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.
All posts by william-davis

Dr. Bill Blanchet: A ray of sunshine

26. June 2008 William Davis (4)
Another heated discussion is ongoing at The Heart.org, this one about Tim Russert's untimely death: Media mulls Russert's death as cardiologists weigh in

Although I posted a couple of brief comments there, I quickly lost patience with the tone of many of the other respondents. Should you choose to read the comments, you will see that many still cling to old notions like heart attack is inevitable, defibrillators should be more widely available, "vulnerable" plaques cannot be identified before heart attacks, etc.

I quickly lose patience with this sort of outdated rhetoric. However, our good friend, Dr. Bill Blanchet of Boulder, Colorado, has a far stronger stomach for this than I do.

Here, a sample of his wonderfully persuasive comments:


Heart disease cannot be stopped but we can certainly do better!

Goals we must achieve if we hope to solve the Rube Goldberg of coronary disease:

1. Find something more reliable than Framingham risk factors to determine who is at risk. Framingham risk factors are wrong more often than they are right. If you are comfortable treating 40% of the patients destined to have heart attacks, continue to rely on “traditional” risk factors only.

2. Treat to new standards beyond NCEP/ATP-III. These accepted standards prevent at best 40% of heart attacks in patients treated. This is unacceptable, and arguably why Tim is dead today! Why prevention protocols emphasize LDL and more or less ignore HDL, triglycerides and underemphasize blood pressure eludes me.

3. Motivate patients to participate in coronary prevention. Saying “you need to get exercise and lose weight” is not adequate motivation, it hasn't worked to date and probably won't work tomorrow. If you are satisfied saying it is "the patient's fault for not listening to me" so be it, that excuse doesn't work for me!

Currently “good results” consist of being able to convince 50% of patients at risk by traditional risk factors to participate in prevention and hopefully 30% will be treated to goal. Of those treated to goal, 60% of the heart attacks will still happen anyway. Mathematically we can hope to prevent <10% of heart attacks with this approach!

I have personally found a solution to this dilemma. It goes like this:

1. EBT-CAC [electron-beam tomography coronary artery calcium] is the most reliable predictor of coronary events period, the end! Anyone who disagrees has not objectively read the literature. The only test more predictive than the initial calcium score is the follow up score 12 to 36 months later. EBT predicted Tim Russert’s event 10 years before it happened; passing his stress test gave him inappropriate reassurance 2 months before he died. If only Tim had the benefit of a second EBT sometime over the last 10 years he and his doctor would have known that what they were doing was insufficient and improvements could have been made.

2. I treat to the standard of stable calcified plaque by EBT (<15% annualized progression, preferably <1% annualized progression). This correlates with a very low incidence of coronary events. Even the ACC/AHA 2007 position paper agrees with this. This is accomplished with aspirin, omega-3 fatty acids, diet, exercise, weight control, smoking cessation, treatment of sleep apnea, stress reduction, control of HDL, triglycerides and LDL cholesterol and excellent control of BP and insulin resistance plus the recent addition of vit D-3. Meeting an LDL goal of 70 is easy but prevents only a minority of events, treating to the goal of stable CAC by EBT is a challenge but when achieved, the reward is near elimination of heart attacks and ischemic strokes. This has indeed been my personal experience!

3. A picture of plaque in the coronary artery is a monumental motivator for patients to get on board to make things better. The demonstration of progression of that plaque despite our initial therapies gets all but a few suicidal patients interested in doing a better job. I think that similar motivational results can be had with carotid imaging; the difference is that CAC by EBT is clinically validated as being a much stronger predictor of events with progression and non-events with stability than any ultrasound test including IVUS.



Wow! I couldn't have said it better.

Sadly, I doubt even Dr. Blanchet's persuasive words will do much to convince my colleagues on this forum. And the cardiologists on this forum are likely among the more inquisitive and open-minded. The ones stuck in the cath lab day and night, or implanting defibrillators, are even less inclined to entertain such conversations.

While I admire Dr. Blanchet's energy for continuing to argue with my colleagues, the lesson I take is: Take charge of health yourself. If you wait for your doctor to do it for you, you could be in the same situation as poor Tim Russert. This is an age when your physician should facilitate your success, not prevent it or leave you wallowing in ignorance.

The Russert Protocol at work

25. June 2008 William Davis (6)
Without a concerted effort at prevention, heart scan scores (coronary calcium scores) grow like weeds. The average rate of growth is 30% per year.

Keith is an illustrative case. At age 39, Keith's heart scan score was 29, in the 99th percentile due to his young age. (In other words, young people before age 40 have no business having plaque. If they do, it's bad.)

True to conventional practice, Keith's doctor prescribed a cholesterol drug (Zocor), asked him to take a baby aspirin, and prescribed a blood pressure medicine. He asked Keith to cut the fat in his diet. His doctor even exceeded conventional (ATP-III) LDL cholesterol treatment targets.

Keith, an intelligent and motivated businessman, happily complied with his doctor's instructions. Eighteen months later, a 2nd heart scan showed a score of 68, representing an increase of 135%, or 76% per year.

This is the very same approach that the late Mr. Tim Russert's doctors employed: treat (calculated) LDL cholesterol with a statin drug, treat high blood pressure, reduce saturated fat, take aspirin. It was a miserable failure in Keith, whose plaque continued to grow at a frightening rate of 76% per year. It was also an obvious failure in poor Tim Russert.

Further investigation in Keith uncovered:

--Severe small LDL--80% of all LDL was small (despite a favorable HDL of 58 mg/dl)
--Measured LDL particle number (NMR) showed that "true" LDL was actually about 60 mg/dl higher than suggested by the crude calculated LDL
--An after-eating (postprandial) disorder (IDL)
--A pre-diabetic blood sugar and insulin
--Severe vitamin D deficiency
--Very low testosterone

All these patterns were present despite the steps Keith and his doctor had instituted. It's no wonder his plaque was undergoing explosive growth.

The conventional approach to coronary disease prevention is inadequate, more often than not a mindless adherence to one-size-fits-all template crafted to a great degree by drug industry interests and "experts" who often stand at arm's length from real live patients.

Keith's "residual" abnormalities are all readily correctable. He has since made dramatic improvements in all parameters. Among the strategies used is a wheat- and cornstarch-free diet that resulted in 12 lbs lost within the first few weeks of effort.

If you are on the "Russert Protocol," have a serious conversation with your doctor about the continued advisability of remaining on this half-assed approach to heart disease. Or, consider finding another doctor.

Petition to the National Institutes of Health

24. June 2008 William Davis (2)
A petition to the National Institutes of Health (NIH) is being circulated in response to the mis-statement made in an NIH-sponsored study, ACCORD.

The ACCORD Trial included over 10,000 type II diabetics and compared an intensive, multiple-medication group to achieve a target HbA1c of <6.0%, with a less intensively treated group with a target HbA1c of 7-7.9%. (HBA1c is a long-term measure of glucose, averaging approximately the last 3 months glucose levels.) To the lead investigators' surprise, the intensively treated group experienced more death and heart attack than the less intensive group. The conclusion suggested that intensive management of diabetes may not be a desirable endpoint and may result in greater risk for adverse events.

The petitioners argue that the problem was not with intensive glucose control per se, but the use of multiple side-effect-generating medications. Unfortunately, the ACCORD conclusions give the impression that loose control over blood sugar may be desirable.

The petition originates from the Nutrition and Metabolism Society, a non-profit organization seeking to promote carbohydrate restriction.


The petition reads:

National Institute of Health re: the ACCORD Diabetes Study: "Intensively targeting blood sugar to near-normal levels ... increases risk of death. "

This statement is untrue. This study lowered blood glucose levels only by aggressive drug treatment.

Preventative measures and proven non-drug treatments are being ignored by the NIH, ADA and many other governing agencies.

There is abundant scientific evidence proving a carbohydrate restricted diet can be as effective as drugs in lowering blood glucose levels safely. Many times diet is more effective than medication in controlling diabetes - all without side effects or increased risk of death.

I ask that the NIH publicly retract the above statement. It is misleading the public.

I also request that the NIH acknowledge the existing science and fund more research by the experts who have experience with carbohydrate restriction as a means of treatment for diabetes.

For more info, or to help people with diabetes, please e-mail info@nmsociety.org .

Thank you.



I added my comment:

In my preventive cardiology practice, I have been employing strict carbohydrate restriction in both diabetics and non-diabetics. This results in dramatic improvement in lipids and lipoprotein abnormalities, substantial weight loss, and improved insulin sensitivity. This experience has been entirely different from the heart disease-causing and diabetes-causing low-fat diets that I used for years.

I have a substantial number of diabetics who have been to reduce their reliance on prescription medication for diabetes or even eliminate them. In my experience, the power of carbohydrate-restricted diets is profound.

However, better clinical data to further validate this approach is needed, particularly as diabetes and pre-diabetes is surging in prevalence. I ask that more funding to further explore and validate this research be made available if we are to have greater success on a broader basis.



If you are interested in adding your voice, you can also electronically sign the petition. It is optional, but you can also add your own comments regarding your own views or experiences.

Wheat withdrawal

24. June 2008 William Davis (16)
It happens in the hospital every so often: A clean-cut, law-abiding person is hospitalized for, say, pneumonia, kidney stones, knee surgery, etc.

Everything's fine until . . . they're running down the hospital hallway stark naked, screaming about snakes on the wall, accusing nurses of trying to kill him, all while yanking out IV's and monitor patches.

It's called alcohol withdrawal. Alcohol withdrawal can range from tremulousness and sweatiness, all the way to delirium tremens, the full-blown form that leads to disorientation, seizures, fever, even death. Withdrawal can also be associated with a number of chronically used agents, such as sedatives/sleeping pills, pain medication/opiates, among others.

How about wheat?

I wouldn't have believed it, but after witnessing this effect countless times, I am convinced there is such a phenomenon: Wheat withdrawal.

You'll recognize it in someone who previously ate bread and other wheat flour-containing products freely, then eliminates them. This is followed by extreme cravings, usually for bread, cookies, or cake; profound fatigue; shakiness; mental fogginess; blue moods. The syndrome can last for up to one week.

Then, bam! Sufferers of wheat withdrawal report mental clarity superior to their wheat-crazed days, improved energy, decreased appetite and cravings, heightened mood, and, of course, fantastic drops in weight.

Why would removal of wheat from the diet trigger a withdrawal phenomenon? I can only speculate, but I believe that at least part of this response is due to a physical conversion from a glycogen (sugar)-burning metabolism to that of a fatty acid (fat mobilizing) metabolism. People who lived in the up-and-down cycle of craving and eating wheat constantly fed the sugar furnace for years and are enzymatically impaired in fat burning; they've been growing fat stores. Eliminating wheat deprives the body of this easy source of glycogen, forcing it to mobilize fatty acids in the fatty tissues. Sluggish at first, people feel fatigue, mental fogginess, etc. Once the enzymatic capacity for fat mobilization revs up, then these feelings dissipate.

Could it also relate to the opioid sequences apparently present in wheat? I wasn't even aware of this fact until a reader of The Heart Scan Blog, Anne, left this comment:

Wheat protein contains a number of opiod peptides which can be released during digestion. Some of these are thought to affect the central and peripheral nervous systems.

When I gave up gluten, I felt much worse for a few days. This is a very common reaction in those who stop eating gluten cold turkey.

Dr. BG provides a fascinating commentary on the addictive/opioid aspect of wheat addictions in her Animal Pharm Blog.

Whatever the mechanism, I believe it is a real phenomenon. It can, at times, be so overwhelming that about 20% of people who try to eliminate wheat find they are simply unable to do it without being incapacitated. Of course, that might be a lesson in itself: If withdrawal is so profound, it hints that there must be something very peculiar going on in the first place.

The Big Squeeze

20. June 2008 William Davis (5)
Some colleagues of mine brought this scary phenomenon to my attention last evening.

As insurance and Medicare reimbursement to doctors and hospitals fall (Medicare is enacting a series of substantial cuts, which will be followed by the private health insurers), you would expect the use of hospital procedures to drop. Makes sense, right? Less money paid per procedure, less incentive to do them.

Unfortunately, that's not how it's playing out in the real world. Your neighborhood interventional cardiologist or cardiothoracic surgeon is accustomed to a level of income and lifestyle. That lifestyle is now threatened by shrinking reimbursement. True to the Law of Unintended Consequences, rather than reducing use of procedures, diminishing procedural fees are prompting a good number of practitioners to do more.

In other words, if each heart catheterization pays less, why not do more of them, along with more stents, pacemakers, defibrillators, and the like? If four heart catheterizations per day pays less, why not do five to make up the difference?

Voila! Income protected. Of course, it comes at the cost of more work. But I will give one thing to my colleageus: They are a generally hard-working bunch who rarely balk at 12-16 hours days in the hospital.

How do you do more procedures? Easy. Just lower the bar on who to do a procedure on. Use more aggressive criteria for pacemaker implantation. Interpret the always-fuzzy nuclear stress tests weighed more towards abnormal. Use scare tactics: "You never know--that chest pain could be the last warning you're going to have!" Because the criteria for performing procedures is "soft" in the real world, it is easy to bend the criteria any way you want.

It's too early to measure the full impact of this unintended consequence of reduced reimbursement. But don't allow yourself to become a casualty in the reimbursement war. Remain vigilant. Recognize that, despite the fuzziness at the edges, there are still rational reasons for performing heart procedures. Always be armed with information and the right questions. Never submit unquestioningly or without satisfactory answers to your questions.

Tim Russert's heart scan score 210. . .in 1998

18. June 2008 William Davis (10)
Despite the media blathering over how Mr. Russert's tragic death from heart attack could not have been predicted, it turns out that he had undergone a heart scan several years ago.

A New York Times article, A Search for Answers in Russert’s Death, reported:

Given the great strides that have been made in preventing and treating heart disease, what explains Tim Russert’s sudden death last week at 58 from a heart attack?

The answer, at least in part, is that although doctors knew that Mr. Russert, the longtime moderator of “Meet the Press” on NBC, had coronary artery disease and were treating him for it, they did not realize how severe the disease was because he did not have chest pain or other telltale symptoms that would have justified the kind of invasive tests needed to make a definitive diagnosis. In that sense, his case was sadly typical: more than 50 percent of all men who die of coronary heart disease have no previous symptoms, the American Heart Association says.

It is not clear whether Mr. Russert’s death could have been prevented. He was doing nearly all he could to lower his risk. He took blood pressure pills and a statin drug to control his cholesterol, he worked out every day on an exercise bike, and he was trying to lose weight, his doctors said on Monday. And still it was not enough.

“What is surprising,” Dr. Newman said, “is that the severity of the anatomical findings would not be predicted from his clinical situation, the absence of symptoms and his performing at a very high level of exercise.”

Buried deeper in this article, the fact that Mr. Russert had a heart scan score of 210 in 1998 is revealed.

That bit of information is damning. Readers of The Heart Scan Blog know that heart scan scores are expected to grow at a rate of 30% per year. This would put Mr. Russert's heart scan score at 2895 in 2008. But the two doctors providing care for Mr. Russert were advising the conventional treatments: prescribing cholesterol drugs, blood pressure medication, managing blood sugar, and doing periodic stress tests.

Conventional efforts usually slow the progression of heart scan scores to 14-24% per year. Let's assume the rate of increase was only 14% per year. That would put Mr. Russert's 2008 score at 779.

A simple calculation from known information in 1998 clearly, obviously, and inarguably predicted his death. Recall that heart scan scores of 1000 or greater are associated with annual--ANNUAL--risk for heart attack and death of 20-25% if no preventive action is taken. The meager prevention efforts taken by Mr. Russert's doctors did indeed reduce risk modestly, but it did not eliminate risk.

We know that growing plaque is active plaque. Active plaque means rupture-prone plaque. Rupture prone plaque means continuing risk for heart attack and death. Heart attack and death means the approach used in Mr. Russert was a miserable failure.

While the press blathers on about how heart disease is a tragedy, as Mr. Russert's doctors squirm under the fear of criticism, the answers have been right here all alone. It sometimes takes a reminder like Mr. Russert's tragic passing to remind us that tracking plaque is a enormously useful, potentially lifesaving approach to coronary heart disease.

Who needs to go next? Matt Lauer, Oprah, Jay Leno, some other media personality? Someone close to you? Can this all happen right beneath the nose of your doctor, even your cardiologist?

I don't need to remind readers of The Heart Scan Blog that heart disease is 1) measurable, 2) trackable, 3) predictable. Mr. Russert's future was clear as long ago as 1998. Every year that passed, his future became clearer and clearer, yet his doctors fumbled miserably.



Copyright 2008 William Davis, MD

Another failure of conventional cardiac care

15. June 2008 William Davis (5)

Though Tim Russert was widely known and respected for his political commentary, he will likely be better remembered as an example of the gross shortcomings of the conventional approach to heart disease.

Let's face it:

Standard heart disease prevention efforts are a miserable failure.

A Track Your Plaque member brought this interview of Mr. Russert's doctor to my attention.

It appears that his doctor did all the correct conventional things. You know what became of it. In the eyes of the public and of any attorney, or even of my colleagues, no wrong was committed. The blame does not lie with Mr. Russert's hapless doctor. The blame lies on the system that endorses procedures, prescription medications, the blind adherence to dogma dictated by the pharmaceutical industry and FDA, along with a prevailing philosophy of preferring the management of catastrophes to preventing them. Dr. Newman's idea of a solution: Making an automatic defibrillator (AED) more widely available (!!!).

How long does this sort of idiocy have to go on? How many people have to die before the system uses the tools that are already available, tools that could have prevented this tragedy and many more like it?

If you and your doctor subscribe to the program that the unfortunate Mr. Russert was prescribed and the brainwashing, unthinking nonsense that his doctor follows, you are a fool. Shame on you. You therefore likely subscribe to the same variety of marketing BS that issues from food manufacturers about Cheerios, whole grains, and low-fat diets.

Get with the program. Sadly, Mr. Russert is not the first, he's not the last. The tragedies of conventional advice that line the pockets of drug and food manufacturers number in the millions. We're not talking about some obscure, rare disease. We're talking about the number one cause of death in both males and females nationwide.

I deeply wish this message could have reached Mr. Russert before his untimely death. We could all look forward to another Sunday morning with his usual incisive, unforgiving probing of the day's political figures.

Tribute to Tim Russert

14. June 2008 William Davis (11)
The sudden passing of news giant, Tim Russert, yesterday of sudden cardiac death struck a blow to American consciousness.

Perhaps his hard-hitting interviewing style, while making guests squirm, made him seem invincible. But, of course, none of us is invincible. We are all vulnerable to this disease.

We should not allow Mr. Russert's tragic death to occur without taking some lessons. The media have already resorted to interviewing prominent doctors for their opinion.


Douglas Zipes, M.D., former President of the American College of Cardiology,was quoted in the media:

"An automated external defibrillator (AED) could have been a life-saver. AEDs should be as common as fire extinguishers."

This is typical sleight-of-hand, medicine-is-too-complex-for-the-public-to-understand sort of rhetoric that is surely to issue from the conventionally-thinking medical people and the press. Instead, let's cut the BS and learn the real lessons from Mr. Russert's needless death.

It is virtually certain that:

--Mr. Russert ruptured an existing coronary atherosclerotic plaque, prompting rhythm instability, or ventricular fibrillation.

--Making automatic external defibrillators (AED) available might have Band-Aided the ventricular fibrillation, but it would not have stopped the heart attack that triggered it.

--Though full details of Mr. Russert's health program have not been made available, it is quite likely that he was prescribed the usual half-witted and barely effective panoply of "prevention": aspirin, statin drug, anti-hypertensive medication. Readers of The Heart Scan Blog and members of Track Your Plaque know that this conventional approach is as effective as aspirin for a fractured hip.

--It is highly unlikely that all causes of Mr. Russert's heart disease had been identified--did he have small LDL (it's certain he did, given his body habitus of generous tummy), Lp(a), low HDL, pre-diabetic patterns, inflammatory abnormalities, vitamin D deficiency, etc.? You can be sure little or none of this had been addressed. Was he even taking simple fish oil that reduces the likelihood of sudden cardiac death by 45%?

--Far more could have been done to have prevented Mr. Russert's needless death. And I don't mean the idiocy of making AED's available in office buildings. I'm talking about preventing the rupture of atherosclerotic plaque in the first place.

Far more can be done to prevent future similar deaths among all of us.

Our jobs are to use the tragic death of Mr. Russert to help those around us learn that heart disease is identifiable and preventable. Though Mr. Russert did not stand for BS in his political commentary, he sadly probably received it in his health advice. Don't let this happen to you or those around you.

Why do skinny people get heart disease?

13. June 2008 William Davis (9)
There's no doubt about it: The majority of people with heart disease are overweight. They may not be grotesquely overweight, just a few pounds over. But weight plays a crucial role in activating numerous factors that heighten risk for heart disease.

Excess weight reduces HDL cholesterol, raises triglycerides, increases small LDL (enormously), fans the fires of inflammatory responses (CRP, IL-6, TNF-alpha, etc.) raises blood pressure, increases resistance to insulin and raises blood sugar. Overweight people tend to be less physically active, may develop diseases of obesity like sleep apnea, and on and on. You've heard this all before.

But why do slender people develop heart disease? If we can't blame weight, what is to blame? By slender, I mean body mass index (BMI) of <25. (Yes, I know there are other ways, better ways, to gauge healthy weight. But, for simplicity, I'll use BMI.) Let's put aside the two obvious causes of heart disease, cigarette smoking and Type I diabetes. (I'd be shocked if any cigarette smokers read this blog.)

Slender people develop heart disease because:

1) They have lipoprotein(a)--The big, big neglected risk factor. In fact, the Lp(a) genotype is, in my casual observation, associated with a slender phenotype (genotypic expression). The prototypical example that makes headlines is the marathon runner--slender and superbly fit, but develops heart disease anyway. People wax on about the uncertainties of exercise and fitness when they hear about Jim Fixx and Alberto Salazar. But one factor would explain it all: Lp(a).

2) The murky category of the normal weight obesity. These people are generally recognizable by their flaccid tummies despite falling into a favorable BMI <25. Small LDL is the standout red flag in these people.

3) They were previously overweight but lost it.

4) They were former smokers.

5) Vitamin D deficiency--Deficiency of vitamin D is important for everyone's health. But there appears to be some people for whom it is the dominant risk. I believe that one of our great Track Your Plaque success stories, Neal, falls into this group. Some people who are vitamin D deficient develop colon cancer, others develop diabetes, others develop osteoporosis or multiple sclerosis, while others develop coronary heart disease and plaque. The likely reason for the varied expression is variation in vitamin D receptor genotypes (VDR genotypes).

6) The murkiest of all: Hypertension genotypic variants. This is a poorly sorted-out category, and one principally based on my observations along with scattered observations in such things as variations in the angiotensin converting enzyme genotypes. But I am convinced that there is a small percentage of slender people who show variation in some genetic type that predisposes to hypertension and heart disease. They also show a propensity towards enlargement of the thoracic aorta. This group is also among the most difficult to control in the Track Your Plaque approach, i.e., they have difficulty slowing or stopping the growth of heart scan scores. While blood pressure control in this group is important, it does not seem to remove the excess source of risk.

So, yes, being slender does put you into a lower risk for heart disease category. But it does not mean you are immune.

You can also be an overweight person who still harbors some of the features of the slender--you're an overweight slender person. The above list can still therefore apply.

Cardiology Confidential

11. June 2008 William Davis (9)

Okay, so it's a shameless knockoff of chef Anthony Bourdain's titillating Kitchen Confidential.

But the confidences that I've heard whispered in the corridors of health involve something more provocative than how your food was prepared. Any service for humans performed by other humans is subject to the idiosyncrasies and weaknesses of human behavior. That's just life.

In healthcare for your heart, the consequences can be more profound than eating three day old fish on Monday's dinner menu.

Over my 15 years practicing cardiology in a variety of settings in three different cities, I've witnessed just about everything from shocking to sublime. Some of it speaks to the extraordinary commitment of people in healthcare, the unexpected courage people show in the midst of illness, the devotion of family in difficult times. It can also speak of mewling, sobbing carryings-on over the most minor conditions, the meanness that emerges when people are frightened, the vultures circling just waiting for Grandpa to kick the bucket and leave his will declaring the spoils.

For the most part, my cardiology colleagues are a hard-working bunch committed to . . . Uh oh. I was going to say "Saving lives, preserving health." But that's not true. Once upon a time, it was true for many of my colleagues, often revealed over $2-a-pitcher beer-softened, "we're going to save people" conversations in medical school. Ahhh, medical school. I remember walking along the street alongside my medical school in St. Louis, bursting with pride and a sense of purpose.

But, for many of us, something sours our purpose through the years. Maybe it's the smell of money, maybe it's the series of distasteful experiences that show that healthcare providers are, in the midst of health crises, the innocent recipients of anger, frustration, disappointment.

Whatever the genesis, the stage is set for an imperfect scenario that pits healthcare provider against patient in a less-than-perfect system.

This would read as a mindless rant if it wasn't based on such pervasive and pravalent truths, tales of the flawed deliverers of healthcare driven by motives less lofty than "saving people."

Take Dr. S, a doctor who performs a large number of procedures on patients. I'm told he is very capable. He manages an extraordinary amount of heart work--in between jail time for wife beating and Medicare fraud.

Or Dr. C, well-known in the region for his procedural talents, also. Usually acerbic and freely-swearing, he opens up engagingly when drinking--which is most of the time. Paradoxically, as is true for some serious drinkers, he works more effectively while intoxicated.

Or Dr. ST, who proudly admitted to me one evening over dinner that he has accepted 6-figure payments from medical device companies on a number of occasions to use their products.

Or the manic ups and downs of Dr. J, who refers just about every patient he sees for emergency bypass surgery when in his down phase, mangles coronary arteries in daring angioplasties during his up phase.

How about 310-lb Dr. P, who hounds her patients about indulgent lifestyles? That would be excusable as innocent lack of self-insight if it weren't for her propensity to use heart procedures on patients as punishment. "I have no choice but to take you to the hospital."

Dr. M. manages to maintain the appearance of straight-and-narrow during the day, all the way to attending church twice a week with his children. His daytime persona effectively covers up his frequent visits to prostitutes.


We are ALL flawed. My colleagues are no different. But some circumstances cultivate the flaws, fertilize corruptibility, reward it. Such has become the state of affairs in healthcare for heart disease. Why? Is it the excessive potential for money-making that existed until recently? Is there something about the save-the-day mentality of heart disease that attracts imperfect personalities looking for the adrenaline-charged thrill but morphs over time into near-psychopathic lives?

It's not the end of the world. The fact that my colleagues' behavior has reached such extravagant lows signals a bottom: things are about to change.

In the meantime, let me tell you a few more secrets . . .



Copyright 2008 William Davis, MD