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.
All posts by william davis

America: The world’s diet laboratory

Low-fat, low-carb, high-protein, Pritikin, Ornish, Atkins, South Beach, Sonoma, Sugar-Busters, Weight Watchers, vegetarian . . . Have Americans tried them all?

We’ve witnessed the relative success of diet habits in selected regions world-wide: the longevity of the Japanese on a spare soy and fish-based diet; the reduced heart disease incidence of the French despite an indulgent food-centered culture; the extreme heart disease-free lives of the Cretan Greeks.

Contrast this with the startling failure of the American diet experiment: We’re all (speaking for the collective whole) fat, diabetic, and miserably mired in the diseases of obesity. We’ve experimented with every possible iteration of diet from grapefruit or cabbage only, to calorie deprivation (a al Weight Watchers), to restricting this or that element of diet. The “official” organizations have made their contributions, as well: the American Heart Association’s Therapeutic Lifestyle Changes (formerly Step I and II diets), a program eerily similar to what Americans are already eating and resulting in failure; the American Diabetes Association diet, incomprehensibly embracing carbohydrates when they are the root of the nutrition-habit-gone-wrong that caused the disease in the first place; the USDA and their Food Pyramid, encompassing a design that contains the germ of wisdom but is so heavily overweighted in grains that it is a sure-fire way to increase weight and heart disease were you to follow their recommendations.

What have we learned from our grand experiment, our nationwide misadventure in nutrition?

I believe that we’ve learned how not to eat: Processed snack foods, meals delivered in a fast-food setting with the offer to “super-size” your order, make-believe food ingested in your car eaten for the sake of staving off the inevitable hunger pangs. Few would argue that these are certain paths to obesity and poor health.

Certainly, if we’ve learned how not to eat, can we extrapolate just how to eat? And not just for weight loss, since most diets focus just on that, but on health, particularly heart health?

If Americans have so far failed to learn the lessons of the nutritional world, we certainly have not failed at talking about it. From books to blogs, websites, information gurus to infomercials, we certainly celebrate the capacity to share our experiences, our grief over our nutritional “misfortune,” despite a world of plenty.

Yet we swim in a sea of information. Can we sift through the chaff to discover the essential truth?

Let me articulate an extreme (extreme meaning closer to the truth, I hope) interpretation of nutritional wisdom:

--If it requires a label or nutritional analysis, reject it. The wondrous green pepper, or bottle of olive oil, for instance, require no such qualifications. Some exceptions: milk, yogurt, cottage cheese (unless, of course, you purchase straight from a local producer). I am always impressed with the contortions and frustrations people experience trying to decipher labels. Ironically, the healthiest foods don’t even require labels.

--If it is ingested in a rush, it’s likely to add to poor health. True food is meant to be consumed at leisure, not in haste to satisfy some irrational, unthinking impulse.

--Search for natural, whole foods. Natural, whole foods require no marketing. You pay a premium for a company to adorn a product with glitz, glamour, and appeal. Repackage Cocoa Puffs as chocolate flavored, round overly-processed wheat flour, sans marketing spin, and what is left? Processed foods are?intentionally?addictive. They are added to, modified, high-fructose corn syruped, etc. to increase desirability, but also create addiction. Eliminate them just as a smoker eliminates cigarettes.

--A corollary to the above issue: purchase foods that appear as if you had grown it or raised it yourself. If you were to grow corn in your backyard garden, you would eat it on the cob or some similar way. You would not grind it, pulverize, process it, nor serve it as cornstarch and add to a pile of chemicals to make breakfast cereal. Eat foods in their natural state, not the highly processed food-product that requires a colorful package and advertising to sell.

--Don’t keep bags of chips, boxes of breakfast cereal and crackers, frozen dinners, all “just in case.” Don’t allow yourself that opportunity because you will more than likely seize it. An alcoholic who keeps a secret bottle of gin hidden in the cabinet is well aware that it’s there and will eventually give in to impulse.

--When you eat meat, try to find free-range, organic products. Even better, purchase from a local producer who you trust.

--For anyone with patterns like low HDL, small LDL, high triglycerides, and blood sugar >100 mg/dl, following a diet that is as free of wheat products as possible will yield enormous benefits. Wheat is a part of all breads, virtually all breakfast cereals, pretzels, crackers, bagels, cookies, cupcakes, pancakes, waffles, etc. Going wheat-free is also a surprisingly effective weight loss strategy.

That’s just a few thoughts. The approach we use in the Track Your Plaque program helps achieve weight loss, but also helps correct lipoprotein patterns, often dramatically.

Many diets have failed to keep pace with the changing nutritional habits of Americans. In 1960, we ingested close to zero high-fructose corn syrup. We’re now approaching 80 lbs per year per American. Breakfast cereal in 1950 consisted of a handful of products, eaten intermittently; today, it is a staple with enough products to fill a modern supermarket’s entire aisle. Meats have changed, thanks to the factory farm phenomenon feeding its animals corn in inhumanely restricted conditions, a dietary shift for livestock that has modified the fat composition to something far different than 50 years ago, not to mention the antibiotics and other chemicals used to accelerate growth and fight off infection from the artificial, overcrowded conditions.

The American nutritional shift, along with rampant obesity, have also caused a relatively new cause of coronary heart disease to explode: small LDL particles. The contribution of small LDL has been enormously underestimated, since most physicians don’t know what it is, don’t know how to check for it, and don’t know what to do with it. Yet it has emerged as the number one cause for heart attack and heart disease nationwide.

Stay tuned for our rewritten New Track Your Plaque diet to be released as a Special Report on the www.cureality.com website in future.

Dr. Jarvik, is niacin as bad as it sounds?

A popular health newsletter, Everyday Health, carried this headline:

A Cholesterol-Busting Vitamin?

Did you know that niacin, one of the B vitamins, is also a potent cholesterol fighter?
Find out how niacin can help reduce choleseterol.


At doses way above the Recommended Dietary Allowance — say 1,000–2,500 mg a day (1–2.5 grams) — crystalline nicotinic acid acts as a drug instead of a vitamin. It can reduce total cholesterol levels by up to 25%, lowering LDL and raising HDL levels, and can rapidly lower the blood level of triglycerides. It does so by reducing the liver’s production of VLDL, which is ordinarily converted into LDL.


I'd agree with that, except that it is rare to require doses higher than 1000-1500 mg per day unless you are treating lipoprotein(a) and using niacin as a tool for dramatic drops in LDL. But for just raising HDL, shifting HDL into the healthy large class, reducing small LDL, and for reduction of heart attack risk, 1000-1500 mg is usually sufficient; taking more yields little or no further effect.

But after that positive comment comes this:

Niacin is safe — except in people with chronic liver disease or certain other conditions, including diabetes and peptic ulcer. . . However, it has numerous side effects. It can cause rashes and aggravate gout, diabetes, or peptic ulcers. Early in therapy, it can cause facial flushing for several minutes soon after a dose, although this response often stops after about two weeks of therapy and can be reduced by taking aspirin or ibuprofen half an hour before taking the niacin. A sustained-release preparation of niacin (Niaspan) appears to have fewer side effects, but may cause more liver function abnormalities, especially when combined with a statin.


Strange. After a headline clearly designed to pull readers in, clearly stating niacin's benefits, the article then proceeds to scare the pants off you with side-effects.

But look to the side and above the text: Ah . . . two prominent advertisements for Lipitor, complete with Dr. Robert Jarvik's photo. "I've studied the human heart for a lifetime. I trust Lipitor to keep my heart healthy."

Niacin bad. Lipitor good. Even celebrity doc says so. Sounds like bait and switch to me. "You could try niacin--if you dare. But you could also try Lipitor."

Who is Dr. Jarvik, anyway, that he serves as spokesman (or at least figurehead) for this $13 billion dollar a year drug? Of course, he is the 1982 inventor of the Jarvik artificial heart, surely an admirable accomplishment. But does that qualify him to speak about heart disease prevention and cholesterol drugs?

Jarvik has never--never--actually prescribed Lipitor, since he never completed any formal medical training beyond obtaining his Medical Doctor degree, nor has he ever had a license to practice medicine. He does, however, continue in his effort to provide artificial heart devices, principally for implantation as a "bridge" to transplantation, i.e., to sustain a patient temporarily who is dying of end-stage heart failure.

So where does his expertise in heart disease prevention come from? It's beyond me. Perhaps it was the thousands of dollars likely paid to him. That will make an "expert" out of just about anybody.

Robert Bazell, science reporter, for CNBC, made this report on the Jarvik-Lipitor connection in his March, 2007 report, Is this celebrity doctor's TV ad right for you?

Mr. Bazell writes:

On May 16, 1988, an editorial in the New York Times dubbed the artificial heart experiments, “The Dracula of Medical Technology.”

“The crude machines,” it continued, “with their noisy pumps, simply wore out the human body and spirit.”

Since then, in a series of start-up companies, Jarvik has continued his quest to make an artificial heart — as have several other firms. One competitor recently won FDA approval to sell its device for implantation in extreme emergencies.

Perhaps Jarvik’s chances of success with another artificial heart account for his willingness to serve as pitchman for Pfizer. I inquired, without success, to find the going rate for a semi- celebrity like Jarvik to appear in such ads. Thomaselli of Advertising Age said whatever it is, it is “infinitesimal” compared to Pfizer’s expenditures of $11 billion a year on advertising, much of it for Lipitor.

Why spend so much marketing Lipitor?

Because Lipitor is only one of six drugs in the class called statins that lower cholesterol. Many cardiologists say that for the vast majority of people any one of these drugs works just as well as the other. Two of them, Mevacor and Zocor, have already lost their patent protection so they cost pennies a day compared to $3 or more a day for Lipitor.

In 2010, when Lipitor loses its patent protection, it, too, will cost pennies a day, and Pfizer will no longer need Dr. Robert Jarvik.



So, is niacin so bad after all? Or is this Everyday Health report just another clever piece of advertising for Pfizer?

Is niacin as bad as it sounds?

A popular health newsletter, Everyday Health, carried this headline:

A Cholesterol-Busting Vitamin?

Did you know that niacin, one of the B vitamins, is also a potent cholesterol fighter?
Find out how niacin can help reduce choleseterol.


At doses way above the Recommended Dietary Allowance — say 1,000–2,500 mg a day (1–2.5 grams) — crystalline nicotinic acid acts as a drug instead of a vitamin. It can reduce total cholesterol levels by up to 25%, lowering LDL and raising HDL levels, and can rapidly lower the blood level of triglycerides. It does so by reducing the liver’s production of VLDL, which is ordinarily converted into LDL.


I'd agree with that, except that it is rare to require doses higher than 1000-1500 mg per day unless you are treating lipoprotein(a) and using niacin as a tool for dramatic drops in LDL. But for just raising HDL, shifting HDL into the healthy large class, reducing small LDL, and for reduction of heart attack risk, 1000-1500 mg is usually sufficient; taking more yields little or no further effect.

But after that positive comment comes this:

Niacin is safe — except in people with chronic liver disease or certain other conditions, including diabetes and peptic ulcer. . . However, it has numerous side effects. It can cause rashes and aggravate gout, diabetes, or peptic ulcers. Early in therapy, it can cause facial flushing for several minutes soon after a dose, although this response often stops after about two weeks of therapy and can be reduced by taking aspirin or ibuprofen half an hour before taking the niacin. A sustained-release preparation of niacin (Niaspan) appears to have fewer side effects, but may cause more liver function abnormalities, especially when combined with a statin.


Strange. After a headline clearly designed to pull readers in, clearly stating niacin's benefits, the article then proceeds to share the pants off you with side-effects.

But look to the side and above the text: Ah . . . two prominent advertisements for Lipitor, complete with Dr. Robert Jarvik's photo. "I've studied the human heart for a lifetime. I trust Lipitor to keep my heart healthy."

Sounds like bait and switch to me. "You could try niacin--if you dare. But you could also try Lipitor."

Who is Dr. Jarvik, anyway, that he stands as the spokesman (or at least figurehead) for this $13 billion dollar a year drug. Of course, he is the 1982 inventor of the Jarvik artificial heart, surely an admirable accomplishment. But does that qualify him to speak about heart disease prevention and cholesterol drugs? Jarvik has, never actually prescribed Lipitor, since he never completed any formal medical training beyond obtaining his Medical Doctor degree, nor has he ever had a license to practice medicine. He does, however, continue in his effort to provide artificial heart devices, principally for implantation as a "bridge" to transplantation, i.e., to sustain a patient temporarily who is dying of end-stage heart failure.

So where does his expertise in heart disease prevention come from?

Omega-3 fatty acids: Frequency vs. quantity

I believe I have been observing an unexpected phenomenon: When it comes to fish oil and omega-3 fatty acids, the frequency of dosing may be as important, perhaps more important, than the actual dose.

First of all, why advocate omega-3 fatty acids from fish oil? There’s a list of lipid/lipoprotein reasons, including reduction of triglycerides and triglyceride-containing particles (VLDL, intermediate-density lipoproteins), reduction of small LDL, and increase in HDL. There’s also solid benefit in reduction of heart attack risk, reduction in death from heart attack, and reduction in stroke. There are also anti-inflammatory benefits and improvements in mood, reduction in depression.

Fish oil is a crucial ingredient in the Track Your Plaque program. I am honestly uncertain of just how much success we would give up if fish oil were NOT a part of the program, but I am unwilling to find out. The data are simply too compelling to not include omega-3 fatty acids from fish oil. Of course, supplementation of omega-3 fatty acids assumes greater importance in a modern world in which your food has become terribly depleted of the omega-3 fraction of oils. (Cultures that rely heavily on fish or wild game probably would not benefit to the same extent, since these foods contain omega-3 fatty acids.)

But I believe I have observed a curious effect over the past year or two. With the proliferation of many different preparations of fish oil that provide seemingly endless choices—low-potency fish oil, high-potency fish oil, paste forms of fish oil like Coromega, liquids such as Carlson’s, etc.¾I’ve observed that frequency of dosing may exert as much of an effect as the dose.

For example, someone might take the basic, low-potency preparation like Sam’s Club that contains 180 mg EPA and 120 mg DHA per capsule, four capsules per day. That yields a total of 1200 mg EPA and DHA per day. This is our minimum dose that provides the basic heart attack-reducing effect, though with modest effect on triglycerides and associated patterns.

Say someone switches to a high-potency preparation of 360 mg EPA and 240 mg DHA, providing a total of 600 mg omega-3 fatty acids per capsule, or twice the dose of the low-potency preparation. Would you expect double the effect?

Curiously, no. What I have observed, however, is that more frequent dosing may provide a larger effect. The least effective dosing is once per day; twice per day is far more effective. Three times per day¾though cumbersome¾provides even greater effect.

So, which is more important: dose or frequency?

I can’t say for certain, since my observations are informal and have not been obtained by a formal statistical analysis of our data. That will come with time.

For the present, suffice it to say that, if you are struggling with suppression of patterns like increased triglycerides, IDL, or low HDL, then at least twice- or three-times-per-day dosing might be worth considering, even before you increase the dose further.

Best: Greater dose, or higher-potency preparation, combined with higher frequency.

Lipoprotein testing

This is an update of a post I made about a year ago. However, I'm reposting it since the question comes up so often.


How can I get my lipoproteins tested?
This question came up on our recent online chat session and comes up frequently phone calls and e-mails.

If lipoprotein testing is the best way to uncover hidden causes of coronary heart disease, but your doctor is unable, unknowledgeable, or unwilling to help you, then what can you do?

There are several options:

1) Get the names of physicians who will obtain and interpret the test for you. That’s the best way. However, it is also the most difficult. Lipoprotein testing, despite over a decade of considerable scientific exploration and validation in thousands of research publications, still remains a sophisticated tool that only specialists in lipids will use. But this provides you with the best information on you’re your lipoproteins mean.
2) If you don’t have a doctor who can provide lipoprotein testing and interpretation, go to the websites for the three labs that actually perform the lipoprotein tests: www.liposcience.com (NMR); www.berkeleyheartlab.com (electropheresis or GGE); www.atherotech.com (ultracentrifugation). None of them will provide you with the names of actual physicians. They can provide you with the name of a local representative who will know (should know) which doctors in your area are well-acquainted with their technology. I prefer this route to just having a representative identify a laboratory in your area where the blood sample can be drawn, because you will still need a physician to interpret the results¾this is crucial. The test is of no use to you unless someone interprets it intelligently and understands the range of treatment possibilities available. Don’t be persuaded by your doctor if he/she agrees to have the blood drawn but has never seen the test before. This will be a waste of your time. That’s like hoping the kid next door can fix your car just because he says he fixed his Mom’s car once. Interpretation of lipoproteins takes time, education, and experience.

3) Seek out a lipidologist. Lipidologists are the new breed of physician who has sought out additional training and certification in lipid and lipoprotein disorders. Sometimes they’re listed in the yellow pages, or you can search online in your area. One drawback: Most lipidologists have been heavily brainwashed by the statin industry and tend to be heavy drug users.

4) Contact us. I frankly don’t like doing this because I feel that I can only provide limited information through this method and, frankly, it is very time consuming. I provide a written discussion of the implications and choices for treatment with the caveat to discuss them with your doctor, since I can’t provide medical advice without a formal medical relationship. We also charge $75 for the interpretation. But it’s better than nothing.

5) Make do with basic testing. Basic lipids along with a lipoprotein(a), C-reactive protein, fibrinogen, and homocysteine would provide a reasonable facsimile of lipoprotein testing. You’ll still lack small LDL and postprandial (after-eating) information, but you can still do reasonably well if you try to achieve the Track Your Plaque targets of 60-60-60. It’s sometimes a necessary compromise.

Our discussions on the Track Your Plaque Forum have impressed me with the difficulty many people encounter in getting lipoproteins drawn and interpreted. Some of our Members have been very resourceful identifying blood draw laboratories around the country, such as Lab Safe, that will at least provide the blood draw service.

I wish it was easier and we are working on some ideas to facilitate this nationwide. It will take time.

In 20 years, this will be a lot easier when doctors more commonly use lipoprotein testing. But for now, you can still obtain reasonably good results choosing one of the above alternatives.

Is it exercise or diet?

Wayne, a 61-year old retired school superintendent, had been an exercise fanatic all his adult life. If not running long distances and occasional marathons, he'd bike up to 70 miles a day. He did this year-round. In cold weather, he set his bicycle up on an indoor device and also ran on a treadmill and added weight training.

That's why it was kind of surprising that he sported a large belly. At 5 ft 8 inch and 190 lbs, that put his Body Mass Index (BMI) also high at 28.8 (desirable <25). You'd think that vigorous, almost extreme, exercise like this would guarantee a slender build.

Wayne also had lipoproteins to match: triglycerides 205 mg/dl, LDL 176 mg/dl but LDL particle number much higher at 2403 nmol/l (an effective LDL of 240 mg/dl); 75% of LDL particles were small.

I asked Wayne about his diet. "I eat healthy. Cheerios for breakfast usually. Some days I'll skip breakfast. Lunch is almost always a sandwich: tuna, turkey, something like that on whole wheat bread or a whole wheat bagel. Chips, too, but I guess that's not too healthy. Dinners vary and we eat pretty healthy. Almost never pizza or junk like that."

"Pasta?" I asked.

"Oh. sure. Two or three tiems a week. Always whole wheat. With a salad."

Wayne was well aware of the conventional advice for whole grains and, indeed, had been trying to increase his intake, particularly since his basic cholesterol numbers had been high in past. To his surprise, the more he tried at diet, the more LDL seemed to go up, as did triglycerides.

I see this situation every day: The obsession with processed carbohydrate foods, worsened by the message perpetuated by the American Heart Association, the USDA Food Pyramid, Kraft, Kelloggs, Post, etc. Eat more fiber, eat whole grains.

NY Times columnist, Jane Brody, chronicles her (embarassing) mis-adventure following the same mis-guided advice in Cutting Cholesterol, an Uphill Battle.

According to the USDA Food Pyramid, Wayne is not getting enough grains and whole grains, particularly since he is highly physically active. Consistent with the message given by the food industry: "Eat more!"

The food industry-supported Whole Grain Council advises:

Whole Grains at Every Meal
The US Dietary Guidelines recommend meeting the daily requirement by eating three "ounce-equivalents" of breads, rolls, cereals or other grain foods made with 100% whole grains. A slice of bread or a serving of breakfast cereal usually weighs about an ounce.

Want an easier way to think about it? Just look at your plate at each meal, and make sure you've included some source of whole grains. That's why our slogan is "Whole Grains at Every Meal."



By this scheme, if you are overweight, it's because you lack fiber and you're too inactive. "Get up and go!" It's not the diet, they say, it's you!

See through this for what it is: Nonsense. Wayne was overweight, packing 20 extra pounds in his abdomen from his over-dependence on processsed carbohydrates--"whole grains"--not from inactivity.

Instant heart disease reversal


What if reversal of heart disease--regression of coronary atherosclerotic plaque--were achievable instantly? Just add water and--voila!!

To my knowledge, it is not--yet. But I sometimes play with this idea in my head. I could imagine that such a program would consist of a few essential elements:

--A fast or semi-fast, or at least a very spare diet, over a period like 10 days to promote net catabolism. It is also supremely anti-inflammatory to restrict calories.

--High-dose vitamin D, e.g., 20,000 units per day of D3 to fully replenish depleted stores and achieve all the metabolism-correcting effects of D3 restoration.

--EPA + DHA at a higher than usual dose with frequent throughout-the-day dosing to encourage replacement of cellular lipid constituents with the more stable omega-3 fraction of fatty acids.

Beyond this, I'm uncertain. What role l-arginine, statins, niacin . . . conjugated linoleic acid? ApoA1 Milano infusions?

This is simply whimsical at this point. I don't know if such an approach would work. But if it did, you might imagine that it would offer an opportunity--for the properly motivated--as an alternative treatment for angina, advanced coronary disease, a means to pull someone back from the brink.

With the insights gained from our slow-but-powerful Track Your Plaque approach, perhaps we will also gain insights into how to accelerate such a process of reversal so that it is achievable in days, rather than months or years.

The small LDL epidemic

Ten years ago, small LDL was fairly common, affecting approximately 50% of the patients I'd see. For instance, an LDL particle number of 1800 nmol/l would be 40-50% small LDL in about half the people.

But in the last few years, I've witnessed an explosion in the proportion of people with small LDL, which now exceeds 80-90% of people. The people who show small LDL also show more severe patterns. 80-90% small LDL is not uncommon.

Why the surge in the small LDL pattern? Two reasons: 1) The extraordinary surge in excess weight and obesity, both of which favor formation of small LDL particles, and 2) over-reliance on processed carbohydrates, especially wheat-based convenience foods.

The constant media din that parrots such nonsense as the report on CNN Health website, Healthful Breakfast Tips to Keep You Fueled All Day, helps perpetuate this misguided advice. The dietitian they quote states:

"If you don't like what you're eating, you won't stick with it. If your choices aren't the most nutritious, small tweaks can make them more healthful. For example, if you have a sweet tooth in the morning, try a piece of nutty whole-grain bread spread with a tablespoon each of almond butter (it's slightly sweeter than peanut butter) and fruit preserves instead of eating foods that offer sweetness but little nutritional benefit, like doughnuts or muffins. If you enjoy egg dishes but don't have time to prepare your favorite before work, try microwaving an egg while toasting two slices whole wheat or rye (whole-grain) bread. Add a slice of low-fat cheese for a healthful breakfast sandwich that's ready in minutes. And don't overlook leftovers. If you feel like cold pizza (which contains antioxidant-filled tomato sauce, calcium-rich cheese, and lots of veggies), have it. It's a good breakfast that's better than no breakfast at all."

It sure sounds healthy, but it's same worn advice that has resulted in a nation drowning in obesity. The food choices advocated by this dietitian keep us fat. It also perpetuates this epidemic of small LDL particles.

If you have small LDL and its good friend, low HDL, it's time for elimination of wheat products, not some politically-correct silliness about increasing fiber by eating whole grains. Whole grains create small LDL! Or, I should say, what passes as whole grains on the supermarket shelves.

For some helpful commentary on this issue, see Fanatic Cook's latest post, Playing with Grains.

Mini-dose CTA?

I caught this little news report in the online edition of Canyon News , an LA paper, under the title Cedars-Sinai Develops Test to Prevent Heart Attacks .

They report that Dr. Daniel S. Berman M.D., chief of Cardiac Imaging and Nuclear Cardiology at Cedars-Sinai, reports that a new method of performing CT coronary angiography, "mini-dose CTA," has been developed that allows both coronary calcium scoring as well as CT coronary angiography (CTA) at a dose as low as 10% of standard dose. No technical details were provided.

Now, that may be worth knowing more about. If this is true, then CTA may indeed be useful as a "screening" procedure. However, we are going to need to know more: What devices are capable of doing this, what settings on the devices were used, etc. It does indeed come from a reputable source in Dr. Dan Berman, who is well known in nuclear cardiology circles.

We will try and dig for info. Stay tuned.