The Paleo approach to meal frequency

24. November 2009 William Davis (12)
Furthering our discussion of postprandial (after-eating) phenomenona, including chylomicron and triglyceride "stacking" (Grazing is for cattle and Triglyceride and chylomicron stacking), here's a comment from the recent Palet Diet Newsletter on the closely related issue, meal timing and frequency:


We are currently in the process of compiling meal times and patterns in the worlds historically studied hunter-gatherers. If any single picture is beginning to emerge, it clearly is not three meals per day plus snacking ala the typical U.S. grazing pattern. Here are a few examples:

--The Ingalik Hunter Gatherers of Interior Alaska: 'As has been made clear, the principal meal and sometimes the only one of the day is eaten in the evening.'
--The Guayaki (Ache) Hunter Gatherers of Paraguay: 'It seems, however, that the evening meal is the most consistent of the day. This is understandable, since the day is generally spent hunting for food that will be eaten in the evening."
--The Kung Hunter Gatherers of Botswana. "Members move out of camp each day individually or in small groups to work through the surrounding range and return in the evening to pool the collected resources for the evening meal."
--Hawaiians, Tahitians, Fijians and other Oceanic peoples (pre-westernization). 'Typically, meals, as defined by Westerners, were consumed once or twice a day. . . Oliver (1989) described the main meal, usually freshly cooked, as generally eaten in the late afternoon after the day’s work was over."

The most consistent daily eating pattern that is beginning to emerge from the ethnographic literature in hunter-gatherers is that of a large single meal which was consumed in the late afternoon or evening. A midday meal or lunch was rarely or never consumed and a small breakfast (consisting of the remainders of the previous evening meal) was sometimes eaten. Some snacking may have occurred during daily gathering, however the bulk of the daily calories were taken in the late afternoon or evening. This pattern of eating could be described as intermittent fasting relative to the typical Western pattern, particularly when daily gathering or hunting were unsuccessful or marginal. There is wisdom in the ways of our hunter gatherer ancestors, and perhaps it is time to re-think three squares a day.


In other words, the notion of "grazing," or eating small meals or snacks throughout the day, is an unnatural situation. It is directly contrary to the evolutionarily more appropriate large meal followed by periods of no eating or small occasional meals.

I stress this point because I see that the notion of grazing has seized hold of many people's thinking. In my view, grazing is a destructive practice that is self-indulgent, unnecessary, and simply fulfills the perverse non-stop hunger impulse fueled by modern carbohydrate foods.

Eliminate wheat, cornstarch, and sugars and you will find that grazing is a repulsive impulse that equates with gorging.


The full-text of the Paleo Diet Newsletter can be obtained through www.ThePaleoDiet.com. You can also read and/or subscribe to the new Paleo Diet Blog, just launched in November, 2009.

Even mummies do it

20. November 2009 William Davis (16)

Lady Rai, nursemaid to Queen Nefertari of Egypt, died in 1530 BC, somewhere between the age of 30 and 40 years. Her mummy is preserved in the Egyptian National museum of Antiquities in Cairo.

A CT scan of her thoracic aorta revealed calcium, representing aortic atherosclerosis, reported by Allam et al (including my friend from The Wisconsin Heart Hospital, Dr. Sam Wann, who provided me a blow-by-blow tale of this really fascinating project). Ladi Rai and 14 other Egyptian mummies were found to have vascular calcification of a total of 22 mummies scanned. (The hearts of the mummies were too degenerated to make out any coronary calcium.)

But why would people of that age have developed atherosclerosis?

The authors of the study comment that "Our findings that atherosclerosis was not infrequent among middle-aged and older ancient Egyptians of high social status challenges the view that it is a disease of modern humans. . . Although ancient Egyptians did not smoke tobacco or eat processed food or presumably lead sedentary lives, they were not hunter-gatherers. [Emphasis mine.] Agriculture was well established in ancient Egypt and meat consumption appers to have been common among those of high social status."

Fascinating. But I don't think that I'd blame meat consumption. Egyptians were also known to have cultivated grains, including wheat, and frequently consumed such sweet delicacies as dates and figs. Egyptians were also apparently beer drinkers. Unfortunately, no beer steins were seen in any of the scans.

Life Extension article on iodine

17. November 2009 William Davis (25)
Here's a link to my recent article in Life Extension Magazine on iodine:

Halt on Salt Sparks Iodine Deficiency

Iodized salt, a concept introduced into the U.S. by the FDA in 1924, slowly eliminated goiter (enlarged thyroid glands), along with an enormous amount of thyroid disease, heart attack, mental impairment, and death. The simple addition of iodine to salt ensured that salt-using Americans obtained enough iodine sufficient to not have a goiter.

Now that the FDA, goiters long forgotten from their memories, urges Americans to reduce salt, what has happened to our iodine?

I talk at length about this issue in the Life Extension article.

The healthiest people are the most iodine deficient

16. November 2009 William Davis (19)
Here's an informal observation.

The healthiest people are the most iodine deficient.

The healthier you are, the more likely you are to:

--Avoid junk foods--30% of which have some iodine from salt
--Avoid overuse of iodized salt
--Exercise--Sweating causes large losses of iodine.

So the healthy-eating, exercising person is the one most likely to show iodine deficiency: gradually enlarged thyroid gland (in the neck), declining thyroid function. Over time, if iodine deficiency persists, excessive sensitivity to iodine develops, as well as abnormal thyroid conditions like overactive nodules.

Even subtle levels of thyroid dysfunction act as a potent coronary risk factor.

It's the score, stupid

14. November 2009 William Davis (4)
Sal has had 3 heart scans. (He was not on the Track Your Plaque program.) His scores:

March, 2006: 439

April, 2007: 573

October, 2009: 799

Presented with the 39% increase from April, 2007 to October, 2009, Sal's doctor responded, "I don't understand. Your LDL cholesterol is fine."

This is the sort of drug-driven, cholesterol-minded thinking that characterizes 90% of primary care and cardiologists' practices: "Cholesterol is fine; therefore, you must be fine, too."

No. Absolutely not.

The data are clear: Heart scan scores that continue to increase at this rate predict high risk for cardiovascular events. Unfortunately, when my colleagues hear this, they respond by scheduling a heart catheterization to prevent heart attack--a practice that has never been shown to be effective and, in my view, constitutes malpractice (i.e., performing heart procedures in people with no symptoms and with either no stress test or a normal stress test).

It's the score, stupid! It's not the LDL cholesterol. Pay attention to the increasing heart scan score and you will know that the disease is progressing at an alarming rate. Accepting this fact will set you and your doctor on the track to ask "Why?"

That's when you start to uncover all the dozens of other reasons that plaque can grow that have nothing to do with LDL cholesterol or statin drugs.

Heart Scan Blog Redux: Cheers to flavonoids

13. November 2009 William Davis (32)
Because in Track Your Plaque we've been thinking a lot about anthocyanins, here's a rerun of a previous Heart Scan Blog post about red wine. (Anthocyanins are among the interesting flavonoids in red wine, along with resveratrol and quercetin.)


The case in favor of healthful flavonoids seems to grow bit by bit.

Flavonoids such as procyanadins in wine and chocolate, catechins in tea, and those in walnuts, pomegranates, and pycnogenol (pine bark extract) are suspected to block oxidation of LDL (preventing its entry into plaque), normalize abnormal endothelial constriction, and yield platelet-blocking effects (preventing blood clots).

Dr. Roger Corder is a prolific author of many scientific papers detailing his research into the flavonoids of foods, but wine in particular. He summarizes his findings in a recent book, The Red Wine Diet. Contrary to the obvious vying-for-prime-time title, Dr. Corder's compilation is probably the best mainstream discussion of flavonoids in foods and wines that I've come across. Although it would have been more entertaining if peppered with more wit and humans interest, given the topic, its straightfoward, semi-academic telling of the story makes his points effectively.

Among the important observations Corder makes is that regions of the world with the greatest longevity also correspond to regions with the highest procyanidin flavonoids in their wines.




Regarding the variable flavonoid content of wines, he states:

Although differences in the amount of procyanidins in red wine clearly occur because of the grape variety and the vineyard environment, the winemaker holds the key to what ends up in the bottle. The most important aspect of the winemaking process for ensuring high procyanidins in red wines is the contact time between the liquid and the grape seeds during fermentation when the alcohol concentration reaches about 6 percent. Depending on the fermentation temperature, it may be two to three days or more before this extraction process starts. Grape skins float and seeds sink, so the number of times they are pushed down and stirred into the fermenting wine also increases extraction of procyanidins. Even so, extraction is a slow process and, after fermentation is complete, many red wines are left to macerate with their seeds and skins for days or even weeks in order to extract all the color, flavor, and tannins. Wines that have a contact time of less than seven days will have a relatively low level of procyanidins. Wines with a contact time of ten to fourteen days have decent levels, and those with contact times of three weeks or more have the highest.

He points out that deeply-colored reds are more likely to be richer in procyanidins; mass-produced wines that are usually "house-grade" served at bars and restaurants tend to be low. Some are close to zero.

Wines rich in procyanidins provide several-fold more, such that a single glass can provide the same purported health benefit as several glasses of a procyanidin-poor wine.

So how do various wines stack up in procyanidin content? Here's an abbreviated list from his book:

Australian--tend to be low, except for Australian Cabernet Sauvignon which is moderate.

Chile--only Cabernet Sauvignon stands out, then only moderate in content.

France--Where to start? The French, of course, are the perennial masters of wine, and prolonged contact with skins and seeds is usually taken for granted in many varieties of wine. Each wine region (French wines are generally designated by region, not by variety of grape) can also vary widely in flavonoid content. Nonetheless, Bordeaux rate moderately; Burgundy low to moderate (except the village of Pommard); Languedoc-Roussillon moderate to high (and many great bargains in my experience, since these producers live in the shadow of its northern Bordeaux neighbors); Rhone (Cote du Rhone) moderate to high, though beware of their powerful "barnyard" character upon opening; decanting is wise.

Italy--Much red Italian wine is made from the Sangiovese grape and called variously Chianti, Valpolicella, and "super-Tuscan" when blended with other varietals. Corder rates the southern Italian wines from Sicily, Sardinia, and the mainland as high in procyanidins; most northern varieties are moderate.

Spain--Moderate in general.

United States--Though his comments are disappointingly scanty on the U.S., he points out that Cabernet Sauvignon is the standout for procyanidin content. He mentions only the Napa/Sonoma regions, unfortunately. (I'd like to know how the San Diego-Temecula and Virginian wines fare, for instance.)

The winner in procyanidin content is a variety grown in the Gers region of southwest France, a region with superior longevity of its residents. The wines here are made with the tannat grape within the Madiran appellation; wines labeled "Madiran" must contain 40% or more tannat to be so labeled (such is a quirk of French wine regulation). Among the producers Dr. Corder lists are Chateau de Sabazan, Chateau Saint-Go, Chateau du Bascou, Domaine Labranche Laffont, and Chateau d'Aydie. (A more complete list can be found in his book.)

How does this all figure into the Track Your Plaque program? Can you succeed without red wine? Of course you can. I doubt you could do it, however, without some attention to flavonoid-rich food sources, whether they come from spinach, tea, chocolate, beets, pomegranates, or red wine.

Though my wife and I love wine, I confess that I've never personally drank or even seen a French Madiran wine. Any wine afficionados with some advice?

Can wheat elimination cure ulcerative colitis?

13. November 2009 William Davis (0)
Tammy is a 36-year old mother of three young children. Since age 20, she has suffered with the debilitating symptoms of ulcerative colitis: constant, gnawing abdominal pain; frequent diarrhea, often bloody.



Tammy has had to take several medications, some with significant side-effects, all of which provided only partial relief from the pain and diarrhea. Her gastroenterologist and surgeon were planning a colectomy (removal of the colon) with creation of an ileostomy (rerouting of the small intestine to the abdominal surface, which would require Tammy to wear an ileostomy bag under her clothes for the rest of her life).



Although Tammy had previously tested negative for celiac disease (an allergic sensitivity to the gluten in wheat products), I urged her to attempt a trial of a wheat-free diet. Having witnessed many people experience relief from irritable bowel syndrome, acid reflux, and other common gastrointestinal complaints, all while trying to reduce blood sugar and small LDL, I'd hoped that Tammy would obtain at least some small improvement in her terrible symptoms.



I therefore urged Tammy to try it. After all, what was there to lose? Tammy grudgingly agreed.



She returned 6 months later. Her report: She had lost 38 lbs, virtually all of it within the first 6-8 weeks. Her diarrhea and cramping were not better, but gone. She was down to a single medicine from her former list of drugs.



I am unsure what proportion of people with ulcerative colitis or other inflammatory bowel diseases like Crohn's will experience a result like Tammy's. Perhaps it's only a minority. But I take this another piece of evidence that this enormously destructive thing called wheat has no place in the human diet.



We have no facts or figures on the prevalence of various forms of wheat intolerance in the U.S. When I contacted the Celiac Disease Foundation, they had no figures on the number of fatalities per year in the U.S. from celiac disease. But if there are 2-3 million Americans with celiac disease, there are probably 100 times that many people with various forms of wheat intolerance.



Postprandial pile-up with fructose

12. November 2009 William Davis (20)
Heart disease is likely caused in the after-eating, postprandial period. That's why the practice of grazing, eating many small meals throughout the day, can potentially increase heart disease risk. Eating often can lead to the phenomenon I call triglyceride and chylomicron "stacking," or the piling up of postprandial breakdown products in the blood stream.

Different fatty acid fractions generate different postprandial patterns. But so do different sugars. Fructose, in particular, is an especially potent agent that magnifies the postprandial patterns. (See Goodbye, fructose.)

Take a look at the graphs from the exhaustive University of California study by Stanhope et al, 2009:



From Stanhope KL et al, J Clin Invest 2009. Click on image to make larger.

The left graphs show the triglyceride effects of adding glucose-sweetened drinks (not sucrose) to the study participants' diets. The right graphs show the triglyceride effects of adding fructose-sweetened drinks.

Note that fructose causes enormous "stacking" of triglycerides, meaning that postprandial chylomicrons and VLDL particles are accumulating. (This study also showed a 4-fold greater increase in abdominal fat and 45% increase in small LDL particles with fructose.)

It means that low-fat salad dressings, sodas, ketchup, spaghetti sauce, and all the other foods made with high-fructose corn syrup not only make you fat, but also magnifies the severity of postprandial lipoprotein stacking, a phenomenon that leads to more atherosclerotic plaque.

Track Your Plaque: Safer at any score

11. November 2009 William Davis (0)
Imagine two people.

Tom is a 50-year old man. Tom's initial heart scan score was 500--a concerning score that carries a 5% risk for heart attack per year.

Harry is also 50 years old. His heart scan score is 100--also a concerning score, but not to the same degree as Tom's much higher score.

Tom follows the Track Your Plaque program. He achieves the 60:60:60 lipid targets; chooses healthy foods, including elimination of wheat; takes fish oil at a therapeutic dose; increase his blood vitamin D level to 60-70 ng/ml, etc. One year later, Tom's heart scan score is 400, representing a 20% reduction from his starting score.

Harry, on the other hand, doesn't understand the implications of his score. Neither does his doctor. He's casually provided a prescription for a cholesterol drug by his doctor, a brief admonition to follow a low-fat diet, and little else. One year later, Harry's heart scan score is 200, a doubling (100% increase) of the original score.

At this point, we're left with Tom having a score of 400, Harry with a score of 200. That is, Tom has twice Harry's score, 200 points higher. Who's better off?

Tom with the score of 400 is better off. Even though he has a significantly higher score, Tom's plaque is regressing. Tom's plaque is therefore quiescent with active components being extracted, inflammation subsiding, the artery in a more relaxed state, etc.

Harry's plaque, in contrast, is active and growing: inflammatory cells are abundant and producing enzymes that degrade supportive tissue, constrictive factors are released that cause the artery to pinch partially closed, fatty materials accumulate and trigger a cascade of abnormal responses.

So it's not just the score--the quantity of atherosclerotic plaque present--but the state of activity of the plaque: Is it growing, is it being reduced? Is there escalating or subsiding inflammation? Is plaque filled with degradative enzymes or quiescent?

Following the Track Your Plaque program therefore leads us to the notion that it's not the score that's most important; the most important thing is what you're doing about it. We sometimes say that Track Your Plaque makes you safer at any score.

Throw away total cholesterol!

17. May 2006 William Davis (1)
Richard's total cholesterol without treatment was 186 mg/dl. "That's great!" his doctor declared, referring to the conventional dictum that total cholesterols less than 200 carry low risk. Several fingersticks in a mall kiosk set up by a local hospital to check total cholesterols confirmed Richard's low number.

But after Richard's unexpected hospitalization and two stents for severe coronary blockages, he demanded better answers.

Tragically, the answer was there all along: Despite a "favorable" total cholesterol, his HDL ("good") cholesterol was a miserable 32 mg (ideal >60 mg).

Total cholesterol is actually the sum total of HDL cholesterol, LDL cholesterol, with a contribution from triglycerides. That's why a low total cholesterol can conceal a low HDL.

This situation is quite common. And low HDL is accompanied by a constellation of other undesirable causes of heart disease, most notably small LDL.

Don't accept total cholesterol as your sole measure of risk. It's nearly worthless. If you live in Bangladesh or a third world country, well perhaps that's the best you can get. But if you live in the U.S. or developed world, it's absurd to rely on total cholesterol.

Smart Start not so smart

15. May 2006 William Davis (2)



Kellogg's has crafted a campaign to support the American Heart Association featuring acress Sela Ward. Her attractive face, familiar to many TV and movie viewers, does add a comforting face to their efforts.

What's in this cereal made by the manufacturers of Pop-Tarts, Cheez-It, Rice Krispies, and Chips Deluxe cookies?

There are, indeed, some healthy ingredients: oat bran, potassium; you can even get a version made with soy protein. But there's sugar listed as the second ingredient. High-fructose corn syrup is also listed prominently. (Remember this issue? High-fructose corn syrup causes overwhelming sugar cravings, causes your triglycerides to skyrocket, and is probably among the principal food ingredients that make you obese.)

Upon detailed questioning of my patients struggling to lose weight, this and products like it are often among the "healthy" foods they've gravitated towards. We spend a great deal of time dissuading them of this idea.

A one-cup serving of Smart Start is low in fat (1 gram) but contains 43 grams of carbohydates, of which there are 14 grams of sugar. There are a meager 3 grams of fiber. To me, this sounds like a cupcake.

The Kellogg's people are exceptionally clever marketers. Partner with the American Heart Association and movie stars? Brilliant!

You should trust food manufacturer advertising about as much as you trust drug manufacturer advertising, which is to say not at all.

Kellogg's sold $10 billion dollars of food products last year. They are the world's leading producer of breakfast cereals. They are a leading producer of convenience foods: cookies, crackers, cereal bars, and frozen waffles under the brands Keebler, Pop-Tarts, Eggo, Cheez-It, Nutri-Grain, Rice Krispies, Famous Amos, and Kashi.

Can they cash in on healthy trends? They'll certainly try.

Does anybody have a normal vitamin D level?

15. May 2006 William Davis (0)
We now routinely check everyone's vitamin D blood level at the start of the program. (The measure to obtain is 25-OH-Vitamin D3. This is not to be confused with 1,25-OH2-vitamin D3, which is a kidney function measure.)

Of the 10 people with levels drawn today, none were even close to normal levels (which we define as 50 ng/ml)--not a single one.

The majority were in the range of severe deficiency (<20 ng/ml). Only two had levels in the 30s. None had higher. (Remember: I'm talking about people in Wisconsin, a terribly sunlight-deprived area much of the year. This might not apply quite as vigorously to Florida residents or others in sun-exposed regions.)

Curiously, I've also seen several people this week who had extraordinary quantities of coronary plaque on their heart scans (scores >1000), all of whom had extremely low vitamin D levels. One of these people had fairly unimpressive lipoproteins, with very minimal abnormalities identified. (This is quite unusual, by the way.) It makes you wonder if a profound deficiency of vitamin D is sufficient to act on its own as an instigator of coronary plaque.

The more we examine the issue of vitamin D deficiency, the more fascinating it gets. I suspect we've just scratched the surface and there's a lot more to learn about this tremendously interesting nutrient. Nonetheless, with what we're seeing in our experience, I'm urging everyone to get a blood vitamin D level.

Don't believe your LDL cholesterol!

14. May 2006 William Davis (0)
Harry's case is typical. For years, his doctor told him his LDL cholesterol of 123 mg was okay. But a heart scan score of 490 (90th percentile at age 52) made him question just where his coronary plaque came from.

Lipoprotein analysis told a very different story: His LDL particle number was 2400 nmol, meaning his trueLDL was more like 240 mg, nearly double the value of LDL obtained through his doctor. Harry had other sources of risk, too, but the LDL particle number was a clear stand-out.

Why does this happen? How can LDL cholesterol be so terribly inaccurate?

LDL cholesterols obtained in virtually all labs are not measured, they're calculated. The calculation was developed in the 1960s by Dr. Friedewald at the National Institutes of Health and therefore goes by his name (the Friedewald calculation). Dr. Friedewald derived this simple calculation to permit doctors across the U.S. to obtain LDL cholesterols, which were technically difficult to measure in those days by using measured HDL, total cholesterol and triglycerides.

Doctors were told that the only time that the Friedewald calculated LDL was inaccurate was when triglycerides exceeded 400 mg. So most family practitioners and internists still believe that calculated LDL's are, for the most part, quite accurate.

Nothing could be further from the truth. When LDL's are actually meaured, you find that LDL is rarely accurate. In fact, in our experience, inaccuracy of 30-50% is the rule, sometimes 100%. The one telltale hint that calculated LDL is wrong is when HDL is <50 mg--that's nearly everybody.

So what's your LDL? You won't really know unless it's measured. Our preferred method is NMR (LipoScience) LDL particle number, probably the most accurate of all. Second best: apoprotein B, direct measured LDL, and non-HDL. (We'll cover this issue much more extensively in an upcoming report on the www.cureality.com website in an extensive Special Report.)

Are you the exception?

14. May 2006 William Davis (0)

I read about 40 heart scans this morning. In the stack was a 41-year old man with a heart scan score of 841.

That's terribly high for anyone, let alone a 41-year old person. He's lucky to find out about this before catastrophe strikes.

People like this worry me. In general, we advise men to consider a heart scan age 40 and older; women 50 and older. If there's anything exceptional about your family history or your own history, then you might notch these numbers down another 5-10 years. For instance, if your Dad had a heart attack at age 43, you might consider a scan at age 35. Or, if you've had diabetes for several years and you're a 42-year old woman, you might think about a scan. (Men tend to develop measurable plaque by heart scans 10 years before women.)

There are no hard and fast rules. It's unusual for a male to have a score >0 before age 40. Likewise, it's very uncommon for a woman to have a score >0 before age 50. But there are occasional exceptions--but they can be very important exceptions.

Our 41-year old man with the score of 841, for instance, probably had a high score since his mid-30s. I've seen several women without any obvious risk factors with scores in the several hundred range in their early 40s.

My rule: When in doubt, opt for safety. Every day, I still read about people in their 30s, 40s, and 50s dying of heart attacks. It shouldn't happen.

When in doubt, get the heart scan. The most you'll lose is the cost of the scan and a modest exposure to radiation. If your score is zero, you know you're safe for the next 5 or more years. But if you have an exceptional score at a young age, take preventive action.

Self-empowerment in health: The new wave in health care

12. May 2006 William Davis (0)
Track Your Plaque is just one facet of the broad and powerful emerging wave of self-empowerment in health.

Hospitals, drug and device manufacturers, and the medical establishment don't like this idea. People managing their own health? That's ridiculous! Dangerous! But mostly unprofitable.

Self-empowerment means having easy access to simple, safe, and inexpensive diagnostic tests like heart scans, carotid scans, bone densitometry (for osteoporosis), cholesterol tests, abdominal ultrasound, even brain scans (e.g., CT or MRI) for people with a family history of brain aneurysm.

Opponents of this idea worry about the "false-positives" that come about with broad testing, i.e, detection of abnormalities that are artifactual. Our experience is that false-positives are only an occasional problem with any test. Instead, we find that most people have many true-positives. In CT heart scanning, for example, we find many unsuspected enlarged aortas (potential future aneurysms), valve disorders, and aortic calcium. These are all important in a preventive program. Unfortunately, your doctor's definition of false-positive often means that no corrective procedure or operation is required.

Other evidence that self-empowerment in health is growing:

--The nutritional supplement movement. What better example of power in managing your own health is there than the fabulous array of nutritional supplements available?

--Medications moving to over-the-counter status. Gradually, more and more medications are trickling into availability for you to obtain without a doctor's prescription.

--What I call "retail imaging", i.e. screening ultrasound, heart scans, full body scans, etc. that are available in most states without a doctor's order.

--The Internet. The rapidity and depth of information available on the Internet today is mind-boggling. It will fuel the self-empowerment movement by providing sophisticated information to the health care consumer previously available only through your physician.

--High-deductible health insurance plans. If health care consumers will bear more and more of the costs of health care, they will seize greater responsibility for early identification and prevention to minimize long-term costs.

There are more. But the movement is powerful and broad--and unstoppable. Let the establishment with vested interests in preserving the status quo fuss and complain, just like horse and buggy manufacturers did in the early 1900's when the autmobile came along.

Vitamin D deficiency is rampant

12. May 2006 William Davis (0)
Today alone I've seen several people with severe deficiencies of vitamin D.

We're now checking everyone's blood vitamin D level at the start of the program. The measure that most accurately reflects your vitamin D status is 25-OH-vitamin D3. This is very confusing to many physicians, who traditionally have thought of 1,25-di-Hydroxy vitamin D3 as the standard test to measure. What they're failing to recognize is that this second measure is a kidney product, not a reflection of vitamin D status.

Using 25-OH-vitamin D3, several people today alone had levels of <10 ng/ml, clearly in the category of severe deficiency (generally regarded as <20ng/ml).

The majority of people we see in the office are Wisconsin residents. It's no wonder they're deficient. Although it's mid-May, we've seen the sun only a handful of days this year. And most of the days have been too chilly to wear short sleeves and shorts to permit sufficient surface area for UV exposure.

Living in a sunny climate, however, is no guarantee that you have sufficient blood vitamin D levels. Two recent studies have shown that 30-50% of the residents of sunny southern Florida and Hawaii are also deficient. (Why, I'm not sure.)

Although our experience thus far is anecdotal in several hundred people, my impression is that people who have normal blood levels of vitamin D (we regard normal as 45-50 ng/ml) have a far easier time of halting or regressing coronary plaque.

Vitamin D is among the most exciting nutritional tools we've come across in a long time. The conversation is making the media, which impresses me tremendously, given the fact that nobody stands to profit financially to any significant degree through vitamin D supplementation.

For a wonderful collection of discussions on vitamin D, go to Dr. John Cannell's website, www.vitaminDcouncil.com. You'll find a huge quantity of scientific background and conversation on the whole idea. I believe you will be thoroughly impressed with just how powerful the argument in favor of vitamin D has become.

What if wheat products were illegal?

11. May 2006 William Davis (3)
Imagine if anything made of wheat were illegal: bread, bagels, crackers, pasta, pretzels, donuts, Shredded Wheat cereal, Raisin Bran, pastry, cookies, cakes, cupcakes. . . Your grocery store would then be unable to carry any of these products.

How empty would the grocery store shelves be?

There would be very little. The stores would be filled instead with vegetables and fruits, meats, and dairy products. But aisle after aisle would be empty. There'd be no cereal aisle. There'd be no snack chip aisle. The ordinarily overcrowded bread shelves wouldn't be there.

Bakery? Nope, not there either. Pasta and noodles? Empty. How about cakes and pastries? Also gone.

Getting the picture? American groceries are dominated by wheat products. What would happen to your health and the health of your family if wheat were abruptly removed from your choices? Would you be less healthy?

No. In fact, your health would be hugely improved. You'd lose a significant quantity of weight. Extraordinary numbers of people would lose diabetic or pre-diabetic tendencies. Feelings of sluggishness, sleepiness, and moodiness would dissolve. Blood pressure would be reduced. The incidence of cancer, skin disease, and inflammatory diseases would plumet.

From a plaque control perspective, your HDL cholesterol would rise, triglycerides drop. Small LDL would improve dramatically.

The message: Slash wheat products from your diet. Yes, you'll miss the smell and taste of freshly baked bread. But you'll do it for many more healthy years. And you may do it without a 14 inch scar in your chest.

The sobering tale of small LDL

10. May 2006 William Davis (0)
Every day, I learn to respect small LDL more and more.

Small LDL particles, and its evil partner, low HDL, is among the most common reasons why someone fails to fully gain control of coronary plaque and heart disease risk.

Just yesterday, I saw a slender businessman (6 feet 1 inch in height, 186 lb.) whose small pattern persisted despite niacin, fish oil, oat bran, and raw almonds. We generally think of small LDL as an overweight person's pattern, but in some people the genetics are quite powerful and it can be expressed even in slender people.

The solution: More physical activity and exercise; cut back on processed carbohydrates, particularly wheat products like breads, pasta, crackers, breakfast cereals; think about magnesium (see our two recent reports on magnesium on the www.cureality.com membership website, the latest report to be posted this week); be sure sleep is adequate (gauge this by whether you're energetic during the day and don't fall asleep watching TV or movies). Lack of sufficient physical activity in people with sedentary jobs is probably among the most common reason the small LDL pattern persists.

Ignore small LDL and it can be like a hidden cancer in your body, growing and metastasizing (not literally, of course), fueling coronary plaque growth. Be sure your doctor assesses whether you have small LDL if you hope to gain control of your coronary risk.

Burn off the fat

9. May 2006 William Davis (0)

If you've ever wondered just how many calories you're burning with various activities like yard work, driving, climbing stairs, etc. go to this great website that will calculate it for you: http://www.caloriecontrol.org/exercalc.html.

Here are some examples:


Dancing for 30 minutes(fast, e.g., tango): 193 calories
Yoga for 30 minutes: 204 calories
Washing the car for 30 minutes: 173 calories
Vacuuming for 30 minutes: 88 calories

(All are for a 170 lb person.)

As you see, physical activity does not necessarily have to consist of exercise. It doesn't require fancy equipment or expensive outfits. But it does require you to keep moving. Sedentary work is among the most common reasons I see in my patients for failing to control weight and its associated lipoprotein patterns, like low HDL and small LDL.

If your work is sedentary, then a minimum of 60 minutes of physical activity per day is necessary to begin to correct weight-related patterns. If you gauge by calories burned, then a useful goal is 500 calories per day in physical activity--at a minimum.
All posts by william-davis

Medicine ain't what it used to be

15. June 2011 William Davis (0)
The practice of medicine ain't what it used to be.

For instance:

White coats are out-of-date--Not only do they serve as filthy reservoirs of microorganisms (since they hang unwashed after repeated use week after week), they only serve to distance the practitioner from the patient, an outdated notion that should join electroshock therapy to treat homosexuality and other "disorders" in the museum of outdated medical practices.

Normal cholesterol panel . . . no heart disease?

15. June 2011 William Davis (19)
I often hear this comment: "I have a normal cholesterol panel. So I have low risk for heart disease, right?"

While there's a germ of truth in the statement, there are many exceptions. Having "normal" cholesterol values is far from a guarantee that you won't drop over at your daughter's wedding or find yourself lying on a gurney at your nearest profit-center-for-health, aka hospital, heading for the cath lab.

Statistically, large populations do indeed show fewer heart attacks at the lower end of the curve for low total and  LDL cholesterol and the higher end of HDL. But that's on a population basis. When applied to a specific individual, population observations can fall apart. Heart attack can occur at the low risk end of the curve; no heart attack can occur at the high risk end of the curve.

First of all, to me a "normal" lipid panel is not adhering to the lax notion of "normal" specified in the lab's "reference range" drawn from population observations. Most labs, for instance, specify that an HDL cholesterol of 40 mg/dl or more and triglycerides of 150 mg/dl or less are in the normal ranges. However, heart disease can readily occur with normal values of, say, an HDL of 48 mg/dl and triglycerides of 125 mg/dl, both of which allow substantial small oxidation-prone LDL particles to develop. So "normal" may not be ideal or desirable. Look at any study comparing people with heart disease vs. those without, for instance: Typical HDLs in people with heart attacks are around 46 mg/dl, while HDLs in people without heart attacks typically average 48 mg/dl--there is nearly perfect overlap in the distribution curves.

There are also causes for heart disease that are not revealed by the lipid values. Lipoprotein(a), or Lp(a), is among the most important exceptions: You can have a heart attack, stroke, three stents or bypass surgery at age 40 even with spectacular lipid values if you have this genetically-determined condition. And it's not rare, since 11% of the population express it. How about people with the apo E2 genetic variation? These people tend to have normal fasting cholesterol values (if they have only one copy of E2, not two) but have extravagant abnormalities after they eat that contribute to risk. You won't know this from a standard cholesterol panel.

Vitamin D deficiency can be suggested by low HDL and omega-3 fatty acid deficiency suggested by higher triglycerides, but deficiencies of both can exist in severe degrees even with reasonably favorable ranges for both lipid values. Despite the recent inane comments by the Institute of Medicine committee, from what I've witnessed from replacing vitamin D to achieve serum 25-hydroxy vitamin D levels of 60-70 ng/ml, vitamin D deficiency is among the most powerful and correctable causes of heart disease I've ever seen. And, while greater quantities of omega-3 fatty acids from fish oil are associated with lower triglycerides, they are even better at reducing postprandial phenomena, i.e., the after-eating flood of lipoproteins like VLDL and chylomicron remnants, that underlie formation of much atherosclerotic plaque--but not revealed by fasting lipids.

I view standard cholesterol panels as the 1963 version of heart disease prediction. We've come a long way since then and we now have far better tools for prediction of heart attack. Yet the majority of physicians and the public still follow the outdated notion that a cholesterol panel is sufficient to predict your heart's future. Nostalgic, quaint perhaps, but as outdated as transistor radios and prime time acts on the Ed Sullivan show.

 

Idiot farm

11. June 2011 William Davis (10)
The notion of genetic modification of foods and livestock is a contentious issue. The purposeful insertion or deletion of a gene into a plant or animal's genome to yield specific traits, such as herbicide resistance, nutritional composition, or size, prompted the Codex Alimentarius Commission, an international effort to regulate the safety of foods, to issue guidelines concerning genetically-modified foods.

The committee is aware of the concept of unintended effects, i.e., effects that were not part of the original gene insertion or deletion design. In their report, last updated in 2009, they state that:

Unintended effects can result from the random insertion of DNA sequences into the plant genome, which may cause disruption or silencing of existing genes, activation of silent genes, or modifications in the expression of existing genes. Unintended effects may also result in the formation of new or changed patterns of metabolites. For example, the expression of enzymes at high levels may give rise to secondary biochemical effects or changes in the regulation of metabolic pathways and/or altered levels of metabolites.

They make the point that food crops generated using techniques without genetic modification are released into the food supply without safety testing:

New varieties of corn, soybean, potatoes and other common food plants are evaluated by breeders for agronomic and phenotypic characteristics, but generally, foods derived from such new plant varieties are not subjected to the rigorous and extensive food safety testing procedures, including studies in animals, that are typical of chemicals, such as food additives or pesticide residues, that may be present in food.

In other words, conventional plant breeding techniques, such as hybridization, backcrossing, and introgression, practices that include crossing parental plants with their progeny over and over again or crossing a plant with an unrelated plant, yield unique plants that are not subject to any regulation. This means that unintended effects that arise are often not identified or tested. Plant geneticists know that, when one plant is crossed with another, approximately 5% of the genes in the offspring are unique to that plant and not present in either parent. It means that offspring may express new characteristics, such as unique gliadin or gluten proteins in wheat, not expressed in either parent and with new immunological potential in consuming humans.

Dr. James Maryanski, the FDA's Biotechnology Coordinator, stated during Congressional testimony in 1999 that:

The new gene splicing techniques are being used to achieve many of the same goals and improvements that plant breeders have sought through conventional methods. Today's techniques are different from their predecessors in two significant ways. First, they can be used with greater precision and allow for more complete characterization and, therefore, greater predictability about the qualities of the new variety. These techniques give scientists the ability to isolate genes and to introduce new traits into foods without simultaneously introducing many other undesirable traits, as may occur with traditional breeding. [Emphasis mine.]

Efforts by the Codex Alimentarius and FDA are meant to control the introduction and specify safety testing procedures for genetically modified foods. But both organizations have publicly stated that there is another larger problem that has not been addressed that predates genetic modification. In other words, conventional methods like hybridization techniques, the crossing of different strains of a crop or crossing two dissimilar plants (e.g., wheat with a wild grass) have been practiced for decades before genetic modification became possible. And it is still going on.

In other words, the potential hazards of hybridization, often taken to extremes, have essentially been ignored. Hybridized plants are introduced into the food supply with no question of human safety. While hybridization can yield what appear to be benign foods, such as the tangelo, a hybrid of tangerines and grapefruit, it can also yield plants containing extensive unintended effects. It means that unique immunological sequences can be generated. It might be a unique gliadin sequence in wheat or a unique lectin sequence in beans. None are tested prior to selling to humans. So the world frets over the potential dangers of genetic modification while, all along, the much larger hazard of hybridization techniques have been--and still are--going on.

Imagine we applied the hybridization techniques applied by plant geneticists to humans, mating an uncle with his niece, then having the uncle mate again with the offspring, repeating it over and over until some trait was fully expressed. Such extensive inbreeding was practiced in the 19th century German village of Dilsberg, what Mark Twain described as "a thriving and diligent idiot factory."

Eat triglycerides

8. June 2011 William Davis (31)
Dietary fats, from olive oil to cocoa butter to beef tallow, are made of triglycerides.

Triglycerides are simply three ("tri-") fatty acids attached to a glycerol backbone. Glycerol is a simple 3-carbon molecule that readily binds fatty acids. Fatty acids, of course, can be saturated, polyunsaturated, and monounsaturated.

Once ingested, the action of the pancreatic enzyme, pancreatic lipase, along with bile acids secreted by the gallbladder, remove triglycerides from glycerol. Triglycerides pass through the intestinal wall and are "repackaged" into large complex triglyceride-rich (about 90% triglycerides) molecules called chylomicrons, which then pass into the lymphatic system, then to the bloodstream. The liver takes up chylomicrons, removes triglycerides which are then repackaged into triglyceride-rich very low-density lipoproteins (VLDL).

So eating triglycerides increases blood levels of triglycerides, repackaged as chylomicrons and VLDL.

Many physicians are frightened of dietary triglycerides, i.e, fats, for fear it will increase blood levels of triglycerides. It's true: Consuming triglycerides does indeed increase blood levels of triglycerides--but only a little bit. Following a fat-rich meal of, say, a 3-egg omelet with 2 tablespoons of olive oil and 2 oz whole milk mozzarella cheese (total 55 grams triglycerides), blood triglycerides will increase modestly. A typical response would be an increase from 60 mg/dl to 80 mg/dl--an increase, but quite small.

Counterintuitively, it's the foods that convert to triglycerides in the liver that send triglycerides up, not 20 mg/dl, but 200, 400, or 1000 mg/dl or more. What foods convert to triglycerides in the liver? Carbohydrates.

After swallowing a piece of multigrain bread, for instance, carbohydrates are released by salivary and gastric amylase, yielding glucose molecules. Glucose is rapidly absorbed through the intestinal tract and into the liver. The liver is magnificently efficient at storing carbohydrate calories by converting them to the body's principal currency of energy, triglycerides, via the process of de novo lipogenesis, the alchemy of converting glucose into triglycerides for storage. The effect is not immediate; it may require many hours for the liver to do its thing, increasing blood triglycerides many hours after the carbohydrate meal.

This explains why people who follow low-fat diets typically have high triglyceride levels--despite limited ingestion of triglycerides. When I cut my calories from fat to 10% or less--a very strict low-fat diet--my triglycerides are 350 mg/dl. When I slash my carbohydrates to 40-50 grams per day but ingest unlimited triglycerides like olive oil, raw nuts, whole milk cheese, fish oil and fish, etc., my triglycerides are 50 mg/dl.

Don't be afraid of triglycerides. But be very careful with the foods that convert to triglycerides: carbohydrates.

 

 

 

 

 

 

 

You've come a long way, baby

3. June 2011 William Davis (16)
In 1945, the room-sized ENIAC vacuum tube computer was first turned on, women began to smoke openly in public, and a US postal stamp cost three cents. And this was the US government's advice on healthy eating:



 

 

 

 

 

 

 

 

 

 

 

 

 

Green and yellow vegetables; oranges, tomatoes, grapefruit; potatoes and other vegetables and fruits; followed by milk and milk products; meat, poultry, fish, or eggs; bread, flour, and cereals, butter and fortified margarine.

In 2011, the computing power of the ENIAC can be performed by a microchip a few millimeters in width, smoking is now banned in public places, and a first class postage stamp has increased in price by 1466%. And this is the new USDA Food Plate for Americans:



 

 

 

 

 

Have we made any progress over the past 65 years? We certainly have in computing power and awareness of the adverse effects of smoking. But have US government agencies like the USDA kept up with nutritional advice? Compare the 2011 Food Plate with the dietary advice of 1945.

It looks to me like the USDA has not only failed to keep up with the evolution of nutritional thought, but has regressed to something close to advising Americans to go out and buy stocks on the eve of the 1929 depression. Most of us discuss issues like the genetic distortions introduced into wheat, corn, and soy; the dangers of fructose; exogenous glycoxidation and lipoxidation products yielded via high-temperature cooking; organic, free-range meats and the dangers of factory farming, etc. None of this, of course, fits the agenda of the USDA.

My advice: The USDA should stay out of the business of offering nutritional advice. They are very bad at it. They also have too many hidden motives to be a reliable source of unbiased information.

 

 

Fasting with green tea

1. June 2011 William Davis (34)
I've been playing around with brief (18-24 hour) fasts with the use of green tea. Of the several variations on fasting, such as juice "fasts,"  I've been most impressed with the green tea experience.

While the weight loss effects of daily green tea consumption are modest, there seems to be a specific satiety effect that has now been demonstrated in multiple studies, such as this and this. In other words, green tea, through an uncertain mechanism, reduces hunger. The effect is not just due to volume, since the effect cannot be reproduced with hot water alone.

I therefore wondered whether green tea might be a useful beverage to consume during a fast, as it might take the "edge" off of hunger. While hunger during a fast in the wheat-free is far less than wheat-consuming humans, there is indeed an occasional twinge of hunger felt.

So I tried it, brewing a fresh 6-8 oz cup evert two hours or so. I brewed a pot in the morning while at home, followed by brewing single cups using my tea infuser at the office. Whenever I began to experience a hunger pang, I brewed another cup and sipped it. I was pleasantly surprised that hunger was considerably reduced. I sailed through my last 18 hours, for instance, effortlessly. The process was actually quite pleasant.

I brew loose Chinese bancha, sencha, and chunmee teas and Japanese gyokuro tea. Gyokuro is my favorite, but also the most expensive. Bancha is more affordable and I've used that most frequently.

If anyone else gives this a try, please report back your experience.

Dreamfields pasta is wheat

28. May 2011 William Davis (11)
An active question on the blogosphere and elsewhere is whether Dreamfields pasta is truly low-carb. Dr. Andreas Eenfeldt of Diet Doctor detailed his high blood glucose experience with it. Jimmy Moore of Livin' La Vida Low Carb had a similar experience, observing virtually no difference when compared to conventional pasta.

The Dreamfields people make the claim that "Dreamfields' patent-pending recipe and manufacturing process protects all but 5 grams of the carbohydrates per serving from being digested and therefore lessens post-meal blood glucose rise as compared to traditional pasta." They call the modified carbohydrates "protected" carbs.



In other words, they are making the claim that they've somehow modified the amylopectin A and amylose molecules in durum wheat flour to inhibit conversion to glucose.

I'd like to add something to the conversation: Dreamfields pasta is wheat. It is a graphic demonstration that, no matter how you cut it, press it, sauce it up, "protect" it, it's all the same thing: wheat. (It reminds me of a bad girlfriend I had in my 20s: She'd put on makeup, a pretty dress, I'd take her out someplace nice . . . She was still an annoying person who whined about everything.)

Wheat is more than a carbohydrate. It is also a collection of over 1000 proteins, including gliadins, glutens, and glutenins. Gliadins, for instance, are degraded to polypeptide exorphins that underlie the addictive potential of wheat, as well as its withdrawal phenomenon on halting consumption. Gliadin-derived exorphins are also the triggers of auditory hallucinations and paranoid delusions in schizophrenia, as well as behavioral outbursts in children with ADHD and autism.

Wheat is a source of lectins that have the curious effect of "unlocking" the proteins of the intestinal lining, the oddly-named "zonulin" proteins, that protect you from ingested foreign molecules. Ingest wheat lectins and all manner of foreign molecules gain entry into your bloodstream. Cholera works by a similar mechanism. (How about a love story: Bread in the time of cholera?)

Glutens, of course, are responsible for triggering celiac disease, the devastating small intestinal disease that now afflicts 3 million Americans, although 2.7 million don't even know it. Glutens are also responsible for neurologic conditions like cerebellar ataxia, peripheral neuropathy, and dementia ("gluten encephalopathy") and the skin condition, dermatitis herpetiformis.

Then there are the conditions for which the active wheat components have not been identified, including acid reflux, irritable bowel syndrome, asthma (excepting "bakers' asthma), rheumatoid arthritis, edema and fluid retention, and a long list of skin conditions from alopecia to gangrene.

My point: Yeah, Dreamfields pastas, from these instructive experiences, acts a lot like conventional durum wheat pasta. But, even if Dreamfields or somebody else perfects the low-carb aspect of it, it's still wheat. Modern wheat is the genetically tarted-up version of Triticum aestivum, the product of genetic shenanigans from the 1960s and 1970s.

Bet you can't fast

26. May 2011 William Davis (28)
People who continue to consume the world's most destructive grain, i.e., wheat, can rarely endure fasting--not eating for an extended period--except by mustering up monumental willpower. That's because wheat is a powerful appetite stimulant through its 2-hour cycle of exaggerated glycemia followed by a glucose low, along with its addictive exorphin effect. Wheat elimination is therefore an important first step towards allowing you to consider fasting.

Why fast? I regard fasting as among the most underappreciated and underutilized strategies for health.

In its purest form, fasting means eating nothing while maintaining hydration with water alone. (Inadequate hydration is the most common reason for failing, often experienced as nausea or lightheadedness.) You can fast for as briefly as 15 hours or as long as several weeks (though I tell people that any more than 5 days and supervision is required, as electrolyte distortions like dangerously low magnesium levels can develop).

Among its many physiological benefits, fasting can:

  • Reduce blood pressure. The blood pressure reducing effect can be so substantial that I usually have people hold some blood pressure medications, especially ACE inhibitors and ARB agents, during the fast since blood pressure will drop to normal even without the drugs. (A fascinating phenomenon all by itself.)

  • Reduce visceral fat, i.e., the fat that releases inflammatory mediators and generates resistance to insulin.

  • Reduce inflammatory measures

  • Reduce liver output of VLDL that cascades into reduced small LDL, improved HDL "architecture," and improved insulin responsiveness. (The opposite of fasting is "grazing," the ridiculous strategy advocated by many dietitians to control weight. Grazing, or eating small meals every two hours, is incredibly destructive for the opposite reason: flagrant provocation of VLDL production.)

  • Accelerate weight loss. One pound per day is typical.


Beyond this, fasting also achieves unique subjective benefits, including reduced appetite upon resumption of eating. You will find that as single boiled egg or a few slices of cucumber, for example, rapidly generate a feeling of fullness and satisfaction. Most people also experience greater appreciation of food--the sensory experience of eating is heightened and your sense of texture, flavors, sweetness, sourness, etc. are magnified.

After decades of the sense-deadening effects of processed foods--over-sugared, over-salted, reheated, dehydrated then just-add-water foods--fasting reawakens your appreciation for simple, real food. On breaking one of my fasts, I had a slice of green pepper. Despite its simplicity, it was a veritable feast of flavors and textures. Just a few more bites and I was full and satisfied.

Once you've fasted, I believe that you will see why it is often practiced as part of religious ritual. It has an almost spiritual effect.

More on fasting to come . . .

Total cholesterol 220

24. May 2011 William Davis (17)
Talking about total cholesterol is like wearing a tie-dyed t-shirt with the peace sign emblazoned on the front: So totally 60s and out of date.

But talk of total cholesterol somehow keeps on coming back. After I spend 45 minutes discussing a patient's lipoprotein patterns, for instance, they'll asking something like, "But what's my total cholesterol?"

To help put this ridiculous notion of total cholesterol to rest, let me paint several pictures of what total cholesterol can tell you. Let's start with a theoretical, but very common, total cholesterol value of 220 mg/dl. Recall that:

LDL cholesterol = total cholesterol - HDL cholesterol - triglycerides/5

Note that LDL cholesterol is nearly always a calculated value. (Yes, your doctor has been treating a calculated, what I call "fictitious," value.)

Rearranging the equation:

Total cholesterol = LDL cholesterol + HDL cholesterol + Triglycerides/5

This relationship means that a great many variations are possible, all under total cholesterol = 220 mg/dl. For example:

LDL 95 mg/dl + HDL 105 mg/dl + Triglycerides 100 mg/dl

(a relatively low-risk pattern for heart disease)

LDL 160 mg/dl + HDL 50 mg/dl + Triglycerides 50 mg/dl

(an indeterminate risk pattern, potentially moderate risk)

LDL 120 mg/dl + HDL 30 mg/dl + Triglycerides 350 mg/dl

(a potentially high-risk pattern)

LDL 60 mg/dl + HDL 25 mg/dl + Triglycerides 675 mg/dl

(an indeterminate risk pattern)

 

That's just a sample of the incredible variation of patterns that can all fall under this simple observation, total cholesterol 220 mg/dl.

Total cholesterol is an outdated concept, one ready long ago for the junk heap of outdated ideas. It's time to throw total cholesterol out in the trash along with beliefs like high-fat intake causes diabetes, whole grains are healthy, and the tooth fairy will leave you money when you leave your molars under the pillow.

Scientists are freakin' liars

14. May 2011 William Davis (3)
So says Tom Naughton, referring to the frequent misinterpretations or misrepresentations of data that characterize much medical research. Dr. Andreas Eenfeldt posted Tom Naughton's recent wonderfully engaging and hilarious talk from Jimmy Moore's Low-Carb Cruise on his Diet Doctor blog.

Comedian and blogger Tom Naughton, also the filmmaker of the movie Fat Head, has brought humor and personality into the low-carb movement. I told my wife to watch it and I could hear her laughing from 30 feet away while watching her laptop.

Dr. Eenfeldt is a sensation of sorts himself, making a big low-carb splash in Sweden. While I missed the cruise this year (due to time pressures), it's clear that Eenfeldt and Naughton have contributed substantially to helping people understand the nonsense that passes as dietary advice in the U.S. and the world.

I watched Naughton's talk while eating my three eggs scrambled with ricotta cheese. I almost spit my eggs out at the computer screen I was laughing so hard.

 

Why do the Japanese have less heart disease?

24. April 2011 William Davis (49)
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?

20. April 2011 William Davis (52)
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

18. April 2011 William Davis (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?

12. April 2011 William Davis (67)
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

9. April 2011 William Davis (30)
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

7. April 2011 William Davis (37)
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?

7. April 2011 William Davis (17)
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

5. April 2011 William Davis (0)
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

4. April 2011 William Davis (5)
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

3. April 2011 William Davis (13)
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

In heart disease prevention, shoot for perfection

12. April 2006 William Davis (0)
It really struck me today that it's the people who've chosen to compromise their prevention program who end up with trouble--heart procedures, heart attack, even heart failure.

Take Bob, for example. Bob is 73 years old and had a bypass operation in 2000. The procedure went well and Bob enjoyed 6 years of seemingly trouble-free life. Bob had a seriously low HDL cholesterol for which he as taken a modest dose of niacin, but was unwilling to do much more. His HDL cholesterol was thererefore "stalled" at around 40 mg. (We aim for 60 mg or greater.) We talked repeatedly about the options for increasing HDL but Bob was content with his results. After all, since his bypass operation, he'd felt well and could do all he wanted without physical limitation.

But Bob underwent a stress test for surveillance purposes (which we routinely do 5 or more years after bypass surgery). The test was markedly abnormal with two major areas of poor blood flow to his heart (signalling potential heart attack in future). Bob ended up getting 5 stents to salvage two bypass grafts, both of which showed signs of substantial degeneration.

I've seen this scenario repeatedly: A person is unwilling to go the extra mile to obtain perfection in lipid/lipoprotein patterns, lifestyle changes, and taking the basic, required supplements. Compromises eventually catch up to you in the form of another heart attack, more procedures, heart failure, physical disability, even death.

The message: Don't draw compromises in heart disease prevention. Coronary plaque is a chronic process. It will take advantage of you if you ever let your guard down.

The epidemic of small LDL

11. April 2006 William Davis (0)
Of the patients I saw in my office yesterday, virtually EVERYONE had small LDL.

Small LDL is emerging as an extraordinarily prevalent lipoprotein pattern that drives coronary plaque growth. Previous estimates have put small LDL as affecting only 20-30% of people with coronary disease. However, in my experience in the last few years, I would estimate that greater than 80% of people with measurable coronary plaque have small LDL.

If you have a heart scan score >zero, chances are you have it, too.

I call small LDL a "modern" disease because it has skyrocketed in prevalence recently because of the great surge in inactivity in Americans.

When's the last time you walked to the grocery store and back, lugging two bags of groceries? How many years has it been since you've push-mowed your lawn? All the small conveniences of life have permeated further and further into our activities. Most of us spend the great majority of our day right where you are now--on your duff.

On the bright side, small LDL in most people is reducable by simply getting up and going. But the old teaching of 30 minutes of activity per day is now outdated. This was true when the other hours of your life included physical activities, like housework or a moderately active job. However, if the other 23 1/2 hours of your day are sedentary, then 30 minutes a day won't do it. An hour or more of activity, whether exercise or physical labor of some variety will get you better small LDL-suppressing results.

For most people with small LDL, fish oil and niacin are also necessary to fully suppress small LDL to the Track Your Plaque goal of <10 mg/dl.

A great discussion on vitamin D

10. April 2006 William Davis (0)
If you need better convincing that vitamin D is among the most underappreciated but crucial vitamins for health, see Russell Martin's review of vitamin D and its role in cancer prevention. You'll find it in March, 2006 Life Extension Magazine or their www.LEF.org website at:

http://search.lef.org/cgi-src-bin/MsmGo.exe?grab_id=0&page_id=1308&query=vitamin%20d&hiword=VITAM%20VITAMER%20VITAMERS%20VITAMI%20VITAMINA%20VITAMINAS%20VITAMINC%20VITAMIND%20VITAMINE%20VITAMINEN%20VITAMINES%20VITAMINIC%20VITAMINK%20VITAMINS%20d%20vitamin%20

Our preliminary experience over the past year suggests that vitamin D may be the crucial missing link in many people's plaque control program. We've had a handful of people who, despite an otherwise perfect program (LDL<60, HDL>60, etc.; vigorous exercise, healthy food selection, etc.--I mean perfect)continued to show plaque growth. The rate of growth was slower than the natural expected rate of 30% per year, but still frightening rates of 14-18% per year--until we added vitamin D. All of a sudden, we saw dramatic regression of 7-25% in 6 months to a year.

This does not mean that vitamin D all by itself regresses plaque. I believe it means that vitamin D exerts a "permissive" effect, allowing all the other treatments (fish oil, LDL reduction, HDL raising, correction of small LDL, etc.) to exert their full benefit. So please don't stop everything and just take D. This will not work. However, adding vitamin D to your program on top of the basic Track Your Plaque approach--that's the best way I know of.

MSNBC Report: We need more heart procedures!

10. April 2006 William Davis (0)
A recent headline from MSNBC by Robert Bazell reads:

NEW YORK - Angioplasty, bypass surgery and cholesterol-lowering medications are among the many interventions that have brought a sharp decrease in heart disease deaths in recent years. But, as Dr. Sharon Hayes of the Mayo Clinic points out, there is one big problem.

“The death rates in women have not declined as much as they have in men,” she says.

The piece goes on to suggest that women are getting short-ended in the diagnosis of heart symptoms and heart attack. The solution: More testing to assess the need for procedures like bypass.

This is typical of the device and medication-dominated media consciousness: More procedures, more medication, more devices. Who's paying for advertising, after all? The money at stake is huge. But is this what you want?

Don't be swayed by media reporters with limited understanding of the real issues (at best), consciousness of who's paying for advertising (at worst). Yes, heart disese is often underestimated or misdiagnosed in women. The answer is better detection earlier in life followed by efforts to halt the process--effective, safe treatments for people's benefit, not just profit.

What role cholesterol medication?

10. April 2006 William Davis (0)
A frequent conversation point among my patients, as well as participants in the www.cureality.com program, is "Are cholesterol medications really necessary?"

No, they are not. What IS necessary is to correct all manifest and hidden causes of coronary plaque. Among these causes, in my view, is LDL cholesterol of 60 mg/dl or greater. There are many other causes of coronary plaque--e.g., small LDL particles, unrecognized hypertension, Lp(a), hidden diabetic patterns, etc.--but reducing LDL to 60 mg is still an important part of a plaque-reversing effort.

Insofar as we wish to get LDL to this goal, the statin cholesterol drugs like Lipitor, Zocor, Crestor, etc. may play a role. However, they should only be considered after a full effort dietary program is pursued. Don't follow the American Heart Association's diet unless you want to fail. It's nonsense.

For a more detailed discussion of how to use nutrition and nutritional supplements to reduce LDL cholesterol, go to www.lef.org, the website for the Life Extension Foundation. I wrote an article for their magazine called "Cholesterol and Statin Drugs: Separating Hype from Reality". You'll find the article at http://search.lef.org/cgi-src-bin/MsmGo.exe?grab_id=0&page_id=1295&query=davis%20cholesterol%20natural&hiword=CHOLESTEROLA%20CHOLESTEROLS%20DAVI%20DAVID%20DAVIE%20DAVIES%20DAVIN%20DAVIO%20DAVISON%20DAVISS%20DAVIT%20NATURALBASED%20NATURALES%20NATURALIZED%20NATURALLY%20NATURALS%20NATURE%20NATURES%20cholesterol%20davis%20natural%20.)

Can your plaque-reversal efforts succeed without statin drugs? It depends on your causes. For instance, someone with small LDL and Lp(a) only may do great on our basic program and then add niacin. Unfortunately, another person with a starting LDL cholesterol of 240 mg/dl--sky high--will have more success with these drugs.

Believe me, I am no blind supporter of drug companies and their flagrantly profit-seeking practices which, in my view, are cut-throat, shoving anyone and anything out of their way to increase profits and market share. I share many of Dr. Dave Warnarowski's views on how vicious their tactics can be; see his recent Blog post at http://www.drdavesbest.com/blog/ called "I smell a rat".

Nonetheless, the deep and well-funded research of the pharmaceutical industry does yield some useful tools. You don't have to love the insect exterminator, but if your house is being eaten by termites, his services can be useful. Same thing with these drugs. Useful--not the complete answer, not even close, but nonetheless useful in the right situations. Sometimes antibiotics are necessary, even life saving. That's how cholesterol drugs are, too.

Take it all in the proper perspective. Your goal is not cholesterol reduction, per se, but plaque control, preferably reversal.

Supplement Mania!

9. April 2006 William Davis (3)
Ever hear of "polypharmacy"? That's when someone takes too many medicines. People will have lists of 15-20 prescription medicines, for instance, with crazy interactions and oodles of side-effects.

Well, how about "poly-supplments"? That's when someone takes a large number of nutritional supplements.

Let me tell you about a 45 year old man I met.

In an effort to rid himself of risk for heart disease that he felt was likely shared with his family (brother and father diagnosed with heart attacks in their late 40s), Steve followed a program of nutritional supplementation. You name it, he took it: hawthorne, anti-oxidant mixtures, vitamins C, E, B-complex, saw palmetto, 7-keto DHEA, velvet deer antler, gingko biloba, policosanol, chronium picolinate, green tea, pine bark extract, St. John's Wort, CoEnzyme Q10, papain and other digestive enzymes...He became a distributor for a nutritional supplement company to allow him to afford his own extraordinary program.

To satisfy himself that he had indeed "cured" himself of heart disease, he got himself a CT heart scan. His score: 470, in th 99th percentile. Steve's heart attack risk based on this score was around 10% per year. High risk, no question.

For weeks after his scan, Steve admitted walking around in a daze, not knowing what to do. Years of telling himself that he had effectively dealt with his heart disease risk, now all down the drain.

When we met, I persuaded him that to think that this collection of supplements would reverse heart disease was magical thinking. We trimmed his list down to the essentials and got him on the right track.

Heart disease is controllable and reversible, but not this way. Don't fool yourself into thinking that some collection of supplements will be enough to stamp out your heart disease risk. Just like taking an antibiotic when you don't have an infection achieves nothing, so does taking the wrong supplements.

What does heart scanning mean to you?

8. April 2006 William Davis (0)
CT heart scans can mean different things to different people.


What does a heart scan mean to you? There are several possibilities:

1) A way of reducing uncertainty in your future.

2) A tool to crystallize your commitment to health.

3) A device to help you track how successful your heart disease prevention program is.

4) A trick to get you in the hospital.

5) A moneymaking tool for unscrupulous physicians hoping to profit from "downstream" testing, particularly heart catheterizations.


Like anything, heart scans can be used for both good and evil. How can you be sure that your heart scan is put to proper use--for your benefit and not someone else's profit?

Simple: Get educated. Understand the issues, be armed with informed questions.

If, for instance, you're a 55-year old female with a heart scan score of 90, active without symptoms, and you're told to have a heart catheterization right off the bat---run the other way. This is bad advice. A heart procedure like catheterization at this score in an asymptomatic woman is very rarely necessary. That decision can only be made after a step-by-step series of decisions are made by a truly interested, unbiased party. (A stress test is almost always required in this situation before the decision can be made to proceed with a catheterization.)

Unfortunately, in 2006, getting unbiased advice from your doctor is still a struggle. That's why we started Track Your Plaque---unbiased information, uncolored by drug or device company support, with an interest in the truth.

Coronary disease is drying up!

7. April 2006 William Davis (1)
I had an interesting conversation with a device representative this morning. He was a sales representative for a major medical manufacturer of stents, defibrillators, and other such devices for heart disease.

Since I'm still involved with hospital heart care and cardiac catheterization laboratories, this representative asked me if I was interested in getting involved with some of the new cardiac devices making it to market over the next year or two. "The coronary market is drying up, what with coated stents and such. We've got to find new profit sources."

Well, doesn't that sum it up? If you haven't already had this epiphany, here it is:

HEART DISEASE IS A PROFITABLE BUSINESS!

Why else can hospitals afford billboards, $10 million dollar annual ad campaigns, etc.? They do it for PROFIT. Likewise, device and drug manufacturers see the tremendous profit in heart disease.

The representative's comments about the market "drying up" simply means that the use of coated stents has cut back on the need for repeat procedures. It does NOT mean that coronary disease is on the way out. On the contrary, for the people and institutions who stand to profit from heart care, there's lots of opportunity.

Track Your Plaque is trying to battle this trend. Heart disease should NOT be profitable. For the vast majority of us, it is a preventable process, much like house fires and dental cavities.

Mammogram for your heart

6. April 2006 William Davis (0)
With the booming popularity of "64-slice CT scans", there's a lot of mis-information about what these tests provide.

These tests are essentially heart scans with added x-ray dye injected to see the insides of the arteries. However, to accomplish this, a large quantity of radiation is required. In addition, the test is not quantitative, that is, it is not a precise measure that can be repeated year after year.

It is okay to have a 64-slice CT coronary angiogram. It is NOT okay to have one every year. That's too much radiation. However, a heart scan can be repeated every year, if necessary, to track progression or regression. Once stabilization (zero change) or reduction is achieved, then you're done (unless your life takes a major change, like a 20 lb weight gain).

The tried-and-true CT heart scan is the gold standard--easy, inexpensive, precise, and repeatable. Not true for 64-slice angiograms.

Is your doctor using "leeches"?

4. April 2006 William Davis (0)
What if you went to your doctor for a problem and he/she promptly placed leeches on your body?

Yeccchhhh! Would you go back? I'd bet that you'd run the other way as fast as your bleeding legs could take you. Outdated health practices like "bleeding" are outdated for good reason.

Then why would you allow your doctor to approach your heart disease prevention program by checking cholesterol and then waiting for symptoms to appear? That miserable approach leads to tragedy and death all too often--ask Bill Clinton! He might as well have had leeches!

Don't allow your doctor's ignorance or disinterest impede your prevention program. Get your coronary plaque measured, then attack it from all sides by knowing all causes, hidden and obvious. That's why Track Your Plaque is such an effective program.

I often wonder why more doctors aren't using this unbelievably powerful approach to deal with heart disease. But when I see colleagues implanting stents, defibrillators, and the like for many thousands of dollars per patient, the answers are obvious. Given a choice of a rational, effective program of prevention that pays the doctor a few hundred dollars for his time, versus $2000 to $10,000 for a procedure, you can see that the temptation is irresistible for many physicians.

The battle for natural hormones

18. April 2007 William Davis (0)
The battle for preservation of availability of compounded natural hormones goes on.

It started with pharmaceutical manufacturer, Wyeth, who petitioned the FDA to disallow the mixing of pharmaceuticals, especially natural human hormones, by specially trained pharmacists at what are called "compounding pharmacies." These are pharmacies that have special equipment and where trained pharmacists can mix up specific preparations for dispensing. These are available by prescription.

For instance, I have been prescribing natural human testosterone and progesterone for nearly 10 years. I have found service to be excellent, with lots of learning materials provided to patients by the pharmacy. The pharmacists I've spoken to have been courteous and knowledgeable. Compounded hormones are also shockingly less expensive. While a testosterone patch from a pharmaceutical company costs around $4.00 per day, the same quantity of testosterone cream formulated by a compouding pharmacy costs around $0.50 per day--87.5% less.

Wyeth hides behind a smoke screen of concern over quality. But the price differences tells the entire story: they want to eliminate the inexpensive competition and hold us all hostage to the far more expensive, often inferior products that they produce. They'd sooner force a woman to use horse-derived Premarin than to allow her access to human estrogens and progesterone.

To me, this is an outrageous affront to our freedom of choice, both as consumers as well as a physician. If you feel as strongly as I do about opposing the unfair and bullying ways of Wyeth Pharmaceuticals and the FDA, the P2C2 association of compounding pharmacists makes writing a letter to your Senator easy by going to

http://iacprx.convio.net/site/PageServer?pagename=P2C2

Just enter your info and personalize the comments, and the e-mails will be generated for you.

Lipitor and memory

17. April 2007 William Davis (2)
At first, I was skeptical. A book from a nutty author and physician named Duane Graveline kept on coming up in conversations with patients. His book, Lipitor: Thief of Memory , details his personal experience with dramatic changes in memory and thought while taking Lipitor.



Now this is a drug that I've seen used thousands of times. But I've now seen about a dozen people who have had distinct struggles with memory and clarity of thinking while taking Lipitor. Most took doses of 40 mg per day or more, though an occasional person takes as little as 10 mg. The association seems to be undeniable, since it improves after two weeks off the drug, recurs when resumed. Just today, I saw two people where this effect may be an issue.

Curiously, I've not seen it with any other statin agent. Unfortunately, uncovering any scientific data on the issue is a hopeless quest. Either it's very uncommon or, worse, the data has been suppressed.

Any way, I believe that Dr. Graveline was right: Lipitor, in a small number of people, does indeed seem to exert real detrimental effects on the mind.

If you take Lipitor, should you stop it in fear of long-term effects on your mental capacity? I think it's premature to toss the drug out based on this relatively uncommon relationship. This particular effect is likely to be idiosyncratic, i.e., peculiar to an occasional person but does not seem to apply to the majority, probably by some quirk of metabolism or penetrability of the barrier between the blood and nervous system tissue.

If, however, you feel that your thinking and memory have deteriorated on the drug, please speak to your doctor.

EKG's and heart disease

16. April 2007 William Davis (6)

How helpful are EKG's for detecting hidden heart disease?

I pose this question because several patients asked this question just this week. It's also a frequent point of confusion and misperception.

Your EKG is nothing more than an expression of the surface electrical activity emitted by heart muscle activity. Multiple (12) leads are attached to the body simply to provide various "views" of this electical activity. EKG, or sometimes "ECG", is short for "electrocardiogram".

What modifies this surface electrical activity? Anything that modifies the electrical activity within the heart itself, or interferes with the detection of the activity. An old heart attack modifies the patterns of electrical conduction in the heart and that can change your EKG. An ongoing heart heart attack likewise. High blood pressure commonly creates changes in the EKG, as does lung disease. A bellyache can change your EKG, as can a stroke. (These non-heart-related phenomena probably are often due to changes in autonomic, or "automatic," nervous system activity.) The heart generates electrical activity in a predictable sequence that generates the heart beat, or "rhythm". EKG's are useful for monitoring heart rhythm, also.

Does having plaque in your coronary arteries have any effect on the EKG? None whatsoever, unless plaque rupture caused heart attack or is about to cause heart attack. So, you can have a horrendous CT heart scan score of, say, 3000, yet maintain a perfectly normal EKG, as long as the heart muscle is normal.

Then why bother with these iffy tests? They are indeed useful to diagnose the cause of active symptoms. For instance, go to the ER with chest pain and an EKG could show changes suggesting that the chest pain is a heart attack. EKG's are also useful for future comparison. Any change in EKG can suggest certain things, like new heart rhythm disturbances unrelated to coronary plaque.

Think of your EKG as just like buying a used car. Say I'm trying to sell you my 1999 Buick Century. It looks pretty good from the outside and I tell you that it has 70,000 miles and runs well. You ask to open the hood, look in the interior and take it out for a drive. I tell you no, you can't do that.

Would you buy the car? Of course you wouldn't. You were permitted only a very superficial examination of the car. You have no idea what's going on inside. Just because the paint job looks brand new doesn't mean the engine and transmission are good.

The same with your EKG: It's a superficial look at one aspect of this used car called your heart. If the EKG is normal, that's good, just like a good exterior on the Buick. But you cannot assume that the heart is otherwise normal.

View the EKG as a simple, superficial test that can only provide minimal reassurance, no matter how often you have it done.

A new Track Your Plaque record

14. April 2007 William Davis (0)
Neal, a 40-year old school principal, and his young wife were terrified on learning of his CT heart scan score of 339, a concerningly high score for any age, particularly age 40.

To make matters worse, all of Neal's plaque was located in the critical left mainstem coronary artery, the shared stem of two of the three coronary arteries. A heart attack in this location is instantly fatal.

So, it was especially gratifying that Neal has set the Track Your Plaque record for largest magnitude of plaque reversal: 51% in his first year.

Studies that show a reduction in heart attack make the news. They talk about 1, 2, up to 6% regression, all achieved with high doses of statin drugs. Yet we are seeing huge, extraordinary quantities of heart disease reversal that haven't yet made headlines, amounts that far exceed those featured in the news. We should be encouraged by experiences like Neal's.

Watch for the upcoming Track Your Plaque newsletter for more details on Neal's story--how he came to the program, how he accomplished this huge effect, and why his experience was such a success. If you haven't yet subscribed, go to the www.cureality.com homepage and click on the upper right hand corner.

The Plavix Scam

12. April 2007 William Davis (3)
Periodically, I'll see a flurry of TV ads for Plavix. It comes with a polished computer-animated cartoon that shows how platelets clump and form a blood clot, causing heart attack.

Imagine there's a pile of oil-soaked rags in a corner of your garage. I come by and tell you to get a good fire extinguisher to keep next to the rag pile in case they spontaneously ignite.

Does that make sense to you?

Wouldn't it be better to get rid of the oily rags and forget about the fire extinguisher?

Plavix is the fire extinguisher. The oil rags are your coronary plaque. The solution is to gain control over plaque behavior. Unfortunately, the TV ads (intentionally, I suspect) give the impression that blood clots just form out of the blue for no reason. Of course that's not true. It requires active, growing, inflamed atheroslcerotic plaque that ruptures, uncovering the "angry" and platelet-adhering material underneath the thin covering or endothelial lining.

Urging everybody to take Plavix is absurd. The TV ads urge many people who have no business taking the drug to take it. There are, without a doubt, groups of people who are better off taking Plavix and aspirin: people who are in the midst of heart attack, people who have unstable plaque, people with recent stents or bypass. Perhaps people at high risk for plaque rupture, e.g., extensive coronary plaque that has continued to grow.

These tactics are consistent with the experiences I've had with the sales representatives from the company (when I used to actually talk to sales reps; my office is now barred from them). The reps very aggressively would urge me to consider having everyone take Plavix. No kidding.


For us, i.e., for people who just have a heart scan score but interested in engaging in a powerful program of prevention and reversal, Plavix rarely provides any advantage. The answer is, just like our oily rag analogy, control the plaque, not put out the fire.

Lipoprotein(a) and small LDL

11. April 2007 William Davis (0)
You won't find a lot of scientific validation for this, but it is my firm impression that small LDL, by some crazy means, has the capacity to "turn on" or "turn off" lipoprotein(a), Lp(a).

Recall that Lp(a) is a specific genetic trait, passed to us (if you have it) by mother or father. It falsely elevates LDL cholesterol and escalates heart disease risk more than just about any other known abnormality.

A frequent hint that Lp(a) might be present is a comment I hear often from patients: "My doctor said statin cholesterol drugs don't work for me. I tried them all and my cholesterol won't go down." Or, the result was substantially less than expected. That's because, when Lp(a) is lurking in your cholesterol value, it is unaffected by the statins.

It's been my in-the-trenches observation that, the more fully expressed the small LDL pattern becomes, the worse the Lp(a) behaves. In other words, if small LDL is suppressed effectively, Lp(a) doesn't seem to carry the same dangers as in someone who has plenty of small LDL. I don't know why this is. (I expect that the answer will come from someone like Dr. Marcovina at Stanford, who is at the forefront of Lp(a) structural research. Lp(a) is a complex molecule with several components. How and why it interacts with other particles remains a mystery.)

There are a little bit of data to confirm this. The Quebec Cardiovascular Study has presented some data to this effect, that the combination of small LDL particles and Lp(a) are a particularly lethal combination. We are trying to correlate our data from a CT heart score perspective to discern any statistical relationships.

This raises a very important therapeutic issue if you have Lp(a): the worst thing you can do if you have Lp(a) is become overweight. Excess abdominal fat is a huge trigger to create small LDL particles. Even though being overweight itself has no effect on the measured level of Lp(a), it activates small LDL which, in turn, throws gasoline on the Lp(a) fire.

If you have Lp(a), stay skinny.

Optimal medical therapy

9. April 2007 William Davis (6)
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

9. April 2007 William Davis (0)
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?

9. April 2007 William Davis (1)
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

8. April 2007 William Davis (1)
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.