Why do the Japanese have less heart disease?

We should look to the Japanese to teach us a few lessons about preventing heart disease. A Japanese male has only 65% of the risk of an American male (despite 40% of Japanese men being smokers), while a Japanese woman has 80% less risk than an American woman. While the U.S. is near the top of the list of nations with highest cardiovascular risk, Japan is the lowest.

What are they doing right?

There is no one explanation, but several. Genetics probably does not play a substantial role, by the way, as demonstrated by observations of Japanese people who emigrate to Western cultures. People of Japanese heritage living in Hawaii, for instance, develop the same cardiovascular risk as non-Japanese living in Hawaii. They also develop obesity and diabetes.

Among the factors that likely contribute to reduced risk in Japanese people:

--A style of eating that does not include a lot of sweet foods. No breakfast cereal or donuts for breakfast, for instance, but miso soup with tofu, fish, green onions, and daikon (as takuan, or pickled radish).
--Seaweed--It's probably a combination of the green phytonutrients and iodine. Typical daily iodine intake is in the neighborhood of 5000 mcg per day from nori, kombu, wakame, and other seaweed forms. (The average American obtains 125 mcg per day of iodine from diet.)
--Seafood--Fish in many forms not seen in the U.S. are popular.
--Green tea--Consumption of green tea has been confidently linked to reduced cardiovascular risk, probably via visceral fat-reducing, anti-oxidative, and anti-inflammatory effects. Although tea in Japan is often the less flavonoid-rich oolong tea, softer benefits from this form are likely.
--Soy--Tofu, miso, and soy sauce are staples. It's not clear to me whether soy is intrinsically beneficial or whether it is beneficial because it serves to replace unhealthy alternatives. (Genetic modification may change this effect.)
--Reduced exposure to cooked animal products (except seafood). This is not a saturated fat issue, but probably an advanced glycation end-product/lipoxidation issue that result from cooking.
--The lack of a "eat more healthy whole grain" mentality, the advice that has plunged the entire U.S. into the depths of a diabetes and obesity crisis (along with high-fructose corn syrup and sugar). Noodles like udon and ramen do have a place in their diet, as do some dessert foods. But the overall wheat exposure is less--no bagels, sandwiches, and breakfast cereals.
--Less overweight and obesity--The above eating style leads to less weight gain.

Japanese foods have a unique taste, consistency, and mouth-feel that go well with saltiness, thus the downside of their diet: salt consumption. On a broad scale, high salt consumption has been associated with hypertension and gastric cancer. But the tradeoff has, on the whole, been a favorable one.


One study trying to find some answers:

Dietary patterns and cardiovascular disease mortality in Japan: a prospective cohort study.

Shimazu T, Kuriyama S, Hozawa A et al.
Division of Epidemiology, Department of Public Health and Forensic Medicine, Tohoku University Graduate School of Medicine, Japan.


We prospectively assessed the association between dietary patterns among the Japanese and CVD mortality. Dietary information was collected from 40 547 Japanese men and women aged 40-79 years without a history of diabetes, stroke, myocardial infarction or cancer at the baseline in 1994.
During 7 years of follow-up, 801 participants died of CVD.

Factor analysis (principal component) based on a validated food frequency questionnaire identified three dietary patterns: (i) a Japanese dietary pattern highly correlated with soybean products, fish, seaweeds, vegetables, fruits and green tea, (ii) an 'animal food' dietary pattern and (iii) a high-dairy, high-fruit-and-vegetable, low-alcohol (DFA) dietary pattern. The Japanese dietary pattern was related to high sodium intake and high prevalence of hypertension. After adjustment for potential confounders, the Japanese dietary pattern score was associated with a lower risk of CVD mortality (hazard ratio of the highest quartile vs the lowest, 0.73; 95% confidence interval: 0.59-0.90; P for trend = 0.003). The 'animal food' dietary pattern was associated with an increased risk of CVD, but the DFA dietary pattern was not.

The Japanese dietary pattern was associated with a decreased risk of CVD mortality, despite its relation to sodium intake and hypertension.

Niacin: What forms are safe?

Niacin, or vitamin B3, remains a confusing issue for many people. It shouldn't be.

It doesn't help that most physicians and many pharmacists also do not understand the basic issues surrounding niacin. The only reason why there is any level of prevailing knowledge about niacin is that Kos Pharmaceuticals managed to "pharmaceuticalize" a niacin preparation, prescription Niaspan, that provided the revenue to fund professional "education."

Niacin can be helpful to increase HDL, reduce small LDL particles and shift them towards the more benign large particles, reduce triglycerides, and reduce lipoprotein(a).

So here's a brief description of the various forms that you will find niacin:

Immediate-release niacin--Also called crystalline niacin or just niacin. This is the original niacin that releases within minutes of ingestion. Because it releases rapidly, it triggers the most intense "hot flush." While this form of niacin works wonderfully well, is the safest, and is dirt cheap, the majority of people are simply unable to tolerate the intense flush. It also works best taken twice a day, generating two intolerable flushes per day.

Slow-release niacin--These preparations were popular in the 1980s, since the slow 12 to 24 hour pattern of release minimized the annoying hot flush. But, with prolonged use, it also became apparent that an unnaceptable frequency of liver toxicity developed. Unfortunately, this means that any niacin preparation that trickles niacin out over an extended period, including many of the slow-release preparations now sold in health food stores and pharmacies, have potential for liver toxicity. These preparations should be avoided.

6-hour release niacin--Releasing niacin more slowly than immediate-release niacin but more rapidly than slow-release niacin, 6-hour release (or what the Niaspan people call "extended-release" niacin) is nearly as effective as immediate-release niacin with approximately the same low potential for liver toxicity. It is far less liver toxic than slow-release niacin. 6-hour release niacin therefore offers the best balance between effectiveness and safety. Preparations that show this pattern of release include Niaspan ($180 per month), the poorly-named Sloniacin (about $8 per month), and Enduracin (about $7 per month) for 1000 mg per day. (Some Track Your Plaque Members have also determined that several other over-the-counter preparations have been demonstrated to share a similar pattern of release.)

Then there are the scam products that have no useful effect at all:

Flush-free or no-flush niacin--Inositol hexaniacinate, or 6 niacin molecules bound to the sugar, inositol, has no effect in humans, at least not with the dozen or so preparations that I've seen used. Nor are there any data to document the effectiveness of flush-free niacin. It's also more expensive.

Nicotinamide--This niacin derivative likewise has no effect on the usual targets for niacin treatment.

While I used to prescribe Niaspan, the ridiculous pricing and aggressive marketing really turned me off. I now advise my patients and our online followers to use only Sloniacin or Enduracin, unless you can tolerate immediate-release niacin.

Introduction to the New Track Your Plaque book, version 2.0


Out with the old,
in with the new  



“I believe that you are suffering from what is called a fatty degeneration of the heart.”

Dr. Tertius Lydgate to Mr. Casaubon on making a diagnosis with the new medical device, the stethoscope.

George Elliot
Middlemarch, 1871





Old notions in medicine have a peculiar way of lingering.

In 1882, Dr. Robert Koch discovered the tubercle bacillus in tissues of people with “consumption.” By connecting a bacterium with the disease, he usurped the long held notion that tuberculosis was a degenerative disease caused by lack of fresh air. But, for decades after Dr. Koch’s revelation, the “bad air” belief persisted. Surgical collapse of the lung, a painful and barbaric treatment for tuberculosis, persisted well into the 1960s, years after effective antibiotics were discovered in 1947.

The medical community of the 19th century viewed mental illness as the hereditary end-product of ancestral nervousness, alcoholism, prostitution and criminal behavior, a bias that remained widespread well into the mid-20th century. Nazi physicians invoked the theory of heritable “mental degeneration” to justify wholesale extermination of schizophrenics. Electro-convulsive therapy (ECT, or “electroshock therapy”) was widely applied to treat schizophrenia, depression, homosexuality, and criminal behavior for over 30 years, gradually abandoned (at least in its original form) after years of abusive application to subdue patients, demonized in the 1975 movie, “One Flew Over the Cuckoo’s Nest,” depicting the author’s real-life experience with ECT.

Long after a theory or practice has been discredited, it can persist, refusing to die. The new and improved may not be adopted into mainstream practice for years, even decades.

Back to the 21st century: What if you realized that, by quirks of human nature and the uneven adoption of health information, your doctor practiced medicine appropriate for 1985? 1975?

While digital information nowadays is transmitted at the speed of light, disseminating as fast as it takes the next juicy tidbit to be “virally” reproduced via social networking websites, it’s the human factor that still operates with the inertia of human behavior. Habits and attitudes slow the adoption of new information in time measured not in seconds, but in years or decades.

A century ago, 20 years were required for the new technology of blood pressure measurement to be adopted after its introduction in the U.S. in 1910, since physicians were long comfortable with the practice of “pulse palpation” (feeling the pulse). (The arcane language of pulse palpation persists to this day, terms like “pulsus parvus et tardus,” the slow rising pulse of a stiff aortic valve; and the "water-hammer" pulse of a leaking aortic valve.)

The discovery of new, health-changing information today in the 21st century disseminates through the ranks of modern healthcare providers at much the same pace as measuring blood pressure did in the early 20th century.

It’s also tempting to paint American medicine as a fiefdom intent on maintaining exclusive rein over health information. Look back over the hierarchical relationship of medicine over nursing in the past century: When blood pressure measurement was adopted on a broad scale in the 1930s, it was practiced only by physicians, since nurses were deemed incapable. (Modern-day nurses should surely have a hearty laugh over this.) Stethoscopes, around even longer than blood pressure cuffs, weren’t permitted to fall into the hands of nurses until the 1960s, since the medical community feared that nurses might command too much control over patient care. Even after nurses were permitted to have their own stethoscopes, great pains were taken to be certain the nurses’ version was readily distinguishable from the “real” tool wielded by physicians; nurses’ stethoscopes were therefore labeled “nurse-o-scopes,” or “assistoscopes,” and were required to be smaller and flimsier.

Old and ineffective doesn’t always give way to new and better at once; it is slowed by habit as well as an unwillingness to relinquish control.

Somehow technology marches on. But it does so unevenly, sweeping some along in its first wave, others in its wake, some never at all.

Just as effective antibiotics to cure tuberculosis were available for 20 years while surgeons continued to remove patients’ lungs, so better solutions to heart disease are already available but not yet employed by your neighborhood physician. The primary care physician may have heard about some of the newest means to prevent heart disease, but is too overwhelmed with the day-to-day of sore throats, diarrhea, and rashes. Cardiologists, intent on inserting the next best stent or defibrillator, have little but passing interest in strategies that might halt or reverse the heart disease that can be “managed,” no matter how imperfectly, with procedural solutions like angioplasty and bypass surgery. We should bear these flawed human tendencies in mind as we explore the world of heart disease prevention.

We need look no farther than the front page of the newspaper to find evidence of the failure of present-day heart disease detection and management. Over the past several years, headlines have carried the likes of Tim Russert, Bill Clinton, Larry King, Dick Cheney, David Letterman, Tommy Lasorda, Ed Bradley, Mike Ditka, Walter Cronkite, Alberto Salazar, all heart disease sufferers. Some, like talk show host David Letterman, survived their brush with heart catastrophe and underwent successful bypass surgery. Others, like marathoners Fixx and Salazar, raised none of the conventional red flags for heart disease. All received standard, “modern” medical care . . . all the way up to their heart attack, bypass surgery, or untimely death.

Like the sphygnomanometer (blood pressure) cuffs of 1910, Track Your Plaque represents an example of the new. But, unlike the simple practice of taking blood pressure in the early 20th century, Track Your Plaque represents an entirely new way to look at coronary heart disease: a new way to measure it, a new way to identify its causes, and a new way to seize control over it, often to the point of achieving reversal of the process. It also puts control over much of this process into your hands and away from hospitals, cardiologists, and heart procedures. 

I could speak of revealing “secrets,” but that’s not true. In Track Your Plaque, I simply convey information about heart disease that you were likely unaware existed, strategies that doctors fail to discuss. I assemble them into a “package” that, together, create an enormously empowering unique approach to prevent heart disease and heart attack.

Track Your Plaque also challenges the high-tech status quo, practices that occupy exalted places in the enormous cardiovascular healthcare machine that has dominated American healthcare for the past 40 years. I propose that high-tech hospital procedures should join the practice of ECT for homosexuality and insanity¾and become yet another relic of the past.

What are "normal" triglycerides?

Among the most neglected yet enormously helpful values on any standard cholesterol panel is the triglyceride value.

Triglycerides traverse the bloodstream by hitching a ride on water (serum)-soluble lipoproteins, or lipid-carrying proteins. We measure triglycerides as an indirect index of triglyceride-containing lipoproteins.

Triglycerides are a basic currency of energy. While the average American ingests around 300 mg of cholesterol per day, he or she also ingests 60,000-120,000 mg (60-120 grams) of triglycerides, i.e., 200 to 400 times greater amounts, from fat intake. Zero triglycerides in the diet or in the bloodstream is not an option.

But what represents too much triglycerides in the bloodstream? There are several observations to help us make this determination:

1) When fasting triglycerides are 133 mg/dl or greater, 80% of people will show show at least some degree of small LDL particles.

2) When fasting triglycerides are 60 mg/dl or less, most (though not all, since genetic factors enter into the picture) people will show little to no small LDL particles.

3) When fasting triglycerides are 200 mg/dl or greater, small LDL particles will dominate and large LDL particles will be in the minority or be gone entirely.

4) When triglycerides are 88 mg/dl or greater after eating, then risk for heart attack is doubled. Non-fasting triglycerides in the 400+ mg/dl range are associated with 17-fold greater risk for heart attack.



From Austin et al 1990. "Phenotype A" means that large LDL particles dominate; "phenotype B" means that small LDL particles dominate.

Note that conventional "wisdom" (i.e., NCEP ATP-3 guidelines) is that triglycerides of up to 150 mg/dl are okay, a level that virtually guarantees expression of small LDL particles and increased cardiovascular risk.

Based on observations like these, in the Track Your Plaque program we aim for fasting triglycerides of no higher than 60 mg/dl and postprandial (after-meal) triglycerides of no more than 90 mg/dl.

Curiously, while fat intake (i.e., triglyceride intake) plays a role in determining postprandial triglyceride blood levels, it's carbohydrate intake that plays a much larger role. That will be an issue for another day.

1985: The Year of Whole Grains

In 1985, the National Cholesterol Education Panel delivered its Adult Treatment Panel guidelines to Americans, advice to cut cholesterol intake, reduce saturated fat, and increase "healthy whole grains" to reduce the incidence of heart attack and other cardiovascular events.

Per capita wheat consumption increased accordingly. Wheat consumption today is 26 lbs per year greater than in 1970 and now totals 133 lbs per person per year. (Because infants and children are lumped together with adults, average adult consumption is likely greater than 200 lbs per year, or the equivalent of approximately 300 loaves of bread per year.) Another twist: The mid- and late-1980s also marks the widespread adoption of the genetically-altered dwarf variants of wheat to replace standard-height wheat.

In 1985, the Centers for Disease Control also began to track multiple health conditions, including diabetes. Here is the curve for diabetes:


Note that, from 1958 until 1985, the curve was climbing slowly. After 1985, the curve shifted sharply upward. (Not shown is the data point for 2010, an even steeper upward ascent.) Now diabetes is skyrocketing, projected to afflict 1 in 3 adults in the coming decades.

You think there's a relationship?

Have some more

Wheat, via exorphin effects, is an appetite stimulant. Eat a whole wheat bagel or bran muffin, you want another. You also want more of other foods. You also want something to eat every two hours due to widely-swinging insulin-glucose responses: blood sugar high followed by a sharp downturn that triggers a powerful impulse to eat (thus the cravings for a snack at 9 and 11 a.m. after a 7 a.m. breakfast).

If wheat is a stimulant of appetite, then removing it should yield reduced appetite and reduced calorie intake. That is precisely what happens.

When wheat products are removed from the diet--without calorie restriction, without counting fat or carbohydrate grams, no exercise program, no cleansing regimen, no skipping meals . . . nothing--calorie intake drops 350 to 400 calories per day. This calorie figure remains curiously consistent across multiple studies in which wheat was eliminated.

400 calories per day results in 21 lbs lost over 6 months, based just on calories. (3500 calories per pound lost.) That is what happens in wheat elimination diets: 21-26 lbs lost over 6 months.

Wheat is the processed food industry's nicotine, a means of ensuring repeat food purchases. It's also low-cost (subsidized by the U.S. government), high-yield, an ingredient that even has its very own withdrawal syndrome should you miss a "hit."

When MIGHT statins be helpful?

I spend a lot of my day bashing statin drugs and helping people get rid of them.

But are there instances in which statin drugs do indeed provide real advantage? If someone follows the diet I've articulated in these posts and in the Track Your Plaque program, supplements omega-3 fatty acids and vitamin D, normalizes thyroid measures, and identifies and corrects hidden genetic sources of cardiovascular risk (e.g., Lp(a)), then are there any people who obtain incremental benefit from use of a statin drug?

I believe there are some groups of people who do indeed do better with statin drugs. These include:

Apoprotein E4 homozygotes

Apoprotein E2 homozygotes

Familial combined hyperlipidemia (apoprotein B overproduction and/or defective degradation)

Cholesteryl ester transfer protein homozygotes (though occasionally manageable strictly with diet)

Familial heterozygous hypercholesterolemia, familial homozygous hypercholesterolemia

Other rare variants, e.g., apo B and C variants

The vast majority of people now taking statin drugs do NOT have the above genetic diagnoses. The majority either have increased LDL from the absurd "cut your fat, eat more healthy whole grains" diet that introduces grotesque distortions into metabolism (like skyrocketing apo B/VLDL and small LDL particles) or have misleading calculated LDL cholesterol values (since conventional LDL is calculated, not measured).

As time passes, we are witnessing more and more people slow, stop, or reverse coronary plaque using no statin drugs.

Like antibiotics and other drugs, there may be an appropriate time and situation in which they are helpful, but not for every sneeze, runny nose, or chill. Same with statin drugs: There may be an occasional person who, for genetically-determined reasons, is unable to, for example, clear postprandial (after-eating) lipoproteins from the bloodstream and thereby develops coronary atherosclerotic plaque and heart attack at age 40. But these people are the exception.

Advanced topics in nutrition

Nutrition in the modern world has become an increasingly problematic topic. From genetic modification to commercialized methods of mass production, we are having to navigate all manner of complex issues in food choices, particularly if ideal health, including maximal control over coronary plaque, is among our goals.

We will therefore be releasing a series of discussions on the Track Your Plaque website in the coming months, a series I call "Track Your Plaque Advanced Topics in Nutrition." These will be, as the series title suggests, discussions for anyone interested in more than the "eat a balanced diet" nonsense that issues from "official" sources. Among the topics to be covered:

1)Advanced Glycation End-products--both endogenous and exogenous, including peripheral issues like lipoxidation and acrylamides.

2)Dietary influences on LDL oxidation--including the concept of "glycoxidation." Protection from oxidative phenomena is not just about taking antioxidants.

3) Foods you MUST eat--We've talked a lot about foods that you shouldn't eat. How about foods you should eat?

The New Track Your Plaque Guide now available

The New Track Your Plaque Guide is now available!

The Track Your Plaque program has evolved over its 8 year history. While the original Track Your Plaque book reflected the program details that got the program started back in 2003-2004, plenty has changed.

This new version of the book, what I call the program Guide, represents version 2.0 of Track Your Plaque and includes:

--Updated lipoprotein treatment strategies--including new and expanded treatment choices for small LDL and lipoprotein(a).

--An entire chapter on vitamin D and its crucial role in cardiovascular health and plaque control.

--A new and expanded diet--All the reasons why the New Track Your Plaque Diet can achieve spectacular improvement in lipids/lipoproteins, reversal of insulin resistance/pre-diabetes/diabetes, weight loss, reduction in blood pressure, etc. are discussed in considerable detail. The diet is crafted to achieve maximum control over both metabolic responses and coronary plaque.

--An entire chapter on the role of omega-3 fatty acids is included.

--A detailed discussion on the role of iodine and thyroid health--One of the newest additions to the Track Your Plaque menu of strategies is to achieve and maintain ideal thyroid health. This tips the scales in your favor for improved control over lipids/lipoproteins, weight, blood sugar, and coronary plaque.


The new guide, as well as our new Member kits that include the new Track Your Plaque Recipe Book, At-Home Lab Test kits, and nutritional supplements, are all available in the Track Your Plaque Marketplace.

Don't wet yourself

While there is more to wheat's adverse effects on human health than celiac disease, studying celiac disease provides important insights into why and how wheat--the gluten component of wheat, in this case--is so destructive to human health.

Modern wheat, in particular, is capable of causing "celiac disease" without intestinal symptoms---no cramping or diarrhea--but instead shows itself as brain injury (ataxia, dementia), peripheral nervous system damage (peripheral neuropathy), joint and muscle inflammation (rheumatoid arthritis, polymyalgia rheumatica and others), and gastrointestinal cancers.

One neurological manifestation of wheat's effect on the human brain is a condition called cerebellar ataxia. This is a condition that can affect adults (average age 48 years) and children and consists of incoordination, falls, and incontinence.

Because brain tissue has limited capacity for healing and regeneration, symptoms of cerebellar ataxia usually improve slowly and modestly with meticulous elimination of wheat and other gluten sources.

Such observations are relevant even to people without celiac disease. Celiac disease sufferers are more susceptible to such extra-intestinal phenomena, but it can also happen in people without positive celiac antibodies.



Some references:

Neurological symptoms in patients with biopsy proven celiac disease

A total of 72 patients with biopsy proven celiac disease (CD) (mean age 51 +/- 15 years, mean disease duration 8 +/- 11 years) were recruited through advertisements. All participants adhered to a gluten-free diet. Patients were interviewed following a standard questionnaire and examined clinically for neurological symptoms. Medical history revealed neurological disorders such as migraine (28%), carpal tunnel syndrome (20%), vestibular dysfunction (8%), seizures (6%), and myelitis (3%). Interestingly, 35% of patients with CD reported of a history of psychiatric disease including depression, personality changes, or even psychosis. Physical examination yielded stance and gait problems in about one third of patients that could be attributed to afferent ataxia in 26%, vestibular dysfunction in 6%, and cerebellar ataxia in 6%. Other motor features such as basal ganglia symptoms, pyramidal tract signs, tics, and myoclonus were infrequent. 35% of patients with CD showed deep sensory loss and reduced ankle reflexes in 14%. Gait disturbances in CD do not only result from cerebellar ataxia but also from proprioceptive or vestibular impairment.



Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristics

Two hundred and twenty-four patients with various causes of ataxia from North Trent (59 familial and/or positive testing for spinocerebellar ataxias 1, 2, 3, 6 and 7, and Friedreich's ataxia, 132 sporadic idiopathic and 33 clinically probable cerebellar variant of multiple system atrophy MSA-C) and 44 patients with sporadic idiopathic ataxia from The Institute of Neurology, London, were screened for the presence of antigliadin antibodies. A total of 1200 volunteers were screened as normal controls. The prevalence of antigliadin antibodies in the familial group was eight out of 59 (14%), 54 out of 132 (41%) in the sporadic idiopathic group, five out of 33 (15%) in the MSA-C group and 149 out of 1200 (12%) in the normal controls. The prevalence in the sporadic idiopathic group from London was 14 out of 44 (32%). The difference in prevalence between the idiopathic sporadic groups and the other groups was highly significant (P < 0.0001 and P < 0.003, respectively). The clinical characteristics of 68 patients with gluten ataxia were as follows: the mean age at onset of the ataxia was 48 years (range 14-81 years) with a mean duration of the ataxia of 9.7 years (range 1-40 years). Ocular signs were observed in 84% and dysarthria in 66%. Upper limb ataxia was evident in 75%, lower limb ataxia in 90% and gait ataxia in 100% of patients. Gastrointestinal symptoms were present in only 13%. MRI revealed atrophy of the cerebellum in 79% and white matter hyperintensities in 19%. Forty-five percent of patients had neurophysiological evidence of a sensorimotor axonal neuropathy. Gluten-sensitive enteropathy was found in 24%. HLA DQ2 was present in 72% of patients. Gluten ataxia is therefore the single most common cause of sporadic idiopathic ataxia.
All posts by william-davis

Be patient with niacin

Mel's HDL started at 37 mg/dl one year ago. Mel had several other abnormal lipoprotein patterns along with his HDL (inc. small LDL and Lp(a)), but HDL was clearly a crucial factor in his panel.

With a heart scan score of 1166, we needed to raise Mel's HDL to the Track Your Plaque target of 60 mg/dl. So Mel started niacin, our number one method to raise HDL, in addition to reducing his exposure to wheat products and other high glycemic index foods; increasing his physical activity; trying to reduce his excess tummy fat; fish oil; dark chocolate (2 oz per day) and red wine (1-2 glasses per day, preferably dark French reds). The form of niacin we often choose is SloNiacin (Upsher Smith), available over-the-counter for about $12-14 per 100 tablets.

Mel started out with niacin 500 mg per day at dinner, increased to 1000 mg at dinner after four weeks. Although this is usually too soon to reassess HDL, Mel insisted. His HDL 41 mg/dl. Mel's disappointment was palpable. He was the usual type A personality: he wanted his HDL higher--now! So Mel insisted that we increase niacin to 1500 mg per day. (We never go higher than this if low HDL or small LDL is the indication for niacin; only when Lp(a) is present do we go higher.)

Six months into this process, HDL: 45 mg/dl. Still a sluggish response.

One year later, HDL: 68 mg/dl. Finally!

That is typical for niacin, as well as combination of lifestyle changes Mel made. None of them result in an immediate rise in HDL; all take months to 1-2 years to exert full HDL-raising effect.

Think of HDL as the 82-year old grandma who takes a long time to cross the street-she does get there!

Note: Doses of niacin >500 mg per day should be taken with medical supervision.

Can vitamin D be a SOLE risk factor?

Here's a crazy question. It occurred to me as I was talking to Drew, a slender, active 54-year old dentist with no bad habits including no smoking.

Drew's heart scan score was 222. His lipoprotein analysis mostly revealed a lot of nothing, which is unusual. The only pattern that showed up was a modestly high LDL of 122 mg/dl with a very slight excess of small LDL. That's it. I would not be satisfied that these were sufficient cause for Drew's level of coronary plaque.

Drew's 25-OH-vitamin D3 level: 15 ng/ml--severe deficiency--despite the fact that his doctor had suggested that he take a vitamin D2 preparation. In other words, Drew had been profoundly deficient, probably for years.

Given the unimpressive cholesterol and lipoprotein values, could vitamin D serve as a trigger for coronary plaque all by itself?

I don't have an answer and know of nobody else who does. However, my opinion is that vitamin D is indeed a potent risk that can cause heart disease as a sole risk factor.

Perhaps it's another piece of circumstantial evidence suggesting that vitamin D has an enormous influence on health, including coronary plaque. Interestingly, the only other health problem Drew has had is prostate cancer, treated a few years ago with prostate removal and radiation. Good evidence suggests that vitamin D deficiency escalates risk of prostate cancer substantially.

By the way, I've seen people taking vitamin D2 preparations, called "ergocalciferol," who are every bit as deficient as those who take no vitamin D at all. Avoid D2 or ergocalciferol preparations: they're worthless.

Does fish oil raise LDL cholesterol?

Katie had an LDL (conventionally calculated) of 87 mg/dl, HDL of 48 mg/dl.

She added fish oil, 6000 mg per day. Three months later her LDL was 118 mg/dl, HDL 54 mg/dl. In other words, LDL increased by 31 mg. What gives?

Several studies have, indeed, shown that fish oil raises LDL cholesterol, usually by 5-10 mg/dl. Occasionally, it may be as much as 20-30.

Unfortunately, many physicians often assume that it's the (minor) cholesterol content of fish oil capsules, or some vague, undesirable effect of fish oil. It's nothing of the kind.

Since we based Katie's program on (NMR) lipoprotein analysis, not conventional lipids (HDL, calculated LDL, triglycerides, total cholesterol), I knew that Katie also had a severe excess of intermediate-density lipoprotein, or IDL, and very-low density lipoproteins, VLDL. This signifies that after a meal, dietary fats persist for 12, 24,or more hours. Fish oil is a very effective method to clear IDL and VLDL, though sometimes it also causes a shift of some IDL and VLDL into the LDL class. Thus, the apparent increase in LDL.

Another contributor: Conventional LDL is a calculated value, not measured. The calculation for LDL is thrown off by any reduction in HDL or rise in triglycerides. In Katie's case, the rise in HDL from 48 to 54 means that calculated LDL is becoming more accurate and rising towards the true measured value. At the start, Katie's true measured LDL was 122 mg/dl, 35 mg higher than the calculated value. Calculated LDL is therefore approximating measured LDL more accurately as HDL rises.

The most important lesson to learn is that, if LDL rises significantly on fish oil and you haven't had lipoproteins formally measured, there may have been a substantial postprandial abnormality like IDL that was unrecognized.

Heart disease is everywhere

If you ever need convincing that heart disease is everywhere, you should do what I do: subscribe to Google Alerts and have them forward news anytime the search phrase "heart attack" crosses the web. (Just go to Google, click on "more" to the right of the search bar, and follow the links.)


Some recent samples:


Workmates resuscitate driver after heart attack

A woman coal mine truck driver had a heart attack and required resuscitation with a defibrillator 3 times on the way to the hospital.





Heart attack kills groom at reception
A 34-year old man died during his wedding reception, leaving behind his 26-year old new wife.






Heart attack ruled as cause of crash

An Alabama man drove his pick-up truck into oncoming traffic while suffering a heart attack.






Heart-attack victim to return to Hamburg stage


Country music artist, Michael Harding, suffered a heart attack and cardiac arrest during a performance. He is apparently recovered and returning to the stage.



That's just a sample from the last two days. While you and I are carry on a conversation on reversal of heart disease, our neighbors and friends drop over every day. Even though I witness successful heart disease reversal routinely, the rest of the world is not participating.

Pass it on: Coronary disease is identifiable, preventable, controllable, and reversible.

Watch your weight plummet:Be a super vegetarian

Here's a neat trick for losing weight: Become a strict vegetarian for 3 days.

Before you yawn or say "Yecchhhh!", let me elaborate.

Pick some time period. It doesn't have to be 3 days. It could be 2 days, or 5 days, or two weeks. But, for the period you choose, eat only vegetables. No meat, cereals, breads, milk, cookies, etc.

Vegetables alone could get monotonous, so make them interesting. Possibilities include:


--Hummus--add a little bit of olive-oil, chopped garlic, paprika, red pepper.

--Tabouleh--I get mine from Trader Joe's and it's delicious.

--Salsa--Low in calories, rich in lycopene and other flavonoids, with no nutritional downside. Also, pico de gallo--chopped tomatoes, onions, jalapeno chiles, cilantro, cucumbers.

--Mustards--hot, yellow, brown, spicy, gourmet, horseradish, etc.

--Cocktail sauce--i.e., ketchup and horseradish. Use the low-carb ketchup made without high fructose corn syrup.

--Tapenades--e.g., olive tapenade made with chopped olives, capers, and olive oil.
--Pesto-made with basil, garlic, and olive oil.

--Spices and herbs--basil, arugula, peppers, mustard powder, garlic, cilantro, ginger, etc.

--Vinegars--wine, Balsamic, rice, apple cider.

--Infused olive oils--infused with garlic is especially delicious,e.g., added to hummus.

--Bean dips--white bean dip, roasted bean dip, etc.





With the varieties of ways to jazz up your vegetables, you couldn't possibly be bored.

For example, for breakfast on day 1, eat sliced cucumbers and green peppers dipped in garlic-infused olive oil hummus and a handful of almonds. For a snack, some walnuts, sunflower seeds, sliced zucchini dipped in salsa. For lunch, a salad with an olive oil and balsamic vinegar dressing. For dinner, tablouleh, a cucumber and tomato salad, celery sticks dipped in pico de gallo.

All vegetables can be eaten without restricting portion size, since calorie content of vegetables are so low compared to other calorie-dense foods. (See The Heart Scan Blog from a few days back, "One bit or many mouthfuls?" at http://heartscanblog.blogspot.com/2007/01/one-bite-or-many-mouthfuls.html.)

This approach works nearly as well as fasting. A half-pound per day weight loss or more is common and painless. You'll also feel great living on low glycemic index foods.

(Photos courtesy Wikipedia.)

Dr. Agatston to the rescue


Dr. Arthur Agatston, author of wildly successful South Beach Diet, has just released a new book titled The South Beach Heart Program. Dr. Agatston has started on a media speaking circuit to promote his book and concepts.


A reporter from Time, who interviewed Dr. Agatston, commented:

". . .not enough doctors prescribe niacin for their heart patients, even though the medicine is a proven treatment for raising 'good' cholesterol. Physicians are reluctant, Agatston suggests, because niacin requires diligent follow-up to watch for side effects, taking time that most primary-care practices cannot afford. On the other hand, he says, too many doctors are performing heart operations that represent a financial windfall for hospitals. Bottom line: there isn't as much money to be made in prevention as in treatment."

Amen.

Dr. Agatston echoes many of the concepts that the Track Your Plaque program advocates. His notoriety is going to help disseminate the idea that 1) CT heart scans are the #1 method to identify hidden atherosclerotic coronary plaque, 2) taking control of your heart scan score is the best way to seize hold of your future, and 3) the present-day popularity of heart procedures like stents and bypass is intolerable, inexcusable, and needs to be reined back.

Agatston also brings great credibility and fairness to the conversation and his comments will gain tremendous attention in the press and with the public.

When is a vitamin not a vitamin?

When it's a hormone.

That's the stand that several researchers in vitamin D have taken and I think they're right. Dr. John Cannell has made a fuss over this in his www.vitamindcouncil.com website.

Structurally, vitamin D is most closely related to testosterone, estrogen, and cortisol. You wouldn't call testosterone vitamin T, would you?

Vitamins are also meant to be obtained from food. Yes, vitamin D is in milk but only because humans are required to put it there to prevent childhood rickets. Otherwise, the only substantial food source of vitamin D is in oily fish like salmon and then only a modest quantity.

Vitamin D is cholecalciferol, a hormone. Deficiencies of hormones can have catastrophic consequences. Imagine that every winter your thyroid gland shuts down and produced no thyroid hormone. You'd get very ill, gain 30 lbs, lose your hair, feel awful.

That's what happens when you're sun deprived and thereby deficient in cholecalciferol--you're deficient in a hormone. And it happens to most of us every year for many months.

I continue to witness spectacular effects by bringing 25-OH-vitamin D3 blood levels to 50 ng/ml with supplementation, including an apparent surge in success dropping heart scan scores.

An epidemic of heart disease reversal

Heart disease reversal is nothing new in my office. However, I have to admit that it's not something that generally happens each and every day.

As our approach is refined, we are witnessing an unprecedented frequency of plaque reversal. Since Monday (today is Tuesday), I've seen four people who have regressed their coronary plaque and dropped their heart scan score.

Pat was the most recent addition to this list. At age 53, I was honestly surprised at the ease of dropping her heart scan score from 128 to 42 in the space of a year. I was surprised because among her lipoprotein patterns was the dreaded combination of lipoprotein(a) and small LDL, probably the most aggressive risk for heart disease I know of and also among the most difficult to gain control over. She also suffered a deep personal tragedy in her family, an emotional convulsion that can sometimes wipe out any hope of plaque reversal.

I'm hopeful that this virtual epidemic of heart disease reversal continues. And I hope that you participate in it.

Second heart scan and heart attack risk

At first, Joe felt disappointed, defeated, and frightened. After his heart scan, a radiologist at the center told him that his score of 264 was moderately high. He told Joe that he was at moderate risk for heart attack and that a nuclear stress test was going to be required.

This left Joe feeling confused. After all he'd had a heart scan 18 months earlier and his score was 278, 5% higher.

I reassured Joe that the radiologist had not been aware that Joe had a prior heart scan. The radiologist didn't know that Joe's heart scan score had actually been reduced.

In fact, Joe's risk for heart attack was not moderate--it is now very low, since his score was 5% lower. While growing plaque is active plaque, shrinking plaque is inactive plaque and thereby at far less risk for heart attack.

I wrote about this phemonenon in a previous Blog: When is a heart scan score of 400 better than 200? at http://heartscanblog.blogspot.com/2006_09_01_archive.html. When you've had more than one scan, the risk for heart attack suggested by the score takes a back seat to the rate of change of your score. In other words, even though Joe's score of 264 represented a moderate risk (of approximately 3% per year, roughly 30% over 10 years), this no longer held true, since it actually represented a 5% decrease over a previous score.

Joe's risk for heart attack is probably close to zero. ALWAYS view your second (or any subsequent) heart scan score in the context of your previous score, not in isolation.

Track Your Plaque newsletter subscribers: We will detail more of Joe's story in the coming January 2007 newsletter. If you'd like to read or subscribe to the newsletter, go to http://www.cureality.com/f_scanshow.asp.

Heart scan curiosities #5

Despite the controversy over drug-coated stents, I maintain that the best stent is no stent at all.

Yes, there are indeed times when such things are necessary, but not with the frequency that they are implanted nowadays.

Another reason why stents are an undesirable phenemenon is that they muck up your heart scan. Take a look:





The long white object in the center is a stent in the left anterior descending artery of this 60 year old man. Just beyond the stent (at about 1 o'clock from the stent) is a plaque that could be scored. However, you can see that, with the presence of the stent, the bulk of this artery is no longer "scorable". If this man wishes to "track his plaque", he will have to be content with tracking only the circumflex and right coronary arteries, the other two arteries without stents.

The stainless steel or similar metallic materials of current stents simply prevent us from seeing through them for plaque scoring purposes. It's best if you can simply avoid getting one for this and other reasons.

Track Your Plaque Members: Watch for the upcoming editorial by our Heart Hawk on drug-eluting stents.

Wheat brain

Among the most common effects of wheat are those on the brain.

Consume wheat and susceptible individuals will experience a subtle euphoria. Others experience mental cloudiness or sleepiness. (This is what I personally get.)

It gets worse. Children with ADHD and autism have difficulty concentrating on a task and have behavioral outbursts after a cookie. Schizophrenics experience paranoid delusions, auditory hallucinations, and worsening of social detachment. People with bipolar disorder can have the manic phase triggered by a breadcrumb. All these effects are blocked by administering drugs that block the brain's opiate receptors. (This is why, by the way, a drug company is planning to release an oral agent, naltrexone, formerly administered to heroin addicts to help control addiction, for weight loss: block the euphoric effect, take away the temptation, lose weight.)

Here is Heart Scan Blog reader, Nicole's, mental fog story:

I have been grain-free (no gluten free grains either) for quite a long time (about a year and a half). Earlier this week, I decided to try white bread and pasta. The experiment only lasted two days. I had horrible terminal insomnia both nights, causing me on the second night to wake up at 2:30 am unable to get back to sleep at all. I felt drugged and in a mind-fog all the next day and even dozed off a few times! Luckily I had the day off work.

I had very bad forgetfulness also. I forgot that I left my bag and groceries at work, so I had to go back for them. Then I had to use my husband's keys to get in because I thought my keys were in my bag, but it turns out they were in my pocket. Then I got my bag, set the alarm, locked the door and then realized I forgot my groceries. So I had to re-open the door, unset the alarm, and go back for the groceries. Then I locked the door, forgetting to set the alarm, so I had to unlock it, open up and set the alarm. It was just ridiculous, I am NEVER like that!

In addition to the insomnia and forgetfulness, I also had horrible anxiety and paranoia, almost to the point of panic. Which I NEVER have, I am usually very easy-going, even-tempered, and worry-free. But this was horrible, I really was quite paranoid and anxious about everything. Weird!

And the worst, was that in just two days of eating wheat, I gained 4 lbs and 2% bodyfat!! It's two days wheat-free now, and it's finally going back down, but wow. Just two days of wheat-eating caused that much weight and fat gain!

Anyway, I've learned my lesson and will continue to avoid grains (including gluten free grains) entirely.


Eat more "healthy whole grains"? Modern dwarf Triticum aestivum, perverted even further by agricultural geneticists and modern agribusiness, subsidized by the U.S. government to permit $5 pizza, is better than any terrorist plot to discombobulate the health and performance of the American people.

The Westman Diet

Dr. Eric Westman has been a vocal proponent of carbohydrate restriction to gain control over diabetes, as have Drs. Richard Bernstein, Mary Vernon, Richard Feinman, and Jeff Volek.

Several studies over the years have demonstrated that reductions in carbohydrate content of the diet yield reductions in weight and HbA1c (glycated hemoglobin, a reflection of average blood glucose over the preceding 60-90 days).

Among the more important recent clinical studies is a small experience from Duke University's Dr. Eric Westman. In this study, obese type 2 diabetics reduced carbohydrate intake to 20 grams per day or less: no wheat, oats, cornstarch, or sugars. Participants ate nuts, cheese, meats, eggs, and non-starchy vegetables.

After 6 months, average weight loss was 24.4 lbs, BMI was reduced from 37.8 to 34.4. At the end of the study, 95% of participants on this severe carbohydrate restriction reduced or eliminated their diabetes medications.

That was only after 6 months. Note that the ending BMI was still quite well into the obese range. Imagine what another 6-12 months would do, or achieving BMI somewhere closer to ideal.

Curiously, this idea of severe low-carbohydrate restriction to cure or minimize diabetes is not new. Sir William Osler, one of the founders of Johns Hopkins Hospital and author of the longstanding authoritative text, Principles and Practice of Medicine, advocated an diet identical to Dr. Westman's diet. So did Dr. Frederick Banting, discoverer of the pancreatic extract, insulin, to treat childhood diabetics. Before insulin, Banting and his colleagues at the University of Toronto used carbohydrate elimination (less than 10 g per day) to prolong the lives of children with diabetes.

This lesson was also learned many times during war time, when staples like bread were unavailable. The Siege of Paris in 1870 yielded cures for diabetes in many (or at least they stopped passing urine that tasted--yes, tasted--sweet and attracted flies), only to have it recur after the siege was over.

These are lessons we will have to relearn. As long as the American Diabetes Association and most physicians continue to advocate a diet of reduced fat, increased carbohydrate that includes plenty of "healthy whole grains," diabetics will continue to be diabetics, taking their insulin and multiple medications while developing neuropathy (nervous system degeneration), nephropathy (kidney disease and failure), atherosclerosis and heart attack, cataracts, and die 8 to 10 years earlier than non-diabetics.

All the while, we've had the combined wisdom from antiquity onwards: Carbohydrates cause diabetes; elimination of carbohydrates cures diabetes.

(This applies, of course, only to adult overweight type 2 diabetics, not type 1 or some of the other variants.)

Handy dandy carb index

There are a number of ways to gauge your dietary carbohydrate exposure and its physiologic consequences.

One of my favorite ways is to do fingerstick blood sugars for a one-hour postprandial glucose. I like this because it provides real-time feedback on the glucose consequences of your last meal. This can pinpoint problem areas in your diet.

Another way is to measure small LDL particles. Because small LDL particles are created through a cascade that begins with carbohydrate consumption, measuring them provides an index of both carbohydrate exposure and sensitivity. Drawback: Getting access to the test.

For many people, the most practical and widely available gauge of carbohydrate intake and sensitivity is your hemoglobin A1c, or HbA1c.

HbA1c reflects the previous 60 to 90 days blood sugar fluctuations, since hemoglobin is irreversibly glycated by blood glucose. (Glycation is also the phenomenon responsible for formation of cataracts from glycation of lens proteins, kidney disease, arthritis from glycation of cartilage proteins, atherosclerosis from LDL glycation and components of the arterial wall, and many other conditions.)

HbA1c of a primitive hunter-gatherer foraging for leaves, roots, berries, and hunting for elk, ibex, wild boar, reptiles, and fish: 4.5% or less.

HbA1c of an average American: 5.2% (In the population I see, however, it is typically 5.6%, with many 6.0% and higher.)

HbA1c of diabetics: 6.5% or greater.

Don't be falsely reassured by not having a HbA1c that meets "official" criteria for diabetes. A HbA1c of 5.8%, for example, means that many of the complications suffered by diabetics--kidney disease, heightened risk for atherosclerosis, osteoarthritis, cataracts--are experienced at nearly the same rate as diabetics.

With our wheat-free, cornstarch-free, sugar-free diet, we have been aiming to reduce HbA1c to 4.8% or less, much as if you spent your days tracking wild boar.

Battery acid and oatmeal

Ever notice the warnings on your car's battery? "Danger: Sulfuric acid. Protective eyewear advised. Serious injury possible."

Sulfuric acid is among the most powerful and potentially harmful acids known. Get even a dilute quantity in your eyes and you will suffer serious burns and possibly loss of eyesight. Ingest it and you can sustain fatal injury to the mouth and esophagus. Sulfuric acid's potent tendency to react with other compounds is one of the reasons that it is used in industrial processes like petroleum refining. Sulfuric acid is also a component of the harsh atmosphere of Venus.

Know what food is the most potent source of sulfuric acid in the body? Oats.

Yes: Oatmeal, oat bran, and foods made from oats (you know what breakfast cereal I'm talking about) are the most potent sources of sulfuric acid in the human diet.

Why is this important? In the transition made by humans from net-alkaline hunter-gatherer diet to net-acid modern overloaded-with-grains diet, oats tip the scales heavily towards a drop in pH, i.e., more acidic.

The more acidic your diet, the more likely it is you develop osteoporosis and other bone diseases, oxalate kidney stones, and possibly other diseases.

Here's one reference for this effect.

What'll it be: Olive oil or bread?

We frequently discuss the advisability of consuming fats, carbohydrates, and various types within each category.

But what's the worst of all? Combining fats with carbohydrates.

Putting aside the wheat-is-worst form of carbohydrate issue and treating bread as a prototypical carbohydrate, let's play out a typical scenario, a make-believe feeding study in which a theoretical person is fed specific foods.

John is our test person, a 40-year old, 5 ft 10 inch, 210 lb, BMI 27.7 (roughly the mean for the U.S.) He starts with an average American diet of approximately 55% carbohydrates and 30% fat. Starting lipoproteins (NMR):

LDL particle number 1800 nmol/L
Small LDL 923 nmol/L


(The LDL particle number of 1800 nmol/L translates to measured LDL cholesterol of 180 mg/dl, i.e., drop last digit or divide by 10.)

Also, calculated LDL cholesterol is 167 mg/dl (yes, underestimating "true" measured LDL), HDL 42 mg/dl, triglycerides 170 mg/dl.

We feed him a diet increased in carbohydrates and reduced in fat, especially saturated fat, with more breakfast cereals, breads and other wheat products, pasta, fruit juices and fruit, and potatoes. After four weeks:

LDL particle number 2200 nmol/L
Small LDL 1378 nmol/L

Note that LDL particle number has increased by 400 nmol/L due entirely to the increase in small LDL particles triggered by carbohydrate consumption. Lipids show calculated LDL cholesterol 159 mg/dl--yes, a decrease, HDL 40 mg/dl, triglycerides 189 mg/dl. (At this point, if John's primary care doctor saw these numbers, he would congratulate John on reducing his LDL cholesterol and/or suggest a fibrate drug to reduce triglycerides.)

John takes a rest for four weeks during which his lipoproteins revert back to their starting values. We then repeat the process, this time replacing most carbohydrate calories with fats, weighed heavily in favor of saturated fats like fatty red meats, butter and other full-fat dairy products. After four weeks:

LDL particle number 2400 nmol/L


Let's

Chocolate peanut butter cup smoothie

Here's a simple recipe for chocolate peanut butter cup smoothie.

The coconut milk, nut butter, and flaxseed make this smoothie exceptionally filling. If you are a fan of cocoa flavonoids for reducing blood pressure, then this provides a wallop. Approximately 10% of cocoa by weight consists of the various cocoa flavonoids, like procyanidins (polymers of catechin and epicatechin) and quercetin, the components like responsible for many of the health benefits of cocoa.


Ingredients:
1/2 cup coconut milk
1 cup unsweetened almond milk
2 tablespoons cocoa powder (without alkali)
2 tablespoons shredded coconut (unsweetened)
1 tablespoon ground flaxseed
1 teaspoon almond extract
1 1/2 tablespoons natural peanut, almond, or sunflower seed butter
Non-nutritive sweetener to taste (stevia, Truvia, sucralose, xylitol, erythritol)
4 ice cubes

Combine ingredients in blender. Blend and serve.

If you plan to set any of the smoothie aside, then leave out the flaxseed, as it absorbs water and will expand and solidify if left to stand.

For an easy variation, try adding vanilla extract or 1/4 cup of sugar-free (sucralose) vanilla or coconut syrup from Torani or DaVinci and leave out the added sweetener.

The compromise I draw here is the use of non-nutritive sweeteners. Beware that they can increase appetite, since they likely trigger insulin release. However, this smoothie is so filling that I don't believe you will experience this effect with this recipe.

Letter from the insurance company

Claudia got this letter from her health insurance company:

Dear Ms. ------,

Based on a recent review of your cholesterol panel of January 12, 2011, we feel that you should strongly consider speaking to your doctor about cholesterol treatment.

Reducing cholesterol values to healthy levels has been shown to reduce heart attack risk . . .


Okay. So the health insurer wants Claudia to take a cholesterol drug in the hopes that it will reduce their exposure to the costs for her future heart catheterization, angioplasty and stent, or bypass surgery. This is understandable, given the extraordinary costs of such hospital services, typically running from $40,000 for a several hour-long outpatient catheterization procedure, to as much as $200,000 for a several day long stay for coronary bypass surgery.

So what's the problem?

Here are Claudia's most recent lipid values:

LDL cholesterol 196 mg/dl
HDL 88 mg/dl
Triglycerides 37 mg/dl
Total cholesterol 291 mg/dl

By the criteria followed by her health insurer, both total and LDL cholesterol are much too high. Note, of course, that LDL cholesterol was a calculated value, not measured.

Here are Claudia's lipoproteins, drawn simultaneously with her lipids:

LDL particle number 898 nmol/L
Small LDL particle number less than 90 nmol/L (Values less than 90 are not reported by Liposcience)

LDL particle number is, by far and away, the best measure of LDL particles, an actual count of particles, rather than a guesstimate of LDL particles gauged by measuring cholesterol in the low-density fraction of lipoproteins (i.e., LDL cholesterol). It is also measured and is highly reproducible.

To convert LDL particle number in nmol/L to an LDL cholesterol-like value in mg/dl, divide by ten (or just drop the last digit).

Claudia's measured LDL is therefore 89 mg/dl--54% lower than the crude calculated LDL suggests.

This is because virtually all of Claudia's LDL particles are large, with little or no small. This situation throws off the crude assumptions built into the LDL calculation, making it appear that she has very high LDL cholesterol.

Do you think that Big Pharma advertises this phenomenon?

Healthy smoothies

I've now seen several people who have either caused themselves to be diabetic or to have other phenomena associated with excessive consumption of carbohydrates, all by innocently indulging in a carbohydrate-packed smoothie every morning.

Kay, for instance, has a smoothie of a half-pint blueberries, a banana, a scoop of whey, low-fat yogurt, a cup of milk every morning. The rest of her diet was fairly healthy: salads with oil-based dressing for lunch, salmon and asparagus for dinner, only an occasional carbohydrate indulgence outside of her morning smoothie ritual. Yet she had a HbA1c (a reflection of prior 60 to 90 days average blood sugar) at the near-diabetic range of 5.9%.

The mistake most people make when making smoothies is relying too heavily on carbohydrates like fruit. A smoothie like the one made by Kay can easily top 50, 60, or 70 grams carbohydrates per serving, more than sufficient to send blood sugars up to 150 mg/dl or more.

So what can you put in your smoothie and not send you over the edge to diabetes, small LDL, and all the other undesirable phenomena of excessive carbohydrates? Here's a list:

--coconut milk, unsweetened almond milk. Less desirable: milk, full-fat soymilk
--ground flaxseed
--oils: flaxseed oil, coconut oil (melted), extra-light olive oil, walnut oil
--dried coconut
--extracts: vanilla, almond, coconut, cherry, hazelnut
--spices: cinnamon, nutmeg, ginger
--herbs: mint leaves, cilantro
--cocoa powder (unsweetened)
--nut or seed butters (peanut butter, almond butter, sunflower seed butter)
--tofu
--exotic ingredients (ingredients you wouldn't expect in a smoothie): spinach, kale, cucumber

How do you sweeten a smoothie? This is what trips up most people. If you resort to fruit like bananas, pineapple, or apple, you will readily send your blood sugar skyward. Honey, agave syrup, and sugar, of course, all increase blood sugar and/or have the adverse effects of fructose. Be careful of yogurt, also, for similar reasons.

Therefore, to sweeten your smoothie, consider:

--Small servings of berries, e.g., 8-10 blueberries, 2 strawberries, a few wedges of apple, half a kiwi
--Non-nutritive sweeteners like stevia, Truvia, sucralose, xylitol, erythritol. Also, sugar-free (sucralose-based) syrups like those from DaVinci and Torani are useful. (Just be aware that non-nutritive sweeteners can increase appetite--use sparingly.)

Also, note that, if you have divorced yourself from wheat, cornstarch, and sugars, your desire for sweet should be much reduced. Foods other people find just right will taste sickeningly sweet to you. You might therefore find that foods like peanut butter or coconut milk have a mild natural sweetness; added sweetness is only minimally necessary.

Coming next: I'll share a smoothie recipe or two of mine. Anyone want to share a recipe?

Insulin secretagogue

Dairy products have the peculiar property of triggering pancreatic release of insulin. The research group at Lund University in Sweden have contributed the most to documenting this phenomenon:




Mean (±SEM) incremental changes (?) in serum insulin in response to equal amounts of carbohydrate from a white-wheat-bread reference meal (x) and test meals of whey (?), milk (?), cheese (?), cod (?), gluten-low (?), and gluten-high (?) meals. From Nilsson 2004.

Note that it is the area under the curve (AUC), not the peak value, that assumes greatest importance.

Dairy products, especially milk, whey, and yogurt, are insulin secretagogues: they stimulate pancreatic release of insulin. The effect is likely due to amino acids and/or polypeptides in dairy products. (The effect is less prominent with cheese. Also see this study.)

By conventional wisdom, this may be a good thing, since the excess insulin will blunt the glucose rise after consumption. However, in my book, this is not such a good thing, since most of us have tired, beaten, overworked pancreatic beta cells from our decades of carbohydrate overconsumption. I fear that the effect of dairy products just take us a bit closer to beta cell failure: diabetes.

Good news: The effect is least with cheese.

Be gluten-free without "gluten-free"

While I've discussed this before, it is such a confusing issue that I'd like to discuss it again.

I advocate wheat elimination because consumption of products made from modern dwarf Triticum aestivum:

--Triggers formation of extravagant quantities of small LDL and LDL particle number (or apoprotein B)
--Triggers inflammatory phenomena like c-reactive protein, increases leptin resistance, and reduction of the protective adipocytokine, adiponectin.
--Encourages accumulation of deep visceral fat ("wheat belly") that is inflammatory and causes resistance to insulin
--Increases blood sugar more than nearly all other foods--higher than a Milky Way bar, higher than a Snickers bar, higher than table sugar.
--Is being linked to a growing number of immune-mediated diseases, including celiac disease (quadrupled over past 50 years), type 1 diabetes in children, and cerebellar ataxia and peripheral neuropathies.

This last group of wheat-related phenomena are primarily due to gluten, the collection of 50+ proteins found in each wheat plant. For this reason, people diagnosed with celiac disease are advised to eliminate gluten from wheat and other sources (barley, rye, triticale, bulgur) and to eat gluten-free foods.

Gluten-free has therefore come to be viewed as wheat-free and problem-free. It ain't so.

Among the few foods that increase blood glucose higher than wheat: cornstarch, rice starch, potato starch, and tapioca starch--Yup: the ingredients commonly used to replace wheat in gluten-free foods. They are also flagrant triggers of the small LDL pattern, along with increased triglycerides, reduced HDL, increased visceral fat, increased blood pressure. In short, gluten-free foods lack the immune and brain effects of wheat gluten, but still make you fat, hypertensive, and diabetic.

I tell patients to view gluten-free foods like jelly beans: Gluten-free pancakes, muffins, breads, etc. are indulgences, not healthy replacements for wheat. It's okay to have a few jelly beans now and then. But they should not be part of a frequent or daily routine. Same with gluten-free foods.
All posts by william-davis

Optimal medical therapy

I was re-reading some of the details behind the recently announced COURAGE Trial comparing angioplasty/stent in 1100 people compared to "optimal" medical therapy in another 1100. You'll recall that no difference was found.

In particular, over approximately 5 years, 20% of participants in each group died, experienced heart attacks, or strokes. Of those treated with "timal" medical therapy, 32% ended up getting a procedure like stents or bypass anyway due to deteriorating symptoms.

What is "optimal" medical therapy? I bring this up again because the study investigators in COURAGE, as well as in similar trials, say this with a straight face. Optimal medical therapy means aspirin and/or Plavix (the anti-platelet, aspirin-like blood thinner); "aggressive" statin drug therapy to reduce LDL cholesterol to 60-85 mg/dl; and "anti-ischemic" therapy (that reduces angina and the phenomena of poor coronary blood flow) using nitroglycerin preparations, beta blockers, and other drugs.

I do give credit to the investigators for having the courage to perform this trial in a world hell bent on doing procedures and still reporting the neutral outcome. But the notion of "optimal" medical therapy begs for comment.

Indeed, this is regarded as optimal by most practitioners. Some would even argue excessive, based on the low LDL target achieved. Would you be satisfied with a 20% likelihood of heart attack, stroke, or death or 5 years, a 1 in 5 roll of the dice? I would not. Recall that we aim for near-total elimination of risk.

What could have been further "optimized"? Plenty. For instance:

--What is the real LDL, not the fabricated, calculated LDL? The two can be commonly 100 mg/dl different.

--How about raising HDL to 60 mgd/?

--What about reducing the proportion of small LDL particles? After all, small LDL is the number one cause of heart disease in the U.S., not high LDL.

--What is Lp(a)? If you treat LDL with a statin drug, Lp(a) is unaffected and continues to trigger huge plaque growth. You will fail if this is not identified and corrected.

--What is vitamin D3? One of the most powerful facilitators of plaque reversal I know of.

--What are triglycerides? Triglycerides create hidden particles in the blood like intermediate-density lipoprotein, potent triggers for coronary plaque growth. Speaking of intermediate-density lipoprotein, that's another very important pattern to identify, the after-eating persistence of dietary fats.

--Why aren't they taking fish oil? With a 28% reduction in heart attack and 45% reduction in sudden death from heart attack, this alone would have halved the number of "events" in the "optimal" medical treatment group.

Of course, there's more. But the idea that aspirin, statins, and anti-ischemic therapy is somehow optimal is silly and sad at the same time. But that's the bias. The COURAGE Trial does represent a step forward, a step away from the "stent everyone and everything" mentality that motivates my colleagues, aided and abetted by their co-conspirators, the hospitals. But you and I know better. "Optimal" medical therapy, in truth, can mean a far better approach that can dramatically reduce, perhaps eliminate, risks for events like heart attack. The conventional "optimal" medical therapy will suffice only if you're content with a 20% likelihood of heart attack, death or stroke, or a 32% likelihood of an urgent procedure in your future.

Niacin, postprandial patterns

For a detailed report on the very important postprandial (after eating) patterns that contribute hugely to heart disease risk, read my recent article in Life Extension Magazine, available (no cost) at:

Uncovering a Hidden Source of Cardiovascular Disease Risk
at http://www.lef.org/magazine/mag2007/mar2007_report_heart_01.htm


For a report on using niacin to reduce risk of heart disease, see another report in the same issue of Life Extension:

Ask the Doctor: Using Niacin to Improve Cardiovascular Health
at
http://www.lef.org/magazine/mag2007/mar2007_atd_01.htm.

Also, keep your eyes open for a lengthy report focused exclusively on the Track Your Plaque program in an upcoming issue of Life Extension. I'll provide links in this Blog when it comes out.

What's better than fish oil?

One of the recent questions on our Track Your Plaque Forum related to what to do about a triglyceride level of 101 mg/dl while on fish oil.

Recall that, contary to conventional thinking like that articulated in the ATP-III cholesterol treatment guidelines, we aim to reduce triglycerides to 60 mg/dl or less. This is important to suppress the formation of abnormal triglyceride-containing lipoprotein particles, especially small LDL, reduced HDL, lack of healthy large HDL, VLDL. ATP-III advises a level of 150 mg/dl or less. Unfortunately, triglyceride levels this high guarantee appearance of all these undesirable particles and an increasing heart scan score.

What's better than 4000 mg of fish oil for its 1200 mg of EPA and DHA (omega-3 fatty acids)? More fish oil. In other words, the 4000 mg fish oil providing 1200 mg EPA + DHA is our minimum. A simple increase to 6000 mg to provide 1800 mg EPA + DHA is usually all that is necessary to reduce triglycerides and put a halt to the cascade of abnormal lipoprotein particles that trigger plaque growth. Occasionally, a somewhat higher dose may be required. Doses are best divided into two, with meals (e.g., three capsules twice a day).

Another important issue: An over-reliance on wheat products can also increase triglycerides. This includes any flour product like breads (regardless of whether it's white, whole wheat, or whole grain--they all raise triglycerides), pretzels, bagels, breakfast cereals, and pasta. A dramatic reduction in wheat-containing products will reduce triglycerides substantially, help you reduce your abdominal fat, reduce blood pressure, raise HDL and reduce small LDL, clear your mind, provide more energy, avoid afternoon "fogginess" . . . Huge benefits.

Valve disease and vitamin D

There are two common forms of heart valve disease: aortic valve stenosis (stiffness) and insufficiency (leakiness), and mitral anular calcification.

Both valve issues are regarded as evidence of senescence, or aging--the older you are, the more likely you will have one or both. Both conditions involve progressive calcium deposition and, to some degree, cholesterol deposition. They might be regarded as phenomena of "wear and tear" just like hip arthritis.

There are no known therapies to stall or stop the development of mitral anular calcification. However, several attempts have been made over the years to identify treatments that can slow or stop the progression of aortic valve disease, which is becoming increasingly common and is addressed by surgical valve replacement when severe. The most recent trials have examined whether high-dose Lipitor (80 mg) has any effect (it did not) and high dose Crestor (40 mg), which slowed but did not stop the deterioration of stiff valves.

It's been my suspicion that vitamins D and K2 may play a crucial factor in valve health. After all, vitamin D is the master controller of calcium deposition. Preliminary data also suggest that people who are intentionally made vitamin K deficient with the drug, Coumadin, develop twice the calcium deposition on aortic valves that non-Coumadin takers develop.

I saw a patient Friday, Marianne. In addition to a moderate heart scan score of 379 at age 71, Marianne had a leaky (insufficient) aortic valve. By an echocardiogram 18 months ago, the valve was moderately leaky. I put Marianne on vitamin D, 4000 units, to raise her blood level to 50 ng/ml.

Last week, I asked Marianne to have another echocardiogram. This time, no leakiness whatsoever--none. I have never seen this happen before. Although Marianne is only one example and we don't want to extrapolate too far from the experience of one person, it's hard not to attribute this phenomenal response to vitamin D supplementation.

I wonder what would have happened if we had added vitamin K2, as well?

Anyway, just another potential wonderful effect of vitamin D restoration.

Homocysteine and coronary plaque

If you’ve watched the news over the past year, you know that doubt has been cast over the idea that reducing homocysteine blood levels with high doses of B vitamins (B6, B12, and folic acid, or B9) results in reduced risk for heart attack.

Is the homocysteine concept dead? Shall we empty our bottles of costly B vitamins into the trash and move on?

I don’t think so. As detailed in one of our Track Your Plaque Special Reports from a few months ago, I think the homocysteine issue still deserves lots of respect and further investigation. After all, hundreds of clinical studies have connected higher homocysteine levels with greater risk for heart disease, stroke, and aneurysm. Numerous studies, for example, have repeatedly and consistently demonstrated a tripling of heart attack risk when homocysteine levels exceed 14 ?mol/l. Can we dismiss this association because several more recent studies—NORVIT, HOPE, and VISP—suggested that, when starting homocysteine levels are 12.5, that B vitamin supplementation does not reduce heart attack risk?

I think there’s lots more to know about the homocysteine connection. That said, I have never seen a patient who I thought had heart disease strictly because homocysteine was increased.

I believe that we can at least use homocysteine as an index of lifestyle: the higher the homocysteine, the poorer the diet, or the less effective the absorption of B vitamins (especially vitamins B12 and folic acid). Homocysteine levels of <9 micromol/l suggest both adequate intake and absorption of these B vitamins.

If homocysteine is tightly connected with risk for heart disease, yet supplementation of B vitamins fails to reduce risk, might there be another means of connection? Or, could both homocysteine and heart disease be connected in some way that has nothing to do with B vitamins?

Don’t close the book on homocysteine. Just because conventional experience fails to draw connection does not necessarily mean that none exists. If it’s any consolation, taking B vitamins has been correlated with better memory, concentration, and other health benefits, even if no reduction in heart disease develops.

Big heart scan scores drop

High heart scan scores of, say, greater than 1000 are more difficult to reduce than lower scores.

I learned this lesson early in the experience of trying to drop scores. In the first few years of trying to drop scores, I saw relatively modest scores of 20, 50, or 100 drop readily, even when the usual targets were not fully achieved, and even before the incorporation of some of the more exciting recent additions to the Track Your Plaque program, like vitamin D.

But big scores of 1000, 2000, or 3000 are a tougher nut to crack. In the first few years, what I usually saw was a slowing , or "deceleration," of growth from the expected rate of annual score increase of 30% that would continue for a year or two, followed by zero change. In the first year of effort, for example, a score increase of 18% was common. 10% was common in year two, then finally zero change in year three. Somehow, the more plaque you begin with, the more "momentum" in growth is present and the longer it takes to stop it. Kind of like stopping a compact car versus stopping a freight train.

But more recently, I'm seeing faster drops. Today, Charlie came to the office to discuss his second heart scan. 18 months earlier, Charlie's first scan showed a score of 3,112, high by anybody's standard.

His repeat score: 3,048. While the drop is relatively small on a percentage basis and may even fall within the expected rate of error for heart scans (which tends to be <2% at this high a score), I told Charlie that it still represented a huge success. Not only did he not increase his score by the expected 30% per year, he also brought a charging locomotive to a rapid stop.

Next year, Charlie is targeting a big drop. Given the tools he now has available, I'm optimistic that he will succeed.

Watch for the Track Your Plaque May, 2007 Newsletter in which we will detail Charlie's story further.

Does the American Heart Association diet reduce heart disease?

If you have a heart attack and land in the hospital where, invariably, you will have a heart procedure. Or, if you get a stent or coronary bypass operation, sometime before your discharge from the hospital, a well-meaning hospital staff dietitian will provide instruction in the American Heart Association (AHA) diet.

Does this diet reduce the risk of heart disease?

The answer depends on where you start. If you begin with a conventional American diet that is enormously influenced by convenience, food manufacturers like Nabisco, General Mills, Quaker Oats, ADM, and Cargill, or food distributors like McDonald’s, Pizza Hut, and Taco Bell, then the American Heart Association diet is indeed an improvement. But just a small one. If LDL cholesterol is the yardstick, the average reduction in LDL is between 10 and 15 mg/dl. This is the same amount of change you’d experience by adding 1 tablespoon of oat bran to your diet. Hardly worth boasting about. HDL, triglycerides, blood glucose, and body weight do not change.

The diet could be substantially better. After all, it’s become common knowledge that other diets, such as the so-called Mediterranean diet, the South Beach Diet, and similar broad projects result in far greater changes than the AHA diet dispensed by your hospital and cardiologist. These diets more effectively reduce LDL, raise HDL, reduce triglycerides, reduce C-reactive protein, reduce blood pressure. Diets like South Beach also yield substantial weight loss and reversal of diabetic tendencies, with the magnitude of benefit dependent on the amount of weight lost.

Why this stubborn adherence to the outdated concepts articulated in the AHA diet? Cardiologists would argue that insufficient data has been generated to permit widespread application of these diets. They also differ on whether they really work. Of course, the majority remain ignorant and dismiss them as fad diets.

A little digging into the financial disclosures of the AHA suggests another, more malignant influence: who is paying the bills? Until recently, drug manufacturers were major contributors to the AHA. However, more recently AHA administrators have become sensitive to the public perception that they might be nothing more than a voice box for the drug industry. They have since limited contributions from the drug companies to 8% of annual charitable revenues.

The drug manufacturers have been replaced by the food industry. In addition to food manufacturers that make the cereals on your grocery shelf, it includes the multi-national conglomerates that produce unimaginable revenues and carry enormous political clout, like ADM and Cargill. Ever wonder how it is that Honey Nut Cheerios received a “Heart Healthy” endorsement from the AHA?

The AHA diet does not provide the answers we’re looking for, not even close. It is a perversion from an organization that has its strings pulled by industry. The answers to health will not come from the AHA, AMA, the American College of Cardiology, the American Hospital Association, and it won’t come from your doctor. It won’t come from a titillating report on the evening news or Good Morning America. It will come from collective and expanding wisdom placed directly into the hands of the public. It will be untainted by the temptation of drug industry dollars. It will not be dirtied by million dollar contributions, or the multi-million dollar behind-closed-doors lobbying of the food manufacturers. It will come from the truth relayed to the healthcare-consuming public. I hope you recognize it when you see it.

If you want a healthy diet for your heart, throw away the pamphlets from the AHA unless you are partial to bread, breakfast cereals, corn, and the supporters of their misguided nutritional advice.

Vitamin K2 and coronary plaque

The vitamin K2 story, though still preliminary, is becoming increasingly interesting from the perspective of CT heart score reduction.

The origin of this concept came from some unexpected observations. One, the observation that osteoporosis (lack of bone calcium that leads to fractures) arises from deficiency of vitamin K2. Two, deficiency of K2 leads to unrestrained calcium deposition in animal models, leading to heart attack in just weeks.

Vitamin K2 has been largely ignored for years, since the more widely understood K1 is rarely deficient. K1 deficiency can occur from prolonged antibiotic use, or from severe malnutrition. But deficiency in otherwise well people is very uncommon. Vitamin K2, however, may be a different story. Deficiency may be common.

The Rotterdam Heart Study of cheese-eating Dutch showed that greater K2 intakes resulted in a halving of heart attacks. Cheese (traditional varieties, not Velveeta or other make-believe cheese products) is a modest source of K2, as is the Japanese native food, natto. (If you've ever seen natto, I dare you to eat it. I have a pretty strong stomach and curiousity for food, but natto is the one thing I could not eat--it is truly horrible.)

The weight of evidence suggests that vitamin K2 supplementation may prove to be a useful addition to your coronary plaque control program. Clearly, more data are needed, particulary therapeutic obserations, i.e., observing people who take dose X of a K2 prepartion and tracking some feedback measure, e.g., bone density, CT heart scan score, "events" like heart attack, etc.

Nonetheless, the K2 story is clearly worth reading about, perhaps even considering supplementation. Please watch for the Special Report on the www.cureality.com website in the coming days.

Exercise and blood pressure

The media has gotten a hold of a case report from the University of Maryland describing a 51-year old physician who, despite being a long distance runner, had a high heart scan score.

An example of the report can be found at

Heart Disease In A Marathon Runner: Is Too Much Exercise A Bad Thing?

http://www.sciencedaily.com/releases/2007/03/070315091100.htm in Science Daily.



"The mystery was all the more intriguing because his resting blood pressure and fasting cholesterol levels, the usual measures of cardiovascular health, were in the normal range."


When this man was put on a treadmill for a stress test, his blood pressure skyrocketed from a normal 118/78 to 230/78--extremely high, even for exercise. The physicians reporting the case raised the question of whether long-distance running represents a risk for heart disease and if the high blood pressure with exercise is a contributor or cause of the high heart scan score.

These are phenomena we are very familiar with. We have stressed the importance of exercise blood pressure as a trigger for coronary plaque for years. While 230/78 is clearly too high, we find that any blood pressure over 170/80 with exercise adds to the fire and can trigger plaque growth.

However, I think it is absurd to suggest that marathon running itself is a trigger of coronary plaque. I think it is far more likely that the person described in the report had lipoprotein(a), a potent trigger for both exercise-induced hypertension and high CT heart scan scores in seemingly well people. He likely also suffered from a deficiency of vitamin D deficiency, another contributor. There's no need to indict exercise.

If you are in the Track Your Plaque program, you know that stress tests are of questionable helpfulness for the detection of hidden heart disease. But they are useful for assessment of blood pressure responses during exercise. If BP exceeds 170/80 at 10 mets (a measure of exercise effort achieved by walking 3.4 mph at a 14% grade for 3 minutes), then blood pressure may be a contributor to your heart scan score.

"Fish oil is stupid"

"Fish oil is a waste of time and money. It's stupid. Just stop it."

So a patient of mine was advised by another physician when he complained that he occasionally experienced a fishy aftertaste.

This attitude perplexes me. After all the confirmatory data that support the enormous health benefits of omega-3 fatty acid supplementation, including the 11,000 participant GISSI-Prevenzione Trial, you'd think this attitude would be history. What's a little fish aftertaste when heart attack risk is slashed 28%?

Perhaps the tendency to pooh-pooh fish oil is because it's available as a nutritional supplement. This shouldn't make fish oil appear inconsequential. Far from it.

If you witness the extraordinary power for fish oil to reduce triglycerides, you will be immediately convinced of its effectiveness. The ability of omega-3 fatty acids from fish to eliminate intermediate-density lipoprotein (IDL), the persistent abnormal lipoprotein which signals an inability to clear dietary fats from the blood, can also convince you. More than 90% of people with excessive IDL have it completely eliminated by 4000-6000 mg of fish oil (providing 1200-1800 mg EPA + DHA) per day.

The fact that fish oil is available as a prescription "medication," as well as an over-the-counter supplement, causes some physicians to dismiss the power of the supplemental form. This is nonsense. The over-the-counter form is every bit as effective as the prescription form.

The makers of prescription Omacor also make the claim that their preparation is safer and purer. That may be true, but I'd like to see independent verification from the FDA, USDA, or an unbiased organization like Consumer Reports before I accept their marketing as fact--particularly at $120 to $240 per month! If Omacor proves to contain substantially less mercury and pesticide residues, then that will need to be factored in. (Please note that both Consumer Reports and Consumer Labs measured no substantial mercury or pesticide residues in their analyses of 16 and 41 brands, respectively.)

I try to persuade my colleagues that the idea of taking supplements is a wonderful trend that allows people to express ownership of their own health. What people need is guidance, not salesmanship for a more expensive version, nor dismissal of nutritional preparations that actually possess considerable benefits.