective for approximately 70 conditions, ranging from schizophrenia and autism to cancer. This provides them with numerous reasons to ignore any trial that finds chelation ineffective for CAD.

--Biochemical literature, either not cited or misrepresented in the TACT protocols, has demonstrated that the heavy metals hypothesis is implausible. Antithetically, it also demonstrates that the chelation mixture used in the TACT has pro-oxidant effects in vitro.

--In our opinion, TACT literature -- including 2 versions of the protocol, the consent form, information posted on the NCCAM Web site, and 2 editorials co-authored by the PI -- has misrepresented chelation, its risks, and the facts of the study. It has exaggerated the value of supportive case series, not only by ignoring evidence of bias and incompetence, but by misrepresenting citations and reporting erroneous data. It has minimized the dangers, both by understatements and by omissions of specific, published complications. It has not acknowledged the deaths mentioned above. It has repeatedly conflated disodium EDTA and a different drug, calcium-sodium EDTA.

--The TACT includes nearly 100 "chelation site" co-investigators who, in our opinion, are unsuitable to care for human subjects or to report trial data. Most espouse implausible health claims while denigrating proven methods; several have been disciplined, for substandard practices, by state medical boards; several have been involved in insurance fraud; at least 3 are convicted felons. Several were members of the ACAM or GLACM IRBs mentioned above. Few appear to have real expertise, required by TACT literature, in treating patients with CAD or in conducting clinical trials. Most continue to promote chelation while the TACT is in progress, contrary to good science, to human studies ethics, and to US Federal Code.


While the criticism itself does not prove the point one way or another, as a clinical trial should, anyone contemplating chelation therapy would be well-advised to read the document first. Another reference: EDTA chelation therapy for cardiovascular disease: a systematic review.


The authors of the exhaustive discussion are:
Kimball C. Atwood IV, MD, Anesthesiologist, Newton-Wellesley Hospital, Newton, Massachusetts; Assistant Clinical Professor, Tufts University School of Medicine, Boston, Massachusetts; Associate Editor, Scientific Review of Alternative Medicine
Author's email: katwood@partners.org

Elizabeth Woeckner, AB, MA, President, CIRCARE (Citizens for Responsible Care and Research), Columbia, Maryland

Robert S. Baratz, MD, DDS, PhD, Medical Director, South Shore Health Center, Inc., Braintree, Massachusetts; Assistant Clinical Professor of Medicine, Boston University School of Medicine, Boston, Massachusetts; President, National Council Against Health Fraud, Inc.

Wallace I. Sampson, MD, Clinical Professor of Medicine (Emeritus), Stanford University, Stanford, California; Senior Attending Physician and formerly Chief of Medical Oncology, Santa Clara Valley Medical Center, San Jose, California; Editor-in-Chief, Scientific Review of Alternative Medicine



The authors provided the following disclosures:


Disclosure: Kimball C. Atwood IV, MD, has disclosed no relevant financial relationships in addition to his employment.

Disclosure: Elizabeth Woeckner, AB, MA, has disclosed that she has received compensation for consulting in civil litigation and professional disciplinary actions.

Disclosure: Robert S. Baratz, MD, DDS, PhD, has disclosed that he has been retained by state licensing boards, the Office of the US Attorney, and plaintiff counsel as an expert in disciplinary proceedings and litigation with regard to chelation therapy and associated matters. He is compensated only for his time and has no commercial interest in the outcome of the proceedings or litigation.

Disclosure: Wallace I. Sampson, MD, has disclosed no relevant financial relationships in addition to his employment.

American Diabetes Association


These are actual quotes from the American Diabetes Association website:


Myth #2 (from list of Diabetes Myths): People with diabetes can't eat sweets or chocolate.
If eaten as part of a healthy meal plan, or combined with exercise, sweets and desserts can be eaten by people with diabetes. They are no more “off limits” to people with diabetes, than they are to people without diabetes.



Myth #5: If you have diabetes, you should only eat small amounts of starchy foods, such as bread, potatoes and pasta.
Starchy foods are part of a healthy meal plan. What is important is the portion size. Whole grain breads, cereals, pasta, rice and starchy vegetables like potatoes, yams, peas and corn can be included in your meals and snacks. The key is portions. For most people with diabetes, having 3-4 servings of carbohydrate-containing foods is about right. Whole grain starchy foods are also a good source of fiber, which helps keep your gut healthy.





How can I have sweets and still keep my blood glucose on target?
The key to keeping your blood glucose on target is to substitute small portions of sweets for other carb-containing foods in your meals and snacks. Carb-containing foods include bread, tortillas, rice, crackers, cereal, fruit, juice, milk, yogurt, potatoes, corn, and peas. For many people, having about 45 to 60 grams at meals is about right. Serving sizes make a difference. To include sweets in your meal, you can cut back on the other carb foods at the same meal.

For example, you’d like to have cookies with your lunch. Your lunch is a turkey sandwich with two slices of bread. Your first step is to identify the carb foods in your meal. Bread is a carb. You decide to swap two slices of bread for two slices of low-calorie bread and have the cookies -- it’s an even trade. Your total amount of carbohydrate remains the same for the meal.



Can I eat foods with sugar in them?
For almost every person with diabetes, the answer is yes! Eating a piece of cake made with sugar will raise your blood glucose level. So will eating corn on the cob, a tomato sandwich, or lima beans. The truth is that sugar has gotten a bad reputation. People with diabetes can and do eat sugar. In your body, it becomes glucose, but so do the other foods mentioned above. With sugary foods, the rule is moderation. Eat too much, and 1) you'll send your blood glucose level up higher than you expected; 2) you'll fill up but without the nutrients that come with vegetables and grains; and 3) you'll gain weight. So, don't pass up a slice of birthday cake. Instead, eat a little less bread or potato, and replace it with the cake. Taking a brisk walk to burn some calories is also always helpful.


Or take a look at the recipes for breads, muffins, cakes, pies, cookies, and pizza.


My point? As I often say, while the "official" organizations like the American Diabetes Association, the American heart Association, and the USDA dominate the message provided to mainstream Americans, to those of us who know better, they have become irrelevant. You can see how obviously boneheaded their advice is. I'd go so far as to say that, if you want diabetes, follow the American Diabetes Association diet. If you have diabetes, and you'd like to accelerate complications like kidney disease, heart disease, and neuropathy, then follow the American Diabetes Association diet.

I'm going to bet that American Diabetes Association sponsors like Lilly, Novo Nordisk, Merck, Pfizer, Abbott ($1 million or more annual contributions) and Cadbury Schweppes (3-year, multi-million dollar support for Weight Loss Matters program) will continue to charge full-speed ahead to maintain the status quo. Cadbury Schweppes are the proud makers of Dr. Pepper, Hawaiian Punch, Snapple, Motts' Apple Juice, and Hires Root Beer--you know, the foods and drinks that you can have as long as you adjust your insulin dose or talk to your doctor about adjusting your diabetes medications. And if you gain, say, 30 or 40 lbs eating these foods. . . well, we've got a treatment for that. Merck's Januvia , for instance, can help you out for only about $200 a month!

Looking at the facts this way, and it seems like some cheap conspiracy theory: They're all out to get us. Dispense information that virtually guarantees propagation of the disease, and all your friends and cronies profit. I don't know if it is or it isn't, but it sure smells like it sometimes.
All posts by william-davis

Heart health for stupid people

I'm kidding.

What I'm referring to is the incredibly lame information I come across that passes as "heart health" on the internet, magazines, and other media. Just to keep abreast of what is being said, I subscribe to multiple newsletters and magazines and I witness the sorts of advice offered to the reading public.

A recent long-winded article on a popular website listed the "exciting" strategies available for a healthy heart:

Eat healthy--by eating a "balanced" diet low in saturated fat

Don't smoke

Exercise

Don't ignore chest pain symptoms or breathlessness

Know your numbers! meaning your cholesterol numbers. "If your cholesterol is high, you may need to speak to your doctor about medication to reduce it."


Surely they must all believe we're stupid. Otherwise, why would they repeat the same obvious information over and over again? Quit smoking? Gee, you think so?

How about some real heart healthy advice:

Get a heart scan--since we have to accept that cholesterol values are a miserable failure in detecting hidden heart disease. So is waiting for symptoms to appear.

If you have any measure of coronary plaque, ask your doctor to assess lipoproteins, not lipids (cholesterol).

Take fish oil for omega-3 fatty acids--At a dose of 1000 mg or more of EPA + DHA, heart attack risk is reduced by at least 28%.

Eliminate wheat and other processed carbohydrates --Small LDL has emerged as the number one cause of coronary plaque, not high cholesterol from saturated fat.

Get vitamin D assessed--The effects are huge--HUGE. There's already a study in a kidney disease population that showed a substantial reduction in mortality with vitamin D supplementation. More data are coming, including our own.


That's a start--truly effective, practical heart healthy strategies that go way beyond the conventional bland advice.


Copyright 2007 William Davis, MD

Money, money, money, money

I've been asked the question numerous times:

Why aren't heart scans more popular?

First, let me qualify by saying that heart scan have indeed grown in popularity over the past decade. I think the real question is:

Given the enormous usefulness of CT heart scanning to detect hidden, asymptomatic coronary atherosclerotic plaque, why haven't they more readily been incorporated into conventional medical practice?

That's easy: There's no money in it.


Say, for instance, your doctor orders a heart scan and somehow receives a $1000 for the test. Scan centers would be scanning 100 people a day, falling over themselves to do scans.

This would be similar to a heart catheterization. Order a catheterization, do 30 minutes of work, and get $1000. Or, order a nuclear stress test. Depending on how its done and where, $1800-4000 is paid by the insurer.

Order a CT heart scan and how much is paid to the doctor? Usually nothing. At most, a nominal fee might be paid if the doctor reads the scan.

With heart scans, there simply is no big payoff.

We learned the implications of this situation 10 years ago when I was trying to help my friend, Steve Burlingame, the owner of Milwaukee Heart Scan. (I am NOT and NEVER WAS an owner.) Steve was trying to let everybody know about this great new $2 million dollar heart scan device in the Milwaukee area.

The first few years were tough for Steve: Carrying the substantial expense of this device while doctors essentially gave the technology the cold shoulder. It simply did not fit into the financial equation. Why change the way things were, particularly when there was virtually no financial reason to do so? To counter this, Milwaukee Heart Scan followed the model many other scan centers have followed and marketed directly to the public.

I see this as yet another example of why people need to take control of health care away from doctors and hospitals, the current controllers of the system who are providing a disservice to the public they are supposed to be serving. These institutions, for the most part, serve their self-serving financial interests, not your health interests. It's the same equation that drives food manufacturers to make more and more processed carbohydrate foods that they sell for substantial markups, not green peppers and cucumbers that make little money.

I regard heart scans as among the greatest self-empowering tools in health ever conceived. It was that way in 1997; it remains that way in 2007.

The many faces of LDL

Ginnie came in for an opinion about her heart scan score of 393. At age 57, this put her in the 99th percentile, a high score.

As usual, we did a lipoprotein analysis by NMR (Liposcience). Some numbers:

LDL cholesterol: 96 mg/dl
This value puts Ginnie's LDL in the most favorable 25% in the country.


LDL particle number: 2140 nmol/l
This value is in the worst 25% of the country and is the equivalent of an LDL cholesterol of 214 mg/dl (take off the zero).

In addition, over 90% of Ginnie's LDL particles fell into the small class.

Had we run some other values, how would they have turned out? These are my estimates (since we didn't actually run them in Ginnie), but having run side-by-side numbers in past, reasonable estimates would have put:

Apoprotein B somewhere in the 120 to 140 mg/dl range

Direct LDL 100-130 mg/dl range.


In other words, conventional calculated LDL is the least reliable of all the ways of examining low-density lipoprotein.

It can also go the other way: High calculated LDL, low LDL particle number or ApoB or direct LDL. And, indeed, these other measures have proven superior in their ability to predict "events" like heart attack over conventional calculated LDL.

Unfortunately, relying on conventional LDL is like a broken speedometer on your car. You really can't gauge accurately how fast you're going; sometimes you could be way off. While insurance companies and many physicians still continue to balk at this argument, the data have already been generated that show that lipoprotein analysis (my bias is NMR) is not just superior, but enormously superior for accuracy and event prediction.

In addition, lipoprotein analysis has proven a crucial tool that accounts for our extraordinary success in reducing and controlling CT heart scan scores in the Track Your Plaque program. I doubt that we could have achieved the same level of success using conventional lipids.

I'm also aware of the logistical difficulties obtaining lipoprotein testing in a world enthusiastically supportive of hospital procedures and smugly ignorant of superior prevention tools like lipoprotein analysis. I've learned just how difficult it can be in our Track Your Plaque Member Forum; I've also learned about some strategies for obtaining these tests that I hadn't been aware of, thanks to the resourcefulness of our Members.

We will be working on some solutions in the coming months.


Copyright 2007 William Davis, MD

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

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

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

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

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

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

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

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

Is health the absence of disease?

It sounds like a word game, but is health the absence of disease?

In other words, if you're not sick, you must be well. If you don't have cancer, heart disease (overtly, that is, like angina and heart attack), the flu, diarrhea, fevers, pain someplace . . . well then, you must be well.

Of course, most of us would disagree. You can be quite unhealthy yet have no overt, explicit disease. Yet this is the philosophy followed in conventional medicine when it comes to many aspects of health.

With regards to heart disease, if you have no chest pain or breathlessness, you don't have heart disease. "Oh, all right, we'll perform a stress test to be sure." Track Your Plaque followers, as well as former President Bill Clinton, recognize the enormous pitfalls of this approach: It fails to identify the vast majority of hidden heart disease. In heart disease, the apparent lack of overt, sympatomatic "disease" does NOT equal the true absence of disease, even life-threatening.

How about nutritional supplements? Vitamin D is a perfect example. Blood levels of vitamin D of 10 ng/ml--profound deficiency--are common, yet people feel fine. Beneath the surface, blood sugar rises because of poor insulin response, hidden inflammatory responses are magnified, HDL is lower and triglycerides are higher, coronary plaque grows at an accelerated rate, colon cancer activity is heightened . . . Though you feel fine.

Can an abnormal "endothelial response" be present while you feel fine? You bet it can. This refers to the abnormal constrictive behavior of arteries that is present in many people who have hidden coronary plaque or risk for coronary plaque, but is entirely beneath consciousness.

How about a triglyceride level of 200 mg/dl, fatally high from the Track Your Plaque experience? (We aim for <60 mg/dl.) This is typical in people who follow the diets endorsed by agencies like the American Heart Association and the American Diabetes Association, organizations too eager to keep the money flowing from corporate sponsors and thereby offer us their advice based more on politics and less on health. Triglyceride levels of 200 mg/dl cause no symptoms.


At so many levels, the absence of disease is NOT the same as health. Health is something that is expressed by, yes, feeling good, but it's also measured by so many other factors hidden beneath the surface. An annual physical is one lame effort to address this aspect of "health." But it needs to go farther, much farther.

Heart scan, lipoprotein testing, vitamin D blood level--those are the basic requirements to go beyond the shortsighted practice of the conventional approach in the world of heart disease.

Cuckoo for Cocoa Puffs





Take a look at the list of ingredients in Cocoa Puffs: corn, sugar, corn syrup--all high glycemic index foods.

In other words, Cocoa Puffs is the physiologic equivalent of pure table sugar. Sure, it comes packaged with this wacky bird and the back of the box usually has fun games and offers. There's also the clever, fast-paced TV commercials to remind you of how fun Cocoa Puffs can be.


What is the actual consequence of a breakfast of a food like Cocoa Puffs in a cup of skim milk? That's easy: A big surge in insulin and blood sugar (from the corn and sugar), a drop in HDL cholesterol, surge in triglycerides (from the sugar and sugar-equivalents), increase in small LDL. Beyond this, you raise blood pressure and experience an insatiable increase in appetite. Then you get fat.

Obviously, none of this is desirable. Then why does the American Heart Association allow its Heart CheckMark endorsement on the package?

The Heart Association is trapped in 1982. Low-fat was in, saturated fat was the sole enemy of heart disease.

In 1982, the evils of small LDL, for instance, were unappreciated. LDL cholesterol was LDL cholesterol--all of it was bad and saturated fats seem to raise LDL. But the story has evolved enormously since then: LDL is not all the same. Small LDL is among the principal culprits in heart disease, the same small LDL hugely magnified by Cocoa Puffs and other similar products that fill 70% of supermarket shelves.

The American Heart Association needs to get with the times. The conversation on healthy diets has progressed considerably. Yet garbage foods that wreak havoc on health like Cocoa Puffs continue to be endorsed by an organization that still carries substantial clout with the American consumer.

My advice: Until they change their tune, anything that carries the endorsement of the American Heart Association should be eliminated from your diet.

Further validation of the Track Your Plaque 60:60:60 targets

The latest analysis of the data from Treat to New Targets (TNT) Trial shows that higher HDL cholesterol values are associated with reduced risk of heart attack, even in those with low LDL cholesterol values.

This counters the argument that some have made that, if a person takes a statin drug, raising HDL adds no additional benefit.

In the 9770-participant trial (randomized, double-blind), participants were given atorvastatin (Lipitor®) 10 mg or 80 mg per day. The study was sponsored by Pfizer, the manufacturer of Lipitor®. All participants were survivors of heart attacks, significant coronary disease by heart catheterization, or had previously undergone coronary angioplasty, stent placement, or bypass surgery—a high-risk group.

At the third month of enrollment, lipid (cholesterol panel) values were obtained and used as the basis for analysis. Participants on 80 mg atorvastatin achieved an average LDL cholesterol (Friedewald) of 77 mg/dl; participants taking 10 mg achieved a level of 101 mg/dl. Using these values, 8.7% of participants taking the higher dose of drug experienced an event, compared to 10.9% on the lower dose (which the investigators called a 22% relative reduction).

However, when the groups were re-analyzed by HDL cholesterol levels, higher HDLs remained predictive of less heart attack and other events, with the group having the highest HDL of =55 mg/dl experiencing 25% less events. Most interestingly, this effect was upheld even in participants with very low LDL cholesterols of <70 mg/dl.

I'm always a bit leery of drug company-sponsored studies, especially ones in which virtually all the participants tolerated a drug like Lipitor 80 mg, a dose in my experience that is very poorly tolerated for more than a few months. (Muscle aches are, in my experience, inevitable. I do not even recommend this dose.) In other words, the data are, in that respect, too good to believe.

Anyway, despite my reservations about these big money studies, there was nothing to gain from the HDL observation. (Of course, at one time, there would have been, given Pfizer's efforts to commercialize the now-kaput torcetrapib, scrapped because of excess mortality in phase II trials.)

Thankfully, there's other data that likewise suggest that the higher the HDL, the better. Yet more validation for the Track Your Plaque lipid targets of LDL 60 mg/dl, triglycerides 60 mg/dl or less, HDL 60 mg/dl or greater.



Copyright 2007 William Davis,MD

My sister called today . . .

My younger sister, aged 48 years (sorry, sis), called this morning.

"I'm going to my doctor today. What labs should I tell him to draw?" she asked.

"Why do you have to tell him? Can't you just ask him what he thinks should be drawn?"

"No," she said. "He just draws what I tell him to."


Maybe my sister is bossier than most. But I've heard this from many patients, as well. They go to their primary care physician and end up requesting this or that test. Sometimes their doctor complies. Often, they resist and refuse to do so.

I've heard many complaints from patients about doctors refusing to order even fairly benign tests like a vitamin D blood level or lipoproteins, even a C-reactive protein.

The number of these sorts of complaints seems to be growing. Ten years ago, it rarely happened. Today, I hear this nearly every day.

I think it is symptomatic of the growing discontent we all have with the status quo in healthcare. We are all expected to submit to the paternalistic, what-can-you-possibly-know mentality that still rules the day in medical offices. Only 40-50 years ago, if you wanted to look at a medical book, you'd have to ask the librarian for special permission so that they could make sure you weren't just a pervert trying to look at naked bodies. Today, every manner of medical and health information can be found online. Quite a contrast.

We are entering a new age, one in which people are far better informed, have surfed the internet and read media reports on health topics, have been exposed to drug company advertising, and know a fair amount about nutritional supplements. I think the system needs to change to accommodate this rapidly growing hyper-knowledgeable society.

In past, when a health problem turned up, you'd turn to your doctor first. I predict that,in the next few years, we will use the doctor as a place of last resort, the person we turn to when all else has failed, after you've exhausted your information sources.

I hope that the Track Your Plaque process will become one of the engines of change, an information resource that provides empowering tools that don't replace your doctor, but provide many information tools that are superior and may minimize your reliance on a health care provider.


Copyright 2007 William Davis, MD

Failure to diagnose

I picked up a hospital publication today. Featured prominently on the cover was a glossy photo of an attorney and his wife, both smiling.

The headline: "Atorney grateful for the lifesaving work of the ______ Hospital."

The story detailed the near-tragic story of how this 59-year old man was exercising at his local gym, only to lose consciousness after stepping off one of the exercise machines. Bystanders--hospital employees, as luck would have it--checked the man's pulse: none. They performed CPR. Ambulance called, blah blah blah.

Severe coronary disease discovered, extensive atherosclerotic plaque in all three coronary arteries, a 12-inch chest incision later and he and his wife are eternally grateful for the fine work done at X hospital. And so they should be for a job well done.

But wait a minute. After the urgent hospital dust settled, did anyone ask the one crucial question: Why wasn't this man's far-advanced heart disease identified? Why did he have to die and be resuscitated before his disease was recognized?

If this man was an indigent, homeless alcoholic . . . well, perhaps it would be no surprise. Health is neglected in this population. But a successful attorney?

Detecting hidden coronary atherosclerotic plaque simply isn't that tough. In Milwaukee, $199 would have diagnosed his disease unequivocally.

Unfortunately, we still have to set off drumrolls and crash cymbals to even begin to get the attention of the practicing physicians around us who continue to fail to diagnose hidden coronary disease. I wouldn't be at all surprised to hear if this man had a $4000 nuclear stress recently that was normal. Why would a nuclear stress test be normal? Easy: Wrong test.

The hidden message: The failure to diagnose paid somebody and some hospital over $100,000. So, why bother detecting disease before the payoff?

The profit motive in all this is all too obvious. The only other explanation is the enormous, repetitive, and systematic stupidity of the conventional approach to heart disease detection. You have the solution, at least for you and the people around you, in a CT heart scan and in the Track Your Plaque program.


Copyright 2007 William Davis, MD

Interview with world heart scan authority, Dr. John Rumberger












Dr. John Rumberger has, from its start, been a good friend of the Track Your Plaque program.

We are very proud to have his friendship. Dr. Rumberger is not only a world-renowned scientist in the world of cardiac imaging and heart scanning, but also a humanitarian and gentleman. From the very first day I met Dr. Rumberger many years ago, when he answered my many silly and naive questions about heart scans, I came to appreciate his deep and genuine interest in improving the world of heart disease detection.

I tracked Dr. Rumberger down from his busy schedule, now on a new project at the Princeton Longevity Center in Princeton, New Jersey.




TYP: Dr. Rumberger, we understand that your career has taken a new direction. Can you tell us about your current project?

Dr. Rumberger: I have not really taken a new direction, but further expanded on my opportunities.

I remain Medical Director of PrevaHealth Wellness Diagnostic Center (formerly Healthwise) in Columbus, Ohio. At that center, we see patients referred by their doctors for further refinement in cardiac risk stratification using heart and body scanning. However, by only doing scans alone there are limited opportunities for me to react in a meaningful way with the individual patients and thus I miss opportunities to do direct one-on-one teaching.

Currently, I spend most of my time in Princeton, NJ as Director of Cardiac Imaging for the Princeton Longevity Center. At the PLC, we perform comprehensive medical examinations along with screening CT scans, blood work, fitness and diet consultation to affect a more thorough one-on-one experience. Each patient then receives a comprehensive de-briefing.

In addition, since I have been involved with cardiac CT for now nearly 24 years, the PLC also affords me an opportunity to develop a CT coronary angiography training program for cardiologists and radiologists (www.cardiaccta.us). Together, these new efforts are merely an extension of my interests in prevention, patient care, and teaching.



TYP: Based on your book, The Way Diet, we understand that you advocate gravitating away from processed foods and incorporating more nuts, monounsaturated oils, lean proteins like fish, and a reduction in processed carbohydrates. You’ve also been a proponent of the Mediterranean diet that demonstrated a dramatic reduction in cardiovascular events in the Lyon Heart Study.

Has your philosophy or practice regarding nutritional strategies evolved or changed in any way since your book was published?

Dr. Rumberger: No, the strategies put forward in The Way Diet have, if anything, been reinforced by further and further research in selecting foods that are naturally high in anti-oxidants with lean sources of protein and reduced intake of processed sugar-containing preparations. The book, however, is what I call a ‘philosophy’ book which looks at three major aspects: proper diet, adequate exercise, and stress management. I also include some recipes which follow the dietary plans, but are done using ingredients that are commonly found in the average home.



TYP: We regard you as the source of much of the wisdom in heart scanning as the basis for early heart disease detection. Much of the original and subsequent scientific data, in fact, bears your name. Can you touch on some of the new directions your research has taken over the past couple of years?

Dr. Rumberger: We have come a long way from the beginning and there is a long way to go to get this incorporated into routine preventive care in the United States.

The most recent research has provided not so much more information as continuing to reinforce the old research. As I always say: if your research continues to show the same thing, then maybe there is a clear pattern here! The biggest challenge is getting this message into the mainstream and also trying to get cardiologists (and internists and, in fact, the general public) away from ‘stenosis’ detection to define the real cause of heart attacks (plaque) and into ‘plaque detection.’ This is where basic heart scanning has the greatest potential to reduce the expanding burden of heart disease.

You may be aware of our SHAPE initiave in which an international group of cardiologists and scientists have advocated getting a heart scan FIRST and then, if abnormal, checking your cholesterol values; rather than using cholesterol (which is valuable, but highly variable in predictive power) to determine who needs medications or further testing. The heart scan can define the current level of plaque and THEN you can determine what to do about it. [See the Track Your Plaque report on the release of the Shape Guidelines at SHAPE Guidelines]



TYP: We understand that you are performing CT coronary angiography in your center. What are your thoughts on the role of CTA in 1) screening for coronary disease, and 2) its role in the diagnostic process?

Dr. Rumberger: CT coronary angiography (CTA) is an incredible method to really define the extent of disease, beyond just coronary calcium. Its role is most appropriate in ruling OUT a significant ‘stenosis’ while really defining the absence or presence (and thus ‘how much’) of plaque. It is the ultimate ‘plaque detector’. CTA is best used in patients who have some symptoms, but in whom the clinician feels may NOT have clear cardiac chest pain. By risk-stratifying using CTA, we also gain information about heart size, heart function, whether there is prior heart damage, as well as other important information. This then becomes a very universal means to risk-stratifying individuals.



TYP: Thanks for your wonderful insights, Dr. Rumberger! We look forward to hearing about your future projects and research directions.





About John Rumberger, PhD, MD:

Dr. Rumberger is among the world's leading authorities on cardiac and vascular imaging using EBT and CT Scanning. Dr. Rumberger was among the first to pioneer the use of new CT technologies for heart scanning. He currently serves as Director of Cardiac Imaging at the Princeton Longevity Center, Princeton, NJ.

Dr. Rumberger is formerly Professor of Medicine and Consultant in the Department of Cardiovascular Diseases at the Mayo Clinic in Rochester, Minnesota. Dr. Rumberger received his doctorate in engineering from The Ohio State University in 1976 and graduated from the University of Miami School of Medicine in 1978.

During his over 20 year career as a clinician, educator, and researcher, Dr. Rumberger has published nearly 500 scientific papers and book chapters. He has lectured worldwide on EBT, early heart disease diagnosis, and wellness. He is an Established Investigator of the American Heart Association and a Founding Member of the International Society of Atherosclerosis Imaging. Dr Rumberger is an active Reviewer for the Journal of the American Medical Association, Archives of Internal Medicine, and the New England Journal of Medicine.

Homocysteine and coronary plaque

If you’ve watched the news over the past year, you know that doubt has been cast over the idea that reducing homocysteine blood levels with high doses of B vitamins (B6, B12, and folic acid, or B9) results in reduced risk for heart attack.

Is the homocysteine concept dead? Shall we empty our bottles of costly B vitamins into the trash and move on?

I don’t think so. As detailed in one of our Track Your Plaque Special Reports from a few months ago, I think the homocysteine issue still deserves lots of respect and further investigation. After all, hundreds of clinical studies have connected higher homocysteine levels with greater risk for heart disease, stroke, and aneurysm. Numerous studies, for example, have repeatedly and consistently demonstrated a tripling of heart attack risk when homocysteine levels exceed 14 ?mol/l. Can we dismiss this association because several more recent studies—NORVIT, HOPE, and VISP—suggested that, when starting homocysteine levels are 12.5, that B vitamin supplementation does not reduce heart attack risk?

I think there’s lots more to know about the homocysteine connection. That said, I have never seen a patient who I thought had heart disease strictly because homocysteine was increased.

I believe that we can at least use homocysteine as an index of lifestyle: the higher the homocysteine, the poorer the diet, or the less effective the absorption of B vitamins (especially vitamins B12 and folic acid). Homocysteine levels of <9 micromol/l suggest both adequate intake and absorption of these B vitamins.

If homocysteine is tightly connected with risk for heart disease, yet supplementation of B vitamins fails to reduce risk, might there be another means of connection? Or, could both homocysteine and heart disease be connected in some way that has nothing to do with B vitamins?

Don’t close the book on homocysteine. Just because conventional experience fails to draw connection does not necessarily mean that none exists. If it’s any consolation, taking B vitamins has been correlated with better memory, concentration, and other health benefits, even if no reduction in heart disease develops.

Big heart scan scores drop

High heart scan scores of, say, greater than 1000 are more difficult to reduce than lower scores.

I learned this lesson early in the experience of trying to drop scores. In the first few years of trying to drop scores, I saw relatively modest scores of 20, 50, or 100 drop readily, even when the usual targets were not fully achieved, and even before the incorporation of some of the more exciting recent additions to the Track Your Plaque program, like vitamin D.

But big scores of 1000, 2000, or 3000 are a tougher nut to crack. In the first few years, what I usually saw was a slowing , or "deceleration," of growth from the expected rate of annual score increase of 30% that would continue for a year or two, followed by zero change. In the first year of effort, for example, a score increase of 18% was common. 10% was common in year two, then finally zero change in year three. Somehow, the more plaque you begin with, the more "momentum" in growth is present and the longer it takes to stop it. Kind of like stopping a compact car versus stopping a freight train.

But more recently, I'm seeing faster drops. Today, Charlie came to the office to discuss his second heart scan. 18 months earlier, Charlie's first scan showed a score of 3,112, high by anybody's standard.

His repeat score: 3,048. While the drop is relatively small on a percentage basis and may even fall within the expected rate of error for heart scans (which tends to be <2% at this high a score), I told Charlie that it still represented a huge success. Not only did he not increase his score by the expected 30% per year, he also brought a charging locomotive to a rapid stop.

Next year, Charlie is targeting a big drop. Given the tools he now has available, I'm optimistic that he will succeed.

Watch for the Track Your Plaque May, 2007 Newsletter in which we will detail Charlie's story further.

Does the American Heart Association diet reduce heart disease?

If you have a heart attack and land in the hospital where, invariably, you will have a heart procedure. Or, if you get a stent or coronary bypass operation, sometime before your discharge from the hospital, a well-meaning hospital staff dietitian will provide instruction in the American Heart Association (AHA) diet.

Does this diet reduce the risk of heart disease?

The answer depends on where you start. If you begin with a conventional American diet that is enormously influenced by convenience, food manufacturers like Nabisco, General Mills, Quaker Oats, ADM, and Cargill, or food distributors like McDonald’s, Pizza Hut, and Taco Bell, then the American Heart Association diet is indeed an improvement. But just a small one. If LDL cholesterol is the yardstick, the average reduction in LDL is between 10 and 15 mg/dl. This is the same amount of change you’d experience by adding 1 tablespoon of oat bran to your diet. Hardly worth boasting about. HDL, triglycerides, blood glucose, and body weight do not change.

The diet could be substantially better. After all, it’s become common knowledge that other diets, such as the so-called Mediterranean diet, the South Beach Diet, and similar broad projects result in far greater changes than the AHA diet dispensed by your hospital and cardiologist. These diets more effectively reduce LDL, raise HDL, reduce triglycerides, reduce C-reactive protein, reduce blood pressure. Diets like South Beach also yield substantial weight loss and reversal of diabetic tendencies, with the magnitude of benefit dependent on the amount of weight lost.

Why this stubborn adherence to the outdated concepts articulated in the AHA diet? Cardiologists would argue that insufficient data has been generated to permit widespread application of these diets. They also differ on whether they really work. Of course, the majority remain ignorant and dismiss them as fad diets.

A little digging into the financial disclosures of the AHA suggests another, more malignant influence: who is paying the bills? Until recently, drug manufacturers were major contributors to the AHA. However, more recently AHA administrators have become sensitive to the public perception that they might be nothing more than a voice box for the drug industry. They have since limited contributions from the drug companies to 8% of annual charitable revenues.

The drug manufacturers have been replaced by the food industry. In addition to food manufacturers that make the cereals on your grocery shelf, it includes the multi-national conglomerates that produce unimaginable revenues and carry enormous political clout, like ADM and Cargill. Ever wonder how it is that Honey Nut Cheerios received a “Heart Healthy” endorsement from the AHA?

The AHA diet does not provide the answers we’re looking for, not even close. It is a perversion from an organization that has its strings pulled by industry. The answers to health will not come from the AHA, AMA, the American College of Cardiology, the American Hospital Association, and it won’t come from your doctor. It won’t come from a titillating report on the evening news or Good Morning America. It will come from collective and expanding wisdom placed directly into the hands of the public. It will be untainted by the temptation of drug industry dollars. It will not be dirtied by million dollar contributions, or the multi-million dollar behind-closed-doors lobbying of the food manufacturers. It will come from the truth relayed to the healthcare-consuming public. I hope you recognize it when you see it.

If you want a healthy diet for your heart, throw away the pamphlets from the AHA unless you are partial to bread, breakfast cereals, corn, and the supporters of their misguided nutritional advice.

Vitamin K2 and coronary plaque

The vitamin K2 story, though still preliminary, is becoming increasingly interesting from the perspective of CT heart score reduction.

The origin of this concept came from some unexpected observations. One, the observation that osteoporosis (lack of bone calcium that leads to fractures) arises from deficiency of vitamin K2. Two, deficiency of K2 leads to unrestrained calcium deposition in animal models, leading to heart attack in just weeks.

Vitamin K2 has been largely ignored for years, since the more widely understood K1 is rarely deficient. K1 deficiency can occur from prolonged antibiotic use, or from severe malnutrition. But deficiency in otherwise well people is very uncommon. Vitamin K2, however, may be a different story. Deficiency may be common.

The Rotterdam Heart Study of cheese-eating Dutch showed that greater K2 intakes resulted in a halving of heart attacks. Cheese (traditional varieties, not Velveeta or other make-believe cheese products) is a modest source of K2, as is the Japanese native food, natto. (If you've ever seen natto, I dare you to eat it. I have a pretty strong stomach and curiousity for food, but natto is the one thing I could not eat--it is truly horrible.)

The weight of evidence suggests that vitamin K2 supplementation may prove to be a useful addition to your coronary plaque control program. Clearly, more data are needed, particulary therapeutic obserations, i.e., observing people who take dose X of a K2 prepartion and tracking some feedback measure, e.g., bone density, CT heart scan score, "events" like heart attack, etc.

Nonetheless, the K2 story is clearly worth reading about, perhaps even considering supplementation. Please watch for the Special Report on the www.cureality.com website in the coming days.

Exercise and blood pressure

The media has gotten a hold of a case report from the University of Maryland describing a 51-year old physician who, despite being a long distance runner, had a high heart scan score.

An example of the report can be found at

Heart Disease In A Marathon Runner: Is Too Much Exercise A Bad Thing?

http://www.sciencedaily.com/releases/2007/03/070315091100.htm in Science Daily.



"The mystery was all the more intriguing because his resting blood pressure and fasting cholesterol levels, the usual measures of cardiovascular health, were in the normal range."


When this man was put on a treadmill for a stress test, his blood pressure skyrocketed from a normal 118/78 to 230/78--extremely high, even for exercise. The physicians reporting the case raised the question of whether long-distance running represents a risk for heart disease and if the high blood pressure with exercise is a contributor or cause of the high heart scan score.

These are phenomena we are very familiar with. We have stressed the importance of exercise blood pressure as a trigger for coronary plaque for years. While 230/78 is clearly too high, we find that any blood pressure over 170/80 with exercise adds to the fire and can trigger plaque growth.

However, I think it is absurd to suggest that marathon running itself is a trigger of coronary plaque. I think it is far more likely that the person described in the report had lipoprotein(a), a potent trigger for both exercise-induced hypertension and high CT heart scan scores in seemingly well people. He likely also suffered from a deficiency of vitamin D deficiency, another contributor. There's no need to indict exercise.

If you are in the Track Your Plaque program, you know that stress tests are of questionable helpfulness for the detection of hidden heart disease. But they are useful for assessment of blood pressure responses during exercise. If BP exceeds 170/80 at 10 mets (a measure of exercise effort achieved by walking 3.4 mph at a 14% grade for 3 minutes), then blood pressure may be a contributor to your heart scan score.

"Fish oil is stupid"

"Fish oil is a waste of time and money. It's stupid. Just stop it."

So a patient of mine was advised by another physician when he complained that he occasionally experienced a fishy aftertaste.

This attitude perplexes me. After all the confirmatory data that support the enormous health benefits of omega-3 fatty acid supplementation, including the 11,000 participant GISSI-Prevenzione Trial, you'd think this attitude would be history. What's a little fish aftertaste when heart attack risk is slashed 28%?

Perhaps the tendency to pooh-pooh fish oil is because it's available as a nutritional supplement. This shouldn't make fish oil appear inconsequential. Far from it.

If you witness the extraordinary power for fish oil to reduce triglycerides, you will be immediately convinced of its effectiveness. The ability of omega-3 fatty acids from fish to eliminate intermediate-density lipoprotein (IDL), the persistent abnormal lipoprotein which signals an inability to clear dietary fats from the blood, can also convince you. More than 90% of people with excessive IDL have it completely eliminated by 4000-6000 mg of fish oil (providing 1200-1800 mg EPA + DHA) per day.

The fact that fish oil is available as a prescription "medication," as well as an over-the-counter supplement, causes some physicians to dismiss the power of the supplemental form. This is nonsense. The over-the-counter form is every bit as effective as the prescription form.

The makers of prescription Omacor also make the claim that their preparation is safer and purer. That may be true, but I'd like to see independent verification from the FDA, USDA, or an unbiased organization like Consumer Reports before I accept their marketing as fact--particularly at $120 to $240 per month! If Omacor proves to contain substantially less mercury and pesticide residues, then that will need to be factored in. (Please note that both Consumer Reports and Consumer Labs measured no substantial mercury or pesticide residues in their analyses of 16 and 41 brands, respectively.)

I try to persuade my colleagues that the idea of taking supplements is a wonderful trend that allows people to express ownership of their own health. What people need is guidance, not salesmanship for a more expensive version, nor dismissal of nutritional preparations that actually possess considerable benefits.

More Vitamin D and HDL

I’m seeing more and more of it and I am convinced that there is a relationship: significant boosts in HDL cholesterol from vitamin D supplementation.

To my knowledge this remains an undescribed and uncharacterized phenomenon. There have been several observers over the last two decades who have noticed that total cholesterol shows a seasonal fluctuation: cholesterol goes up in fall and winter, down in spring and summer; year in, year out. This phenomenon was unexplained but makes perfect sense if you factor in vitamin D fluctuations from sun exposure.

I have come across no other substantiating evidence about fluctuations of HDL. But I am convinced that I am seeing it. Replace vitamin D to a blood level of 50 ng/ml, and HDL goes up if it is low to begin with. If HDL is high to begin with, say, 63 mg/dl, it doesn’t seem to change.

But, say, starting HDL is 36 mg/dl. You take niacin, 1000 mg; reduce high-glycemic index foods like breakfast cereals, breads, cookies, bagels, and other processed carbohydrate foods; exercise four days a week; add a glass of red wine a day; even add 2 oz of dark chocolate. You shed 15 lbs towards your ideal weight. After 6 months, HDL: 46 mg/dl. Better but hardly great.

Add vitamin D at a dose of, say, 4000-6000 units per day (oil-based gelcap, of course!), and re-check HDL two or three months later: 65 mg/dl.

I’ve seen it happen over and over. It doens't occur in everybody but occurs with such frequency that it’s hard to ignore or attribute to something else. What I’m not clear about is whether this effect only occurs in the presence of the other strategies we use to raise HDL, a “facilitating” effect, or whether this is an independent benefit of HDL that would occur regardless of whatever else you do. Time will help clarify.

We are tracking our experience to see if it holds up, how, and to what degree on a more formal basis. Until then, a rising HDL is yet another reason—-among many!-—to be absolutely certain your 25-OH-vitamin D3 level is at 50 ng/ml or greater.

How high is an ideal vitamin D blood level? If 50 ng is good, is 60 or 70 ng even better? Probably not, but there are no data. We have to wait and see. Unlike a drug that enjoys plentiful “dose-response” data, there are no such observations for vitamin D into this higher, though still “physiologic,” range.

Thin ice

How long can an industry built on ignorance and deception continue its practices in the new Information Age?

I don’t think it can for long. I talk to hospital administrators who believe that their source of competition is the hospital across town, battling for the same patients. I speak to my colleagues, the cardiologists, who believe that the current model is sustainable—take every willing body to the catheterization laboratory or operating room for heart procedures, the revenue-generating engine of income and expanding heart programs.

I speak to primary care physicians, who are dumbfounded and perplexed and have no idea which way things are going. They are trapped in a peculiar position: most have signed contracts and are employees of the hospital. They are legally bound to support the cardiologists who take anybody possible to the catheterization laboratory or direct patients to other profit-making procedures.

Much of this system depends on the willingness of the participant, meaning you and the health care seeking public. What happens when the truth comes out and disseminates widely through the thinking populace? What happens to hospitals and physicians and the vast structures they’ve built when the bottom drops out for 50% of their “market?

The proverbial cow manure will hit the fan. Upheavals in the medical industry will rival the changes that the automobile or telephone brought early in the last century. Cardiologists, immense hospital heart programs, and the vast economic infrastructure they spawned will go the way of stage coach manufacturers and the telegraph.

What form will the broad exposure of detailed information in health take? I’m not sure, but it will certainly come. The collaborative efforts that created the Linux operating system and have challenged the monopoly of Microsoft Windows, or the emergence of the extraordinary Wikipedia as a repository of human knowledge that dwarfs the venerated Encylopedia Brittanica, will eventually overtake the American medical system, the heart disease industry in particular.

If you base your future on the welfare of your local hospital or the manufacturers of stents, operating room equipment for heart bypass, or similar industries, watch out. The ice is thin. And as the spring warms the air around you, it gets thinner.

The Track Your Plaque program is our first step in broadcasting the message of self-empowerment in heart health care and an attempt to wrestle control away from the profit-seeking forces that dominate. As we grow, we not only hope to broadcast the message more widely, but expand the message to other areas of health. I predict that the collaborative, let’s-all-pitch-in-and-help spirit of the Information Age, “version 2.0,” will spark the change.

Vitamin D and cancer

Although this is a Blog about heart scans and heart disease, I came across a helpful video from Dr. Joseph Mercola about vitamin D and cancer that's worth viewing. Though I do not agree with many of Dr. Mercola's on-the-edge views, he does come up with some good thoughts and, in this instance, a useful educational tool about vitamin D.

You can view his video (which he claims crashed his server, due to the excessive demand for downloads) by cutting and pasting the address into your URL bar (above):

http://v.mercola.com/blogs/public_blog/How-to-Reduce-Your-Risk-of-Cancer-By-50--8790.aspx

Also, for my many patients who I've directed to look in my Blog for Dr. Reinhold Vieth's webcast presentation on vitamin D, here's the address:

http://tinyurl.com/f93vl

Perhaps I carry on too much about vitamin D. But I've come to respect this "nutrient" as among the most powerful strategies I've seen for dramatically improving control over coronary plaque growth as well as other aspects of health, as Drs. Mercola and Vieth eloquently detail.

Lipoprotein(a), menopause, and andropause

Lipoprotein(a) is a curious lipoprotein. Not only is it a genetic pattern with numerous variations, it is also one that shows a predictable age-dependent rise.

Women in particular are prone to this effect, men to a lesser degree. As we age, many hormones recede, particularly growth hormone, testosterone, the estrogens (estradiol, estriol, estrone), progesterone, and DHEA, among others. This is not a disease but the process of senescence, or aging.

When we're young, estrogens, testosterone, and DHEA all exert suppressive effects to keep lipoprotein(a), Lp(a), at bay. But as a woman proceeds through her pre-menopausal and menopausal years, and as a male passes through his fourth decade, there is an accelerated decline of these hormones. As a result, Lp(a) crawls out of its cave and starts to sniff around.

Typically, a woman might have a Lp(a) of 75 nmol/l (approximately 30 mg/dl) at age 38. Ten years later, at age 48, her Lp(a) might be 125 nmol/l (app. 50 mg/dl), all due to the decline of estrogens and DHEA. A parallel situation develops in males due to the drop in testosterone. For this reason, it may be necessary to re-check Lp(a) once after the fourth decade of life if you've had a level checked in your younger years.

This opens up some interesting therapeutic possibilities. If receding hormones are responsible for unleashing Lp(a), hormones can be replenished to reduce it. In males, this is relatively straightforward: supplement human testosterone and Lp(a) drops about 25%.

In women, however, it's a bit murkier, thanks to the negative experince reported using horse estrogens (AKA Premarin) in the HERS Trial and Women's Health Initiative. You'll recall that women who take horse estrogens and progestins (synthetic progesterone) do not experience less heart attack and develop a slightly increased risk of endometrial and breast cancer. There was, however, a poorly-publicized sub-study that showed that women with Lp(a) experience up to 50% fewer heart attacks on the horse/synthetic combination.

Wouldn't it be nice to have a large trial examining the safety/advisability of human estrogens and progesterone? To my knowledge, no such confident study in a significant number of women exists, since there's so little money to be made with human hormonal preparations.

For these reasons, we use lots of DHEA, generally at doses of 25 to 50 mg per day. It makes most people feel good, boosts energy modestly, increases muscle, and reduces Lp(a) up to 18% in women, a lesser quantity in men.

Stents, defibrillators, and other profit-making opportunities

As a practicing cardiologst, every day I receive a dozen or more magazines or newspapers targeting practicing physicians, not to mention the hundreds of letters, postcards, invitations to "talks", etc. that I receive. All of these materials share one common goal: To get the practicing cardiologist/physician to insert more of a manufacturer's stents, defibrillators, prescribe more of their drugs, etc.

This is a highly effective and profitable area. Pfizer's Lipitor, for instance, generated $12.2 billion just last year alone. This kind of money will fund an extraordinary amount of marketing.

I'm on the www.heart.org mailing list, a website for cardiologists. I'd estimate that 90% or more of their content is device-related: discussions of situations in which to insert stents, the expanding world of implantable devices, the ups and downs of various drugs. Rarely are discussions of healthy lifestyles, exercise, nutritional supplements, part of the dialogue.

How can you protect yourself from the brainwashed physician, flooded with visions of all the devices he can put in you, all the drugs that can "cure" your disease? Simple: information. Be better informed. Ask pointed questions. The idiotic lay press tells you to ask a doctor about his education. That's not generally the problem. Some of the best educated doc's I know are also the most flagrantly guilty of profiteering medicine.

Ask your doctor about his/her philosphy about the use of medications, devices, etc. If their word is God, take it or leave it, run the other way.

Will radiation kill you?

Several people have asked me lately if radiation is truly dangerous. These conversations were sparked by an editorial comment made on a column I wrote for Life Extension Magazine's April, 2006 issue on "Three ways to detect hidden heart disease".

Among the methods that were discussed in this piece was, of course, CT heart scanning. Anyone who is involved with CT heart scans Quickly recognizes the spectacular power of this test to uncover hidden, unsuspected heart disease, literally within seconds. In 2006, there's really nothing like it for the every day person to have hidden heart disease detected and precisely quantified.

Yet, the "rebuttal" to my article claimed that the broad use of heart scans was only my personal view and that, in truth, radiation kills people.

NONSENSE! If an ovarian cancer is discovered by a CT scan of the abdomen, is that unwise use of radiation? If pneumonia or lung cancer is discovered on a chest x-ray with minimal radiation exposure, have we performed a disservice. Of course not. In fact, these are often lifesaving applications of radiation.

Can radiation be used unwisely with excessive exposure? Of course. The 64 slice CT angiograms are just an example of this. Dr. Mehmet Oz announced on Oprah recently that this was a test to be used for broad screening of women for heart disease. This is wrong. The radiation required for a full 64 slice CT angiogram test is truly excessive for a screening application. You wouln't want to get breast cancer from your mammogram, would you? The radiation from a 64-slice CT angiogram is similar to that of a heart catheterization in the hospital--too much for screening. This is not to be confused with a CT heart scan for a calcium score performed on a 64 slice device. I think this can be performed with acceptable radiation exposure.

Think about what would happen, for instance, if you had your heart disease undetected, had a heart attack, and went to the hospital? During your hospitalization, you'd likely get five chest x-rays, a heart catheterization, perhaps one or more nuclear imaging tests, maybe even a full CT scan (with far more radiation than a screening heart scan). The amount of radiation of a heart scan is trivial compared to what you obtain in a hospital.

So take it all in perspective. The low level of radiation required for a simple heart scan (not an angiogram) does not by itself substantially add to your lifetime risk of radiation exposure. It may, in fact, save your life or reduce your life long exposure to radiation.

Are you using bogus supplements?

I consider nutritional supplements an important, many times a critical,part of a coronary plaque control program.

But use the wrong brand or use it in the wrong way, and you can obtain no benefit. Occasionally, you can even suffer adverse effects.

Take coenzyme Q10, for instance. (Track Your Plaque Members: A full, in-depth Special Report on coenzyme Q10 will be on the website in the next couple of weeks.) Take the wrong brand to minimize the likelihood of statin-related muscle aches, and you may find taking Lipitor, Zocor, Crestor, etc. intolerable or impossible. However, take a 100 mg preparation from a trusted manufacturer in an oil-based capsule, and you are far more likely to avoid the inevitable muscle aches. (Though, of course, consult with your doctor, for all it's worth, if you develop muscle aches on any of these prescription agents.)

Unfortunately, you and I often don't truly know for a fact if a bottle from the shelf of a health food store or drugstore is accurately labeled, pure, free of contaminants, and efficacious.

One really great service for people serious about supplements is the www.consumerlab.com website. They are a membership website (with dues very reasonable) started by a physician interested in ensuring supplement quality. Consumer Lab tests nutritional supplements to determine whether it 1) contains what the label claims, and 2) is free of contamination. (I have no reason to pitch this or any other site; it's just a great service.) They recently found a supplement with Dr. Andrew Weil's name on it to have excess quantities of lead!

What Consumer Lab does not do is determine efficacy. In other words, they do a responsible job of reporting on what clinical studies have been performed to support the use of a specific supplement. However, true claims of efficacy of supplement X to treat symptom or disease Y can only come with FDA approval. Supplements rarely will be put through the financial rigors of this process.

If you're not a serious supplement user, but just need a reliable source, we've had good experiences with:

--GNC--the national chain
--Vitamin Shoppe--also a national chain
--www.lifeextension.com or www.lef.org--A great and low-priced source, but they do charge a $75 annual membership that comes with a subscription to their magazine, Life Extension (which I frequently write for) and several free supplements that you may or may not need. Again, I'm not pitching them; they are simply a good source.
--Solgar--a major manufacturer
--Vitamin World
--Nature's Bounty
--Sundown

There are many others, as well. Unfortunately, it's only the occasional manufacturer or distributor that permits unnacceptable contamination with lead or other poisons, or inaccurately labels their supplement (e.g., contains 1000 mg of glucosamine when it really contains 200 mg). I have not come across any manufacturer/distributor who has systemtically marketed uniformly bad products.

It really helps to have someone to lean on

Among my patients are several husband and wife teams, both of whom have heart disease by some measure. Several couples, for instance, consist of a huband who's received a stent, survived a heart attack, or has some other scar of the conventional approach. The wives generally have a substantial heart scan score in the several hundred range.

There are a few couples for which the roles are reversed: wife with bypass, heart attack, etc. and husband with a substantial quantity of coronary plaque by CT heart scan.

From them all, however, I've learned the power of teamwork. When both wife and husband (or even "significant other") are committed to the effort of controlling or reversing heart disease risk, the likelihood of success is magnified many-fold. Everything is easier: shopping for and choosing foods, incorporating supplements in the budget, taking vacations with a healthy focus, following through and sticking with your program.

Several of the couples have succeeded in obtaining regression of plaque for both man and woman. Both have reduced their heart scan scores and, as a result, dramatically reduced the potential for future heart attack and procedures.

Unfortunately, I will also see the opposite situation: One spouse committed to the program but the other indifferent. They may say such things as "You can't control what happens in the future." Or, "There's no way you can get rid of risk for heart disease. My doctor says it's hereditary." Or, "I've eaten this way since I was a kid. I'm not changing now for you or for anybody else."

Such negative commentary can't help but erode your commitment to health. Most of us recognize these sorts of comments as self-fulfulling and self-defeating.

What should you do if you have an unsupportive partner? Not easy. But it really can help to seek out a supportive partner, whether it's a friend, relative, or other significant person in your life. Of course, not everybody can find such a person. Perhaps that's another way our program can help.

I'd like to hear from anyone who does obtain substantial support of someone close, or if you are struggling to do so.

Five foods that can booby trap your heart disease prevention program

There are several foods that commonly come up on people's lists of habitual foods that are truly undesirable for a heart disease prevention program. Curiously, people choose these foods because of the mis-perception that they are healthy. My patients are often shocked when I tell them that they are not healthy and are, in fact, detrimental to their program.

I'm not talking about foods that are obviously unhealthy. You know these: fried foods, greasy cheeseburgers, French fries, bacon, sausage, etc. Nearly everyone knows that the high saturated fat content, low fiber, and low nutritional value of these foods are behind heart disease, hypertension, and a variety of cancers.

I'm talking about foods that people say they eat because they view them as healthy--but they're not.

Here's the list:

1) Low-fat or non-fat salad dressings--Virtually all brands we've examined have high-fructose corn syrup as one the main ingredients. What does high fructose corn syrup do? Triggers sugar cravings, makes your triglycerides skyrocket (causing formation of abnormal lipoproteins like small LDL), and causes diabetes. The average American now ingests nearly 80 lbs of this evil sweetener per year. You're far better off with olive, canol, grapeseed, or flaxseed based salad dressings.

2) Breakfast cereals--If you've been following these discussions, you know that the majority of breakfast cereals are sugar. They may not actually contain sugar, but they contain ingredients that are converted to sugar in your body. They may be cleverly disguised as healthy--Raisin Bran, Shredded Wheat, etc.

3) Pretzels--"A low-fat snack". That's right. A low-fat snack that raises blood sugar like eating table sugar from the bowl.

4) Margarine--Forget this silly argument about which is worse, butter or margarine. Which is worse, strychnine or lead? Both are poisons to the human body. Who cares which is worse? Fortunately, there are now healthy "margarines" like Smart Balance and Benecol that lack the saturated fat or hydrogenated fat of either.

4) Bananas--Bananas are not all that intrinsically unhealthy. The problem is that people will say to me, "Oh sure, I eat fruit. Two bananas a day." What I hear is "I don't really eat fruit with high nutrient value, fiber, and reduced sugar release. I reach for only bananas which yield extreme sugar rises in my blood and are low fiber." Aren't they high in potassium? Yes, but there are better sources. Cut back if you are a banana freak.


Why the mis-perceptions? A holdover from the low-fat diet days and marketing from food manufacturers are the principal reasons. Of course, foods are meant to be enjoyed, but be informed about it. Choose foods for the right reasons, not because of some cleverly-crafted marketing campaign.

Breakfast of champions?

I spend time every day educating or reminding patients that breakfast cereals are not health foods.

I see jaws drop in shock when I tell them that, in my opinion and despite the marketing claims, Cheerios, Raisin Bran, Shredded Wheat, and the like do not yield health benefits. In fact, they do the the opposite: dramatically raise blood sugar and trigger an adverse cascade of events that eventually leads to diabetes and heart disease.

Why the health claims in advertising? Because these products contain insoluble fiber, the sort that makes your bowels regular. Yes, your bowels are important to health, too. But the benefits end there.

Breakfast cereals are a highly refined, processed food that are not good for your plaque control program. What they are is a highly profitable, multi-billion dollar business, deeply entrenched in American culture ("They'rrrre grrrrrreat!"--Tony the Tiger; "There's a whole scoop of raisins in every box of Post Raisin Bran!" Bet you remember them all.)

I find it particularly upsetting when I see the stamp of approval from the American Heart Association on some products. Gee, if the Heart Association says it's good for you, it must be true! Don't you believe it. The American Heart Association relies on corporate donations, just like any other charity.

If you must eat breakfast cereals, refer to www.glycemicindex.com for a full database of glycemic indexes. You can look up a specific product and it will list its glycemic index, or sugar-releasing properties. You should try to keep glycemic index of the foods you choose below 50.

For a revealing discussion of the influence of food marketers on our perceptions of food, see Track Your Plaque nutrition expert, Gay Riley's discussion The Marketing of Food and Diets in America at her website, www.netnutritionist.com.

In heart disease prevention, shoot for perfection

It really struck me today that it's the people who've chosen to compromise their prevention program who end up with trouble--heart procedures, heart attack, even heart failure.

Take Bob, for example. Bob is 73 years old and had a bypass operation in 2000. The procedure went well and Bob enjoyed 6 years of seemingly trouble-free life. Bob had a seriously low HDL cholesterol for which he as taken a modest dose of niacin, but was unwilling to do much more. His HDL cholesterol was thererefore "stalled" at around 40 mg. (We aim for 60 mg or greater.) We talked repeatedly about the options for increasing HDL but Bob was content with his results. After all, since his bypass operation, he'd felt well and could do all he wanted without physical limitation.

But Bob underwent a stress test for surveillance purposes (which we routinely do 5 or more years after bypass surgery). The test was markedly abnormal with two major areas of poor blood flow to his heart (signalling potential heart attack in future). Bob ended up getting 5 stents to salvage two bypass grafts, both of which showed signs of substantial degeneration.

I've seen this scenario repeatedly: A person is unwilling to go the extra mile to obtain perfection in lipid/lipoprotein patterns, lifestyle changes, and taking the basic, required supplements. Compromises eventually catch up to you in the form of another heart attack, more procedures, heart failure, physical disability, even death.

The message: Don't draw compromises in heart disease prevention. Coronary plaque is a chronic process. It will take advantage of you if you ever let your guard down.

The epidemic of small LDL

Of the patients I saw in my office yesterday, virtually EVERYONE had small LDL.

Small LDL is emerging as an extraordinarily prevalent lipoprotein pattern that drives coronary plaque growth. Previous estimates have put small LDL as affecting only 20-30% of people with coronary disease. However, in my experience in the last few years, I would estimate that greater than 80% of people with measurable coronary plaque have small LDL.

If you have a heart scan score >zero, chances are you have it, too.

I call small LDL a "modern" disease because it has skyrocketed in prevalence recently because of the great surge in inactivity in Americans.

When's the last time you walked to the grocery store and back, lugging two bags of groceries? How many years has it been since you've push-mowed your lawn? All the small conveniences of life have permeated further and further into our activities. Most of us spend the great majority of our day right where you are now--on your duff.

On the bright side, small LDL in most people is reducable by simply getting up and going. But the old teaching of 30 minutes of activity per day is now outdated. This was true when the other hours of your life included physical activities, like housework or a moderately active job. However, if the other 23 1/2 hours of your day are sedentary, then 30 minutes a day won't do it. An hour or more of activity, whether exercise or physical labor of some variety will get you better small LDL-suppressing results.

For most people with small LDL, fish oil and niacin are also necessary to fully suppress small LDL to the Track Your Plaque goal of <10 mg/dl.

A great discussion on vitamin D

If you need better convincing that vitamin D is among the most underappreciated but crucial vitamins for health, see Russell Martin's review of vitamin D and its role in cancer prevention. You'll find it in March, 2006 Life Extension Magazine or their www.LEF.org website at:

http://search.lef.org/cgi-src-bin/MsmGo.exe?grab_id=0&page_id=1308&query=vitamin%20d&hiword=VITAM%20VITAMER%20VITAMERS%20VITAMI%20VITAMINA%20VITAMINAS%20VITAMINC%20VITAMIND%20VITAMINE%20VITAMINEN%20VITAMINES%20VITAMINIC%20VITAMINK%20VITAMINS%20d%20vitamin%20

Our preliminary experience over the past year suggests that vitamin D may be the crucial missing link in many people's plaque control program. We've had a handful of people who, despite an otherwise perfect program (LDL<60, HDL>60, etc.; vigorous exercise, healthy food selection, etc.--I mean perfect)continued to show plaque growth. The rate of growth was slower than the natural expected rate of 30% per year, but still frightening rates of 14-18% per year--until we added vitamin D. All of a sudden, we saw dramatic regression of 7-25% in 6 months to a year.

This does not mean that vitamin D all by itself regresses plaque. I believe it means that vitamin D exerts a "permissive" effect, allowing all the other treatments (fish oil, LDL reduction, HDL raising, correction of small LDL, etc.) to exert their full benefit. So please don't stop everything and just take D. This will not work. However, adding vitamin D to your program on top of the basic Track Your Plaque approach--that's the best way I know of.

MSNBC Report: We need more heart procedures!

A recent headline from MSNBC by Robert Bazell reads:

NEW YORK - Angioplasty, bypass surgery and cholesterol-lowering medications are among the many interventions that have brought a sharp decrease in heart disease deaths in recent years. But, as Dr. Sharon Hayes of the Mayo Clinic points out, there is one big problem.

“The death rates in women have not declined as much as they have in men,” she says.

The piece goes on to suggest that women are getting short-ended in the diagnosis of heart symptoms and heart attack. The solution: More testing to assess the need for procedures like bypass.

This is typical of the device and medication-dominated media consciousness: More procedures, more medication, more devices. Who's paying for advertising, after all? The money at stake is huge. But is this what you want?

Don't be swayed by media reporters with limited understanding of the real issues (at best), consciousness of who's paying for advertising (at worst). Yes, heart disese is often underestimated or misdiagnosed in women. The answer is better detection earlier in life followed by efforts to halt the process--effective, safe treatments for people's benefit, not just profit.

Put lipstick on a dwarf

Today, virtually all wheat products are produced from the Triticum aestivum dwarf mutant.

You might call it "multi-grain bread,""oat bread," or "flaxseed bread." You could call it "organic," "pesticide-free," "non-GMO," or "no preservatives." It might be shaped into a ciabatta, bruschetta, focaccia, or panini. It might be sourdough, unleavened, or sprouted. It could be brown, black, Pumpernickel, or white. It could be shaped into a roll, bun, bagel, pizza, loaf, pretzel, cracker, pancake, brioche, baguette, or pita. It could be matzah, challah, naan, or Communion wafers.

No matter what you call it, it's all the same. It's all from the dwarf mutant Triticum aestivum plant, the 18-inch tall product of hybridizations, backcrossings, and introgressions that emerged from genetics research during the 1960s and 70s.

According to Dr. Allan Fritz, Professor of Wheat Breeding at Kansas State University, and Dr. Gary Vocke at the USDA, over 99% of all wheat grown today is the dwarf variant of Triticum aestivum. (For you genetics types, Triticum aestivum is the hexaploid, i.e., 3 combined genomes, product of extensive hybridizations, while ancestral einkorn is a diploid, i.e., a single genome, grass. Hexaploid Triticum aestivum contains the especially hazardous "D" genome, the set of genes most commonly the recipient of genetic manipulations to modify the characteristics of flour, such as gluten content. Einkorn contains only the original "A" genome.)

No matter what you call it, add to it, how you shape it, etc., it's all the same. It's all the dwarf mutant product of tens of thousands of hybridizations.

You can put lipstick on a pig, but it's still a pig. By the way, lipstick may contain wheat.

What the Institute of Medicine SHOULD have said

The news is full of comments, along with many attention-grabbing headlines, about the announcement from the Institute of Medicine that the new Recommended Daily Allowance (RDA) for vitamin D should be 600 units per day for adults.

What surprised me was the certainty with which some of the more outspoken committee members expressed with their view that 1) the desirable serum 25-hydroxy vitamin D level was only 20 ng/ml, and 2) that most Americans already obtain a sufficient quantity of vitamin D.

Here's what I believe the Institute of Medicine SHOULD have said:

Multiple lines of evidence suggest that there is a plausible biological basis for vitamin D's effects on cancer, inflammatory responses, bone health, and metabolic responses including insulin responsiveness and blood glucose. However, the full extent and magnitude of these responses has not yet been fully characterized.

Given the substantial observations reported in several large epidemiologic studies that show an inverse correlation between 25-hydroxy vitamin D levels and mortality, there is without question an association between vitamin D and mortality from cancer, cardiovascular disease, and all cause mortality. However, it has not been established that there are cause-effect relationships, as this cannot be established by epidemiologic study.

While the adverse health effects of 25-hydroxy vitamin D levels of less than 30 ng/ml have been established, the evidence supporting achieving higher 25-hydroxy vitamin D levels remains insufficient, limited to epidemiologic observations on cancer incidence. However, should 25-hydroxy vitamin D levels of greater than 30 ng/ml be shown to be desirable for ideal health, then vitamin D deficiency has potential to be the most widespread deficiency of the modern age.

Given the potential for vitamin D's impact on multiple facets of health, as suggested by preliminary epidemiologic and basic science data, we suggest that future research efforts be focused on establishing 1) the ideal level of 25-hydroxy vitamin D levels to achieve cancer-preventing, bone health-preserving or reversing, and cardiovascular health preventive benefits, 2) the racial and genetic (vitamin D receptor, VDR) variants that may account for varying effects in different populations, 3) whether vitamin D restoration has potential to exert not just health-preserving effects, but also treatment effects, specifically as adjunct to conventional cancer and osteoporosis therapies, and 4) how such vitamin D restoration is best achieved.

Until the above crucial issues are clarified, we advise Americans that vitamin D is a necessary and important nutrient for multiple facets of health but, given current evidence, are unable to specify a level of vitamin D intake that is likely to be safe, effective, and fully beneficial for all Americans.


Instead of a careful, science-minded conclusion that meets the painfully conservative demands of crafting broad public policy, the committee instead chose to dogmatically pull the discussion back to the 1990s, ignoring the flood of compelling evidence that suggests that vitamin D is among the most important public health issues of the age.

Believe it or not, this new, though anemic, RDA represents progress: It's a (small) step farther down the road towards broader recognition and acceptance that higher intakes (or skin exposures) to achieve higher vitamin D levels are good for health.

My view: Vitamin D remains among the most substantial, life-changing health issues of our age. Having restored 25-hydroxy vitamin D levels in over 1000 people, I have no doubt whatsoever that vitamin D achieves substantial benefits in health with virtually no downside, provided 25-hydroxy vitamin D levels are monitored.

Coronary calcium: Cause or effect?

Here's an interesting observation made by a British research group.

We all know that coronary calcium, as measured by CT heart scans, are a surrogate measure of atherosclerotic plaque "burden," i.e., an indirect yardstick for coronary plaque. The greater the quantity of coronary calcium, the higher the heart scan "score," the greater the risk for heart attack and other unstable coronary syndromes that lead to stents, bypass, etc.

But can calcium also cause plaque to form or trigger processes that lead to plaque formation and/or instability?

Nadra et al show, in an in vitro preparation, that calcium phosphate crystals are actively incorporated into inflammatory macrophages, which then trigger a constellation of inflammatory cytokine release (tumor necrosis factor-alpha, interleukins), fundamental processes underlying atherosclerotic plaque formation and inflammation.

Here's the abstract of the study:
Proinflammatory Activation of Macrophages by Basic Calcium Phosphate Crystals via Protein Kinase C and MAP Kinase Pathways:

A Vicious Cycle of Inflammation and Arterial Calcification?


Basic calcium phosphate (BCP) crystal deposition underlies the development of arterial calcification. Inflammatory macrophagescolocalize with BCP deposits in developing atherosclerotic lesionsand in vitro can promote calcification through the release of TNF alpha. Here we have investigated whether BCP crystals can elicit a proinflammatory response from monocyte-macrophages.BCP microcrystals were internalized into vacuoles of human monocyte-derived macrophages in vitro. This was associated with secretion of proinflammatory cytokines (TNF{alpha}, IL-1ß and IL-8) capable of activating cultured endothelial cells and promoting capture of flowing leukocytes under shear flow. Critical roles for PKC, ERK1/2, JNK, but not p38 intracellular signaling pathways were identified in the secretion of TNF alpha, with activation of ERK1/2 but not JNK being dependent on upstream activation of PKC. Using confocal microscopy and adenoviral transfection approaches, we determined a specific role for the PKC-alpha isozyme.

The response of macrophages to BCP crystals suggests that pathological calcification is not merely a passive consequence of chronic inflammatory disease but may lead to a positive feed-back loop of calcification and inflammation driving disease progression.



This observation adds support to the notion that increasing coronary calcium scores, i.e., increasing accumulation of calcium within plaque, suggests active plaque. As I say in Track Your Plaque, "growing plaque is active plaque." Active plaque means plaque that is actively growing, inflamed and infiltrated by inflammatory cells like macrophages, eroding its structural components, and prone to "rupture," i.e., cause heart attack. Someone whose first heart scan score is, say, 100, followed by another heart scan score two years later of 200 is exposed to sharply increasing risk for cardiovascular events which may, in part, be due to the plaque-stimulating effects of calcium.

Conversely, reducing coronary calcium scores removes a component of plaque that would otherwise fuel its growth. So, people like our Freddie, who reduced his heart scan score by 75%, can be expected to enjoy a dramatic reduction of risk for cardiovascular events.

Less calcium, less plaque to rupture, less risk.

Wheat one-liners

If you're having difficulty convincing a loved one or someone else that wheat should be eliminated from the human diet, here are some useful one-liners to use:

Wheat makes your boobs big.
(This is true. Priceless for women to use on their husbands.)

Wheat causes dementia.
(And confirmed on examination of brain tissue at autopsy. Yes, autopsy.)

Wheat makes you look pregnant.
(The visceral fat of a wheat belly does a darn good imitation of a near-term infant.)

The first sign of wheat intolerance can be wetting your pants.
(Cerebellar ataxia, i.e., destruction and atrophy of the cerebellum, caused by wheat leads to loss of coordination and bladder control. Average age of onset: 53 years old.)

White flour bad, whole grain better; just as Marlboros are bad, Salems are better.
(The flawed syllogism that led to the "eat more healthy whole grain" colossal blunder.)

Wheat is the only food with its very own mortality rate.
(Celiac disease, osteoporotic hip fractures, and the neurologic diseases triggered by wheat can be fatal.)

"Wheat" is no longer wheat; it's the dwarf mutant that came from genetics research in the 1960s.
(Over 99% of all wheat today comes from the 18-inch tall dwarf mutant.)

Wheat increases blood sugar higher than nearly all other foods.
(Higher than Milky Way bars, higher than Snickers bars, higher than table sugar.)


There you have it: A full arsenal of one-liners to shoot at your husband, wife, or friend when they roll their eyes at your refusal to consume this thing called "wheat."

The happy homeotherm

If you were a "cold blooded" poikilotherm unable to regulate internal body temperature, you would have to sun yourself on rocks to raise your body temperature, just like turtles and snakes. When it got cold, your metabolic rate would slow and you might burrow into the mud to hide.

You and I, however, are homeotherms, terrestrial animals able to regulate our own internal body temperature. Principal responsibility for keeping your body temperature regulated falls with the thyroid gland, your very own thermoregulatory "thermostat."

But internal body temperature, even in a homeotherm, varies with circadian rhythm: Highest temperature occurs in the early evening around 8 p.m.; the low temperature nadir occurs at around 4 a.m.

The notion that normal human temperature is 98.6 degrees Fahrenheit is a widely-held fiction, a legacy of the extraordinary experience of 19th century German physician, Carl Reinhold August Wunderlich, who claims to have measured temperatures of one million people using his crude, uncalibrated thermometer to obtain axillary (armpit) body temperatures.

Dr. Broda Barnes was a 20th century American proponent of using the nadir body temperature to gauge thyroid function. Like Wunderlich, Barnes also used axillary temperatures.

Modern temperature assessments have employed radiotransmitting thermistors that are swallowed, with temperatures tracked as the thermistor travels through the stomach, duodenum, small intestine, large intestine, rectum, then peek-a-boos back out. Such internal "core temperature" assessments have shown that:

--Axillary temperatures do not track with internal core temperatures very well, often veering off course due to external factors.
--Axillary temperatures are subject to ambient temperatures, such as room temperature, and are affected by clothing.
--Axillary temperatures are more susceptible to physical activity, e.g., increased with exercise or physical work.

Even right vs. left axillary temperatures have been shown to vary up to 2 degrees Fahrenheit.

Studies such as this demonstrate that normal oral temperature upon arising is around 97.2-97.3 degrees Fahrenheit. While we lack data correlating thyroid function with circadian temperature variation, the a.m. nadir does indeed, as Dr. Barnes originally suggested, seem to track thyroid status quite well: lower with hypothyroidism, higher with normal or hyperthyroidism.

I have been using 97.3 degrees F orally as the cutoff for confirming or uncovering thyroid dysfunction, particularly when symptoms or blood tests (TSH, free T3, free T4) are equivocal, a value that has held up well in the majority of cases. I find it helpful when, for instance, someone complains of cold hands and feet and has normal TSH (1.5 mIU/L or less in my view) but low free T3. An a.m. oral temperature of, say, 95.7 degrees F, suggests that there will be a favorable response to T3 supplementation. And it nearly always plays out that way.

Wouldn't it be interesting to know if there was insight into thyroid status provided by also examining the circadian behavior of temperature (e.g., height or timing of the peak)?

Statin buster?

Merck recently reported preliminary results with its drug-in-development, anacetrapib.

After six months of treatment, participants showed:

LDL cholesterol was reduced from 81 mg/dl to 45 mg/dl in those taking anacetrapib, and from 82 mg/dl to 77 mg/dl in the placebo group.

HDL increased from 41 mg/dl to 101 mg/dl in the drug group, from 40 mg/dl to 46 mg/dl in those on placebo.

As you'd expect, the usual line-up of my colleagues gushed over the prospects of the drug, salivating over new speaking opportunities, handsomely-paid clinical "research" trials, and plenty of nice trips to exotic locales.

Anacetrapib is a cholesteryl-ester transfer protein inhibitor, or CETP inhibitor, much like its scrapped predecessor, torcetrapib . . . you know, the one that went down in flames in 2006 after 60% excess mortality occurred in people taking the drug compared to placebo. The hopes of many investors and Pfizer executives were dashed with torcetrapib's demise. The data on torcetrapib's lipid effects were as impressive as Merck's anacetrapib.

These drugs block the effects of the CETP enzyme, an enzyme with complex effects. Among CETP's effects: mediating the "heteroexchange" of triglycerides from triglyceride-rich VLDL particles that first emerge from the liver for cholesterol from LDL particles. This CETP-mediated process enriches LDL particles with triglycerides, which then make LDL a target for action by another enzyme, hepatic lipase, that removes triglycerides. This yields a several nanometer smaller LDL particle, now the number one most common cause of heart disease in the U.S., thanks to conventional advice to cut fat intake and increase consumption of "healthy whole grains."

With effects like this, anacetrapib, should it hold up under the scrutiny of FDA-required trials and not show the same mortality-increasing effects of torcetrapib, will be a huge blockbuster for Merck if release goes as scheduled in 2015. It will likely match or exceed sales of any statin drug. Statin drugs have achieved $27 billion annual sales, some of it deserved. Anacetrapib will likely handily match or exceed Lipitor's $12 billion annual revenue.

More than increasing HDL, CETP inhibition is really a strategy to reduce small LDL particles.

As with many drugs, there are natural means to achieve similar effects with none of the side-effects. In this case, similar effects to CETP inhibition, though with no risk of heightened mortality, is . . . elimination of wheat, in addition to an overall limitation of carbohydrate consumption. Not just low-carb, mind you, but wheat elimination on the background of low-carb. For instance, eliminate wheat products and limit daily carbohydrate intake to 50-100 grams per day, depending on your individual carbohydrate sensitivity, and small LDL drops 50-75%. HDL, too, will increase over time, not as vigorously as with a CETP inhibitor, but a healthy 20-30% increase, more with restoration of vitamin D.

Eliminating wheat and adjusting diet to ratchet down carbs is, of course, cheap, non-prescription, and can be self-administerd, criteria that leave the medical world indifferent. But it's a form of "CETP inhibition" that you can employ today with none of the worries of a new drug, especially one that might share effects with an agent with a dangerous track record.

Why does wheat cause arthritis?

Wheat causes arthritis.

Before you say "What the hell is he saying now?", let me connect the dots on how this ubiquitous dietary ingredient accelerates the path to arthritis in its many forms.

1) Wheat causes glycation--Glycation is glucose-modification of proteins in the body that occurs when blood glucose exceeds 100 mg/dl. Cartilage cells are especially susceptible to glycation. The cartilage cells you had at age 18 are the very same cartilage cells you have at age 60, since they lack the ability to reproduce and repair themselves. Proteins in cartilage are highly susceptible to glycation, which makes them stiff and brittle. Stiff, brittle cartilage loses its soft, elastic, lubricating function. Damaged cartilage cells don't regenerate nor produce more protective proteins. This allows destruction of cartilage tissue, inflammation, and, eventually, bone-on-bone arthritis.

Because wheat, even whole wheat, sends blood sugar higher than almost all other foods, from table sugar to Snickers bars, glycation occurs after each and every slice of toast, every whole wheat bagel, every pita wrap.

2) Wheat is acidifying--Humans are meant to consume a diet that is net alkaline. While hunter-gatherers who consume meat along with plentiful vegetables and fruits live a net alkaline diet (urine pH 7 to 9), modern humans who consume insufficient vegetables and too much grain (of which more than 90% is usually wheat) shift the body towards net acid (urine pH 5 to 7). Wheat is The Great Disrupter, upsetting the normal pH balance that causes loss of calcium from bones, resulting in decalcification, weakness, arthritis and osteoporotic fractures.

3) Wheat causes visceral fat--The extravagant glucose-insulin surges triggered by wheat leads to accumulation of visceral fat: wheat belly.

Visceral fat not only releases inflammatory mediators like tumor necrosis factor and various interleukins, but is also itself inflamed. The inflammatory hotbed of the wheat belly leads to inflammation of joint tissues. This is why overweight and obese wheat-consuming people have more arthritis than would be explained by the burden of excess weight: inflammation makes it worse. Conversely, weight loss leads to greater relief from arthritis pain and inflammation than would be explained by just lightening the physical load.

We need a name for this wheat effect. How about "bagel bones"?

Why do morphine-blocking drugs make you lose weight?

Naloxone (IV) and naltrexone (oral) are drugs that block the action of morphine.

If you were an inner city heroine addict and got knifed during a drug deal, you'd be dragged into the local emergency room. You're high, irrational, and combative. The ER staff restrain you, inject you with naloxone and you are instantly not high. Or, if you overdosed on morphine and stopped breathing, an injection of naloxone would reverse the effect immediately, making you sit bolt upright and wondering what the heck was going on.

So what do morphine-blocking drugs have to do with weight loss?

An odd series of clinical studies conducted over the past 40 years has demonstrated that foods can have opiate-like properties. Opiate blockers, like naloxone, can thereby block appetite. One such study demonstrated 28% reduction in caloric intake after naloxone administration. But opiate blocking drugs don't block desire for all foods, just some.

What food is known to be broken down into opiate-like polypeptides?

Wheat. On digestion in the gastrointestinal tract, wheat gluten is broken down into a collection of polypeptides that are released into the bloodstream. These gluten-derived polypeptides are able to cross the blood-brain barrier and enter the brain. Their binding to brain cells can be blocked by naloxone or naltrexone administration. These polypeptides have been named exorphins, since they exert morphine-like activity on the brain. While you may not be "high," many people experience a subtle reward, a low-grade pleasure or euphoria.

For the same reasons, 30% of people who stop consuming wheat experience withdrawal, i.e., sadness, mental fog, and fatigue.

Wouldn't you know that the pharmaceutical industry would eventually catch on? Drug company startup, Orexigen, will be making FDA application for its drug, Contrave, a combination of naltrexone and the antidepressant, buproprion. It is billed as a blocker of the "mesolimbic reward system" that enhances weight loss.

Step back a moment and think about this: We are urged by the USDA and other "official" sources of nutritional advice to eat more "healthy whole grains." Such advice creates a nation of obese Americans, many the unwitting victims of the new generation of exorphin-generating, high-yield dwarf mutant wheat. A desperate, obese public now turns to the drug industry to provide drugs that can turn off the addictive behavior of the USDA-endorsed food.

There is no question that wheat has addictive properties. You will soon be able to take a drug to block its effects. That way, the food industry profits, the drug industry profits, and you pay for it all.

Heart scan tomfoolery 2

In the last Heart Scan Blog post, I discussed the significance of the apparent discrepancy between Steve's heart scan score and volume score. This post addresses his second question, also a FAQ about heart scan scores.

Steve noted that his second scan compared to his first showed:

- Left Main volume went up from 22.4 to 35.6
- LAD went down from 95.2 to 91.3
- LCX volume went down from 23.2 to 0
- RCA volume went up from 0 to 9.3

So there are apparent divergences in behavior in the left main that increased and both LAD (left anterior descending) and LCX (left circumflex) that decreased.

The explanation is simple: When heart scans are "scored," they are viewed in horizontal "slices." When the heart is viewed as horizontal slices, the LAD and LCX originate from the common left main stem. In other words, it's like a tree with the left mainsteam representing the trunk, the LAD and LCX representing two main branches.

Plaque can form, obviously, in all three arteries, but it can do so by starting in the left main, for instance, and extending into either the LAD or LCX, or both. The left main plaque can therefore bridge any 2 or all 3 arteries.

When the plaque is "scored" by taking the computer mouse and circling the calcified plaque in question (to allow the computer program to generate the calcium score and volume score of that particular plaque), the plaque that may extend from left main into the LAD and/or LCX might be labeled "left main," or it might be labeled "LAD" or "LCX." There is no reliable way to "dissect" apart the plaque into the three arteries, since the plaque is coalescent and continuous. So the scoring technologist or physician simply arbitrarily declares the artery "LAD," for instance.

The problem comes when two different interpretation methods are used: Perhaps it's a new technologist or physician, or there was no attention paid to how the previous scan was read. One reader calls it "left main" and the next calls it "LCX."

So the apparent discrepancy has to do with flaws in the methods of segregating plaque location, as well as inattention to scoring techniques. The total score, however, remains unaffected.

Nonetheless, Steve has enjoyed a modest reduction in the score of the left main/LAD/LCX from his original 140.8 down to a second left main/LAD/LCX score of 126.9.

The right coronary artery (RCA), however, is not subject to this difficulty and Steve score shows a modest increase in score. (Why the divergent behavior between left main/LAD/LCX and RCA? There is no clear explanation for this, unfortunately.)

All in all, the news for Steve is good: He achieved these results on his own using nutritional techniques. Because he, in all practicality, stopped the progression of his heart scan score and avoided the "natural" rate of increase of 30% per year, all he needs to do is "tweak" his program a bit to achieve reversal, i.e., reduction of score.


Here's an image from another previous Heart Scan Blog post (about the relationship of osteoporosis and coronary disease) that shows such a plaque that starts in the left mainstem yet extends into both the LAD and LCX:

Heart scan tomfoolery

Heart Scan Blog reader, Steve, sent these interesting questions about his heart scan experience. (I sometimes forget that this blog is called "The Heart Scan Blog" and was originally--several years ago--meant to discuss heart scans. It has evolved to become a much broader conversation.)

The answers are a bit lengthy, so I'll tackle Steve's questions in two parts, the second in another blog post.

Dr. Davis,

I had a heart scan last year. The score was 96. While not a horrible score, it
was a wake up call, and I changed my lifestyle.

I had another scan this year and the heart scan score went up to 105, but the
volume score went down from 141 to 136.

The report I received said this:

'The calcium volume score is less in the current study as compared with the
original or reference study. This is an excellent coronary result and indicates
that there has been a net decrease in coronary plaque burden. The current
prevention program is very effective and should be continued.'

This is all well and good, but I have two questions:

1. Am I really going in the right direction even though the heart scan score
went up 9%?

2. Here are results that make no sense to me:
- Left Main volume went up from 22.4 to 35.6
- LAD went down from 95.2 to 91.3
- LCX volume went down from 23.2 to 0
- RCA volume went up from 0 to 9.3

Why would there be so much variation from year to year, and why would the plaque
move from site to site?

Steve


Questions like Steve's come up with some frequency, so I thought it would be worthwhile to discuss in a blog post.

First of all, the conventional heart scan score, or "calcium score" or "Agatston score" (after Dr. Arthur Agatston, developer of the simple algorithm for calcium scoring, as well as South Beach Diet fame), is the product of the area of the plaque in a single CT "slice" image
multiplied by a density coefficient, i.e., a number ranging from 1 to 4 that grades the x-ray density of the plaque. (1 is least dense; 4 is most dense.) A density coefficient of 1 therefore signifies some calcium within plaque, with higher density coefficients signifying increasing calcium content and density. Incidentally, "soft" plaque, i.e., non-calcified, would fall in the less than 1 range, even the negative range (fatty tissue within plaque).

The volume, or "volumetric," score is the brainchild of Drs. Paulo Raggi and Traci Callister, who expressed concern that, if we cause plaque to shrink in volume, the density coefficient used to calculate the calcium score would increase (since they believed that calcium could not be reduced, contrary to our Track Your Plaque experience, thereby leading to misleading results. They therefore developed an algorithm that did not rely on density coefficients, but used the same two-dimensional area obtained in the standard heart scan score, but replaced the density coefficient with a (mathematically interpolated) vertical axis (z-axis) measure of plaque "height." This 3-dimensional volumetric value therefore provided a method to generate a measure of calcium volume. In their original publication, the volume score proved more reproducible than the standard calcium score. This way, any reduction in plaque volume would not be influenced by the misleading effects of calcium density, but reflect a real reduction in volume.

Callister and Raggi's study also highlighted that calcium scoring in any form is subject to variability. Back in 1998 (when their study was published), there was a bit more variation than today due to the image acquisition methods used. But, even today, there is about 9% variation in scoring even if performed repeatedly (with less percentage variation the higher the score).

Unfortunately, volume scoring never caught on and the calcium score has been the most commonly used value by most heart scan centers and in most clinical studies. And, in all practicality, the two values nearly always track together: When calcium score increases, volume score increases in tandem; when calcium score decreases, volume score decreases in tandem.

Steve is therefore an exception to the general observation that calcium score and volume score travel together. Steve's calcium score increased, while his volume score decreased. From the above discussion, you can surmise a few things about Steve's experience:"

1) In all likelihood, the changes in both calcium score and volume score could simply be due to variability, i.e., variation in the placement of his body on the scan table, variation in position of the heart, variation in data acquisition, etc. There is a high likelihood that neither value changed; both are essentially unchanged.

2) If the changes are not due to scan variability, but are real, then it could be that the calcified plaque is reduced in volume but increased in density. If true, this is probably still a favorable phenomenon, since plaque volume is a powerful predictor of coronary "events" and an increase in plaque density is likely a benign phenomenon. It would also raise questions about the adequacy of vitamin D and vitamin K2 status, both major control factors over calcium deposition and metabolism.

So, in all likelihood, Steve's apparent discrepant results are modest good news, especially since calcium scores can ordinarily be expected to increase at the rate of 30% per year if no action is taken. Experiencing no change in score, calcium or volumetric, carries a very excellent prognosis, with risk for heart attack approaching zero. (I'm impressed that Steve accomplished this on his own, something the majority of my colleagues haven't the least bit of interest doing.)

Part 2 of Steve's question will be tackled in a separate post.

Restaurant eating: A fructose landmine

There is no remaining question that fructose is among the worst possible things humans can consume.

Followers of the Heart Scan Blog already know this, from conversations like The LDL-Fructose Disconnect, Where do you find fructose?, and Goodbye, fructose.

But fructose, usually as either high-fructose corn syrup (44%, 55%, occasionally higher percentage fructose) or sucrose (50% fructose), is ubiquitous. I've seen it in the most improbable places, including cole slaw, mustard, and dill pickles.

It's reasonably straightforward to avoid or minimize fructose exposure while eating at home, provided you check labels and focus on foods that don't require labels (like green peppers, salmon, and olive oil, i.e., unprocessed foods). But when you choose to eat at a restaurant, then all hell can break loose and fructose exposure can explode.

So what are some common and unsuspected fructose sources when eating at a restaurant?

Salad dressings--Dressings in all stripes and flavors are now made with high-fructose corn syrup and/or sucrose. This is especially true of low-fat, non-fat, or "lite" dressings, meaning oils have been replaced by high-fructose corn syrup. It can also be true of traditional non-low-fat dressings, too, since high-fructose corn syrup is just plain cheap.

Olive oil and vinegar are still your safest bets. I will often use salsa as a dressing, which works well.

Sauces and gravies--Not only can sauces be thickened with cornstarch, many pre-mixed sauces are also made with high-fructose corn syrup or sweetened with sucrose. Barbecue sauce is a particular landmine, since it is now a rare barbecue sauce not made with high-fructose corn syrup as the first or second ingredient. Sauces for dipping are nearly always high-fructose corn syrup-based.

Ketchup--Yup. Good old ketchup even is now made with high-fructose corn syrup. In fact, you should be suspicious of any condiment.

Highball, Bloody Mary, Margarita, Daiquiri, beer--Even the before-dinner or dinner drink can have plenty of fructose, particularly if a mix is used to make it. While Blood Marys seem the most benign of all, adorned with celery, pickle, and olive, just take a look at the ingredient label on the mix used: high-fructose corn syrup.

Fructose is a stealth poison: It doesn't immediately increase blood sugar; it doesn't trigger any perceptible effect like increased energy or sleepiness. But it is responsible for an incredible amount of the health struggles in the U.S., from obesity, to diabetes, to hyperlipidemias and heart disease, to arthritis, to cataracts.

A glycation rock and a hard place

Advanced Glycation End-products, or AGEs, the stuff of aging that mucks up brains, kidneys, and arteries, develop via two different routes: endogenous (from within the body) and exogenous (from outside the body).

Endogenous AGEs develop via glycation. Glycation of proteins in the body occurs when there are glucose excursions above normal. For instance, a blood glucose of 150 mg/dl after your bowl of stone-ground oatmeal causes glycation of proteins left and right, from the proteins in the lens of your eyes (cataracts), to the proteins in your kidneys (proteinuria and kidney dysfunction), to skin cells (wrinkles), to cartilage (brittle cartilage followed by arthritis), to LDL particles, especially small LDL particles (atherosclerosis).

At what blood sugar level does glycation occur? It occurs even at "normal" glucose levels below 100 mg/dl (with measurable long-term cardiovascular effects as low as 83 mg/dl). In other words, some level of glycation proceeds even at blood glucose levels regarded as normal.

There's nothing we can do about the low-level of glycation that occurs at low blood sugar levels of, say, 90 mg/dl or less. However, we can indeed do a lot to not allow glycation to proceed more rapidly, as it inevitably will at blood sugar levels higher than 90 mg/dl.

How do you keep blood sugars below 90 mg/dl to prevent excessive glycation? Avoid or minimize the foods that cause such rises in blood sugar: carbohydrates.

What food increases blood sugar higher than nearly all other known foods? Wheat.

Is einkorn the answer?

People ask: "What if I would like a piece of bread or other baked product just once in a while? What is safe?"

Eli Rogosa, Director of The Heritage Wheat Conservancy, believes that a return to the wheat of our ancestors in the Fertile Crescent, circa 10,000 years ago, is the answer.

Former science teacher, now organic farmer, farm researcher, and advocate of sustainable agriculture, Eli has been reviving "heritage" crops farmed under organic conditions, some of her research USDA-funded.

In particular, Eli has been cultivating original 14-chromosome ("diploid") einkorn wheat. Although einkorn contains gluten (in lesser quantities despite the higher total protein content), the group of proteins that trigger the immune abnormalities of celiac disease and other immune phenomena, Eli tells me that she has witnessed many people with a variety of wheat intolerances, including celiac disease, tolerate foods made with einkorn wheat. (The variety of glutens in einkorn differ from the glutens of the dwarf mutant that now dominate supermarket shelves.)

Eli travels to Israel every year, returning with "heritage" seeds for wheat and other crops. She formerly worked in the Israel GenBank as Director of the Ancient Wheat Program. She has written a brochure that describes her einkorn wheat.

Eli sent me 2 lb of her einkorn grain that nutritionist, Margaret Pfeiffer, and I ground into bread. Our experience is detailed here. My subsequent blood sugar misadventure, comparing einkorn bread to conventional organic whole wheat bread is detailed here, followed by the odd neurologic effects I experienced here.

Anyone else wishing to try this little ancient wheat experiment with einkorn can also obtain either the unground grain or ground flour through Eli's website, www.growseed.org. Most recently, einkorn pasta is being retailed under the Jovial brand at Whole Foods Market.

If anyone else makes bread or any other food with Eli's einkorn wheat, please let me know:

1) Your blood sugar response (before and 1 hour after consumption)
2) Whether you experienced any evidence of wheat intolerance similar to what you experienced with conventional wheat, e.g., rash, acid reflux, gas and cramping, moodiness, asthma, etc.

But remember: Wheat effects or no, einkorn is still a grain. My belief is that humans do best with little or no grain. The einkorn experience is an effort to identify reasonable compromises so that you and I can have a piece of birthday cake once a year without getting sick.

Genetic incompatibility

Peter has lipoprotein(a), or Lp(a), a genetic pattern shared by 11% of Americans.

It means that Peter inherited a gene that codes for a protein, called apoprotein(a), that attaches to LDL particles, forming the combined particle Lp(a). It also means that his overall pattern responds well to a high-fat, high-protein, low-carbohydrate diet: The small LDL particles that accompany Lp(a) over 90% of the time are reduced, Lp(a) itself is modestly reduced, other abnormalities like high triglycerides (that facilitate Lp(a)'s adverse effects) are corrected. Small LDL particles are, by the way, part of the genetic "package" of Lp(a) in most carriers.

Peter also has another gene for Apo E4, another genetically-determined pattern shared by 19% of Americans. (Another 2% of Americans have two "doses" of Apo E4, i.e., they are homozygotes for E4.) This means that the Apo E protein, normally responsible for liver uptake and disposal of lipoproteins (especially VLDL), is defective. In people with Apo E4, the higher the fat intake, the more LDL particles accumulate. (The explanation for this effect is not entirely clear, but it may represent excessive defective Apo E-enriched VLDL that competes with LDL for liver uptake.) People with Apo E4 therefore drop LDL (and LDL particle number and apoprotein B) with reductions in fat intake.

This is a genetic rock-and-a-hard-place, or what I call a genetic incompatibility. If Peter increases fat and reduces carbohydrates to reduce Lp(a)/small LDL, then LDL measures like LDL particle number, apoprotein B, and LDL cholesterol will increase. Paradoxically, sometimes small LDL particles will even increase in some genetically predisposed people.

If Peter decreases fat and increases carbohydrates, LDL particle number, apoprotein B, and LDL cholesterol will decrease, but the proportion of small LDL will increase and Lp(a) may increase.

Thankfully, such "genetic incompatibilities" are uncommon. In my large practice, for instance, I have about 5 such people.

The message: If you witness paradoxic responses that don't make sense or follow the usual pattern, e.g., reductions in LDL particle number, apoprotein B, and small LDL with reductions in their dietary triggers (i.e., carbohydrates, especially wheat), then consider a competing genetic trait such as Apo E4.

The folly of an RDA for vitamin D

Tom is a 50-year old, 198-lb white male. At the start, his 25-hydroxy vitamin D level was 28.8 ng/ml in July. Tom supplements vitamin D, 2000 units per day, in gelcap form. Six months later in January (winter), Tom's 25-hydroxy vitamin D level: 67.4 ng/ml.

Jerry is another 50-year old white male with similar build and weight. Jerry's starting summer 25-hydroxy vitamin D level: 26.4 ng/ml. Jerry takes 12,000 units vitamin D per day, also in gelcap form. In winter, six months later, Jerry's 25-hydroxy vitamin D level: 63.2 ng/ml.

Two men, similar builds, similar body weight, both Caucasian, similar starting levels of 25-hydroxy vitamin D. Yet they have markedly different needs for vitamin D dose to achieve a similar level of 25-hydroxy vitamin D. Why?

It's unlikely to be due to variation in vitamin D supplement preparations, since I monitor vitamin D levels at least every 6 months and, even with changes in preparations, dose needs remain fairly constant.

The differences in this situation are likely genetically-determined. To my knowledge, however, the precise means by which genetic variation accounts for it has not been worked out.

This highlights the folly of specifying a one-size-fits-all Recommended Daily Allowance (RDA) for vitamin D. The variation in need can be incredible. While needs are partly determined by body size and proportion body fat (the bigger you are, the more you need), I've also seen 105 lb women require 14,000 units and 320-lb men require 1000 units to achieve the same level of 25-hydroxy vitamin D.

An RDA for everyone? Ridiculous. Vitamin D is an individual issue that must be addressed on a person-by-person basis.

Heart scan: Standard of care?

If coronary disease is easy to detect by measuring coronary calcium, shouldn't this represent the standard of care?

In other words, if you've been seeing your doctor and he/she has been monitoring cholesterol levels and, inevitably, talks about statin drugs, then you have a heart attack, unstable angina, or die--yet never knew you had heart disease--isn't this negligence?

Coronary calcium, and thereby coronary atherosclerotic plaque, are markers for the disease itself. Unlike cholesterol, high blood pressure, etc., that represent risk factors for coronary atherosclerotic plaque, coronary calcium is a measure of total plaque: "soft" elements like lipid collections, necrotic tissue, fibrous tissue, as well as "hard" elements like calcium. Because calcium occupies 20% of total atherosclerotic plaque volume, it can be used as an indirect "dipstick" for total plaque.

So why isn't an unexpected heart attack, hospitalization for unstable heart symptions, emergency bypass, etc., not regarded as potential malpractice? These are not benign events, but potentially life-threatening.

The costs of doing drug business?

Here's a telling situation.

Liz had been on prescription niacin, Niaspan, 1500 mg per day (3 x 500 mg tablets) for several years to treat her severe small LDL pattern and familial hypertriglyceridemia (triglycerides 500-1000 mg/dl). Because her health insurance had been paying for the "drug," she insisted on taking the prescription form.

A change in insurance, however, meant that the Niaspan was no longer covered. Her pharmacy wanted to charge $227 per month.

Liz came to the office in tears, worried that she was going to have to choke up $227 per month. I reminded her that, as I had told her several years ago, she could easily replace the Niaspan with over-the-counter Sloniacin or Enduracin. Both release niacin over approximately 6 hours, just like Niaspan.

Here are the prices I've seen with Sloniacin, 100 tablets of 500 mg:

Walgreens: $15.99
Walmart: $12.99
Costco: $8.99

So the most expensive source, Walgreens, would cost Liz just under $15.99 per month to take 1500 mg per day.

$15.99 versus $227.00 per month for preparations that are highly similar. Hmmmmmm.

I wonder what the $211.01 extra per month goes towards? Admittedly, Abbott Labs, the current company selling Niaspan (after Abbott acquired Kos), has invested in a few clinical trials, such as ARBITER-HALTS6. But does supporting research justify this much difference, a difference that amounts to $2532 over a year? If just 100,000 patients are prescribed Niaspan at this dose (a typical dose), this generates $253 million.

Is the cost of developing and marketing a supplement-turned-drug that great? Is this justifiable? Is it any wonder that our health insurance premiums continue to balloon?

I use Sloniacin and Enduracin almost exclusively.

Measurement

A crucial component of self-empowerment in healthcare is to be able to measure various health parameters. More and more measurement tools are entering the direct-to-consumer arena.

Quantification of various phenomena is important in managing many aspects of health. Imagine a carpenter trying to build a house without the use of a tape measure, level, or other measuring tools. In health, as in building a house, measurement, adjustment, and correction are critical.

Among the most helpful health measurement tools:

Blood glucose meters--Blood glucose meters aren't just for diabetics. They are among the most powerful weight loss tools available.

Blood pressure cuffs--There's no better way to assess blood pressure than to assess it under all the varied conditions of life: When you're tired, when you're excited, when you're upset, when you're happy, hungry, stomach full, morning, night. This is a lot better than the one isolated measure in the doctor's office.

Digital thermometers--Your first a.m. oral temperature is a great way to assess thyroid status. We aim to maintain first a.m. oral temperature around 97.3 degrees F, the normal human temperature upon arising that reflects normal thyroid function. (No, Dr. Broda Barnes fans, axillary temperatures should NOT be used due to flagrant variation from right armpit to left armpit, modifying effects of clothing and ambient temperature, etc. Oral temperature tracks internal, "core," temperature fluctuations reliably, including circadian variation, far better than axillary temperatures.)

Fingerstick blood tests--An incredible number of blood tests are now available just by performing a simple fingerstick in your kitchen or bathroom. You can get 25-hydroxy vitamin D, lipids, thyroid measures (TSH, free T3, free T4), hormones (DHEA, testosterone, estrogens). And the list is growing rapidly. Salivary tests are also growing in number for many of the same measures.

A variation on fingerstick blood tests are devices like CardioChek that allow you to do a fingerstick, but also run the test on your own device at home. (The CardioChek device tests total cholesterol, triglycerides, and HDL.)

Urine pH--You can dipstick your own urine to assess the relative acidity or alkalinity of your lifestyle. Acid pH (7 or below) suggests that diet is weighed too heavily in favor of animal products and grains. An alkaline pH (above 7) suggests plentiful vegetables and fruits, not counteracted by animal products and grains.

There are many more, including the ZEO device to monitor sleep quality, RESPeRATE for reduction of blood pressure, HeartMath to manage stress and augment the parasympathatic (relaxation) response. We've come a long way compared to the health monitoring devices of just 25-30 years ago.

Anyway, that's a partial list. Given the rapid advances in technology that allow such home tests, I anticipate a much longer list in the coming few years.

For some perspective on how far these devices have come, here's a great graphic of an early sphygmomanometer, or blood pressure gauge.


Courtesy Wellcome Library, London

I lost 37 lbs with a fingerstick

Jack needed to lose weight.

At 5 ft 7 inches, he weighed in at 273 lbs, putting his BMI at a sobering 42.8. (A BMI of 30 or above is classified as "obese.") In addition to lipoprotein(a), Jack had an extravagant quantity of small LDL (the evil "partner" of lipoprotein(a)), high triglycerides, and blood sugars in the diabetic range. With a heart scan score of 1670, Jack had little room for compromises.

Try as he might, Jack could simply not stick to the diet I urged him to follow. Three days, for instance, of avoiding wheat was promptly interrupted by his wife's tempting him with a nice BLT sandwich. This triggered his appetite, with diet spiraling downward in short order.

So I taught Jack how to check his blood sugars using a fingerstick device, what I call the most important weight loss tool available. I asked Jack to check his pre-meal blood glucose and his one-hour after-meal blood glucose and not allow the after-meal blood glucose to rise any higher than the pre-meal. For example, if blood glucose pre-meal was 115 mg/dl, after-meal blood glucose should be no higher than 115 mg/dl.

If any food or combination of foods increase blood glucose more than the pre-meal value, then eliminate the culprit food or reduce the portion size. For example, if dinner consists of baked salmon, asparagus, and mashed potatoes, and pre-meal blood glucose is 115 mg/dl, post-meal 155 mg/dl, reduce or eliminate the mashed potatoes. If slow-cooked, stone ground oatmeal causes blood glucose to increase from 115 mg/dl to 185 mg/dl (a typical response to oatmeal), then eliminate it.

Having immediate feedback on the effects of various foods finally did it for Jack: It identified foods that were triggering excessive blood sugar rises (and thereby insulin) and foods that did not.

What Jack did not do is limit or restrict calories. In fact, I asked him to eat portion sizes that left him comfortable. There was no need to reduce calories, push the plate away, etc. Just don't allow blood sugars to rise.

Six months later, Jack came back 37 lbs lighter. And he got there without calorie-counting, without regulating portion sizes, without hunger.

The two kinds of small LDL

You won't find this in any publication nor description (at least ones that I've come across) about the ubiquitous small LDL particles. It's an observation I've made having obtained thousands of advanced lipoprotein panels of the sort that break lipoproteins down by size. I've discussed this issue previously here. But small LDL is so ubiquitous, not addressed by conventional strategies like statin drugs or fat restriction (it is made worse, in fact, by reducing fat in the diet), that it is worth keeping at the top of everyone's consciousness.

(Because most of the lipoprotein analyses performed in my office are done via NMR, I will discuss in terms relevant to NMR. This does not necessarily mean that similar observations cannot be made with centrifugation, i.e, VAP from Atherotech, or gel electropheresis from Berkeley, Boston Heart Lab, Spectracell, and others).

There are two basic varieties of small LDL particles:

1) Genetically-programmed--e.g., via cholesteryl-ester transfer protein (CETP) activity
2) Acquired--via carbohydrate consumption


It means that people with acquired small LDL from carbohydrate consumption can reduce small LDL to zero with reduction of carbohydrates, especially the most small LDL-provoking foods of all: wheat, cornstarch, and sucrose.

It also means that people who have small LDL for genetically-determined reasons can only minimize, not eliminate, small LDL. By NMR, we struggle to keep small LDL in the 300-600 nmol/L range when genetically-determined. (People typically start with 1400-3000 nmol/L small LDL particles prior to diet changes and other efforts.) We can only presumptively identify genetically-determined small LDL when all the appropriate efforts have been made, including reduction in weight to ideal, yet small LDL persists.

Here is where we need better tools: when you've done everything possible, yet small LDL persists.

While we break LDL particles (NOT LDL cholesterol, the crude and misleading way of viewing atherosclerosis causation) down by size, it's really about all the undesirable characteristics that accompany small size:

--Distortion of Apo B conformation--i.e., the primary protein that directs LDL particle fate is distorted, making it less likely to be cleared by the liver but more likely to be taken up by inflammatory (macrophages) in the artery wall, creating plaque. It means that small LDL particles linger for a longer time than larger particles.

--Small LDLs are more oxidation-prone. Oxidized LDL are more avidly taken up by inflammatory macrophages.

--Small LDLs are more glycation-prone.

--Small LDLs are more adherent to structural tissues, e.g., glycosaminoglycans, that reside in the artery wall.

You and I cannot measure such phenomena, so we resort to distinguishing LDL particles by size.

The drug industry believes it may have a solution to small LDL in the form of CETP-inhibiting drugs, like anacetrapib. In the way of nutritional solutions beyond carbohydrate reduction, weight loss/exercise, niacin, vitamin D normalization, and omega-3 fatty acid supplementation, there are exciting but very preliminary data surrounding the possibility that anthocyanins may inhibit CETP activity. Having toyed with this concept for the past 6 months, I remain uncertain how meaningful the effect truly is, but it is harmless, since we obtain anthocyanins from foods colored purple or purplish, such as blackberries, blueberries, cherries, red leaf lettuce, red cabbage, etc.

I welcome any unique observations on this issue.
All posts by william-davis

"You've got 10 minutes"

There's a new trend in office healthcare in Milwaukee: Time-restricted office visits.



I'm told by several physicians who are employed by a major healthcare system here in town that they are peridically watched--physically watched by an administrator--to make sure that they do not exceed the allotted 10 minutes of time. My cardiologist colleagues, I gather, were at first incredulous at such intrusions into their practices, but apparently had no choice: They were employees.



Goiter, goiter everywhere

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

The question:

Do you used iodized salt?

The responses:

Yes, I use iodized salt every day
94 (28%)

Yes, I use iodized salt occasionally
56 (16%)

No, I do not use any iodized salt
41 (12%)

No, I use a non-iodized salt (sea salt, Kosher)
126 (37%)

No, I use a non- or low-sodium substitute
15 (4%)


Thanks for your responses.

If only 28% of people are regular users of iodized salt, that means that the remainder--72%--are at risk for iodine deficiency if they are not getting iodine from an alternative source, such as a multivitamin or multimineral.

Even the occasional users of salt can be at risk. The common perception is that occasional use is probably sufficient to provide iodine. This is probably not true and not just because of the lower quantity of ingestion. Occasional users of salt tend to have their salt canister on the shelf for extended periods. The iodine is then lost, since iodine is volatile. In fact, iodine is virtually undetectable four weeks after a package is opened.

In my office, now that I'm looking for them much more systematically and carefully, I am finding about 2 people with goiters every day. They are not the obvious grotesque goiters of the early 20th century (when quack therapies like the last post, the Golden Medical Discovery, were popular). The goiters I am detecting are small and spongy. Yesterday alone I found 5 people with goiters, one of them visible to the eye and very distressing to the patient.

It seems to me that iodine deficiency is more prevalent than I ever thought. It is also something that is so simple to remedy, though not by increasing salt intake. Kelp tablets--cheap, available--have been working quite well in the office population. My sense is that the Recommended Daily Allowance of 150 mcg per day for adults is low and that many benefit from greater quantities, e.g., 500 mcg. What is is the ideal dose? To my knowledge, nobody has yet generated that data.

Thyroid issues being relatively new to my thinking, I now find it incredible that endocrinologists and the American Thyroid Association are not broadcasting this problem at the top of their lungs. This issue needs to be brought to the top of everyone's attention, or else we'll have history repeating itself and have goiters and thyroid dysfunction galore.

For more on this topic, see the previous Heart Scan Blog post, "Help keep your family goiter free."

Goiter and the Golden Medical Discovery


Thick neck, or goitre . . . consists of an enlargement of the thyroid gland, which lies over and on each side of the trachea, or windpipe, between the prominence known as "Adam's apple" and the breast bone. The tumor gradually increases in front and laterally, until it produces great deformity, and often interferes with respiration and the act of swallowing. From its pressure on the great blood vessels running to and from the head, there is a constant liability to engorgement of blood in the brain, and to apoplexy, epilepsy, etc.

The causes of the affection are not well understood. The use of snow water, or water impregnated with some particular saline or calcareous matter, has been assigned as a cause. It has also been attributed to the use of water in which there is not a trace of iron, iodine, or bromine. . . The disease is often due to an impeded circulation in the large veins of the neck, from pressure of the clothing, or from the head being bent forward, a position which is often seen in school children.



Treatment

We have obtained excellent results in many cases, not too far advanced, by a method of treatment which consists in the employment of electrolysis. . . Many cases at the present time are operated upon with entire success.

Those who are afflicted with this disease and unable to avail themselves of special treatment cannot do better than to take Doctor Pierce's Alterative Extract, or Golden Medical Discovery, and apply over the skin around the tumor, night and morning, the following, which may be prepared at any drug store:

Resublimed Iodine--One dram
Iodide of Potassium--Four drams
Soft Water--Three ounces 


Apply to the tumor, twice daily, with feather or camel hair pencil.


From The People's Common Sense Medical Adviser by R.V. Pierce, MD; 1918.

Magnesium and you-Part I

If this were 10,000 B.C., you'd get your drinking water from streams, rivers, and lakes, all rich in mineral content. Humans became reliant on obtaining a considerable proportion of daily mineral needs from natural water sources.

21st century: We obtain drinking water from a spigot or plastic bottle. Pesticides and other chemicals seep into the water supply. Municipal water purification facilities have intensified water purification in most communities to remove contaminants like lead, pesticide residues, and nitrates. (For a really neat listing of the water quality of various cities, the University of Cincinnati makes this data available.)

But intensive water treatment also removes minerals like calcium and magnesium.

Many people have added water filters or purifiers to their homes,, like reverse osmosis and distillation, that are efficient at extracting any remaining minerals, converting “hard” into “soft” water. In fact, manufacturers of such devices boast of their power to yield pure water free of any “contaminant,” minerals like magnesium included. The magnesium content of water after passing through most commercial filters is zero.

Modern enthusiasm for bottled water has compounded the problem. Americans consumed a lot of bottled water, nearly 8 billion gallons last year. In the U.S., nearly all bottled water has little or no magnesium.

The result is that we can no longer rely on drinking water to provide magnesium. The Recommended Daily Allowance (RDA)—the amount required to prevent severe deficiency—for magnesium is 420 mg per day for men, 320 mg/day for women. In cities with the highest magnesium water content, only 30% of the RDA can be obtained by drinking two liters of tap water per day. In most cities, only a meager 10–20% of the daily requirement can be obtained. That leaves between 70–90% that needs to come from other sources. As a result, the average American ingests substantially less than the RDA.

Blast triglycerides

The conventional answers to high triglycerides levels are generally: low-fat diet, a fibrate drug (Tricor, Lopid), a statin drug, and--most recently--prescription fish oil.

This is the regimen to take if you want the drug industry to get even richer and more powerful than they already are. After all, what CEO of a pharmaceutical company can stand to have his salary and benefits slashed to below $200 million this year? It's outrageous!

If you really want to blast the heck out of your triglycerides and achieve numbers like 50 mg/dl, then the regimen to consider consists of:

--Elimination of sugars, wheat, and cornstarch
--Fish oil--Sam's Club would do fine at $8 for 350 capsules, or the high-potency at $14.99 for 180 capsules (at 680 mg EPA +DHA, nearly the same potency as prescription Lovaza at 842 mg)
--Vitamin D supplementation sufficient to achieve normal blood levels (60-70 ng/ml)

Those three strategies alone can reduce triglycerides far more than any drug combination. In fact, it is rare for someone with triglycerides as high as 900 mg/dl to not reduce them to the <100 mg/dl range.

Cheerios: Prescription required?

Followers of The Heart Scan Blog know my feelings about Cheerios:


Can you say "sugar"?

Cheerios and heart health


There's an interesting tussle going on between the makers of Cheerios, General Mills, and the FDA.

The FDA says that the Cheerios' package claims of:

• "you can Lower Your Cholesterol 4% in 6 weeks"
• "Did you know that in just 6 weeks Cheerios can reduce bad cholesterol by an average of 4 percent? Cheerios is ... clinically proven to lower cholesterol. A clinical study showed that eating two 1 1/2 cup servings daily of Cheerios cereal reduced bad cholesterol when eaten as part of a diet low in saturated fat and cholesterol."

constitute a medical claim, i.e., trying to promote Cheerios as a drug.

I'm glad that the FDA has come down on General Mills. But I find this entire episode laughable: The debate is over the purported health benefits of what I would regard as pure junk food, no better in my view than claiming that a cupcake has health benefits, or a carton of ice cream.

In my experience, Cheerios does not 1) reduce risk for heart disease, nor 2) reduce cholesterol.

It does, however, cause blood sugar to skyrocket and increase the small type of LDL--you know, the type that causes heart disease.

"Placebos are frequently of value"

The treatment of angina pectoris, generally speaking, is unsatisfactory.

Any procedure that relieves mental tension is valuable. Since patients suffer particularly during the winter, I encourage winter vacations in a southern climate.

I insist that obese patients lose weight, and have found small doses of benzedrine, 10 to 20 mg. daily, helpful in curbing the appetite.

I generally forbid smoking. This is a particularly disturbing task for many patients to carry out. In such cases, I suggest that 3 or 4 cigarettes be smoked daily, knowing full well that regardless of what I say or recommend, the patients is going to continue to smoke.

Innumerable drugs, most of which are of questionable value, have been used to prevent attacks of angina pectoris. In fact, placebos are frequently of value.

Testosterone--The male sex hormone has been effective in my experience. Whether it acts as a vasodilator or merely by promoting a sense of well-being is not known.

Alcohol--Alcohol (whiskey, brandy, rum) has been used for many years in the treatment of angina pectoris. I have prescribed it in moderate quantity--an ounce several times a day--and while I have not made alcoholics of any of my patients, I also have not cured any of them with it. Preparations, such as creme de menthe, are of value in relieving "gas" of which so many patients complain.


From Heart Disease Diagnosis and Treatment
Emanuel Goldberger, MD
1951

Iodine is not salt

I've noticed a point of confusion recently, something I hadn't noticed in my patients before: Because of the public health advice from the FDA, American Heart Association, and Surgeon General's office to reduce sodium/salt intake, people have thought this meant reducing iodine, too.

I believe that people have drawn an equation in their minds:


Sodium = iodine


Of course, they are two entirely unrelated things.

Recall that the only reason iodine is added to many (not all) salt products is because it was a public health solution to solve the substantial nationwide iodine deficiency prevalent during the 20th century. But it was a solution conceived in 1924, when the FDA thought this was the best way to get iodine into Americans. And it worked.

Unfortunately, sodium does indeed present adverse effects in some people. As a result, "get your iodine from salt" has evolved into "reduce your sodium intake." Everyone forgot about the iodine: They forgot about the large disfiguring goiters, the poor school performance in iodine-deficient schoolchildren, the mentally-impaired offspring of iodine-deficient mothers.

So don't confuse sodium with iodine. You may need less of the former, but more of the latter.

For more on this, see "Help keep your family goiter free."

"You can't reduce coronary plaque"

"I told my cardiologst that I stumbled on a program called 'Track Your Plaque' that claims to be able to help reduce your coronary calcium score.

"My cardiologist said, 'That's impossible. You cannot reduce coronary plaque. I've never seen anyone reduce a heart scan score."

Who's right here?

The commenter is right; the cardiologist is wrong.

I would predict that the cardiologist is among the conventionally-thinking, "statins drugs are the only solution" group who follows his patients over the years to determine when a procedure is finally "needed." In fact, I know many of these cardiologists personally. The primary care physicians are completely in the dark, usually expressing an attitude of helplessness and submitting to the "wisdom" of their cardiology consultants.

Quantify and work to reduce the atherosclerotic plaque? No way! That's work, requires thinking, some sophisticated testing (like lipoprotein testing), even some new ideas like vitamin D. "They didn't teach that to me in medical school (back in 1980)!"

Welcome to the new age.

Atherosclerotic plaque is 1) measurable, 2) trackable, and 3) can be reduced.

We do it all the time. (Amy still holds our record: 63% reduction in plaque/heart scan score.)

Though I pooh-pooh the value of statin drug studies, there's even data from the conventional statin world documenting coronary plaque reversal. The ASTEROID Trial of rosuvastatin (Crestor), 40 mg per day for one year, demonstrated 7% reduction of atherosclerotic plaque using intracoronary ultrasound.

I have NEVER seen a heart attack or appearance of heart symptoms (angina, unstable angina) in a person who has reversed coronary plaque (unless, of course, they pitched the whole effort and returned to bad habits--that has happened). Stick to the program and coronary risk, for all practical purposes, been eliminated.

A heart scan score is not a death sentence. It is simply a tool to empower your prevention program, a measuring stick to gauge plaque progression, stabilization, or regression. Don't accept anything less.

Lethal lipids

There's a specific combination of lipids/lipoproteins that confers especially high risk for heart disease. That combination is:

Low HDL--generally less than 50 mg/dl

Small LDL--especially if 50% or more of total LDL

Lipoprotein(a)--an aggressive risk factor by itself



This combination is a virtual guarantee for heart disease, often at a young age. It's not clear whether each risk factor exerts its own brand of undesirable effect, or whether the combined presence of each cause some adverse interaction.

For instance, lipoprotein(a), or Lp(a), by itself is the most aggressive risk factor known (that nobody's heard about--there's no blockbuster revenue-generating drug for it). Each Lp(a) molecule is a combination of an LDL cholesterol molecule with a specific genetically-determined protein, apoprotein(a). If the LDL component of Lp(a) is small, then the combination of Lp(a) with small LDL is somehow much worse, kind of like the two neighborhood kids who are naughty on their own, but really bad when they're together.

Interestingly, the evil trio responds as a whole to many of the same corrective treatments:

Niacin--increases HDL, reduces small LDL, and reduces Lp(a)

Elimination of wheat, cornstarch, and sugars--Best for reducing small LDL; less potent for Lp(a) reduction.

High-fat intake--Like niacin, effective for all three.

High-dose fish oil--Higher doses of EPA + DHA north of 3000 mg per day also can positively affect all three, especially Lp(a).


If you have this combination, it ought to be taken very seriously. Don't let anybody tell you that it is uncorrectable--just because there may be no big revenue-generating drug to treat it on TV does
not mean that there aren't effective treatments for it. In fact, some of our biggest successes in reducing heart scan scores have had this precise combination.