All posts by william-davis

Wheat causes arthritis.

Before you say "What the hell is he saying now?", let me connect the dots on how this ubiquitous dietary ingredient accelerates the path to arthritis in its many forms.

1) Wheat causes glycation--Glycation is glucose-modification of proteins in the body that occurs when blood glucose exceeds 100 mg/dl. Cartilage cells are especially susceptible to glycation. The cartilage cells you had at age 18 are the very same cartilage cells you have at age 60, since they lack the ability to reproduce and repair themselves. Proteins in cartilage are highly susceptible to glycation, which makes them stiff and brittle. Stiff, brittle cartilage loses its soft, elastic, lubricating function. Damaged cartilage cells don't regenerate nor produce more protective proteins. This allows destruction of cartilage tissue, inflammation, and, eventually, bone-on-bone arthritis.

Because wheat, even whole wheat, sends blood sugar higher than almost all other foods, from table sugar to Snickers bars, glycation occurs after each and every slice of toast, every whole wheat bagel, every pita wrap.

2) Wheat is acidifying--Humans are meant to consume a diet that is net alkaline. While hunter-gatherers who consume meat along with plentiful vegetables and fruits live a net alkaline diet (urine pH 7 to 9), modern humans who consume insufficient vegetables and too much grain (of which more than 90% is usually wheat) shift the body towards net acid (urine pH 5 to 7). Wheat is The Great Disrupter, upsetting the normal pH balance that causes loss of calcium from bones, resulting in decalcification, weakness, arthritis and osteoporotic fractures.

3) Wheat causes visceral fat--The extravagant glucose-insulin surges triggered by wheat leads to accumulation of visceral fat: wheat belly.

Visceral fat not only releases inflammatory mediators like tumor necrosis factor and various interleukins, but is also itself inflamed. The inflammatory hotbed of the wheat belly leads to inflammation of joint tissues. This is why overweight and obese wheat-consuming people have more arthritis than would be explained by the burden of excess weight: inflammation makes it worse. Conversely, weight loss leads to greater relief from arthritis pain and inflammation than would be explained by just lightening the physical load.

We need a name for this wheat effect. How about "bagel bones"?

Naloxone (IV) and naltrexone (oral) are drugs that block the action of morphine.

If you were an inner city heroine addict and got knifed during a drug deal, you'd be dragged into the local emergency room. You're high, irrational, and combative. The ER staff restrain you, inject you with naloxone and you are instantly not high. Or, if you overdosed on morphine and stopped breathing, an injection of naloxone would reverse the effect immediately, making you sit bolt upright and wondering what the heck was going on.

So what do morphine-blocking drugs have to do with weight loss?

An odd series of clinical studies conducted over the past 40 years has demonstrated that foods can have opiate-like properties. Opiate blockers, like naloxone, can thereby block appetite. One such study demonstrated 28% reduction in caloric intake after naloxone administration. But opiate blocking drugs don't block desire for all foods, just some.

What food is known to be broken down into opiate-like polypeptides?

Wheat. On digestion in the gastrointestinal tract, wheat gluten is broken down into a collection of polypeptides that are released into the bloodstream. These gluten-derived polypeptides are able to cross the blood-brain barrier and enter the brain. Their binding to brain cells can be blocked by naloxone or naltrexone administration. These polypeptides have been named exorphins, since they exert morphine-like activity on the brain. While you may not be "high," many people experience a subtle reward, a low-grade pleasure or euphoria.

For the same reasons, 30% of people who stop consuming wheat experience withdrawal, i.e., sadness, mental fog, and fatigue.

Wouldn't you know that the pharmaceutical industry would eventually catch on? Drug company startup, Orexigen, will be making FDA application for its drug, Contrave, a combination of naltrexone and the antidepressant, buproprion. It is billed as a blocker of the "mesolimbic reward system" that enhances weight loss.

Step back a moment and think about this: We are urged by the USDA and other "official" sources of nutritional advice to eat more "healthy whole grains." Such advice creates a nation of obese Americans, many the unwitting victims of the new generation of exorphin-generating, high-yield dwarf mutant wheat. A desperate, obese public now turns to the drug industry to provide drugs that can turn off the addictive behavior of the USDA-endorsed food.

There is no question that wheat has addictive properties. You will soon be able to take a drug to block its effects. That way, the food industry profits, the drug industry profits, and you pay for it all.

In the last Heart Scan Blog post, I discussed the significance of the apparent discrepancy between Steve's heart scan score and volume score. This post addresses his second question, also a FAQ about heart scan scores.

Steve noted that his second scan compared to his first showed:

- Left Main volume went up from 22.4 to 35.6
- LAD went down from 95.2 to 91.3
- LCX volume went down from 23.2 to 0
- RCA volume went up from 0 to 9.3

So there are apparent divergences in behavior in the left main that increased and both LAD (left anterior descending) and LCX (left circumflex) that decreased.

The explanation is simple: When heart scans are "scored," they are viewed in horizontal "slices." When the heart is viewed as horizontal slices, the LAD and LCX originate from the common left main stem. In other words, it's like a tree with the left mainsteam representing the trunk, the LAD and LCX representing two main branches.

Plaque can form, obviously, in all three arteries, but it can do so by starting in the left main, for instance, and extending into either the LAD or LCX, or both. The left main plaque can therefore bridge any 2 or all 3 arteries.

When the plaque is "scored" by taking the computer mouse and circling the calcified plaque in question (to allow the computer program to generate the calcium score and volume score of that particular plaque), the plaque that may extend from left main into the LAD and/or LCX might be labeled "left main," or it might be labeled "LAD" or "LCX." There is no reliable way to "dissect" apart the plaque into the three arteries, since the plaque is coalescent and continuous. So the scoring technologist or physician simply arbitrarily declares the artery "LAD," for instance.

The problem comes when two different interpretation methods are used: Perhaps it's a new technologist or physician, or there was no attention paid to how the previous scan was read. One reader calls it "left main" and the next calls it "LCX."

So the apparent discrepancy has to do with flaws in the methods of segregating plaque location, as well as inattention to scoring techniques. The total score, however, remains unaffected.

Nonetheless, Steve has enjoyed a modest reduction in the score of the left main/LAD/LCX from his original 140.8 down to a second left main/LAD/LCX score of 126.9.

The right coronary artery (RCA), however, is not subject to this difficulty and Steve score shows a modest increase in score. (Why the divergent behavior between left main/LAD/LCX and RCA? There is no clear explanation for this, unfortunately.)

All in all, the news for Steve is good: He achieved these results on his own using nutritional techniques. Because he, in all practicality, stopped the progression of his heart scan score and avoided the "natural" rate of increase of 30% per year, all he needs to do is "tweak" his program a bit to achieve reversal, i.e., reduction of score.

Here's an image from another previous Heart Scan Blog post (about the relationship of osteoporosis and coronary disease) that shows such a plaque that starts in the left mainstem yet extends into both the LAD and LCX:

Heart Scan Blog reader, Steve, sent these interesting questions about his heart scan experience. (I sometimes forget that this blog is called "The Heart Scan Blog" and was originally--several years ago--meant to discuss heart scans. It has evolved to become a much broader conversation.)

The answers are a bit lengthy, so I'll tackle Steve's questions in two parts, the second in another blog post.

Dr. Davis,

I had a heart scan last year. The score was 96. While not a horrible score, it
was a wake up call, and I changed my lifestyle.

I had another scan this year and the heart scan score went up to 105, but the
volume score went down from 141 to 136.

The report I received said this:

'The calcium volume score is less in the current study as compared with the
original or reference study. This is an excellent coronary result and indicates
that there has been a net decrease in coronary plaque burden. The current
prevention program is very effective and should be continued.'

This is all well and good, but I have two questions:

1. Am I really going in the right direction even though the heart scan score
went up 9%?

2. Here are results that make no sense to me:
- Left Main volume went up from 22.4 to 35.6
- LAD went down from 95.2 to 91.3
- LCX volume went down from 23.2 to 0
- RCA volume went up from 0 to 9.3

Why would there be so much variation from year to year, and why would the plaque
move from site to site?

Steve

Questions like Steve's come up with some frequency, so I thought it would be worthwhile to discuss in a blog post.

First of all, the conventional heart scan score, or "calcium score" or "Agatston score" (after Dr. Arthur Agatston, developer of the simple algorithm for calcium scoring, as well as South Beach Diet fame), is the product of the area of the plaque in a single CT "slice" image
multiplied by a density coefficient, i.e., a number ranging from 1 to 4 that grades the x-ray density of the plaque. (1 is least dense; 4 is most dense.) A density coefficient of 1 therefore signifies some calcium within plaque, with higher density coefficients signifying increasing calcium content and density. Incidentally, "soft" plaque, i.e., non-calcified, would fall in the less than 1 range, even the negative range (fatty tissue within plaque).

The volume, or "volumetric," score is the brainchild of Drs. Paulo Raggi and Traci Callister, who expressed concern that, if we cause plaque to shrink in volume, the density coefficient used to calculate the calcium score would increase (since they believed that calcium could not be reduced, contrary to our Track Your Plaque experience, thereby leading to misleading results. They therefore developed an algorithm that did not rely on density coefficients, but used the same two-dimensional area obtained in the standard heart scan score, but replaced the density coefficient with a (mathematically interpolated) vertical axis (z-axis) measure of plaque "height." This 3-dimensional volumetric value therefore provided a method to generate a measure of calcium volume. In their original publication, the volume score proved more reproducible than the standard calcium score. This way, any reduction in plaque volume would not be influenced by the misleading effects of calcium density, but reflect a real reduction in volume.

Callister and Raggi's study also highlighted that calcium scoring in any form is subject to variability. Back in 1998 (when their study was published), there was a bit more variation than today due to the image acquisition methods used. But, even today, there is about 9% variation in scoring even if performed repeatedly (with less percentage variation the higher the score).

Unfortunately, volume scoring never caught on and the calcium score has been the most commonly used value by most heart scan centers and in most clinical studies. And, in all practicality, the two values nearly always track together: When calcium score increases, volume score increases in tandem; when calcium score decreases, volume score decreases in tandem.

Steve is therefore an exception to the general observation that calcium score and volume score travel together. Steve's calcium score increased, while his volume score decreased. From the above discussion, you can surmise a few things about Steve's experience:"

1) In all likelihood, the changes in both calcium score and volume score could simply be due to variability, i.e., variation in the placement of his body on the scan table, variation in position of the heart, variation in data acquisition, etc. There is a high likelihood that neither value changed; both are essentially unchanged.

2) If the changes are not due to scan variability, but are real, then it could be that the calcified plaque is reduced in volume but increased in density. If true, this is probably still a favorable phenomenon, since plaque volume is a powerful predictor of coronary "events" and an increase in plaque density is likely a benign phenomenon. It would also raise questions about the adequacy of vitamin D and vitamin K2 status, both major control factors over calcium deposition and metabolism.

So, in all likelihood, Steve's apparent discrepant results are modest good news, especially since calcium scores can ordinarily be expected to increase at the rate of 30% per year if no action is taken. Experiencing no change in score, calcium or volumetric, carries a very excellent prognosis, with risk for heart attack approaching zero. (I'm impressed that Steve accomplished this on his own, something the majority of my colleagues haven't the least bit of interest doing.)

Part 2 of Steve's question will be tackled in a separate post.

As more and more people are eliminating wheat from their diet and losing their "wheat bellies," i.e., the muffin top around their waists along with the visceral fat beneath, I am frequently seeing something I haven't seen in years: the linea alba.

Linea alba, or "white line," refers to the band of connective tissue running vertically from sternum to pubic area. It underlies the depression that separates the horizontal abdominal rectus muscles of the "six pack" abdomen.

It's like digging in your closet and finding something you thought you'd lost years earlier. Surprise! It's been there all along. Buried deep beneath the abdominal fat from dozens of deep-crust pizzas, whole wheat pasta, and whole grain sandwiches is this pleasing anatomical feature long lost from most peoples' anteriors.

Can you see your linea alba?

Here's my 12-year old standing next to dwarf wheat grown near my house. The wheat is full-grown, harvested about 2 weeks after I took this photo.

Wheat is no longer the 4-foot tall "amber waves of grain" of the 20th century. Over 99% of all wheat grown worldwide is now the 18- to 24-inch tall dwarf. New size, new biochemistry, new effects on humans. I call it dwarf "mutant" wheat despite its lack of extra limbs or eyes because of the dramatic transformation required to breed this unique synthetic plant.

Short-stature means less stalk, faster growing. The stockier stalk also means that the heavy seed head won't cause the plant to "buckle," as 4-foot tall wheat used to.

The thousand-plus proteins of wheat that have been transformed to generate this dwarf mutant also changed wheat's relationship to consuming humans.

I received this detailed email from an unexpected source: a 3rd-year medical student.

In her email, Theresa describes her frustrations in what she is witnessing for the first time, proceeding through her training and getting exposed to the realities of medical life.

Medical training, particularly clinical training from the 3rd and 4th years of medical school, onwards through internship, residency, and fellowship training, consists largely of bullying, "pimping" (meaning rapid-fire grilling of questions at trainees), and sleep deprivation. It is an extended hazing period meant to demoralize and inculcate the trainee into following the lead of superiors. Buck the system and you're . . . out. Imagine you've just sunk $190,000 and 8 years of college into getting to your internship. You are not going to chance being thrown out on principle. So you just swallow your pride, go along with the game, and echo all the answers they want you to repeat.

While Theresa laments the sad state of modern American pharmaceutical- and procedure-obsessed medicine, she provides me with hope that some young people training to practice medicine today will carve out their own paths, not the one laid for them by the pharmaceutical industry, nor fall for the temptation of higher-paying procedural specialties like orthopedics and cardiology. I am impressed with her ability to see this so early in her career.

Dr. Davis,

I am a 3rd year medical student at ________ University. I came across
your blog today, and I'm very glad I did. I appreciate the value of your time,
so I want to be as succinct as possible while still getting across what I'm
really thinking and feeling:

From what I gathered exploring your blog for a while this afternoon, the
wellness strategies you incorporate into your practice are some of the exact
things I want to do with my future patients. Personally, I strongly believe in
staying healthy by eating right, staying active, etc. For instance, I don't eat
grains or much in the way of starches and sugars. So I love the fact that you
are helping your patients make these powerful and foundational changes in their
lives.

As I'm sure was your experience, a full appreciation of nutrition and lifestyle
as a first-line health strategy is not something that was taught to me in
medical school. I came to school with this deep conviction already in my heart
and mind, and now, on my 3rd year rotations, I am still conflicted and at a loss
as to how I'm going to be able to practice medicine the way I want to, which is
to incorporate these all-important principles into the care of my patients.

What I've come to understand about the medical field today is that the
information that exists is primarily subsidized by the pharmaceutical industry,
and dictated to medical professionals as "evidence-based" treatment guidelines
and recommendations by organizations with sincere and official sounding names
like American Heart Association and American Cancer Society. Add to that the
pressure of potential malpractice litigation and the complexities of the
insurance reimbursement game, and it seems to me like what you get is a bunch of
diagnostic and medication management algorithms that any half-trained monkey
could follow. In his sleep. Which I guess would be alright if at least they
weren't algorithms based on misguided, self-serving, profit-seeking Big Pharma,
Food Inc, insurance conglomerates, and agri-politics (I think I just made that
word up.)

A lot of well-intentioned physicians are just parroting the party
line, as their patients dutifully and gratefully chomp down their statins and
diabetes drugs and blood pressure pills. And I'm sorry, but "diabetes
education" programs with curriculum put together by drug companies? How is that
even legal? Massive corporations raking in massive profits that are dependent
on uncontrolled blood sugars telling people how to best control their blood
sugars?!

Anyway, forgive my rant. What I'm getting at is this: How can I practice
medicine, with the freedom to educate/coach/treat my patients with diet and
lifestyle changes to mitigate/reverse their chronic health conditions? Without
feeling like I automatically have to first and foremost prescribe the litany of
drugs dictated by "evidence-based" guidelines? Without excessive fear of
litigation or loss of credibility among my peers? Without having to lie through
my teeth to my patients, and tell them that eating low-fat and heart-healthy
whole grains is the best way (implication also being the only scientifically
proven way) to control their diabetes, lower their cholesterol, etc, etc, etc?

I want my patients to have the full benefit of honest nutrition and lifestyle
information, and medications and surgery as necessary. I'm afraid that there
isn't room for this kind of holistic emphasis in the medical profession today.
Are there residencies that include this kind of training or at least respect
these "unconventional" philosophies? Are there clinics or practice groups that
would allow me to practice with this emphasis, or is there a bias against docs
who do not necessarily conform to the party position? Will I have no other
option but to go it alone under the auspices of my own shingle? How do you
handle these kinds of issues in your professional life?

Sincerely,
Theresa M.

A ray of hope! Perhaps Theresa is just the first among many more medical students who refuse to submit to the brainwashing practices of the pharmaceutical industry, the same mind manipulation that has hopelessly turned most of my colleagues into their unwitting puppets.

I'll be interested in watching how Theresa's experience unfolds. I've asked her to keep us informed every so often.

The effusive Jimmy Moore of Livin' La Vida Low-Carb asked me to help get the word out about his new podcast subscription service, The Livin' La Vida Low-Carb Show Fan Club.

Jimmy has been The Great Connector for the low-carb discussion, from his ubiquitous online and social media presence, to his annual low-carb cruise. He has also broadcast first class interviews of nutritional notables like Gary Taubes, Dr. Robert Lustig, and blogger Stephan Guyenet. His Fan Club expands listener involvement in the podcast process and, potentially, greater access to his guests:

My faithful listeners have long been asking me about how they can become even more engaged in the behind-the-scenes workings of the show to get the inside scoop about what’s coming next. I’ve heard people ask specifically for access to transcripts of the most popular podcasts, a listing of the interviews I’m currently working on with the ability to ask questions of those guests, to have sneak peek of audio from not-yet-released interviews and more. My amazing podcast producer, Kevin Kennedy-Spaein, and I have been discussing how to best do this for a while in an effort to meet the demands of our biggest fans and we think we’ve got just the answer for you. Introducing The Livin’ La Vida Low-Carb Show Fan Club!

This is for all intents and purposes the quintessential destination for people who can’t get enough of this podcast that goes much deeper than discussion about the low-carb lifestyle. Yes, I speak with a lot of people who are supporters of carbohydrate-restricted diets, but I also talk with fitness gurus, people who support alternative eating plans, those who have interesting theories and beliefs regarding health and much more. Wouldn’t you love to have a chance to know who’s coming up in my schedule to be able to ask them questions BEFORE I interview them? Keep in mind that my interviews are pre-recorded and air sometimes as much as 5-6 months afterwards. Members of the “fan club” would know all about who’s coming and likely will have their question asked on the air just for signing up to be a part of this exciting new addition to “The Livin’ La Vida Low-Carb Show.”

Jimmy is the guy who is bringing this disparate and widely-spread community together. He's the guy we all know, he knows "everybody." I'm looking forward to seeing how this new project makes a more involved, personal delivery of interaction possible.

The record for the largest drop in heart scan score (by percentage of starting score) has been held for around three years, with 63% reduction in score.

Well, the longstanding record was broken this week: 75% reduction in score.

At the start, Freddie has disastrous lipid values:

LDL cholesterol 263 mg/dl
HDL 26 mg/dl
Triglycerides 323 mg/dl
Total cholesterol 354 mg/dl

Lipoproteins (NMR) were worse:

LDL particle number 3360 nmol/L
Small LDL 2677 nmol/L

Heart scan score: 732

Interestingly, Freddie had virtually no vitamin D in his body, with a 25-hydroxy vitamin D level that was unmeasurable.

Freddie was miserably intolerant to statin drugs, with even the smallest dose resulting in intolerable muscle aches. That's when his doctor sent him to me.

Because I felt that the dominant abnormality in Freddie's lipids and lipoproteins was small LDL particles, representing 80% of total LDL particle number, we focused his program on correcting this parameter. Freddie's program was therefore focused elimination of wheat, cornstarch, oats, and sugars, along with an eventual vitamin D dose of 20,000 units to finally achieve a 25-hydroxy vitamin D level of 66 ng/ml. No statin drug in sight.

43 lbs of weight loss and 18 months later, a second heart scan score: 183--a 75% reduction.

While the rest of the world continues to insist that coronary calcium (heart scan) scores cannot be reduced, I am seeing records being broken. I add Freddie's experience to the rapidly growing list of people who have not just stopped coronary plaque from growing, but are seizing control and reducing it, sometimes to dramatic degrees.

Advanced Glycation End-products, AGEs, are a diverse collection of compounds that have been associated with endothelial dysfunction, cataracts, kidney disease, and atherosclerosis in both animal models and human studies. Not all involve glycation nor glucose, but the catch-all name has stuck.

There are a number of actively-held theories of aging, such as the idea that aging is the result of accumulated products of oxidative injury; a genetically pre-programmed script of declining hormones and other phenomena; genetic "mis-reading" that results in disordered gene expression, debris, and uncontrolled cell proliferation (e.g., cancer); among others.

One of the fascinating theories of aging is, cutely, the AGEing theory of aging, i.e., the accumulation of AGE debris in various tissues. Such AGEs have been recovered in lenses from the eyes, atherosclerotic plaque in arteries, kidney and liver tissue, even brain tissue of people with Alzheimer's dementia. AGEs perform no known useful physiologic function: They are relatively inert once formed (especially polymeric AGEs), they do not participate in communication, they make no contribution of significance. They simply gum up the works--debris. (AGEs are to health as the USDA food pyramid is to dietary advice: material for the junkyard.)

There are two general ways to develop AGEs:

1) Endogenous--High blood glucose (any blood sugar above 100 mg/dl) will permit glycation of the various proteins of the body. The higher the blood glucose, the more glycation will proceed. Glycation also occurs at low velocity at blood glucose levels below 100 mg/dl, though this would therefore represent the "normal," expected rate of glycation. Endogenous glycation explains why people with diabetes appear to age and develop all the phenomena of aging faster than non-diabetics (kidney disease, eye diseases, atherosclerosis, dementia, etc.). Hemoglobin A1c, HbA1c, is a readily-obtainable blood test that can show how enthusiastically you have been glycating proteins (hemoglobin, in this case) over the last 2 to 3 months.

A low-carbohydrate diet is the nutritional path that limits endogenous glycation leading to AGE formation. Restricting the most obnoxious carbohydrates, the ones that increase blood sugar the most, such as wheat, cornstarch, rice starch, potato starch, tapioca starch, and sucrose, will limit endogenous AGE formation.

2) Exogenous--AGEs (here especially is where the "AGE" label is misleading, since many other reactions besides glycation lead to such compounds) are formed with cooking at high temperatures, especially meats and animal products. Therefore, a rare steak will have far less than a well-done steak. A thoroughly baked piece of salmon will have greater AGE content than sashimi.

The forms of cooking that increase AGE content the most: roasting,deep-frying, and barbecuing. Temperatures of 350 degrees Fahrenheit and greater increase AGE formation.

Therefore, cooking foods at lower temperature (e.g., baking, sauteeing, or boiling), eating meats rare whenever possible (not chicken or pork, of course), eating raw foods whenever possible (e.g., nuts) are all strategies that limit exogenous AGE exposure. And minimize or avoid butter use, if we are to believe the data that suggest that it contains the highest exogenous AGE content of any known food.

If we connect the dots and limit exposure to both endogenous and exogenous AGEs, we will therefore not trigger this collection of debris that is likely associated with disease and aging. So following a low-AGE diet may also be an anti-aging strategy.

The New Track Your Plaque Diet, soon to be released on the Track Your Plaque website, has incorporated strategies to limit both endogenous as well as exogenous AGEs.

Just a muse.

Endogenous substances are those that are already contained within our bodies. They are part of basic human equipment.

Exogenous substances are those that come from outside of our bodies. This includes various substances in foods, drugs (most, though not all), and pesticides.

I often mull over all of the tools we use in the Track Your Plaque program to achieve control over this thing called coronary plaque. It struck me that just about all the supplements we use that seem to provide outsized benefits are all endogenous substances themselves:

--Omega-3 fatty acids from fish oil
--Vitamin D
--l-arginine
--Niacin (vitamin B3)

Many of the other substances, though not directly relevant to our plaque-control efforts, but are among the most effective nutritional supplements, also supplement endogenous levels: calcium pyruvate, creatine, acetylcarnitine, DHEA, testosterone, progesterone, growth hormone, pregnenolone, phenylalanine, tyrosine, melatonin, etc.

Curiously, most drugs are not meant to directly supplement endogenous levels, but are designed either to enhance or block an enzyme (e.g., acetylcholinesterase inhibitors that block breakdown of acetylcholine; HMG CoA reductase inhibitors to block cholesterol synthesis; angiotensin converting enzyme inhibitors to reduce blood pressure), to exert toxic effects on an organism (antibiotics, antivirals), or to exert an entirely unique effect that does not ordinarily occur in the human body (some anti-cancer drugs, for instance). (This is an admitted, vast over-simplification.)

That's not to say that any endogenous substance is desirable or safe when supplemented. Cortisol, thyroid hormone, and estrogens are three examples of endogenous substances that have downsides when administered at slightly more than physiologic concentrations.

Nonetheless, it makes me wonder if the world of endogenous substance supplementation has not been fully explored. Are there other endogenous substances that are as potent and wonderful, for instance, as vitamin D but not yet fully appreciated? I'm sure there are.

Reprinted here is the unfailingly informative Vitamin D Newsletter from Dr. John Cannell. Although there's little here specifically about heart disease, there's so much great information about vitamin D that I thought most would still appreciate it.

The Vitamin D Newsletter

May, 2008

Yesterday's Washington Post article, Too-Good-To-Be-True Nutrient?, sums up the April 9th vitamin D symposium at UCSD in San Diego, which was nothing short of spectacular. Carole Baggerly outdid herself organizing it and explaining how she got involved. Make no mistake; Carole is both serious and energetic. She told about her efforts to introduce resolutions at upcoming meetings of various professional groups. Then she introduced the volunteers from the San Diego Black Nurses Association who made sure the conference went off without a hitch. Then Carole introduced the four speakers. The slides of each speaker are available at Grassroots Health.

Before I tell you the highlights of the conference, I'd like to tell you about another conference, this one in Germany, this May 17th and 18th. It is the Third International Symposium on Vitamin D Analogs in Cancer Prevention and Therapy. Readers know how I feel about giving analogs to vitamin D deficient patients instead of vitamin D but speakers include Michael Holick, Reinhold Veith, Bill Grant, Tai Chen, Heidi Cross, David Feldman, and Roger Bouillon, all of whom know the importance of the nutrient. Most of this conference is for scientists, not lay people. However, Michael Holick is the first speaker and if you have not heard his latest talk about vitamin D, it might be worth a trip to Germany.

The first San Diego speaker was Dr. William Grant. Since leaving NASA to begin a full-time career as a vitamin D researcher, Bill has published dozens of studies and has another dozen in the works. Using ecological studies (from Greek oikos, house + German -logie, study or studying your own house) of UVB irradiance and cancer, Bill reported that 15 cancers (colon, esophageal, gallbladder, gastric, pancreatic, rectal, small intestinal, bladder, kidney, prostate, breast, endometrial, ovarian, Hodgkin's lymphoma, and non-Hodgkin's lymphoma) are associated with lower UVB light. He concluded that 257,000 cancer deaths in 2007 in the USA were accounted for by inadequate vitamin D levels. Of course the problem with ecological studies is that it easy to be vitamin D deficient in Miami, all you have to do is listen to your doctor's advice and stay out of the sun. Recently, a group from the Arizona Cancer Center found almost 80% of Arizonians had levels below 30 ng/ml. So much for sunny spots.

Jacobs ET, et al. Vitamin D insufficiency in southern Arizona. Am J Clin Nutr. 2008 Mar;87(3):608-13.

The next speaker was Professor Cedric Garland. I found myself wondering how he did it. I became convinced that vitamin D prevents cancer five years ago. Cedric and his brother Frank and his colleague Ed Gorham knew it 30 years ago! I know what it is like to tell someone that vitamin D prevents cancer and see them think, "Here we go again, another miracle vitamin." I know what it is like to try and explain and watch people die unnecessarily. But I've only had that experience for five years. Cedric has dealt with that frustration for thirty years. Almost thirty years ago, Cedric and Frank Garland published evidence that vitamin D prevents cancer. In fact, it was Cedric's first publication. Thankfully, the paper was recently recognized as being so important that it was republished in 2006 by the International Journal of Epidemiology. You can read the entire paper for free by clicking on the second link below and then clicking on "free final text", courtesy of Oxford Journals.

Garland CF, Garland FC. Do sunlight and vitamin D reduce the likelihood of colon cancer? Int J Epidemiol. 1980 Sep;9(3):227-31.

Garland CF, Garland FC. Do sunlight and vitamin D reduce the likelihood of colon cancer? Int J Epidemiol. 2006 Apr;35(2):217-20.

Cedric began by showing the incidence of type-1 diabetes and multiple sclerosis by latitude. I had no idea that the latitudinal data was so strong for type 1 diabetes in children. This disease is almost nonexistent around the equator. Type-1 diabetes is but one of the three modern childhood epidemics caused by the sunlight-hating dermatologists, the other two, I think, are autism and asthma. Next he showed latitude and 25(OH)D levels, which reminded me to be suspicious of high levels, unless they use accurate methods of detecting 25(OH)D. Some methods used, even in this country, are over detecting vitamin D and telling patients their levels are above 50 ng/ml when they are, in reality, much lower. Cedric's data showed Thailand had mean levels of 70 ng/ml, which I doubt and suspect were due to inaccurate 25(OH)D tests. He then reviewed evidence of the 25(OH)D levels needed to prevent numerous cancers. The safest levels are somewhere above 50 ng/ml. Cedric spent most of his time presenting an entirely new theory of carcinogenesis, one dependent on vitamin D maintaining cellular junctions. I suspect this paper will also be reprinted in 20 years. The only disagreement I have is with his recommendation for cancer patients to start at fairly low doses. For reasons I recently explained, the risk benefit analysis indicates cancer patients should take 5,000 to 10,000 IU per day and they may have no time to lose. Why worry about the phantom of vitamin D toxicity if you may be dying of cancer? Just have your calcium checked along with frequent 25(OH)D levels. Get your levels up to 70-90 ng/ml if you have cancer.

Does vitamin D treat cancer?

The next speaker was Professor Bruce Hollis. He reviewed basic physiology of vitamin D and emphasized that the entire system is designed to deal with an excess not with an insufficiency of vitamin D. Numerous mechanisms are available in your body to prevent vitamin D toxicity but few are available to deal with insufficiency. Then he briefly mentioned one of the most important discoveries about vitamin D in the last few years, one where Professor Neil Binkley of the University of Wisconsin was senior author. (In the last four years, Professor Binkley has become a prolific vitamin D expert and I hope Carol Baggerly is able to get him to speak at some of the upcoming conferences she hopes to sponsor.) As I have pointed out before, Hollis and Binkley's crucial discovery was that the body doesn't start storing the parent compound, cholecalciferol, until 25(OH)D levels reach about 50 ng/ml. They showed, using basic steroid pharmacology, that 50 ng/ml should be considered the lower limit of adequate 25(OH)D levels.

Hollis BW, Wagner CL, Drezner MK, Binkley NC. Circulating vitamin D3 and 25-hydroxyvitamin D in humans: An important tool to define adequate nutritional vitamin D status. J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):631-4.

Bruce kept the audience enthralled with a review of all the disease states that indicate 25(OH)D levels need to be much higher than they are now, that is, the multiple biomarkers that suggest the lower limit of 25(OH)D levels should be above 40 ng/ml and closer to 50 ng/ml. Then Professor Hollis spoke of his ongoing study in pregnant women and how he got approval to use 4,000 IU of vitamin D per day back in 2003, quite an accomplishment. He also reviewed another one of his research projects, one that answered an age old question, why is breast milk a poor source of vitamin D? How were prehistoric infants supposed to get their vitamin D, by lying out in the sun where saber tooth tigers would eat them? No, they were hidden in caves and had to have another source or the human race would have died out long ago because rickets destroys a woman's and infant's chance to live through childbirth due to rachitic deformations of the mother's pelvis. Carol Wagner and Bruce Hollis, together with their colleagues, answered that age old question, human breast milk is a poor vitamin D source because virtually all modern mothers are vitamin D deficient. That is, when pregnant women keep their levels where we think prehistoric human levels were, about 50 ng/ml, breast milk becomes a rich source of vitamin D. First Carol and Bruce gave 2,000 IU per day, then 4,000 IU per day and finally 6400 IU of D3 per day to lactating women. Only at 6400 of D3/day did the women maintain both their own 25(OH)D levels and the levels of their breast feeding babies above 50 ng/ml. On 6400 IU/day, the vitamin D activity of the breast milk went from about 80 to 800 IU/L. Quite a discovery, and another reason for all of us to keep our levels above 50 ng/ml.

Wagner CL, Hulsey TC, Fanning D, Ebeling M, Hollis BW. High-dose vitamin D3 supplementation in a cohort of breastfeeding mothers and their infants: a 6-month follow-up pilot study. Breastfeed Med. 2006 Summer;1(2):59-70.

Professor Robert Heaney went last, discussing 74 slides. So much of what we know about vitamin D today is due to Robert's unceasing dedication to vitamin D, the most recent example being his and Joanne Lappe's randomized controlled trial showing that increasing baseline levels from 29 to 38 ng/ml reduced the risk of getting cancer by around 70%. He again pointed out that the body does not begin to consistently store much vitamin D until your levels get to around 50 ng/ml. He also went through multiple biomarkers of vitamin D. That is, what level or intakes do you have to have to reduce the incidence of multiple diseases? He covered calcium absorption, osteoporosis, risk of falling, muscle function, death and disability of the aged, TB, influenza, cardiovascular disease, hypertension, diabetes, cancer, multiple sclerosis, and gum disease. How can one vitamin be involved in so many diseases? Simple said Dr. Heaney, "vitamin D is the key that unlocks the DNA library." He then reviewed toxicity and concluded there is no evidence that it occurs at levels below 200 ng/ml or with intakes (total) below 30,000 IU per day. Of course, we have no reason to think anyone needs 30,000 IU per day or levels of 200 ng/ml, which would be irresponsible. But someone with a serious cancer should consider getting their level up to 70-90 ng/ml and that may take 10,000 IU per day or even more in some people. As a rule of thumb, 1,000 IU will raise 25(OH)D levels by about 10 ng/ml.

Then Professor Heaney addressed a public health question. How much would we have to give all Americans to get 98% of people above 32 ng/ml without causing toxicity in anybody? The answer: 2,000 IU per day. Of course 32 ng/ml is not adequate but it would be a great first step. Furthermore, of the people left out, a high percentage would be African Americans. In fact, Dr. Talwar recently reported that 40% of African American women fail to achieve a level of 30 ng/ml even after taking 2,000 IU/day for a year.

Talwar SA, Aloia JF, Pollack S, Yeh JK. Dose response to vitamin D supplementation among postmenopausal African American women. Am J Clin Nutr. 2007 Dec;86(6):1657-62.

He also discussed his recent study giving healthy adults 100,000 IU as a single dose. If you start with a baseline level of 28 ng/ml and take 100,000 IU as a single dose, mean levels will remain above 32 ng/ml for two months. If you rely on such stoss doses, but you start with a lower level, or want your levels above 50 ng/ml, how often do you need to take 100,000 IU? We don't know the answer to the last question but we know that Grey et al gave 50,000 IU per week for four weeks then 50,000 per month for a year to 21 patients with hyperparathyroidism. Blood levels rose from a mean of 11 ng/ml at baseline to 30 ng/ml at one year and levels did not continue to rise after six months. Remember, that means half the patients had levels lower than 30 ng/ml at the end of the year. Also remember that the metabolic clearance (how quickly you use it up) might be higher in certain disease states.

Grey A, et al. Vitamin D repletion in patients with primary hyperparathyroidism and coexistent vitamin D insufficiency. J Clin Endocrinol Metab. 2005 Apr;90(4):2122-6.

That last point, metabolic clearance, is only one of a number of reasons that patients vary in their response to vitamin D. Remember, a surprising number of patients will tell their physician they are taking vitamin D when they are not, some will be taking preparations that have less in it than the label says, some will not absorb it, and some people weigh more than others. As Dr. Heaney points out, even if you know patients took 100,000 IU, great variably exists in individual response. At the end of two months some will have shown a minimal response and other much more. This is a field where little is known. Do different disease states use up vitamin D quickly? The answer is probably yes. Furthermore, variability also exists in how one metabolizes and catabolizes (breaks down) vitamin D. Also, what is the interactive effect of drugs that use the same liver enzymes for catabolism? We just don't know and that is why vitamin D blood testing is crucial. Remember, the only test to have is a 25-hydroxy-vitamin D. Do not let anyone get a 1,25-dihydroxy-vitamin D; it will not tell you if you are vitamin D deficient and is usually only indicated in evaluating high blood calcium.

As far as 25(OH)D levels go, many of you have written complaining about the high cost of a 25(OH)D levels at some labs. I've got some good news. For the next month, Life Extension Foundation is having a sale on their 25(OH)D blood tests, only $32.25, including the fee for drawing the blood. (No, we don't get funding from Life Extension, I wish we did.) Life Extension uses LabCorp, which, in turn, uses an accurate method to determine 25(OH)D levels, the DiaSorin Laiason method. The only problem is that DiaSorin, LabCorp, and Life Extension all say that 30 ng/ml is acceptable. It is not. Take enough vitamin D or get enough UVB radiation to get your levels above 50 ng/ml. To order the test, call Life Extension at 800 208-3444. Unfortunately, this offer is not available in New York, New Jersey or Rhode Island.

Also, Dr. James Dowd has written a fine book about vitamin D, The Vitamin D Cure. Get this, he is board certified in internal medicine, adult rheumatology, and pediatric rheumatology, an associate professor at Michigan State University, and runs his own Arthritis Institute and the Michigan Arthritis Research Center. He gives a formula for how much vitamin D you need but stresses the importance of testing to know for sure. He uses the formula of 2000 IU for every 100 pounds of body weight, which is as accurate an estimation as one can make without knowing baseline levels. Of course it depends on so many things, as Dr. Dowd points out, such as percentage body fat, latitude, skin type, sun exposure and age. He gives case after case examples of how vitamin D not just prevents disease, but seems to have a treatment effect. He also stresses three other things I've written about before, acid base balance, magnesium and potassium. If you can't get eat enough fruits and green leafy vegetables to obtain your potassium and magnesium and to get rid of low-grade chronic metabolic acidosis, then you should consider magnesium supplements and potassium bicarbonate supplements.

With these four experts and with this month's vitamin D news articles about breast cancer, brain function, artery blockage in the legs, soft skulls in babies, peripheral neuropathy in diabetics, childhood type-1 diabetes, colon cancer, and stress fractures and with the increasing number of scientists around the world jumping on the vitamin D express, why doesn't the government do something? What will it take? Like Carole says it will take a grassroots effort.

The first thing to do is tell your family and friends about vitamin D. Tell your doctor. Get your family's 25(OH)D tested, including your children. Once people begin to see it works, they will get their family and friends to take it. They will feel better and then the word will spread. All the government can do is make vitamin D illegal or limit the amount in each pill. The first is unlikely but not the second. With 5,000 IU capsules widely available, many people give no thought to taking one a day. But if the government limits the sale of anything over 400 IU and people had to take 12 of the 400 IU tablets, instead of one of the 5,000 IU, they might balk at so many pills. Before our officials in Washington take such a step, let's hope they read the Washington Post.

John Cannell, MD
The Vitamin D Council

This is a periodic newsletter from the Vitamin D Council, a non-profit trying to end the epidemic of vitamin D deficiency. This newsletter is not copyrighted. Please reproduce it and post it on Internet sites. We are a nonprofit tax-exempt educational organization and depend on your donations.

The Vitamin D Council
9100 San Gregorio road
Atascadero, CA 93422

Judging by the conversations here, in the Track Your Plaque Forums, and elsewhere, it's clear that many people are searching for the perfect diet.

Should we reconsider the role of saturated fat? Are there fractions of fatty acids in saturated fat that are more or less harmful? How about the role of fats on cancer risk? How about the role of proteins like casein on cancer risk? Are there flavonoid sources, or combinations of flavonoids, that yield outsized health benefits? Is there a ceiling for omega-3 fatty acid supplementation? Is there a role for linolenic acid sources in cardiovascular disease prevention? And on and on.

All important issues, to be sure, ones that we've all zig-zagged through over the past 30 years.

I also see patients every day, however, who are not interested in micro-managing their diet. Their goals are less ambitious: lose 20 lbs, feel good, raise HDL, reduce triglycerides and small LDL, all while meeting all the other responsibilities in their lives, like children, spouses, maintaining a household and jobs.

So, if your interest is not to consider whether we should distinguish myristic acid sources from palmitic, or if epigallocatechin is better when combined with quercetin, then the biggest bang from your nutritional buck can come from one single strategy:

Eliminate wheat flour products

Secondarily, avoiding corn starch products and "goodies" (candy, fruit juices, fruit drinks, cookies, potato chips, etc.--you know what they are) is important, as well.

It means weighing your diet more heavily in favor of vegetables and fruits; lean meats; healthy oils; and raw nuts and seeds, all in unlimited quantities. Dairy products should be limited, however, because of sugar effects.

Of course, this advice clearly contradicts the pronouncements of the USDA Food Pyramid (6-8 servings of grains per day), the American Heart Association, and the diabetes-causing American Diabetes Association diabetic diets.

But, follow this approach, a diet strategy that appears too simple to be effective, and the majority of people lose dramatic amounts of weight, raise HDL, reduce triglycerides, reduce small LDL, reduce C-reactive protein and other inflammatory measures, reduce blood pressure, and raise self-esteem.

It's also a lot easier than it sounds (after habits are broken) because the appetite stimulating effect of wheat is removed. Many, if not most, people also experience increased energy, including elimination of the afternoon "slump," improved sleep, less mood swings, less intestinal problems.

It may not be perfect, but if your interest is to get the most with a modest amount of effort, it works like a charm for the majority of people.

Copyright 2008 William Davis, MD

You're going to hate this.

Dr. Romero-Corral and colleagues from the Mayo Clinic presented an analysis of the National Institutes of Health-funded National Health and Nutrition Examination Survey (NHANES-3) at the recent American College of Cardiology meetings. (Science Daily also has some coverage on this report.)

Their analysis identified 2127 adults from the NHANES database who had normal body-mass indexes (BMI) between 18.5 and 24.9 units), average age 41 years old. When broken down by percent body fat (measured with bioimpedance, meaning a small electrical current is passed through the body, much like what the store-bought Tanita devices do), with normal-weight obesity defined as >20% body fat in males, >30% body fat in females, 55% of participants met criteria for designation as normal-weight obesity.

Compared to people with similar BMI's but who fell below these body fat percentage cut-offs, the normal-weight obese men had increased ratios of Apo B to Apo A1; were much more likely to have increased blood sugars or be diabetic; have higher C-reactive protein (CRP); were several-fold more likely to meet other criteria for diagnosis of metabolic syndrome; had lower HDL cholesterols; and had higher blood pressure. Women with normal-weight obesity were four-fold more likely to have coronary disease.

While preliminary, this suggests that a substantial number of people with apparently favorable body weights and BMIs are, in actuality, overweight when judged by metabolic parameters. This then probably leads to increased risk for heart disease. We can then fairly readily extrapolate the argument that a reduction in weight to even lower BMIs likely reduces or corrects these patterns.

This argument is similar to that proposed by several others, arguing that BMI is a flawed measure, since it does not incorporate muscle mass or skeletal factors ("big- or small-boned"). Instead, they have argued that waist circumference is preferable.

The normal-weight obesity syndrome was originally identified by Dr. Antonio de Lorenzo and colleagues at the University of Tor Vergata, Rome, Italy, and reported in Normal weight obese (NWO) women: an evaluation of a candidate new syndrome. Their studies of women with this "syndrome" have suggested that heightened measures of inflammation are present despite apparently normal body weight and BMIs. One such report, Normal-weight obese syndrome: early inflammation?, is available in full-text.

Is there a lesson to be learned for the Track Your Plaque program? I believe there is. I believe it means that, if you have any weight-sensitive parameter, such as low HDL, small LDL, high triglycerides, high CRP, high blood sugar, high blood pressure, etc., then further weight loss might be considered, even if BMI is around 25. Obviously, there is a rational limit to how far you can push this concept. (Anorexia is not good for you either.)

I find this a useful concept. It provides yet another potential strategy to pursue when the above patterns are encountered. Perhaps it's also a way to cap reliance on niacin, whose effects closely mimic that of weight loss.

Now that's a lot more preferable to more and more statin drug, isn't it?

Copyright 2008 William Davis, MD

Since vitamin D has been the topic of a fair amount of media coverage, I've received many questions about this fascinating "nutrient." A day doesn't go by without several nurses, friends, even fellow physicians stopping me to ask about vitamin D.

When I inform them that the average dose for females in this region (upper Midwest) is 4000-5000 units per day, 5000-6000 units per day for males, they are all surprised. "Then why did they say just take your multivitamin every day, or just drink your milk on the news?"

Many people are even more surprised, sometimes completely turned off, when they hear that, to be truly confident of adequate vitamin D dosing, a blood level of 25(OH) vitamin D3 needs to be checked. Now we're talking real hassle!

But there is no other way to do it. In order to obtain the full potential benefits of vitamin D, such as reduction in blood sugar and sensitization to insulin, reduction in cancer risk (especially prostate, colon, and breast), reductions in blood pressure, increased bone density, not to mention markedly increasing the likelihood of stopping or reducing your heart scan score, then achieving a desirable blood level of 25(OH) vitamin D is necessary.

Checking a blood level of vitamin D is no more difficult than having a cholesterol test, unless, of course, your doctor balks at the idea. (Time for a new doctor if that occurs.)

All too often, someone will be convinced they are taking a sufficient dose of vitamin D of, say 2000 units per day, only to discover that their blood level of 25(OH) vitamin D is something like 17 ng/ml--severe deficiency, sufficient to leave them exposed to all the undesirable consequences of vitamin D deficiency. Even though 2000 units per day represents 500% of the Institute of Medicine's recommended Adequate Intake for adults, to those familiar with the Track Your Plaque program it likely sounds like a child's dose.

Many variables enter into the equation in your body that determines your need for vitamin D: body size (heavier or larger people need more, with obese people often requiring enormous doses); sex (men need more than women); age (aging results in dramatic loss of ability to activate vitamin D in the skin); race; skin color (darker skinned people require more). Trying to guess your need is a fool's game. It's also a game that can seriously compromise your health and your hopes of ever stopping or reducing your heart scan score.

The message is clear: You cannot guess what your vitamin D need is. You cannot properly judge your vitamin D requirement by your age, body size, sex, or any other characteristic. Having a tan or a lack of a tan is a lousy indicator, as well. A simple blood level of 25(OH) vitamin D is an absolute necessity to gauge your vitamin D status, both before starting and while on your supplement.

Members of Track Your Plaque: Watch for the 30-some page booklet, The Track Your Plaque Complete Handbook on Vitamin D and Heart Health, which will be released in the next day or two.

Copyright 2008 William Davis, MD

According to the poll just completed by 80 participants on The Heart Scan Blog, 50% of respondents said they were less likely to take a drug after viewing an advertisement for it. A whopping 3 (4%) said that they would be more likely to take the drug after viewing an advertisement.

I find that interesting. If half the people responding are less likely to become customers of a drug company, then how does the drug industry justify running around-the-clock, every-few-minute ads? Spending by the drug industry for direct-to-consumer (DTC) advertising has ballooned over the past few years, and is now well over $30 billion dollars per year.

Unfortunately, despite the views of the highly-educated, curious, think-for-yourself, health information-seeking sorts of people who read this blog, drug companies still come out on top by DTC advertising. Estimates vary, with a 2006 U.S. Government Accountability Office study reporting that, for every $1 DTC advertising, sales are increased by $2.20. A 2000 Harvard study showed a higher return of $4.40 for every advertising dollar spent.

I'm sure the drug companies themselves have a very tight accounting handle on their own set of figures. We may not be terribly fond of these people and their often suspect tactics, but they're not stupid. They are certainly not stupid when it comes to making money.

Interestingly, 80% of the funds spent on DTC advertising focus on the 20 or so most popular drugs, all of which are used for treatment of chronic conditions like high cholesterol and high blood pressure, markets that are large and long-term. It pays very little to advertise drugs that may serve small markets for a short period. The implicit message is that this is not at all about informing the public. It is about advertising to grow revenues and profits--pure and simple.

It makes me wonder what the results of our poll would have been had we conducted it in 2000 before many people hadn't yet been brought to the brink of vomiting from the endless onslaught of commercial after commercial, complete with smarmy spokespeople (a la Lipitor's Dr. Robert Jarvik). What will it show in two years? Will the broader public join the more informed people who read this blog and become increasingly inured to the hard sell tactics?

For further discussion of this topic, click here for a reprint of an August, 2007 New England Journal of Medicine study, A Decade of Direct-to-Consumer Advertising of Prescription Drugs provides background, along with commentary on the impact of DTC drug marketing since the FDA allowed it 10 years ago. (Because it is a study and not an editorial, the editors fall short of making any recommendations for improvement or calling for a moratorium.)

Copyright 2008 William Davis, MD

Anna responded to the Heart Scan Blog post, Can you say "sugar"? with the following wonderfully telling comment:

A measured bowl of Cheerios and a bit of milk (whole, because it's what I had), equal to 75 grams of carbohydrate, gave me the highest ever blood glucose reading from a food (not counting glucose solution from a Glucose Tolerance Test). I was attempting a "homemade" version of a 3 hr GTT before going to my doctor with my concerns about my BG.

My BG started to rise very fast within 15 minutes after eating the cereal, peaked at about 250 mg/dL at 45 minutes, then slowly dropped. By about 60-75 minutes, I experienced strong hunger and carb cravings as the BG began to slowly drop, and by about 2.5 hours after eating, my BG had suddenly dropped quite low (in the low 70s) and I had developed a nasty hypoglycemic feeling (shaky, irritable, craving sugary foods, headache, etc.).

It's hard for me to see "heart healthy" Cheerios (or any other highly processed breakfast cereal) as anything other than a bowl of pre-digested sugar that contributes to roller coaster blood glucose and insulin levels, which a great way to start anyone's day. Certainly, I don't do well with Cheerios because I clearly have a damaged glucose regulatory system (probably a diminished or absent first phase insulin response, but I can't imagine that it is doing any good for people with healthy glucose regulation, either.

I banned prepared cold cereals from our house. If my 9 yr old son gets cereal at all at home, it's whole groats (not even rolled or steel cut because those aren't truly "whole grain" anymore), soaked overnight in some water and a tsp of plain yogurt (soaking neutralizes phytates and reduces cooking time), then cooked about 8-10 minutes (water added as necessary). Sometimes I add a bit of quinoa or almond meal prior to soaking to boost the protein content a bit. I garnish with a pat of butter, some heavy cream, and a dusting of cinnamon. If I'm feeling *really* indulgent, I drizzle about 1 tsp of Grade B maple syrup on top (Grade B is stronger in flavor and so less can be used). I don't eat this cereal myself, and truthfully, I'd rather my son not, either, but he sometimes wants cereal. It's the least damaging compromise I can come up with that we can both live with.

I have also seen diabetic effects from Cheerios: rises in blood sugar, exagerration of small LDL, drops in HDL, rises in triglycerides. Yes, it may reduce LDL a small quantity, but so what?

The Cheerios "heart healthy" claim is based on a piece of research apparently performed by Dr. Donald Hunninghake at the University of Minnesota and reported in 1998:

A study conducted at the University of Minnesota Heart Disease Prevention Clinic and published as "Cholesterol-Lowering Benefits of a Whole Grain Oat Ready-to-Eat Cereal" in the May issue of the Nutrition in Clinical Care journal in 1998, showed that people can lower their blood cholesterol by an average of 3.8% over six weeks by enjoying 3 cups of cold cereal made with 100% whole grain oats everyday as part of the meals and snacks in a healthy lower-fat diet.

(Unfortunately, I could not locate the actual publication. It doesn't mean it doesn't exist; I just couldn't locate it. Perhaps it's in a small journal not entered into the online publication database.)

The purported effects of Cheerios should not be confused with that of actual, intact oat bran, as suggested by studies such as those of Brenda Davy et al, High-fiber oat cereal compared with wheat cereal consumption favorably alters LDL-cholesterol subclass and particle numbers in middle-aged and older men, in which significant reductions in LDL particle number and small LDL (NMR) were obtained. (This study was also supported by Quaker Oats.) Several studies have shown that oat bran does indeed reduce LDL cholesterol, sometimes as much as 30-50 mg/dl. Cheerios can not even come close to this.

If Cheerios were nothing more than finely pulverized oats, then perhaps it wouldn't be so bad. But add corn starch and sugar, and you have ingredients that have potential to distort LDL particle size and yield blood sugar-escalating effects like those described by Anna.

The gravity of perpetuating these myths is brought home by a testimonial posted on the website for Cheerios:

“I had unexpected open heart surgery a year ago. As I adopted heart health habits during my recovery, I realized that I should have been eating the Cheerios cereal I carried around in a plastic baggie so many years for my kids!”

Beverly
Scotch Plains, NJ

It makes me shudder.

Copyright 2008 William Davis, MD

There's a wonderful blog called The IF Life: Intermittent Fasting and Instant Freedom. It is written by personal trainer (and apparently former corporate bigshot), Mike O'Donnell.

Mike has a great take on brief, intermittent fasting that I found helpful and I believe you will also.

Intermitent Fasting 101: How to Start, Part I

The biggest question people have is how to effectively use IF (intermittent fasting) to achieve their goals and maximum results. These results and goals can vary by each person with fat loss, muscle gain, better health, improved performance in your sport of choice and more. With that comes the individuality of what is a person’s insulin resistance, current body composition (bodyfat%), daily lifestyle, eating habits, macronutrient ratios (carbs/protein/fat), type of exercise program, frequency and volume of training, recovery demands, and so forth. You are unlikely to find 2 people with the same set of parameters and same exact responses to an IF protocol. What does this mean? Well just that we need to start with a basic IF program, and then learn how to monitor results and adjust as we go. Even down the road things will change as you will improve health, lower insulin resistance and maybe change performance and recovery needs. So nothing is ever just one set way. Life is dynamic (always changing and evolving) and so should be the way we see our own journey for health and fitness.

What is IF?

For those that may not be familiar to the term, intermittent fasting is just taking times of fast (no food) and working them into your lifestyle. This can be either daily or a couple times a week (will get into that more below). Benefits include improving insulin resistance (which you will hear alot about as being the #1 key marker in so many health factors including weight loss, muscle gain, performance, recovery, anti-ageing and disease prevention) and giving the body a chance to do some internal cleaning (or housework), which can lead to improved immune function and overall health. If you want to see studies of all the benefits of IF/CR, please the resources page.

How do I begin to IF?

Is there only one set way in which to do IF? No. I could easily come up with 10 different IF protocols based on 10 people’s individual’s needs, lifestyle, exercise, goal, macronutrient ratios, and so forth. We will keep it simple and give the 2 most frequent and basic options.

Daily Fasting: Typically done every day and only giving the person a smaller eating window in which to get their calories. (for example, a 18hr daily fast would mean someone would only eat every day between the hours of Noon and 6pm). You will see varying times from 15-19 hours for daily fasting.
Fasting 1-3x a week: This could also be called alternate day fasting/calorie restriction (for those doing it every other day). This is just fasting of usually longer periods 18-24 hours but only 1-3x a week. Many variations to play with here.
“But which one is better and how to I do it now if I want…….”. Whoa, slow down. I know many have questions but let’s still try to keep this simple for now and expand into more specifics later. So far many people have experimented with both types of IF and have seen great results. But you also have to take into account all the other variables such as what is the person eating in that window? Is is junk food? Is it low carb? How many times a week are they doing it? Are they overweight and wanting just fat loss? Are they lower bodyfat but looking for improved performance and health? How many times a week are they exercising? What kind are they doing and what intensity? The list can go on and on, but let’s start to analyze the 2 types of IF and let you decide which one best suits your lifestyle.

Daily Fasting (15-19 hours):

The Advantages are:

--simple eating strategies for every day
--even people that may not eat 100% clean foods can see weight loss due to the smaller window and lower calorie total per day

The Disadvantages are:

--Can possibly lower metabolism if calories are too low for too long (not what you want if your #1 goal is weight loss)
--Not getting enough food in the smaller window may also lead to muscle loss for more active people (not good)
Fasting 1-3x a week:

The advantages are:

--Allows a person to make sure they are getting enough calories on the non-fasting days, and then just keeps to a simple small feed window (if any) on the IF days.
--Simple thinking for people who do not have experience in how to eat clean to eat one day, and then eat in a smaller window the following day (alternate day fasting/CR). This can achieve fat loss for people who are mostly overweight and may not be too active. (of course don’t get me wrong, that eating healthy is our main goal but this can be a good step for some people to start their weight loss jounrey and learn how to make better choices as they go)

Disadvantages:

--Doesn’t force a person to make better choices with their food (as one could probably eat junk one day, and then fast the next and still lose weight). Not something we want long term because this is not going to improve your other health markers (diseases prevention, insulin resistance) like a good IF program on healthy foods.

Again I can’t say it enough, as there are so many variables to play with in an IF program. Some people may say “well it didn’t work for me” or “I didn’t gain any muscle”. Well unless I know everything about what you do for exercise daily, your total calories, when you eat and your macronutrient ratios (protein/carbs/fats), I can’t even begin to help. IF is a simple tool to start with, but you have to take full responsibility for your own health and progress and learn when it is not working and when to change things up! Like I said, if it is NOT working then stop IF and rethink your attack plan (or get a professional to coach you on it).

So to sum up, here are some examples of what you can play with:

Daily Fasting of 15-19 hours. I would highly suggest that if you do this make sure you are recovering from your exercise and start only Mon-Fri and give yourself the weekends to eat all day (hopefully with healthy choices of course)

Fast 1-2x a week to start if you have never done any fasting or do not know how to eat healthy and control your macronutrients. Start with 1-2 days a week with fasts of 18-20 hours (I wouldn’t start with 24 hr fasts to begin as most people can not handle the hunger cravings and in turn will just end up eating all the wrong foods when they do eat) and say eat only from say 1pm-6pm for example. Drink lots of water (add lemon, your liver will appreciate it! and it will help with the hunger). For example, fast Wed and Sun (or whatever days fit into your schedule)

Or you can do a mixed approach and fast every other day for a small eating window. For example eat all day Mon, only 12-6pm on Tues, all day Wed, 12-6pm on Thurs, etc. Start with bigger eating windows and make them smaller as you get used to fasting. This approach may work for people who have alot of weight to lose and can not (I should really say “will not” as everything is a choice!) eat 100% healthy for the moment. This approach may not work for more advanced people who have a high activity level unless you are getting a ton of health calories in that fasting window.
“So What Do I Eat on the Fasting Days?”

That’s the best part, you should be able to eat unlimited healthy foods (healthy proteins, fats, veggies, fruit, nuts…see Paleo Diet in the resources page). If you are eating more processed foods, breads and other high calorie intakes then you may have to monitor and control portions. Please know this is NOT about chronic calorie restriction or starving yourself. When I do weeks of eating 1-7pm, I am eating a ton of protein and veggies (complex carbs pwo also). I am hardly starving myself. I am not taking in 4000 cal a day however, so my daily average of say 2200-2500 cal is still low compared to the alternative. If you want to lose weight of course you will need a calorie deficit to pull the “stored energy” out of fat cells. That is the advantage to eating “Paleo”, you can’t over eat on protein, healthy fats, fruits (in moderation) and veggies. If you are making bad choices or starving yourself on IF, you may lose the effectiveness or slow progress. All goes back to the fact that if it is not working, then change something up! (there is always something that can be changed…and food choices is the #1 place to start!) I don’t count calories, and by eating natural foods that have been around for 100s of years….I don’t need to! (eating healthy natural foods will not only help you lose weight but also improve your health and lower your risks of diseases….so eating for health should always be the #1 goal in any program)

Hopefully this will give a good overview while trying to keep it simple. Remember it’s your journey to take, measure progress and adjust things that are not working. Start with one approach, and modify it. Who knows, your approach may change every couple months and that is ok. Life is always changing and so should your approach to health and fitness (as the body always responds better to change than sticking with the same eating/exercise approach for a long period of time).

All of these products bear the American Heart Association Check Mark of approval emblem, signifying that they are "heart healthy":

Kellogg's Frosted Mini-Wheats cereal

Ingredients:WHOLE GRAIN WHEAT, SUGAR, STRAWBERRY FLAVORED CRUNCHLETS (SUGAR, CORN CEREAL, CORN SYRUP, MODIFIED CORN STARCH, PARTIALLY HYDROGENATED COTTONSEED AND/OR SOYBEAN OIL, CITRIC ACID, GLYCERIN, NATURAL AND ARTIFICIAL FLAVOR, RED #40, BLUE #2), NATURAL AND ARTIFICIAL STRAWBERRY AND CREME FLAVOR, SORBITOL, GELATIN, REDUCED IRON, NIACINAMIDE, ZINC OXIDE, RED #40, PYRIDOXINE HYDROCHLORIDE (VITAMIN B6), RIBOFLAVIN (VITAMIN B2), THIAMIN HYDROCHLORIDE (VITAMIN B1), FOLIC ACID, BLUE #1, AND VITAMIN B12. TO MAINTAIN QUALITY, BHT HAS BEEN ADDED TO THE PACKAGING.

Orville Redenbacher popcorns

Dora the Explorer Cereal

Cheerios

The following requirements must be met to gain approval of the Check Mark program:

1) total fat 3.0 grams or less per serving

2) saturated fat 1.0 gram or less per serving

3) 20 grams or less cholesterol per serving

4) 480 mg or less sodium per serving

5) "Jelly Bean Rule": 10% of the Daily Value of 6 nutrients (e.g., fiber, vitamins A and C, etc.) must also be contained in each serving.

Had the Check Mark program focused on genuine nutrition and rated products by:

1) Healthy oil content

2) Sugar content or sugar-equivalents, i.e., glycemic index or load

3) Impact on HDL, small LDL, triglycerides

none of these products would have made the list, not even close.

Gilbert is a 58-year old high school science teacher.

When I first met Gil, he'd been having bouts of atrial fibrillation and had required various medications to suppress recurrences of the rhythm. However, because his rhythm proved somewhat difficult to control, his electrophysiologist (heart rhythm specialist) prescribed warfarin to reduce the risk of stroke. With atrial fibrillation, because of blood stagnation (in the left atrial appendage) in the heart, there is a stroke risk of approximately 8% per year. Warfarin reduces this risk substantially, to about 2%.

I met Gil because he had a cholesterol disorder. In my practice, the first step in gauging the implications of a lipid or lipoprotein disorder is to obtain a heart scan. If the heart scan score is zero, great. It means that we have plenty of time to treat the disorder since risk for cardiovascular events is near zero also; it means less intensive efforts less intensive efforts are necessary. But if the heart scan score is, say, 1200, then an aggressive approach in short order is required, since the risk for heart attack may as high as 20-25% per year, even in the absence of symptoms.

Gil's heart scan score: 787--high and posing a risk for heart attack of about 5-10% per year without preventive efforts. Gil did indeed prove to have a complex lipoprotein disorder, as well as high blood pressure, vitamin D deficiency, and several other potential contributors to coronary plaque.

Gil did just about everything right: He exercised, followed the recommended diet, achieved better than the Track Your Plaque 60-60-60, lost 18 lbs of abdominal fat.

Gil's rhythm stabilized for several months, only to have atrial fibrillation break through again. So Gil's electrophysiologist re-prescribed warfarin.

18 months later, Gil's 2nd heart scan score: 1410--a near doubling. Unsettling to Gil and to us, to say the least.

How can this happen in the face of perfect lipids/lipoproteins, correction of hidden causes like lipoprotein(a) and inflammation, along with a vigorous lifestyle effort?

I fear that the culprit might be warfarin.

Warfarin, better known by its brand name, Coumadin, may have some effects that intersect with the Track Your Plaque mission of reducing coronary plaque.

It is no secret that, beyond the obvious risk of bleeding from blood thinning, warfarin also may:

--Accelerate aortic valve calcification
--Accelerate calcification of the framework of the mitral valve (the mitral "anulus")
--Accelerate osteoporosis
--Induce an artificial situation of vitamins K1 and K2 deficiency.

The vitamin K1 deficiency is the route by which blood thinning is achieved. However, the K2 deficiency may have undesirable consequences, among which are the above list of various pathologic calcifications.

I therefore wonder if warfarin dramatically accelerated the coronary calcium that we track to gauge the progression of coronary atherosclerosis. One experience is hardly sufficient reason to sound the alarm. It is also difficult to pinpoint the cause of the explosive growth in Gil's coronary calcium specifically on warfarin.

That all said, I am quite certain it was the warfarin.

Unfortunately, some people are unavoidably committed to warfarin, such as those with specific genetic blood clotting disorders, prosthetic valves, prior deep vein thromboses and pulmonary emboli, etc.--serious reasons. Until an alternative emerges, warfarin remains a necessity for some people. (No, nattokinase is NOT an alternative, at least not one that would permit survival.)

My personal policy is that warfarin be used only when absolutely necessary and the gains markedly outweight the risks--including that of possible accelerated calcification of multiple sites.

Whether we will be able to get Gil off warfarin and potentially gain control over his coronary disease/plaque/calcium remains to be seen. I sure hope so.

Caraballo PJ, Heit JA, Atkinson EJ et al. Long-term use of oral anticoagulants and the risk of fracture. Arch Intern Med 1999; 159 (15): 1750–6. PMID 10448778.

Pilon D, Castilloux AM, Dorais M, LeLorier J. Oral anticoagulants and the risk of osteoporotic fractures among elderly. Pharmacoepidemiol Drug Saf 2004;13(5): 289–294.PMID 15133779.

Gage BF, Birman-Deych E, Radford MJ, Nilasena DS, Binder EF. Risk of osteoporotic fracture in elderly patients taking warfarin: results from the National Registry of Atrial Fibrillation 2. Arch Intern Med 2004; 166(2):241–246.PMID 16432096.

Copyright 2008 William Davis, MD

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