And you thought gasoline was expensive

In 1995, the Palmaz coronary stent was introduced, the brainchild of Drs. Julio Palmaz and Richard Schatz. Medical device manufacturer, Johnson & Johnson, priced the device at $2500 per stent.

Let's put this into perspective: At just 0.05 grams per 15 millimeter stent, that put the price of the common stainless steel used to manufacture the stent at $22,650,000 per pound.

Only after several competing stents finally made it to market did J&J reduce its price to its bargain price of $1200, or $10,872,000 per pound. And to think that most of us were shocked to find out that the U.S. military paid $200 for a hammer.

Since 1995, a competitive market for stents has developed, pushing prices down. Now, you can purchase a brand-new coronary stent for as little as $4,000,000 per pound.

Medical device manufacturers have been guilty of a degree of greed that would make many Wall Street bankers blush. That's why I call medical devices "the industry of infinite markups."

"Hey buddy, wanna buy some exorphins?"

Dr. Christine Zioudrou and colleagues at the National Institutes of Mental Health got this conversation going back in 1979 with their paper, Opioid peptides derived from food proteins: The exorphins.

Exorphins are exogenously-derived peptides (i.e., short amino acid sequences obtained from outside the body) that exert morphine-like properties. Mimicking the digestive process that occurs in the gastrointestinal tract using the gastric enzyme, pepsin, and hydrochloric acid (stomach acid), Zioudrou et al isolated peptides from wheat gluten with morphine-like activity. They followed this research path because of the apparent association of wheat and mental illness.

In the bioassays used, wheat-derived exorphins competed successfully with the endogenous opiate, met-enkephalin. Interestingly, casein-derived (i.e., casein milk protein) exorphins were also identified that also displayed opiate-binding activity, though less powerfully. The morphine-like activity was also blocked by the drug, naloxone (the same stuff given to people exposed to morphine overdose).

Among the many devastating effects of celiac disease , the immune disease that develops from wheat gluten exposure, are mental and emotional effects, such as anxiety, fatigue, mental "fog," depression, bipolar illness, and schizophrenia, that disappear with removal of gluten. Many parents of autistic children also advocate wheat-free diets for similar reasons.

Among the many wonderful comments posted on the last Heart Scan Blog post, "I can't do it," was Anne's:

I am not the Anne in your post, but I was addicted to wheat. It was my favorite food. I lived on and for breads. Then I discovered I was gluten sensitive and I did go through a withdrawal of about 4 days. After 4 days I noticed my health problems were disappearing. Depression, brain fog and joint pain are 3 of the many symptoms that disappeared. That was 6 yrs ago.

Tell Anne that I had dreams about bread in the beginning - they will pass. Now the donuts, breads, cookies and cakes in the stores and at work don't even look good. In fact, I don't like the smell of bread anymore. It takes time, but the cravings do pass.



Combine wheat"s exorphin-driven addictive potential with its flagrant blood sugar-increasing properties, and you have a formula that:

1) makes you fat
2) increases likelihood of diabetes, and
3) makes you want to keep on doing it.

Reminds me of nicotine.

My personal view: I have absolutely no remaining doubt that wheat products have no place in the human diet. Not only does the research provide a plausible basis for its adverse health effects, but having asked hundreds of people to remove it from their habits has yielded consistent and remarkable health benefits. Just read the reader comments here and here.

"I can't do it"

Anne sat across from me, bent over and sobbing.

"I can't do it. I just can't do it! I cut out the breads and pasta for two days, then I start dreaming about it!

"And my husband is no help. He knows I'm trying to get off the wheat. But then he brings home a bunch of Danish or something. He knows I can't help myself!"

Having asked hundreds of people to completely remove wheat from their diet, I witness 30% of them go through such emotional and physical turmoil, not uncommonly to the point of tears. For about 10-20% of people who try, it is as hard as quitting cigarettes.

Make no mistake about it: For many people, wheat is addictive. It meets all the criteria for an addictive product: People crave it, consuming it creates a desire for more, lacking it triggers a withdrawal phenomenon. If wheat were illegal, there would surely be an active underground trafficking illicit bagels and pretzels.

Withdrawal consists of fatigue and mental fogginess that usually lasts 5-7 days. Just like quitting smoking, wheat withdrawal is harmless but no less profound in severity.

People who lack an addictive relationship with wheat usually have no idea what I'm talking about. To them, wheat is simply a grain, no different than oats.

But wheat addicts immediately know who they are. They are the ones who can't resist the warm dinner rolls served at the Italian restaurant, need to include something made of wheat at every meal, and crave it every 2 hours (matching the cycle of blood sugar peaks and valleys, the "valley" triggering the craving). When they stop the flow of immediately-released glucose that comes from wheat (with blood sugar peaks that occur higher and faster than table sugar), irresistible cravings kick in. Then watch out: They'll bite your hand off if you reach for that roll before they do.

Break the cycle and the body is confused: Where's the sugar? The body is accustomed to receiving a constant flow of easily-digested sugars.

Once the constant influx of sugars ceases, it takes 5-7 days for metabolism to shift towards fat mobilization as a source of energy. But along with fat mobilization comes a shrinking tummy, reducing the characteristic wheat belly.

If you try to quit smoking, you've got "crutches" like nicotine patches and gum, Zyban, Chantix, hypnosis, and group therapy sessions. If you try and quit wheat, what have you got? Nothing, to my knowledge. Nothing but sheer will power to divorce yourself from this enormously destructive, diabetes-causing, small LDL-increasing, inflammation-provoking, and addictive substance.

Spontaneous combustion, vampires, and goitrogens

What do the following have in common:

Lima beans
Flaxseed
Broccoli
Cabbage
Kale
Soy
Millet
Sorghum?

They are all classified as goitrogens, or foods that have been shown to trigger goiter, or thyroid gland enlargement. Most of them do this either by blocking iodine uptake in the thyroid gland or by blocking the enzyme, thyroid peroxidase. This effect can lead to reduction in thyroid hormone output by the thyroid gland, which then triggers increased thyroid stimulating hormone (TSH) by the pituitary; increased TSH acts as a growth factor on the thyroid, thus goiter.

Add to this list of goitrogens the flavonoid, quercertin, found in abundance in red wine, grapes, apples, capers, tomatoes, cherries, raspberries, teas, and onions. Most of us obtain around 30 mg per day from our diet. Quercetin, often touted as a healthy flavonoid alongside resveratrol (e.g., Yang JY et al 2008), has been shown to be associated with reduced risk for heart disease and cancer. Many people even take quercetin as a nutritional supplement.

Quercetin has also been identified as a goitrogen (Giuliani C et al 2008).

What to make of all this?

Most of these observations have been made in in vitro ("test tube") preparations or in mice. Rabbits who consume a cabbage-only diet can develop goiter.

How about humans? The few trials conducted in humans have shown little or no effect. In most instances, the adverse effects of goitrogens have been eliminated with supplemental iodine. In other words, goitrogens seem to exert their ill thyroid effects when iodine deficiency is present. Restore iodine . . . no more goitrogens (with rare exceptions).

Should we as humans adopt a diet that avoids apples, grapes, tomatoes, red wine, tea, onions, soy etc. on the small chance that we will develop goiter?

I believe that we should avoid these common food-sourced goitrogens with as much enthusiasm as we should be worried about spontaneous combustion of humans or the appearance of vampires on our front porches. We are as likely to suffer low thyroid activity from quercetin or other "goitrogens" as we are to experience the "mitochondrial explosions" that are purported to set innocent people afire.

Magnesium and you-Part II

Blood magnesium levels are a poor barometer for true body (intracellular) magnesium.

Only 1% of the body’s magnesium is in the blood, the remaining 99% stored in various body tissues, particularly bone and muscle. If blood magnesium is low, cellular magnesium levels are indeed low—very low.

If blood magnesium is normal, cellular or tissue levels of magnesium may still be low. Unfortunately, tissue magnesium levels are not easy to obtain in living, breathing humans. In all practicality, a blood magnesium test only helps if it’s low, while normal levels don’t necessarily mean anything and may provide false reassurance.

Short of performing a biopsy to measure tissue magnesium levels, several signs provide a tip-off that magnesium may be low:

• Heart arrhythmias—Having any sort of heart rhythm disorder should cause you to question whether magnesium levels in your body are adequate, since low magnesium levels trigger abnormal heart rhythms. In fact, in the hospital we give intravenous magnesium to quiet down abnormal rhythms.
• Low potassium— Low magnesium commonly accompanies low potassium. Potassium is another electrolyte depleted by diuretic use and is commonly deficient in many conditions (e.g., excessive alcohol use, hypertension, loss from malabsorption or diarrhea). Like magnesium, potassium may not be fully replenished by modern diets.
• Muscle cramps— Magnesium regulates muscle contraction. Leg cramps, or “charlie-horses”, painful vise-like cramps in calves, fingers, or other muscles, are a common symptom of magnesium deficiency. (Leg cramps that occur with physical activity, such as walking, are usually due to atherosclerotic blockages in the leg or abdominal arteries, not low magnesium.)
• Migraine headaches—Reflective of magnesium’s role in regulating blood vessel tone, low magnesium can trigger vascular spasm in the blood vessels of the brain. In some emergency rooms, they will actually administer intravenous magnesium to break a migraine.
• Metabolic syndrome—Magnesium plays a fundamental role in regulating insulin responses. Metabolic syndrome (low HDL, high triglycerides, small LDL, high blood pressure, increased blood sugar, excessive abdominal fat, etc.) is triggered by insulin responses gone awry and is clearly linked to low magnesium levels.

The absence of any of these tell-tale signs does not necessarily mean that tissue levels of magnesium are normal.

Then how do you really know? There really is no easy, available method to gauge body magnesium. As a practical solution, we therefore have aimed for maintaining serum levels of >2.1 mg/dl or RBC magnesium (a surrogate for tissue levels) of >6.0 mg/dl. (Going too high is not good either, so occasional monitoring really helps. However, I've only seen this once in a psychotic woman who drank ungodly amounts of magnesium-containing antacids for no apparent reason; she almost ended up on a respirator due to respiratory suppression by the magnesium level of 11 mg/dl!)

In all practicality, because of magnesium’s crucial role in health, its widespread deficiency in Americans, and the growing depletion of magnesium in water, supplemental magnesium is necessary for nearly everyone to ensure healthy levels.

More on magnesium to come.

Lethal Lipids II

I call the combination of low HDL, small LDL, and lipoprotein(a) "lethal lipids," since the trio is an exceptionally potent predictor for heart disease. Uncorrected, the combination is a virtual guarantee of heart disease.

Ed is a perfect example of someone who came to my office recently with this pattern. His starting values:

HDL: 34 mg/dl

Small LDL: 78% of total LDL
NMR: Small LDL 1655 nmol/L; total LDL particle number 2122 nmol/L)

Blood sugar lessons from a Type I diabetic

A friend of mine is a Type I, or childhood onset, diabetic. He's had it for nearly 50 years, since age 6. He's also in the health industry and is a good observer of detail.

He made the following interesting comments to me recently when talking about the effects of various foods on blood sugar:

"When I eat normally, like some vegetables or salad and meat, I dose up to 10 units of insulin to control my blood sugar.

"If I eat a turkey sandwich on two slices of whole wheat, I usually dose 15 units. The bread makes my blood sugar go to 300 if I don't.

"If I eat a Cousins's Sub [a local submarine sandwich chain], I dose 15 units. The bread really makes my blood sugar go up.

"I can only eat a Quarter Pound from McDonald's once a year, because it make my blood sugar go nuts. I dose 15-20 units before having it, and I feel like crap for two days afterwards.

"If I eat Mexican food, I have to dose 15-20 units. For some reason, it's gotten worse over the years, and I need to dose higher and higher.

"Chinese food is the absolute worst. I dose 20-25 units before eating Chinese. I'll often have to dose more afterwards, because my blood sugar goes so berserk."


Nothing beats the real-world observations on the impact of various foods on blood sugar than the observations of people with Type I diabetes. All the insulin they get is in a syringe. Dosing needs to match intake.

Personally, though I love the taste of Americanized Chinese food, I've always been suspicious of what exactly goes into these dishes. But I was unaware of the blood sugar implications.

The impact of Mexican I believe can be attributed to the cornstarch used in the tacos and tortillas, though I also wonder if there are other starches being snuck in, as well.

Lessons about omega-3s from Japan















Image courtesy of apc33.

Japan provides a useful "laboratory" for studying the effect of a culture that relies heavily on eating fish.

The JELIS Trial, the topic of a previous Heart Scan Blog post, showed that supplementation with the single omega-3 fatty acid, EPA, 1800 mg per day (the equivalent of 10 capsules of 'standard' fish oil that contains 180 mg per day of EPA, 120 mg of DHA) significantly reduced heart attack in a Japanese population. Interestingly, this benefit was additive to the already substantial intake of omega-3 fatty acids among the general Japanese population, a population with a fraction of the heart attacks found in western populations like the U.S. (approximately 3% over 5 years in Japanese compared to several-fold higher in a comparable American group).

While there may be genetic and other cultural and lifestyle reasons behind the dramatically reduced cardiovascular risk in Japanese, it is undeniably at least partially due to the increased intake of omega-3 fatty acids from fish. Incidentally, the purported benefits of omega-3 fatty acids provide a vigorous counter-argument to the idea that all humans should be vegetarians.

Anyway, if we were to take some lessons from the Japanese and their greater habitual intake of omega-3 fatty acids from fish, they might include:

--Rural and coastal Japanese are the sub-populations with the highest reliance on fish, about a quarter-pound a day. (Gives new meaning to the idea of a "Quarter Pounder," doesn't it?) This is at least five-times greater than the intake of an average American.

--Likewise, the blood level of omega-3s in the blood of Japanese is 5-fold higher than in Americans.

--The average intake of omega-3s (EPA + DHA) among a broadly-selected population of Japanese is 850 mg per day (320 mg EPA; 520 mg DHA). Intake ranges from 300 mg per day all the way up to 3100 mg per day.

--Greater omega-3 intake (EPA + DHA) is associated with lesser carotid intimal-medial thickness, an index of body-wide atherosclerosis.

--Japanese have far less heart attack and stroke despite greater prevalence of smoking (nearly half of Japanese) and drinking.

--Total fat intake (percent of calories) is nearly identical between Americans and Japanese. It's the proportion of fat calories from omega-3 that is greater, the proportion of omega-6 that is less in Japanese.


The Japanese eat their fish in ways that we do not: As sashimi (raw, as with sushi in its various forms like Nigiri and Chirashi); fried in tempura; shaved, dried fish sprinkled on about anything you can imagine (it's not as bad as it sounds); as a snack, as in dried cuttlefish (which you can purchase in packages as a portable, sweetened fish that you eat on-the-run--I know it sounds awful, but don't poke fun at it until you've tried it); in "soups" with soba noodles. Fish is commonly consumed with rice and soy sauce, as well as other soy-based foods, such as tofu, miso (soy bean paste), or natto. 


I believe that there are some lessons to take from the Japanese and their fish-consuming habits:

1) An omega-3 fatty acid intake of at least 1000 mg per day yields measurable cardiovascular benefits. 

2) Despite the fears over mercury and pesticide residues in fish, this seems to not have played out to be a real-life effect in the Japanese, who consume five-fold greater quantities of fish. 

3) My mother was right after all when she encouraged us to eat more fish. 


DIRECT Study result: Low-carb, Mediterranean diets win weight-loss battle

Drs. Iris Shai and colleagues released results of a new Israeli study, the Dietary Intervention Randomized Controlled Trial (DIRECT) Trial, that compared three different diet strategies. Of those tested, a low-carbohydrate diet was most successful at achieving weight loss.

You can find the full-text of the study on the New England Journal of Medicine website.

322 participants followed one of three diets over two year period. Compared head-to-head, the (mean) weight loss in each group was:

• 2.9 kg (6.4 lbs) for the low-fat group
• 4.4 kg (9.7 lbs) for the Mediterranean-diet group
• 4.7 kg (10.3 lbs) for the low-carbohydrate group

(Average age 52 years at start; average body-mass index, or BMI, 31.)

The conclusion was that the low-carb diet performed the best, with 60% greater weight loss, with the Mediterranean diet a close second.


The diets

The low-fat diet was based on the American Heart Association diet, with 30% of calories from fat (10% from saturated fat) and food choices weighted towards low-fat grains, vegetables, fruits, and legumes and limited additional fats, sweets, and high-fat snacks; calorie intake of 1500 kcal per day for women and 1800 kcal per day for men was encouraged.

The Mediterranean diet was a moderate-fat diet rich in vegetables, with reduced red meat, and poultry and fish replacing beef and lamb. Total calories from fat of 35% per day or less was the goal, with most fat calories from olive oil and a handful of nuts. Like the low-fat program, calories were limited to 1500 kcal per day for women, 1800 kcal per day for men.

The low-carbohydrate diet was patterned after the popular Atkins’ program, with 8% participants achieving the ketosis that Dr. Atkins’ advocated as evidence that a fat-burning metabolism was activated, rather than sugar-burning as fuel. For the 2-month “induction phase,” 20 grams of carbohydrates per day was set as the goal, followed by 120 grams per day once the weight goal was achieved. Unlike the other two diets, calories, protein and fat were unlimited.


Weight loss, lipids, inflammation

You can see from the weight loss graph that the low-carb approach exerted the most dramatic initial weight loss. Interestingly, much of the weight-loss benefit was lost as the carbohydrate intake increased, by study design, back to 120 mg per day. However, the other two diet approaches showed similar phenomena of “giving back” some of the initial weight loss.

The low-carbohydrate diet exerted the greatest change in cholesterol, or lipid, panels: increased HDL 8.4 mg/dl vs. 6.3 mg/dl on low-fat; the triglyceride response was the most dramatic, with a reduction of 23.7 mg/dl vs. 3.7 mg/dl on low-fat. Interestingly, the LDL cholesterol-reducing effect of all three diets was modest, with the most reduction achieved by the Mediteranean diet.

The inflammatory measure, C-reactive protein (CRP), was reduced most effectively by the low-carb and Mediterranean diets, least by the low-fat diet. HbA1c, a measure of long-term blood sugar, dropped significantly more on the low-carb diet.

When the final dietary composition was examined, interestingly, there really were only modest differences among the three diets, with 8% less calories from carbs, 8% greater calories from fat, comparing low-carb to low-fat, with Mediterranean intermediate.



Taken at face value, this useful exercise quite clearly shows that, from the perspective of weight loss and correction of metabolic parameters like triglycerides, HDL,CRP, and blood sugar, low-carbohydrate wins hands down, with Mediterranean diet a close second.

It also suggests that a return to a carbohydrate intake of 120 mg/day allows a partial return of initial weight lost, as well as deterioration of metabolic parameters after the initial positive changes.

Although the study has already received some criticism for such potential flaws as the modest number of Atkins’ followers achieving ketosis (8%), suggesting lax adherence, and the reintroduction of the 120 mg/day carbohydrate advice, I can suspect that these may have been compromises drawn to satisfy some Institutional Review Board. (Whenever a study is going to be conducted involving human subjects, a study needs to pass through the review of an Institutional Review Board, or IRB. IRB’s, while charged to protect human subjects from experimental abuses, also tend to be painfully conservative and will block a study or demand changes even if they are not dangerous, but just veer too far off the mainstream.)


However, several unanswered questions remain:

1) How would the diets have compared if the carbohydrate restriction were continued for a longer period, or even indefinitely? (The divergences would likely have been dramatic.)
2) Will low-carb exert the same cardiovascular event reduction that the Mediterranean approach has shown in the Lyon study and others?
3) Are there effects on health outside of the measures followed that differ among the three diets, such as cancer? (I doubt it, especially given the modest real differences over time. But this will be the objection raised by various "official" organizations.)


I would further propose that:

Low-fat diets are dead

The AHA will cling to their version of low-fat diet, based on difficulty in changing course for any large, consensus-driven organization, not to mention the substantial ($100’s of millions) revenues derived from endorsing low-fat manufactured products. The AHA will also point to the lack of difference in LDL cholesterol among the three, since they cannot get beyond the fact that there’s more to coronary risk—a lot more—than LDL.


Off-the-shelf diets achieve off-the-shelf results

If you just need a T-shirt, a medium might fit fine. But if you’d like a nicely fitting suit or dress, then tailoring to your individual proportions is needed. When aiming towards maximizing benefits on lipoproteins and coronary risk, none of these diets achieve the kinds of changes we often need for coronary plaque reversal, as in the Track Your Plaque program. That requires making dietary changes that exert maximal effects on lipoprotein patterns.

Do I sell heart scans?

I came across a criticism of the Track Your Plaque program recently that suggested that it was nothing more than a program to sell CT heart scans.

Huh?

I suppose if you say that the Track Your Plaque program is nothing more than a way to sell heart disease prevention, omega-3 fatty acids from fish oil, vitamin D, better nutrition, and better identification of causes of heart disease . . . well, I believe that would be true.

But is the program a "front" to sell heart scans?

No, it is not, nor has it ever been.

I've heard about these peculiar suspicions about the program before. Though I've never taken them seriously, let me clear up any lingering uncertainty:


--I have no relationship with any heart scan center, scanning facility, or hospital other than to interpret heart scans.

I do not own a scanner, I have no financial interest in a scanner or scanning center, nor have I ever had any interest. I also have no plans to do so in the future. Let business people in the imaging business do that. I want no part of it. I have seen what these people go through and, frankly, I want no part of it, nor do I want the appearance that I am advocating scans to make money. I'm accused of trying to make money from scans even when I do not have any financial interest!


--I do not sell heart scans or imaging packages, nor have I ever done so.

You can't buy a scan through Track Your Plaque, The Heart Scan Blog, or through me. To me, heart scans are simply a measuring tool to identify the extent of coronary plaque, as well as a tracking tool to follow its course. Without it, there would be no Track Your Plaque. But there is also no alternative. The closest alternative would be carotid intimal-medial thickness, a technique, while useful, is a distant second choice to indirectly gauge coronary plaque by examining the thickness of the carotid lining (not carotid plaque). Perhaps in 10 years, a better measure to gauge and track coronary plaque will emerge that has superior aspects over CT heart scanning. If reasonable, safe, accessible, and quantitative, then Track Your Plaque may adopt that technology as its measuring tool.

Track Your Plaque is not about heart scanning; Track Your Plaque is about measuring and tracking plaque that, in 2008, is still best accomplished with CT heart scans.


--I make loads of money from heart scans and Track Your Plaque.

Yeah, right.

Track Your Plaque is a volunteer venture for my team; none of us get paid a penny for doing all we do, including me. We charge a membership fee on the website (somewhere around $6-7 a month) to pay our expenses, such as code writing for our proprietary software (much of it remains under development), printing costs, modest legal costs, the costs of doing business (e.g., accountant). Despite the fact that Track Your Plaque and the Heart Scan Blog occupies a substantial part of the day of the Track Your Plaque team, none of us are reimbursed for our time. I do believe, however, that this concept is so enormously powerful that it will, someday, pay us all enough to allow us to devote more time and effort to it.

Personally, I can't wait to devote more time and effort to this concept that is simple, logical, and effective. More research is needed, more development is needed, more discussion is needed. Right now, it is all accomplished outside of our busy schedules, including my full-time cardiology practice. I continue to have 7 am procedures, middle-of-the-night calls, weekend hospital rounds and emergencies (though virtually none of these are the patients involved in prevention, but the "other" people: atrial fibrillation, elderly heart failure patients, rhythm disorders, cardiomyopathies, pulmonary hypertension, peripheral vascular disease, the non-compliant).


--The book, Track Your Plaque, is a gimmick to sell you a heart scan.

No, it's a program that relies on this technology. But there's no special deal, no discounts, no steering to heart scan centers that I have a special arrangement with. No such thing exists, nor has there ever been such an arrangement.


I've heard it all. Early on, when I was helping my friend, Steve Burlingame and his wife, Nancy, set up Milwaukee Heart Scan, I helped by providing medical oversite, education of physicians and public, and interpreting heart scans. After all, in the "early days," nobody knew anything about heart scans. It was a long, hard climb against ignorance, habit, entrenched thinking, stubbornness, and stupidity. I've been paid next to nothing for all this. I told Steve long ago that, given the extraordinary expenses of maintaining an independent scanning center, that he should first pay his expenses, pay his technologists, receptionists, and nurse, pay himself, then pay me for reading scans if he had any money left over. Most of the time, Steve had nothing left over and I was paid nothing.

So, while some of my colleagues were assuming that I was rolling in money from "promoting" heart scans, the reality was that I was doing nearly everything for free. (It certainly wasn't the high life I was living; I don't drive a Mercedes, take fancy vacations, none of that. In fact, I work about 51 weeks a year.)

Why do I do this if it doesn't yield a big flow of money? Because I believe in it as a superior path to the conventional. If I were simply interested in making more money--I wouldn't do it. I would simply do what all my cardiology colleagues are doing: more heart catheterizations, more angioplasties and stents, learning how to do carotid stents, iliac stents, peripheral angioplasty, renal stents, acquiring the skills to put in defibrillators, new device insertion like umbrellas in the interatrial septum, etc. There's plenty more money in that. It's also not that hard. I know, because that is my background: high-risk cardiac interventions. That's what I was trained to do, that's what I did from a number years, until I started to see that this was nothing more than "putting out fires" in people who became increasingly ill and reliant on bail-out procedures. It makes lots of money, but it is also fundamentally wrong.

So, no, I do not sell heart scans, nor is the Track Your Plaque program or The Heart Scan Blog meant to promote heart scans except as a tool for tracking this disease.

That's it, pure and simple.

Plaque is the new cholesterol

Which is more important: cholesterol or coronary plaque?

Ask what Dr. Michael Eades' calls "statinators," and you will likely receive a befuddled look. Or, you might receive comments like "Measuring plaque has never been shown to reduce mortality."

While risk factors for heart disease are important, no doubt (my office practice is about half lipid consultation and complex hyperlipidemia management), for many they have become an end in themselves. In other words, LDL cholesterol in particular dominates thinking so much that it has caused many to exclude the fact that plaque---coronary atherosclerotic plaque---is the disease itself.

Dozens of studies, from the St. Francis Heart Study to the 25,000-participant UCLA registry, to the recently-released MESA database (ethic differences, women, as well as superiority to carotid measures) have repeatedly shown that heart scan scores (coronary artery calcium scores) are superior to conventional risk factors (usually via the Framingham risk score) for predicting future heart attack and other events. And the differences are not minor incremental differences. The predictive power of plaque measurement via heart scanning is multiples better: 4 times, 10 times, 20 times or more in various subgroups.

Much of what we do in medicine is not based on long-term studies of outcome, pitting some diagnostic measure or treatment against placebo. It is already standard practice to measure plaque via heart catheterization, crudely via stress testing, and increasingly popular CT coronary angiography. None of these methods have been subjected to studies comparing testing vs. not testing in a large population, followed by some program of prevention to assess differences in mortality, heart attack, and other events.

Why should heart scan be held to such a standard?

Dr. Scott Grundy, lipid guru and one of the experts who sat on the Adult Treatment Panel-II for lipid management guidelines, recently stated [emphasis added]:

"Imaging has at least 3 virtues. It individualizes risk assessment beyond use of age, which is a less reliable surrogate for atherosclerosis burden; it provides an integrated assessment of the lifetime exposure to risk factors; and it identifies individuals who are susceptible to developing atherosclerosis beyond established risk factors. Also of importance, in the absence of detectable atherosclerosis, short-term risk appears to be very low."

Well said, and from a vocal statinator, to boot.

Sadly, Dr. Grundy goes on to say how plaque imaging can serve to better determine who will benefit from statin drug use.

Of course, you and I know that there is far more to reduction of cardiovascular risk applied to a framework of serial plaque quantification ("tracking plaque"!) than statin drugs. I doubt that a man as intelligent as Dr. Grundy truly believes this. I suspect that he is simply stating what he knows what will be published without resistance in the standard medical literature, trying to achieve a modest incremental success just by raising consciousness about heart scanning and plaque imaging: first things first.

Maybe next will be a plaque-tracking, or even a plaque-reducing, mainstream conversation, just like the one we've been conducting for the past four years.

Track Your Plaque success story blows it

Joe was a Track Your Plaque Success Story. With a starting heart scan score of 278, he dropped it 12 months later to 264, a 5% reduction. Though not a huge reduction, Joe's risk for a heart attack or other coronary event was virtually zero. I was very proud of Joe.

Among the culprit lipoprotein patterns that caused Joe's plaque was lipoprotein(a), or Lp(a). Niacin was therefore crucial to his program. It was among the principal reasons he dropped his heart scan score and reduced his risk for heart attack so dramatically.

Since he retired, Joe has been freewheeling around the country, traveling and having a great time. He consequently stopped thinking about his heart disease and Lp(a). He also tired of the occasional hot flushes he'd experienced with niacin. Though the flushes were promptly aborted by drinking two glasses of water, he simply didn't want to be bothered.

So when Joe saw this interesting and tantalizing "flush-free niacin" on the store shelf, he grabbed it.

Joe came back to the office. His blood pressure was 190/94, so high that he was having occasional chest pains from it (which can happen when something called "left ventricular diastolic dysfunction" develops from hypertension). His lipoprotein patterns were terrible, including a big upward jump in Lp(a) and drop in HDL. So I asked him to have another heart scan right away: Score 371, a 40% increase. In other words, his program went down the toilet.

Why?

Simple: Flush-free niacin. I've said it before (No flush = No effect and No flush niacin kills) and I'll say it again:

Flush-free or No-flush niacin is a complete, unadulterated, completely ineffective SCAM.

Flush-free or no-flush niacin is not a substitute for niacin. Joe is yet another example of how dangerous this scam can be. It turned one of our great success stories into a failure.

Please, please, please do not fall for this misleading and potentially dangerous scam product. While the product itself is not intrinsically dangerous, it denies you the benefits of the real thing: niacin.

Thankfully, the mistake in Joe's program was caught before a heart attack or other catastrophe. He did manage to pass a stress test, though with a flagrantly out-of-control blood pressure response. We'll get him back on track--but with niacin, the real thing.

Dr. Cannell comments on vitamin D lab tests

As always, Dr. John Cannell of The Vitamin D Council continues to teach us new lessons about vitamin D.

Apparently, Dr. Cannell is swamped with the attention that vitamin D is drawing, largely due to his efforts to publicize the enormous deficiency of Americans and his great talent for articulating the science. The most current newsletter, while a bit haphazard, makes some excellent new points that I reprint here.

(I did not reprint his conversation about "any form of vitamin D" being acceptable. My experience differs: In nearly 1000 patients who have taken vitamin D supplements, my experience is that most tablet forms are inconsistently absorbed, sometimes not absorbed at all. I therefore advocate only use of gelcaps or liquids. I'm told by members of Track Your Plaque, however, that they are witnessing reliable increases in blood levels of vitamin D by taking the powdered form of Bio Tech Pharmacal's product.)


Does it matter what reference lab my doctor uses?

Yes, it might make a huge difference. A number of methods exist to measure 25(OH)D in commercial labs. The two most common are mass spectrometry and a chemiluminescence method, LIAISON. The first, mass spectrometry, is highly accurate in the hands of experienced technicians given enough time to do the test properly. However, in the hands of a normally trained technician at a commercial reference lab overwhelmed with 25(OH)D tests, it may give falsely elevated readings, that is, it tells you are OK when in fact you are vitamin D deficient. The second method, chemiluminescence, LIAISON, was recently developed and is the most accurate of the screening, high throughput, methods; LabCorp uses it. Quest Diagnostics reference lab uses mass spec. Again, both Quest and LabCorp are overwhelmed by 25(OH)D requests. The problem is that the faster the technicians do the mass spec test, the more inaccurate it is likely to be. If your 25(OH)D blood test says "Quest Diagnostics" on the top, do not believe you have an adequate level (> 50 ng/ml). You may or may not; the test may be falsely elevated. Let me give you an example. A doctor at my hospital had Quest Diagnostics do a 25(OH)D. It came back as 99 ng/ml of ergocalcifero All posts by william-davis

Goodbye, Dr. Jarvik

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

Pfizer pulls Lipitor ads featuring Dr Robert Jarvik in HeartWire

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

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

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


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

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



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

Hammers and nails

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

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


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

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

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

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

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

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

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

My message: Don't get nailed.

What is abnormal?

What is abnormal?

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

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

Diameter of the thoracic aorta: 4.5 cm

Mild coronary plaque by heart catheterization

Carotid plaque of 30-50%


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

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

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

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

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

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

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

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

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

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

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


Copyright 2008 William Davis, MD

Niacin and hydration

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

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

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

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

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

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

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

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

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

Let me float an idea

I'd like to float an idea.

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

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

Actos, Avandia, and vitamin D

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

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

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

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

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

--Reduces small LDL

--Reduces triglycerides

--Reduces c-reactive protein

--Reduces blood pressure

--Reduces blood sugar

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

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

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

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

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

What if heart scans become obsolete?

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

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

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

Simple: Then we will convert to that measure.

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

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

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

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

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

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

Scare tactics

Does the media engage in scare tactics?

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

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

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

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

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

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

A sampling:

Stress test could help prevent sudden heart attack

DAWN ZERA Times Leader Correspondent

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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



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

ABC News

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

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

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

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

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

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

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

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



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


By Ed Edelson

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

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

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

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

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

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

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

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

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

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

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

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

More information

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




Heart Attack Threatens Young, Old

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

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

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

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

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

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


The messages I take from such stories:

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

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

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


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

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

Heart disease detectable decades before disaster

Or:

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



Copyright 2008 William Davis, MD

Which statin is best?

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

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

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

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

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

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

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

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

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

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

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

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


Copyright 2008 William Davis, MD

Lipoprotein(a)--neglected and unappreciated


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

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

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

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

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

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

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

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

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

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

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



Copyright 2008 William Davvis, MD

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That's easy: NONE.

(Although I've addressed this previously, the question has come up again many times and I thought it'd be worth repeating.)

In other words, no heart scan score--100, 500, 1000, 5000--should lead automatically to procedures in someone who underwent a heart scan but has no symptoms.

This question is a common point of confusion.

In other words, is there a specific cut-off that automatically triggers a need for catheterization?

In my view, there is no such score. We can't say, for instance, that everybody with a score above 1000 should have a catheterization. It is true that the higher your score, the greater the likelihood of a plaque blocking flow. A score of 1000 carries an approximately 25-30% likelihood of reduced blood flow sufficient to consider a stent or bypass. This can nearly always be settled with a stress test. Recall that, despite their pitfalls for uncovering hidden heart disease in the first place, stress tests are useful as gauges of coronary blood flow.

But even a score of 1000 carries a 70-75% likelihood that a procedure will not be necessary. This is too high to justify doing heart catheterizations willy-nilly.

Unfortunately, some of my colleagues will say that any heart scan score justifies a heart cath. I believe this is absolutely, unquestionably, and inexcusably wrong. More often than not, this attitude is borne out of ignorance, laziness, or a desire for profit.

Does every lump or bump justify surgery, radiation, and chemotherapy on the chance it could represent cancer? Of course not. There is indeed a time and place for these things, but judgment is involved.

In my view, no heart scan score should automatically prompt a major heart procedure like heart catheterization in a person without symptoms. If a stress test is normal, signifying normal coronary flow (and there are no other abnormal phenomena, such as abnormal left ventricular function), then there is no defensible rationale for heart procedures. Heart procedures like stents and bypass cannot prevent heart attacks in future; they can only restore flow when flow is poor, or stop the heart attack that is about to occur.

However, EVERY heart scan score above zero is a reason to engage in a program of prevention.

"It's genetic"

At 53, Sam had been through the wringer with heart disease. After his first heart attack at age 50, he'd undergone four heart catheterizations, 5 stents, and, most recently, a bypass operation. He came to us to see if there was a better solution.

After hearing Sam's story, I asked,"Did your doctors suggest to you why you had heart disease?"

"Well, they said it was genetic, since my father went through the same thing in his early 50s, though he died after his second heart attack at age 54. They said it was bad luck and nothing could be done about it."

Though Sam's case is more dramatic than most, I hear this argument every day: Risk for heart disease is genetic.

It's true: There are indeed multiple reasons for inheriting causes for coronary heart disease, genes that heighten inflammatory responses, oxidative responses, modify lipoprotein particles, increase blood pressure, etc. There has even been some excitement over developing chromosomal markers for heightened risk.

That's all well and fine, but what can we do about it today?

In practical life, many inherited genetic patterns can be expressed in ways that you and I can identify--and correct. They are not chromosomal markers, but end products of genetic patterns. (Although there are indeed identifiable chromosomal markers, they have not yet led to meaningful treatments to my knowledge.)

These readily identifiable patterns include:

--Lipoprotein(a)--Clearly genetically transmitted, passed from mother or father to each child with a 50% likelihood, then you onto your children if you have it.

--Small LDL--Although small LDL is amplified by high-carbohydrate diets and obesity, it can also occur in slender people who do not indulge in carbohydrates --i.e., a genetic tendency. Or, it can be a combination of poor lifestyle magnifying the genetic tendency for small LDL.

--Low HDL--Particularly the extremes of low HDL below 30 mg/dl. (Although, interestingly, I am seeing more of these people, though not all, respond to vitamin D replacement. Perhaps an important subgroup of low HDL people are really Vitamin D Receptor (VDR) variants.)

--ApoE--Two variants are relevant: ApoE2 and ApoE4. In my experience, it's the E2 that carries far greater significance, though the data are somewhat scanty. ApoE4 people are more sensitive to the fats in their diet (greater rises in LDL with fats; thus, some people advocate a tighter saturated fat restriction with this pattern, though I am not convinced that is the best solution), while ApoE2 people are exceptionally sensitive to carbohydrates, develop extravagant increases in triglycerides, and are very diabetes-prone with even the most minimal weight gain. If two "doses" of the E2 gene are present (homozygotic), then the tendencies are very exagerrated. E4 people are also subject to greater likelihood of Alzheimer's, though it is not a certain risk in a specific individual.

--Postprandial disorders--We use the fasting intermediate-density lipoprotein (IDL) as an easy, obtainable index of the ability to clear after-eating byproducts of meals from the blood. Increased IDL has been related to increased coronary, carotid, and aortic aneurysmal disease.

--Hypertriglyceridemia-i.e., increases in triglycerides, While not all forms of high triglycerides confer risk for atherosclerosis, many do, particularly if associated with IDL, small LDL, increased LDL particle number and/or apoB.


There are more, but you get the point. There are clear-cut genetically-transmitted reasons for greater risk for cardiovascular disease. Some, like lipoprotein(a), yield very high risk. Others, like increased triglycerides, yield mixed levels of risk.

Importantly, all of these patterns--ALL--are identifiable and are treatable. Treatment may not always be the easiest thing, but they are treatable nonetheless. While lipoprotein(a), for instance, is the most difficult pattern to correct in the above list, I remind everyone that our current "record holder" for reversal of plaque and heart scan scores--63% reduction--has lipoprotein(a) that we corrected.

If you've been told that your risk for cardiovascular disease or coronary plaque is "genetic" and thereby uncorrectable and hopeless, run the other direction as fast as you can. Get another opinion from someone willing to take the modest effort to tell you precisely why.

Tim Russert Revisited

A Heart Scan Blog reader brought this piece by Dr. MacDougall to my attention.

Dr. MacDougall created a fictitious posthumous conversation between himself and the late Tim Russert. MacDougall paints a picture of a hardworking, hard-living man who adhered to an overindulgent lifestyle of excessive eating. He concludes that a vegetarian, low-fat diet would have saved his life.

Beyond being disrespectful, I would differ with Dr. MacDougall’s assessment. In fact, I’ve heard an interview with Mr. Russert’s primary care physician in which the doctor claimed that Mr. Russert had been counseled on the need for a low-fat diet and, in fact, adhered to it quite seriously. Far from being an overindulgent, overeating gourmand, he followed the dictates of conventional dietary wisdom according to the American Heart Association. The low-fat diet articulated by Dr. MacDougall is simply a little more strict than that followed by Mr. Russert.

What exactly could Mr. Russert have done to prolong his life? Several basic strategies:

--Added fish oil. This simple strategy alone would have reduced the likelihood of dying suddenly by almost half.

--Eliminated wheat and cornstarch—Mr. Russert developed diabetes in the last few years of his life. By definition, diabetes is an inability to handle sugars and sugar-equivalents. Wheat and cornstarch yield immediate and substantial surges in blood sugar greater than table sugar; elimination causes weight to plummet, blood sugar to drop, and diabetes (at least in its early phases) can be eliminated in many people, particularly those beginning with substantial excess weight.

Just those two strategies alone would more than likely have avoided the tragic death that brought Mr. Russert’s wonderful life and career to an abrupt end.

Of course, he could have even taken his heart health program even further, as we do in the Track Your Plaque program. While the conversation has focused on how to avoid tragic events like sudden cardiac death, why not take it a step farther and ask, "How can coronary plaque be measured, tracked, and reversed?"

In that vein, Mr. Rusert could have restored vitamin D to normal levels; identified all hidden sources of heart disease using lipoprotein testing (though he had small LDL without a doubt, given his generous waist size, HDL of 36 mg/dl and high triglycerides); considered niacin. Simple, yet literally lifesaving efforts, that make reversal much more likely.

Those simple steps, in fact, would have tipped the scales heavily in Mr. Russert’s favor, making a heart attack and/or sudden death from heart disease exceptionally unlikely.

Water: Bottled vs. tap

The Fanatic Cook has a great post discussing the findings of the Environmental Working Group (EWG) on the quality of bottled water.

The full text of the study from the EWG can be viewed here.

They report that "the bottled water industry promotes an image of purity, but comprehensive testing by the Environmental Working Group (EWG) reveals a surprising array of chemical contaminants in every bottled water brand analyzed" . . . After analyzing 10 brands, they conclude that "tests strongly indicate that the purity of bottled water cannot be trusted. Given the industry's refusal to make available data to support their claims of superiority, consumer confidence in the purity of bottled water is simply not justified."

"EWG's study has revealed that bottled water can contain complex mixtures of industrial chemicals never tested for safety, and may be no cleaner than tap water. Given some bottled water company's failure to adhere to the industry's own purity standards, Americans cannot take the quality of bottled water for granted. Indeed, test results like those presented in this study may give many Americans reason enough to reconsider their habit of purchasing bottled water and turn back to the tap."


For these reasons, as well as environmental reasons (plastic bottles filling up dumpsites), I think it is becoming clearer and clearer that bottled water is something we should only use in a pinch, not habitually.

Can CRP be reduced?

The JUPITER study has sparked a lot of discussion about c-reactive protein, or CRP.

If we follow the line of reasoning that prompted this study, reducing CRP may correlate with reduction of cardiovascular events. Thus, in the JUPITER study, Crestor 20 mg per day reduced cardiovascular events by nearly half.

From a CRP perspective, starting values were 4.2 mg/dl in the Crestor group of the trial, 4.3 mg/dl in the placebo group. After 24 months, CRP in the Crestor group was 2.2 mg/dl, 3.5 mg/dl in the placebo group, representing a 37% reduction.

Now, in our Track Your Plaque program--an experience that has yielded the virtual ELIMINATION of cardiovascular events--we aim for a CRP level of 1.0 mg/dl or less, ideally 0.5 mg/dl or less. The majority of people achieve these ambitious levels. In fact, it is a rare person who does not.

How do we achieve dramatic reductions in CRP? We use:

--Weight loss through elimination of wheat and cornstarch--This yields impressive reductions.

--Vitamin D--I have no doubt whatsoever of vitamin D's capacity to exert potent anti-inflammatory effects. I am not entirely sure why this happens (enhanced sensitivity to insulin, reduced expression of tissue inflammatory proteins like matrix metalloproteinase and others, etc.), but the effect is profound.

--Elimination of junk foods--like candies, cookies, pretzels, rice cakes, potato chips, etc.

--Exercise--Amplifies the benefits of diet on CRP reduction.

--Not allowing saturated fats to dominate--Yes, yes, I know. The demonization of saturated fat conversation has been largely replaced by the Taubesian saturated fat has not been confidently linked to heart disease conversation. But controlled feeding studies, in which a single component of diet is manipulated (e.g., saturated vs. monounsaturated vs. polyunsaturated fat) have clearly shown that saturated fats do activate several factors in the inflammatory response.

--Fish oil--Though I am a firm believer in the huge benefits of omega-3 fatty acid supplementation/restoration, the anti-inflammatory effect is modest from a CRP perspective. However, there are anti-inflammatory benefits beyond that of simple CRP (via normalization of eicosanoid metabolism and other pathways).

--Weight loss--A BIG effect. Weight loss drops CRP like a stone. The CRP-reducing effect is especially large if achieved via carbohydrate reduction.

Of course, this is much more complicated than taking a pill. But it is effective to achieve health benefits outside of cardiovascular risk, is enormously useful as part of a weight loss effort, and doesn't cost $1400 per year like Crestor.

In short, if CRP reduction is the goal, it certainly does not have to involve Crestor.