Cureality | Real People Seeking Real Cures

How long should it take to stop or reverse coronary plaque growth? How long will it require to stop your heart scan score of, say, 350, from increasing at the expected rate of 30% per year, slow it down (we say "decelerate") to less than 30%, or stop it altogether? Or, actually reduce your score?

It can vary widely. Several simple patterns do seem to emerge, however. Our experience is that lower scores, particularly less than 100 at the start, are easier to gain control over. Scores of 50 or less, in fact, commonly can return to zero.

Higher scores, particularly those >1000, are more difficult to slow or reduce, though we've done it many times. You'll generally have to try harder and it may take longer. It's not uncommon to not stop plaque growth with a starting score this high until your 2nd or 3rd year of effort.

Sometimes it may take even longer. An occasional person requires four or five years to gain control. And there are, unfortunately, some people who never really gain complete control. They slow plaque growth compared to what it would have been with conventional efforts, but never completely halt growth. Why? Sometimes it's a matter of less than full commitment. Other times, we just don't know. Thankfully, these especially difficult cases are few and the majority enjoy substantial slowing or reversal.

Since, in some people, success may take time, you've got to stick it out. Have you ever gotten lost in a strange city only to find out later that the place you were looking for was right around the corner? It can be the same way with stopping coronary plaque growth. If you start with a score of 1000 and, after two years of effort, you've only slowed growth to 11% per year and then give up in frustration, you may have missed the opportunity to have stopped growth entirely in your third year.

All we can do is tip the scales heavily in your favor. We provide you with the best tools known. You've got to provide the commitment, the consistent effort of taking your supplements or medication, making the lifestyle changes, choosing the right foods and avoiding the wrong ones. But you've got to go the distance and not give up too easily.

Where can you find an expert in health?

In my experience, they're hard--very hard--to find.

Your hospital? Certainly not the hospitals I know. The hospitals I know are experts in disease, but not in health. Hospitals are helpful when you're sick. But if you're well and would like to stay that way, there's no reason to hang around a hospital. Prevent cancer, prevent heart disease, stay well? There's no place for this conversation in a hospital.

In fact, hospital staff are among the most unhealthy people I come across. Obesity is a nationwide problem affecting millions of Americans. But it's especially a problem among people who work in hospitals. I shudder in horror when I go to a hospital cafeteria and witness the sorts of food they serve in hospitals and see what the staff eat. Should they be regarded as experts in health?

How about doctors? If you associate with physicians like the ones I know, most have lots of knowledge about disease, but little understanding of health. A rare one has insight and interest in health.

I went to a recent meeting with my cardiology colleagues. Food served: pizza, Coca-Cola, spaghetti, fried onion rings, white bread with butter. They all dug in without hesitation. Over half were miserably overweight. Several were, in fact, diabetic; several more, pre-diabetic. I know that at least several are smokers. Experts in health?

Drug companies? Well, they're interested in health only as far as it provides profits. But health for its own sake? Ask anybody from a drug manufacturer about their views on the nutritional supplement movement and watch them sneer.

Food manufacturers? You mean like Coca-Cola, Pepsi-Cola, Nabisco, and General Mills? How about fast-food operations like McDonald's, Pizza Hut, and KFC?

The message: Know where to look for genuine information on health. You won't get it from hospitals. You won't get it from drug company marketing. For the most part, you can't even get it from your physician.

Instead, you're going to witness a broad movement towards self-empowerment in health, fueled by the internet and services like ours (Track Your Plaque). These are information resources that are not driven by profit, intent on providing truth, and not afraid to reject prevailing views.

It does not mean that hospitals are unnecessary, or that food manufacturers are evil, or that fast food should be legislated out of existence. We live in a capitalistic society, driven by supply and demand. Hopefully, demand is borne from educated choices from informed consumers. That's where information that's reliable, credible, and not profit driven come in.

It's been my suspicion for some time that the combination of lipoprotein(a), or Lp(a), in combination with small LDL particles is a really bad risk for heart disease. People with this combination seem to have much higher heart scan scores for age than others. This seems to be a pattern that we'll see in the occasional woman less than 50 years old who already has a high heaert scan score. (It's unusual for women to have detectable coronary plaque before age 50.)

Very little data exists to support this idea and we are in the process of performing a small study to see whether it's true or not. My gut sense: it's among the most potent causes of coronary plaque around.

Case in point: Even though I spend a great deal of my time and energy advocating heart disease prevention, I still maintain my hospital privileges and skills. I had to cover one of the emergency rooms in town this past weekend (a requirement to maintain my hospital privileges).

One of the patients I saw was a 40-year old man--we'll call him Roland-- suffering a very large heart attack, a so-called "anterior myocardial infarction", or a heart attack involving the most important front portion of the heart. Thankfully, he came to the ER within 45 minutes after his chest pain started. The situation was immediately obvious and I was called to the ER. We quickly took him to the cardiac catheterization laboratory and put a stent in the left anterior descending artery and flow was restored. His chest pain dissipated over the next few minutes.

Nonetheless, Roland was left with a large area of reduced contraction of his heart muscle. Only time will tell how much recovery he'll have.

Roland was extremely lucky. The majority of people with closure of the artery that he'd experienced die within minutes. He did, in fact, "arrest" briefly, i.e., his heart became electrically unstable, though he recovered promptly.

Along with the multiple tubes of blood we required to run tests for his heart attack management, we had Roland's lipids and other measures sent off, as well. Wouldn't you know: Lp(a) and small LDL. This may have accounted for a heart attack at age 40.

Keep a lookout for this when you have lipoprotein testing. Conveniently, niacin can be used to treat both patterns, though higher doses are generally required for the Lp(a) part of the pattern. It's also my belief that the sort of Lp(a) measurement performed by the Liposcience laboratory (www.liposcience.com) is superior. They use a particle number based measure, not a weight-based measure. It is therefore independent of particle size, which can vary. Further work will, I believe, reveal some very important insights into the dreaded Lp(a).

I overheard this recent conversation between a CT technologist and a 53-year old woman (who I'll call Joan) who just had a scan at a heart scan center:

CT Tech: It appears to me that you have a moderate quantity of coronary plaque. But you should know that this is a lot of plaque for a woman in your age group. A cardiologist will review your scan after it's been put through a software program that allows us to score your images.

Joan: (Sighing) I guess now I know. I've always suspected that I would have some plaque because of my mother. I just don't want to go through what she had to.

CT Tech: Then it's really important that you discuss these results with your doctor. If you wrote your doctor's name on the information sheet, we'll send him the results.

Joan: Oh, no! Don't send my doctor the results! I already asked him if I should get a scan and he said there was no reason to. He said he already knew that my cholesterol was kind of high and that was everything he needed to know. He actually got kind of irritated when I asked. So I think it's best that he doesn't get involved.

This is a conversation that I've overheard many times. (I'm not intentionally an eavesdropper; the physician reading station at the scan center where I interpret scans--Milwaukee Heart Scan--is situated so that I easily overhear conversations between the technologists and patients as they review images immediately after undergoing a scan.)

If Joan feels uncomfortable discussing her heart scan results with her doctor, where can she turn? Get another opinion? Rely on family and friends? Keep it a secret? Read up about heart disease on the internet? Ignore her heart scan?

I've seen people do all of these things. Ideally, people like Joan would simply tell their doctor about their scan and review the results. He/she would then 1) Discuss the implications of the scan, 2) Identify all concealed causes of plaque, and then 3) Help construct an effective program to gain control of plaque to halt or reverse its growth. Well, in my experience, fat chance. 98% of the time it won't happen.

I think it will happen in 10-20 years as public dissatisfaction with the limited answers provided through conventional routes grows and compels physicians to sit up and take notice that people are dying around them every day because of ignorance, misinformation, and greed.

But in 2006, if you're in a situation like Joan--your doctor is giving you lame answers to your questions or dismissing your concerns as neurotic--then PLEASE, PLEASE, PLEASE take advantage of the universe of tools in the Track Your Plaque program.

People tell me sometimes that our program is not that easy--it requires reading, thinking, follow-through, and often asking (persuading?) your doctor that some extra steps (like blood work) need to be performed. The alternative? Take Lipitor and keep your mouth shut? Just accept your fate, grin and bear it, hoping luck will hold out? To me, there's no rational choice here.

I see a great many people in my practice who come for a 2nd opinion regarding their coronary disease.

When I ask patients whether they ever asked their primary doctor or cardiologist why they have heart disease in the first place, I get one of several responses:

1) My doctor said it from high cholesterol.

2) My doctor said it was "genetic" or "part of your family history" and so unidentifiable and uncorrectable. Tough luck.

3) I didn't ask and they didn't tell me.

Let's talk about each of these.

Can heart disease be only from high cholesterol and, if so, can taking a statin cholesterol drug be a "cure"? In the vast majority of cases, in my experience, cholesterol by itself is rarely the only identifiable cause of coronary disease.

Most people have a multitude of causes (e.g., small LDL, low HDL, vitamin D deficiency, concealed pre-diabetic patterns, etc.). This explains why many people with high LDL don't have heart disease and why others with low HDL do have heart disease. High LDL cholesterol is only part of the cause.

Does "genetic" or being part of your family's history also mean unidentifiable and uncorrectable? Absolutely not.

What your doctor is really saying is "I don't know enough to diagnose the causes because I haven't kept up with the scientific literature", or "I don't want to be bothered with this because it takes a lot of time and pays me very little money; I'd rather wait until you need a stent ", or "The drug representatives haven't told me about any new drugs". This is ignorance and laziness at best, greed and profiteering at worst. Don't fall for it. I hope that by now you recognize that the great majority of causes of heart disease are identifiable and correctable.

If you didn't think to ask, now you know that you should. If you and your doctor don't think about why you have coronary plaque in the first place, how can you develop a program to control it?

You need to ask. And you need to get confident answers. "I don't know" or "It's genetic" and the like are unacceptable.

Have you read the latest cover story from Forbes magazine? It's entitled "Pill Pushers: How the drug industry abandoned science for salesmanship".

It's great reading. (A condensed version is available at the www.forbes.com website: http://www.forbes.com/business/forbes/2006/0508/094a.html. They require you to provide your e-mail address though it's free.)

Drug industry advertising has raised consciousness of all the prescription therapies available for us--that's good. However, they've gone so far overboard trying to squeeze more and more revenues out of drugs that they've cost this country a huge amount in increased health care costs and even lost lives. (Forbes does a great job of summarizing some of these instances.)

Drugs like Lipitor, Crestor, Zocor; diabetes agents; anti-hypertensive agents, etc., that is, medications taken chronically, a huge financial bonanzas for drug companies. Not only do they get $100-200 per month, but they get it month after month after month. That's per drug.

Now not all medications are bad or unnecessary. There are times when they can be truly necessary and beneficial. But don't rely on drug company advertising to tell us when.

I've recently observed that more and more of our patients on the Track Your Plaque program seem to be stopping or reducing their heart scan scores. And they're doing it faster, in less time, and with larger drops in score.

I'm not entirely sure why the sudden surge in success. However, I do wonder if adding therapeutic levels of vitamin D--at least in our generally sun-deprived Wisconsin participants--is responsible. However, we've also gotten a lot smarter on how to correct the parameters that seems to have outsized effects on plaque growth, especially small LDL.

Yesterday alone, we had two people we added to our list of successes. One, an attorney, stopped his score in one year, with no change (compared to the expected increase of 30%). Another, a woman from the northeast, dropped her score 10% in one year. Her story is remarkable for beginning at a score >1000. In general, the higher your starting score, the longer it takes to stop or reduce it.

These are just two examples. It seems to be happening at an accelerating pace.

I can only hope that our surge in success (not 100%--yet!) will continue. But, every week, we're adding more and more people to our list of success stories.

Imagine that, every day, a parade of used-car salesmen knock on your front door to sell you a special "deal". Day in, day out they knock, expecting you to hear about their offers openly.

Is there any doubt about their intentions or motives? Of course not. They're just trying to profit from selling you a car.

That's how it is in a medical office nowadays. Drug representatives, 5, 6, or more each and every day, promoting drugs. Except that the profits from drugs are far greater than a used automobile, and there's a third party involved in the transaction: you.

Today, a pushy representative came to my office. My staff and I tried to tell him that I was not interested in speaking to him. But he proved such a nuisance that I finally came out to tell him that I objected to the idea of drug reps just hanging around trying to hawk their wares.

He blurted, "Doctor, do you have patients with angina? Our new drug, ranolazine, is perfect. Forget about nitroglycerin, beta blockers, and all that. Here's the latest study proving it's better." He tried to shove a reprint of the study at me.

Getting to the bottom line, I asked, "What does it cost the patient?"

"Well, the co-pay is between $40 and $60. We're not yet well covered by insurance, so it'll cost patients around $200 a month."

Need I say more? Here's a drug that does little more than help relieve anginal chest pains. It doesn't reverse coronary plaque. It won't avoid heart attack, death, or procedures. It just modestly cuts back on the frequency of chest pain. And all for the cost of a single heart scan--a heart scan that could have prevented the entire cascade of symptoms/procedures/medication/hospitalization etc.

Hospitals, drug companies, medical device manufacturers. They're all businesses that thrive on your doctor's failure to detect and control your coronary plaque. Sometimes, even your doctor is part of this conspiracy to squeeze dollars out of human disease. Don't fall for it.

I met Agnes 18 months ago after she underwent a heart scan that revealed a scary score of over 1100. Although in her mid-70s, this was still a very high score. (Recall that a score this high carries a risk for heart attack and death of 25% per year.) Poor Agnes was a wreck over this unexpected result. "I can't sleep, I can't stop thinking about it!"

She'd undergone the scan because her 44-year old son had a heart scan score of 2200! Unfortunately, he ended up with a bypass operation for very severe disease.

Despite having been seeing a cardiologist in Boston for the last 8 years for a murmur, we uncovered multiple hidden lipoprotein patterns, many of which she shared with her son. Her most notable abnormalities were a low HDL and small LDL. Nearly 100% of all LDL particles were, in fact, small. This pattern also caused her LDL cholesterol to be underestimated by over 40%.

18 months on the Track Your Plaque program and Agnes came into town to get a repeat scan. Her score was 10.2% lower. She'd learned to live with the idea that she had hidden heart disease missed by her doctor and cardiologist for many years. But knowledge of the substantial reversal she'd achieved in the 18 months on the program gave Agnes tremendous peace of mind.

Agnes left the office with a big smile.

If you've read Track Your Plaque, you already know my feelings about smoking and coronary plaque. Smoke, and you will lose the battle for control over coronary plaque growth--it will grow and grow until catastrophe strikes.

Nonetheless, this is not sufficiently motivating for some people.

If you need more motivation to quit smoking, just take a look at your heart scan sometime, accompanied by either one of the doctors or technicians at the scan center you choose. After you've had an opportunity to look at your coronary arteries, take a look at the lungs. The heart is in the middle and the lungs are the two large black areas on either side of the heart. (They're not really black; that's just the way the images are color-coded.)

Smokers will see large cavities in their lungs--literally, half-inch to one-inch wide holes that contain only air. Many of them. These represent remnants of lung tissue, digested away and now useless from the damage incurred through smoking.

Non-smokers should see uniform lung tissue without such cavities.

What surprised me early on in my heart scan experience was how little smoking exposure was required to generate these cavities. A 40-year old, for instance, who smoked a half-pack per day for 10 years would have them. Heavier smokers, of course, showed far more extensive cavities.

Officially, these cavities are called "emphysematous blebs", meaning the scars of the lung disease, emphysema.

When I've pointed out these cavities or emphysematous blebs to patients, 9 out of 10 times they immediately become non-smokers. Commonly, they'd exclaim, "I had no idea I was really damaging my lungs!" Most admitted that they were awaiting some bona fide evidence that they were truly doing some harm to their bodies. Well, that's it.

Give it a try if you're struggling.

Most of us already know that the intake of omega-6 fatty acids in the American diet has gone overboard, much at the expense of the omega-3 fraction. This occurred as a result of the misguided advice of the 1970s and 1980s to eat polyunsaturated oils like corn, sunflower, and safflower, because of their presumed cholesterol-reducing properties compared to saturated fats. However, more recent examinations of this advice have suggested that the omega-6 fraction of oils present in polyunsaturated oils may amplify arachidonic acid and other inflammatory patterns despite the reduction in cholesterol (total and LDL).

Dr. Artemis Simopoulos of the Center for Genetics, Nutrition and Health in Washington, D.C. has written extensively on the role of omega-6 and omega-3 fatty acids in diet.

In a review entitled The Importance of the Omega-6/Omega-3 Fatty Acid Ratio in Cadiovacular Disease and Other Chronic Disease , Dr. Simopoulos collects the following comparison of omega-6 to omega-3 ratios from various populations:

Paleolithic humans 0.79
Greece (prior to 1960) 1.00-2.00
Current Japan 4.00
Current India, rural 5-6.1
Current United Kindom and northern Europe 15.00
Current United States 16.74
Current India, urban 38-50

(The numbers refer to the ratio of omega-6 to omega-3 intake.)

If we believe the observations of Dr. Loren Cordain and others, while paleolithic man died of trauma and infectious diseases, they did not die of heart disease. Paleolithic human intake of omega-3 exceeded that of omega-6.

Likewise, the traditionally low cardiac event regions of the world like Japan and Greece have less omega-3 intake than Paleolithic man, but still many times more than the U.S. and U.K.

Worst of all with an enormous preponderance of omega-6 over omega-3 are urban Indians, who experience among the highest rates of heart disease in the world.

Just for perspective, let's assume you eat an 1800 calorie per day diet, of which 30% of calories come from fat. This would amount to 540 calories per day from fat. With 9 calories per gram of fat, this means that there are 60 grams, or 60,000 mg, of fat in your diet per day.

Paleolithic man has been found to have existed on a diet consisting of 21% of calories from fats. Again assuming an 1800 calorie per day diet, that comes to 42 grams of fat per day (42,000 mg).

If we were to try to recreate the Paleolithic fat composition of diet, we would ingest 21,000 mg of omega-3 fatty acids (EPA, DHA, linolenic acid) per day. Even recreating a Japanese experience with a 4:1 ratio, it would mean 8400 mg of omega-3 per day. (Curiously, this does not agree with all estimates of Japanese intake of omega-3s.)

No matter how you look at it, cultures with lower rates of cardiovascular disease take in greater--much greater--quantities of omega-3 fatty acids.

So don't complain about your six fish oil capsules (usually containing 6000 mg of total oil, 1800 mg omega-3s)!

A Heart Scan Blog reader brought the following tidbit to my attention.

Cardiologist and now writer for U.S. News and World Report, Dr. Bernadine Healy, wrote this editorial, a glowing endorsement of heart scans:

The approach is beautifully simple. Calcium accumulates in advanced plaques, so calcium visible in the heart's arteries indicates atherosclerosis. An exploding number of studies in the past few years have unequivocally shown that the calcium score predicts both heart attack and sudden death. As a generalization, patients with scores between 100 and 400 face three to four times the risk of a heart attack or death compared with others at the same age with a zero score. Over 400, that elevated risk more than doubles.

Most doctors rely instead on the Framingham calculator, which estimates a symptom-free person's risk of a heart attack in the next 10 years based on smoking history, blood pressure, cholesterol levels, sex, and age. It's available free online from the National Institutes of Health. Most people taking the test will have minimal or no coronary disease, though risk estimates over 9 percent should inspire vigorous preventive efforts. For some, however, coronary heart disease is sneaky, and Framingham will underestimate what lies ahead. Roughly half of those who suffer a major heart attack or sudden coronary death are symptom free. Calcium scores are additive to Framingham; they pick up the individual surprises by using X-ray vision to look inside the heart. No wonder insurance companies are scrambling to use coronary calcium scores—life insurers, that is.

Dr. Bernadine Healy is no small-time player. In addition to her academic credentials, she is former chief of the National Institutes of Health (the first woman to hold the influential post), former head of the American Red Cross, and former deputy director of the White House Office of Science and Technology Policy under the Reagan administration. An endorsement of CT heart scans, though written under the guise of a probing editorial, will do an enormous amount of good to overcome the hurdles in gaining wider acceptance of heart scans.

Those of us applying heart scans in everyday practice have long appreciated their enormous power to detect and track coronary plaque. Framingham scoring can't even touch the certainty and quantification provided by heart scans in day-to-day life. Hundreds of studies have validated their use, but they still suffer from lying in the shadows of the procedural bullies aiming to boost the number of heart catheterizations, angioplasties, stents, bypass surgeries.

Dr. Healy, a voice with great weight, not just a political figure but also a cardiologist and scientist, has done a great service to broadcast the message of heart scanning.

As time passes, the dose of fish oil advocated in the Track Your Plaque program is going upward.

While epidemiologic studies, like the Chicago Western Electric Study and the Nurses' Health Study suggest that decreases in mortality from heart disease begin by just eating fish a couple times per month, there are newer data that suggest greater quantities confer greater benefits.

In the last Heart Scan Blog post, I discussed the recently-released ERA JUMP Study that demonstrated a relationship between higher omega-3 fatty acid blood content and reduced quantities of carotid and coronary plaque. The JELIS Study demonstrated a 19% reduction in cardiovascular events when fish-consuming Japanese added 1800 mg of EPA (only).

However, the suggestion that increased quantities of fish oil potentially yield greater protection from heart attack and facilitate coronary plaque regression is also stirring up worries about mercury exposure. So I dug up a Heart Scan Blog post from a year ago that discussed this issue and reprint it here.

I often get questions about the mercury content in fish oil. I've even had patients come to the office saying their primary care doctor told them to stop fish oil to avoid mercury poisoning.

Manufacturers of fish oil also make claims that this product or that ("super-concentrated", "pharmaceutical grade", "purified", etc.) is purer or less contaminated than competitors' products. The manufacturers of the "drug" Omacor [now Lovaza], or prescription fish oil, have added to the confusion by suggesting that their product is the most pure of all, since it is the most concentrated of any fish oil preparation (900 mg EPA+DHA per capsule). They claim that "OMACOR is naturally derived through a unique, patented process that creates a highly concentrated, highly purified prescription medicine. By prescribing OMACOR® (omega-3-acid ethyl esters), a prescription omega-3, your doctor is giving you a concentrated and reliable omega-3. Each OMACOR capsule contains 90% omega-3 acids (84% EPA/DHA*). Nonprescription omega-3 dietary supplements typically contain only 13%-63% EPA/DHA."

How much truth is there in these concerns?

Let's go to the data published by the USDA, FDA, and several independent studies. Let's add to that the independent (and therefore presumably unbiased) analyses provided by Consumer Reports and Consumer Labs (www.consumerlab.com). How much mercury has been found in fish oil supplements?

None.

This is different from the mercury content of whole fish that you eat. Predatory fish that are at the top of the food chain and consume other fish and thereby concentrate organic methyl mercury, the toxic form of mercury. Thus, shark, swordfish, and King mackerel are higher in mercury than sardines, herring, and salmon.

The mercury content of fish oil capsules have little to do with the method of processing and much more with the animal source of oil. Fish oil is generally obtained from sardines, salmon, and cod, all low in mercury. Fish oil capsules are not prepared from swordfish or shark.

Thus, concerns about mercury from fish oil--regardless of brand--are generally unfounded, according to the best information we have. Eating whole fish--now that's another story for another time. But you and I can take our fish oil to reduce triglycerides, VLDL, IDL, small LDL, and heart attack risk without worrying about mercury.

I am not advocating ad libitum eating of fish. Sadly, this may be related to excessive accumulation of contaminants. I am suggesting that greater quantities of omega-3 fatty acids from relatively contaminant- and mercury-free fish oil capsules.

More on this in an upcoming webinar on the Track Your Plaque website: Fish Oil and the Track Your Plaque Program - Is More Better?

The results of the uniquely-constructed ERA JUMP Study were just released, a fascinating study of the relationship of omega-3 fatty acids to coronary and carotid plaque.

The study adds insight into why the Japanese experience only one third of the heart attacks of Americans, and why Japan occupies the bottom of the list for least heart attacks among all developed countries.

The Electron-Beam Tomography, Risk Factor Assessment Among Japanese and U.S. Men in the Post-World War II Birth Cohort Study (ERA JUMP), a collaborative U.S.-Japanese effort, compared three groups of men:

-- 281 Japanese men living in Japan
-- 306 non-Japanese men living in the U.S. (Pittsburgh, Pennsylvania)
-- 303 Japanese Americans (having both parents Japanese without “ethnic admixture”) living in Hawaii.

The last group represents a group that is genetically similar to the group in Japan, but exposed to an American diet and lifestyle.

Three main measures were compared:

-- Blood levels of omega-3 fatty acids, EPA and DHA)
-- Carotid intimal-medial thickness (CIMT, the thickness of the carotid artery lining that can serve as an index of body-wide atherosclerosis)
-- Coronary calcium (heart scan) scores.

Interestingly, at the start of the study, the Japanese men possessed an overall cardiovascular risk profile worse than the Americans: Though more slender (BMI 23.6), Japanese men were more likely to be smokers, alcohol drinkers, had more high blood pressure, and were less likely to take cholesterol medications. The Americans, conversely, although heavier (BMI 27.9), were less likely to be smokers and drinkers, and had a four-fold greater use of cholesterol medications.

The Japanese Americans were the most likely to be hypertensive, diabetic, with a similar proportion of overweight as the non-Japanese Americans.

Despite the overall greater heart disease risk for profile for Japanese men, compared to non-Japanese Americans they had 10% less CIMT. In addition, only 9.3% of Japanese men had abnormal coronary calcium scores vs. 26.1% of non-Japanese Americans. Japanese-Americans were the worst, however, with nearly 10% more CIMT than non-Japanese Americans and 31.4% with abnormal calcium scores.

The most intriguing finding of all was the fact that, of all the various groups and degrees of atherosclerosis, whether gauged via CIMT or coronary calcium scores, the blood level of omega-3 fatty acids was inversely related, i.e., the greater the omega-3 blood level, the less plaque by either measure was detected.

Japanese men had the highest omega-3 blood levels: twice that of the non-Japanese Americans. The Japanese-Americans had levels only slightly greater than non-Japanese Americans.

While other studies, like the GISSI Prevenzione study, have persuasively demonstrated that omega-3 fatty acids substantially reduce heart attack, a weak link in the omega-3 argument has been a study that links greater omega-3 intake with less atherosclerosis. The unique construction of the ERA JUMP Study, employing two groups with sharply different omega-3 intakes, very powerfully argues for the plaque-inhibiting effects of this fraction of fats.

How much omega-3 fatty acids do Japanese people eat? Estimates vary, depending on part of the country, coastal vs. inland, age, etc., but Japanese tend to ingest anywhere from 5 to 15-times more omega-3 fatty acids than Americans. The actual intake of omega-3 fatty acids (EPA +DHA) in Japanese ranges from 850 to 3100 mg per day.

Data such as that from the Lyon Heart Study have demonstrated that a so-called Mediterranean diet substantially reduces risk for heart attack.

But there are aspects of the Mediterranean diet and lifestyle that are not entirely sorted out.

For instance, what specific component(s) of the diet provide the benefit? Is it olive oil and linolenic acid? Is it red wine? Is it the reduced exposure to processed snack foods that Americans are indundated with? Is it their more slender builds and greater tendency to walk? How about exposure to the Mediterranean sun? What about the inclusion of breads, since in the Track Your Plaque program I advocate elimination of wheat products for many abnormalities?

Anyway, here's a wonderfully thoughtful set of observations from Anna about her experiences traveling Italy, trying to understand the details of the Mediterranean diet while also trying to keep blood sugar under control.

I just returned from a two week stay in Italy, doing a bit of my own "Mediterranean Diet" experiments. When practical, we sought out food sources and places to eat that were typical for the local area, and tried as much as possible/practical to stay away from establishments that mostly catered to tourist tastes. I was really curious to see how the mythical "Mediterranean Diet" we Americans are urged to follow compared to the foods really consumed in Italy.

The first week, we stayed in a rural Tuscan farmhouse apartment (agriturismo), so many, if not most of our meals were prepared by me with ingredients I bought at the local grocery store (Coop) or the outdoor market in Siena. In addition, I purchased really fantastic free-range eggs from the farm where we were staying. (Between some language issues and seasonality, eggs and wine were what we could buy from them - though I was tantalized by the not-quite-ripe figs heavy on many trees). Mostly, our meals consisted of simple and easily prepared fresh fruits and vegetables, rustic cured meats (salami, proscuitto, pancetta, etc.) hand-sliced at the deli down the road, fresh sausages, various Italian cheeses, plus plenty of espresso. It was a bit disappointing to find underripe fruit & tomatoes as well as old green beans in the grocery stores, not to mention too many low fat and highly processed foods, but all over Europe the food supply is becoming more industrialized, more centralized, and homogenous, so I'm not too surprised that it happens even in Italy. But even with the smaller grocery store size, the amount of in-season produce was abundant, yet one still was better off shipping from the perimeter of the store, venturing into the aisles only for spices, olive oil, vinegar, coffee, etc. Without the knowledge of where to go and the language to really talk in depth about food with people, I wasn't able to find truly direct and local sources for as many foods as I would have liked, but still, we ate well enough!

The first week I maintained blood sugar levels very similar to those I get at home, because except for the Italian specialties, we ate much like we always do. A few rare exceptions to my normal BG tests were after indulging in locally made gelato or a evening limoncello cordial, but even then, the BG rise was relatively modest and to me, acceptable under the circumstance. Even with the gelato indulgences, it felt like I might have even lost a few pounds by the end of the first week and my FBG didn't rise much over 100.

The second week we stayed in two cities (Florence & Rome), and I didn't prepare any of my own food because I didn't have a kitchen/fridge. I found it impossible to get eggs anywhere for breakfast, and the tickets our hotels provided for a "continental" breakfast at a nearby café/bar was always for a coffee or hot chocolate drink and some sort of bread or roll (croissant, brioche, danish, etc.). At first I just paid extra for a plate of salami and cheese if that was available - or went to a small grocery store for some plain yogurt, but then I decided to go off low-carb and conduct a short term experiment, though I didn't consume nearly as many carbs as a typical Italian or tourist would.

So I breakfasted with a brioche roll or plain croissant for breakfast with my cappuccino, but unfortunately no additional butter was available. I didn't feel "full" enough with such a breakfast and I was usually starving an hour or two later. Additionally, when I ate the "continental" breakfast, I noticed immediate water retention - my ankles, lower legs, and knees looked like someone else's at the end of a day walking and sightseeing, swollen heavy. Exercising my feet and lower legs while waiting in lines or sitting didn't seem to help.

Food is much more expensive in Europe than in the US, and the declining US$ made everything especially expensive (not to mention the higher cost of dining out rather than cooking at home), so we tried to manage food costs by eating simple lunches at local take-away places, avoiding the corporate fast food chains. I was getting tired of salami/proscuitto & cheese plates, but the typical "quick" option was usually a panini (sandwich). At first I tried to find alternatives to paninis, but the available salads were designed for side dishes, not main meals and rarely had any protein, and the fillings of the expensive sandwiches were too skimpy to just eat without the bread. So I started to eat panini, although I sometimes removed as much as half of the bread (though it was nearly always very excellent quality pan toasted flatbreads or crusty baguette rolls, not sliced America bread). So of course, my post-prandial BGs rose, as did my FBG. I also found my hunger tended to come back much too soon and I think overall I ate more than usual in terms of volume.

Then we deviated from the "Italian" lunch foods and found a better midday meal option (quick, cheaper, and easier to customize for LC) - stopping at one of the numerous kebab shops and ordering a kebab plate with salad, hold the bread (not Italian, but still Mediterranean, I guess). I felt much better fueled on kebab plates (more filling and enough protein) than paninis, though I must say I still appreciated the taste of caprese paninis (slices of fresh mozzerella and tomato, basil leaves, mustard dressing on crusty, pan-toasted flat bread). If I followed my appetite, I could have eaten two caprese paninis.

We had some great evening dinners, at places also frequented by locals. This often was a fixed price dinner of several courses ("we feed you what we want you to eat"). Multi-course meals included house wine, and invariably consisted of antipasta (usually LC, such as a cold meat and cheese plate), pasta course (much smaller servings than typical US pasta dishes), main course plus some side vegetables, and dessert/coffee. These were often the best meals we experienced, full of local flavor and tradition (sometimes with a grandmotherly type doing the cooking), and definitely of very good quality, though we noticed the saltiness overall tended to be on the high side. I ate from every course, including some of the excellent bread (dipped in plenty of olive oil) and usually about half of the pasta served (2 oz dry?), plus about half of the dessert. After these meals I always ran BGs higher than usual, varying from moderately high (120-160 - at home I would consider this very high for me) to very high (over 180). By late in the week, my FBG was into the 115 range every morning (usually I can keep it 90-100 on LC food). Nearly everything that week was delicious, well-prepared food, but the high carb items definitely were not good for my BG control in the long run.

And most days I was doing plenty of walking, sprinting for the Metro subway trains, stair climbing (4th and 5/6th floor hotel rooms!), etc. but since I didn't have my usual housework to do, it probably wasn't too different from my usual exertion level.

So it was very interesting to experience the "Mediterranean Diet" first hand. Meats and cheeses were plentiful, fruits and vegetables played a much more minor role (main courses didn't come with vegetables other than what was in the sauce, but had to be ordered as additional items), but the overall carbs were decidedly too many. As I expected, it wasn't nearly as pasta-heavy as is portrayed in the US media/health press, but it is still full of too much grain and sugar, IMO. Low fat has become the norm in many dairy products, sadly, and if the grocery stores are any indication, modern families are gravitating towards highly processed, industrial foods. Sugar seems to be in everything (I quickly learned to order my caffe freddo con panno or latte sensa zuccero - iced coffee with cream or milk without sugar) after realizing that adding lots of sugar was the norm).

And, after several days of breakfasting at the café near our Rome hotel (where carbs were the only option in the morning), I learned that our very buff, muscular, very flat-stomached, café owner doesn't eat pasta (said as he proudly patted his 6 pack abs). I probably could have stuck closer to the carb intake I know works better for my BG control, but I figured if I was going to go off my LC way of eating and experiment, this was the time and place.

And yes, there were far fewer really obese people than in the US and lots of very slender people, but I could still see there were *plenty* of overweight, probably pre-diabetic and diabetic Italians (very visible problems with lower extremities, ranging from what looked like diabetic skin issues, walking problems, acanthosis nigricans, etc.). Older people do seem to be generally more fit than in the US (fit from everyday life, not exercise regimes), but there were plenty of "wheat bellies" on men old and young, even more young women with "muffin tops", and simply too many overweight children (very worrisome trend). So it may well be more the relaxed Italian way of living life (or a combination of other factors such as less air conditioning, strong family bonds, lots of sun, etc?) that keeps Italian CVD rates lower than the American rates, more than the mythical "Mediterranean diet".

Primary care physicians are the initial entry point for healthcare for the majority of Americans.

Develop pneumonia; go to your family or internal medicine physician (internist) to be prescribed an antibiotic. Need your blood pressure or cholesterol checked? Develop a sore knee or swelling in your leg? Once again, go to your primary care physician.

Image courtesy Dedde'

Primary care physicians are a patient’s guide to a bewildering array of technology and specialists. If you require a specific diagnostic test or consultation with a specialist, your primary care physician will help you navigate through the maze, choosing the path that is best for you. He or she will order a chest x-ray for a cough and fever, provide vaccines to prevent flu or pneumococcal pneumonia, perform an annual physical. If you require hospitalization, your primary care physician will admit you. He or she will order diagnostic tests like MRI’s, ultrasounds, x-rays, and blood testing, usually performed in the hospital or a hospital-owned facility. If you require the services of a gastroenterologist, orthopedist, general surgeon, or neurologist, your primary care physician will refer you to the appropriate specialist.

That’s how it’s supposed to work, at least in principle. In fact, during the first eight decades of the 20th century, it did work that work way for the most part. Your primary care physician acted not just as a provider of healthcare, but as your advocate, someone who knew you and worked to protect your welfare. Your family doctor often knew your parents, maybe even delivered you at birth, and cared for your children. His children often went to the same schools as your children. He and his family lived in the same town and sometimes went to the same church.

That hardly happens any more. It’s more likely you got the name of your primary care physician from a doctor referral service provided by a hospital. Or you picked a name off a list provided by your health insurer. It’s also common to see one doctor, only to see another a year later. Two, three, or more different primary care physicians over a five-year period are common. Doctors come and go, since physician turnover in clinics and practices has been on the increase for years. Insurance companies frequently force policyholders to change doctors, requiring you to choose from a list.

The end result of this shuffling of primary care is increasing impersonality of the relationship. You probably don’t know your primary care physician outside of the 10-minute interaction you had six months ago. She probably never met your mother and will likely not care for your children. Two years from now, she will likely not be your doctor any more, replaced by someone else who obtains the details of your health from a chart. Your chart is more likely to be electronic, with the details of your health history listed in a checklist. There’s little room to detail the idiosyncrasies and quirks of your unique personality or health profile. Throw into this impersonal equation the fact that many doctors have become scared of patients because of potential for lawsuits, often over the most trivial of issues, or because of an error of oversight or misdiagnosis.

This flawed and impersonal system, though emotionally unsatisfying, can still work if each doctor who assumes a patient’s care maintains the ethic of putting health and welfare above all.

But what if your primary care physician is not just an advocate for your welfare, but is a representative of the hospital? What if there are hidden, unspoken financial incentives paid to your doctor to direct you to the hospital for diagnostic testing, hospitalization, and referral to specialists? If a headache becomes a $4800 MRI, or chest pain becomes a $4200 nuclear stress test, then a $14,000 heart catheterization, your primary care physician becomes the purveyor of far greater financial opportunity for the hospital. The entire interaction, founded on the proposition that your doctor actually cares about you, collapses in a heap of financially motivated testing and procedures. It appears to work, and you and your family can still obtain access to healthcare. The problem is that you’re likely to get too much of it.

This message has not been lost on the shrewd administrators at hospitals. Take a look at the ranks of primary care physicians who refer patients to some of your local hospitals. It is typical that a hospital system maintains several hundred primary care physicians on their payroll, all of whom are expected to refer patients to the hospital, cardiologists, and other proceduralists. Why so many?

Most primary care physicians today have signed contracts with a hospital. In other words, they are employees of the hospital. This practice is not unusual: the American Medical Association reported that 4 of 5 primary care physicians are now bound by such employment arrangements across the U.S. In effect, 80% of primary care physicians are legally bound by contract to direct patients to cardiologists who work at hospitals.

On top of contractual obligations, there are financial incentives for the volume of procedures that are generated as a result of referrals. The more procedures generated from an internist’s or family practitioner’s practice, the greater the end-of-year productivity bonus will be, not uncommonly totaling tens of thousands of dollars. Dr. Ted Phillips (not his real name, since he declined to allow me to use it) received a bonus check of $9,437 this year for his “productivity,” defined murkily as the return on specialist referrals. While the bonus may have helped him pay for his son’s college tuition, it clearly was a situation that made him acutely uncomfortable when asked.

Several primary care physicians are also quietly dismissed every year from the ranks of employed physicians for not maintaining a minimum flow of patients into the system.

Another hazardous point of entry: Many patients enter the hospital through the emergency room (ER). A patient in the emergency room is at his or her most vulnerable, seeking help for an urgent complaint and usually willing to accept whatever the ER physician advises. Hospitals know this. That’s why many systems insist that the ER physicians be employees of the hospital, with their practice habits subject to control. A patient goes to the ER with chest pain or breathlessness. The worst thing that can happen from a financial standpoint is for the patient to be evaluated and discharged. For this reason, a growing number of hospitals employ ER physicians, then proceed to legislate practice patterns. Consulting a cardiologist is strongly encouraged, since they generally provide access to the downstream revenue-producing procedures offered in the hospital. That way, what might have been a four hour, $2500 ER visit is converted into a $10,000 to $40,000 hospital stay, even when nothing was wrong in the first place. There are millions of people nationwide who have the hospital bills to prove it after being discharged with a diagnosis of indigestion.

Caveat emptor: Buyer beware.

Like many scams, this one follows a predictable formula.

It is a formula widely practiced among food manufacturers, ever since food products began to jockey for position based on nutritional composition and purported health benefits.

First, identify a component of food, such as wheat fiber or oat bran, that confers a health benefit. Then, validate the healthy effect in clinical studies. Wheat fiber, for instance, promotes bowel regularity and reduces the likelihood of colon cancer. Oat bran reduces blood cholesterol levels.

Second, commercialize food products that contain the purported healthy ingredient. Wheat bran becomes Shredded Wheat, Fiber One, and Raisin Bran cereals and an endless choice of “healthy” breads. Oat bran becomes Honey Bunches of Oats, Quaker’s Instant Oatmeal, and granola bars. Even if many unhealthy components are added, as long as the original healthy product is included, the manufacturer continues to lay claim to healthy effects.

Third, as long as the original healthy ingredient remains, get an agency like the American Heart Association to provide an endorsement: “American Heart Association Tested and Approved.”

The last step is the easiest: just pay for it, provided the product meets a set of requirements, no matter how lax.

You will find the American Heart Association certification on Quaker Instant Oatmeal Crunch Apples and Cinnamon. Each serving contains 39 grams carbohydrate, 16 grams sugar (approximately 4 teaspoons), and 2.5 grams fat of which 0.5 grams are saturated. Ingredients include sugar, corn syrup, flaked corn, and partially hydrogenated cottonseed oil. Curiously, of the 4 grams of fiber per serving, only 1 gram is the soluble variety, the sort that reduces cholesterol blood levels. (This relatively trivial quantity of soluble fiber is unlikely to impact significantly on cholesterol levels, since a minimum 3 grams of soluble fiber is the quantity required, as demonstrated in a number of clinical studies.) Nonetheless, this sugar product proudly wears the AHA endorsement.

Thus, a simple component of food that provides genuine benefit mushrooms into a cornucopia of new products with added ingredients: sugar, high fructose corn syrup, corn starch, carageenan, raisins, wheat flour, preservatives, hydrogenated oils, etc. What may have begun as a health benefit can quickly deteriorate into something that is patently unhealthy.

There’s a clever variation on this formula. Rather than developing products that include a healthy component, create products that simply lack an unhealthy ingredient, such as saturated or trans fats or sodium.

Thus, a ¾-cup serving of Cocoa Puffs cereal contains 120 calories, no fiber, 14 grams (3 ½ teaspoons) of sugar—but is low in fat and contains no saturated fat. Proudly displayed on the box front is an American Heart Association stamp of approval. It earned this stamp of approval because Cocoa Puffs was low in saturated, trans, and total fat and sodium. Likewise, Cookie Crisp cereal, featuring Chip the Wolf, a cartoon wolf in a red sweater (“The great taste of chocolate chip cookies and milk!”), has 160 calories, 26 grams carbohydrate and 19 grams (4½ teaspoons) of sugar per cup, and 0 grams fiber—but only 1.0 gram fat, none saturated, thus the AHA check mark. (Promise margarine, made with hydrogenated vegetable oil and therefore containing significant quantities of trans fats, was originally on the list, as well, but removed when the trans fat threshold was added to the AHA criteria.)

It is this phenomenon, the sleight of hand of taking a healthy component and tacking on a list of ingredients manageable only by food scientists, or asserting that a product is healthy just because it lacks a specific undesirable ingredient, that is a major factor in the extraordinary and unprecedented boom in obesity in the U.S. Imagine the chemical industry were permitted such latitude: “Our pesticide is deemed safe by the USDA because it contains no PCBs.” Such is the ill-conceived logic of the AHA Heart-Check program the "Heart Healthy" claims.

It’s best we keep in mind the observations of New York University nutritionist and author of the book, Food Politics, Marion Nestle, that “food companies—just like companies that sell cigarettes, pharmaceuticals, or any other commodity—routinely place the needs of stock holders over considerations of public health. Food companies will make and market any product that sells, regardless of its nutritional value or its effect on health. In this regard, food companies hardly differ from cigarette companies. They lobby Congress to eliminate regulations perceived as unfavorable; they press federal regulatory agencies not to enforce such regulations; and when they don’t like regulatory decisions, they file lawsuits. Like cigarette companies, food companies co-opt food and nutrition experts by supporting professional organizations and research, and they expand sales by marketing directly to children, members of minority groups, and people in develop countries—whether or not the products are likely to improve people’s diets.”

Qualms over just how heart-healthy their products are? Doubtful.

Once upon a time, the tobacco industry was guilty of conducting a widespread, systematic, highly organized campaign to deliver their product to as much of the unsuspecting public as possible.

As clinical data mounted linking smoking and health problems like cancer and heart disease, tobacco producers labored fiercely to counter these claims despite darkening public sentiment. When individual company executives were questioned on why they continued to perpetuate the industry’s scandalous practices, the invariable justification offered was “Well, I had to pay my mortgage.” That tidy ends-justifies-the-means rationalization has a familiar ring when you examine the behavior of those in the heart "industry."

Things are not what they seem. The hospital, once an institution to serve the sick, a place for clergy, volunteers, and other altruists, has evolved into a business serving a thriving bottom line. You are the “product” they seek. The cardiologist, ostensibly in the service of alleviating heart disease, instead seeks to grow his checkbook by performing procedures that have nothing to do with lessening the burden of heart disease. He dives into the water to save drowning victim after drowning victim, but fails to simply toss in the life preserver that has been close at hand all along.

The woeful family practitioner, who is expected to bear undue responsibility for the broad spectrum of health, ignorantly permits heart disease to grow under his or her nose and, by default, allows heart disease to become the exclusive province of the proceduralist. Worse, the family practitioner or internist in the employ of the hospital (a situation that has quietly grown to encompass 80% of all primary care physicians) labors to fatten hospital business by directing patients into hospital services. The comparative lowly incomes of the primary care physician are substantially supplemented by participating in this huge revenue-generating machine called heart care.

The astounding grasp of the system has caused one of every 10 adults in the U.S. to have undergone a heart procedure. The lemming-like procession to the hospital creates a crowd mentality among some sectors of the frightened public. “My friends and neighbors have all had bypass operations. Sooner or later I guess it’s going to be my turn.”

Tragically, the system has grown through the exploitation of trust. The faith we have in doctors, hospitals, and the institutions and people associated with healthcare has been subverted into the service of profit. Many practitioners and institutions choose to operate under the guise of doing good, but instead capitalize on the public’s willingness to accept as fact the need for major heart procedures and all its associated costly trappings.

"When banks compete, you win.”

The TV ad opens with a 60-something man sitting in his living room, talking to a three-piece suit-clad, 30-something banker. The older man is explaining to the dismayed younger man why he’s going to use Lending Tree loan service for a home loan.

“But Dad, I’m you’re son!” the younger whines.

Many of Lending Tree’s clients have collaborated in filing a multi-million dollar class action suit against the company, claiming “bait and switch” tactics. They claim that home buyers are lured by low interest rates or low closing costs on a home loan. Once the buyer concludes the hassle of filling out numerous forms, the suit accuses Lending Tree of making a switch to a costlier loan.

Bait and switch is among the oldest con games around. If you’ve ever bought a car from a car dealer, chances are you’ve had your own little brush with this deception. The ad promises the SUV you’ve wanted for only $299 per month. Only, once you get there, the salesman informs you that only a limited number of special deals were available and they’ve run out. But he’s still got a really good deal right over here!

Most of us recognize that we’ve been hookwinked. Yet we still go along and buy a car from the dealer.

What if it’s not a sleazy salesman behind the pitch, but a physician. If it’s hard to resist the sales pitch at the car dealership, it can be near impossible to ignore the advice of your doctor. But the truth is often loud and clear: in many instances, it is a genuine, bona fide, and fully-certified scam.

Among the most common bait-and-switch heart scams: Your cholesterol is high. The sequence of subsequent testing is well-rehearsed. “Gee, Bob, I’m worried about your risk for heart disease. Let’s schedule you for a nuclear stress test.”

The stress test, like 20% or more of them, is “falsely positive,” meaning abnormal even though there’s nothing wrong with you. Another 30% are equivocal, not clearly abnormal but also not clearly normal. Now up to 50% of people tested “need” a heart catheterization in the hospital to clarify this frightening uncertainty. You might end up with a stent or two, even bypass surgery. Your simple $20 cholesterol panel has metamorphosed into $100,000 in hospital procedures.

That familiar sequence is followed thousands of times, seven days a week, 365 days a year.

Congestive heart failure is among the most common diagnoses in the hospital nowadays.

Congestive heart failure is the result of injury to the heart muscle such as that occurring during heart attack, viral infections of the heart (myocarditis), poorly controlled high blood pressure, and a smattering of other rare causes. Eight million Americans with congestive heart failure account for over one million hospital admissions annually (AHA Update, 2007). It has become so common, in fact, that it has ranked as number one cause for hospital admission for the last several years.

Heart failure is a frightening condition causing the sufferer to gasp for breath. Excess fluid accumulates in the lungs, amplifying the work of breathing and imparting a feeling of unease. Some heart failure sufferers struggle to the point of blacking out or requiring mechanical ventilation on a respirator.

There are a number of standard treatments for heart failure that usually rapidly rescue the patient from the brink of respiratory failure. These generally consist of intravenous diuretics that force the kidney to clear excess water rapidly, medications to increase heart muscle strength, and other treatments. It’s not uncommon for a heart failure patient to drop 10–20 lbs. in water weight with treatment. The treatments are quite effective for the majority of patients with rapid relief of the breathlessness generally obtained within hours.

However, the problem with congestive heart failure is not generally the rapidity or effectiveness of acutely providing relief, it is the chronic recurring nature of the disease. Someone can come to the hospital, obtain prompt treatment with relief of the breathlessness within 48–72 hours, only to return to the hospital in several weeks with a recurrence of the same process.

As common as congestive heart is in hospitals, it has also presented the perennial problem: how to convert this frequent reason for hospitalization into a profit opportunity. Some people who experience heart failure will undergo the usual sequence of heart procedures of heart catheterization, stents, bypass surgery, valve surgery, etc. But, because heart failure tends to be a repeatedly recurring event, even patients tire of the “need” for heart procedures. Then how can more heart failure occurrences be converted into profitable events?

A unique principle operates in the medical device market: If a disease lacks a procedure . . . create one.

Several problems are solved by such a principle. First, procedures are much more generously reimbursed by insurers than standard medical care without procedures. Two, the physician is provided an opportunity to also bill at a higher level. Third, patients often love the more dramatic, heroic nature of procedures, whether or not there is true benefit.

To the rescue of the poorly reimbursed area of congestive heart failure walks a Minnesota company called CHF Solutions, Inc., manufacturers of the Aquadex device.

Cost? $14,500 plus $900 per filter every time a patient gets one treatment. The Aquadex works by a decades-old process called ultrafiltration, used for many years but used principally for kidney failure not severe enough to require regular dialysis. New York cardiologist Howard Levin simply adapted the process, using smaller catheters inserted into the arm veins, in 2000. As in conventional ultrafiltration, blood is taken from the body from a catheter, passed through a filter that removes excess water, then returned to the body.

This is a serious effort. Dr. Levin raised $51 million in venture backing on top of $12 million seed capital. The device sailed through the Food & Drug Administration in June 2002, since it was labeled a newer form of ultrafiltration, thereby obtaining approval through the FDA’s 501k rule, a minor modification of existing technology. (Many truly technologically unique devices do come to market and therefore require the full process of FDA approval, a generally lengthy and costly process for devices. However, there’s another way: bill a device as “substantially equivalent” to an existing technology and the approval process is relatively quick and easy.)

In an industry publication, Cath Lab Digest, Dr. Levin was interviewed in February, 2003, and proclaimed, “We can treat many of the symptoms of heart failure, but we’re a long ways off from a cure. That’s why new technologies are so exciting, such as LVADs for the very sickest heart failure patients; biventricular pacing for the small subset of patients who seem to benefit from it; and simplified ultrafiltration such as the System 100 that can be applied to a broad range of congestive heart failure patients with fluid overload. “

What does this have to do with heart scans and heart disease reversal? Nothing-directly. I highlight this phenomenon because it caricatures how things work in medicine and health care in general, more so in cardiovascular diseases in which the profit motive is especially deeply ingrained. Focus on a need, then generate a profitable treatment for it. Profits are what drive growth, marketing, sales, and expansion into new revenue-generating niches.

Sadly, the reverse principle does not work: Replace profitable procedures with unprofitable strategies, regardless of their effectiveness. Replacing coronary angioplasty and coronary stent implantation, or bypass surgery, with intensive prevention efforts is no easy matter. Just witness the enormous resistance to the concept of early heart disease detection achieved with heart scans. A day doesn’t go by without a major media outlet bashing heart scans, or confusing them with CT coronary angiograms with claims of excessive radiation.

But the mounting volume of criticisms against heart scans also means that they are gaining some traction in mainstream thinking. But will there be a day when they replace the need for profitable procedures? I believe they will, when coupled with a powerful program of prevention, but don’t hold your breath.

We should look to the Japanese to teach us a few lessons about preventing heart disease. A Japanese male has only 65% of the risk of an American male (despite 40% of Japanese men being smokers), while a Japanese woman has 80% less risk than an American woman. While the U.S. is near the top of the list of nations with highest cardiovascular risk, Japan is the lowest.

What are they doing right?

There is no one explanation, but several. Genetics probably does not play a substantial role, by the way, as demonstrated by observations of Japanese people who emigrate to Western cultures. People of Japanese heritage living in Hawaii, for instance, develop the same cardiovascular risk as non-Japanese living in Hawaii. They also develop obesity and diabetes.

Among the factors that likely contribute to reduced risk in Japanese people:

--A style of eating that does not include a lot of sweet foods. No breakfast cereal or donuts for breakfast, for instance, but miso soup with tofu, fish, green onions, and daikon (as takuan, or pickled radish).
--Seaweed--It's probably a combination of the green phytonutrients and iodine. Typical daily iodine intake is in the neighborhood of 5000 mcg per day from nori, kombu, wakame, and other seaweed forms. (The average American obtains 125 mcg per day of iodine from diet.)
--Seafood--Fish in many forms not seen in the U.S. are popular.
--Green tea--Consumption of green tea has been confidently linked to reduced cardiovascular risk, probably via visceral fat-reducing, anti-oxidative, and anti-inflammatory effects. Although tea in Japan is often the less flavonoid-rich oolong tea, softer benefits from this form are likely.
--Soy--Tofu, miso, and soy sauce are staples. It's not clear to me whether soy is intrinsically beneficial or whether it is beneficial because it serves to replace unhealthy alternatives. (Genetic modification may change this effect.)
--Reduced exposure to cooked animal products (except seafood). This is not a saturated fat issue, but probably an advanced glycation end-product/lipoxidation issue that result from cooking.
--The lack of a "eat more healthy whole grain" mentality, the advice that has plunged the entire U.S. into the depths of a diabetes and obesity crisis (along with high-fructose corn syrup and sugar). Noodles like udon and ramen do have a place in their diet, as do some dessert foods. But the overall wheat exposure is less--no bagels, sandwiches, and breakfast cereals.
--Less overweight and obesity--The above eating style leads to less weight gain.

Japanese foods have a unique taste, consistency, and mouth-feel that go well with saltiness, thus the downside of their diet: salt consumption. On a broad scale, high salt consumption has been associated with hypertension and gastric cancer. But the tradeoff has, on the whole, been a favorable one.

One study trying to find some answers:

Dietary patterns and cardiovascular disease mortality in Japan: a prospective cohort study.

Shimazu T, Kuriyama S, Hozawa A et al.
Division of Epidemiology, Department of Public Health and Forensic Medicine, Tohoku University Graduate School of Medicine, Japan.

We prospectively assessed the association between dietary patterns among the Japanese and CVD mortality. Dietary information was collected from 40 547 Japanese men and women aged 40-79 years without a history of diabetes, stroke, myocardial infarction or cancer at the baseline in 1994.
During 7 years of follow-up, 801 participants died of CVD.

Factor analysis (principal component) based on a validated food frequency questionnaire identified three dietary patterns: (i) a Japanese dietary pattern highly correlated with soybean products, fish, seaweeds, vegetables, fruits and green tea, (ii) an 'animal food' dietary pattern and (iii) a high-dairy, high-fruit-and-vegetable, low-alcohol (DFA) dietary pattern. The Japanese dietary pattern was related to high sodium intake and high prevalence of hypertension. After adjustment for potential confounders, the Japanese dietary pattern score was associated with a lower risk of CVD mortality (hazard ratio of the highest quartile vs the lowest, 0.73; 95% confidence interval: 0.59-0.90; P for trend = 0.003). The 'animal food' dietary pattern was associated with an increased risk of CVD, but the DFA dietary pattern was not.

The Japanese dietary pattern was associated with a decreased risk of CVD mortality, despite its relation to sodium intake and hypertension.

Niacin, or vitamin B3, remains a confusing issue for many people. It shouldn't be.

It doesn't help that most physicians and many pharmacists also do not understand the basic issues surrounding niacin. The only reason why there is any level of prevailing knowledge about niacin is that Kos Pharmaceuticals managed to "pharmaceuticalize" a niacin preparation, prescription Niaspan, that provided the revenue to fund professional "education."

Niacin can be helpful to increase HDL, reduce small LDL particles and shift them towards the more benign large particles, reduce triglycerides, and reduce lipoprotein(a).

So here's a brief description of the various forms that you will find niacin:

Immediate-release niacin--Also called crystalline niacin or just niacin. This is the original niacin that releases within minutes of ingestion. Because it releases rapidly, it triggers the most intense "hot flush." While this form of niacin works wonderfully well, is the safest, and is dirt cheap, the majority of people are simply unable to tolerate the intense flush. It also works best taken twice a day, generating two intolerable flushes per day.

Slow-release niacin--These preparations were popular in the 1980s, since the slow 12 to 24 hour pattern of release minimized the annoying hot flush. But, with prolonged use, it also became apparent that an unnaceptable frequency of liver toxicity developed. Unfortunately, this means that any niacin preparation that trickles niacin out over an extended period, including many of the slow-release preparations now sold in health food stores and pharmacies, have potential for liver toxicity. These preparations should be avoided.

6-hour release niacin--Releasing niacin more slowly than immediate-release niacin but more rapidly than slow-release niacin, 6-hour release (or what the Niaspan people call "extended-release" niacin) is nearly as effective as immediate-release niacin with approximately the same low potential for liver toxicity. It is far less liver toxic than slow-release niacin. 6-hour release niacin therefore offers the best balance between effectiveness and safety. Preparations that show this pattern of release include Niaspan ($180 per month), the poorly-named Sloniacin (about $8 per month), and Enduracin (about $7 per month) for 1000 mg per day. (Some Track Your Plaque Members have also determined that several other over-the-counter preparations have been demonstrated to share a similar pattern of release.)

Then there are the scam products that have no useful effect at all:

Flush-free or no-flush niacin--Inositol hexaniacinate, or 6 niacin molecules bound to the sugar, inositol, has no effect in humans, at least not with the dozen or so preparations that I've seen used. Nor are there any data to document the effectiveness of flush-free niacin. It's also more expensive.

Nicotinamide--This niacin derivative likewise has no effect on the usual targets for niacin treatment.

While I used to prescribe Niaspan, the ridiculous pricing and aggressive marketing really turned me off. I now advise my patients and our online followers to use only Sloniacin or Enduracin, unless you can tolerate immediate-release niacin.

Out with the old,

in with the new

“I believe that you are suffering from what is called a fatty degeneration of the heart.”

Dr. Tertius Lydgate to Mr. Casaubon on making a diagnosis with the new medical device, the stethoscope.

George Elliot

Middlemarch, 1871

Old notions in medicine have a peculiar way of lingering.

In 1882, Dr. Robert Koch discovered the tubercle bacillus in tissues of people with “consumption.” By connecting a bacterium with the disease, he usurped the long held notion that tuberculosis was a degenerative disease caused by lack of fresh air. But, for decades after Dr. Koch’s revelation, the “bad air” belief persisted. Surgical collapse of the lung, a painful and barbaric treatment for tuberculosis, persisted well into the 1960s, years after effective antibiotics were discovered in 1947.

The medical community of the 19^th century viewed mental illness as the hereditary end-product of ancestral nervousness, alcoholism, prostitution and criminal behavior, a bias that remained widespread well into the mid-20^th century. Nazi physicians invoked the theory of heritable “mental degeneration” to justify wholesale extermination of schizophrenics. Electro-convulsive therapy (ECT, or “electroshock therapy”) was widely applied to treat schizophrenia, depression, homosexuality, and criminal behavior for over 30 years, gradually abandoned (at least in its original form) after years of abusive application to subdue patients, demonized in the 1975 movie, “One Flew Over the Cuckoo’s Nest,” depicting the author’s real-life experience with ECT.

Long after a theory or practice has been discredited, it can persist, refusing to die. The new and improved may not be adopted into mainstream practice for years, even decades.

Back to the 21^st century: What if you realized that, by quirks of human nature and the uneven adoption of health information, your doctor practiced medicine appropriate for 1985? 1975?

While digital information nowadays is transmitted at the speed of light, disseminating as fast as it takes the next juicy tidbit to be “virally” reproduced via social networking websites, it’s the human factor that still operates with the inertia of human behavior. Habits and attitudes slow the adoption of new information in time measured not in seconds, but in years or decades.

A century ago, 20 years were required for the new technology of blood pressure measurement to be adopted after its introduction in the U.S. in 1910, since physicians were long comfortable with the practice of “pulse palpation” (feeling the pulse). (The arcane language of pulse palpation persists to this day, terms like “pulsus parvus et tardus,” the slow rising pulse of a stiff aortic valve; and the "water-hammer" pulse of a leaking aortic valve.)

The discovery of new, health-changing information today in the 21^st century disseminates through the ranks of modern healthcare providers at much the same pace as measuring blood pressure did in the early 20^th century.

It’s also tempting to paint American medicine as a fiefdom intent on maintaining exclusive rein over health information. Look back over the hierarchical relationship of medicine over nursing in the past century: When blood pressure measurement was adopted on a broad scale in the 1930s, it was practiced only by physicians, since nurses were deemed incapable. (Modern-day nurses should surely have a hearty laugh over this.) Stethoscopes, around even longer than blood pressure cuffs, weren’t permitted to fall into the hands of nurses until the 1960s, since the medical community feared that nurses might command too much control over patient care. Even after nurses were permitted to have their own stethoscopes, great pains were taken to be certain the nurses’ version was readily distinguishable from the “real” tool wielded by physicians; nurses’ stethoscopes were therefore labeled “nurse-o-scopes,” or “assistoscopes,” and were required to be smaller and flimsier.

Old and ineffective doesn’t always give way to new and better at once; it is slowed by habit as well as an unwillingness to relinquish control.

Somehow technology marches on. But it does so unevenly, sweeping some along in its first wave, others in its wake, some never at all.

Just as effective antibiotics to cure tuberculosis were available for 20 years while surgeons continued to remove patients’ lungs, so better solutions to heart disease are already available but not yet employed by your neighborhood physician. The primary care physician may have heard about some of the newest means to prevent heart disease, but is too overwhelmed with the day-to-day of sore throats, diarrhea, and rashes. Cardiologists, intent on inserting the next best stent or defibrillator, have little but passing interest in strategies that might halt or reverse the heart disease that can be “managed,” no matter how imperfectly, with procedural solutions like angioplasty and bypass surgery. We should bear these flawed human tendencies in mind as we explore the world of heart disease prevention.

We need look no farther than the front page of the newspaper to find evidence of the failure of present-day heart disease detection and management. Over the past several years, headlines have carried the likes of Tim Russert, Bill Clinton, Larry King, Dick Cheney, David Letterman, Tommy Lasorda, Ed Bradley, Mike Ditka, Walter Cronkite, Alberto Salazar, all heart disease sufferers. Some, like talk show host David Letterman, survived their brush with heart catastrophe and underwent successful bypass surgery. Others, like marathoners Fixx and Salazar, raised none of the conventional red flags for heart disease. All received standard, “modern” medical care . . . all the way up to their heart attack, bypass surgery, or untimely death.

Like the sphygnomanometer (blood pressure) cuffs of 1910, Track Your Plaque represents an example of the new. But, unlike the simple practice of taking blood pressure in the early 20^th century, Track Your Plaque represents an entirely new way to look at coronary heart disease: a new way to measure it, a new way to identify its causes, and a new way to seize control over it, often to the point of achieving reversal of the process. It also puts control over much of this process into your hands and away from hospitals, cardiologists, and heart procedures.

I could speak of revealing “secrets,” but that’s not true. In Track Your Plaque, I simply convey information about heart disease that you were likely unaware existed, strategies that doctors fail to discuss. I assemble them into a “package” that, together, create an enormously empowering unique approach to prevent heart disease and heart attack.

Track Your Plaque also challenges the high-tech status quo, practices that occupy exalted places in the enormous cardiovascular healthcare machine that has dominated American healthcare for the past 40 years. I propose that high-tech hospital procedures should join the practice of ECT for homosexuality and insanity¾and become yet another relic of the past.

Among the most neglected yet enormously helpful values on any standard cholesterol panel is the triglyceride value.

Triglycerides traverse the bloodstream by hitching a ride on water (serum)-soluble lipoproteins, or lipid-carrying proteins. We measure triglycerides as an indirect index of triglyceride-containing lipoproteins.

Triglycerides are a basic currency of energy. While the average American ingests around 300 mg of cholesterol per day, he or she also ingests 60,000-120,000 mg (60-120 grams) of triglycerides, i.e., 200 to 400 times greater amounts, from fat intake. Zero triglycerides in the diet or in the bloodstream is not an option.

But what represents too much triglycerides in the bloodstream? There are several observations to help us make this determination:

1) When fasting triglycerides are 133 mg/dl or greater, 80% of people will show show at least some degree of small LDL particles.

2) When fasting triglycerides are 60 mg/dl or less, most (though not all, since genetic factors enter into the picture) people will show little to no small LDL particles.

3) When fasting triglycerides are 200 mg/dl or greater, small LDL particles will dominate and large LDL particles will be in the minority or be gone entirely.

4) When triglycerides are 88 mg/dl or greater after eating, then risk for heart attack is doubled. Non-fasting triglycerides in the 400+ mg/dl range are associated with 17-fold greater risk for heart attack.

From Austin et al 1990. "Phenotype A" means that large LDL particles dominate; "phenotype B" means that small LDL particles dominate.

Note that conventional "wisdom" (i.e., NCEP ATP-3 guidelines) is that triglycerides of up to 150 mg/dl are okay, a level that virtually guarantees expression of small LDL particles and increased cardiovascular risk.

Based on observations like these, in the Track Your Plaque program we aim for fasting triglycerides of no higher than 60 mg/dl and postprandial (after-meal) triglycerides of no more than 90 mg/dl.

Curiously, while fat intake (i.e., triglyceride intake) plays a role in determining postprandial triglyceride blood levels, it's carbohydrate intake that plays a much larger role. That will be an issue for another day.

In 1985, the National Cholesterol Education Panel delivered its Adult Treatment Panel guidelines to Americans, advice to cut cholesterol intake, reduce saturated fat, and increase "healthy whole grains" to reduce the incidence of heart attack and other cardiovascular events.

Per capita wheat consumption increased accordingly. Wheat consumption today is 26 lbs per year greater than in 1970 and now totals 133 lbs per person per year. (Because infants and children are lumped together with adults, average adult consumption is likely greater than 200 lbs per year, or the equivalent of approximately 300 loaves of bread per year.) Another twist: The mid- and late-1980s also marks the widespread adoption of the genetically-altered dwarf variants of wheat to replace standard-height wheat.

In 1985, the Centers for Disease Control also began to track multiple health conditions, including diabetes. Here is the curve for diabetes:

Note that, from 1958 until 1985, the curve was climbing slowly. After 1985, the curve shifted sharply upward. (Not shown is the data point for 2010, an even steeper upward ascent.) Now diabetes is skyrocketing, projected to afflict 1 in 3 adults in the coming decades.

You think there's a relationship?

Wheat, via exorphin effects, is an appetite stimulant. Eat a whole wheat bagel or bran muffin, you want another. You also want more of other foods. You also want something to eat every two hours due to widely-swinging insulin-glucose responses: blood sugar high followed by a sharp downturn that triggers a powerful impulse to eat (thus the cravings for a snack at 9 and 11 a.m. after a 7 a.m. breakfast).

If wheat is a stimulant of appetite, then removing it should yield reduced appetite and reduced calorie intake. That is precisely what happens.

When wheat products are removed from the diet--without calorie restriction, without counting fat or carbohydrate grams, no exercise program, no cleansing regimen, no skipping meals . . . nothing--calorie intake drops 350 to 400 calories per day. This calorie figure remains curiously consistent across multiple studies in which wheat was eliminated.

400 calories per day results in 21 lbs lost over 6 months, based just on calories. (3500 calories per pound lost.) That is what happens in wheat elimination diets: 21-26 lbs lost over 6 months.

Wheat is the processed food industry's nicotine, a means of ensuring repeat food purchases. It's also low-cost (subsidized by the U.S. government), high-yield, an ingredient that even has its very own withdrawal syndrome should you miss a "hit."

I spend a lot of my day bashing statin drugs and helping people get rid of them.

But are there instances in which statin drugs do indeed provide real advantage? If someone follows the diet I've articulated in these posts and in the Track Your Plaque program, supplements omega-3 fatty acids and vitamin D, normalizes thyroid measures, and identifies and corrects hidden genetic sources of cardiovascular risk (e.g., Lp(a)), then are there any people who obtain incremental benefit from use of a statin drug?

I believe there are some groups of people who do indeed do better with statin drugs. These include:

Apoprotein E4 homozygotes

Apoprotein E2 homozygotes

Familial combined hyperlipidemia (apoprotein B overproduction and/or defective degradation)

Cholesteryl ester transfer protein homozygotes (though occasionally manageable strictly with diet)

Familial heterozygous hypercholesterolemia, familial homozygous hypercholesterolemia

Other rare variants, e.g., apo B and C variants

The vast majority of people now taking statin drugs do NOT have the above genetic diagnoses. The majority either have increased LDL from the absurd "cut your fat, eat more healthy whole grains" diet that introduces grotesque distortions into metabolism (like skyrocketing apo B/VLDL and small LDL particles) or have misleading calculated LDL cholesterol values (since conventional LDL is calculated, not measured).

As time passes, we are witnessing more and more people slow, stop, or reverse coronary plaque using no statin drugs.

Like antibiotics and other drugs, there may be an appropriate time and situation in which they are helpful, but not for every sneeze, runny nose, or chill. Same with statin drugs: There may be an occasional person who, for genetically-determined reasons, is unable to, for example, clear postprandial (after-eating) lipoproteins from the bloodstream and thereby develops coronary atherosclerotic plaque and heart attack at age 40. But these people are the exception.

Nutrition in the modern world has become an increasingly problematic topic. From genetic modification to commercialized methods of mass production, we are having to navigate all manner of complex issues in food choices, particularly if ideal health, including maximal control over coronary plaque, is among our goals.

We will therefore be releasing a series of discussions on the Track Your Plaque website in the coming months, a series I call "Track Your Plaque Advanced Topics in Nutrition." These will be, as the series title suggests, discussions for anyone interested in more than the "eat a balanced diet" nonsense that issues from "official" sources. Among the topics to be covered:

1)Advanced Glycation End-products--both endogenous and exogenous, including peripheral issues like lipoxidation and acrylamides.

2)Dietary influences on LDL oxidation--including the concept of "glycoxidation." Protection from oxidative phenomena is not just about taking antioxidants.

3) Foods you MUST eat--We've talked a lot about foods that you shouldn't eat. How about foods you should eat?

The New Track Your Plaque Guide is now available!

The Track Your Plaque program has evolved over its 8 year history. While the original Track Your Plaque book reflected the program details that got the program started back in 2003-2004, plenty has changed.

This new version of the book, what I call the program Guide, represents version 2.0 of Track Your Plaque and includes:

--Updated lipoprotein treatment strategies--including new and expanded treatment choices for small LDL and lipoprotein(a).

--An entire chapter on vitamin D and its crucial role in cardiovascular health and plaque control.

--A new and expanded diet--All the reasons why the New Track Your Plaque Diet can achieve spectacular improvement in lipids/lipoproteins, reversal of insulin resistance/pre-diabetes/diabetes, weight loss, reduction in blood pressure, etc. are discussed in considerable detail. The diet is crafted to achieve maximum control over both metabolic responses and coronary plaque.

--An entire chapter on the role of omega-3 fatty acids is included.

--A detailed discussion on the role of iodine and thyroid health--One of the newest additions to the Track Your Plaque menu of strategies is to achieve and maintain ideal thyroid health. This tips the scales in your favor for improved control over lipids/lipoproteins, weight, blood sugar, and coronary plaque.

The new guide, as well as our new Member kits that include the new Track Your Plaque Recipe Book, At-Home Lab Test kits, and nutritional supplements, are all available in the Track Your Plaque Marketplace.

While there is more to wheat's adverse effects on human health than celiac disease, studying celiac disease provides important insights into why and how wheat--the gluten component of wheat, in this case--is so destructive to human health.

Modern wheat, in particular, is capable of causing "celiac disease" without intestinal symptoms---no cramping or diarrhea--but instead shows itself as brain injury (ataxia, dementia), peripheral nervous system damage (peripheral neuropathy), joint and muscle inflammation (rheumatoid arthritis, polymyalgia rheumatica and others), and gastrointestinal cancers.

One neurological manifestation of wheat's effect on the human brain is a condition called cerebellar ataxia. This is a condition that can affect adults (average age 48 years) and children and consists of incoordination, falls, and incontinence.

Because brain tissue has limited capacity for healing and regeneration, symptoms of cerebellar ataxia usually improve slowly and modestly with meticulous elimination of wheat and other gluten sources.

Such observations are relevant even to people without celiac disease. Celiac disease sufferers are more susceptible to such extra-intestinal phenomena, but it can also happen in people without positive celiac antibodies.

Some references:

Neurological symptoms in patients with biopsy proven celiac disease

A total of 72 patients with biopsy proven celiac disease (CD) (mean age 51 +/- 15 years, mean disease duration 8 +/- 11 years) were recruited through advertisements. All participants adhered to a gluten-free diet. Patients were interviewed following a standard questionnaire and examined clinically for neurological symptoms. Medical history revealed neurological disorders such as migraine (28%), carpal tunnel syndrome (20%), vestibular dysfunction (8%), seizures (6%), and myelitis (3%). Interestingly, 35% of patients with CD reported of a history of psychiatric disease including depression, personality changes, or even psychosis. Physical examination yielded stance and gait problems in about one third of patients that could be attributed to afferent ataxia in 26%, vestibular dysfunction in 6%, and cerebellar ataxia in 6%. Other motor features such as basal ganglia symptoms, pyramidal tract signs, tics, and myoclonus were infrequent. 35% of patients with CD showed deep sensory loss and reduced ankle reflexes in 14%. Gait disturbances in CD do not only result from cerebellar ataxia but also from proprioceptive or vestibular impairment.

Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristics

Two hundred and twenty-four patients with various causes of ataxia from North Trent (59 familial and/or positive testing for spinocerebellar ataxias 1, 2, 3, 6 and 7, and Friedreich's ataxia, 132 sporadic idiopathic and 33 clinically probable cerebellar variant of multiple system atrophy MSA-C) and 44 patients with sporadic idiopathic ataxia from The Institute of Neurology, London, were screened for the presence of antigliadin antibodies. A total of 1200 volunteers were screened as normal controls. The prevalence of antigliadin antibodies in the familial group was eight out of 59 (14%), 54 out of 132 (41%) in the sporadic idiopathic group, five out of 33 (15%) in the MSA-C group and 149 out of 1200 (12%) in the normal controls. The prevalence in the sporadic idiopathic group from London was 14 out of 44 (32%). The difference in prevalence between the idiopathic sporadic groups and the other groups was highly significant (P < 0.0001 and P < 0.003, respectively). The clinical characteristics of 68 patients with gluten ataxia were as follows: the mean age at onset of the ataxia was 48 years (range 14-81 years) with a mean duration of the ataxia of 9.7 years (range 1-40 years). Ocular signs were observed in 84% and dysarthria in 66%. Upper limb ataxia was evident in 75%, lower limb ataxia in 90% and gait ataxia in 100% of patients. Gastrointestinal symptoms were present in only 13%. MRI revealed atrophy of the cerebellum in 79% and white matter hyperintensities in 19%. Forty-five percent of patients had neurophysiological evidence of a sensorimotor axonal neuropathy. Gluten-sensitive enteropathy was found in 24%. HLA DQ2 was present in 72% of patients. Gluten ataxia is therefore the single most common cause of sporadic idiopathic ataxia.

You can always count on Dr. John Cannell for unique perspectives on vitamin D. I reprint here his unfailingly entertaining and informative Vitamin D Newsletter on whether vitamin D replacement enhances physical performance.

The whole vitamin D "discovery" sometimes worries me. Vitamin D has proven to be an unbelievable, remarkable, dramatic boon to health, including facilitation in dropping CT heart scan scores. Yet the answer was always right in front of us. It worries me that you and I might have the answer to important questions right within our grasp all along--but don't know it. What if the same were true, say, for cancer? That is, a profound answer is right there, but our eyes just pass right over it.

Anyway, we should all keep our eyes open and perhaps you and I will continue to identify the most powerful tools available that return control over heart disease to us and take it away from the perverse, procedural hospital formula that still reigns.

If you haven't done so already, be sure to visit Dr. Cannell's website, www.vitamindcouncil.com.

The Vitamin D Newsletter
March, 2007

Peak Athletic Performance and Vitamin D

"No way doc." I had just finished telling my patient about the benefits of vitamin D, telling him he should take 4,000 IU per day, using all the techniques I had learned in 30 years of medical practice to convince someone proper treatment is important. But, he knew the U.S. government said he only needed 200 IU per day, not 4,000. He also knew the official Upper Limit was 2,000 IU a day. "What are you trying to do doc, kill me?" I told him his 25(OH)-vitamin D blood test was low, only 13 ng/ml. He had read about that too, in a medical textbook, where it said normal levels are between 10 and 40 ng/ml. "I'm fine doc;" adding "Are you in the vitamin business?" I explained I was not; that the government used outdated values; that recent studies indicate ideal 25(OH)D levels are about 50 ng/ml; and that they indicated that he needed about 4,000 IU per day to get his level up to 50. "No thanks doc, I'm fine."

So I tried a different tact. I brought him copies of recent press articles. "Look," I said, "look at these." Science News called vitamin D the Antibiotic Vitamin. The Independent in England says vitamin D explains why people die from influenza in the winter, and not the summer. U.S. News and World Report says almost everyone needs more. Newsweek says it prevents cancer and helps fight infection. In four different recent reports, United Press International says that: it reduces falls in the elderly, many pregnant women are deficient , it reduces stress fractures, and that it helps heals wounds.

He glanced at the articles, showing a little interest in stress fractures. Then he told me what he was really thinking. "Look doc, all this stuff may be important to old guys like you. I'm 22. All I care about are girls and sports. When I get older, maybe I'll think about it. I'm too young to worry about it. I'm in great condition." I couldn't argue. He was in good health and a very good basketball player, playing several hours every day, always on indoor courts.

What could I do to open his eyes? As an African American, his risk of early death was very high, although the risk for blacks doesn't start to dramatically increase until their 40's and 50's. Like all young people, he saw himself as forever young. The U.S. government was no help, relying on a ten-year-old report from the Institute of Medicine that is full of misinformation.

I tired to tell him that the 200 IU per day the U.S. government recommends for 20-year-olds is to prevent bone disease, not to treat low vitamin D levels like his. I pointed out the U.S. government's official current Upper Limit of 2,000 IU/day is the same for a 300 pound adult as it is for a 25 pound toddler. That is, the government says it's safe for a one-year-old, 25-pound, child to take 2,000 IU per day but it's not safe for a 30-year old, 300-pound, adult to take 2,000 and one IU a day. I mean, whoever thought up these Upper Limits must have left their thinking caps at home. Nevertheless, nothing worked. My vitamin D deficient patient was not interested in taking any vitamin D.

What are young men interested in? I remembered that he had told me: "Sex and sports." Two years ago I had researched the medical literature looking for any evidence vitamin D enhanced sexual performance. Absolutely nothing. That would have been nice. Can you imagine the interest?

Then I remembered that several readers had written to ask me if vitamin D could possibly improve their athletic performance? They told me that after taking 2,000 to 5,000 IU per day for several months, they seemed just a little faster, a little stronger, maybe had a little better balance and timing. A pianist had written to tell me she even played a better piano, her fingers moved over the keys more effortlessly! Was vitamin D responsible for these subtle changes or was it a placebo effect? That is, did readers just think their athletic performance improved because they knew vitamin D was a steroid hormone precursor (hormone, from the Greek, meaning "to set in motion")?

The active form of vitamin D is a steroid (actually a seco-steroid) in the same way that testosterone is a steroid and vitamin D is a hormone in the same way that growth hormone is a hormone. Steroid hormones are substances made from cholesterol, which circulate in the body, and work at distant sites by "setting in motion" genetic protein transcription. That is, both vitamin D and testosterone regulate your genome, the stuff of life. While testosterone is a sex steroid hormone, vitamin D is a pleomorphic (multiple function) steroid hormone.

All of a sudden, it didn't seem so silly. Certainly steroids can improve athletic performance although they can be quite dangerous. In addition, few people are deficient in growth hormone or testosterone, so when athletes take sex steroids or growth hormone they are cheating, or doping. The case with vitamin D is quite different because natural vitamin D levels are about 50 ng/ml and, since almost no one has such levels, extra vitamin D is not doping, it's just good treatment. I decided to exhaustively research the medical literature on vitamin D and athletic performance. It took me over a year.

To my surprise, I discovered that there are five totally independent bodies of research that all converge on an inescapable conclusion: vitamin D will improve athletic performance in vitamin D deficient people (and that includes most people). Even more interesting is who published this literature, and when. Are you old enough to remember when the Germans and Russians won every Olympics in the 60's and 70's? Well, it turns out that the most convincing evidence that vitamin D improves athletic performance was published in old German and Russian medical literature.

With the help of my wife and mother-in-law, both of whom are Russian, and with the help of Marc Sorenson, whose book Solar Power is a must read, I finally was able to look at translations of much of the old Russian and German literature. When one combines that old literature with the modern English language literature on neuromuscular performance, the conclusion is inescapable. The readers who wrote me are right.

If you are vitamin D deficient, the medical literature indicates that the right amount of vitamin D will make you faster, stronger, improve your balance and timing, etc. How much it will improve your athletic ability depends on how deficient you are to begin with. How good an athlete you will be depends on your innate ability, training, and dedication. However, peak athletic performance also depends upon the neuromuscular cells in your body and brain having unfettered access to the steroid hormone, activated vitamin D. In addition, how much activated vitamin D is available to your brain, muscle, and nerves depends on having ideal levels of vitamin D in your blood - about 50 ng/ml, to be precise.

Why would I write about such a frivolous topic like peak athletic performance when cancer patients all across this land are dying vitamin D deficient? Like many vitamin D advocates, I have been disappointed that the medical profession and the public don't seem to care about vitamin D. Maybe people, like my young basketball player, will care if it makes better athletes. So, Hey! You jocks! Listen up! I'm talking speed, balance, choice reaction time, muscle mass, muscle strength, squats, reps, etc. Important stuff. Here's the Vitamin D Council's first ever sports quiz.

1. Vitamin D-producing UVB radiation improves athletic performance and may have been widely practiced by German and Russian Olympic athletes in the 1960's and 70's.

True. I found tantalizing evidence the Russians and especially the Germans were on to this during the 60's and 70's when those two nations took turns placing number one and number two in the Olympics every year?

For example, in 1938, Russian researchers reported that a course of ultraviolet irradiations improved speed in the 100-meter dash in college students compared to matched controls, both groups undergoing daily training. Average 100-meter dash times decreased from 13.51 seconds to 13.28 seconds in the non-irradiated controls, but from 13.63 seconds to 12.62 seconds in the irradiated students. Here we see training improved times but training and irradiation improved times much more. Obviously, irradiation or vitamin D would not render the same magnitude of improvements in world-class sprinters, but they would be happy with a few milliseconds.

Gorkin Z, Gorkin MJ, Teslenko NE. [The effect of ultraviolet irradiation upon training for 100m sprint.] The Journal of Physiology of the USSR [Fiziol, z. (RSSR)] 1938; 25: 695-701. (In Russian)

If you want to know what early German thinking was on this, read this summation of the German literature:

"It is a well-known fact that physical performance can be increased through ultra-violet irradiation. In 1927, a heated argument arose after the decision by the German Swimmers' Association to use the sunlamp as an artificial aid, constituting an athletic unfairness, doping, so to speak. In 1926, Rancken had already reported the improving effect of sunlamp irradiation on muscle work with the hand-dynamo-graph. Heib observed an improvement in swimming times after repeated irradiations. In thorough experiments, Backmund showed that a substantial increase in muscle activity happens after radiation of larger portions of the body with an artificial sunlamp; that this performance increase is not caused through local - direct or indirect - effects on the musculature, but through a general effect. This general effect, triggered by ultra-violet irradiation, is caused by a systemic effect on the nervous system." (p. 17)

Parade GW, Otto H. Die beeinflussung der leistungsfahigkeit durch Hohensonnenbestrahlung. Zeitschrift fur Klinische Medizin (Z Klin Med),1940;137:17-21 [In German]

In 1945, two Americans measured the cardiovascular fitness and muscular endurance of 11 male Illinois subjects undergoing training in an indoor physical education class, comparing them to 10 matched controls. Both groups underwent similar physical training. Treatment consisted of ultraviolet irradiation, given in the nude, up to two minutes per session, three times per week, for ten weeks in the late fall and winter. After ten weeks, the treatment group had a 19% standard score gain in cardiovascular fitness compare to a 2% improvement in the control students. To regular readers of this newsletter, it should come as no surprise that the un-irradiated control group reported twice as many viral respiratory infections as the treatment group.

Allen R, Cureton T. Effects of Ultraviolet Radiation on Physical Fitness. Arch Phys Med 1945: 10: 641-44.

In 1952, the German sports medicine researcher, Spellerberg, reported on the effects of wholesale irradiation of athletes studying and training at the Sports College of Cologne - including many elite athletes - with a "central sun lamp." He irradiated the athletes in their bathing suits, on both sides of their bodies, for up to ten minutes, twice a week, for 6 weeks. He reported a "convincing effect" on athletic performance and a 50% reduction in sports injuries. Results were particularly impressive for swimmers, soccer, handball, hockey, and tennis players, as well as for boxers and most track and field athletes. He reported that irradiation leading to burns, further irradiation of athletes having achieved peak performance, and irradiation within 24 hours of competition, all impaired athletic performance. Their results were so convincing, the Sports College of Cologne officially notified the "national German and International Olympic committee." (p. 570)

Spellerberg AE. [Increase of athletic effectiveness by systematic ultraviolet irradiation.] Strahlentherapie 1952; 88: 567-70. [In German]

In 1952, Ronge exposed 120 German schoolchildren to UV lights installed in classrooms and compared them to 120 un-irradiated control children. Over a two-year period - excluding summer vacations - he tested both groups with a series of six cardiovascular fitness tests using a bike ergometer. Un-irradiated children showed a distinct seasonality in fitness, with the highest values right after summer break and the lowest values in the spring. Treated children showed no seasonal differences in physical performance. Differences in work performance between the irradiated and un-irradiated children were most conspicuous in the spring with 56% difference between the two groups. In a final experiment, he gave 30 children in the control classrooms 6.25 mg (250,000 IU) of vitamin D as a single dose in February and found their performance had "increased considerably," one month later but did not report the actual numbers. He concluded that vitamin D, either as a supplement or induced via UV irradiation, improved physical performance.

Ronge HE. [Increase of physical effectiveness by systematic ultraviolet irradiation.] Strahlentherapie 1952; 88: 563-6. [In German]

In 1954, another researcher, at the Max-Planck Institute for Industrial Physiology in Dortmund, Germany, administered three different wavelengths of UV light over 8 weeks to university students. He found that ultraviolet light in the vitamin D-producing UVB range was consistently effective in reducing resting pulse, lowering the basal metabolic rate, and increasing athletic performance. UVA had no effect; interestingly, artificial UVC irradiation (the atmosphere normally completely filters out UVC radiation and thus it's not naturally present on earth) also gave some positive results.

Lehmann G. [Significance of certain wave lengths for increased efficacy of ultraviolet irradiation.] Strahlentherapie. 1954 Nov;95(3):447-53. [In German]

In 1956, Hettinger and Seidel irradiated seven subjects in two different experiments: athletic performance on bike-ergometers and forearm muscle strength. They found that UV radiation induced a significant improvement in both muscle strength and athletic performance.

Hettinger T, Seidl E. [Ultraviolet irradiation and trainability of musculature.] Internationale Zeitschrift für angewandte Physiologie, einschliesslich Arbeitsphysiologie 1956; 16: 177-83. [In German]

Another German researcher, at the Institute for Medical Physics and Biophysics at the University of Gottiingen, studied reaction times (the time needed to recognize a light and switch it off) during October and November in a series of controlled experiments on 16 children and an unspecified number of adults. He first controlled for practice effects (getting better by practicing) and then administered nine full-body UV radiation treatments over three weeks to the two treatment groups, using placebo radiation in the two control groups. UV radiation improved choice reaction time by 25% in children and 20% in adults while reaction time worsened in controls. The improvements in the irradiated groups peaked at the end of the three weeks of UV treatments and reverted to baseline levels three weeks later. In the two control groups, he found distinctly improved reaction times in the sunnier months.

Sigmund R. [Effect of ultraviolet rays on reaction time in man.] Strahlentherapie. 1956; 101: 623-9. [In German]

The next study threw me because it was very well conducted, meticulously designed, and completely negative. In 1963, Berven reported on the effects of ultraviolet irradiation and vitamin D supplementation in a group of 30 Stockholm schoolchildren, aged 10 -11, comparing them to appropriate controls. He found no seasonality of fitness in the control group and no effect from either irradiation or two different vitamin D supplementation protocols (1500 IU of cholecalciferol daily for two months and a single dose of 400,000 IU of ergocalciferol) on performance on a bike ergometer.

Berven H. The physical working capacity of healthy children; seasonal variations and effect of ultraviolet irradiation and vitamin-D supply. Acta paediatrica. Supplementum 1963; 148: 1-22.

However, two things were not right and got me thinking. One, Berven found no seasonality of physical fitness and was the only author who found no such seasonal variations in athletic performance. Second, he found no effect from irradiation, again, the only author. Then I realized he was working with Swedish children in the late 1950's. Supplementation of children with high doses of vitamin D - often as cod liver oil - was routine in Scandinavia in the past, particularly in children. For example, in neighboring Finland, the official recommended daily dose of vitamin D for children - including infants - was 4,000 IU per day until 1964, when authorities reduced it to 2,000 IU/day. (That's right, you read that correctly, 4,000 IU per day for infants, which is too much by the way.)

In 1975, Finnish authorities reduced it to 1,000 IU per day, and, in 1992, to 400 IU per day. I emailed Professor Elina Hypponen who confirmed that the Swedish recommendations were similar to the Finnish ones. Therefore, it seems highly unlikely that many of Berven's Swedish children, studied in 1958 and 1959, all from "families with a good standard of living," were vitamin D deficient. Therefore, this study showed that vitamin D will not improve athletic ability in vitamin D replete people. That's very important because it indicates more is not necessarily better. More is only better if you are not taking enough.

Hypponen E, et al. Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study. Lancet. 2001 Nov 3;358(9292):1500-3.

In the 1960's, three American researchers conducted experiments with university students. Rosentswieg studied the effects of a single six-minute dose of UV light on each side of the trunk in 23 college women, recording changes in various tests of muscle strength at one and five hours. He found a trend towards significance after five hours in white but not African American students. In 1968, Cheatum found that a six-minute administration of UV light, on each side of the trunk, increased the speed of 15 college women in the 30-yard dash. In 1969, Rosentswieg found a six-minute dose of UV light, on each side of the trunk, finding improved performance on a bicycle ergometer in college women. However, unlike the Germans and Russians, I could find no evidence that any of these American findings interested any American professionals involved in the care or training of athletes.

Rosentsweig J. The effect of a single suberythemic biodose of ultraviolet radiation upon the strength of college women. J Assoc Phys Ment Rehabil. 1967 Jul-Aug;21(4):131-3.

Cheatum BA. Effects of a single biodose of ultraviolet radiation upon the speed of college women. Res Q. 1968 Oct;39(3):482-5.

Rosentswieg J. The effect of a single suberythemic biodose of ultraviolet radiation upon the endurance of college women. J Sports Med Phys Fitness. 1969 Jun;9(2):104-6.

2. Athletic performance peaks in the summer when vitamin D levels peak, and is at its lowest in the winter when vitamin D levels are at their lowest.

A. True
B. False

True. The studies below - all I could find in the literature - show tests of physical performance peak in the summer, when vitamin D levels peak, start to decline in early autumn, as vitamin D levels decline, and athletic performance reaches its lowest point in late winter, when vitamin D levels bottom out. However, it is reasonable to assume that any associations between athletic performance and summer season may be due to "reverse causation." That is, improved athletic performance in the summer might be secondary to increased outdoor physical and recreational activity in the warmer weather with an indoor sedentary lifestyle during the colder months. Maybe people have better athletic ability in the summer because they exercise more. If that is true - and using the same logic - athletic performance should not begin to decline until late autumn, because at most temperate latitudes early fall weather is ideal for outdoor physical activities.

However, some of the studies below controlled for seasonal variations in time spent exercising. Furthermore, besides a consistent positive association of summer season with improved athletic performance, the below studies found an abrupt - and unexplained - reduction in athletic performance beginning in the early fall - when vitamin D levels decline - but when the weather is ideal for outdoor activities.

For example, in 1956, German researchers found a distinct seasonal variation in the trainability of musculature, studying wrist flexor strength in 21 German subjects undergoing daily training. They found highly significant seasonal differences with peak performance during the later part of the summer, nadirs in the winter, and an unexplained sharp autumn decline beginning in October.

Hettinger T, Muller EA. Seasonal course of trainability of musculature. Int Z Angew Physiol. 1956;16(2):90-4.

A study of Polish pilots and crew found physical fitness and tolerance to hypoxia were highest in the late summer with an unexplained sharp decline starting in September. The authors hypothesized that seasonal variations in an unidentified hormone best explained their results.

Kwarecki K, Golec L, Klossowski M, Zuzewicz K. Circannual rhythms of physical fitness and tolerance of hypoxic hypoxia. Acta Physiol Pol. 1981 Nov-Dec;32(6):629-36.

Cumulative work ability among 1,835 mainly sedentary Norwegian men during bicycle exercise tests showed an August peak, a sharp decline starting in the autumn, and a wintertime nadir. There were no seasonal changes in body weights, as might be expected if more caloric-demanding recreational activity during the sunnier months explained their results.

Erikssen J, Rodahl K. Seasonal variation in work performance and heart rate response to exercise. A study of 1,835 middle-aged men. Eur J Appl Physiol Occup Physiol. 1979 Oct;42(2):133-40.

Koch and Raschka reviewed the mostly German literature on the seasonality of physical performance, discussing studies indicating that muscle strength and stamina peak in the late summer. The authors then attempted to control for seasonal variations in the time spent exercising by instituting a controlled yearlong training regimen, beginning in December. The training regimen consisted of at least 20 push-ups per day and 2 or 3 long-distances races per week for the entire year. They found the both the number of push-ups and muscle strength peaked in late summer followed by a rapid decline in the fall, and a nadir in the winter, despite continued training. They concluded that seasonal variations in an unidentified hormone best explained their results. In addition, by now we all know that vitamin D is a seasonal hormone, and a steroid hormone precursor to boot.

Koch H, Raschka C. Circannual period of physical performance analysed by means of standard cosinor analysis: a case report. Rom J Physiol. 2000 Jan-Dec;37(1-4):51-8.

3. Vitamin D has direct muscle-building (anabolic) effects.

A. True
B. False

True, but only in vitamin D deficient subjects. Both animal and human studies have found that vitamin D directly affects muscle. That is, vitamin D increases muscle mass.

For example, Birge and Haddad found that vitamin D caused new protein synthesis in rat muscle.

Birge SJ, Haddad JG. 25-hydroxycholecalciferol stimulation of muscle metabolism. J Clin Invest. 1975 Nov;56(5):1100-7.

What about humans? In 1981, Young performed muscle biopsies on 12 severely vitamin D deficient patients before and after vitamin D treatment. They found type-II (fast-twitch) muscle fibers were small before treatment and significantly enlarged after treatment. Sorensen performed muscle biopsies on eleven older patients with osteoporosis before and after treatment with vitamin D. The percentage and area of fast twitch fibers increased significantly after treatment, despite the lack of any physical training.

Young A, Edwards R, Jones D, Brenton D. Quadriceps muscle strength and fibre size during treatment of osteomalacia. In: Stokes IAF (ed) Mechanical factors and the skeleton. 1981. pp 137-145.

Sorensen OH, Lund B, Saltin B, Lund B, Andersen RB, Hjorth L, Melsen F, Mosekilde L. Myopathy in bone loss of ageing: improvement by treatment with 1 alpha-hydroxycholecalciferol and calcium. Clin Sci (Lond). 1979 Feb;56(2):157-61.

Sato reported that two years of treatment with 1,000 IU of vitamin D per day significantly increased muscle strength, doubled the mean diameter, and tripled the percentage of fast-twitch muscle fibers, in the functional limbs of 48 severely vitamin D deficient elderly stroke patients. The placebo control group suffered declines in muscle strength, and in the size and percentage of fast-twitch muscle fibers.

Sato Y, Iwamoto J, Kanoko T, Satoh K. Low-Dose Vitamin D Prevents Muscular Atrophy and Reduces Falls and Hip Fractures in Women after Stroke: A Randomized Controlled Trial. Cerebrovasc Dis. 2005 Jul 27;20(3):187-192 [Epub ahead of print]

These studies clearly show that vitamin D when administered to vitamin D deficient people stimulates the growth and number of those muscle fibers critical to athletic ability, type-2, or "fast twitch," muscle fibers.

4. Many studies have found direct associations between physical performance and vitamin D levels. That is, the higher your vitamin D level, the better your athletic performance.

A. True
B. False

True. I found 13 positive studies of associations between vitamin D levels and various parameters of neuromuscular performance. However, they were all in old people. Of course, old people can be athletes too. Furthermore, age differences in physiology and pharmacology are quantitative, not qualitative. That is, what is true in old people will be true in young people, although the magnitude might be different. Higher vitamin D levels are associated with a wide variety of athletic performance but appear to have the strongest associations with balance, timing, and timed tests of physical performance.

The three largest studies had more than 7,000 elderly subjects. All found evidence of a vitamin D threshold of between 30 - 50 ng/ml, above which further improvements in athletic performance were not seen. Wicherts and her colleagues found a linear correlation between vitamin D and neuromuscular performance; scores were 78% better for those with vitamin D levels greater than 30 ng/ml compared to those with levels less than10 ng/ml.

Bischoff-Ferrari HA, Dietrich T, Orav EJ, Hu FB, Zhang Y, Karlson EW, Dawson-Hughes B. Higher 25-hydroxyvitamin D concentrations are associated with better lower-extremity function in both active and inactive persons aged > or =60 y. Am J Clin Nutr. 2004 Sep;80(3):752-8.

Gerdhem P, Ringsberg KA, Obrant KJ, Akesson K. Association between 25-hydroxy vitamin D levels, physical activity, muscle strength and fractures in the prospective population-based OPRA Study of Elderly Women. Osteoporos Int. 2005 Nov;16(11):1425-31.

Wicherts IS, et al. Vitamin D status predicts physical performance and its decline in older persons. J Clin Endocrinol Metab. 2007 Mar 6; [Epub ahead of print]

Professor Heike Bischoff-Ferrari, now in Switzerland, did the largest study. She and her colleagues found a strong positive correlation and suggestion of a U-shaped curve with athletic performance on one test peaking with vitamin D levels of 50 ng/ml but deteriorating at higher levels. It is interesting to speculate that levels around 50 ng/ml may be optimal for athletic performance as such levels are common in humans living in a "natural" state of sun-exposure, such as lifeguards or tropical farmers.

Bischoff HA, Stahelin HB, Urscheler N, Ehrsam R, Vonthein R, Perrig-Chiello P, Tyndall A, Theiler R. Muscle strength in the elderly: its relation to vitamin D metabolites. Arch Phys Med Rehabil. 1999 Jan;80(1):54-8.

Interestingly, all three studies that looked for an association between mental abilities and vitamin D levels found one. A fourth study, unrelated to athletic function, also found an association. The obvious explanation for these findings is that cognitively impaired patients do not go outdoors as often as higher functioning patients and thus have lower vitamin D levels. However, Dhesi found the association after excluding all but mildly demented patients, making such an explanation more difficult. Flicker and - more recently - Przybelski and Binkley, found the association after controlling for outdoor activities, raising the possibility that the association of vitamin D levels with cognitive abilities is casual. Both the vitamin D receptor and the enzyme necessary to activate vitamin D are present in a wide-variety of human brain tissue. If vitamin D deficiency impairs cognitive abilities, it is likely that such deficiencies will also impair the brain's ability to process the complex circuits needed for peak athletic performance.

Dhesi JK, Bearne LM, Moniz C, Hurley MV, Jackson SH, Swift CG, Allain TJ. Neuromuscular and psychomotor function in elderly subjects who fall and the relationship with vitamin D status. J Bone Miner Res. 2002 May;17(5):891-7.

Kenny AM, Biskup B, Robbins B, Marcella G, Burleson JA. Effects of vitamin D supplementation on strength, physical function, and health perception in older, community-dwelling men. J Am Geriatr Soc. 2003 Dec;51(12):1762-7.

Flicker L, Mead K, MacInnis RJ, Nowson C, Scherer S, Stein MS, Thomasx J, Hopper JL, Wark JD. Serum vitamin D and falls in older women in residential care in Australia. J Am Geriatr Soc. 2003 Nov;51(11):1533-8.

Przybelski RJ, Binkley NC. Is vitamin D important for preserving cognition? A positive correlation of serum 25-hydroxyvitamin D concentration with cognitive function. Arch Biochem Biophys. 2007 Jan 8;

There can be no doubt that higher vitamin D levels are associated with improved athletic performance in the elderly. From what we know of physiology and pharmacology, the same associations should hold true in young people, including young athletes.

5. Numerous studies have found that vitamin D improves physical performance.

A. True
B. False.

True, but, again, most all the studies are in old persons, not young ones, and none of the studies are in world-class athletes. However, there is no medical reason why vitamin D would improve the athletic performance of vitamin D deficient old people but not vitamin D deficient young ones. Eleven studies found vitamin D improved physical performance, mainly on measures of balance and reaction time. The one study of younger subjects showed dramatic physical performance effects in 55 severely vitamin D deficient women.

Sorensen OH, Lund B, Saltin B, Lund B, Andersen RB, Hjorth L, Melsen F, Mosekilde L. Myopathy in bone loss of ageing: improvement by treatment with 1 alpha-hydroxycholecalciferol and calcium. Clin Sci (Lond). 1979 Feb;56(2):157-61.

Gloth FM 3rd, Smith CE, Hollis BW, Tobin JD. Functional improvement with vitamin D replenishment in a cohort of frail, vitamin D-deficient older people. J Am Geriatr Soc. 1995 Nov;43(11):1269-71.

Glerup H, Mikkelsen K, Poulsen L, Hass E, Overbeck S, Andersen H, Charles P, Eriksen EF. Hypovitaminosis D myopathy without biochemical signs of osteomalacic bone involvement. Calcif Tissue Int. 2000 Jun;66(6):419-24.

Prabhala A, Garg R, Dandona P. Severe myopathy associated with vitamin D deficiency in western New York. Arch Intern Med. 2000 Apr 24;160(8):1199-203.

Verhaar HJ, Samson MM, Jansen PA, de Vreede PL, Manten JW, Duursma SA. Muscle strength, functional mobility and vitamin D in older women. Aging (Milano). 2000 Dec;12(6):455-60.

Pfeifer M, Begerow B, Minne HW, Abrams C, Nachtigall D, Hansen C. Effects of a short-term vitamin D and calcium supplementation on body sway and secondary hyperparathyroidism in elderly women. J Bone Miner Res. 2000 Jun;15(6):1113-8.

Bischoff HA, Stahelin HB, Dick W, Akos R, Knecht M, Salis C, Nebiker M, Theiler R, Pfeifer M, Begerow B, Lew RA, Conzelmann M. Effects of vitamin D and calcium supplementation on falls: a randomized controlled trial. J Bone Miner Res. 2003 Feb;18(2):343-51.

Dhesi JK, Jackson SH, Bearne LM, Moniz C, Hurley MV, Swift CG, Allain TJ. Vitamin D supplementation improves neuromuscular function in older people who fall. Age Ageing. 2004 Nov;33(6):589-95.

Sato Y, Iwamoto J, Kanoko T, Satoh K. Low-Dose Vitamin D Prevents Muscular Atrophy and Reduces Falls and Hip Fractures in Women after Stroke: A Randomized Controlled Trial. Cerebrovasc Dis. 2005 Jul 27;20(3):187-192 [Epub ahead of print]

In summary, five converging - but totally separate - lines of scientific evidence leave little doubt that vitamin D improves athletic performance. (I actually left out a sixth line of evidence, something a little more complicated, studies of muscle strength and vitamin D receptor polymorphisms; the two studies I could find were both positive.) Anyway, the scientific evidence that UVB radiation, either from the sun or from sunbeds, will improve athletic performance is overwhelming and the mechanism is almost certainly vitamin D production. Peak athletic performance will probably occur with 25(OH)D levels of about 50 ng/ml, whether from sun, sunbeds, or supplements.

All that is missing is a big-time professional or college team identifying and then treating their elite athletes who are vitamin D deficient. Can you imagine what such performance-enhancing effects would do for basketball players, most of who are African American and who practice and play indoors all winter? Or gymnasts? Or weight lifters?

However, a word of caution. The above studies suggest that taking too much vitamin D (more than 5,000 IU per day) may actually worsen athletic performance. Take the right amount, not all you can swallow. Take enough to keep your 25(OH)D levels around 50 ng/ml, year round. Easier yet, regularly use the sun in the summer and sunbeds in the winter - with care not to burn. Once a week should be about right.

When you think about it, none of this should surprise anyone. Every body builder knows that steroid hormones can improve athletic performance, certainly increase muscle mass. Barry Bonds knows they increase timing and power. Moreover, activated vitamin D is as potent a steroid hormone as exists in the human body. However, unlike other steroids, levels of activated vitamin D in muscle and nerve tissue are primarily regulated by sun exposure. That's right, the rate-limiting step for the cellular function (autocrine) of activated vitamin D is under your control. It depends on how much you put in your both or go into the sun. It's ironic that many athletes now avoid the sun, organized baseball is even promoting sun avoidance and sunblocks. The ancient Greeks knew better; they had there elite athletes train on the beach and in the nude.

The medical literature indicates vitamin D levels of about 50 ng/ml are associated with peak athletic performance. Of course, recent studies show such levels are ideal for preventing cancer, diabetes, hypertension, influenza, multiple sclerosis, major depression, cognitive impairments, etc. But who cares about all that disease stuff old people get, we're talking about something really important: speed, balance, reaction time, muscle mass, muscle strength, squats, reps, etc. And guess who's now taking 4,000 IU/day? Yes he is, and he tells me his timing is better, he can jump a little higher, run a little faster, and the ball feels "sweeter," whatever that means.

John Cannell, MD

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The reason why I've been blogging lightly these past few days is because, as a favor, I'm covering the practice for some colleagues who I'm (very) loosely affiliated with. The time demands have been great.

Nonetheless, it is a good reminder to me just how far wrong conventional cardiology remains. Judging by what I see around me, there is a startling lack of restraint in proceeding to the catheterization laboratory. Curiously, the internists and family practitioners have been brainwashed into accepting this path. I suppose that all it takes is an occasional real "save" for these physicians to develop a fear of ever missing real disease.

What I'm seeing is just how many people presenting with chest pain or similar symptoms end up going to the cath lab. I would crudely estimate 80%. That is, once you make it past the emergency room, there's a four out of five chance that you'll end up with a heart catheterization to "be sure your heart is okay", "make certain you're not going to die of heart disease", "see if there's a ticking time bomb in your chest". You've heard all the clever, scary phrases that get tossed around to scare the pants off you and justify putting catheters in your groin.

Despite the fact that tools for heart disease prevention have improved dramatically, the volume of heart catheterizations continues to grow nationwide.

I find it shocking and unacceptable. We're currently working behind the scenes to help change this situation through education of the public. Persuade a $1 million a year cardiologist that he is overdoing procedures? Unlikely in my experience. Educate the public about the shocking over-reliance on high-revenue procedures? Perhaps more practical.

Garlic May Not Lower Cholesterol
Study Shows No Improvement in Cholesterol Levels From Raw Garlic or Garlic Supplements

Lots of reports continue to hit the press about a small study that hoped to determine whether garlic as whole cloves (4 to 6), an aqueous extract of garlic called Kyolic, or an oil extract called Garlicin (high in allicin), or placebo. No differences in lipid numbers including LDL cholesterol were observed.

(Full text at WebMD at http://www.webmd.com/cholesterol-management/news/20070226/garlic-may-not-lower-cholesterol?ecd=wnl_chl_030507. You may be required to log in or register.)

I believe that the researchers were sincere in their effort to follow an honest, scientfically sound clinical trial design. I'm personally not that surprised. The effect in prior studies has been modest, sometimes none. Does that mean that we should ignore the other studies that suggest there may be modest blood-thinning, anti-inflammatory, blood pressure-reducing, and cancer-preventing properties? No, it does not. Dr. Matt Budoff at UCLA even published a very small study in about 20 people that suggested a slowing of plaque growth by using Kyolic in persons tracked by CT heart scans.

Nonetheless, garlic is, at best, probably no more than a source of small benefits. The biggest fallout from this kind of report, however, is not the neutral results from garlic, but from the open door the drug companies sense when this happens.

If you read the WebMD report, you'll notice all sorts of advertisements from drug companies for statin cholesterol drugs ("Cholesterol health center"; "Understanding Cholesterol Numbers"; "There are two sources of cholesterol: food and family"), Niaspan (which I used to support but have been discouraged by the Kos companies excessively profiteering methods and recent big Wall Street sellout).

It doesn't follow. The failure of one nutritional strategy to reduce LDL does nothave to trigger a run to the drugs. Don't fall for it. Drugs have their place. So do supplements and food choices, which can be very powerful. Drug manufacturers and their marketing people salivate when something like this comes along, an open invitation to say, "If garlic doesn't work, _____ sure does."

Jason came to the office because of chest pain. At 34 years old, he works as manager of a (non-fast food) restaurant, but indulges in lots of the odds and ends. Among his indulgences: Diet Coke.

Every time he'd have a diet Coke, he'd have chest pain. Not drinking diet Coke--no chest pain. If Jason drank coffee, no chest pain. Other foods, no chest pain. Anyway, just eliminating the diet Coke seemed to do the trick. (Aspartame?)

Anyway, that's not why I tell you Jason's story. In the midst of his evaluation, an echocardiogram showed a mildly enlarged aorta, measuring 4.0 cm in diameter. So we obtained lipoproteins. Jason showed lipoprotein(a) and small LDL particles, the dreaded duo. We talked about how to correct this pattern. Among the strategies we discussed was niacin.

But what bothered me was that neither of Jason's parents had a diagnosis of heart disease. Jason had to have gotten Lp(a) from either his mother or father, since you obtain the gene from one or the other parent. You cannot acquire Lp(a). So one of Jason's parents was sitting on a genetic time bomb of unrecognized Lp(a) and hidden heart disease.

Because Jason's paternal grandfather had a heart attack at age 62, only Jason's Dad had the heart scan (though I urged both to get one). Score: 1483. Recall that heart scan scores >1000 carry a risk of death or heart attack of 25% per year if no preventive action is taken. Now, of course, we have to persuade Jason's Dad that a program of prevention--intensive prevention is in order, including a measure of Lp(a).

So that's the curious story of how Diet Coke probably saved Jason's Dad's life. The lesson is that if you or someone you know has Lp(a), think about their children as well as their parents, each of whom carry a 50% chance of having the pattern.

There's a widely-known (among cardiologists) problem with nuclear stress tests. It's called the "false positive." (Nuclear stress tests are known as stress Cardiolites, stress thalliums, stress Myoviews, persantine stress tests, adenosine stress tests)

Stress tests, nuclear and otherwise, are helpful for identifying areas of poor blood flow. If an area of poor blood flow is detected and the area is substantial, then there may be greater risk of heart attack and other undesirable events in the relatively near future.

What "false positive" means is a stress test that shows an abnormality but it's not true--it is falsely abnormal. There are a number of reasons why this can happen. The problem is that this phenomenon is very common. Up to 20% of nuclear stress tests are false positives.

There are indeed situations where there may an abnormality and it is not clear whether it is true or false. This may lead to a justifiable heart catheterization or CT coronary angiogram. But, given the extraordinary number of false positives, there's a lot of gray in interpreting these tests. Hospital staff, in fact, call nuclear medicine "unclear" medicine. It's common knowledge that you can often see just about anything you want to see on a nuclear image of the heart. Abnormalities in the bottom of the heart, the "inferior" wall, are especially common due to the overlap of the diaphragm with the heart muscle, yielding the appearance of reduced blood flow. Defects in the front of the heart heart are common in females with large breasts for the same reasons.

The problem: The uncertainty inherent in nuclear stress tests opens the door to the unscrupulous or lazy practitioner. Any blip, tick, or imperfection on the nuclear images serve as carte blanche to drag you into the hospital for procedures.

This abusive practice is, in my experience, shockingly common for two reasons: 1) It pays better to do heart catheterizations, and 2) Defensive medicine.

What's the disincentive? Only doing the right thing and maintaining a clear conscience. Slim reasons for many of my colleagues--and a lot less money.

If you are without symptoms and feel fine, and a nuclear stress test is advised by your doctor, followed by a discussion of an abnormality, insist on a discussion of exactly what is abnormal, just how abnormal, and what the alternatives might be. If you receive unsatisfactory or incomplete answers despite your best effort, it's time for another opinion.

Magnesium is kind of boring. So most people don't pay too much attention to it.

Magnesium can be important, however. I saw an interesting phenomenon recently. A type I diabetic patient of mine (that is, an adult who developed diabetes as a child), Mitch, was experiencing wide swings in blood sugar: low low's and very high high's (300-400 mg/dl). Mitch's magnesium was only marginally low at 2.0 mEq/L. (Ranges for normal magnesium blood levels are usually 1.3–2.1 mEq/L or 0.65–1.05 mmol/L.) Note that Mitch's blood levels fall within "normal." I do not agree with these "normal" ranges. I shoot for 2.1 to 2.4 mEq/L, which I think is the truly normal range.

In addition to eating plenty of raw nuts and green vegetables, Mitch began supplementing magnesium with magnesium citrate, 200 mg twice a day (our preferred supplement form). He reported that the wide swings in blood sugar were nearly eliminated.

Mitch's dramatic benefit is just a great illustration of how magnesium can help control blood sugar metabolism. A type I diabetic is more sensitive to the effects, but anyone with type II (adult) diabetes, metabolic syndrome, or just a slightly high blood sugar could benefit from magnesium supplementation.

There's a number of ways to accomplish getting sufficient magnesium in your daily regimen. Track Your Plaque members, Be sure to read:

Your water may be killing you at
http://www.cureality.com/library/fl_03-002magnesium.asp

Magnesium: Water to the rescue! at http://www.cureality.com/library/fl_03-010magnesium2.asp

It struck me recently that, for many people, it's not the second but the third heart scan that more commonly shows a reduction in score.

I think this is because many people's reaction to their first heart scan is "This can't be. There's no way my arteries have that much plaque." They then follow a half-hearted program to correct their patterns.

When the second heart scan shows a significantly higher score, that really catches their attention. This is when they finally buckle down and give it their all.

Only the occasional person will, after the first heart scan, seize full control and take their program very seriously. These tend to be highly motivated people.

Don't feel too bad if your second heart scan score shows an increase. Look at it for what it represents: feedback on the adequacy of your program.

Peter started out at age 59 at 248 lbs, standing 6 ft tall (BMI = 33.6!).

Along with his weight, Peter had the entire panel of phenemena of the so-called "metabolic syndrome", or pre-diabetes:

--Triglycerides 238 mg/dl and associated with extremes of excess VLDL and IDL
--High blood pressure
--Blood sugar 115 mg/dl
--High c-reactive protein
--Small LDL particles 99% of total LDL

Interestingly, Peter's HDL was a surprisingly favorable 58 mg/dl (HDL is usually low in this syndrome). However, when broken down by size, he had nearly zero large, healthy HDL (sometimes called HDL2b). Though total HDL was favorable, most of it was simply ineffective.

Peter eliminated snacks and processed foods, particularly bread; increased his reliance on healthy oils and lean proteins; incorporated soy protein; increased vegetables. He added 30 minutes of a rapid walk on a treadmill every day. He added vitamin D to achieve a blood level of 50 ng/dml. He added a magnesium supplement.

Peter has lost 31 lbs. in the last year. Weight 207 lbs., BMI 28.1 (desirable <25). Blood sugar: 96 mg/dl; triglycerides: 56 mg/dl; HDL 71 mg/dl with 35% in the large fraction; small LDL 45% of total. Not perfect, but a damn site better.

Control of metabolic syndrome is an achievable goal for over 90% of people, just with these simple efforts. We haven't yet had a chance to assess the effect on the progression or regression of Peter's heart scan score, but he has, at the very least, spared himself a future of diabetes and all its complications.

This is a "slice" from a normal heart scan in a 58 year old woman. Heart scan score zero. Look at the lungs, the dark areas left and right of the heart in the center. The lungs are also normal. Black represents normal density, healthy lung tissue. The white streaking is just normal lung blood vessels. This person doesn't smoke.

This woman smokes a pack of cigarettes a day and has done so for 45 years ("45 pack-years"). She had a surprisingly low heart scan score (at age 64) of only 71, despite the smoking. However, look at this woman's lungs. It's a little tough to make out, since the computer graphics loses some of the resolution. But you can see the near absence of lung tissue on both sides. This is an advanced phase of the destructive lung disease, emphysema, from smoking. Even if she quit smoking today, the destroyed lung tissue never grows back. She literally has huge gaps or holes in her lungs where lung tissue used to be.

Smoking is among the most destructive, terrible things you can do to your body, short of swallowing strychnine or jumping off a building. Stay as far the heck away from cigarettes as you possibly can. If you are exposed to "secondary" smoke, insist that the person never smoke in your presence. It's not the smell that destroys your lungs or causes coronary plaque (though it is indeed foul), it's the actual smoke.

Do you need to become a vegetarian in order to reduce your heart scan score?

No. Plain and simple. We’ve had many non-vegetarians drop their scores.

That said, are there still advantages to following a vegetarian diet, or some variation on the vegetarian theme?

Yes, there are. Let’s put aside the moral or religious arguments in favor of not eating animals—the need to eliminate killing animals for food, elimination of suffering common in modern livestock practices, Kosher considerations, etc. (Not that there aren’t real arguments here. Our focus for this conversation is not, however, the moral dilemma, but the health argument.)

Some of the most unhealthy people I’ve ever met, mostly males, are proud carnivores who boast of their prodigious capacities to eat meat. Unfortunately, it’s hard to tease out the ill-effects of excessive meat eating, since these same men also tend to be substantially overweight, smoke, drink excessively, and fail to get exercise unless their job is physically demanding. You know the type.

What advantages does a vegetarian obtain? A number of studies have suggested that the reduced saturated fat, reduced exposure to parasites, as well as reduced exposure to the antibiotics and hormones now used routinely in livestock-raising practices, do indeed provide benefits to the vegetarian. Thus, vegetarians tend to be substantially thinner, experience less bowel cancer, have less diabetes and heart disease, and live longer.

(If you are interested in reading or seeing more about just how inhumane modern livestock practices are, take a look at the video, "Meet Your Meat" at meat.org. Be sure not to view this after dinner.)

Of course, some of the disadvantages of eating animal products diminish when free-range livestock are eaten, i.e., livestock not raised in the inhumane cramped, filthy conditions of livestock factories, but in the open, grazing or rooting freely. These animals tend to have different fat compositions and taste different.

The advantages of vegetarianism, however, have blurred in recent years, since many so-called vegetarians have failed to maintain the distinction between naturally-occurring foods and processed foods. So, Ritz Crackers, Oreo cookies, whole wheat bread, and Raisin Bran fit into a vegetarian program, but they’re awful for your health. I’ll occasionally meet a self-proclaimed vegetarian who looks every bit as unhealthy as a conventionally eating American, that is, overweight, pre-diabetic person with a developing heart scan score.

So it is not necessary to be vegetarian to reduce your score. You might consider vegetarianism for other reasons, such as moral considerations, or to reduce your risk for cancer. But it is not necessary to drop your heart scan score. A non-processed food diet? Now that's is worth giving serious consideration.

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