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.

What Mr. Clinton did NOT do

You've likely already heard that former President Bill Clinton underwent a heart catheterization today during which one of the bypass grafts to his coronary arteries was found to be occluded. The original coronary artery was therefore stented.

Dr. Alan Schwartz, Mr. Clinton's cardiologist, announced to the gathered press that Mr. Clinton had followed a good diet, had adopted a regular exercise program, but that his condition is a "chronic disease" like hypertension that is not cured by these efforts.



Needing a stent just 6 years after four bypass grafts are inserted is awfully soon. I would propose that it has less to do with having a "chronic disease" and more to do with all the things that Mr. Clinton likely is NOT doing. (In addition to all the other things that Mr. Clinton did not do.) In other words, in the Track Your Plaque world, procedures are a rarity, heart attacks virtually unheard of. I would wager that Mr. Clinton has been doing none of the following:

--Taking fish oil. Or, if his doctor was "advanced" enough to have advised him to take fish oil, not taking enough.
--Vitamin D--Followers of the Heart Scan Blog already know that vitamin D is the most incredible health find of the last 50 years, including its effects on reducing heart disease risk. Unless Mr. Clinton runs naked in a tropical sun, he is vitamin D deficient. A typical dose for a man his size is 8000 units per day (gelcap only!).
--Eating a true heart healthy diet. I'll bet Mr. Clinton's doctor, trying to do the "right" thing, follows the prudent course of advising a "balanced diet" that is low in fat--you know, the diet that causes heart disease. Judging by Mr. Clinton's body shape (central body fat), it is a virtual certainty that he conceals a severe small LDL pattern, the sort that is worsened by grains, improved with their elimination.
--Making sure that hidden causes are addressed--In addition to the "hidden" small LDL, lipoprotein(a) is another biggie. Lp(a) tends to be the province of people with greater than average intelligence. I believe Mr. Clinton qualifies in this regard. I would not be at all surprised if Mr. Clinton conceals a substantial lipoprotein(a) pattern, worsened in the presence of small LDL.
--Controlling after-meal blood sugars--Postprandial (after-eating) blood sugars are a major trigger for atherosclerotic plaque growth. There are easy-to-follow methods to blunt the after-meal rise of blood sugar. (This will be the subject of an in-depth upcoming Track Your Plaque Special Report.)
--Thyroid normalization--It might be as simple as taking iodine; it might involve a little more effort, such as supplemental T3. Regardless, thyroid normalization is an easy means to substantially reduce coronary risk and slow or stop coronary plaque growth.


It's not that tough to take a few steps to avoid bypass surgery in the first place. Or, if you've already had a procedure, a few additional steps (of the sort your doctor will likely not tell you about) and you can make your first bypass your only bypass.

Magnesium and arrhythmia

Because magnesium is removed during municipal water treatment and is absent from most bottled water, deficiency of this crucial mineral is a growing problem.

Magnesium deficiency can manifest itself in a wide variety of ways, from muscle cramps (usually calves, toes, and fingers), erratic blood sugars, higher blood pressure, to heart rhythm problems. The abnormal heart rhythms that can arise due to magnesium deficiency include premature atrial contractions, premature ventricular contractions, multifocal atrial tachycardia, atrial fibrillation, and even ventricular tachycardia, fibrillation, and Torsade de Pointes (all potentially fatal). Magnesium is important!

Magnesium supplementation is therefore necessary for just about everybody to maintain normal tissue levels. (The exception is people with kidney disorders, who should not take magnesium without supervision, since they retain magnesium.)

Here is a Heart Scan Blog reader's dramatic rhythm-correcting response to magnesium supplementation:



Dr. Davis,

A few months ago, I contacted you inquiring if you had written any articles on arrhythmia. You were generous enough to answer and guide me to an LEF article you'd written in which you stressed fish oil and magnesium. I had been suffering with bad PVCs [premature ventricular contractions] for over 20 years, and they had gotten so bad recently that I was told my next options were ablation or pacemaker!

I was already on fish oil and had not seen any difference, and so I researched the magnesium you suggested more thoroughly and found a huge body of studies supportng its effect on arrhythmia. I also read many posts on heart forums with people having success with it. After getting advice from various bloggers, I tried magnesium taurate in the morning and Natural Calm (an ionized form of mag citrate) in the afternoon and evening. Within three days the PVCs were quite diminished and by 2 weeks totally gone! As long as I keep taking it, they never return---not even one irregular blip---even when I drink strong coffee! The magnesium also cleared up my restless leg syndrome, my eye twitching, and insomnia. (Apparently, I was the poster-girl for magnesium deficiency.)

I am so angry that after all these years of suffering, trying various medications, and seeing at least 4 different cardiologists that NOT ONE ever even mentioned trying magnesium. The generosity of the few minutes you took to answer my email and steer me in a helpful direction brought me total relief.

Thank you SO MUCH!

Warmly,
Catherine C.

Video teleconference with Dr. Davis


Dr. Davis is available for personal
one-on-one video teleconferencing

to discuss your heart health issues.


You can obtain Dr. Davis' expertise on issues important to your health, including:

Lipoprotein assessment

Heart scans and coronary calcium scores

Diet and nutrition

Weight loss

Vitamin D supplementation for optimal health

Proper use of omega-3 fatty acids/fish oil



Each personalized session is 30 minutes long and by appointment only. To arrange for a Video Teleconference, go to our Contact Page and specify Video Teleconference in your e-mail. We will contact you as soon as possible on how to arrange the teleconference.


The cost for each 30-minute session is $375, payable in advance. 30-minute follow-up sessions are $275.

(Track Your Plaque Members: Our Member cost is $300 for a 30-minute session; 30-minute follow-up sessions are $200.)

After the completion of your Video Teleconference session, a summary of the important issues discussed will be sent to you.

The Video Teleconference is not meant to replace the opinion of your doctor, nor diagnose or treat any condition. It is simply meant to provide additional discussion about your health issues that should be discussed further with your healthcare provider. Prescriptions cannot be provided.

Note: For an optimal experience, you will need a computer equipped with a microphone and video camera. (Video camera is optional; you will be able to see Dr. Davis, but he will not be able to see you if you lack a camera.)

We use Skype for video teleconferencing. If you do not have Skype or are unfamiliar with this service, our staff will walk you through the few steps required.

Thinner by Thursday

You want to lose a few pounds . . . Okay, maybe 50 or 75.

Should you exercise? Lengthen you workout? Push the plate away, deny yourself seconds, use a smaller plate?

Of all the weight loss strategies I've tried in patients, there's only one that stands out as a means of obtaining immediate--meaning within 3 days--weight reduction.

Wheat elimination.

Omega-3 Index: 10% or greater?

We've previously considered the question:

What is an ideal level of omega-3 fatty acids in the blood?

Recall that omega-3 levels in red blood cells (RBCs), a measure called the "omega-3 index," have been associated with risk for sudden cardiac death:





In a recent analysis, 265 people experiencing sudden death during a heart attack (ventricular fibrillation, successfully resuscitated) showed an omega-3 index of 4.88%, while 185 people not experiencing sudden death during a heart attack showed an omega-3 index of 6.08%.

We have more ambitious goals than just avoiding sudden death, of course! How about the omega-3 index associated with reduced risk for heart attack? A recent analysis of females from the Harvard School of Public Health suggested that RBC omega-3 levels as high as 8.99% were still associated with non-fatal heart attack (myocardial infarction), compared to 9.36% in those without heart attacks, suggesting that even higher levels are necessary to prevent non-fatal events.

Most recently, another study comparing 50 people after heart attack with 50 controls showed that people with heart attack had an omega-3 index of 9.57% vs 11.81% in controls--even higher. (This study was in a Korean population with higher fish consumption. There was also a powerful contribution to risk from trans fat RBC levels.) The investigators concluded: "The area under the receiver operating characteristic curve of fatty acid profiles was larger than that for traditional risk factors, suggesting that fatty acid profiles make a higher contribution to the discrimination of MI cases from controls compared with modified Framingham risk factors."

The data suggest that, while an omega-3 index of 7.3% is associated with reduced risk for sudden cardiac death, a higher level of 10% or greater is associated with less risk for heart attack. Surprisingly, fish consumption and fish oil intake account for only 47% of the variation in omega-3 index.

I believe the emerging data are becoming increasingly clear: If you desire maximal control over heart health, know your omega-3 index and keep it 10% or higher.

Let's soak 'em with fish oil

If you don't think that charging drug prices for fish oil is wrong, take a look at a letter from an angry Heart Scan Blog reader:


Hello Dr. Davis,

My 44 year old brother had an MI [myocardial infarction, or heart attack] in June. He got pushed around due to "bad government insurance," a state-run program for the "uninsured": government pays 1/3, job pays 1/3, and individual pays 1/3.

What they didn't tell him is that there is no major medical coverage and little to no prescription coverage. We fought for 4 months to get him open heart surgery that the insurance was not going to pay for.

Now, with no assistance, terrible insurance, and no disability he has little to no income. He is a heavy equipment mechanic and is trying to be the "good American"-- take care of his bills, not file bankruptcy, etc.

Anyway, the doctors never seem to pay attention to what they prescribe. Lipitor was not working for him, due to side effects. Now they want to give him Zetia and Lovaza....Zetia at $114, and Lovoza is $169.85! Wow! For dead fish???? I think this is a little fishy! I looked up Lovaza, gee how nice, they will give you a $20 coupon....

Forget it, he can't afford this stuff. So I am enrolling in the Zetia program for him. And trying to get him OTC [over-the-counter] fish oil. The most prevalent fish oil around here (that I take myself is) Omega 3 Fish Oil that has EPA 410mg, DHA 274.

Thanks for your blog. It made me feel better that I wasn't the only one outraged by this stuff. I 've been a nurse for 20 years and it just never seems to get better. Thank you for your wisdom.

Sincerely JP, Tennessee



Had this reader not been aware that her brother could take fish oil as a nutritional supplement, he likely would have been denied the benefit of omega-3 fatty acids in slashing the risk for recurrent cardiovascular events. You and I can buy wonderfully safe and effective fish oil as a nutritional supplement, but there won't be a sexy drug representative to sell it, nor an expensive dinner and payment for a trip to Orlando to hear about it.

Heart scan gone wrong

Those of you reading the Heart Scan Blog, I hope, have come to appreciate the power in measuring atherosclerotic plaque, the stuff of coronary artery disease, and not relying on indirect potential "risk factors," especially the fictitious LDL cholesterol.

However, like all things, even a great thing like heart scans can be misused. Here's a story of how a heart scan should NOT be used, submitted by a reader.


Dr. Davis,

First of all, let me start out by commending you on all of the work you are doing with your website, blogs, etc. You are truly a breath of fresh air at a time when conventional medicine is no longer making any sense. In the last 3 years or so, I have spent a lot of time using the internet to try and find answers . . . and just about every time, when I find things that make "sense," it coincides which the recommendations you provide. Thank You!!

I am 56 years old, and roughly 5 years ago I bought your book, Track Your Plaque, primarily because I had asked my then Internal Medicine physician about why we weren't more "proactive" about determining the state of our cardiovascular health...since the means to do so existed (scans). He was trying to get me to go on a statin because my cholesterol #'s were a little high and at the time I smoked. Other than that, I was in perfectly good health with no side effects or issues. The following year at my annual physical, we again discussed this and he gave me a few options and I ended up having a calcium score done, which showed some blockage, but again, I never had any pains, sweats, or any other symptoms whatsoever, and I am a very active former athlete. This is when I bought your book to try and set a course of plan that wouldn't just include pharmaceuticals.

At the same time, my father was in his last months of life dealing with prostate cancer and the multiple radiation and chemo treatments, so I was making many trips from my home to be with him . . . a 4 hour drive, and very disruptive to family, as I still have 3 kids at home. At what I thought was going to be my last visit with him, I stopped at the cemetery he had planned on being buried to confirm details and such and then started home.

As I was driving, a symptom hit me which I was unfamiliar with (pretty sure it was an anxiety attack now) and I stopped at a friend's house in Chicago, as I didn't want this to be a heart attack while I was driving. This is when I began thinking about the heart scan and the blockage, and ended up driving back later that night and went right to the ER....not because I had any chest pains, but thought it best to be checked out because I did not want to go before my dad did. I ended up staying the night. In the morning the cardiologist PA [physician's assistant] came in with a copy of my calcium scoring and said it was best to have a heart cath...which I was in total agreement with since it would definitively tell me the current condition of my coronary vessels. As I was getting ready to be wheeled into the cath lab, they approached me with a form that would allow them to treat (stent). This is where I became very uncomfortable, in that I had never even met the cardiologist . . . and I didn't like this. No one ever had asked if I was experiencing pains or anything else . . . but I buckled and signed the form.

Before you knew it, I was awake watching my heart being cathed and the cardiologist angry because they did not have all the right sizes of stents, so he had to use a couple extra and I ended up w/5 total . . . and my life changed forever! In looking back, I can't necessarily argue the need for intervention, but in hindsight, it would have been nice to have tried an alternative method of reversing my plaque, especially since I had never experienced any symptoms and didn't appear to be in any imminent danger.

Upon release from the hospital I was put on a cocktail of drugs that typically follow and I then began to search and research. No one talked to me about lifestyle changes other that smoking....but nothing on diet or other means of cholesterol control, etc....in fact, when I had to pick out my meals in the hospital, they wouldn't let me have cheese....but the rice crispy treat was fine....how stupid! They originally told me the Plavix had to last 6 months....and then 12....and then 2 years....I stayed on it for 1-1/2 years and it was the only thing other than a baby aspirin. I went to another cardiologist out of town and he wanted me back on 5 or 6 medications and said that now I had the stents....I would have to be on these for life.....and he was the expert that talked at several main conferences.....my last trip to him.

Now, fast forward to about 6 months ago: I was participating in a father-son soccer scrimmage and was playing goalie. It was wet out and I couldn't catch very well. So being the competitive person I am, I resorted to using my chest on several of the saves and also took a direct blow to my eye ( I wear glasses) and the eye started swelling up pretty good. We then finished and went inside to have pizza and everyone was concerned about my eye. About 30 minutes later I excused myself as i felt some pretty significant sweats and subsequently a pretty severe pain directly in the middle of my chest....I was having a heart attack! Called 911 and went to hospital (2-1/2 years since original stents) and my local cardiologist removed the blockage that was at the anterior portion of my 1st stent causing the blockage. The huge disappointment to me is that I had taken many steps to improve my overall health. But now that I have foreign bodies in my vessels, the chance of further clotting is something that i will most likely always have to live with.

BU, Michigan



This is an example of how heart scans should NOT be used. They should NEVER be used to justify a procedure, no matter how high the score or where the plaque is located. The "need" for procedures is determined by symptoms (BU's symptoms were hardly representative of heart disease), blood findings, EKG, stress testing, and perhaps CT coronary angiography. "Need" for procedures can never be justified simply on the basis of the presence of plaque by a heart scan calcium score.

Unnecessary procedures like the one BU underwent are not entirely benign, as his experience at the soccer game demonstrated.

Heart scans are truly helpful things. But, like many good things, they are subject to misuse in the hands of the uncaring or greedy.

Blood sugar: Fasting vs. postprandial

Peter's fasting blood glucose: 89 mg/dl--perfect.

After one whole wheat bagel, apple, black coffee: 157 mg/dl--diabetic-range.

How common is this: Normal fasting blood sugar with diabetic range postprandial (after-eating) blood sugar?

It is shockingly common.

The endocrinologists have known this for some years, since a number of studies using oral glucose tolerance testing (OGTT) have demonstrated that fasting glucose is not a good method of screening people for diabetes or pre-diabetes, nor does it predict the magnitude of postprandial glucose. (In an OGTT, you usually drink 75 grams of glucose as a cola drink, followed by blood sugar checks. The conventional cut off for "impaired glucose tolerance" is 140-200 mg/dl; diabetes is 200 mg/dl or greater.) People with glucose levels during OGTT as high as 200 mg/dl may have normal fasting values below 100 mg/dl.

High postprandial glucose values are a coronary risk factor. While conventional guidelines say that a postprandial glucose (i.e., during OGTT) of 140 mg/dl or greater is a concern, coronary risk starts well below this. Risk is increased approximately 50% at 126 mg/dl. Risk may begin with postprandial glucoses as low as 100 mg/dl.

For this reason, postprandial (not OGTT) glucose checks are becoming an integral part of the Track Your Plaque program. We encourage postprandial blood glucose checks, followed by efforts to reduce postprandial glucose if they are high. More on this in future.

Diabetes from fruit

Mitch sat in my office, looking much the same as he had on prior visits.

At 5 ft 7 inches, he weighed a comfortable 159 lb, though he did have a small visible "paunch" above his beltline.

I had been seeing Mitch for his heart scan score of 1157 caused by low HDL of 38 mg/dl, severe small LDL (87% of total LDL), and lipoprotein (a).

Part of Mitch's therapeutic program was elimination of wheat, cornstarch, and sugars, the three most flagrant triggers of small LDL particles, and weighing his diet in favor of oils and fats to reduce Lp(a). However, Mitch somehow failed to follow our restriction on fruit, which we limit to no more than two 4 oz servings per day, preferably berries. He thought we said "Eat all the fruit you want." And so he did.

Mitch had a banana, orange, and blueberries for breakfast. For lunch, along with some tuna or soup, he'd typically have half a melon, a pear, and red grapes. For snacks, he'd have an apple or nectarine. After dinner, it wasn't unusual for Mitch to have another piece of fruit for dessert.

Up until Mitch's last visit, he'd had blood glucose levels of 100-112 mg/dl, above normal and reflecting mild insulin resistance and pre-diabetes. Today, on his unlimited fruit diet, his blood sugar: 166 mg/dl--well into diabetes territory.

I helped Mitch understand the principles of our diet better and advised him to reduce his fruit intake to no more than the 2 small servings per day, as well as sticking to our "no wheat, no cornstarch, no sugar" principles.

While fruit is certainly better than, say, a half-cup of gummy bears (84.06 g carbohydrates, 50.12 g sugars), fruit is unavoidably high in carbohydrates and sugars.

Take a look at the carbohydrate content of some common fruits:

Apple, 1 medium (2-3/4" dia)
19.06 g carbohydrate (14.34 g sugar)

Banana, 1 medium (7" to 7-7/8" long)
26.95 g carbohydrate (14.43 g sugar)

Grapes, 1 cup
27.33 g carbohydrate (23.37 g sugar)

Pear, 1 medium
25.66 g carbohydrate (16.27 g sugar)

Source: USDA Food and Nutrient Database

Fruit has many healthy components, of course, such as fiber, flavonoids, and vitamin C. But it also comes with plenty of sugar. This is especially true of modern fruit, the sort that has been cultivated, hybridized, fertilized, gassed, etc. for size and sugar content.

When you hear such conventional advice like "eat plenty of fruits and vegetables," you should hear instead: "eat plenty of vegetables. Eat a small quantity of fruit."

The sniff test

It is well established that omega-3 fatty acids from fish oil are free of mercury, PCBs, furans, and other pesticide residues. Several independent analyses have all agreed: little to none are contained in fish oil. In the Consumer Lab series of assessments, for example, no fish oil supplement failed because of any heavy metal or pesticide residue.

However, oxidative byproducts are a problem. Just as fish that sits on the store shelf or your refrigerator too long starts to smell "fishy," so will fish oil. When fish or fish oil becomes rancid, smelling like rotten fish at its worst, it means that