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.

I had a heart attack--and I don't know why!

Kevin came to my office for another opinion.

A husband and father of two teenagers, Kevin had his first heart attack at age 39. Kevin received two stents to his right coronary artery. The entire process took place in a flurry with little explanation over 48 hours, start to finish.

He smoked a pack of cigarettes a day, but the only history of heart disease in his family was his father, who, also a smoker, had his heart disease uncovered in his late 70s.

His internist subsequently prescribed Zocor even though Kevin's LDL cholesterol was a relatively unimpressive 128 mg/dl.

Kevin subsequently asked his cardiologist, "Where did I get the heart disease from?"

"Cigarettes. And genetics. You can quit the first. There's nothing you can do about the second." End of explanation.

This left Kevin frightened and demoralized. If much of the cause of his heart disease couldn't be identified, why bother quitting smoking? Why not enjoy what time he had left?

Kevin was understandably shocked when I told him that genetic causes were 1)identifiable, 2)quantifiable, and 3) correctable.

Kevin's full lipoprotein analysis subsequently showed the most dire combination that commonly accounts for coronary disease in young people: Lp(a) with small LDL particles. This, along with smoking, fully accounted for this young father of two's heart disease.

Along with starting Kevin on a new program for correction of his patterns, I also persuaded him to get a heart scan. What usefulness is a heart scan after the fact? Plenty. Even though Kevin's right coronary was no longer "scorable" because the steel in the stent obscured our measurements, the two remaining unstented arteries would still yield a score. This provides a baseline for future comparison. Even after a stent, Kevin could "track his plaque".

Butter basics

There’s lot of confusion about butter, margarines, and their substitutes. Butter/margarine substitutes that avoid the negative aspects and provide modest health benefits are available, but I find that people confuse what's what. So here’s a brief primer.


Butter--Avoid it. Plain and simple. Butter is a rich source of saturated fat. Of 11.5 grams total fat per tablespoon, 7.3 grams are saturated. It is not better than margarine, contrary to simple-minded reports from some media sources. Butter raises LDL cholesterol, raises blood pressure, and has been related to various cancers.

Margarine--Not better than butter, arguably worse. Some argue that the trans-fatty acids, or hydrogenated oils, used to solidify vegetable oils to make margarine solid are worse than butter. In addition to the ill-effects of butter, margarine reduces HDL and raises cancer risk, perhaps even more than saturated fats. Hydrogenation yields a very unnatural structure that modifies cellular behavior of the sort that may promote the appearance of cancer cells. More recently, however, some of the major manufacturers, like Blue Bonnet, have produced soft spread products without hydrogenation. These are reasonable substitutes when used sparingly.

Smart Balance--This is a product made with canola oil, a source of monounsaturates (the best oil source after omega-3s), but manufactured without hydrogenation and therefore has no trans-fats. It does have, in my view, a bit too much saturated fat (1.5 gm per tbsp. in the 37% Light Spread; 2.5 gm per tbsp in the 67% regular spread). This is a reasonable product to use in small quantities.

There is also a Smart Balance Omega PLUS product that contains added flaxseed oil and sterol esters. I do not recommend this product because of the sterol content (see below). I also object to the manufacturers who label their products “rich in omega-3s” when they mean linolenic acid (in flaxseed), which is converted to a trivial quantity of omega-3s. Linolenic acid may pose unique benefits of its own, but it should not be listed as an omega-3 source.

Benecol--This is a butter substitute that contains stanol esters, a substance that reduces total and LDL cholesterol. Two tablespoons a day reduces LDL around 20 mg/dl, more or less depending on your starting cholesterol.
There’s a light and regular spread. The light contains 20 calories less per tablespoon but somewhat less monounsaturates, but the same LDL-reducing stanol esters. The manufacturer does hydrogenate the oils, yielding 0.5 mg trans-fats per tablespoon--a small drawback.

Take Control--Similar to Benecol, but made with sterol esters. Take Control also reduces LDL cholesterol. However, data from several high-quality studies from Finland suggest that sterol esters may, in some people, be absorbed into the blood. This is potentially concerning. There is a rare disease called sitosterolemia that results in coronary disease in teenagers and young adults in their 20s from increased absorption of sterol esters. While you can’t acquire this genetic disease, some people have the capacity to absorb sterol esters from their intestines very efficiently. I find it very disturbing and I suggest that you stay away this product and other sterol-containing products like HeartWise orange juice and Smart Balance Omega PLUS until the issue is clarified and safety assured.

Brummel and Brown--A blend of vegetable oils (soybean and partially hydrogenated soybean) with calories and fats reduced by blending in yogurt. This is an okay product. The hydrogenation yields trans-fats below the FDA required declaration limit of 1.0 mg.
There’s also 1.0 mg each of saturated and monounsaturated fats. The calories are relatively low as a consequence of the added yogurt, only 45 calories per tablespoon. This makes the Brummel and Brown a reasonable choice.


Other products are making their way out to supermarkets. Look for the type of oil used. Canola, olive, and flaxseed are the best. Also look for trans-fats and saturated fat content; both should be low, preferably <1.0 mg per tablespoon, ideally none.

The best choice among the above products in my view is Benecol, though it’s also the most expensive. It will yield substantial drops in LDL cholesterol. All the products in our informal tastings taste a lot like butter, or at least as well as we can remember what butter tasted like! The key with all of these products is use in moderation, since they all provide between 45?80 calories per tablespoon.

Let Dr. Friedewald rest in peace

In the 1960s, doctors struggled with the concept of cholesterol and its relationship to heart disease. It was becoming clear that higher levels of cholesterol were predictive of heart disease. It was also becoming clear that the low-density fraction of cholesterol, or LDL, was somewhat better than total cholesterol in predicting heart attack.

Cholesterol was easily measurable in the 1960s. LDL was not. So, Dr. Friedewald, a noted lipid researcher at the National Institutes of Health, proposed an easy method to calculate LDL cholesterol from total choleseterol, HDL, and triglycerides:

LDL cholesterol = Total cholesterol – HDL cholesterol – triglycerides/5

This simple manipulation would put LDL cholesterols into the hands of the practicing physician and the American public. Dr. Friedewald recognized that this calculation only represented an approximation of LDL cholesterol and that it was thrown off, sometimes substantially, by any abnormal rise in triglycerides or reduction in HDL. But it served its purpose at an age when most doctors hadn’t even heard of cholesterol and the public was still sold on whole milk and “farm-fresh” butter, and Chesterfields were the cigarette choice of most doctors.



The world has since changed. Most doctors have heard about cholesterol and, along with the public, have been drowned in drug company marketing for cholesterol-reducing drugs. Most people with some level of common sense and health awareness no longer use butter or whole milk, and no longer believe that the brand of cigarette you choose can be healthy. But we’re still using Dr. Friedewald’s original calculation for LDL cholesterol. When you get an LDL cholesterol from your clinic, doctor, or hospital, >99% of the time it is obtained using Dr. Friedewald’s calculation.

Is it because there’s nothing better available? No, it’s not. There’s two reasons why your neighborhood primary care physician or cardiologist is still using this dinosaur of testing called LDL:

1) The lag in science to practice is 20 years. Accept that most primary care doctors are 20 years behind the times on many issues, LDL cholesterol included.

2) Insurance companies vigorously discourage testing beyond conventional lipids. The array of objections we get from insurance companies is mind-boggling. It would be funny if human life and finances weren’t at stake. These “new” tests are “experimental”, “unproven”, not endorsed by standard guidelines, not approved by some internal committee, or simply “We don’t know what this test is” ?we’ve heard them all.

What are the tests that are superior to Dr. Friendewald’s calculated LDL? There are several, listed here in order of best to worst:

1) LDL particle number--the value generated by NMR lipoprotein testing. This is the gold standard, most reliable test available, and the one I recommend.

2) Apoprotein B--More widely available even from conventional laboratories in hospitals. Not as accurate as NMR LDL particle number, but a pretty good choice. Apo B is the principal protein in LDL, VLDL, and IDL particles, and so it’s a better reflector of risk from all of these lipoprotein fractions, not just LDL.

3) “Direct” LDL--This is LDL that is actually measured. Unfortunately, it ignores the issues of LDL size and has some other pitfalls, but it’s still better than calculated LDL

4) Non-HDL cholesterol--So-called because it incorporates all undesirable cholesterol-containing lipids except good HDL, thus “non-HDL”. This is another calculation, though better than LDL (because it sums up the risk from other apoprotein B-containing lipoproteins). Non-HDL is calculated from Total cholesterol – HDL. It’s therefore available from any standard lipid panel. It’s little used in everyday practice, however, because most people and their physicians find it confusing.

5) Friedewald calculated LDL--You can see that calculated LDL is last on a list of choices. Yet this is the measure that doctors use day in, day out. It’s the measure that drug companies base billions of dollars of revenue and profits on.

It’s an everyday occurrence in my office that calculated LDL is 89 mg/dl, but the real value is somewhere between 160 and 200 mg/dl. That’s a big difference. Imagine your realtor tells you your house’s estimated value is $200,000 and that’s what you sell it for to an eager buyer. After closing, you find out your house was really worth $300,000. You’d be upset. But that’s what you’re often getting with LDL cholesterol?a bum deal.

It’s part of the reason people will say, “My doctor said my cholesterol was fine and that no cause for my heart disease can be found. He said it was genetic.” In reality, they could have sky-high LDL cholesterol revealed by LDL particle number or apoprotein B.

Use LDL cholesterol in a pinch when you’ve got nothing else. It’s also helpful to gauge any treatment effect of diet, functional foods, drugs, etc. But it is a seriously flawed tool to diagnose your initial level of risk.

The key to losing weight

I saw three people this past week, all of whom set off on an effort to lose substantial quantities of weight. And all seriously needed to.

All three started with at least 70 lbs. excess weight; all showed substantial weight-sensitive lipoprotein patterns like low HDL, small LDL, high triglycerides, VLDL, and pre-diabetic levels of blood sugar. They also all shared high blood pressure.

All three also had high heart scan scores. Kate’s score was just over 1200. Tom, a 58-year old real estate developer, had a score of nearly 600. Susan, the youngest of the three at 52, had a heart scan score of 377¾99th percentile at this age. Losing weight was an absolute requirement for their plaque control program. Because their lipoprotein abnormalities and pre-diabetic patterns were triggered by weight, weight loss would provide powerful correction. Each and every one of them would need to lose much of their excess weight¾at least 50 lbs¾if they hoped to halt the relentless progression of their heart scan scores.

All three of them returned after 6-8 weeks, and all had lost between 17-24 lbs: spectacular results.

There’s no secret to weight loss. Each of them achieved their weight loss in slightly different ways. But they also shared several critical ingredients in their weight-loss efforts:

1) All three dramatically slashed their intake of wheat flour-containing foods and other processed carbohydrates and did so consistently. All also avoided the usual high-fat, high caloric-density foods like butter, margarine, fried foods, greasy foods, nuts roasted in oil, etc. They concentrated on vegetables, salads, raw nuts, lean proteins (inc. turkey, chicken, fish, lean red meats, low-fat cottage cheese and yogurt).

2) They stopped using food as a reward or as a consolation tool.

3) Exercise for one hour a day at least 5 days a week. The exercise in 2 of 3 of these people was just walking. It wasn’t strenuous, it wasn’t expensive. The women both liked walking with friends or their spouse. Tom followed a more common male path of more strenuous work on his treadmill, elliptical, and biking at the fitness club. But they all did it religiously and missed rare sessions.

4) They refrained from any and all alcoholic beverages. Yes, there are some advantages to 1-2 glasses of wine per day, but it stalls weight loss efforts.

5) They didn’t allow themselves any major indiscretions. There were no binges, major pig-outs at weddings, barbecues, or all-you-can-eat buffets. They did allow themselves an occasional “treat” but did so in small portions.

That’s it. But for most people, that’s simply too much. Adhering to an effort to lose dramatic weight requires day-after-day consistency. Nobody can lose the equivalent of 70,000 calories (20 lbs.) just by skipping a meal, a 20-minute walk, skipping the mashed potatoes at dinner.

It can be done. You’ve just got to be consistent about it.

How can I get my lipoproteins tested?

This question came up on our recent online chat session and comes up frequently in 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. 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 (VAP or centrifugation). None of them will provide you with the names of actual physicians. They will provide you with the name of a local representative who will know who the doctors in your area who 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.
2) 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.
3) Contact us. I frankly don’t like doing this because I feel that I can only provide limited information through this method. 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 a lot better than nothing.
4) 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.

In 20 years, this will be a lot easier. But for now, you can still obtain reasonably good results choosing one of the above alternatives.

What do you think about those heart scans?

52-year old Jerry came in for a stress test. He displayed the usual apprehension: fidgeting while he sat on the bed, examining his surroundings, asking lots of questions.

“Your doctor asked you have have a stress test?” I asked.

“All the males in my family have had heart attacks by age 56, so my doctor suggested I have a stress test,” Jerry explained.

Jerry went on to tell me that he had exercised vigorously this morning for 45 minutes without symptoms. He had, in fact, gone surfing just several weeks earlier and described how aerobically challenging it was keeping up with the 20 year olds. “But I did it!” he proudly declared.

As he neared the end of his brisk walk on the treadmill, Jerry asked, “What do you think about those heart scans?”

Jerry had asked his primary care physician the same question. His doctor had apparently told him that they were just a gimmick. “We’ll get you a real test.”

Of course, Jerry’s stress test proved entirely normal. The likelihood of an abnormal stress test with his history of vigorous exercise was <2%. I explained to Jerry that not getting heart scan would be a mistake. In fact, a heart scan was the only easily obtainable test that would uncover hidden heart disease. In truth, the stress test was a waste of time—and an unneeded exposure to radiation.

If Jerry’s heart scan score turned out to be zero, great! He was probably spared the genes from the other males in his family, and his risk of heart attack in the next decade was nearly zero.

If his heart scan turned out be 1000, then an urgent scramble to uncover the causes and correct them to create a truly effective prevention program would be crucial for his long term health. Or, perhaps his score lies somewhere in between, but Jerry would then know how far along he stood on his way to heart disease.

Don’t be a victim of the ignorance of your doctor. Despite all the attention heart scans have received, the majority of doctors remain miserably, inexcusably in the dark. I say inexcusable because CT heart scans can uncover the number one killer of Americans, the number one cause of all deaths in any primary care physician’s practices, and it’s laughably easy. How can a physician not advise patients on the value of heart scans?

If given a choice and you’re without symptoms, a heart scan is far and away the superior test.

Olive oil for gourmets

"The finest extra-virgin olive oils should not be used as a medium for hot cooking, but rather as a condiment or a finisher on top of your favorite savory foods. They are expensive, but if stored properly they will last for up to a year..."

You all know that olive oil is among the preferred oils to use: rich in monounsaturates, low in saturates, high in polyphenols.




For a fascinating perspective for the olive oil gourmet, go to www.npr.org, the website for National Public Radio. (Scroll down to the article or enter olive oil into their site search.) Their article, "Like fine wines, fine olive oils boast subtle joys" provides an insightful discussion on squeezing maximum enjoyment out of this wonderful "functional food".

As we emerge from the mis-directed low-fat craze of the past 20 years, we're re-discovering the joys of healthy oils. You'll find some great thoughts here

Vitamin D must be oil-based

As part of the Track Your Plaque coronary plaque reversal program, we advocate vitamin D supplementation. Vitamin D has been shown to reduce blood sugar and reduce pre-diabetic tendencies, reduce blood pressure (it's a renin antagonist, a blood pressure hormone), it's far more important for bone health than calcium, and it may help prevent colon cancer, prostate cancer, and multiple sclerosis.

And, oh yes, it may facilitate coronary plaque regression.

One lesson I've learned is that vitamin D MUST be taken as a oil-based capsule or gelcap. You'll recognize it as a transparent or translucent, sometimes opaque, capsule. The list of ingredients may say something like "cholecalciferol [vitamin D] in a base of soybean oil", indicating that the active ingredient is oil-based. Oil-based vitamin D3 skyrockets blood levels of 25-OH-vitamin D3 in to the normal range reliably and easily.


Tablets are a different story. These are generally white powdery tablets. The rise in blood levels of vitamin D3 are minimal, sometimes none. Women will often say "I get vitamin D with my calcium tablets."


People taking this form almost always have blood levels of vitamin D that are low, as if they were taking nothing.
If you're going to take vitamin D, the oil-based tablets are the way to go. They're not necessarily any more expensive. We've had good experiences with the Nature's Life 2000 unit capsule, as well as preparations from Life Extension. We have had negative experiences with the preparations from GNC, Sam's Club, and Walgreen's, all tablets and non-oil-based.

When is LDL cholesterol NOT LDL cholesterol?

Darlene had a high LDL cholesterol, at times as high as 200 mg/dl. Her primary care doctor first tried Mevacor, then Pravachol, then Zocor, then Lipitor. Every statin drug failed to reduce Darlene's LDL below 160 mg/dl, even when maximum doses were used. The higher doses also resulted in nearly intolerable muscle aches and weakness.

When we sent Darlene's blood sample off for lipoprotein analysis, a surprise came back: she had a high lipoprotein(a), or Lp(a). This explained a lot.

LDL cholesterol is not always just LDL cholesterol. One of the particles that can masquerade as LDL is Lp(a). Darlene's story is typical of many people who've had high cholesterol levels poorly responsive to the statin drugs. That's because their LDL conceals Lp(a), which does not respond to these agents. LDL cholesterol does drop some because there's also some real LDL mixed in.

A poor response to statin agents or to nutritional strategies to reduce LDL is a tip-off that Lp(a) may be hidden. The answer: just measure Lp(a)! If you and your doctor don't measure it, you won't know whether or not you have it. Rather than a statin drug, we put Darlen on niacin. Not only did her Lp(a) drop, but her LDL also plummeted.

What is a desirable triglyceride level?


Though well-intended, the National Cholesterol Education Panel's Adult Treatment Panel, or ATP-III, (whew!) guidelines for cholesterol have been responsible for loads of misinformation.

The intention was to educate the internist or family doctor who treats sore throats, performs Pap smears, administers pneumovax vaccine, treats arthritic knees---and dabbles in heart disease prevention. The ATP-III guidelines are the "Cholesterol for Dummies" approach.

What standard guidelines definitely do not represent are the ideal values to achieve. They do not ensure protection from heart disease. This is particularly true of the ATP-III advice to keep triglycerides at or below the "desirable" level of 150 mg/dl.

In the Track Your Plaque program, we ask "What is necessary to tip the odds in favor of coronary plaque regresion or reduction of heart scan score?" This is not achieved with a triglyceride of 150. In fact, triglycerides at this level are associated with flagrant abnormalities of lipoprotein patterns. It usually means that processed carbohydrates, particularly wheat products, are occupying too prominent a role in your food choices. It could mean that you're making excessive use of processed foods containining high-fructose corn syrup. It will not respond to a low-fat diet. It will, however, respond vigorously to fish oil.

Triglycerides are a crucial aspect of your plaque control program. We aim for 60 mg/dl or less. The ideal level is actually 45 mg/dl. At this level, all abnormal triglyceride-containing lipoproteins finally go away.