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.

Can I stop my Coumadin?

Here I go again.

While I will try to keep this blog on topic, i.e., coronary heart disease prevention and reversal using nutritional and other natural strategies, I believe that a "critical mass" of frequently asked, though off topic, questions keep cropping up.

One such question revolves around Coumadin, or warfarin.

Somehow, my Nattokinase scam blog post draws traffic about Coumadin. I tried to make the point that a conventional blood thinning agent like Coumadin that undoubtedly has undesirable side-effects cannot be replaced by an agent that has an uncertain track record. In the case of nattokinase, no track record.

To illustrate how far wrong the "nattokinase as replacement for Coumadin" idea can go, here is a question from Anna:


I came across your blog while perusing.

I am a bit bummed because I have been on Coumadin (warfarin) for around 22 years since I was 6 years old. I have a mechanical heart valve (St. Jude's), as I have heart-related issues, including hypertrophic obstructive cardiomyopathy.

Well, it is just that the warfarin seems to interact with nearly everything. I feel like I can not get the nutrients my body requires. I desire to consume more raw foods and vegan foods, though I do not want anything to damage my heart valve or risk a stroke/heart attack or internal bleeding.

I have been underweight the majority of my life, malnourished , currently am still somewhat underweight, though enjoying food again, as I had what mimicked Crohn's Disease for several years (horrendous pain), from which I am in remission now. I was diagnosed with osteoporosis, which may or may not be caused from consuming warfarin.

Is it possible to get off of warfarin and effectively keep my blood thinned ? I currently take 1.5 mg to 2 mg dosage. Does the warfarin destroy Vitamin K and if so does that mean while on warfarin I never get the Vitamin K nutrients even if I did consume foods with it in it?

Thank you
Anna


No, sorry, Anna. Stopping Coumadin with your unique issues, i.e., a prosthetic mechanical heart valve (likely mitral, judging by your history of hypertrophic obstructive cardiomyopathy, in which the patterns of blood flow ejected from the heart disrupt the natural mitral valve function) and cardiomyopathy, can be fatal. Without blood thinning, the mechanical heart valve can trigger blood clot formation, since it is a foreign object implanted into the bloodstream.

There are no natural alternatives available with track records confident enough to bet your life on. Aspirin nor Plavix are blood thinners, but platelet inhibitors. These two agents, while they work for other forms of arterial (but not venous) blood clot inhibition, will not work for your unique situation.

Likewise, a purported oral lytic agent like nattokinase should not be substituted for Coumadin. Even if there was plausible science behind it, you should demand substantial evidence that it provides at least blood thinning equivalent to Coumadin. Should a blood clot, even a small one, form in or around the prosthetic valve, the valve can stop working within seconds. This can lead to death within minutes.

I believe it would be foolhardy to bet your life based on the marketing--let me repeat: MARKETING--of a "nutritional supplement" by supplement manufacturers eager to make a buck.

Nor are there any other nutritional supplements that can safely replace the Coumadin. I wish that were NOT true, as I am no stranger to the long-term dangers of Coumadin and I am a big believer, in general, in nutritional supplements. I am a BIGGER believer, however, in the truth. Weighing the options available to us today, there really is no rational choice but to remain on Coumadin.

By the way, I tell my patients to eat a substantial amount of green vegetables while they take Coumadin. I know that conventional advice is to reduce or eliminate green vegetables due to their content of Coumadin-antagonizing vitamin K. I think this is wrong, also. Green vegetables are the best foods on earth. They reduce risk for cancer, diabetes, bone disease, and coronary heart disease.

To obtain the benefits of green vegetables without mucking up your blood thinning (your "protime" or International Normalized Ratio, INR), I advise my patients who take Coumadin to eat green vegetables--but do so every day in relatively consistent quantities, so that the protime or INR is not disrupted and remains reasonably constant. It may mean that your total dose of Coumadin may be somewhat higher, e.g., 3 or 4 mg instead of 2 mg, but the dose is immaterial outside of blood thinning. That way, you obtain all the wonderful health benefits of green vegetables while maintaining fairly consistent blood thinning/protime/INR. Coumadin does not block all the health benefits of vegetables, only those related to vitamins K1 and K2.

With regards to protecting yourself from the osteoporosis promoting effects of Coumadin, I would be sure to follow a program of natural bone health, such as the one I discussed in Homegrown osteoporosis prevention and reversal. You will have to be extra careful, however, with the vitamin K2. Ideally, you have a doctor knowledgeable about vitamin K2 who can assist you in managing K2 intake while on Coumadin. This is something you can definitely NOT manage on your own. (I am a big believer in self-managed care, but this is way beyond the limit.)

Lastly, it is my belief that anyone with an inflammatory bowel condition, such as Crohn's disease or ulcerative colitis, should absolutely, positively, and meticulously AVOID WHEAT and all other gluten sources (such as rye, barley, and oats). Even if you test negative for celiac markers (e.g., anti-gliadin antibodies, emdomysium and transglutaminase antibodies), the enhanced intestinal permeability will allow wheat proteins, such as gluten, to gain ready entry into the bloodstream. Not to mention that wheat should have no place in the human diet anyway, in my view.

Homegrown osteoporosis prevention and reversal

I don't like to stray too far off course from discussions of heart disease and related issues in this blog. But the question of bone health comes up so often that I thought I'd discuss the strategies available to everybody to stop, even reverse, osteoporosis.

Coronary atherosclerotic plaque and bone health are intimately interwoven. People who have coronary plaque usually have osteoporosis; people who have osteoporosis usually have coronary plaque. (The association is strongest in females.) The worse the osteoporosis, the greater the quantity of coronary plaque, and vice versa. The two seemingly unconnected conditions share common causes and thereby respond to similar treatments.

Incredibly, rarely will your doctor tell you about these strategies. Your doctor orders a bone density test, the value shows osteopenia or osteoporosis, and a drug like Fosamax or Boniva is prescribed. As many people are learning, drugs like this can be associated with severe side-effects, such as jaw necrosis (death of the jaw bone), a dangerous and disfiguring condition that leads to loss of teeth and disfigurement, followed by reconstructive surgery of the jaw and face. These are not trivial effects.

Note that drugs are approved by the FDA based on assessment of efficacy and safety, NOT proven equivalence or superiority to natural treatments.

In order of importance (greatest to least), here are strategies that I believe are important to regain or maintain bone health. Indeed, I have seen many women increase bone density using these strategies . . . without drugs of any sort.

1) Vitamin D restoration--Vitamin D is the most important control factor over bone calcium metabolism, as well as parathyroid function. As readers of this blog already know, gelcap forms of vitamin D work best, aiming for a 25-hydroxy vitamin level of 60-70 ng/ml. This usually requires 6000 units per day, though there is great individual variation in need.

2) Vitamin K2--If you lived in Japan, you would be prescribed vitamin K2. While it's odd that K2 is a "drug" in Japan, it means that it enjoys the validation required for approval through their FDA-equivalent. Prescription K2 (as MK-4 or menatetranone) at doses of 15,000-45,000 mcg per day (15-45 mg), improves bone architecture, even when administered by itself. However, K2 works best when part of a broader program of bone health. I advise 1000 mcg per day, preferably a mixture of the short-acting MK-4 and long-acting MK-7. (Emerging data measuring bone resorption markers suggest that lower doses may work nearly as well as the high-dose prescription.)

3) Magnesium--I generally advise supplementation with the well-absorbed forms, magnesium glycinate (400 mg twice per day) or magnesium malate (1200 mg twice per day). Because they are well-absorbed, they are least likely to lead to diarrhea (as magnesium oxide commonly does).

4) Alkaline potassium salts--Potassium as the bicarbonate or the citrate, i.e., alkalinizing forms, are wonderfully effective for preservation or reversal of bone density. Because potassium in large doses is potentially fatal, over-the-counter supplements contain only 99 mg potassium per capsule. I have patients take two capsules twice per day, provided kidney function is normal and there is no history of high potassium.

5) An alkalinizing diet--Animal products are acidic, vegetables and fruits are alkaline. Put them together and you should obtain a slightly net alkaline body pH that preserves bone health. Throw grains like wheat, carbonated soft drinks, or other acids into the mix and you shift the pH balance towards net acid. This powerfully erodes bone. Therefore, avoid grains and never consume carbonated soft drinks. (Readers of this blog know that "healthy, whole grains" should be included in the list of Scams of the Century, along with Bernie Madoff and mortgage-backed securities.)

6) Strength training--Bone density follows muscle mass. Restoring youthful muscle mass with strength training can increase bone density over time. The time and energy needs are modest, e.g., 20 minutes twice per week.

Note that calcium may or may not be on the list. If on the list at all, it is dead last. When vitamin D has been restored, intestinal absorption of calcium is as much as quadrupled. The era of force-feeding high-doses of calcium are long-gone. In fact, calcium supplementation in the age of vitamin D can lead to abnormal high calcium blood levels and increased heart attack risk.

These are benign and easily incorporated strategies. They are also inexpensive. I challenge any drug to match or exceed the benefits of this combination of strategies. Keep in mind that strategies like vitamin D restoration provide an extensive panel of health benefits that range far beyond bone health, an effect definitely NOT shared by prescription drugs.

Your enlarged aorta

The thoracic aorta lives happily within the chest.

The aorta is the main artery of the body that emerges from the heart, located just under the sternum. It is the "tree trunk" from which all the major arteries branch off to the rest of the body: the arms, brain, abdominal organs, pelvis, and legs. The aorta receives the high-pressure blood ejected directly out of the heart muscle.

However, there are evil forces in the body that work to weaken the aorta. When the aorta is weakened, it enlarges. Enlarged aortas also tend to grow atherosclerotic plaque. Plaque in the aorta poses long-term risk for stroke and and mini-strokes ("transient ischemic attacks," or TIAs), due to fragmentation.

There are many enlarged aortas in this world. I see at least several every week. It is fairly common, particularly in people with high blood pressure and cholesterol abnormalities, as well as those who are overweight. Smokers get it really bad.

Conventional thinking is that, once an aorta enlarges, it will inevitably continue to enlarge at the average rate of 2.0 mm per year (resulting in 1.0 cm enlargement over 5 years). For this reason, conventional discussions on the topic of thoracic aortic aneurysms all say something like "Enlarged aortas should be monitored yearly. Surgical replacement should proceed when the aorta reaches a diameter of 5.5 cm."

This is because an aortic diameter of 5.5 cm is associated with much greater likelihood that the aorta will rupture (fatal within minutes) or the internal lining will tear, a "dissection." The surgery is a major undertaking that involves opening the chest and usually replacing the aortic valve and inserting a synthetic aorta. The procedure is high-risk, especially if any branch arteries are involved.

So putting a stop to any further aortic enlargement is a worthwhile goal. Unfortunately, conventional thought is that there is nothing you can do to stop the inevitable growth of the thoracic aorta.

Nonsense. There are a number of efforts you can make to halt further increase in aortic diameter. (My experience in this is anecdotal and unpublished, but now numbers several hundred patients.)

There are two categories of factors that cause the aorta to increase in diameter:

1) Internal pressure--Think of blood pressure as the internal inflating pressure on this "balloon." Keeping the "inflating pressure," i.e., blood pressure, low exerts substantial effect on slowing growth of aortic diameter. I aim for normal BP or lowish BP (less than 130/80, preferably 100/70).

2) Factors that weaken the aortic wall--Processes like inflammation, glycation, lipoprotein deposition, and nutritional deficiencies will serve to weaken the supportive tissue of the aorta. For that reason, correction of lipoprotein abnormalities (e.g., small LDL and lipoprotein(a)), reductions in carbohydrate intake and thereby blood glucose/glycation, and "normalization" of vitamin D, vitamin C supplementation (for collagen crosslinking), and omega-3 fatty acids all play a role.

To push even farther, there may be additional advantage to following strategies that impair the production and activity of a crucial enzyme that lives within the aortic wall: matrix metalloproteinase, or MMP. MMP degrades the collagen and other supportive tissues within the aorta, weakening it and permitting expansion. Blocking MMP may prove to be among the most powerful new strategies to halt aortic expansion.

Compounds that have potential MMP-inhibiting effects include:
--Vitamin D--A substantial effect
--Resveratrol--One of the polyphenols from red wine
--Doxycycline--This old antibiotic often used for acne treatment has, in preliminary studies, shown important MMP-blocking effects and slowed aortic expansion.

Anyway, there you have it. A bit complicated, but a "recipe" that has failed me only rarely.

Extreme carbohydrate intolerance

Here's an interesting example of what you might call "extreme carbohydrate intolerance."

May is a 44-year woman who has now had her 7th stent placed in her coronary arteries. She lives on a diet dominated by breads, breakfast cereals, muffins, rice, corn products, along with some real foods.

Her conventional lipid panel and other lab values:

Total cholesterol 346 mg/dl
Triglycerides: 877 mg/dl
HDL cholesterol: 22 mg/dl
LDL cholesterol: incalculable
(Recall that LDL cholesterol is usually a calculated, not a measured value. The excessively high triglycerides make the standard calculation invalid--more invalid than usual.)

Fasting blood glucose: 210 mg/dl
HbA1c (a reflection of previous 60-90 days average glucose): 7.2% (desirable 4.5% or less)
ALT (a "liver enzyme"): 438 (about five-fold normal)


At 5 ft even and 138 lbs (BMI 27.0), May appears small. But the modest excess weight is all concentrated in her abdomen, i.e., in visceral fat.

By lipoprotein analysis via NMR (Liposcience), May's LDL particle number was 2912 nmol/L, or what I would call a "true" LDL of 291 mg/dl. (Drop the last digit.) Of the 2912 nmol/L LDL particles, 2678 nmol/L, or 92%, were small.

The bad news: This pattern of extremely high triglycerides, extremely high LDL particle number, low HDL, predominant small LDL, and diabetes poses high-risk for heart disease--no surprise. It earned her 7 stents so far. (Unfortunately, she has made no effort whatsoever to correct these patterns, despite repeated advice to do so.)

The good news: This collection is wonderfully responsive to diet. LDL particle number, small LDL, triglycerides, blood glucose, and HbA1c drop dramatically, while HDL increases. Heart disease will at least slow, if not stop.

It's amazing how far off human metabolism can go while indulging in carbohydrates, particularly a genetically carbohydrate-intolerance person. (Actually, I wouldn't be surprised if May's diet, as bad as it seems to you and me, still fits within the dictates of the USDA food pyramid.) The crucial step in diet to correct this smorgasbord of disaster is elimination of carbohydrates, especially that from wheat, cornstarch, and sugars.

What's for breakfast? Egg bake

Heart Scan Blog reader and dietitian, Lisa Grudzielanek, provided this recipe in response to the post, What's for breakfast?

Lisa, by the way, is one of the rare dietitians who understands that organizations like the American Dietetic Association have made themselves irrelevant. She therefore advocates diet principles that work, not just echoing the idiocy that emanates from such organizations, often driven by economics more than science. Lisa works in the Milwaukee area and has proven a useful resource person for my patients who have required extra coaching in the Track Your Plaque diet principles.

Egg Bake
My favorite breakfast is what I call an "egg bake." Others may refer to it as a "quiche."

Take a variety of fresh vegetables. This time of year is great for farmers' markets.

I typically use fresh chopped organic spinach, bell peppers, red & white onions, scallions, broccoli, mushrooms, cherry tomatoes halved and, if desired, meat (nitrite-free ham or leftover chicken breasts).

1) Chop veggies and place in casserole dish.
2) Add meat and handful of cheese of your choice.
3) Scramble 8 eggs & little bit of milk & pepper.
4) Add to casserole dish and mix/coat veggies with egg mixture.
5) Put in oven at 450 degress for 30 minutes.

Yummy, ready to eat breakfast that is so easy for the work week.

What's for breakfast?

If you eliminate wheat from breakfast and otherwise adhere to a low-carbohydrate dietary approach, what is there to eat for breakfast?

If you take out English muffins, bagels, all breakfast cereals, pancakes, waffles, and toast, what's left to eat?

Actually, there's plenty left to eat. It just may not look like the traditional American notion of "breakfast." (The traditional idea of breakfast was is, in part, due to the legacy of Dr. John Harvey Kellogg, who, in the latter part of the 19th century, ran a sanitarium in Battle Creek Michigan. He and his brother, Will Keith Kellogg, discovered the idea of turning grains into flakes, the birth of the breakfast cereal. Subscribe to the idea of breakfast cereal for breakfast and you subscribe to the ideas of a man who would administer four enemas for you today to cure your cancer or rheumatism.)

Here are a few ideas. By no means is this meant to be a comprehensive list, just a starting point for a few new breakfast food ideas.

--Eggs--Of course, eat the yolk. Eat three yolks. Scrambled, "fried," (not really deep-fried, of course), hard-boiled, poached, as an omelette. Add pesto, olive oil, vegetables, mushrooms, salsa.

--Ground flaxseed--As a hot cereal with your choice of water, milk (not my favorite because of insulin effects; the fat is immaterial), full-fat soy milk (yeah, yeah, I know), unsweetened almond milk. Add walnuts, blueberries, etc. Ground flaxseed is the only grain I know of that contains no digestible carbohydrates.

--Lunch and dinner--Yes, if you cannot have breakfast foods for breakfast, then have lunch and dinner, meaning incorporating foods you ordinarily regard as lunch and dinner foods into your day's first meal. This means salads, leftover chicken from last night, soup, raw vegetables dipped in hummus or guacamole, stir fry, etc.

--Cheese--For something quick, grab a chunk of gouda or emmentaler along with a handful of raw almonds, walnuts, or pecans. Because of the excess acidity of cheese (along with meats, among the most acidifying of foods), I usually try to include something like a raw pepper or avocado, foods that are net alkaline.

--Avocados--Cut in half, scoop out contents. They're quick and delicious, when available.

I hesitate to mention it, but I sometimes will have tofu, cubed and flavored with whatever is available--soy sauce, miso, pickled vegetables. My mother was Japanese, so I'm comfortable with this, though many people are not.

Anyway, that's a partial list that nonetheless can get you started on a wheat-free, low-carb breakfast.

If you are just starting out, you will notice a number of fundamental changes. You may first experience the characteristic "withdrawal" effect: mental fog and fatigue that lasts about a week. Energy then picks up, often substantially. This is followed by gradually reduced appetite: You will be far less hungry. You will require less food, less often, since appetite will be driven by physiologic need, not the appetite-stimulating properties of wheat (and cornstarch, high-fructose cornsyrup and sucrose).

By the way, do not skip breakfast unless it's part of an occasional fasting effort. Skip breakfast, wind down metabolism, get fat. I am impressed at how consistent skipping breakfast backfires in those who think that it helps you control weight.

I also welcome any suggestions on what you eat as part of your wheat-free, low-carb breakfast. (Thanks for the great suggestions on the last blog post, Anna.)

Wheat hip

You've heard of wheat belly. How about wheat hip?

Recall that the innocent appearing wheat belly is actually a hotbed of inflammatory activity beneath the surface. The visceral fat of the wheat belly, i.e., fat kidneys, fat liver, fat intestines, fat pancreas, produces abnormal inflammatory signals, such as various interleukins, tumor necrosis factor, and leptin. These are the inflammatory signals that create insulin resistance and diabetes, heart disease, hypertension, and cancer.

These same inflammatory mediators are able to enter the joint spaces, such as those in your hips, knees, and hands. This leads to osteoarthritis, the exceptionally common form of arthritis that affects 1 in 7 Americans. In particular, the level of leptin in joints mirrors that in blood, a phenomenon that has been associated with joint destruction.

The previously widely-held notion that arthritis is simply a wear-and-tear phenomenon due to the mechanical stress of excess weight is proving to be an oversimplification. Arthritis is also part of the carbohydrate-driven, weight-increasing, inflammatory condition of insulin resistance or metabolic syndrome.

Throw into this cytokine storm the fact that glycation, i.e., glucose modification of proteins, also causes cartilage destruction. The cells of human cartilage lack the ability to divide, so the cartilage cells you had at age 18 are the cartilage cells that you will hopefully still have at age 80. However, high blood sugars (glucose) glycate the proteins in cartilage. (Wheat raises blood glucose higher than almost all other foods, higher than a Milky Way bar, higher than a Snickers bar.) The process is irreversible and cumulative. Because cartilage has next to no capacity for repair or regeneration, it becomes brittle. Over years, it essentially crumbles, leading to the "bone on bone" that prompts conversations about total hip and total knee replacement.

So that ciabatta or blueberry muffin in your mouth takes you a step or two closer to joint destruction via heightened inflammation arising from the visceral fat of the wheat belly, worsened by glycation of high blood sugars after carbohydrate consumption.

My solution: Lose the ciabatta.

Men's lingerie is on the second floor

Consume wheat products, like poppyseed muffins, raisin bagels, and whole grain bread, and you trigger the 90- to 120-minute glucose-insulin cycle.

Blood glucose goes way up (more than almost any other known food), triggering insulin release from the pancreas. Glucose enters cells as a result, blood glucose plummets. You get hungry, shaky, and crabby, reach for another wheat or other sugar-generating food to start the roller coaster ride all over again.

Repetitive insulin triggering grows this thing I call a "wheat belly," the protuberant, hang-over-the-belt fat you see everywhere nowadays. Wheat belly fat is really visceral fat. Visceral fat means you have fat kidneys, fat intestines, fat pancreas, and fat liver, all causing the belly to protrude in the familiar way we've all come to recognize.

Visceral fat is special fat. Unlike the fat in the backside, thighs, or arms, visceral fat triggers inflammatory responses that are evident in such measures as tumor necrosis factor, interleukins, and leptin, as well as drops in the protective hormone, adiponectin.

Visceral fat also, oddly, triggers estrogen release. Estrogen triggers growth of breast tissue. That's why females with wheat bellies have up to four-fold (400%) greater likelihood of breast cancer.

Men also experience excess estrogen from the visceral fat wheat belly, causing "man boobs." This B-cup phenomenon means that inflammation is raging beneath the surface, all due to this thing you're wearing around your waist.

I wasn't aware until recently that male breast reduction surgery is a booming business growing at double-digit rates. So are special clothes to help men conceal their expansive breasts.

Perhaps the USDA is in cahoots with Playtex.

10,000 units of vitamin D

Joanne started with a 25-hydroxy vitamin D level of 23 ng/ml--severe deficiency.

What made this starting value even worse was that it was drawn in August after a moderately sunny summer spent outdoors. (Last summer, not this summer.) It therefore represented her high for the year, since vitamin D levels trend lower as fall and winter set in. This suggests that her winter level was likely in the teens or even single digits. In addition, note that, at age 43, Joanne has lost much of her ability to activate vitamin D in the skin.

So I advised that she take 6000 units of an oil-based gelcap per day, a dose likely to generate the desired blood level, which I believe is 60-70 ng/ml.

Four months later, her 25-hydroxy vitamin D level: 39.9 ng/ml--still too low. So I advised her to increase her dose to 10,000 units per day. Several months later, her 25-hydroxy vitamin D level: 63.8 ng/ml--perfect.

However, on hearing that she was taking 10,000 units vitamin D per day, Joanne's primary care physician was shocked: "What? Stop that immediately! You're taking a toxic dose!" So Joanne called me to find out if this was true.

No, of course it's not true. It's not the dose that's toxic, but the blood level it generates. Although it varies, vitamin D toxicity, as evidenced by increased blood calcium levels, generally does not even begin to get underway until at least 120-130 ng/ml, perhaps higher. Rarely, a dose of 2000 units per day will generate a level this high. In others, it may require 24,000 or more units per day to generate such a high level.

So it's not the dose that's toxic, but the blood level of 25-hydroxy vitamin D it generates.

Provided you and/or your doctor are monitoring 25-hydroxy vitamin D blood levels, the dose is immaterial. It's the blood level you're interested in.