Track Your Plaque makes Consumer Reports!

. . . but not in a good way.

The September, 2011 issue of Consumer Reports showcases their Protect Your Heart discussion. Third paragraph: "The website Track Your Plaque warns, 'The old tests for heart disease were wrong--dead wrong.' It says heart scans are 'the most important health test you can get.'"

They go on to expose the overuse of heart procedures like angioplasty and stent implantation and offer their advice on how to manage heart disease risk: lower BP, reduce LDL cholesterol, lose weight, stop smoking, take aspirin. They quote Dr. Paul Ridker who declares heart scans are not useful because the "deposits cardiologists worry about are the less stable plaques that CT scans routinely miss."

I thought I'd been transported back to 1995. Not only is it clear that the Consumer Report writers never looked beyond the homepage of Track Your Plaque, but somehow saw our heart disease prevention and reversal program as promoting heart procedures. Incredible.

Of course, the Track Your Plaque program does the exact opposite: Advocates an approach that virtually eliminates the need for procedures and returns control over heart disease to the participant. That's a critical difference.

And, as I've had to remind my colleagues time and time again, what we are really after is an index of total coronary atherosclerotic plaque. Even in 2011, that index remains the simple coronary calcium score, a gauge of total plaque, not just of "hard," stable plaque. Perhaps in 10 years we will be using a better tool to gauge progression and regression of all the components of coronary atherosclerotic plaque, but today it remains the simple, accessible, mammogram-like coronary calcium score.

Consumer Reports does for the idea of heart disease prevention what food manufacturers do for health and weight loss: Echo conventional wisdom of the sort that generally makes us fatter, more diabetic, leads us to more heart procedures and needless deaths. I might use Consumer Reports to rate MP-3 devices or toasters, but I certainly would not rely on them for insightful health advice.

Paging Dr. Basedow

A 23-year old man came to my office having experienced weeks of extreme anxiety, palpitations, and 19 pounds of weight loss triggered by an overactive thyroid.

It all happened because of a large dose of iodine received during a CT scan using iodine-containing x-ray dye. (X-ray dyes are made visible on x-ray due to the iodine content.) This is a reaction first described in the 19th century by German physician, Karl Adolph von Basedow. (Jod is German for iodine.)[caption id="attachment_4313" align="alignleft" width="217" caption="Dr. von Basedow. Image courtesy Wikipedia"][/caption]

Now, here's the kicker: Jod-Basedow only occurs when there is pre-existing iodine deficiency. Indeed, this young man had an enlarged thyroid, signaling longstanding iodine deficiency (a goiter).

This example is among the more flagrant examples of something I have been witnessing: the return of iodine deficiency. As Americans cut back on their intake of iodized salt and fail to obtain iodine in sufficient quantities from seafood, seaweed, or supplementation, goiters and iodine deficiency are making a return in all its glory, reminiscent of the early 20th century, pre-iodized salt.

This young man's frightening experience is yet another way iodine deficiency can show itself, by the overenthusiastic thyroid response to a large dose of iodine when iodine deficiency has been present for a prolonged period.

Iodine deficiency and goiters have been lost to memory for most people. Even the FDA, in its advice for Americans to reduce salt and sodium intake, have forgotten to remind everyone to obtain iodine from an alternative source. "Those who cannot remember the past are condemned to repeat it."

Get your iodine.

Carb counting

In the recent Heart Scan Blog post, Can I eat quinoa, I discussed how non-wheat carbohydrate sources like quinoa, amaranth, black beans, brown rice, fruit, etc. do not exert the inflammation-provoking, appetite-increasing effects of wheat (since gliadin and gluten are not present), nor do they increase blood glucose as enthusiastically as the amylopectin A of wheat--but non-wheat grains can still increase blood sugar quite substantially.

Of course, any food that triggers blood sugar also trigger hepatic de novo lipogenesis, thereby increasing triglyceride levels and postprandial particles (e.g., chylomicron remnants), which, in turn, triggers formation of small LDL particles.

So these non-wheat carbohydrates, or what I call "intermediate carbohydrates" (for lack of a better term; low-glycemic index is falsely reassuring) still trigger all the carbohydrate phenomena of table sugar. Is it possible to obtain the fiber, B-vitamin, flavonoid benefits of these intermediate carbohydrates without triggering the undesirable carbohydrate consequences?

Yes, by using small portions. Small portions are tolerated by most people without triggering all these phenomena. Problem: Individual sensitivity varies widely. One person's perfectly safe portion size is another person's deadly dose. For instance, I've witnessed many extreme differences, such as 1-hour blood sugar after 6 oz unsweetened yogurt of 250 mg/dl in one person, 105 mg/dl in another. So checking 1-hour blood sugars is a confident means of assessing individual sensitivity to carbs.

Some people don't like the idea of checking blood sugars, however. Or, there might be times when it's inconvenient or unavailable. A useful alternative: Count carbohydrate grams. (Count "net" carbohydrate grams, of course, i.e., carbohydrates minus indigestible fiber grams to yield "net" carbs.) Most people can tolerate around 40-50 grams carbohydrates per day and deal with them effectively, provided they are spaced out throughout the day and not all at once. Only the most sensitive, e.g., diabetics, apo E2 people, those with familial hypertriglyceridemia, are intolerant to even this amount and do better with less than 30 grams per day. Then there are the genetically gifted from a carbohydrate perspective, people who can tolerate 50-60 grams, occasionally somewhat more.

People will sometimes say things like "You don't know what the hell you're talking about because I eat 200 grams carbohydrate per day and I'm normal weight and have perfect blood sugar and lipids." As in many things, the crude measures made are falsely reassuring. Glycation, for instance, from postprandial blood sugars of "only" 140 mg/dl--typical after, say, unsweetened oatmeal--still works its unhealthy magic and will lead long-term to cataracts, arthritis, and other conditions.

Humans were not meant to consume an endless supply of readily-digestible carbohydrates. Counting carbohydrates is another way to "tighten up" a carbohydrate restriction.

One hour blood sugar: Key to carbohydrate control and reversing diabetes

Diabetics are instructed to monitor blood glucose first thing in the morning and two hours after eating. This helps determine whether blood sugar is controlled with medications like metformin, Januvia, Byetta injections, or insulin.

But that's not how you use blood sugar to use to prevent or reverse diabetes. Two-hour blood sugars are also of no help in deciding whether you have halted glycation, or glucose modification of proteins the process that leads to cataracts, brittle cartilage and arthritis, oxidation of small LDL particles, atherosclerosis, kidney disease, etc.

So the key is to check one-hour after-eating (postprandial) blood sugars, a time when blood glucose peaks after consumption of carbohydrates. (It may peak somewhat sooner or later, depending on factors such as how much fluid was in the meal; protein, fat, and fiber content; presence of foods like vinegar that slow gastric emptying; the form of carbohydrate such as amylopectin A vs. amylopectin B, amylose, fructose, along with other factors. Once in a while, you might consider constructing your own postprandial glucose curve by doing fingersticks every 15 minutes to determine when your peak occurs.)

I reject the insane notion that after-eating blood sugars of less than 200 mg/dl are acceptable, the value accepted widely as the cutoff for health. Blood sugars this high occurring with any regularity ensure cataracts, arthritis, and all the other consequences of cumulative glycation. I therefore aim to keep one-hour after-eating glucoses 100 mg/dl or less. If you start in a pre-diabetic or diabetic range of, say, 120 mg/dl, then I advise people to not allow blood glucose to go any higher. A pre-meal blood glucose of 120 mg/dl would therefore be followed by an after-eating blood glucose of no higher than 120 mg/dl.

No doubt: This is strict. But people who do this:

--Lose weight from visceral fat
--Heighten insulin sensitivity
--Drop blood pressure
--Drop HbA1c and fasting glucose over time
--Reduce small LDL and other carbohydrate-sensitive measures

By the way, if you inadvertently trigger a high blood sugar like I did when I took my kids to the all-you-can-eat Indian buffet, go for a walk, bike, or burn the sugar off with a 30-minute or longer physical effort. Check your blood sugar again and it should be back in desirable range. But then learn from your lesson: Eliminate or reduce portion size of the culprit carbohydrate food.

Wheat Belly coming to bookstores!

Anyone following the conversations on these pages know that I have some very serious concerns about this thing being sold to us called "wheat"--cause it ain't wheat! It is the result of incredible genetics shenanigans inflicted on this plant, mostly in the name of increased yield per acre.



I now classify wheat as "Public Enemy #1," the prime nutritional culprit underlying obesity, heart disease, "cholesterol" abnormalities, hypertension, arthritis, psychiatric illness, and on and on. Once you read the full story, I believe that you will agree: Modern Triticum aestivum, the plant that now serves as the source for virtually all the wheat flour products now consumed--organic, whole grain, multigrain, sprouted . . . it makes no difference--does not belong in the human diet. So many people, searching for solutions for their fatigue, weight gain, leg edema, incurable rashes, joint pain, etc., will find their answers here.

Wheat Belly: Lose the wheat, lose the weight and find your path back to health will be on bookstore shelves including Barnes and Noble August 30, 2011 or is available for preorder here at Amazon. Wheat Belly will also be available as a downloadable Kindle book and as unabridged audio CDs.

You can also follow the Wheat Belly conversations on my Wheat Belly Blog. One of my recent posts discusses the herbicide-resistant semi-dwarf wheat strain, Clearfield, that is now making its way to more and more supermarket shelves.

You'll also find more conversation on the Wheat Belly Facebook pages.

The exception to low-carb

I witness spectacular results restricting carbohydrates, both in the office as well as in my online experiences, such as those in Track Your Plaque. Of course, the diet I advocate is not just low-carb; it starts with elimination of wheat (for a long list of reasons). So the diet is wheat-free in the setting of low-carbohydrate.

What does this accomplish? Here's a partial list:

--Weight loss-Specifically, loss of visceral fat, the kind hinted at on the surface as "love handles" or what I call "wheat belly."
--Reduced blood sugar and HbA1c (reflecting prior 60-90 days glucose)
--Marked reduction in small LDL and triglycerides, increased HDL
--Reduced inflammatory measures like c-reactive protein
--Reduced leptin and leptin resistance, increased adiponectin
--Reduced estrogen and prolactin in men, accompanied by shrinkage or loss of enlarged breasts ("man boobs"); reduced estrogen in females accompanied by reduced risk for breast cancer

Pretty impressive. But there's one group of people who can experience unexpected effects with this diet: The 25% of people with apoprotein E4.

Everybody has two genes for apo E; the most common type is apo E 3/3. Around 1 in 4 people have 1, less commonly 2, genes for apo E4.

I hate apo E4. I hate apo E4 because it means I've got to dust off the nonsense I used to tell patients about cutting their fat, cutting their saturated fat. But that's what apo E4 people have to do. But it doesn't end there.

Apo E4 people also typically have plenty of small LDL particles triggered by carbohydrates. Put fats and carbohydrates together and you get an explosion of small LDL particles. Remove fats, small LDL goes down a little bit, if at all. Remove carbohydrates, small LDL goes down but total LDL (mostly large) goes up. The large LDL in apo E4 does seem to be atherogenic (plaque-causing), though the data are fairly skimpy.

So apo E4 creates a nutritional rock and a hard place: To extract full advantage from diet, people with apo E4 have to 1) go wheat-free, low-carb, then 2) not overdo fats, especially saturated fat.

It still gives me the creeps to tell an apo E4 person that they've got to watch their fats, worse than watching Starsky and Hutch reruns.

Can I eat quinoa?

. . . or beans, or brown rice, or sweet potatoes? Or how about amaranth, sorghum, oats, and buckwheat? Surely corn on the cob is okay!

These are, of course, non-wheat carbohydrates. They lack several crucial undesirable ingredients found in our old friend, wheat, including no:

Gliadin--The protein that degrades to exorphins, the compound from wheat digestion that exerts mind effects and stimulates appetite to the tune of 400 additional calories (on average) per day.
Gluten--The family of proteins that trigger immune diseases and neurologic impairment.
Amylopectin A--The highly-digestible "complex" carbohydrate that is no better--worse, in fact--than table sugar.

So why not eat these non-wheat grains all you want? If they don't cause appetite stimulation, behavioral outbursts in children with ADHD, addictive consumption of foods, dementia (i.e., gluten encephalopathy), etc., why not just eat them willy nilly?

Because they still increase blood sugar. Conventional wisdom is that these foods trend towards having a lower glycemic index than, say, table sugar, meaning it raises blood glucose less.

That's true . . . but very misleading. Oats, for instance, with a glycemic index of 55 compared to table sugar's 59, still sends blood sugar through the roof. Likewise, quinoa with a glycemic index of 53, will send blood sugar to, say, 150 mg/dl compared to 158 mg/dl for table sugar--yeah, sure, it's better, but it still stinks. And that's in non-diabetics. It's worse in diabetics.

Of course, John Q. Internist will tell you that, provided your blood sugars after eating don't exceed 200 mg/dl, you'll be okay. What he's really saying is "There's no need for diabetes medication, so you're okay. You will still be exposed to the many adverse health consequences of high blood sugar similar to, though less quickly than, a full diabetic, but that's not my problem."

In reality, most people can get away with consuming some of these non-wheat grains . . . provided portion size is limited. Beyond limiting portion size, there are two ways to better manage your carbohydrate sensitivity to ensure that metabolic distortions, such as high blood sugar, glycation, and small LDL particles, are not triggered.

More on that in the future.


Lipoproteins . . . zero!

With the recent refinements in our approach to correction of the lipoprotein abnormalities that lead to coronary plaque and heart disease risk, I have been witnessing more and more people achieve:

Small LDL particles 0 nmol/L
Lipoprotein(a) 0 nmol/L



For instance, Ted, a 58-year old man I saw in the office today started with:

Small LDL 1673 nmol/L
Lipoprotein(a) 219 nmol/L


In other words, both small LDL particles and lipoprotein(a) are being knocked down to zero values.

Incidentally, the combination of lipoprotein(a) with small LDL is among the most atherogenic (atherosclerotic plaque-causing) patterns known. Despite his athletic, slender build and avoidance of unhealthy habits, Ted's heart scan score was 922--very high.

So Ted followed the diet I advocate, i.e., wheat elimination followed by elimination of cornstarch, oats, and sugars; high-dose fish oil (total daily EPA + DHA of 6000 mg/day); vitamin D supplementation sufficient to achieve a 25-hydroxy vitamin D level of 60-70 ng/ml; iodine supplementation; and thyroid normalization which, in Ted's case, required supplementation with the T3 thyroid hormone, liothyronine, at a small dose.

The result:

Small LDL particles 0 nmol/L
Lipoprotein(a) 0 nmol/L


Not everybody, of course, is achieving these incredible--and previously impossible--results. But the numbers are growing. Ted is the third person to achieve zeroes all around, in fact, over the past 10 days.

Heart disease prevention is getting better and more powerful every day. And it ain't all about Lipitor and low-fat.


Chocolate almond biscotti

Biscotti are twice-baked biscuits or cookies that are perfect for dipping into coffee, latté, or espresso. These wheat-free, low-carb biscotti are rich with the taste of chocolate and almonds.

Yield: approximately 15 biscotti



Ingredients:

2 cups almond meal
½ cup chopped walnuts
1/4 cup cocoa powder (undutched)
½ cup dark chocolate chips
Sweetener equivalent to ½ cup sugar (e.g., liquid stevia, Truvia)
½ cup ricotta cheese, room temperature (replace with coconut milk if lactose intolerant)
4 tablespoons butter, melted (replace with coconut oil if lactose intolerant)
2 large eggs
¼ cup milk, unsweetened almond milk, or soy milk
¼ cup almond, peanut, or sunflower seed butter, room temperature

Preheat oven to 350º F.

Mix almond meal, walnuts, sweetener, cocoa powder, and chocolate chips in bowl. Mix in ricotta, butter, eggs, milk, and nut butter and blend by hand thoroughly.

Pour mix onto baking pan lined with parchment paper or greased with coconut oil or other oil. Shape into loaf approximately 1 inch deep and 3½ to 4 inches in width. Place in oven and bake for 40 minutes.

Remove loaf and allow to cool 15 minutes. Slice into approximately ¾-inch widths and lay each biscotto on its side on baking pan. Put back in oven for 10 minutes.

Remove pan and flip biscotti over. Place back in oven and bake an additional 5 minutes. Remove and cool.

Optional: For a little dark chocolate "icing":
Melt 3-4 oz semisweet or dark chocolate in microwave (in 15 second increments until melted) or in metal bowl placed in heated water. Stir in 1-2 teaspoons butter.
Dip each biscotti into melted chocolate mix or drizzle chocolate mixture over top of each biscotto.

Sun green tea

Here's a great way to enjoy the health benefits of green tea during the summer: sun green tea.


I dropped two green tea bags into approximately one-half gallon of cold water in a clear glass jar. I placed the jar in the sun (with top on) for four hours, then brought it into the kitchen. I served it as iced tea with a slice of lemon and mint leaf.

The sun green tea was a smoother than standard green tea brewed with hot water. Ordinarily, if you brew hot green tea for more than 3-5 minutes, it becomes more bitter or tannic. This sun green tea, despite steeping for four hours, was not the least bit bitter or tannic.

The green tea lasted well for about 48 hours, more than enough to enjoy several glasses per day.

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.