Unexpected effects of a wheat-free diet

Wheat elimination continues to yield explosive and unexpected health benefits.

I initially asked patients in the office to eliminate wheat because I wanted to help them reduce blood sugar and pre-diabetic tendencies.

A patient would come to the office, for example, with a blood sugar of 118 mg/dl (in the pre-diabetic range) and the other phenomena of pre-diabetes or metabolic syndrome (high blood pressure, high inflammation/c-reactive protein, low HDL, high triglycerides, small LDL), and the characteristic wheat belly. Eliminate wheat and, within three months, they lose 30 lbs, blood sugar drops to normal, blood pressure drops, triglycerides drop by several hundred milligrams, HDL goes up, small LDL plummets, c-reactive protein drops.

People also felt better, with flat tummies and more energy. But they also developed benefits I did not anticipate:

--Improved rheumatoid arthritis--I have seen this time and time again. Eliminate wheat and the painful thumbs, fingers, and other joints clear up dramatically. Many former rheumatoid sufferers people tell me that one cracker or pretzel will trigger a painful throbbing reminder that lasts a couple of hours.

--Improved ulcerative colitis--People incapacitated with pain, cramping, and diarrhea of ulcerative colitis (who are negative for the antibodies for celiac disease) can experience marked improvement. I've seen people be able to stop all their nasty colitis medications just by eliminating wheat.

--Reduction or elimination of irritable bowel syndrome

--Reduction or elimination of gastroesophageal reflux

--Better mood--Eliminating wheat makes you happier and experience more stable moods. Just as wheat is responsible for a subset of schizophrenia and bipolar illness (this is fact), and wheat elimination generates dramatic improvement, when you or I eliminate wheat, we also experience a "smoothing" of mood swings.

--Better libido--I'm not sure whether this is a consequence of losing a belly the size of a watermelon or improvement in sex hormones (esp. testosterone) or endothelial responses, but more interest in sex typically develops.

--Better complexion--I'm not entirely sure why, but various rashes will often dissipate, bags under the eyes are reduced, itching in funny places stops.


It's also peculiar how, after someone eliminates wheat for several months, re-exposure of an errant cracker or sandwich results in cramping and diarrhea in about 30% of people.

Obviously, people with celiac disease, who can even die of exposure to wheat, are even worse. What other common food do you know of that makes us sick so often, even occasionally with fatal outcome?

Is Lp(a) part of your legacy to your children?

If you have lipoprotein(a), Lp(a)--the most aggressive known cause of heart disease that no one has heard of--then you need to tell your children.

Lp(a) is a "cleanly" inherited genetic pattern: If either parent has it, there's a 50% chance that you have it. If you have it, then there's a 50% likelihood that each of your children has it. (Note that each child experiences a likelihood of 50%, not 50% of your children. This is because each child is conceived as an independent statistical event. So much for romance!)

The atherogenicity (plaque-causing potential) of Lp(a) also tends to get transmitted. In other words, if your Dad had a heart attack at age 50 due to Lp(a) and you share Lp(a), then you likely share a similar magnitude of risk as your Dad. If your Mom had Lp(a), though passed quietly at age 89 without any overt evidence of heart disease, then you are likely to share the relatively benign form of Lp(a).

For most of us with Lp(a), however, it is best to assume that it has at least some potential for causing heart disease, being the most aggressive cause known. (That is, until we have the ability in everyday clinical practice to characterize Lp(a) by assessing such factors as the size of the apoprotein(a) molecule, the number of kringle "repeats" on the tail, etc. Until then, we need to rely on the crude, though helpful, observation of family history.)

At what age should you inform your children? There's no hard-and-fast rule. However, I generally suggest to patients that they talk about Lp(a) with their children when they reach their 20s or 30s, old enough to begin to understand the implications and begin to think about adopting healthier lifestyles. Is treatment required at, say, age 35? That depends on the pattern of Lp(a)-related heart disease in the family: With exceptionally aggressive forms, it might be reasonable to begin treatment at this relatively early age.

Do "Heart Healthy" sterols cause heart disease?

The sterol question continues to pop up.

Sterols are an ingredient widely added by food manufacturers that allows a "heart healthy" claim, since sterols have been shown to reduce LDL cholesterol (at least transiently). HOWEVER, sterols have also been implicated in possibly increasing risk for heart disease. After all, people with the genetic condition called sitosterolemia absorb sterols into the blood and develop coronary heart disease in their teens and twenties. Those of us without sitosterolemia who increase sterol intake with sterol-enriched foods increase blood levels of sterols several-fold. Is this healthy, or does it contribute to coronary plaque as it does in people with sitosterolemia?

Below, I've reprinted a previous Heart Scan Blog post on sterols.


Sterols should be outlawed

While sterols occur naturally in small quantities in food (nuts, vegetables, oils), food manufacturers are adding them to processed foods in order to earn a "heart healthy" claim.

The FDA approved a cholesterol-reducing indication for sterols , the American Heart Association recommends 200 mg per day as part of its Therapeutic Lifestyle Change diet, and WebMD gushes about the LDL-reducing benefits of sterols added to foods.


Sterols--the same substance that, when absorbed to high levels into the blood in a genetic disorder called "sitosterolemia"--causes extravagant atherosclerosis in young people.

The case against sterols, studies documenting its coronary disease- and valve disease-promoting effects, is building:

Higher blood levels of sterols increase cardiovascular events:
Plasma sitosterol elevations are associated with an increased incidence of coronary events in men: results of a nested case-control analysis of the Prospective Cardiovascular Münster (PROCAM) study.

Sterols can be recovered from diseased aortic valves:
Accumulation of cholesterol precursors and plant sterols in human stenotic aortic valves.

Sterols are incorporated into carotid atherosclerotic plaque:
Plant sterols in serum and in atherosclerotic plaques of patients undergoing carotid endarterectomy.




Though the data are mixed:

Moderately elevated plant sterol levels are associated with reduced cardiovascular risk--the LASA study.

No association between plasma levels of plant sterols and atherosclerosis in mice and men.




The food industry has vigorously pursued the sterol-as-heart-healthy strategy, based on studies conclusively demonstrating LDL-reducing effects. But do sterols that gain entry into the blood increase atherosclerosis regardless of LDL reduction? That's the huge unanswered question.

Despite the uncertainties, the list of sterol-supplemented foods is expanding rapidly:




Each Nature Valley Healthy Heart Bar contains 400 mg sterols.












HeartWise orange juice contains 1000 mg sterols per 8 oz serving.













Promise SuperShots contains 400 mg sterols per container.














Corozonas has an entire line of chips that contain added sterols, 400 mg per 1 oz serving.














MonaVie Acai juice, "Pulse," contains 400 mg sterols per 2 oz serving.














Kardea olive oil has 500 mg sterols per 14 gram serving.










WebMD has a table that they say can help you choose "foods" that are sterol-rich.

In my view, sterols should not have been approved without more extensive safety data. Just as Vioxx's potential for increasing heart attack did not become apparent until after FDA approval and widespread use, I fear the same may be ahead for sterols: dissemination throughout the processed food supply, people using large, unnatural quantities from multiple products, eventually . . . increased heart attacks, strokes, aortic valve disease.

Until there is clarification on this issue, I would urge everyone to avoid sterol-added "heart healthy" products.


Some more info on sterols in a previous Heart Scan Blog post: Are sterols the new trans fat? .

Why obese people can't fast

Why do obese people claim it is impossible to fast?

Most overweight people are terrified at the prospect of facing any period of time without ready access to food. Persuading them to begin a program of intermittent fasting is a hopeless cause. They just refuse.

Contrary to popular opinion, this is not just glutonny at work. It is the effect of what I call "the cycle of hunger," the 2-hour up and down cycle of rising sugar and insulin, followed by their inevitable fall. The precipitous fall of sugar and insulin triggers mental fogginess, fatigue, and insatiable hunger. (By the way, this is the same phenomenon underlying the silly notion of "grazing.")

According to an LA Times article, fasting may be difficult to impossible for some people:

"Ruth Frechman, a registered dietitian in Burbank and spokeswoman for the American Dietetic Assn., says she frequently sees such extreme strategies backfire. 'You're hungry, fatigued, irritable. Fasting is not very comfortable. People try to cut back one day and the next day they're starving and they overeat.'"
(Not surprising, coming from the American Diatetic Assn. They, along with such agencies as the American Diabetes Association, are vocal proponents of low-fat, high-carbohydrate, "healthy whole grain" diets--you know, the diets that make us fat and diabetic.)

Ms. Frechman is correct: Having someone engage in a period of fasting, no matter how brief, when the diet leading up to the fast is filled with "healthy whole grains" and other carbohydrates will result in painful hunger that eventually overcomes any effort. A period of overeating typically follows the aborted attempt.

Fasting cannot work as long as the 2-hour cycle of hunger continues. The first step: Eliminate the 2-hour cycle of hunger by dramatically reducing or eliminating carbohydrates. Our preferred method is to eliminate wheat, cornstarch, and sugars. (Just be aware of wheat withdrawal, the fatigue that develops in the first 5 days after wheat elimination that affects up to 30% of people.)

Once wheat, cornstarch, and sugars are eliminated, hunger reverts to that of physiologic need--appetite will be smaller and less intense, since it is driven by your body's needs, not by abnormal stimulation from wheat, cornstarch, and sugar. The fear of not having food dissolves, the 2-hour cycle of mental fogginess, fatigue, and hunger will be gone.

Intermittent fasting is a wonderful strategy for reducing weight; gaining control over lipids, lipoproteins, and coronary plaque; regaining appreciation for food; reducing appetite. But it's not even worth trying unless you've already eliminated the unnatural appetite triggers that will booby-trap any fasting effort.

Test your own thyroid

134 people responded to the latest Heart Scan Blog poll:


When I ask my doctor to test my thyroid, he/she:

Accommodates me without question 45 (33%)

Questions why, but orders the tests 49 (36%)

Refuses because you seem "healthy" 20 (14%)

Refuses without explanation 4 (2%)

Ridicules your request 16 (11%)



That's better than I anticipated: 69% of physicians complied with this small request. After all, you're not asking for major surgery. You're just asking for a very basic test, as basic as a blood count or electrolytes. 36% of respondents said that their doctor asked why, but still complied; this is simply practicing good medicine--If there is a problem, your doctor would like to know about it.

However, the remainder--31%--were refused in one way or another. Incredibly, 11% were ridiculed.

Although this was not asked in the poll, I believe that it is a safe assumption that you asked with good reason: you're abnormally fatigued, you have been gaining weight for no apparent reason or can't lose weight despite substantial effort, or you feel cold at inappropriate times.

Let's say you're tired. Ever since last summer, you've suffered a gradual decline in energy.

So you ask your doctor to assess your thyroid. He refuses. "You're just fine! There's nothing wrong with you."

You disagree. In fact, you are quite convinced that there is something physically wrong. What do you do?

You could:

--Drink more coffee
--Exercise more in the hopes that it will snap you out of your lethargy
--Sleep more
--Take stimulants of various sorts

Or, you could get your thyroid assessed and settle the issue. But how can you get this done when your doctor won't accommodate you, even though you have perfectly fine health insurance and are simply interested in feeling better and preserving your health?

You could test your thyroid yourself. This is why we're making self-testing kits available. Test kits are available here.

This is yet another facet of the powerful revolution that is emerging: Self-directed health.

Trains, planes, and heart scans

A Heart Scan Blog reader posted the following question:

It is not clear to me why getting a cardiac scan is the necessary first step, if in fact the next step would be to bring down small LDL particles which is revealed on a NMR lipoprofile or VAP test. Why isn't the NMR or VAP test the first thing?

Good question. Think of it this way:

Lipoproteins, as measured via VAP (Vertical Auto Profile) or NMR (Nuclear Magnetic Resonance), provide a snapshot of risk from a metabolic viewpoint at that moment. Lipoproteins shift with the tides of age, menopause, weight changes, even what you ate last evening for dinner (especially small LDL). There are also other factors that cause coronary plaque, as well, not revealed through lipoprotein testing, such as vitamin D deficiency, smoking, high blood pressure, phosopholipase A2, lipoprotein(a), inflammatory factors, thyroid dysfunction, omega-3 fatty acid deficiency, etc.

A heart scan, providing a coronary calcium score, provides an indirect measure of coronary plaque that is the sum total of lipoprotein and other plaque-causing factors that have accumulated up to the time of your scan--regardless of the cause.

It means that two females, each 60 years old, with 70% small LDL, HDL 42 mg/dl, triglycerides 150 mg/dl, and mild hypertension, have identical markers for potential coronary risk, but can have widely different heart scan scores. One might have a score of zero, while the other might have a score of 300.

Why would the same panel of causes measured at one moment yield wildly different quantities of plaque? Several reasons:

1) The lifestyles, eating habits, and weight of each woman differed during their earlier years, not currently reflected in this moment's lipid or lipoprotein patterns. Perhpaps one experienced several years of extraordinary stress from a failed marriage, or suffered through two years of depression that caused her to smoke and overeat.

2) There are hidden factors that affect coronary plaque growth that we are presently not able to detect, e.g., vitamin D receptor genotype, cholesteryl-ester transfer protein variants, variation in inflammatory factors. If we can't measure it, we won't know whether it might influence coronary plaque risk.


With all the changes that occur over a person's life, with the uncertainties of yet-to-be-identified causes for coronary plaque, how can you possible know what your risk for heart disease truly is? Yup--a heart scan. Do it and you will know.

D2 and D3 are two different things

Helena posted this instructive comment in response to the Heart Scan Blog post, Weight loss and vitamin D. It illustrates the confusion common among physicians and pharmacists on the differences between D2 and D3.

(Edited slightly for clarity.)

Not many weeks ago a colleague of mine (let’s call him Eric) asked me if I knew the difference between D2 and D3 and I told Eric that D2 comes from irradiated mushrooms and D3 comes from wool. In other words, D3 is the same kind of vitamin as humans get from the sun. Humans just don’t get enough and we can’t produce it on our own, like the sheep can. (D3 is natural for humans, D2 is not.)

After telling Eric this, he asked me how he would know what he is taking and I gave him the medical definitions of them both (D2 = Ergocalciferol; D3 = Cholecaliciferol). Since I was aware that he had gotten his Vitamin D by prescription, I told him “I am 99.9% sure that you are taking D2, but I would be thrilled to find out I am wrong.”

Eric called his pharmacy right away and got the answer I was expecting: ergocalciferol. On confronting the person Eric was talking to, the answer he got back was that Ergocalciferol is the only Vitamin D they are giving out.

A week later, Eric had a new appointment with his doctor and decided to ask him about the D2/D3 issue. The doctor said he knew that there was a difference in them both, but could not say what, not even the basic facts I mentioned above. But the doctor stamped a post-it with what he had sent to the pharmacy just to show Eric. “Vitamin D3; 50,000IU tab” is what the stamp said.

Eric, off course, got confused and was starting to believe that the pharmacy had made a mistake by giving him Ergocalciferol (D2) since the doctor had given him D3, or at least that is what was stamped on the little note he had.

Today, after getting a refill of his Vitamin D he also got and kept all his paperwork that came along with it. Still believing that stamp the doctor had given Eric earlier, he asked me to double and triple check that my definition of D2 and D3 was correct. I did, just for my own sanity, and I was still right.

One of the sheets Eric brought me today was the “Patient Education Monograph” sheet stating the drugs and how to use it and so on. The thing that jumped out the most to me was this:

Generic Name: Vitamin D – Oral
Common Brand name(s): Drisdol, Maximum D3
Identification: PA140 Green Oval Capsule

This is the Drug Eric was given: Vitamin D 1.25 MG softgel; Generic name: Ergocalciferol

My researching mind went into high concentration mood and I started to dig. And this is what I found:

The brand name Drisdol is Ergocalciferol (D2), not D3. The Brand name Maximum D3 seems to be hard to find out there in cyber space as a brand name. But the ones I found that were called Maximum D3 seems to be the real stuff, however none of them required a prescription.

When trying to find out through the identification number on the pills (PA140) I now know for sure that Eric is taking Vitamin D2 and not the preferred Vitamin D3. The brand name, Drisdol, had the identification W on one side and D92 on the other, but it is still Ergocalciferol.

The only conclusion I can draw from all this is that the medical industry does not know or care about the difference in D2 and D3 – it is all same to them. And as long as the pharmacies only give out D2 it does not matter what the doctor prescribe anyway.

I know that people are most likely to be prescribed a D2 pill than to be told to buy over-the-counter D3. But it was almost heart breaking to see the letter D and number 3 right next to the drug Drisdol, as we know is a D2 vitamin. It just didn’t make sense to me that they can be labeled as the same type of medication, when we know it is not!



Incredible.

Why prescribe plant form D2 when you can get perfectly reliable, safe, effective D3--the human form, at the health food store for about $6?

Once again, it's the peculiar false bias of physicians and pharmacists: If it's prescription, it must be good; if it comes from a health food store, it must be bogus.

Humans need human vitamin D. Plain and simple.

For more on the D2 vs. D3 issue, see the Heart Scan Post, The case against vitamin D2.

Weight loss: Different causes, different solutions

Heart Scan Blog reader, Kris, related this enlightening story of weight loss (slightly edited for clarity).

Kris learned that excess weight is gained through multiple causes. The solutions are therefore multiple, not just one change in diet or two.


I started studying about my thyroid issue much earlier and did lose some weight. But ever since I started following Dr. Davis’s blog, it has given me confidence that I was on the right track. I did have my thyroid and iodine figured out from other sources, but Dr. Davis helped me to understand the issues with not only the thyroid but vitamin D3, fructose, fish oil, niacin, wheat etc. I have lost 43lb in last 14 months.

It seems to me that there are certain percentages of weight connected with different issues. For example, after I gave up alcohol and sugar, I lost about 14lbs from total weight of 243lbs, weight came down to about 229lb. Then it stopped at 229lb, even though I was in the gym almost 5 to 6 days a week with full workouts.

After I changed my thyroid medication to natural thyroid hormones (took synthetic T4 for over 10 years), the weight dropped down further 13lbs or so in matter of few days, shape of the face changed from moon shape/double chin to ordinary long face. Then it kind of stopped at around 213-216 lbs.

After giving up wheat, reducing carbs, increasing protein intake (whey protein, chicken etc. no soya, no fructose) the weight came down another 14lbs. Now it is around 200-202lbs and I am over 6.2 tall with heavy set of bones.

I feel better than I have ever in my life. More stamina, more clarity/no fog, more confidence and 99% of the time relaxed and being able to see the situation from multiple angles.

I use to be able to drink a liter or more jack denial without a problem in one evening but now can’t stand half a can of beer (I miss JD). Drinking alcohol makes me sick. I sleep well and if I wake up in the middle of the night, I have no problem going back to sleep. No more out of breath stair climbing at all.

One other thing: I used to be the most attractive meal to the mosquitoes, but not anymore. This year I haven’t been bitten once. I take my dog to the park everyday and I do not use any mosquito repellent, what a relief. I don’t know if it is because of thyroid, iodine, wheat or something else. Skin texture has changed dramatically. I do not use full soap or shampoo, 20% borax, 10 percent of my soap or shampoo for scent and rest water, mixed in a 500ml bottle. No more dandruff, dry skin, pimples for me.

Dr. Davis I am thankful to people like you who have the ability to see beyond what you have been taught and have the guts to say the way it is. Most of us work to make living on daily basis but some make their living while spreading their knowledge to save lives. Dr Davis you are one of those few people. Please keep it going.

Calling all losers!

I'd like to invite anyone who has followed the Track Your Plaque Break the Weight Barrier program to consider posting their stories and photos on the Heart Scan Blog.

Because our focus is prevention and reversal of coronary heart disease, we have not made an effort to catalog the weight loss experience that people have while on the program. For many, weight loss has been substantial. (Several people this week alone have reported weight loss of 9 to 46 lbs in the past 6 months.)

It would be helpful to hear and see these results.

For those of you who don't mind having a story and photo on this Blog, please come back in future to post your results. You will find this post by entering "weight loss" into the site-specific search bar at the top of the page.

Weight loss and vitamin D

At the start of her program, Penny's 25-hydroxy vitamin D blood level showed the usual deficiency at 22 ng/ml.

She supplemented with 8000 units of vitamin D. Another 25-hydroxy vitamin D blood level several months later showed a level of 67.8 ng/ml, right on target.

But Penny also began our diet, including the elimination of wheat, cornstarch, and sugars, and, over 6 months, lost 34 lbs.

Now a much trimmer 146 lbs (still more to go!), another vitamin D blood level: 111 ng/ml.

Penny's weight loss means that the vitamin D is distributed in a smaller total volume, particularly a lower volume of fat.

This is a common phenomenon with substantial weight loss: lose weight and the need for vitamin D is reduced. The reduction in dose is roughly proportion to the weight lost. Vitamin D should therefore be reassessed with any substantial change in weight of, say, 10 lbs or more, either up or down, because of the influence of fat on vitamin D blood levels.

Some references on this effect:

Men and women over age 65:
Adiposity in relation to vitamin D status and parathyroid hormone levels: a population-based study in older men and women.

Obese women:
Low 25-hydroxyvitamin D concentrations in obese women: their clinical significance and relationship with anthropometric and body composition variables

Obese children:
Hypovitaminosis D in obese children and adolescents: relationship with adiposity, insulin sensitivity, ethnicity, and season.

African-Americans:
Relationship of vitamin D and parathyroid hormone to obesity and body composition in African Americans.

Although the bulk of the effect is most likely due to sequestration by fatty tissue, perhaps less sun exposure in obese people also contributes:
Body mass index determines sunbathing habits: implications on vitamin D levels.
All posts by william-davis

Olive oil for gourmets

"The finest extra-virgin olive oils should not be used as a medium for hot cooking, but rather as a condiment or a finisher on top of your favorite savory foods. They are expensive, but if stored properly they will last for up to a year..."

You all know that olive oil is among the preferred oils to use: rich in monounsaturates, low in saturates, high in polyphenols.




For a fascinating perspective for the olive oil gourmet, go to www.npr.org, the website for National Public Radio. (Scroll down to the article or enter olive oil into their site search.) Their article, "Like fine wines, fine olive oils boast subtle joys" provides an insightful discussion on squeezing maximum enjoyment out of this wonderful "functional food".

As we emerge from the mis-directed low-fat craze of the past 20 years, we're re-discovering the joys of healthy oils. You'll find some great thoughts here

Vitamin D must be oil-based

As part of the Track Your Plaque coronary plaque reversal program, we advocate vitamin D supplementation. Vitamin D has been shown to reduce blood sugar and reduce pre-diabetic tendencies, reduce blood pressure (it's a renin antagonist, a blood pressure hormone), it's far more important for bone health than calcium, and it may help prevent colon cancer, prostate cancer, and multiple sclerosis.

And, oh yes, it may facilitate coronary plaque regression.

One lesson I've learned is that vitamin D MUST be taken as a oil-based capsule or gelcap. You'll recognize it as a transparent or translucent, sometimes opaque, capsule. The list of ingredients may say something like "cholecalciferol [vitamin D] in a base of soybean oil", indicating that the active ingredient is oil-based. Oil-based vitamin D3 skyrockets blood levels of 25-OH-vitamin D3 in to the normal range reliably and easily.


Tablets are a different story. These are generally white powdery tablets. The rise in blood levels of vitamin D3 are minimal, sometimes none. Women will often say "I get vitamin D with my calcium tablets."


People taking this form almost always have blood levels of vitamin D that are low, as if they were taking nothing.
If you're going to take vitamin D, the oil-based tablets are the way to go. They're not necessarily any more expensive. We've had good experiences with the Nature's Life 2000 unit capsule, as well as preparations from Life Extension. We have had negative experiences with the preparations from GNC, Sam's Club, and Walgreen's, all tablets and non-oil-based.

When is LDL cholesterol NOT LDL cholesterol?

Darlene had a high LDL cholesterol, at times as high as 200 mg/dl. Her primary care doctor first tried Mevacor, then Pravachol, then Zocor, then Lipitor. Every statin drug failed to reduce Darlene's LDL below 160 mg/dl, even when maximum doses were used. The higher doses also resulted in nearly intolerable muscle aches and weakness.

When we sent Darlene's blood sample off for lipoprotein analysis, a surprise came back: she had a high lipoprotein(a), or Lp(a). This explained a lot.

LDL cholesterol is not always just LDL cholesterol. One of the particles that can masquerade as LDL is Lp(a). Darlene's story is typical of many people who've had high cholesterol levels poorly responsive to the statin drugs. That's because their LDL conceals Lp(a), which does not respond to these agents. LDL cholesterol does drop some because there's also some real LDL mixed in.

A poor response to statin agents or to nutritional strategies to reduce LDL is a tip-off that Lp(a) may be hidden. The answer: just measure Lp(a)! If you and your doctor don't measure it, you won't know whether or not you have it. Rather than a statin drug, we put Darlen on niacin. Not only did her Lp(a) drop, but her LDL also plummeted.

What is a desirable triglyceride level?


Though well-intended, the National Cholesterol Education Panel's Adult Treatment Panel, or ATP-III, (whew!) guidelines for cholesterol have been responsible for loads of misinformation.

The intention was to educate the internist or family doctor who treats sore throats, performs Pap smears, administers pneumovax vaccine, treats arthritic knees---and dabbles in heart disease prevention. The ATP-III guidelines are the "Cholesterol for Dummies" approach.

What standard guidelines definitely do not represent are the ideal values to achieve. They do not ensure protection from heart disease. This is particularly true of the ATP-III advice to keep triglycerides at or below the "desirable" level of 150 mg/dl.

In the Track Your Plaque program, we ask "What is necessary to tip the odds in favor of coronary plaque regresion or reduction of heart scan score?" This is not achieved with a triglyceride of 150. In fact, triglycerides at this level are associated with flagrant abnormalities of lipoprotein patterns. It usually means that processed carbohydrates, particularly wheat products, are occupying too prominent a role in your food choices. It could mean that you're making excessive use of processed foods containining high-fructose corn syrup. It will not respond to a low-fat diet. It will, however, respond vigorously to fish oil.

Triglycerides are a crucial aspect of your plaque control program. We aim for 60 mg/dl or less. The ideal level is actually 45 mg/dl. At this level, all abnormal triglyceride-containing lipoproteins finally go away.

Super size me in little bits and pieces



Alvin came into the office for consultation on his cholesterol values: LDL 198 mg/dl, HDL, 43 mg/dl, triglycerides 143 mg/dl. He says that he doesn't really try to choose healthy foods but he restricts his overall calorie intake by following the Weight Watcher's exchange approach.

Every morning, 7 days a week, Alvin eats a Sausage McMuffin for breakfast. He justified this by skipping lunch to make up for the 450 calories in the Sausage McMuffin, and not eating anything until dinner.

Can this work? Can you eat foods with unhealthy ingredients but make up the excessive calories by cutting back elsewhere?

The nutritional composition of McDonald's Sausage McMuffin includes 27 grams of total fat (10 gm saturated); 255 mg cholesterol; 950 mg sodium; 31 gm carbohydrate; 2 grams fiber. In other words, it's essentially the same as butter with sugar on it--pure fat, processed wheat, with little fiber or nutritive value.

For Alvin, this is an extremely unhealthy way to eat. His lipid patterns are just the tip of the iceberg: multiple hidden factors are also at work to create heart disease, atherosclerosis in other territories outside the heart, diabetes, high blood pressure, and cancer.

I think the effects are not much different than what Morgan Spurlock achieved in his Super Size Me documentary, but in little bits and pieces. Eating at McDonald's "restaurants" three times a day yielded frightening changes in his lipids, liver function, kidney function, not to mention his appearance and the way he felt. Alvin is doing the same thing, though in less dramatic fashion.

I see this very frequently: people mimicking the experience of Spurlock, just a little at a time, with overindulgence in processed fats and starches.

When you seen a set of Mcdonald's golden arches (or any fast food restaurant, for that matter), run as fast as you can in the other direction. Such indulgences, even in small bits and pieces, still creates a mess of your health.

View from the precipice


Many people, upon first learning of their CT heart scan score, feel like they're on the edge of a sharp drop. It can feel like you're facing a vast, unknown abyss. At the bottom, all those dreaded things that can happen to you: heart attack, heart failure, hospitals, even dying.

I've encountered this "deer in the headlights" look many times. It truly can be frightening to hear that your heart scan score is 300, or 500, or whatever.

What I find truly frightening, however, is when your score prompts the usual array of misinformation commonly dispensed by physicians: "That's so bad you need a heart catheterization", "Nobody knows why people get calcified plaque", or "Reversal is impossible". All absolute bunk.

Let your fear motivate you to do something about your risk for heart disease. Aim for reversal of your coronary plaque and seek out the tools to achieve this. It is possible and, in fact, we do it all the time. I can't claim 100% success, but the majority of people who engage in an effort like the Track Your Plaque program to reverse coronary plaque succeed. Even a substantial slowing of plaque growth from the expected 30% per year is better than submitting to the conventional approach.

At the very least, get both LDL and HDL cholesterol around 60 mg/dl. This alone is a major plus in reducing the risks associated with your heart scan score. It doesn't guaranteee reversal, but it sure tips the odds in your favor.

Organic Rice Krispies?



Breakfast cereal manufacturing giant, Kelloggs, is launching a line of three cereals that will carry the "organic" designation: Organic Rice Krispies, Organic Raisin Bran, and Organic Frosted Mini-Wheats.

This reminds me of the advertisements I've seen for "fresh fried chicken", or "fresh from the can", or "contains only pure cane sugar". How about organic tobacco? Would that make cigarettes healthier?

The TV ad ends with the slogan "Childood is calling!" Oh, those marketers are a shrewd, clever bunch. I worry that they're so clever that most people will fall for these ludicrous tricks.

Don't fall for these thinly-shrouded marketing shenanigans. Organic? Who cares. These foods remain unhealthy whether or not they contain pesticide residues. Take a look at the nutritional composition: Rice Krispies, organic or not, is sugar to your body. It is the sort of food that creates pre-diabetes, diabetes, makes us fat, and fans the flames of lipoprotein patterns like small LDL, VLDL, and postprandial particles, all of which is like throwing cow manure on the weed patch of your coronary plaque.

Nuts as functional foods

Food manufacturers gave nuts a bad name when they started adding evil ingredients to them. "Party mix", "honey-roasted", mixed nuts, etc., are made with added hydrogenated oils, salt, sugar, excessive quantities of raisins, or other added ingredients that turned a healthy food--nuts--into something that made us fat and hypertensive, raised LDL, dropped HDL, and raised blood pressure.

But nuts themselves are, for the most part, very healthy foods. The very best are nuts with a brown fiber coating like almonds, walnuts, and pecans. Nearly all nuts also come rich in monounsaturated oils similar to that in olive oil. Although calorie-dense, nuts tend to be very filling and slash your appetite for other foods. I have never seen anyone gain weight by adding raw nuts to their diet. In fact, I find adding raw nuts cuts craving for sweets.

Nuts are also among the most concentrated sources of magnesium, containing around 150 mg per 1/2 cup serving. As most Americans are at least marginally if not severely deficient in magnesium, this really helps. Magnesium deficiency is a prominent aspect of "metabolic syndrome" and resistance to insulin.




Some nuts have added benefits like the l-arginine content of almonds or the linolenic acid content of walnuts. However, I think the real health "punch" comes from the fiber and monounsaturate content.

Add 1/4-1/2 cup of raw almonds, walnuts, or pecans per day to your diet and what can you expect? The effects that I see every day that are relevant to plaque control/heart scan score-reducing efforts include:

--Reduction in LDL--usually a 20 mg/dl drop, sometimes more.

--Reduction in triglycerides, especially if nuts replace processed carbohydrate calories. This may be because the fiber and monounsaturate content of nuts reduces blood sugar and the effective glycemic index of any accompanying foods.

--Modest blood pressure reduction.

--Though somewhat inconsistent, partial suppression of the dreaded small LDL particle pattern. We struggle with turning off the small LDL pattern in some people, and raw nuts can provide a real advantage.

If that isn't enough, the fiber content also makes your bowels regular.

Unless there's some reason to avoid nuts (e.g., allergy), nuts should be a part of your heart scan score reducing program. Shop around, as prices can vary wildly. I've been paying $12.99 for a 3 lb bag of raw almonds from Sam's Club, though I've seen almonds elsewhere for up to $12.99 per pound.

For additional commentary, go to one of my favorite Blogs, http://fanaticcook.blogspot.com. The Fanatic Cook's recent post, The Season for Walnuts , provides additional discussion on walnuts and the recent study showing how they improve "endothelial function". The nutritionist behind this Blog has fabulous insights into food, including the concept of "functional foods", i.e., using foods as a treatment tool. She is also unfailingly entertaining.

Can you tell the difference?

Stan is 55 years old. He feels fine, is in moderately good physical condition. His LDL cholesterol is 135 mg/dl, HDL 43 mg/dl, triglycerides 167 mg/dl, total cholesterol 211 mg/dl.

Can you tell me whether Stan has heart disease or not?

How about Charles? Charles has an LDL cholesterol of 127 mg/dl, HDL of 44 mg/dl, triglycerides of 98 mg/dl, and total cholesterol of 191 mg/dl. He is also reasonably fit and feels fine. Can you tell whether Charles has heart disease?

If you can't, don't feel bad. Neither can your doctor. But this is the folly of using cholesterol for risk prediction.

Stan's heart scan score: 0

Charles' heart scan score: 978

Look even more closely at Stan's and Charles' cholesterol numbers. Is there some fine distinction we overlooked? What if we calculated total cholesterol to HDL ratio? Or LDL/HDL ratio?

No matter how you squeeze it, shake it, beat it with a stick, you simply cannot use cholesterol numbers to predict heart disease in specific individuals. Yes, the higher your LDL cholesterol and lower your HDL, the higehr your total cholesterol to HDL ratio, the greater the likelihood of heart disease. But you can simply cannot tell in a specific individual at a specific point in time. If you've seen your doctor puzzle over the numbers, understand that he/she is trying to make sense out of something that doesn't make sense, no matter how hard he/she tries.

You simply need to measure the disease itself: get a CT heart scan, the only measure of atherosclerotic coronary plaque that you have access to.

By the way, if you haven't seen it yet, go to the Track Your Plaque website (www.cureality.com) to see the news piece reporting the American Heart Association's much overdue position statement on CT heart scanning. The AHA has finally released a statement which, in effect, provides their "official" endorsement. Blocked by political shenanigans behind the scenes for several years, the guidelines finally made it to press. The only real difference it makes to me is that my patients may finally get their heart scans paid for by insurance, once the insurance companies realize that it's getting tougher and tougher to dodge their responsibility.

Statin agents and muscle aches

How common are muscle aches with the statin drugs?

It depends on who you ask. If you ask the drug manufacturers, they will tell you no more than 2% of people who take them. They back this up with the experience in tens of thousands of people in published clinical trials.

What if we ask people who take them outside of clinical trials. How many then? I estimate, from my large experience, over 80%! In other words, muscle aches are inevitable in nearly everyone who takes them. The longer you take them, the higher your dose, the more likely muscle aches are going to be.

Why the disconnect between published data and real-world experience? I really don't know. In some instances, the differences are dramatic. The ASTEROID trial, for instance, in which Crestor, 40 mg, was given for two years, only resulted in 8% of people dropping out because of side-effects. My experience: everybody--nobody can tolerate this dose for any length of time.

Let me qualify what "muscle aches" mean. It means achiness and/or weakness, usually mild, occasionally moderate to severe, worse upon awakening and less with use. It can affect many muscles or it can involve only one. Rarely is it incapacitating but it is commonly annoying and frightening. It commonly shows up as gradually diminishing strength with exercise. Strength usually returns promptly upon stopping the offending drug.

"Rhabdomyolysis", or true muscle destruction is, fortunately, very unusual in otherwise well people. People with abnormal kidney function, diabetes, and other concurrent illnesses are somewhat more prone. But in reality, rhabdomyolysis is unusual. I've personally seen it twice, both in people sick for other reasons.

Coenzyme Q10 (CoQ10) supplementation has been a godsend for us. At least 4 out of 5 people who require statins and develop muscle aches respond favorably, but it requires 100 mg per day. The preparation must be oil-based to work, not powder in a capsule which exerts no effect. Some people get by with less; some require as much as 300 mg per day. I've had favorable experiences with the CoQ10 from Sam's Club, GNC, Vitamin Shoppe, and Life Extension (www.LEF.org).

The Track Your Plaque target for LDL cholesterol is 60 mg/dl. Many people do indeed use statins to achieve this level, the level of LDL that amplifies your chances of heart disease reversal, i.e., reduction of heart scan score. The only drawback that I'm aware of with CoQ10 replacement is cost. Beyond this, it's a benign supplement that even supplies higher energy for some people who take it.
All posts by william-davis

Niacin scams

In the Track Your Plaque program, we often resort to niacin (vitamin B3 or nicotinic acid) to:

--Raise HDL cholesterol
--Reduce the proportion of small LDL particles
--Shift HDL towards the healthy larger fraction (HDL2b or "large")
--Reduce lipoprotein(a), the most aggressive risk factor known


But niacin comes with a crazy "hot flush," a warm, prickly feeling that usually envelops the upper chest, neck and face that is, without a doubt, annoying. Around 1 in 20 people simply cannot tolerate any amount of niacin >100 mg, while others have no problem even into the 3000 mg per day or more range. (Tolerance to niacin is genetically determined, governed by the rapidity of metabolism to the niacin metabolite, nicotinuric acid.)

The niacin flush has spawned an entire panel of niacin-like scams, agents that sound like niacin or may even contain niacin, but exert no beneficial effect whatsoever:

Flush-free niacin--I have previously posted on this useless but ubiquitous preparation that often costs several times more than conventional niacin. Flush-free niacin, or inositol hexaniacinate, does indeed contain niacin, but it is not released in the human body. You simply pass it out down the toilet, where this preparation belongs in the first place.

Nicotinamide--Also called niacinamide. While the nicotinamide/niacinamide forms of vitamin B3 can be used to treat B3 deficiency ("pellagra"), they do not reproduce the lipid and lipoprotein effects of niacin. For our purposes, they are useless.

Niacin-containing heart-healthy supplements--These are the multi-supplements that contain a little of everything that might be beneficial for the heart, but none at a dose that provides genuine benefit. Don't throw your money away.


There's also a prescription niacin, Niaspan, that costs 20-fold more than the best over-the-counter preparation, Sloniacin. Niaspan has yielded hundreds of millions of dollars for the pharmaceutical industry. Your money, in my view, is far better spent on Sloniacin (around $12-14 per bottle of 100 tablets of 500 mg).

For more on niacin, here's an article I wrote for the Life Extension Magazine people a while back: Using Niacin to Improve Cardiovascular Health.

Deja vu all over again?

HeartHawk brought a report and debate on The Heart.Org website to my attention:

Screening for risk factors or detecting disease? Debate divides the CV community. After landing on theheart.org, paste this onto your URL address:article/883239.do. (Full address: http://www.theheart.org/article/883239.do. I don't know why, but I couldn't go there directly.)

Some interesting comments:

Dr. Jay Cohn (University of Minnesota):

"They're saying that we can't identify disease very effectively so let's just stick with risk factors, which we know are very poorly predictive and nonspecific. It boggles my mind as to why they won't open up their minds to the importance of moving forward in finding better strategies to identify the disease that we are treating. It's very strange. They criticize these disease markers because they are not predictive of events, but they are looking at very short-term outcomes. We're interested in lifetime risk. We're screening people in their 40s who are concerned about morbid events in their 60s and 70s, and no trials are going to track them that long."

"You have to accept the pathophysiologic reality that heart attacks don't occur in the absence of coronary disease, and coronary disease doesn't occur in the absence of endothelial dysfunction and vascular disease, all of which now can be identified."

". . . Can we as a society and as a profession accept the idea that there is a link between the vascular abnormalities and the events? "And that that linkage is tight enough that it should allow us to accept slowing of progression of the vascular abnormalities as an adequate marker for slowing disease progression, without waiting for events to occur? As soon as you use the word surrogate, people jump up and say we have all these markers that we know don't work well—things like premature ventricular contractions [PVCs] on the electrocardiogram, LDL, HDL—but those are not the markers we're talking about. We're talking about structural and functional changes in the blood vessel and in the heart."



Wow. The idea may be starting to catch on.

As an interesting aside, Cohn et al use a 10-test panel to screen for vascular disease:

"Named for the center's benefactor, the Rasmussen score includes tests for large and small artery elasticity (compliance), resting blood pressure, blood-pressure response to moderate treadmill exercise, optic fundus photography, carotid intimal-media thickness (IMT), microalbuminuria, electrocardiography, left ventricular (LV) ultrasonography for LV volume and mass, and brain natriuretic peptide (BNP). Each test result is scored out of 10 for low, intermediate, or high risk, and the combined results yields a score that Cohn et al believe is more predictive than any of the existing standalone tests."


The counterarguments in this debate were provided by Dr. Philip Greenland (Northwestern University), who repeated his oft-used argument that, while he accepts that vascular disease can be identified, no one has proven that measuring it improves outcomes:

"We do have that evidence for risk-factor screening. Even though people criticize risk-factor assessment because it is not sensitive enough or not accurate enough, the interesting and curious thing is that we actually have evidence that if you go to the trouble of screening for risk factors and treating them, patients have better outcomes. We do not have that evidence for any of these other tests."


An interesting debate ensues that includes Track Your Plaque friend, Dr. William Blanchet, who characteristically argues persuasively in favor of broad screening for coronary disease with coronary calcium scoring:

"If we were doing our jobs in primary prevention, we would not need to look at improved intervention and secondary prevention to reduce coronary death."


Here's a shock: Dr. Melissa Shirley-Walton, the cardiologist who previously preached the "cath lab on every corner" argument seems to have undergone a change of heart:

"What if I walked up to a gentleman and said, "you are at risk for CAD, take a statin", to which he replies, "I'm afraid of those meds". BUT if he sees his calcium score........he is then convinced to be pro-active. What is so wrong with that? What is so wrong with allowing him to spend 250.00 US out of pocket in order to save the US 150,000.00 US later on?

No hard endpoints you say with intensive therapy for primary prevention? What about extrapolating from trials for secondary prevention like HATS? ARBITER2? And what exactly is the true definition of secondary prevention? Is it truly primary prevention if we already have intima thickness abnormalities, or fatty streaks? That would more likely fall under secondary prevention by today's new standards.

So, I'm all for any visual aid that will encourage compliance with life style change, necessary medical therapy and followup. If the patient is willing to spend 250.00$ to get a calcium score, so be it. Better yet, why not lower the price so everyone can have the option if they are motivated enough to seize an opportunity?"



I have to admit that I thought that Dr. Blanchet was wasting his time trying to persuade Shirley-Walton et al, but perhaps he is having an impact, though having hammered away at them for the last year or so.

These arguments, for me, eerily echo many previous debates I've heard. But I am encouraged by the more favorable treatment the notion of atherosclerosis screening is receiving. Just 5 years ago, all coronary calcium scoring would have received from the conventionalists is "more clinical studies are needed."

So perhaps the cardiology and medical worlds are inching slowly towards broad acceptance of screening for coronary and vascular disease.

BUT, screening is not sufficient. What do you do with the information?

Here is where the conventional-thinkers stop. The question that seems to occupy them: Perhaps we should screen people for hidden coronary and vascular atherosclerosis so we can better decide who needs a statin drug or a procedure.

I would pose a different challenge: We should screen people for hidden coronary and vascular atherosclerosis so we can better decide who needs to engage in an intensive program of disease reversal using natural means and as little medication and procedures as possible.

Well, perhaps in time.

Lead to Gold: The alchemy of transforming nutritional-supplement-to-medication

Here's a recipe to make hundreds of millions of dollars. Others have done it and you can do it, too!

1) Identify a nutritional supplement that works.

Find some agent deemed to fall within the broad allowances of the 1994 Dietary Supplement Health and Education Act . However, because this agent is already in the public domain and is essential non-patent-protectable, you may need to develop some patent protectable aspect of its production, application, or encapsulation. This patent-protected aspect may or may not provide genuine advantage, but that's not your concern. Your concern is protecting your investment and providing the appearance of exclusivity.


2) Identify a medical indication for your product.

Choose a disease or condition that is likely to yield unquestioned efficacy, e.g., omega-3 fatty acids to reduce high triglycerides in people with familial hypertriglyceridemia (triglycerides >500 mg/dl). While this will restrict your ability to make market claims, it will not restrain your ability to sell or allow use of your agent for "off-label" applications. In fact, there are methods to surreptitiously promote the use of your product for off-label use, such as hiring experts to discuss the science behind your product with doctors who can prescribe your product. Ideally, your product's primary indication will provide a substantial market on its own to justify your investment. However, the eventual off-label sales can be substantial, even outstripping the sales generated through your primary indication.


3) Obtain at least $230 million to pay for the clinical trials required to obtain FDA approval.

You will also have to raise the capital to build the business to manufacture, distribute, and sell your product.


4) After FDA approval is obtained, your business is up and running, and distribution begins, start bashing the non-FDA-approved nutritional products that stand to compete in your market.

You could point out that only your product has actually passed through the rigorous FDA process. You could make claims regarding purity, potency, "approved by your doctor," etc., whether or not there is any truth behind the claim.


5) Buy that second vacation home in Aspen and the corporate jet you've been dreaming about! After all the risks you've taken, you deserve it!


That's it, plain and simple. It is a tried-and-true formula that has been applied many times.

It is a formula like this that brought Lovaza-brand omega-3 fatty acids to market, Niaspan brand of niacin, ergocalciferol form of vitamin D, Folbee (prescription combination B vitamins), with a slightly different spin for Synthroid (since the Armour Thyroid it is meant to replace is not a nutritional supplement, but a low-cost, generic thyroid replacement).

Whatever you do, don't EVER run a head-to-head comparative trial of your agent versus the nutritional supplement competition. For instance, NEVER compare Lovaza to supplemental fish oil capsules, matched milligram-for-milligram for EPA and DHA content. NEVER compare Niaspan to over-the-counter Sloniacin. NEVER compare Armour Thyroid to Synthroid. You never know what you might find. (Psssssttt! They might be equivalent!)

The formula is not a foolproof road paved with riches, however. There have been market failures, as well. Folbee, for instance, is hardly a household name. So there's risk involved, no question about it. But, should it all work out, the payoff can be big, VERY big, as it has been for Niaspan and Lovaza.

So, start thinking about how you might follow this formula for:

1) Cholecalciferol (vitamin D3)--e.g., for osteopenia, low HDL, or high c-reactive protein
2) Vitamin K2--also for osteopenia
3) Magnesium--for suppression of ventricular arrhythmias (especially Torsade de Pointes)
4) Iodine--for goiter and iodine deficiency
5) Vitamin C--for uric acid reduction

Who said you can't turn lead into gold?

Another interview with Livin' La Vida Low Carb's Jimmy Moore

I recently provided another interview for Livin' La Vida Low Carb's Jimmy Moore.

You may remember Jimmy as the irrepressible host of the Livin' La Vida Low Carb Show who lost around 200 lbs, dropping from 410 to 230 lbs on a low-carbohydrate diet.

In this hour-long interview, we discussed some of the dietary strategies that we use in the Track Your Plaque program.

Jimmy's website is definitely worth exploring. It's loaded with great interviews, including with Good Calories, Bad Calories author, Gary Taubes.

"Millions of needless deaths"

"Millions of needless deaths" is the title of an editorial by Life Extension Magazine's Bill Faloon.

". . . If vitamin D’s only benefit was to reduce coronary heart attack rates by 142%, the net savings (after deducting the cost of the vitamin D) if every American supplemented properly would be around $84 billion each year. That’s enough to put a major dent in the health care cost crisis that is forecast to bankrupt Medicare and many private insurance plans."

Although I don't agree with all the over-the-top commentary that issues from Mr. Faloon or Life Extension (although I sit on their Medical Advisory Board), I agree with virtually all of the issues he raises with vitamin D.

Despite the enormously compelling observations of vitamin D potential effects in populations, the medical community's reluctance comes from the lack of treatment data. In other words, what we lack are long-term data on vitamin D supplementation vs. placebo on rate of heart attack, vitamin D vs. placebo on risk of colon cancer, etc.

The data that exists connecting vitamin D levels with cardiovascular risk originate from three population observations:

1) The NHANES data in 16,000 participants showed 20% increased risk of cardiovascular events in those with vitamin D levels <20>20 ng/ml after factoring in all standard risk factors.

Another NHANES analysis showed the high prevalence of vitamin D deficiency in those with cardiovascular disease.

2) A German study of 2500 participants that showed showed the lowest quartile of vitamin D levels (<13.3>28.4 ng/ml.

3) The Health Professionals' Follow-Up Study of 18,000 males showed a 2.4-fold increase in cardiovascular events in those with vitamin D levels <15>30 ng/ml.

While we lack treatment data (vitamin D vs. placebo) in a large population, we do have data that Suzie Rockway, Mary Kwasny (both from Rush University, Chicago) and I generated on the effect of vitamin D as a part of a broader treatment program on coronary calcium scores:

Effect of a Combined Therapeutic Approach of Intensive Lipid Management, Omega-3 Fatty Acid Supplementation, and Increased Serum 25 (OH) Vitamin D on Coronary Calcium Scores in Asymptomatic Adults.
Davis W, Rockway S, Kwasny M. Amer J Ther 2008 (Dec 15).

The impact of intensive lipid management, omega-3 fatty acid, and vitamin D3 supplementation on atherosclerotic plaque was assessed through serial computed tomography coronary calcium scoring (CCS). Low-density lipoprotein cholesterol reduction with statin therapy has not been shown to reduce or slow progression of serial CCS in several recent studies, casting doubt on the usefulness of this approach for tracking atherosclerotic progression. In an open-label study, 45 male and female subjects with CCS of >/= 50 without symptoms of heart disease were treated with statin therapy, niacin, and omega-3 fatty acid supplementation to achieve low-density lipoprotein cholesterol and triglycerides /=60 mg/dL; and vitamin D3 supplementation to achieve serum levels of >/=50 ng/mL 25(OH) vitamin D, in addition to diet advice. Lipid profiles of subjects were significantly changed as follows: total cholesterol -24%, low-density lipoprotein -41%; triglycerides -42%, high-density lipoprotein +19%, and mean serum 25(OH) vitamin D levels +83%. After a mean of 18 months, 20 subjects experienced decrease in CCS with mean change of -14.5% (range 0% to -64%); 22 subjects experienced no change or slow annual rate of CCS increase of +12% (range 1%-29%). Only 3 subjects experienced annual CCS progression exceeding 29% (44%-71%). Despite wide variation in response, substantial reduction of CCS was achieved in 44% of subjects and slowed plaque growth in 49% of the subjects applying a broad treatment program.


I also summed up the data as of early 2008 in a Life Extension article:

Vitamin D's Crucial Role in Cardiovascular Protection


I do agree with Mr. Faloon: It's time to take the vitamin D issue very seriously. Personally, I think it is foolhardy to not correct vitamin D deficiency, even in the absence of long-term treatment data.

Should we subject people living in tropical climates with vitamin D blood levels of 90 ng/ml to long-term observation? Though that has not yet been done, it has been done--in effect--through observations on the prevalence of diabetes, heart disease, and various cancers by latitude: the farther away from the equator, the greater the prevalence of these diseases.

That's more than good enough for me.

Thiazide diuretics: Treatment of choice for high blood pressure?

Thiazide diuretics are a popular first-line treatment for hypertension among the primary care set.

This practice became especially well-established with the 2002 publication of the ALLHAT Study (Major Outcomes in High-Risk Hypertensive Patients Randomized to Angiotensin-Converting Enzyme Inhibitor or Calcium Channel Blocker vs Diuretic:The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT)).

ALLHAT showed that an inexpensive diuretic like chlorthalidone (a weak diuretic in the thiazide class, similar to hydrochlorothiazide) as first-line treatment for hypertension achieved equivalent reductions in cardiovascular events (cardiovasular death and heart attack) as non-thiazide antihypertensives, lisinopril (an ACE inhibitor) and amlodipine (a calcium channel blocker, better known as Norvasc).

After 7 years of treatment, there was 14% death or heart attack among all three groups--no difference.

This was interpreted to mean that inexpensive thiazide diuretics like chlorthalidone offer as much benefit as other blood pressure medications at reduced cost.

On the surface, that's great. Anything that detracts from the ubiquitous pharmaceutical industry propaganda of bigger, better, more expensive drugs to replace old, inexpensive, generic drugs is fine by me.

But you knew there'd be more to this issue! If we accept that thiazides are equivalent to other single-drug treatments for high blood pressure, what do we do with the following issues:

--Thiazides deplete body potassium-This effect can be profound. In fact, built into the ALLHAT mortality rate is an expected death rate from potassium depletion. When potassium in the body and blood go low, the heart becomes electrically unstable and dangerous rhythms develop.

--Thiazides deplete magnesium--Similar in implication to the potassium loss, magnesium loss also creates electrical instability in the heart, not to mention exaggeration of insulin resistance, rise in triglycerides, reduction in HDL.

--Thiazides reduce HDL cholesterol

--Thiazides increase triglycerides

--Thiazides increase small LDL particles--You know, the number one cause for heart disease in the U.S.

--Thiazides increase uric acid--Uric acid is increasingly looking like a coronary risk factor: The higher the uric acid blood level, the greater the risk for heart attack. Thiazides have long been known to increase uric acid, occasionally sufficient to trigger attacks of gout (uric acid crystals that precipitate in joints, like rock candy). (Fully detailed Special Report on uric acid coming this week on the Track Your Plaque website.)

What about the advice we commonly give people to hydrate themselves generously? Yet we give them diuretics? Which is it: More hydration or less hydration? You can't have both.

Do thiazides exert an apparent cardiovascular risk reduction in a society due to its flagrant sodium obsession?

Thus, there are a number of inconsistencies in the thinking surrounding thiazides. In my experience, I have seen more harm done than good using these agents. While I cannot fully reconcile the reported benefit seen in ALLHAT with what I see in real life, all too often I see people having to take another drug to make up for a side-effect of a thiazide diuretic (e.g., high-dose prescription potassium to replace lost potassium, allopurinol to reduce uric acid, etc.). I have seen many people get hospitalized, even suffer near-fatal or fatal events from extremely low potassium or magnesium levels.

My personal view: ALLHAT or no, avoid thiazide diuretics like the plague. Sure, it might save money on a population basis, but I suspect that the ALLHAT data are deeply misleading.

What's better than a thiazide, calcium blocker, or ACE inhibitor? How about vitamin D restoration, thyroid normalization, wheat elimination?

"High-dose" Vitamin D

I stumbled on one of the growing number of local media stories on the power of vitamin D.

In one story, a purported "expert" was talking about the benefits of "high-dose" vitamin D, meaning up to 1000, even 2000 units per day.

I regard this as high-dose---for an infant.

Judging by my experiences, now numbering well over 1000 patients over three years time, I'd regard this dose range not as "high dose," nor moderate dose, perhaps not even low dose. I'd regard it as barely adequate.

Though needs vary widely, the majority of men require 6000 units per day, women 5000 units per day. Only then do most men and women achieve what I'd define as desirable: 60-70 ng/ml 25-hydroxy vitamin D blood level.

I base this target level by extrapolating from several simple observations:

--In epidemiologic studies, a blood level of 52 ng/ml seems to be an eerily consistent value: >52 ng/ml and cancer of the colon, breast, and prostate become far less common; <52 ng/ml and cancers are far more likely. I don't know about you, but I'd like to have a little larger margin of safety than just achieving 52.1 ng/ml.

--Young people (not older people >40 years old, who have lost most of the capacity to activate vitamin D in the skin) who obtain several days to weeks of tropical sun typically have 25-hydroxy vitamin D blood levels of 80-100 ng/ml without adverse effect.

More recently, having achieved this target blood level in many people, I can tell you confidently that achieving this blood level of vitamin D achieves:

--Virtual elimination of "winter blues" and seasonal affective disorder in the great majority
--Dramatic increases in HDL cholesterol (though full effect can require a year to develop)
--Reduction in triglycerides
--Modest reduction in blood pressure
--Dramatic reduction in c-reactive protein (far greater than achieved with Crestor, JUPITER trial or no)
--Increased bone density (improved osteoporosis/osteopenia)
--Halting or reversal of aortic valve disease

(I don't see enough cancer in my cardiology practice to gauge whether or not there has been an impact on cancer incidence.)

My colleagues who have bothered to participate in the vitamin D conversation have issued warnings about not going "overboard" with vitamin D, generally meaning a level of >30 ng/ml.

I know of no rational basis for these cautions. If hypercalcemia (increased blood calcium) is the concern, then calcium levels can be monitored. I can reassure them that calcium levels virtually never go up in people (without rare diseases like sarcoid or hyperparathyroidism). Then why any hesitation in recreating blood levels that are enjoyed by tropical inhabitants exposed to plentiful sun that achieve these extraordinary health effects?

For the present, I have applied the target level of 60-70 ng/ml without apparent ill-effect. In fact, I have witnessed nothing but hugely positive effects.

Vitamin D Home Test

The ever-resourceful Dr. John Cannell of the Vitamin D Council has announced the availability of an at-home, self-ordered vitamin D test kit for $65. The Vitamin D Council newsletter is reprinted below.

(However, please note that, as wonderful as the advice Dr. Cannell provides, I don't agree on several small points, such as the lack of need for vitamin D if you use a tanning bed or obtain "sufficient" sun; I have seen many people with dark tans, virtually all over 40 years old, who are still severely deficient. I attribute this to the lost capacity for vitamin D activation as we age.)

I have not used this service. Should anyone choose to try it, please let us know how it goes.



The Vitamin D Newsletter
December 28, 2008

The Vitamin D Council is happy to announce that we have partnered with ZRT Laboratory to provide an inexpensive, $65.00, in-home, accurate, vitamin D [25(OH)D] test. The usual cost for this test is between $100.00 and $200.00.

If you read this newsletter, you know about our interest in accurate vitamin D testing. In the next few weeks, you may read about the Vitamin D Council's quest for accurate vitamin D blood tests in the national media. Before we partnered with ZRT, we verified, repeatedly, that ZRT provides accurate and reliable vitamin D tests and that their method corresponds very well to the gold standard of vitamin D blood tests, the DiaSorin RIA.

Our ZRT service is not just inexpensive, it means no more worrying about your doctor ordering the right test or interpreting it correctly. You buy the test kit on the internet or by phone, a few days later the kit comes in the mail, you or a nurse friend do a finger stick, collect a few drops of blood, and send the blotter paper back to ZRT in the postage paid envelope provided with the kit. A week later you get results back in the mail and know accurate 25-hydroxy-vitamin D levels of you and your family.

For every test you order, ZRT will donate $10.00 to the Vitamin D Council. Please read the new page hyperlinked below on our website as it both explains the procedure and how to order the test.

http://www.vitamindcouncil.org/health/deficiency/am-i-vitamin-d-deficient.shtml

Executive summary: keep your family's 25-hydroxy-vitamin D blood test above 50 ng/ml, year around. Most adults need at least 5,000 IU per day, especially this time of year. Most children need at least 1,000 IU per day per every 25 pounds of body weight. Bio Tech Pharmacal provides high quality and inexpensive vitamin D. Currently Bio Tech Pharmacal is providing vitamin D for numerous scientific studies. To see their prices and for ordering, click the hyperlink below.

http://www.bio-tech-pharm.com/catalog.aspx?cat_id=2

As a gift to our readers for the New Year, Thorne publications have provided a free download to a basic paper about vitamin D. I wrote it earlier this year for educated lay people as well as health care practitioners. Please read this paper carefully, your family's well-being, even lives, may depend on you understanding it.

http://www.thorne.com/altmedrev/.fulltext/13/1/6.pdf

Seasons Greetings
John Cannell, MD
vitamindcouncil.org

Where do Track Your Plaque membership revenues go?

People pay about $90 per year to become Members on the Track Your Plaque website. This provide access to our in-depth Special Reports, guides, webinars, and our proprietary software data tracking tools. Members can also participate in online discussions, such as those in the Track Your Plaque Forum and chats.

Why is there a charge for membership in the program and where does the money go?

Money raised from membership fees goes towards:

1) The costs of doing business, e.g., server fees, software purchases, legal fees. Hosting webinars, for instance, costs us about $99 per month for the GoToWebinar software service.

2) Software development--Our most recent round of software data tracking tools, for instance, cost us nearly $30,000. That may not be a lot from big business standards, but it is onerous enough that obtaining membership dues really helps.

3) Graphics development--A website without graphics would be awfully dull, regardless of the quality of the textual content. Some of the newest tools on the Track Your Plaque website require photography and graphics work, which can add up very quickly.


Where membership fees do NOT go:

1) In our pockets--In fact, except for the various contractors who are paid for their services (e.g., software developers), NOBODY on the Track Your Plaque staff are paid: not me, nor any of the behind-the-scenes staff. Some of the staff overlap with my office staff, but they are paid purely out of the office revenues, not out of Track Your Plaque membership dues.

2) Towards overhead costs beyond those listed above--For example, membership fees do not pay for office lease, utilities, phones, etc.


We rely on membership fees because we have chosen to remain as free of commercial bias as possible. We host no advertising, we have no behind-the-scenes corporate or institutional agendas, we show no favoritism to any business or commercial operation. We believe this permits editorial freedom that few other health websites can enjoy. (In fact, I know of no other that is so free of commercial bias, outside of small blogs or narrow-interest websites.)

If you want to see what damage commercial bias can create, just go to a health website like WebMD. I challenge you to find information that is not flagrantly biased by commercial influence, namely that of the drug industry. (According to the WebMD SEC filings, in fact, the great majority--approximately 80%--of their $331 million revenues (2007) were derived directly or indirectly from the drug industry.) This commercial bias reaches into all of WebMD's related businesses, including MedicineNet.com, RxList.com, Medscape.com, and several others.

Preventing heart disease is not a money maker, sad to say. It is, from the perspective of conventional heart care, a big money loser. Undergo a heart catheterization, hospitalization, stent or bypass for anywhere from $14,000 to well over $100,000---or pay $90 for in-depth health information that dramatically reduces the potential need for the hospital and its procedures, minimizes need for prescription medication (statins alone, of course, are a $27 billion annual revenue phenomenon), and achieves all this by maximizing nutrition, self-purchased nutritional supplements, and inexpensive heart scans. Nobody is going to make a bundle off of this approach.

So that is why we charge a membership fee. I often get a laugh from some of the comments of people on this blog or even in my office who believe that we are rolling in money from the website from membership dues. The opposite is true: We don't pay ourselves. Virtually every penny is reinvested back into the website to better serve the Members.

Green coffee bean extract in AGF Factor I

Track Your Plaque's new and proprietary formulation, AGF Factor I, is designed to to support a program to achieve low levels of endogenous glycation.

Endogenous glycation, discussed at length in a recent Track Your Plaque Special Report, makes LDL particles (especially small LDL particles) more prone to oxidation and thereby more atherogenic, i.e., more likely to contribute to atherosclerotic plaque. Endogenous glycation also exerts unhealthy effects on long-lived proteins in the body, such as the proteins in the lenses of your eyes (cataracts), the lining of arteries (hypertension), and the cartilage cells of joints (brittle cartilage and arthritis).

Endogenous glycation is reduced by slashing carbohydrates in the diet, especially the most offensive carbohydrates of all, the amylopectin A of wheat, sucrose, high-fructose corn syrup and other fructose sources. Endogenous glycation can also be blocked by using blockers of the glycation reaction, such as benfotiamine (lipid-soluble thiamine), pyridoxal-5'-phosphate (a form of vitamin B6 with greater glycation blocking effect), and chlorogenic acid from green coffee beans, all components of AGF Factor I, which also contains Portulaca oleracea (Portusana), or purslane, for reduction of glucose.

Green coffee bean extract, and thereby chlorogenic acid, is receiving increased attention, most recently due to a study demonstrating substantial weight loss with 750-1050 mg green coffee bean extract, providing approximately 325-500 mg chlorogenic acid per day. Participants lost 15.4 pounds over 8 weeks at the higher dose (500 mg chlorogenic acid per day), while participants lost 8.8 pounds over 8 weeks at the lower dose (325 mg chlorogenic acid per day).

AGF Factor I was not formulated for weight loss but, taken twice or three times per day, does indeed mimic the dose of chlorogenic acid from green coffee bean extract used in the weight loss study. If you wish to take advantage of this application of chlorogenic acid/green coffee bean extract, while also maximizing protection from endogenous glycation, our AGF Factor I is one excellent choice to do so.

Lessons learned from the 2012 Low-carb Cruise

I just returned from Jimmy Moore's Low-carb Cruise, a 7-day excursion to Jamaica, Grand Cayman Island, and Cozumel aboard the Carnival Magic. During our 7 wonderful days, a number of authors and experts spoke, each offering their unique perspective on the low-carb world. The focus was the science, experience, and practical application of low-carbohydrate diets.

The event kicked off with a roast by Tom Naughton of Fat Head fame, who entertained with his insightful low-carb humor and predictions of my demise at the hands of Monsanto!

Among the most important lessons provided:

Dr. Andreas Eenfeldt of the Diet Doctor blog discussed how Sweden is leading the world as the nation with the most vigorous low-carbohydrate following, witnessing incredible weight loss and reversal of carbohydrate-related diseases way ahead of the U.S. experience. I spent several hours with Dr. Eenfeldt who, besides being an engaging speaker, is a new father and an all-around gentleman. At 6 ft, 7 inches, he also towered high above all of us.

Dr. Eric Westman of Duke University and author of The New Atkins for a New You, debunked low-carbohydrate myths, such as "low-carb diets are high-protein diets that make your kidneys explode."

Dr. John Briffa, creator of the popular blog, Dr. John Briffa: A Good Look at Good Health, and author of the wonderfully straightforward primer to low-carbohydrate eating, Escape the Diet Trap, stressed the importance of never allowing hunger to rule behavior. Dr. Briffa's serious writing tone conceals an incredible charm and wit that took me by surprise, having spent several thoroughly engaging hours over breakfast, lunch, and dinner with him over the week.

Fred Hahn, exercise expert, founder of Serious Strength and author of Slow Burn Fitness Revolution and Strong Kids, Healthy Kids, debunked a number of trendy exercise methods, boiling many of the purported benefits of exercise down to that of increased strength.

Dr. Chris Masterjohn of The Daily Lipid and supporter of the Weston A. Price Foundation program, provided a comprehensive overview of the data that fails to link saturated fat with heart disease. He also helped me understand the analytical techniques used in studies of advanced glycation end-products.

Denise Minger, brilliant young usurper of China Study dogma and blogger at Raw Foods SOS, proved an engaging speaker and a truly real person (since some critics of her analyses have actually questioned whether there was even such a person!). She also proved every bit as likable as she seems in her captivating blog discussions.

Dr. Jeff Volek, prolific researcher from University of Connecticut, author of over 200 studies validating low-carbohydrate diet effects, and author of the recently released book with Dr. Stephen Phinney, The Art and Science of Low Carbohydrate Living, debunked myths behind carbohydrate dependence and "loading" by athletes. He also talked about how assessing blood ketones may be the gold standard method to ensure low-grade ketosis on a long-term low-carb effort.

Over a bottle of wine, Jimmy Moore and I reminisced over how his modest start with no experience in blogging or media has now ballooned to an audience of over 100,000 readers/viewers.

All in all, Jimmy's Low-carb Cruise experience was worth every minute, with many wonderful lessons and memories!

Chili Sesame Crackers

Looking for something hot and crunchy?

These chili sesame crackers are perfect for dipping into hummus or salsa. As written, the recipe yields a moderately spicy cracker that you can modify readily by increasing or decreasing quantities of cayenne pepper and Tabasco sauce.

This recipe uses sesame seeds as the "flour." Either brown sesame seeds or the lighter version work, though the lighter seeds yield a slightly less bitter flavor with the spices.

For ease of baking, a shallow baking pan measuring 11 x 17 inches works best, as it allows the batter to fill the pan and spread to a cracker thickness. With a smaller pan, you may have to bake in two batches.

Makes approximately 30 chips

2 cups raw sesame seeds
1 cup shredded Parmesan cheese
2 tablespoons extra-virgin olive oil
1 tablespoon chili powder
½ teaspoon cayenne pepper
2 teaspoons onion powder
1 teaspoon garlic powder
1 teaspoon dry mustard
1 teaspoon sea salt
1 teaspoon Tabasco sauce
1¼ cups water

Preheat oven to 350º F.

In food chopper or food processor, grind 1¼ cups sesame seeds to fine meal. Remove and place in large bowl.

Place shredded Parmesan cheese in food chopper or food processor and pulse briefly until reduced to granular consistency. Add to sesame seed meal and mix. Stir in olive oil.

Add remaining (unground) sesame seeds, chili powder, cayenne pepper, onion and garlic powder, mustard, sea salt and mix thoroughly. Add Tabasco sauce and water and mix. Add additional water, if necessary, one tablespoon at a time, to obtain a consistency similar to pancake batter.

Pour mixture into baking pan and smooth to fill pan and obtain a thickness of a cracker. If too thick, remove some batter and re-smooth. Optionally, roll a clean cylindrical glass or bottle over top to smooth and yield a consistent thickness.

Bake for 30 minutes or until edges browned and center firm. If a dry, extra crunchy cracker is designed, bake an additional 10-15 minutes at 250 degrees F.

Remove and allow to cool. Cut with pizza cutter to desired size.

Opiate of the masses

Although it is a central premise of the whole Wheat Belly argument and the starting strategy in the New Track Your Plaque Diet, I fear that some people haven't fully gotten the message:

Modern wheat is an opiate.

And, of course, I don't mean that wheat is an opiate in the sense that you like it so much that you feel you are addicted. Wheat is truly addictive.

Wheat is addictive in the sense that it comes to dominate thoughts and behaviors. Wheat is addictive in the sense that, if you don't have any for several hours, you start to get nervous, foggy, tremulous, and start desperately seeking out another "hit" of crackers, bagels, or bread, even if it's the few stale 3-month old crackers at the bottom of the box. Wheat is addictive in the sense that there is a distinct withdrawal syndrome characterized by overwhelming fatigue, mental "fog," inability to exercise, even depression that lasts several days, occasionally several weeks. Wheat is addictive in the sense that the withdrawal process can be provoked by administering an opiate-blocking drug such as naloxone or naltrexone.

But the "high" of wheat is not like the high of heroine, morphine, or Oxycontin. This opiate, while it binds to the opiate receptors of the brain, doesn't make us high. It makes us hungry.

This is the effect exerted by gliadin, the protein in wheat that was inadvertently altered by geneticists in the 1970s during efforts to increase yield. Just a few shifts in amino acids and gliadin in modern high-yield, semi-dwarf wheat became a potent appetite stimulant.

Wheat stimulates appetite. Wheat stimulates calorie consumption: 440 more calories per day, 365 days per year, for every man, woman, and child. (440 calories per person per day is the average.) We experience this, sense the weight gain that is coming and we push our plate away, settle for smaller portions, increase exercise more and more . . . yet continue to gain, and gain, and gain. Ask your friends and neighbors who try to include more "healthy whole grains" in their diet. They exercise, eat a "well-balanced diet" . . . yet gained 10, 20, 30, 70 pounds over the past several years. Accuse your friends of drinking too much Coca Cola by the liter bottle, or being gluttonous at the all-you-can-eat buffet and you will likely receive a black eye. Many of these people are actually trying quite hard to control impulse, appetite, portion control, and weight, but are losing the battle with this appetite-stimulating opiate in wheat.

Ignorance of the gliadin effect of wheat is responsible for the idiocy that emits from the mouths of gastroenterologists like Dr. Peter Green of Columbia University who declares:

"We tell people we don't think a gluten-free diet is a very healthy diet . . . Gluten-free substitutes for food with gluten have added fat and sugar. Celiac patients often gain weight and their cholesterol levels go up. The bulk of the world is eating wheat. The bulk of people who are eating this are doing perfectly well unless they have celiac disease."

In the simple minded thinking of the gastroenterology and celiac world, if you don't have celiac disease, you should eat all the wheat you want . . . and never mind about the appetite-stimulating effects of gliadin, not to mention the intestinal disruption and leakiness generated by wheat lectins, or the high blood sugars and insulin of the amylopectin A of wheat, or the new allergies being generated by the new alpha amylases of modern wheat.

Jelly beans and ice cream

What if I said: "Eliminate all wheat from your diet and replace it with all the jelly beans and ice cream you want."

That would be stupid, wouldn't it? Eliminate one rotten thing in diet--modern high-yield, semi-dwarf wheat products that stimulate appetite (via gliadin), send blood sugar through the roof (via amylopectin A), and disrupt the normal intestinal barriers to foreign substances (via the lectin, wheat germ agglutinin)--and replace it with something else that has its own set of problems, in this case sugary foods. How about a few other stupid replacements: Replace your drunken, foul-mouthed binges with wife beating? Replace cigarette smoking with excessive bourbon?

Sugary carbohydrate-rich foods like jelly beans and ice cream are not good for us because:

1) High blood sugar causes endogenous glycation, i.e, glucose modification of long-lived proteins in the body. Glycate the proteins in the lenses of your eyes, you get cataracts. Glycate cartilage proteins in the cartilage of your hips and knees, you get brittle cartilage that erodes and causes arthritis. Glycate structural proteins in your arteries and you get hypertension (stiff arteries) and atherosclerosis. Small LDL particles--the #1 cause of heart disease in the U.S. today--are both triggered by blood sugar rises and are 8-fold more prone to glycation (and thereby oxidation).

2) High blood sugar is inevitably accompanied by high blood insulin. Repetitive surges in insulin lead to <em>insulin resistance</em>, i.e., muscles, liver, and fat cells unresponsive to insulin. This forces your poor tired pancreas to produce even more insulin, which causes even more insulin resistance, and round and round in a vicious cycle. This leads to visceral fat accumulation (Jelly Bean Belly!), which is highly inflammatory, further worsening insulin resistance via various inflammatory mediators like tumor necrosis factor.

3) Sugary foods, i.e., sucrose- or high-fructose corn syrup-sweetened, are sources of fructose, a truly very, very bad sugar that is metabolized via a completely separate pathway from glucose. Fructose is 10-fold more likely to induce glycation of proteins than glucose. It also provokes a (delayed) rise in insulin resistance, accumulation of triglycerides, marked increase in formation of small LDL particles, and delayed postprandial (after-eating) clearance of the lipoprotein byproducts of meals, all of which leads to diabetes, hypertension, and atherosclerosis.

I think we can all agree that replacing wheat with jelly beans and ice cream is not a good solution. And, no, we shouldn't have drunken binges, wife beating, smoking or bourbon to excess. So why does the "gluten-free" community advocate replacing wheat with products made with:

rice starch, tapioca starch, potato starch, and cornstarch?

These powdered starches are among the few foods that increase blood sugar (and thereby provoke glycation and insulin) higher than even the amylopectin A of wheat! For instance, two slices of whole wheat bread typically increase blood sugar in a slender, non-diabetic person to around 170 mg/dl. Two slices of gluten-free, multigrain bread will increase blood sugar typically to 180-190 mg/dl.

The fatal flaw in thinking surrounding gluten-free junk carbohydrates is this: If a food lacks some undesirable ingredient, then it must be good. This is the same fatally flawed thinking that led people to believe, for instance, that Snack Well low-fat cookies were healthy: because they lacked fat. Or processed foods made with hydrogenated oils were healthy because they lacked saturated fat.

So gluten-free foods made with junk carbohydrates are good because they lack gluten? No. Gluten-free foods made with rice starch, tapioca starch, potato starch, and cornstarch are destructive foods that NOBODY should be eating.

This is why the recipes for muffins, cupcakes, cookies, etc. in this blog, the Track Your Plaque website, and the Track Your Plaque Cookbook are wheat- and gluten-free and free of gluten-free junk carbohydrates. And put that bottle of Jim Beam down!

Diet by LDL

Conventional notions of heart healthy diets, such as that advocated by the American Heart Association, are largely based on observations of total and LDL cholesterol.

So, cut the saturated fat in the diet, cut the overall fat content, and replace them with polyunsaturated oils like safflower, corn, and vegetable oils and increase consumption of whole grains and total and LDL cholesterol show a modest downturn. Thus, diets like the American Heart Association Total Lifestyle Change approach advocate limiting total fat to no more 25 to 35% of calories and saturated fat to no more than 7% of calories.

Orange Cream Cookies

If you loved Creamsicles as a kid, you'll love these Orange Cream Cookies. (Sorry, no photo: We ate them up before I realized we hadn't taken the photo. And, worse, we did it twice!)

Ingredients:
2 cups almond meal
2 tablespoons coconut flour
1 teaspoon baking soda
½ teaspoon sea salt
¼ cup golden raisins
½ cup chopped pecans
Sweetener equivalent to 1 cup sugar
2 tablespoons finely-grated orange rind
1 large egg
2 tablespoons coconut oil, melted
½ cup whipping cream (or coconut milk)
1 tablespoon vanilla extract

Preheat oven to 350º F.

Combine almond meal, coconut flour, baking soda, salt, raisins, pecans, sweetener and orange zest in bowl and mix.

In separate bowl, whisk egg, then add coconut oil, whipping cream, vanilla extract and mix together. Pour wet mix into dry and blend by hand thoroughly.

Spoon onto parchment paper-lined baking pan (or oiled pan) and flatten with spoon to ½-¾ inch thickness. Bake for 20-25 minutes or until toothpick withdraws dry.

Why are heart attacks still happening?

I'm a cardiologist. I see patients with heart disease in the form of coronary artery disease every day.

These are people who have undergone bypass surgery, received one or more stents or undergone other forms of angioplasty, have survived heart attacks or sudden cardiac death, or have high heart scan scores. In short, I see patients every day who are at high-risk for heart attack and death from heart disease.

But I see virtually no heart attacks. And nobody is dying from heart disease. (I'm referring to the people who follow the strategies I advocate, not the guy who thinks that smoking a pack of cigarettes a day is still okay, or the woman who thinks the diet is unnecessary because she's slender.)

Two high-profile deaths from heart attacks occurred this week:

Davy Jones--The iconic singer from the 1960s pop group, the Monkees, suffered sudden cardiac death after a large heart attack, just hours after experiencing chest pain.

Andrew Breitbart--The conservative blogger and controversy-generating media personality suffered what was believed to be sudden cardiac death while walking.

It's a darn shame and it shouldn't happen. The tools to identify the potential for heart attack are available, inexpensive, and simple. The strategies to reduce, even eliminate, risk are likewise available, inexpensive, and cultivate overall health.

The followers of the Track Your Plaque program who

1) get a heart scan that yields a coronary calcium score (for long-term tracking purposes)
2) identify the causes such as small LDL particles, lipoprotein(a), vitamin D deficiency, and thyroid dysfunction
3) correct the causes

enjoy virtual elimination of risk.

My letter to the Wall Street Journal: It's NOT just about gluten

The Wall Street Journal carried this report of a new proposed classification of the various forms of gluten sensitivity: New Guide to Who Really Shouldn't Eat Gluten

This represents progress. Progress in understanding of wheat-related illnesses, as well as progress in spreading the word that there is a lot more to wheat-intolerance than celiac disease. But, as I mention in the letter, it falls desperately short on several crucial issues.

Ms. Beck--

Thank you for writing the wonderful article on gluten sensitivity.

I'd like to bring several issues to your attention, as they are often neglected
in discussions of "gluten sensitivity":

1) The gliadin protein of wheat has been modified by geneticists through their
work to increase yield. This work, performed mostly in the 1970s, yielded a form
of gliadin that is several amino acids different, but increased the
appetite-stimulating properties of wheat. Modern wheat, a high-yield, semi-dwarf
strain (not the 4 1/2-foot tall "amber waves of grain" everyone thinks of) is
now, in effect, an appetite-stimulant that increases calorie intake 400 calories
per day. This form of gliadin is also the likely explanation for the surge in
behavioral struggles in children with autism and ADHD.
2) The amylopectin A of wheat is the underlying explanation for why two slices
of whole wheat bread raise blood sugar higher than 6 teaspoons of table sugar or
many candy bars. It is unique and highly digestible by the enzyme amylase.
Incredibly, the high glycemic index of whole wheat is simply ignored, despite
being listed at the top of all tables of glycemic index.
3) The lectins of wheat may underlie the increase in multiple autoimmune and
inflammatory diseases in Americans, especially rheumatoid arthritis and
inflammatory bowel diseases (ulcerative colitis, Crohn's).

In other words, if someone is not gluten-sensitive, they may still remain
sensitive to the many non-gluten aspects of modern high-yield semi-dwarf wheat,
such as appetite-stimulation and mental "fog," joint pains in the hands, leg
edema, or the many rashes and skin disorders. This represents one of the most
important examples of the widespread unintended effects of modern agricultural
genetics and agribusiness.

William Davis, MD
Author: Wheat Belly: Lose the wheat, lose the weight and find your path back to health
All posts by william-davis

Are you hungry?

Eliminate modern high-yield semi-dwarf Triticum aestivum . . . and what is the effect on appetite?

A reduction in appetite is among the most common and profound experiences resulting from wheat elimination. I know that I have personally felt it: Wake up in the morning, little interest in breakfast for several hours. Lunch? Maybe I'll have a few bites of something. Dinner . . . well, I'd like to exercise first.

The wheatless report that:

--Appetite diminishes to the point where you can't remember whether you've eaten or not. It is not uncommon to miss a meal, perfectly content. Calorie intake drops by 400 calories per day, on average, calories you otherwise would not have needed but all went to . . . you know where.
--Hunger feels different: It's not the gnawing, rumbling hunger that plagues you every 2 hours. In its place, you will find that hunger feels like a soft reminder that, gee, maybe it's time to have something to eat because you haven't had anything in--what?--4 to 6 hours. And it's a subtle reminder, not a desperate hunt that makes you knock people aside at the food bar, steal coworkers' lunches stored in the refrigerator, salivating at the mere thought of food.
--The simplest foods satisfy--It no longer requires an all-you-can-eat buffet to satisfy, but a few small pieces of healthy food. (Yeah, but what happens to revenues at Kraft, Nabisco, and Kelloggs, not to mention the revenues at agribusiness giants ADM and Monsanto? Slash consumption by, say, 30%, you likewise slash revenues by 30%. What would shareholders say?)
--Even prolonged periods of not eating, i.e., fasting, is endured with ease.

Hunger and the relentless search for something to eat disappear for most people. By eliminating the appetite-stimulating properties of wheat, we return to a natural state of eating for sustenance, to satisfy physiologic need. We are no longer victims of this incredibly powerful appetite-stimulant called gliadin from wheat.

This is why many diets fail: They fail to remove this powerful appetite stimulant. You might eat only lean meats, limit your calories, and exercise 90 minutes per day, but as long as the gliadin protein is pushing your appetite button, you will want to eat more or you will have to mount monumental willpower to resist it. You can lose 20 pounds on phase 1 of the South Beach diet, for instance, only to regain it in phases 2 and 3 when "healthy whole grains" are added back.

So the key is to remove the gliadin protein from your life, i.e., eliminate all things wheat.

 

Chocolate . . . for adults only

If you've got a serious chocolate addiction and you'd like to make it as healthy as possible, give this X-rated dark chocolate a try.
I call it X-rated because it is certain to not satisfy young, sugar-craving palates, but is appropriate for only the most serious chocolate craver. This is a way to obtain the rich flavors and textures of cocoa, the health benefits (e.g., blood pressure reduction, antioxidation) of cocoa flavonoids, while obtaining none of the sugars/carbohydrates . . . and certainly no wheat!

It is easy to make, requiring just a few ingredients, a few steps, and a few minutes. Set aside and save for an indulgence, e.g., dip into natural peanut or almond butter.

Ingredients:
8 ounces 100% unsweetened cocoa
5 tablespoons coconut oil, melted
1/2 cup dry roasted pistachios
1/4 cup whole flaxseeds or chia seeds
Truvia or other non-aqueous sweetener

Using double-boiler method, melt cocoa. Alternatively, melt cocoa in microwave in 15-20 second increments. Stir in coconut oil, pistachios, and flaxseeds or chia seeds. Stir in sweetener, mixing thoroughly. (Note that the sweetener must be non-aqueous, as water-based sweeteners will separate in the oils.)

Lay a sheet of parchment paper out on a large baking pan. Pour chocolate mixture slowly onto paper, tilting pan carefully to spread evenly until thickness of thick cardboard obtained. Place pan in refrigerator or freezer for 20 minutes.

Remove chocolate and break by hand into pieces of desired size.

"Friday is my bad day"

At the start, Ted had a ton of small LDL particles. His starting (NMR) lipoprotien values:

LDL particle number: 2644 nmol/L

Small LDL: 2301 nmol/L

In other words, approximately 85% of all LDL particles were abnormally small. I showed Ted how to use diet to markedly reduce small LDL particles, including elimination of wheat, limiting other carbohydrates, and even counting carbohydrates to keep the quantity no higher than 15 grams per meal ("net" carbs).

Ted comes back 6 months later, having lost 14 pounds in the process (and now with weight stabilized). Another round of lipoproteins show:

LDL particle number: 1532 nmol/L

Small LDL: 799 nmol/L

Better, but not perfect. small LDL persists, representing nearly 50% of total LDL particle number.

So I quiz Ted about his diet. "Gee, I really stick to this diet. I have nothing made of wheat, no sugars. I count my carbs and I almost never go higher . . . except on Fridays."

"What happens on Friday?" I asked.

"That's when I'm bad. Not really bad. Maybe just a couple of slices of pizza. Or I'll go out for a big custard cone or something. That wouldn't do it, would it?"

That's the explanation. Your liver is well-equipped to recognize normal, large LDL particles. Large LDL particles therefore "live" for only a couple of days in the bloodstream. But the human liver does not recognize the peculiar configuration of small LDL particles, so it lets them pass--over and over and over again. The result: Once triggered by, say two slices of pizza, small LDL particles persist for 5 days, sometimes longer.

So Ted's one "bad" day per week is enough to allow a substantial quantity of small LDL particles to persist. While a fat indulgence (if there is such a thing) pushes large LDL up, the effect is relatively short-lived. Have a carbohydrate indulgence, on the other hand, and small LDL particles persist for up to a week. It means that Ted's one "bad" day per week is enough to allow his small LDL particles to persist at this level, preventing him from gaining full control over coronary plaque.

It also means that, if you have blood drawn for lipoprotein analysis but had a carbohydrate goodie within the previous week, small LDL particles may be exaggeratedly high.

HDL 80 mg/dl

More and more people in my clinic are showing HDL cholesterol values of 80 mg/dl or higher, males included.

Think about it: Nationwide, average HDL for males is 42 mg/dl and for females 52 mg/dl. Even though these average values are generally regarded as favorable, HDL cholesterol values at these levels are nearly always associated with higher levels of triglycerides, postprandial (after-eating) lipoprotein abnormalities, and excessive quantities of small LDL particles.

HDL particles are, of course, protective and are powerfully anti-oxidative. Higher levels of HDL have been associated with reduced potential for cancer, as well as reduced risk for heart disease.

Following the simple regimen that we follow to gain control over coronary plaque has therefore increased levels of HDL to heights that are uncommon in the rest of the population, levels that readily top 80, 90, or 100 mg/dl. That regimen includes:

1) Elimination of all wheat--Yes, consumption of "healthy whole grains" sets you up to have lower HDL levels; elimination of wheat increases HDL.
2) Limited carbohydrate consumption--While eliminating wheat is a powerful nutritional strategy to increase HDL, non-wheat carbohydrates like quinoa, millet, beans, rice, and fruit can still cause high triglycerides that lead to reduced levels of HDL. Limited exposure helps keep HDL at higher levels.
3) Omega-3 fatty acid supplementation--Because omega-3 fatty acids reduce both triglycerides and blunt the postprandial rise in lipoproteins that can cause HDL degradation, HDL rises with omega-3s from fish oil.
4) Vitamin D supplementation--The effect is slow, but it is BIG. HDL just goes up and up and up over about 2 years of supplementation. Before vitamin D, HDL levels of 60 mg/dl were the best I could hope for in most people. Now 80 mg/dl is an everyday occurrence.

Other factors can also be used to increase HDL levels, such as weight loss, red wine and alcohol, exercise, cocoa flavonoids, green tea, and niacin. But following the regimen above sends HDL through the roof in the majority.

Lessons from the 20-year statin experience

Readers of the Heart Scan Blog know that, while I recognize that statins are useful in a small segment of the population with genetically-determined disorders, they are wildly overused, misused, and abused. In my view, the majority of people taking statins have no business doing so and could, in fact, obtain superior results by following some of the strategies advocated in these pages.

Nonetheless, the 30-year long statin experience has taught us some important lessons. Statin drugs have enjoyed more "research" than any other class of drugs ever conceived. They have received more media attention and embraced by more physicians than any other class of drugs. Combine these social phenomena and I believe that several lessons can be learned:

Small LDL particles and increased HbA1c--An evil duo

Small LDL particles are triggered by consumption of carbohydrates. Eat more "healthy whole grains," for instance, and small LDL particles skyrocket.

Increased hemoglobin A1c, HbA1c, a reflection of the last 60-90 days' blood sugars, is likewise a reflection of carbohydrate consumption. The greater the carbohydrate consumption and/or carbohydrate intolerance, the greater the HbA1c. Most regard a HbA1c of 6.5% or greater diabetes; values of 5.7-6.4% pre-diabetes. However, note that any value of 5.0% or more signifies that the process of glycation is occurring at a faster than normal rate. Recall that endogenous glycation, i.e., glucose modification of proteins, ensues whenever blood sugars increase over the normal range of 90 mg/dl (equivalent to HbA1c of 4.7-5.0%). Glycation is the fundamental process that leads to cataracts, arthritis, and atherosclerosis.

Put the two together--increased quantity of small LDL particles along with HbA1c of 5.0% or higher--and you have a powerful formula for heart disease and coronary plaque growth. This is because small LDL particles are not just smaller; they also have a unique conformation that exposes a (lysine residue-bearing) portion of the apoprotein B molecule contained within that makes small LDL particles uniquely glycation-prone. Compared to large LDL particles, small LDL particles are 8-fold more prone to glycation.

So glycated small LDL particles are present when HbA1c is increased above 5.0%. Small, glycated LDL particles are poorly recognized by the liver receptor that ordinarily picks up and disposes LDL particles, unlike large LDL particles, meaning small LDL particles "live" much longer in the bloodstream, providing more opportunityt to do its evil handiwork. Curiously, small LDL particles are avidly taken up by inflammatory white blood cells that can live in the walls of arteries, where they are oxidized--"glycoxidized"--and add to coronary atherosclerotic plaque.

The key is therefore to tackle both small LDL particles and HbA1c.

Unforgiving small LDL particles

Small LDL particles are triggered by carbohydrates in the diet: Eat carbohydrates, small LDL particles go up. Cut carbohydrates, small LDL particles go down.

A typical scenario would be someone starts with, say, 2000 nmol/L small LDL (by NMR) because they've been drinking the national Kool Aid of eating more "healthy whole grains" and consuming somewhere around 200 grams carbohydrates per day, including the destructive amylopectin A of wheat. This person slashes wheat followed by limiting other carbohydrates and takes in, say, 40-50 grams per day. Small LDL: 200 nmol/L.

In other words, reducing carbohydrate exposure slashes the expression of small LDL particles, since carbohydrate deprivation disables the liver process of de novo lipogenesis that forms triglycerides. Abnormal or exaggerated postprandial (after-eating) lipoproteins that are packed with triglycerides are also reduced. Because triglycerides provide the first lipoprotein "domino" that cascades into the formation of small LDL particles, carbohydrate reduction results in marked reduction in small LDL particle formation.

So let's say you are doing great and you've slashed carbohydrates. Small LDL particles are now down to zero--no small LDL whatsoever. What LDL particles you have are the more benign large variety, say, 1200 nmol/L (LDL particle number), all large, none small. You are due for some more blood work on Thursday. On Tuesday, however, you have four crackers because, what the heck, you've been doing great, you've lost 43 pounds, and have been enjoying dramatic correction of your lipoprotein abnormalities.

Your next lipoprotein panel: LDL particle number 1800 nmol/L, small LDL 700 nmo/L--substantially worse, with a major uptick in small LDL.

That's how sensitive small LDL particles can be to carbohydrate intake. And the small LDL particles can last for up to several days, since small LDL particles are not just smaller in size, they also differ in conformation, making them unrecognizable by the normal liver receptor. The small LDL particles triggered by the 4 crackers therefore linger, outlasting the normal-conformation large LDL particles that are readily cleared by the liver.

This phenomenon is responsible for great confusion when following lipoprotein panels, since a 98% perfect diet can yield dismaying results just from a minor indulgence. But, buried in this simple observation is the notion that small LDL particles are also extremely unforgiving, being triggered by the smallest carbohydrate indulgence, lasting longer and wreaking their atherosclerotic plaque havoc.

I eliminated wheat . . . and I didn't lose weight!

Elimination of wheat is a wonderfully effective way to lose weight. Because saying goodbye to wheat means removing the gliadin protein of wheat, the protein degraded to brain-active exorphins that stimulate appetite, calorie consumption is reduced, on average, 400 calories per day. It also means eliminating this source of high blood sugar and high blood insulin and the 90-minutes cycles of highs and lows that cause a cyclic need to eat more at the inevitable low. It means that the high blood sugar and insulin phenomena that trigger accumulation of visceral fat are now turned off. It may possibly also mean that wheat lectins no longer block the leptin receptor, undoing leptin resistance and allowing weight loss to proceed. And weight loss usually results effortlessly and rapidly.

But not always. Why? Why are there people who, even after eliminating this appetite-stimulating, insulin-triggering, leptin-blocking food, still cannot lose weight? Or stall after an initial few pounds?

There are a list of reasons, but here are the biggies:

1) Too many carbohydrates--What if I eliminate wheat but replace those calories with gluten-free breads, muffins, and cookies? Then I've switched one glucose-insulin triggering food for another. This is among the reasons I condemn gluten-free foods made with rice starch, cornstarch, tapioca starch, and potato starch. Or perhaps there's too many potatoes, rices, and oats in your diet. While not as harmful as wheat, they still provoke phenomena that cause weight loss to stall. So cutting carbohydrates may become necessary, e.g., no more than 12-14 grams per meal.

2) Fructose--Fructose has become ubiquitous and has even assumed some healthy-appearing forms. "Organic agave nectar" is, by far, the worst, followed by maple syrup, honey, high-fructose corn syrup, sucrose,and fruit--yes, in that order. They are all sources of fructose that causes insulin resistance, visceral fat accumulation or persistency, prolongation of clearing postprandial (after-meal) lipoproteins that antagonize insulin, and glycation. Lose the fructose sources--as much of it as possible. (Fruit should be eaten in very small portions.) Watch for stealth sources like low-fat salad dressings--you shouldn't be limiting your fat anyway!

3) Thyroid dysfunction--A real biggie. Number one cause to consider for thyroid dysfunction: iodine deficiency. Yes, it's coming back in all its glory, just like the early 20th century before iodized salt made it to market shelves. Now, people are cutting back on iodized salt. Guess what's coming back? Iodine deficiency and even goiters. Yes, goiters, the disfiguring growths on the neck that you thought you'd only see in National Geographic pictures of malnourished native Africans. Number two: Exposure to factors that block the thyroid. This may include wheat, but certainly includes perchlorate residues (synthetic fertilizer residues) on produce, pesticides, herbicides, polyfluorooctanoic acid residues from non-stick cookware, polybrominated diphenyl ethers (flame retardants), and on and on. If you are iodine-deficient, it can even include goitrogenic iodine-blocking foods like broccoli, cauliflower, and soy. Thyroid status therefore needs to be assessed.

4) Cortisol--Not so much excess cortisol as disruptions of circadian rhythm. Cortisol should surge in the morning, part of the process to arouse you from sleep, then decline to lower levels in the evening to allow normal recuperative sleep. But this natural circadian cycling is lost in many people represented, for instance, as a flip-flopping of the pattern with low levels in the morning (with morning fatigue) and high levels at bedtime (with insomnia), which can result in stalled weight loss or weight gain. Cortisol status therefore needs to be assessed, best accomplished with salivary cortisol assessment.

5) Leptin resistance--People who are overweight develop an inappropriate resistance to the hormone, leptin, which can present difficulty in losing weight. This can be a substantial issue and is not always easy to overcome. It might mean assessing leptin levels or it might mean taking some steps to overcome leptin resistance.

Okay, that's a lot. Next: More on how to know when thyroid dysfunction is to blame.

Do the math: 41.7 pounds per year

Consumers of wheat take in, on average, 400 calories more per day. Conversely, people who eliminate wheat consume, on average, 400 calories less per day.

400 calories per day multiplied by 365 days per day equals 146,000 additional calories over the course of one year. 146,000 calories over a year equals 41.7 pounds gained per year. Over a decade, that's 417 pounds. Of course, few people actually gain this much weight over 10 years.

But this is the battle most people who follow conventional advice to "cut your fat and eat more healthy whole grains" are fighting, the constant struggle to subdue the appetite-increasing effects of the gliadin protein of wheat, pushing your appetite buttons to consume more . . . and more, and more, fighting to minimize the impact.

So, if you eat "healthy whole grains" and gain "only" 10 pounds this year, that's an incredible success, since it means that you have avoided gaining the additional 31.7 pounds that could have accumulated. It might mean having to skip meals despite your cravings, or exercising longer and harder, or sticking your finger down your throat.

400 additional calories per day times 365 days per year times 300,000,000 people in the U.S. alone . . . that's a lot of dough. Is this entire scenario an accident?

Or, of course, you could avoid the entire situation and kiss wheat goodbye . . . and lose 20, 30, or 130 pounds this year.

We got the drug industry we deserve

A biting commentary on just who is writing treatment guidelines for diabetes and cardiovascular disease was published in the British Medical Journal, summarized in theHeart.org's HeartWire here.

"About half the experts serving on the committees that wrote national clinical guidelines for diabetes and hyperlipidemia over the past decade had potential financial conflicts of interest (COI), and about 4% had conflicts that were not disclosed.

"Five of the guidelines did not include a declaration of the panel members' conflicts of interest, but 138 of the 288 panel members (48%) reported conflicts of interest at the time of the publication of the guideline. Eight reported more than one conflict. Of those who declared conflicts, 93% reported receiving honoraria, speaker's fees, and/or other kinds of payments or stock ownership from drug manufacturers with an interest in diabetes or hyperlipidemia, and 7% reported receiving only research funding. Six panelists who declared conflicts were chairs of their committee.

"Of the 73 panelists who had a chance to declare a conflict of interest but declared none, eight had undeclared COI that the researchers identified by searching other sources. Among the 77 panel members who did not have an opportunity to publicly declare COI in the guidelines documents, four were found to have COI.
"

The closing quote by Dr. Edwin Gale of the UK is priceless:
"Legislation will not change the situation, for the smart money is always one step ahead. What is needed is a change of culture in which serving two masters becomes as socially unacceptable as smoking a cigarette. Until then, the drug industry will continue to model its behavior on that of its consumers, and we will continue to get the drug industry we deserve."

It's like having Kellogg's tell us what to each for breakfast, or Toyota telling us what car to drive. The sway of the drug industry is huge. Even to this day, I observe colleagues kowtow to the sexy sales rep hawking her wares. But that's the least of it. Far worse, even the "experts" who we had trusted to have objectively reviewed the evidence to help the practitioner on Main Street appears to be little more than a hired lackey for Big Pharma, hoping for that extra few hundred thousand dollars.