Why do the Japanese have less heart disease?

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: What forms are safe?

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.

Introduction to the New Track Your Plaque book, version 2.0


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 19th 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-20th 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 21st 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 21st century disseminates through the ranks of modern healthcare providers at much the same pace as measuring blood pressure did in the early 20th 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 20th 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.

What are "normal" triglycerides?

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.

1985: The Year of Whole Grains

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?

Have some more

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."

When MIGHT statins be helpful?

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.

Advanced topics in nutrition

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 now available

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.

Don't wet yourself

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.
Cureality | Real People Seeking Real Cures

An exercise in optimism

Followers of the Track Your Plaque program already know that maintaining an optimistic viewpoint is important in gaining control over coronary plaque.

In fact, I believe that, in many cases, a sense of optimism may make or break your CT heart scan score-reducing efforts. Pessimists rarely drop their score, while optimists do so all the time.

This week posed a challenge to my optimism. I spent the last week on jury duty hearing the details of a murder case. For four days, I listened to blow-by-blow testimony about the totally pointless, unprovoked death of a young man by a drug-dealing thug. Much of the witness testimony was from people who shared the hopeless, violent world of the defendant.

I was, however, completely impressed by the dedication of the prosecuting attorney, a 50-some year old man who was clearly deeply dedicated to his mission and didn't once provide any indication that he was grandstanding or looking for some personal glory. He was doing his job and trying to obtain justice for the fallen victim. I was equally impressed by the judge, who seemed unfazed by the events but carefully explained why the system worked the way it did. After the trial, he provided some further insights to us jury members and I saw him as a human being who, like the prosecutor, was trying to make a small contribution to making the world better.

Though many of the witnesses who testified against the defendant shared his world, I was impressed with their courage in coming forward. They face the threat of reprisals, I'm sure, for coming forward to the law and testifying against a known career criminal. Several of them said that they were not after any reward, but simply wished to do the right thing and provide testimony that proved damning against the defendant.

I acted as the jury foreman and I was proud of how the jury members listened carefully, asked intelligent and probing questions, and then helped us render a confident and expeditious sentence: guilty.

If anything, despite the tragic circumstances, I was much heartened at how all the participants in this process played their part and justice (at least in the legal sense) was served.

Let optimism prevail, even in dire circumstances.

No need to re-invent the wheel

I seem to be repeating myself lately, but I think this does bear repeating:

There's no need to re-invent the wheel when it comes to gaining control over your heart scan score.

The Track Your Plaque program is the most powerful approach known to help you gain control over your coronary atherosclerotic plaque and CT heart scan score, bar none. While 100% of people do not drop their score, more and more people every week are doing so. (One of the admitted weaknesses of the Track Your Plaque website is our failure to list more success stories; we're working on it.)

The basic program is quite simple:

--The Rule of 60 for lipids (LDL 60 mg/dl; HDL 60 mg/dl or greater; triglycerides 60 mg/dl or less)

--Identify hidden causes of plaque, esp. small LDL, Lp(a), and IDL, followed by specific corrective action

--Fish oil--minimum 1200 mg per day of EPA + DHA

--Normal vitamin D3 blood levels (We aim for 25-OH-vitamin D3 of 50-60 ng/ml)

--Normal blood sugar (<100 mg/dl)

--Normal blood pressure (<130/80)

--An optimistic attitude



Much of the other stuff--vitamin K, matrix metalloproteinase reducing strategies, flavonoid strategies, exercise-induced hypertension, etc.--are, for the majority, fluff. Their real role is in people who may have failed in stopping the rise of their heart scan score just doing the basics of the program.

If you neglect the basics, hoping to find some magic potion, I'm afraid the overwhelming likelihood is that you will fail. I've seen it happen time and again. Someone will come to my office with an extraordinary list of supplements--hawthorne, dozens of anti-oxidants, EDTA, concentrated flavonoid preparations, and on and on. Not only is it shockingly expensive to do this, it's also unnecessary and foolhardy. This kind of unfocused, hocus-pocus in the hopes of getting it right fail time after time.

The Track Your Plaque program, while not foolproof, is the best I know of. Stick to the basics and wander off when the basics fail. But there's extraordinary power in just achieving the basics.

Are we a front for drug companies?

I was shocked recently when someone accused me and the Track Your Plaque website of being nothing more than a front for the drug industry, that we are promoting concepts with the hidden pharmacuetical agenda behind us.

Don't make me laugh. How in the world that kind of impression could be gotten from either the Heart Scan Blog or the Track Your Plaque website is beyond me.

But I occasionally do need to state explicity: We do not promote drugs, neither this Blog nor the Track Your Plaque website has ever sought nor been backed by pharmaceutical money. The only money that supports this website is our own and that from paying Track Your Plaque members.

In fact, I am quite proud of the unbiased content and commentary on both venues. I challenge anyone to point out how and where there is any suggested relationship to a hidden source of commercial backing. I assure you, there is none.

If I say a drug is worth you and your doctor considering, then I say so with a true belief in it, not because somebody or some company paid me to say so. If I say a drug stinks, I believe that too. If we use a specific supplement in the program, it's because we believe it truly adds value to a plaque-reversal program. We receive no money from drug, supplement, or other commercial interests to promote their products. Period.

What is "normal"?

When it comes to laboratory values and medical testing, a common dilemma is knowing what is "normal." Let me explain.

First of all, when you receive a laboratory result for a test, a "reference range" or "normal range" is usually provided. Where did that range come from?

It varies from test to test. For instance, a low potassium is easy, because low potassium levels can lead to life threatening consequences, e.g., dangerous heart rhythms. High potassium likewise, because dangerous phenomena develop when potassium generally exceeds 5.5 mg/dl or so.

But what about something like HDL or LDL. Here's where confusion reigns. Often, "normal" is obtained by taking the average and saying that any value plus or minus two standard deviations (remember that painful class?) represents normal or reference range.

If that were true, what if we applied that principle to body weight. If we weighed several thousand adult women, the average would be in the neighborhood of 172 lbs (no kidding). Does that mean that 172 lbs plus or minus two standard deviations is normal? No, of course not.

There is therefore a distinction between "normal" and "desirable". For HDL cholesterol, your laboratory report might say that an HDL cholesterol of 40-60 mg/dl is normal. But is it desirable? I don't think so. The most frequent HDL level for a male with a heart attack is 42 mg/dl--hardly desirable.

Let's take triglycerides. The average triglyceride level in the U.S. is somewhere around 140 mg/dl. For those of us who do a lot of lipoprotein testing, we can tell you that triglycerides at this level, though generally regarded as being within the normal range, are associated with flagrant and obvious excesses of several abnormal lipoprotein particles that contribute to coronary plaque growth (VLDL and often IDL; small LDL; drop in HDL and shift towards small HDL).

So, always take the so-called "normal" or "reference" values on a lab report as crude guidelines that often have little or nothing to do with health or desirability. Unfortunately, many physicians are not aware of this and will declare any value within the normal or reference range as okay. An HDL of 40 mg is not okay. A triglyceride level of 140 mg is also not okay.

What is okay? What is desirable? That depends on the parameter being examined. From a basic lipid standpoint, of course, we regard desirable as 60-60-60. Desirability from a lipoprotein standpoint we will cover in a more thorough Track Your Plaque Special Report in future.

The wisdom of the masses

My sister sent me these quotes:



"We don't like their sound, and guitar music is on the way out."

Decca Recording Co. rejecting the Beatles, 1962


"Stocks have reached what looks like a permanently high plateau."

Irving Fisher, Professor of Economics, Yale University, 1929


"Airplanes are interesting toys but of no military value."

Marechal Ferdinand Foch, Professor of Strategy, Ecole Superieure de Guerre, France


"Everything that can be invented has been invented."

Charles H. Duell, Commissioner, US Office of Patents, 1899



No doubt, conventional wisdom can often be laughably (tragically?) wrong. The problem is that, as absurd as all the above sentiments seem to us now and in retrospect, they represented the view of many people years ago. These views were held by many, including many people in positions of power and decision-making responsibility.

A more relevant but nonetheless laughable and widely held belief in 2007: coronary heart disease should be treated with hospital procedures.

Why is a disease that requires 30 years to develop treated only at the final moments with a procedure? Do you only change your car's oil when the engine is on its last legs? Or, do periodic, relatively effortless oil changes during the life of the car make better sense?

I witness just how brainwashed the public has become with this crazed notion when I meet someone socially at, say a fundraiser or cocktail party. When they ask what I do, I tell them I'm a cardiologist. The invariable response: "Oh, what hospital do you work out of?"

I tell them I don't, that I take care of the majority of heart disease right from the office. 99% of the time I get a puzzled look. If we had comic bubbles above our heads revealing our internal thoughts, it would read "Yeah, right. What a kook."

The notion that coronary heart disease is something that is manageable with simple tools for the majority of us in the early stages is entirely foreign to almost everybody. The hospitals and the medical industry have so succeeded in dazzling the public with images of staff in scrubs, rushing from emergency to emergency, lights flashing, scalpels flying. . . how can you possibly accomplish this at home or anywhere outside of the high-tech world of the hospital?

Well, I'm a cardiologist and I do it every day. We all need a figurative dose of electroshock therapy to shake ourselves of this crazy notion.

How important is l-arginine?

Perhaps more than any other supplement, l-arginine causes frustration and confusion. It’s difficult to find, sometimes quite expensive, and some preparations cause loose stools.

Just how necessary is it?

L-arginine, you’ll recall, is a source of nitric oxide, or NO. Though it’s the same stuff as in car exhaust, NO provides a critical signaling role in your body’s cells that regulate a multitude of functions. Among the important roles of NO is to powerfully dilate, or relax, arteries. A constant flow of NO is required for health, particularly since each molecule persists only a few seconds.

L-arginine is the body’s source of nitric oxide. In addition, a peculiar but very effective blocker of l-arginine called asymmetric dimethylarginine, or ASDM, has recently been discovered to prevent the production of NO. Varied conditions like hypertension, diabetes, high cholesterol, excessive saturated fat or processed carbohydrate intake all lead to heightened levels of ASDM, often several-fold greater levels, and thereby effectively blocking NO production.

The “Arginine Paradox” is the name that some researchers in this field have given to the unusual property of l-arginine supplementation to “overpower” the blocking effects of ASDM. This is somewhat unusual in biologic systems in that an agent that blocks a receptor cannot usually be outmuscled by providing excess material for a reaction. Kind of like hoping that your car runs faster simply by topping up the gas tank.

Concrete observable benefits have been made for l-arginine in clinical trials, such as arterial relaxation that results in arterial enlargement (which can actually be seen in the cath lab); anti-inflammatory effects; reduction of blood pressure; enhancement of insulin responses, etc. All of these effects can be connected to beneficial properties that may facilitate atherosclerotic plaque regression and, indeed, there are limited data to document that this is true.

Drug companies may be greedy, but they’re not stupid. They’ve been vigorously pursuing this line of research for some years, a research path that led inadvertently to the erectile dysfunction agent, sildenafil (Viagra), and all its subsequent competitors. (Erectile dysfunction is another expression of endothelial dysfunction, since male erections are driven by the ability to dilate penile arteries.) The wonderful properties of NO enhancement continue to occupy research labs around the world.

Wow. So what’s the reluctance? In the early years of the Track Your Plaque program (meaning just a short 7-8 years ago), I was thoroughly convinced that l-arginine was a crucial, necessary part of a plaque regression program. Without it, you would rarely succeed. With it, the odds were tipped in your favor.

However, something curious has emerged recently. I’ve seen more and more people dropping their heart scan scores. Not just a little bit, but a huge amount. Witness our most recent record holder, Neal, who dropped his score 51% in 15 months. Just five years ago, this magnitude of reversal was unimaginable. Granted, Neal is our record holder, but others are obtaining 10, 18, 24, 30% drops in scores all the time. Many have done it without l-arginine.

Now, how about the people who have failed to stop a rising score? Would they do better with l-arginine as part of the mix? I believe so, but sometimes we never quite know except in retrospect. It has been a great dilemma for us trying to predict from the starting gate who will or who won’t drop their heart scan score.

My view from the trenches is that l-arginine packs its greatest atherosclerosis-fighting punch in the first year or two of use, when “endothelial dysfunction” is likely to be present (abnormal artery constriction). But as all other strategies take hold—fish oil, correction of lipid and lipoprotein abnormalities, weight loss (big effect), vitamin D (another very big effect), etc.—endothelial behavior improves over time. Perhaps l-arginine becomes a less necessary component over time.

There’s no doubt that uncertainty still surrounds the use and science surrounding l-arginine. However, if you’re interested in stacking the odds in your favor, particularly during the first year or two of your plaque-reducing efforts, I think that l-arginine is worth considering. It is cumbersome, it can be expensive, some preparations may even be foul. But in the big picture of life, with hospitals trying every possible ploy to get your body on a table for a procedure, doctors perverting their mission by signing employment contracts with hospitals and agreeing to usher you into the hospital as a paying patient whenever possible, and drug companies viewing you and me as a market for medications which may or may not be helpful, l-arginine is surely not that big a burden.

Track Your Plaque and non-commercialism

If you're a Track Your Plaque Member or viewer, you may know that we have resisted outside commercial involvement. We do not run advertising on the site, we do not allow drug companies to post ads, we do not covertly sponsor supplements. We do this to main the unbiased content of the site.

We've seen too many sites be tempted by the money offered by a drug company only to see content gradually drift towards providing nothing more than cleverly concealed drug advertising. I personally find this deceptive and disgusting. Ads are ads and everyone knows it. But when you subvert content, secretly driven by a commercial agenda, that I find abhorrent.

That said, however, I do wonder if we need the participation of some outside commercial interests to help our members. In other words, many (over half) of the questions and conversations we have with people is about what supplement to take, or what medication to take. While we cannot offer direct medical advice online (nor should we) because of legal and ethical restrictions, I wonder if could facilitate access to products.

Many people struggle, for instance, with trusted sources for l-arginine, vitamin D, fish oil. Other people struggle with finding a heart scan center because of the changing landscape of the CT scanning industry. Could we somehow provide a clear-cut segment of the website that clearly demarcates what is commercial and non-Track Your Plaque-originated, yet at least provides a starting place for more info?

Ideally, we would have personally tried and investigated everything there is out there applicable to the program. But that's simply impossible at this stage.

I feel strongly that we will never run conventional ads on the site. Nor will we ever permit any outside commercial interest to dictate what and how we say something. The internet world is full of places like that. Look at WebMD. I find the site embarassing in the degree of commercial bias there. We will NEVER sell out like that, regardless of the temptation. People with heart disease are all conducting a war with the commercial forces working to profit from them--hospitals, cardiologists, drug companies, medical device companies (yes, even they advertise to the public, e.g., implantable defibrillators--no kidding). Genuine, honest, unbiased information is sorely needed and not from some kook who either knows nothing about real people with real disease, or has a hidden agenda like selling you chelation.

I'd welcome any feedback either through this Blog or through the contact@cureality.com.

The nattokinase scam

A conversation about vitamin K2 commonly leads to confusion. Several people have asked about something called nattokinase.

The scientific data on the potential role of vitamin K2 deficiency in causing both osteoporosis and vascular calcification is fascinating. Along with vitamin D3, vitamin K2 may be an important factor in regulation of calcium metabolism. Supplementation may prove to be a major strategy for inhibition of vascular calcification.

Obtaining K2 in the diet is tricky, since it's present in just a handful of foods: egg yolks, liver, traditional cheeses, and natto. This is where the confusion starts.

Natto is a Japanese fermented soy product. I've had it and it's quite disgusting. Nonetheless, Japanese who eat natto experience less fracture. (A parallel study in heart disease has not been performed.) Natto is also a source of another substance called nattokinase.

Advocates (otherwise often known as supplement distributors) claim that nattokinase is a "fibrinolytic", or blood clot-dissolving, preparation that "improves blood flow, protects from blood clots, and prevents heart attacks and strokes."

Don't you believe it. This is patent nonsense. There are several problems with this rationale:

--Any oral fibrinolytic agent is promptly degraded in the highly acid environment of the stomach. That's why all medically used fibrinolytics are given intravenously. Drug companies have struggled for years to encapsulate, modify, or somehow protect protein (or polypeptide) products taken orally from degrading this way. They've never succeeded. That's why, for instance, growth hormone (a polypeptide) remains an injection, not an oral agent. An oral growth hormone, by the way, would sell like mad, so the drug companies would very much like to figure out how to bypass the degradative effects of stomach acid. One of the "researchers" behind the nattokinase claims boasts that he has single-handedly figured out how to protect the nattokinase molecule in the gastrointestinal tract. However, he won't tell anybody how he does it. Right.

--Fibrinolytic agents are extremely dangerous. In years past, we used to treat heart attacks with intravenous fibrinolytic agents like tissue plasminogen activator, urokinase, streptokinase, and others. They have fallen by the wayside, for the most part, because of limited effectiveness and the unavoidable dangers of their use. Fibrinolytics are "dumb": they dissolve blood clots in both good places and bad. While they might dissolve the blood clot causing your heart attack, they also degrade the tiny clot in your cerebral (brain) circulation that was protective. That's why fatal brain hemorrhages, bleeding stomach ulcers, and blood oozing from strange places can also occur with fibrinolytic administration. Believe me, I've seen it happen, and I've watched people die from them.

The idea that a small dose taken orally is healthy is ridiculous. Even if nattokinase worked, why the heck would you take an agent that has known dangerous and very real consequences?

Don't let this idiocy reflect poorly on the K2 conversation, which, I believe, holds real merit and is backed by legitimate science. This is symptomatic of a larger difficulty with the supplement industry: Insane and unfounded claims about one supplement erodes credibility for the entire industry. It gives regulation-crazed people like the FDA ammunition to go after supplements, something none of us need. You and I have to sift through the nonsense to uncover the real gems in this rockpile, real gems like vitamin D3, omega-3 fatty acids from fish oil, and, perhaps, vitamin K2. But not nattokinase.

Blood pressure with exercise

Here's a frequently neglected cause for an increasing CT heart scan score: High blood pressure with exercise. Let me explain.

Paul's blood pressure at rest, sitting in the office or on arising in the morning, or at other relatively peaceful moments: 110/75 to 130/80--all in the conventional normal range.

We put Paul on the treadmill for a stress test. At 10 mets of effort (on the protocol used, this means 3.4 mph treadmill speed at 14 degree incline), Paul's blood pressure skyrockets to 220/105. That's really high.

Now, blood pressure is expected to increase with exercise. If it doesn't rise, that's abnormal and may, in fact, be a sign of danger. Normally, blood pressure should rise gradually in a stepwise fashion with increasing levels of exercise. But any blood pressure exceeding 170/90 is clearly too high with exercise. (Not to be confused with high blood pressures not involving exercise.) A handful of studies have suggested that a "breakpoint" of 170/90 also predicts heightened risk of heart attack over a long period.)

I see this phenomenon frequently--normal blood pressure at rest, high with exercise. This also suggests that when Paul is stressed, upset, in traffic congestion, under pressure at work, etc., his blood pressure is high during those periods, as well. I wouldn't be surprised to see other phenomena of underappreciated high blood pressure, like abnormally thick heart muscle (left ventricular hypertrophy), an enlarged thoracic aorta (visible on your heart scan), left atrium, perhaps even an abnormal EKG or abnormal kidney function (evidenced by an elevated creatinine on a standard blood panel).

Unfortunately, the treatments that reduce blood pressure are "stupid," i.e., they have no appreciation for what you are doing and they reduce blood pressure all the time, whether or not you're stressed, exercising, or sleeping.

Blood pressure reduction should begin with weight loss, exercise, reduction of saturated fats and processed carbohydrates (esp. wheat), magnesium replacement, vitamin D replacement. Think about CoQ10. After this, blood pressure medication might be necessary.

The message: Watch out for the blood pressures when you have a stress test. Or, if you have a friend who is adept at getting blood pressures, get a blood pressure immediately upon ceasing exercise. It should be no higher than 170/90.

Vitamin D2 vs. vitamin D3

An interesting question came up on the Track Your Plaque Member Forum about vitamin D2 vs. vitamin D3. This often comes up among our patients, as well.

Vitamin D is measured in the blood as 25-OH-vitamin D and is distinct from 1,25-diOH-vitamin D, a kidney measure, a test you do not need unless you have kidney failure.

The human form of vitamin D is cholecalciferol and is usually obtained via activation of a precursor molecule in the skin on activation by the sun. You can also take cholecalciferol and it increases blood levels of 25-hydroxy vitamin D reliably.

However, there is a cheap, plant-sourced, alternative to vitamin D3, called vitamin D2, or ergocalciferol. D2 has far less effect in the body. Taking D2 or ergocalciferol orally is an extremely inefficient way to get D. Unfortunately, it's the form often used in milk and many supplements, even the prescription form of D. About half the multivitamins and calcium supplements I've looked at contain ergocalciferol rather than cholecalciferol.

Taking vitamin D2 yields very little conversion to the effective D3. This particular issues is maddening, as the USDA requires dairy farmers to add 100 units of vitamin D to milk, and D2 is often used. In other words, the D in many dairy products barely works at all. There are many children who rely on D from dairy products who are at risk for rickets and are not getting the D they need from dairy products because of this cost-saving switch. Do not rely on milk for vitamin D for your children.

D2 or ergocalciferol is often included in the blood measures of vitamin D along with vitamin D3. The only reason it's checked with blood work is to ensure "compliance,", i.e., see whether or not you're taking a prescribed ergocalciferol. Beyond this, it has no usefulness.

25-OH-vitamin D3, or cholecalciferol, is both the blood measure and the supplement you need. This is the one that packs all the punch. Keep in mind also that it is the oil-based gelcap you want, with more consistent and efficient absorption. Tablets usually barely work at all, even if it contains cholecalciferol. Most people who take calcium tablets with D, or multivitamin with D, not only are getting a powdered form of D, but also in trivial doses. It's the pure vitamin D3, cholecalciferol, in gelcap form you want if you desire all the spectacular benefits of vitamin D.