Are endogenous nutritional supplements better?

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.

Vitamin D Newsletter reprinted

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

Biggest bang for your nutritional buck

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

Can skinny be fat?

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

Fatal underdose

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

Is direct-to-consumer drug marketing a failure?

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

Cheerios and heart health



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

The IF Life: Intermittent fasting

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).

Can you say "sugar"?

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.

Warfarin is scary stuff

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
Cureality | Real People Seeking Real Cures

Rerun: To let low-carb right, you must check POSTPRANDIAL blood sugars

Checking postprandial (after-eating) blood sugars yields extraordinary advantage in creating better diets for many people.

This idea has proven so powerful that I am running a previous Heart Scan Blog post on this practice to bring any newcomers up-to-date on this powerful way to improve diet, lose weight, reduce small LDL, reduce triglycerides, and reduce blood pressure.



To get low-carb right, you need to check blood sugars

Reducing your carbohydrate exposure, particularly to wheat, cornstarch, and sucrose (table sugar), helps with weight loss; reduction of triglycerides, small LDL, and c-reactive protein; increases HDL; reduces blood pressure. There should be no remaining doubt on these effects.

However, I am going to propose that you cannot truly get your low-carb diet right without checking blood sugars. Let me explain.

Carbohydrates are the dominant driver of blood sugar (glucose) after eating. But it's clear that we also obtain some wonderfully healthy nutrients from carbohydrate sources: Think anthocyanins from blueberries and pomegranates, vitamin C from citrus, and soluble fiber from beans. There are many good things in carbohydrate foods.

How do we weigh the need to reduce carbohydrates with their benefits?

Blood sugar after eating ("postprandial") is the best index of carbohydrate metabolism we have (not fasting blood sugar). It also provides an indirect gauge of small LDL. Checking your blood sugar (glucose) has become an easy and relatively inexpensive tool that just about anybody can incorporate into health habits. More often than not, it can also provide you with some unexpected insights about your response to diet.

If you’re not a diabetic, why bother checking blood sugar? New studies have documented the increased likelihood of cardiovascular events with increased postprandial blood sugars well below the ranges regarded as diabetic. A blood sugar level of 140 mg/dl after a meal carries 30-60% increased (relative) risk for heart attack and other events. The increase in risk begins at even lower levels, perhaps 110 mg/dl or lower after-eating.

We use a one-hour after eating blood sugar to gauge the effects of a meal. If, for instance, your dinner of baked chicken, asparagus brushed with olive oil, sauteed mushrooms, mashed potatoes, and a piece of Italian bread yields a one-hour blood sugar of 155 mg/dl, you know that something is wrong. (This is far more common than most people think.)

Doing this myself, I have been shocked at the times I've had an unexpectedly high blood sugar from seemingly "safe' foods, or when a store- or restaurant-bought meal had some concealed source of sugar or carbohydrate. (I recently had a restaurant meal of a turkey burger with cheese, mixed salad with balsamic vinegar dressing, along with a few bites of my wife's veggie omelet. Blood sugar one hour later: 127 mg/dl. I believe sugar added to the salad dressing was the culprit.)

You can now purchase your own blood glucose monitor at stores like Walmart and Walgreens for $10-20. You will also need to purchase the fingerstick lancets and test strips; the test strips are the most costly part of the picture, usually running $0.50 to $1.00 per test strip. But since people without diabetes check their blood sugar only occasionally, the cost of the test strips is, over time, modest. I've had several devices over the years, but my current favorite for ease-of-use is the LifeScan OneTouch UltraMini that cost me $18.99 at Walgreens.

Checking after-meal blood sugars is, in my view, a powerful means of managing diet when reducing carbohydrate exposure is your goal. It provides immediate feedback on the carbohydrate aspect of your diet, allowing you to adjust and tweak carbohydrate intake to your individual metabolism.

LDL glycation

The proteins of the body are subject to the process of glycation, modification of protein structures by glucose (blood sugar). In the last Heart Scan Blog post, I discussed how glycated hemoglobin, available as a common test called HbA1c, can serve as a reflection of protein glycation (though it does not indicate actual Advanced Glycation End-products, or AGEs, just a surrogate indicator).

There is one very important protein that is subject to glycation: Apoprotein B.

Apoprotein B, or Apo B, is the principal protein of VLDL and LDL particles. Because there is one Apo B molecule per VLDL or LDL particle, Apo B can serve as a virtual VLDL/LDL particle count. The higher the Apo B, the greater the number of VLDL and LDL particles.

Because Apo B is a protein, it too is subject to the process of glycation. The interesting thing about the glycation of Apo B is that its "glycatability" depends on LDL particle size: The smaller the LDL particle, the more glycation-prone the Apo B contained within.

Younis et al have documented an extraordinary variation in glycatability between large and small LDL, with small LDL showing an 8-fold increased potential.

Think about it: Carbohydrates in the diet, such as wheat products and sugars, trigger formation of small LDL particles. Small LDL particles are then more glycation-prone by up to a factor of 8. Interestingly, HbA1c is tightly correlated with glycation of Apo B. Diabetics with high HbA1c, in particular, have the greatest quantity of glycated Apo B. They are also the group most likely to develop coronary atherosclerosis, as well as other consequences of excessive AGEs.

No matter how you spin it, the story of carbohydrates is getting uglier and uglier. Carbohydrates, such as those in your whole grain bagel, drive small LDL up, while making them prone to a glycating process that makes them more likely to contribute to formation of coronary atherosclerotic plaque.

High HbA1c: You're getting older . . . faster

Over the years, we all accumulate Advanced Glycation End-products, or AGEs.

AGEs are part of aging; they are part of human disease. AGEs are the result of modification of proteins by glucose. AGEs form the basis for many disease conditions.

Accumulated AGEs have been associated with aging, dementia, cataracts, osteoporosis, deafness, cancer, and atherosclerosis. Most of the complications of diabetes have been attributable to AGEs.

There's one readily available method to assess your recent AGE status: HbA1c.

Hemoglobin is the oxygen-carrying protein of red blood cells. Like other proteins, hemoglobin becomes glycated in the presence of glucose. Hemoglobin glycation increases linearly with glucose: The higher the serum or tissue glucose level, the more glycation of hemoglobin develops. Glycated hemoglobin is available as the common test, HbA1c.

Ideal HbA1c is 4.5% or less, i.e., 4.5% of hemoglobin molecules are glycated. Diabetics typically have HbA1c 7.0% or greater, not uncommonly greater than 10%.

In other words, repetitive and sustained high blood glucose leads to greater hemoglobin glycation, higher HbA1c, and indicates greater glycation of proteins in nerve cells, the lens of your eye, proteins lining arteries, and apoprotein B in LDL cholesterol particles.

If AGEs accumulate as a sign of aging, and high blood sugars lead to greater degrees of glycation, it only follows that higher HbA1c marks a tendency for accelerated aging and disease.

Indeed, that is what plays out in real life. People with diabetes, for instance, have kidney failure, heart disease, stroke, cataracts, etc. at a much higher rate than people without diabetes. People with pre-diabetes likewise.

The higher your HbA1c, the greater the degree of glycation of other proteins beyond hemoglobin, the faster you are aging and subject to all the phenomena that accompany aging. So that blood glucose of 175 mg/dl you experience after oatmeal is not a good idea. 

The lesson: Keep HbA1c really low. First, slash carbohydrates, the only foods that substantially increase blood glucose. Second, maintain ideal weight, since normal insulin responsiveness requires normal body weight. Third, stay physically active, since exercise and physical activity exerts a powerful glucose-reducing effect. Fourth, consider use of glucose-reducing supplements, an issue for another day.

While HbA1c cannot indicate cumulative AGE status, it can reflect your recent (preceding 60 to 90 days) exposure to this age-accelerating thing called glucose.

If your doctor refuses to accommodate your request for a HbA1c test, you can perform your own fingerstick test.

Slash carbs . . . What happens?

Cut the carbohydrates in your diet and what sorts of results can you expect?

Carbohydrate reduction results in:

Reduced small LDL--This effect is profound. Carbohydrates increase small LDL; reduction of carbohydrates reduce small LDL. People are often confused by this because the effect will not be evident in the crude, calculated (Friedewald) LDL that your doctor provides.

Increased HDL--The HDL-increasing effect of carbohydrate reduction may require 1-2 years. In fact, in the first 2 months, HDL will drop, only to be followed by a slow, gradual increase. This is the reason why, in a number of low-carb diet studies, HDL was shown to be reduced.--Had the timeline been longer, HDL would show a significant increase.

Decreased triglycerides--Like reduction of small LDL, the effect is substantial. Triglyceride reductions of several hundred milligrams are not at all uncommon. In people with familial hypertriglyceridemia with triglyceride levels in the thousands of milligrams per deciliter, triglyceride levels will plummet with carbohydrate restriction. (Ironically, conventional treatment for familial hypertriglyceridemia is fat restriction, a practice that can reduce triglycerides modestly in these people, but not anywhere near as effectively as carbohydrate restriction.) Triglyceride reduction is crucial, because triglycerides are required by the process to make small LDL--less triglycerides, less small LDL.

Decreased inflammation--This will be reflected in the crude surface marker, c-reactive protein--Yes, the test that the drug industry has tried to convince you to take statins drugs to reduce. In my view, it is an absurd notion that you need to take a drug like Crestor to reduce risk associated with increased CRP. If you want to reduce CRP to the floor, eliminate wheat and other junk carbohydrates. (You should also add vitamin D, another potent CRP-reducing strategy.)

Reduced blood pressure--Like HDL, blood pressure will respond over an extended period of months to years, not days or weeks. The blood pressure reduction will be proportion to the amount of reduction in your "wheat belly."

Reduced blood sugar--Whether you watch fasting blood sugar, postprandial (after-meal) blood sugars, or HbA1c, you will witness dramatic reductions by eliminating or reducing the foods that generate the high blood sugar responses in the first place. Diabetics, in particular, will see the biggest reductions, despite the fact that the American Diabetes Association persists in advising diabetics to eat all the carbohydrates they want. Reductions in postprandial (after-eating) blood sugars, in particular, will reduce the process of LDL glycation, the modification of LDL particles by glucose that makes them more plaque-causing.


You may notice that the above list corresponds to the list of common plagues targeted by the pharmaceutical industry: blood pressure, diabetes (diabetes being the growth industry of the 21st century), high cholesterol. In other words, high-carbohydrate, low-fat foods from the food industry create the list of problems; the pharmaceutical industry steps in to treat the consequences.

In the Track Your Plaque approach, we focus specifically on elimination of wheat, cornstarch, and sugars, the most offensive among the carbohydrates. The need to avoid other carbohydrates, e.g., barley, oats, quinoa, spelt, etc., depends on individual carbohydrate sensitivty, though I tend to suggest minimal exposure.

Normal fasting glucose with high HbA1c

Jonathan's fasting glucose: 85 mg/dl
His HbA1c: 6.7%

Jonathan's high HbA1c reflects blood glucose fluctuations over the preceding 60-90 days and can be used to calculate an estimated average glucose (eAG) with the following equation:

eAG = 28.7 X A1c – 46.7

(For glucose in mmol/L, the equation is eAG = 1.59 × A1C - 2.59)

Jonathan's HbA1c therefore equates to an eAG of 145.59 mg/dl--yet his fasting glucose value is 85 mg/dl. 

This is a common situation: Normal fasting glucose, high HbA1c. It comes from high postprandial glucose values, high values after meals. 

It suggests that, despite having normal glucose while fasting, Jonathan experiences high postprandial glucose values after many or most of his meals. After a breakfast of oatmeal, for instance, he likely has a blood glucose of 150 mg/dl or greater. After breakfast cereal, blood glucose likely exceeds 180 mg/dl. With two slices of whole wheat bread, glucose likewise likely runs 150-180 mg/dl. 

The best measure of all is a postprandial glucose one hour after the completion of a meal, a measure you can easily obtain yourself with a home glucose meter. Second best: fasting glucose with HbA1c.

Gain control over this phenomenon and you 1) reduce fasting blood sugar, 2) reduce expression of small LDL particles, and 3) lose weight.  

Can you handle fat?

No question: Low-carbohydrate diets generate improved postprandial lipoprotein responses.

Here's a graph from one of Jeff Volek's great studies:



Participants followed a low-carb diet of less than 50 g per day carbohydrate ("ketogenic") with 61% fat.   The curves were generated by administering a 123 g fat challenge with triglyceride levels assessed postprandially. The solid line represents the postprandial response at the start; dotted line after the 6-week low-carb effort.

Note that:

1) The postprandial triglyceride (area-under-the-curve) response was reduced by 29% in the low-carb diet.  That's a good thing.

2) The large fat challenge generated high triglycerides of greater than 160 mg/dl even in the low-carb group. That's a bad thing. 

In other words, low-carb improves postprandial responses substantially--but postprandial phenomena still occur. Postprandial triglycerides of 88 mg/dl or greater are associated with greater heart attack risk because they signify the presence of greater quantities of atherogenic (plaque-causing) postprandial lipoproteins.

A full discussion of these phenomena can be found in the Track Your Plaque Special Report, Postprandial Responses: The Storm After the Quiet!, part of a 3-part series on postprandial phenomena.

Statin stupid

If we followed the lead of the pharmaceutical industry and my cardiology colleagues, we would all subscribe to the "statins for all" philosophy. There is now $2 billion of clinical "research" to back up this "evidence-based" practice.

I do not endorse this "statins for all" philosophy. I believe it is a product of the raw profiteering of the pharmaceutical industry, who are adept at recruiting physicians to their cause.

But lost in the confusion of tainted studies and over-the-top media saturation is the fact that there are small groups of people who likely do obtain benefit from statin drugs. They would certainly benefit from better informed scrutiny of their lipoprotein and metabolic abnormalities. But treatment may involve statins.

This is entirely distinct from the "statins for all" argument, the simpleminded rule that primary care physicians and cardiologist are told to follow.

Groups who may indeed benefit from statin therapy include:

Homozygous or heterozygous familial hypercholesterolemia--Lacking a receptor for LDL particles, LDL piles up to very high levels in these people. LDLs of 300+ are common and lead to heart disease and stroke at relatively young ages.

Combined mixed hyperlipidemia--Among the one or more genetic defects underlying this condition involves excessive production of apoprotein B and VLDL particles. This leads to high risk for heart disease.

People unable to follow a diet to correct their lipid disorder--I have 80+-year old patients, for instance, who say, "I've eaten this way for 82 years. I'm not going to change now!" In the absence of diet and other efforts (e.g., omega-3 fatty acids from fish oil), drugs may be the answer.

In other words, of the $27 billion annual bill for statin drugs, perhaps a tiny fraction is truly necessary. The majority of people taking statin drugs would not really need them if they had the real answers. But don't let that confuse us: There are some people who do indeed benefit.

Butter and insulin

In a previous post, Atkins Diet: Common Errors, I commented on butter's unusual ability to provoke insulin responses. I offer this as a possible reason why, after a period of effective weight loss on a low-carbohydrate program, inclusion of some foods, such as butter, will trigger weight gain or stall weight loss efforts.

This develops because of butter's insulin-triggering effect, doubling or tripling insulin responses (postprandial area-under-the-curve). If insulin is triggered, fat gain follows.

Here's one such study documenting this effect: Distinctive postprandial modulation of ß cell function and insulin sensitivity by dietary fats: monounsaturated compared with saturated fatty acids

López et al 2008


From Lopez et al 2008. Mean (± SD) plasma glucose, insulin, triglyceride, and free fatty acid (FFA) concentrations during glucose and triglyceride tolerance test meal (GTTTM) with no fat (control), enriched in monounsaturated fatty acids (MUFAs) from refined olive oil (ROO meal), with added butter, with a mixture of vegetable and fish oils (VEFO) or with high-palmitic sunflower oil (HPSO). N = 14.

The postprandial (after-eating) area-under-the-curve is substantially greater when butter is included in the mixed composition meal. This effect is not unique to butter, but is shared by most other dairy products.

Fat, in general, does not make you fat. But butter makes you fat.

Vitamin D as a cardiovascular risk factor gains ground

If you were reading The Heart Scan Blog back in 2007, or read my Life Extension article on vitamin D deficiency as a cardiovascular risk factor, you already knew that vitamin D deficiency is rampant and adds to cardiovascular risk.

Results of a study from the Intermountain Medical Center Heart Institute in Utah bolster the concept that vitamin D deficiency is a cardiovascular risk factor, vitamin D normalization/supplementation reduces cardiovascular risk.

Science Daily reported:

For the first study, researchers followed two groups of patients for an average of one year each. In the first study group, over 9,400 patients, mostly female, reported low initial vitamin D levels, and had at least one follow up exam during that time period. Researchers found that 47 percent of the patients who increased their levels of vitamin D between the two visits showed a reduced risk for cardiovascular disease.


In the second study, researchers placed over 31,000 patients into three categories based on their levels of vitamin D. The patients in each category who increased their vitamin D levels to 43 nanograms per milliliter of blood or higher had lower rates of death, diabetes, cardiovascular disease, myocardial infarction, heart failure, high blood pressure, depression, and kidney failure. Currently, a level of 30 nanograms per milliliter is considered "normal."


Over the past 4 years, people in our program have been enjoying the extravagant benefits of vitamin D restoration. Cardiovascular benefits are becoming better documented and the bone health, cancer-preventing, insulin-normalizing, mood-adjusting, and anti-inflammatory effects likewise.

Atkins Diet: Common errors

No doubt: The diet approach advocated by the late Dr. Robert Atkins was a heck of a lot closer to an ideal diet than the knuckleheaded advice emitting from the USDA, American Heart Association, American Diabetes Association, and the Surgeon General's office.

But having just spent a week with Atkins low-carbers, here are some common errors that I see many make, errors that I believe have long-term health consequences, including impairment of weight loss.

Excessive consumption of animal products--Non-restriction of fat often leads to over-reliance on animal products. Higher intakes of red meats (heme proteins?) have been strongly associated with increased risk for colon and other gastrointestinal tract cancers. It is not a fat issue; it is an animal product issue. We should consume less meat, more vegetables and other plant-sourced foods.

Consumption of cured meats--Cured, processed meats, such as sausage, hot dogs, salami, bologna, and bacon, have a color fixative called sodium nitrite, an additive that has been confidently linked to gastrointestinal cancers. Risk is likely dose-dependent: The more you ingest, the greater the long-term risk.

Overconsumption of dairy products--Dairy products, especially milk, yogurt, cottage cheese, and butter, are potent insulinotropic foods, i.e., foods that trigger insulin release. There can be up to a tripling of insulin (area-under-the-curve) levels. This is not good in a world populated with tired, overworked pancreases, exhausted from a lifetime of high-carbohydrate eating.

Too many calories--While I agree that "a calorie is a calorie" and "calories in, calories out" are faulty concepts, I have anecdotally observed that long-time low-carbers often trend towards unlimited consumption of food, a phenomenon that seems to result in weight gain, especially in the sedentary. I wonder if this is a reflection of the insulinotropic action of dairy products and other proteins, compounded by the poor insulin responsiveness that develops with lack of physical activity. Factor into this conversation that lower calorie intake extends life, probably substantially (Sirt-2 activation and related phenomena, a la resveratrol). If lower calorie intake extends life, unlimited calorie intake likely shortens life.

Please don't hear this as low-carb bashing--it is not. It is a call to improve diets and not stumble into common traps that can impair heart health, weight loss, and longevity.
All posts by william-davis

When meat is not just meat


The edgy nutrition advocate, Mike Adams, over at NewsTarget.com came up with this scary photo tour of a processed meat product from Oscar Mayer: Mystery Meat Macrophotography: A NewsTarget PhotoTour by Mike Adams







Along with increasingly close-up photographs of this meat-product, Adams lists the ingredients in Oscar Mayer's Cotto Salami:


Beef hearts
Pork
Water
Corn syrup
Beef

Contains less than 2% of:
Salt
Sodium lactate
Flavor
Sodium phosphates
Sodium diacetate
Sodium erythorbate
Dextrose
Sodium nitrite
Soy lecithin
Potassium phosphate
Potassium chloride
Sugar


As I reconsider the role of saturated fat in diet, given the startlingly insightful discussion by Gary Taubes of Good Calories, Bad Calories, I am reminded that not all meat is meat, not all saturated fat sources are equal.

I am concerned in particular about sodium nitrite content, a color-fixer added to cured meats that caused a stir in the 1970s when data suggesting a carcinogenic effect surfaced. The public's effort to remove sodium nitrite from the food supply was vigorously opposed by the meat council and it remains in cured meats like sausage, hot dogs, and processed meats like Cotto Salami. A 2006 meta-analysis (combined analysis of studies) of 63 studies did indeed suggest that sodium nitrite was related to increased risk of gastric cancer. This argument is plausible from animal models of cancer risk, as 40 animal models have likewise suggested the same carcinogenic association.

Also, fructose? This is most likely added for sweetness. Recall that fructose heightens appetite and raises triglycerides substantially.

I personally have a natural aversion to meat. I don't like the taste, the look, smell, and the thought of what the animal went through to make it to the supermarket. But, considered from the cold, carnivorous viewpoint of the question, "Is meat okay to eat?", among the issues to consider is whether the meat has been cured or processed, and does that process include addition of sodium nitrite.

Cotto Salami and similar products are not, of course, what carnivorous humans in the wild ate. This is a processed, modified product created from factory farm animals raised in cramped conditions and fed corn and other cheap, available foods. It is not created from free-ranging animals wandering their pastures or pens, eating diets nature intended. This results in modified fat composition, not to mention hormones and antibiotics added. These are not listed on the ingredients. Wild meat does not contain fructose or color-fixers, either.

So don't mistake "meat" in your grocery store for meat. It might look and smell the same--until you look a little closer.



Copyright 2007 William Davis, MD

Don't lament no OTC mevacor

After Merck's third go at FDA approval for over-the-counter (OTC) status for its statin cholesterol drug, Mevacor (lovastatin), the FDA advisory board suggested that its request be denied. They expressed concern that too many people would not understand how the drugs would be used and that misuse would be common.

Similar sentiments were echoed by Dr. Sidney Wolfe, director of the Health Research Group at Public Citizen; the American Medical Association (though the AMA always fights anything that threatens to erode physician control over health); and the de facto spokesman for cardiologists, Dr. Steven Nissen of the Cleveland Clinic.

Although I am a supporter for tools and legislation that yield greater self-empowerment in health care to the public, there is no need to lament the failed OTC status for Mevacor. For one, Merck had no plans to reduce the price on its OTC preparation. For many people, this would have meant an increase in cost, since health insurers would surely not cover a non-prescription agent.

Second, OTC status sends the implicit message that cholesterol is the most common cause of heart disease; it is not. (Small LDL particles are the number one cause, a pattern only partially addressed by any statin drug and a pattern largely responsible for the failure of statin drugs to "cure" heart disease despite pharmaceutical manufacturer's attempts to increase doses to take up any slack in effect.)

Thirdly, you can achieve the same effect--no, a superior effect--by incorporating several simple strategies into your life. These strategies are superior to Mevacor because they do more than just reduce LDL cholesterol. You can achieve similar LDL-reducing effect to Mevacor, 20 mg, just by adding:

--2 tablespoons oat bran or ground flaxseed per day (choose flaxseed if you have sugar problems or small LDL; flaxseed contains no digestible sugars, only protein and fiber)
--Raw almonds or walnuts--at least a handful, though more is fine and will not make you fat. (It's nuts like party mixes, mixed nuts roasted in unhealthy oils, and honey-roasted nuts that make us fat, not raw.)
--Soy protein sources--probably the weakest effect of all foods listed, but a contributor that can be obtained in a variety of forms, such as tofu, soy protein powders, and soy milk.
--Other foods that reduce LDL include pectin sources (e.g., citrus rind), flavonoids (e.g., green tea); stanol esters found in butter substitute Benecol (recall that sterol-containing products like Take Control and the flood of new products on the market like HeartWise orange juice might have potential for allowing sterol esters to enter the blood, so I do NOT recommend them); and, of course, niacin.

Many of these strategies also reduce small LDL, raise HDL, reduce triglycerides, and reduce blood sugar, effects that go beyond that achieved with Mevacor. Of course, a combination strategy is not as easy as popping one pill a day, it's better for you.

I will certainly not shed any tears for Merck and its relentless efforts to gain a stronger foothold in the "transform conditions into diseases" marketing strategy, the same strategy that classifies shyness, toe fungus, and sadness into medical conditions necessitating medication. While I do generally support efforts to increase public access to strategies that increase their health care power, this one was not necessarily all good.

Members of Track Your Plaque can read the complete report, Unique nutritional strategies to Reduce cholesterol naturally on the Track Your Plaque website.



Copyright 2007 William Davis, MD

Damage control

Medical device manufacturer, Cordis, is launching a new marketing program to promote its Cypher drug-coated stent. You can view the details at www.CypherUSA.com , including the slick TV commercial that HeartHawk posted a blog about.

The campaign opens with:

When you open up your heart, you open up your life.

Lives hampered by angina. By shortness of breath. By restricted blood flow. These lives are changing. Because of a state-of-the-art advancement. One that can have a huge impact on arteries around your heart. The CYPHER® Stent. It can open up your arteries. Increase flow of blood and oxygen. And change your restricted life. To an active life worth living. Your new life is...

Life Wide Open


Direct-to-consumer drug advertising has been around for a few years. While it has increased awareness of drugs and the "conditions" they are supposed to treat, it has also highlighted the aggressive profit-motive of the drug industry. This is not health care for the needy and sick, but health care for profit.

So now we're beginning to see the emergence of direct-to-consumer (DTC) advertising for medical devices. There was also a brief, though unsuccessful, foray into DTC advertising for implantable defibrillators, of all things, by Medtronic a couple of years ago, also.

What is the purpose of Cordis' marketing effort? Is it to educate and inform the public who might unknowingly receive non-drug coated stents and be deprived of the restenosis-inhibiting advantage of a drug-coated device? Is it meant to right a systematic wrong, a failure of cardiologists to insert the technologically, biologically, and ethically superior coated stents?

I find that doubtful. A more likely motive is damage control. With some of the (both deserved and undeserved) negative press the drug-coated stents have received lately, Cordis, eager to protect their $20 billion (annual revenues, 2006) medical device franchise, came up with this DTC strategy. After viewing the smiling faces of people , elated because of their "wide open" arteries and lives, Cordis hopes to see people going to their doctors insisting on the stent that is "opening millions of lives," since, "when your arteries narrow, so does your life."

Cool, trendy, liberating. That's the message they wish to deliver. Cool music, beautiful people, flashy high-tech images. Who wouldn't want a Cypher stent?

Beyond damage control, it's a familiar marketing theme: You're slender, glamorous, and sexy if you drink Coke, you're a caring mother if you feed your children Jif peanut butter, you're health conscious and smart if you eat Total cereal . . . you're cool and know what you want from life if you insist on a Cypher stent.

I don't object to advertising. It's part of the capitalistic economic system. It drives awareness and grows businesses. I do get concerned when advertising is so slick and effective that the people who are not properly armed with information can be duped into thinking that they need something that they don't really need.

Or, for which there are powerful, viable alternatives. Even hear about "prevent the disease in the first place?"

Low expectations

The Framingham Risk Calculator is a standard method used by many physicians to predict risk for heart attack or death from heart disease over a 10-year period. Low-risk is defined as <10% risk of heart attack or cardiac death over 10 years; high-risk is defined as 20% or more over 10 years; intermediate-risk is in between.

Let's put it to the test:

Amy is a 53-year old businesswoman. She is 5 ft 4 inches, weighs 150 lbs. Her father had a heart attack in his early 50s followed by the usual list of hospital procedures including bypass surgery at age 60.

What is Amy's risk for heart attack or death from heart disease over the next 10 years? If we enter her data into the Framingham risk calculator, the following result is returned:

Information about your risk score:
Age: 53
Gender: female
Total Cholesterol: 198 mg/dL
HDL Cholesterol: 74 mg/dL
Smoker: No
Systolic Blood Pressure: 120 mm/Hg
On medication for HBP: No
Risk Score: 1% Means 1 of 100 people with this level of risk will have a heart attack in the next 10 years.


So, according to the Framingham calculation, Amy has <1% risk for heart attack or death from heart disease over the next 10 years. Most primary care physicians would, at most, prescribe a statin drug and talk about a reduction in saturated fat.

Thankfully, Amy didn't fall for that bit of conventional mis-information. She instead got a CT heart scan, principally because of her father's history. Her score: 117. At age 53, this put her into 90th percentile, in the worst 10% of scores for women in her age group (50-55). By heart scan criteria, her risk for heart attack is probably more like 4-5% per year, or approximately 40-50% over the next 10 years.

Let's do just a bit more math. If Amy hadn't known about her heart scan score and no preventive action was taken, the expected progression of her heart scan scores would likely be:

Start: 117
Year 1: 152
Year 2: 198
Year 3: 257
Year 4: 335
Year 5: 436
Year 6: 567
Year 7: 737
Year 8: 958
Year 9: 1245
Year 10: 1618

In fact, given Amy's starting heart scan score of 117, it is highly unlikely that she survives the next 10 years without heart attack or a fatal heart event. Yet the Framingham risk calculator puts Amy's risk at less than 1%. Could anything be more wrong?

The folly of the Framingham calculator was highlighted by a recent publication from the large Multi-Ethnic Study of Atherosclerosis (MESA), in which 3600 women (45-84 years), all of whom fell into the "low-risk" category by the Framingham calculator--just like Amy--were tracked over approximately 3 3/4 years. This study generated several observations:

1) 30% of the "low-risk" women had positive heart scan scores.
2) 5% of the "low-risk" women had scores of 300 or greater (very significant for a woman). 8.6% of these women experienced a cardiovascular event like heart attack or death over the period. Women with a heart scan score of 300 or greater had a 22-fold greater event risk compared to women with zero heart scan scores.
3) Women with heart scan scores of 1 to 299 had a cardiovascular event risk of approximately 5-fold greater risk over the period.


Across the U.S., 90% of women younger than 70 years old fall into the Framingham "low-risk" category. Yet this fiction is accepted as the prevailing standard, along with LDL and total cholesterol, for determination of risk in women and men.

In my view, using the Framingham risk calculator is a misguided, misleading path, one that will mis-classify a substantial number of women who could otherwise be spared from heart attack and catastrophe.

By the way, Amy is also the Track Your Plaque program record holder (by percentage drop), with a 63% drop in heart scan score over a 15 month period.

Niacin vs. low-carb weight loss

Niacin:

--Raises HDL and shifts HDL towards the healthier large (HDL2b) subclass.
--Reduces total LDL.
--Reduces small LDL particles.
--Reduces triglycerides and triglyceride-containing particles like VLDL and IDL (intermediate-density lipoprotein).
--Reduces fibrinogen.
--Reduces inflammatory responses.


Weight loss achieved through a low-carbohydrate (read "wheat-free") diet:

--Raises HDL and shifts HDL towards the healthier large (HDL2b) subclass.
--Reduces total LDL.
--Reduces small LDL particles.
--Reduces triglycerides and triglyceride-containing particles like VLDL and IDL (intermediate-density lipoprotein).
--Reduces fibrinogen.
--Reduces inflammatory responses.


Curious, isn't it? Niacin achieves virtually the same effect as weight loss achieved through a low-carbohydrate diet, particularly if free of wheat products. The only major difference is that niacin also reduces lipoprotein(a), though even that distinction shrinks if monounsaturated fat sources like almonds are included in a low-carbohydrate program.

So which should you do first if you have any of the above patterns? Well, it's a question of 1) severity, 2) how carbohydrate-rich your starting diet is, 3) how much weight you could stand to lose, and 4) how urgent your program is (determined largely by your heart scan score).

Niacin can also be very helpful if you've taken full advantage of weight loss through a carbohydrate-restricted program, yet still retain some of the abnormal lipoprotein patterns that could continue to grow coronary plaque. For instance, if HDL cholesterol rises from 28 to 40 mg/dl by eliminating wheat and reducing carbohydrates and losing weight, niacin could raise HDL to 50 mg/dl or higher.

As much as I love and use niacin for its broad array of plaque-controlling effects, a low-carbohydrate, wheat-free diet can achieve many of the same effects. Use this strategy to full advantage.

Explosive plaque growth

Every once in a while, we will see someone experience more-than-expected rate of coronary plaque growth, a sudden jump in heart scan scores. I'm talking about increases in score of 50%, even 100%, sometimes despite favorable lipid and lipoprotein patterns.

It's not always easy to pin this phenomenon down, since we often detect it after a year or more on a repeat heart scan. It would be wonderfully insightful to perform heart scans more frequently and track plaque growth more precisely, but of course, radiation exposure is the most important limiting factor, as is cost.

So this list is, admittedly, speculative. It is based on observation, on presumptive associations between events and heart scan scores. But, judging from what we do confidently know about coronary atherosclerotic plaque, I think these observations make physiologic sense.

These are the sorts of increases in heart scan score that can scare the heck out of you, silent yet explosive growth of coronary atherosclerotic plaque that can grow with no warning whatsoever.



Image courtesy Wikipedia and the United States Geological Survey.









Factors which I have observed to possibly be responsible for explosive plaque growth include:

--Overwhelming tragedy such as death of a loved one, financial ruin, divorce. One of my early and catastrophic failures was a young man in his early 40s who, in the space of just a few months, suffered the loss of his mother, a brother, and his mother-in-law, while working a high-stress job. His heart scan score doubled from around 100 to 200 in one year, despite perfect lipoproteins. He had a heart attack shortly after the second score, despite a normal stress test just months earlier. (Pessimism is tragedy's weak cousin, but one that still holds power to corrupt our otherwise best efforts at plaque reversal.)

--Substantial weight gain. In the early years of the Track Your Plaque program, before it was even called "Track Your Plaque," I witnessed a man more than double his score from 1100 to 2400 in 18 months just by allowing himself to gain 40 lbs. (I don't know what became of him. His life apparently suffered other disasters, as well, and we lost track of him.)

--Poorly-controlled diabetes. High blood sugars out of control have yielded explosive growth.

--Kidney disease--However, I am uncertain of how much this overlaps with a deficiency of vitamin D's active form, 1,25-OH-vitamin D3, the form that is often deficient in people with dysfunctional kidneys.

--An inflammatory disease that is out of control, e.g., rheumatoid arthritis.

--This is very speculative, but I've witnessed explosive growth after vaccine administration that yielded strange viral-like symptoms. In this one instance, the man was getting heart scans (on his own) every three to six months and described a severe illness following a vaccine administered in preparation for travel out of the U.S.

--Unrecognized low thyroid function--i.e., hypothyroidism. This is easily corrected with thyroid hormone replacement.


These factors can also be relative and they can be overcome. Look at our current Track Your Plaque reversal record-holder: a 53-year old woman who dropped her heart scan score an amazing 63% despite the loss of a loved one during the 15 months of her program. Despite an overwhelming tragedy, she overcame the potential adverse effects and set a record, probably a record for the entire world.

Dr. Cannell on "How much vitamin D?"

In his most recent Vitamin D Council Newsletter (reprinted in its entirety below, minus clickable links, as Dr. Cannell apparently lost his webmaster and this issue of the newsletter is therefore not posted on the Vitamin D Council website; if you would like to either donate money to the Vitamin D Council or pitch in with help with his website, go to www.vitamindcouncil.com), Dr. John Cannell once again enlightens us with some new insights into vitamin D and its enormous role in health. In this issue, he discusses the role of vitamin D in people diagnosed with cancer (treatment, not prevention).

While cancer is not our focus on the Heart Scan Blog, Dr. Cannell's always insightful comments provide some helpful thoughts for our management of vitamin D doses and blood levels.

Dr. Cannell cites a recent study from vitamin D research expert, Dr. Bruce Hollis:

In the first study of its kind, Professor Bruce Hollis of the Medical University of South Carolina gave all of us something to think about. He asked and answered a simple question: How much vitamin D do you have to take to normalize the metabolism of vitamin D?

Remember, unlike other steroid hormones, vitamin D has very unusual metabolism in most modern humans, called first-order, mass action, kinetics. All this means is that the more vitamin D you take, the higher the 25(OH)D level in your blood, and the higher the 25(OH)D level in your blood, the higher the levels of activated vitamin D in your tissues. No other steroid hormone in the body behaves like this. Think about it: would you like your estrogen level to be dependent on how much cholesterol you ate? Or your cortisol level? (I'd ask the same about testosterone levels but I know men well enough not to ask.) No, the body must tightly regulate powerful steroid hormones through substrate inhibition, that is, if an enzyme turns A into B, when the body has enough B, B inhibits the enzyme and so limits its own production.

Not so with vitamin D, at least at modern human vitamin D levels. Professor Reinhold Vieth was the first to write about this and Vieth's Chapter 61 in Feldman, Pike, and Glorieux's wonderful textbook, Vitamin D (Elsevier, 2005, second edition), is a great reason to buy the textbook or have your library do so. (I'm glad to see Amazon is out of stock of the new ones (someone must be reading about vitamin D) but you can still buy used editions.)

Why would the kinetics of vitamin D be different from all other steroids? Maybe they are not, Hollis reasoned, like Vieth before him. Maybe vitamin D levels are so low in modern humans that its metabolic system is on full blast all the time in an attempt to give the body all the vitamin D metabolites it craves. So Hollis asked, Is vitamin D's metabolism different in populations in the upper end of 25(OH)D levels (a population of sun-exposed people and a group of women prescribed 7,000 IU per day)? Note, the Hollis study is free on Medline, you can download the entire paper on the right hand of the PubMed page below.

Hollis BW, et al. 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):631-634.

If you look at the two graphs, Figures 1 and 2 of Hollis' paper, you find vitamin D's kinetics can be normalized, made just like all other steroid hormones in the body, but you have to get enough sunshine or take enough vitamin D to get your 25(OH)D level above 50 ng/ml, and 60 ng/ml would be better. Then your body starts to store cholecalciferol in the body without much further increase in 25(OH)D levels. The reaction becomes saturable. This is a remarkable discovery and it implies levels of 30 and 40 ng/ml are usually not sufficient. It also implies actual vitamin D levels (cholecalciferol levels), not just 25(OH)D levels, may be useful in diagnosing and treating deficiency. Note, that not all of the sun-exposed individuals or women prescribed 7,000 IU/day achieved such levels. That's because the sun-exposed individuals were tested after an Hawaiian winter and because prescribing and taking are two different things.

In answer to the question, "How much vitamin D should someone with cancer take?," Dr. Cannell advises:
"Take enough to get your 25(OH)D level above 60 ng/ml, summer and winter." In doing so, you will have normalized the kinetics of vitamin D and stored the parent compound, cholecalciferol, in your tissues. In the absence of sunshine, you need to take about 1,000 IU/day per 30 pounds of body weight to do this. A 150 pound cancer patient may need to take 5,000 IU per day, a 210 pound cancer patient about 7,000 IU per day, all this in the absence of sunlight.

Dr. Cannell, no stranger to the resisitance among many practicing physicians unaware of the expanding and robust literature on vitamin D, advises people with cancer that:
In the end, if you have cancer and your physician won't do a risk/benefit analysis, do it yourself. The risk side of that equation is easy. Both Quest Diagnostics and Lab-Corp, the two largest reference labs in the USA, report the upper limit of 25(OH)D normal is 100 ng/ml and toxic is above 150 ng/ml, so 60 ng/ml is well below both. The reason levels up to 100 ng/ml are published normals is because there is no credible evidence in the literature that levels of 100 ng/ml do any harm and because sun worshipers often have such levels. (If you don't believe me, go to the beach in the summer for one month, sunbath every day for 30 minutes on each side in your bathing suit, and go home and have a 25(OH)D level.) By getting your level above 60 ng/ml, all you are doing is getting your levels into the mid to upper range of laboratory reference normals. Little or no risk.



For readers wishing to read the entire text of Dr. Cannell's newsletter, it is reprinted below:

The Vitamin D Newsletter
January, 2008


The January newsletter is coming early as I will be out of touch for awhile. If you remember, the last newsletter was on preventing cancer, not treating it. Below is a sampling of the tragic emails the last newsletter generated:


"Dr. Cannell, I was just diagnosed with breast cancer, how much vitamin D should I take?"

"My mother has colon cancer, how much vitamin D should she take?"

"I've had prostate cancer for four years, is there any reason to think vitamin D would help?"

"Dr. Cannell, my son has leukemia, should I give him vitamin D?"


It's one thing to talk about evidence vitamin D may prevent cancer but something quite different to discuss evidence vitamin D might help treat cancer. I used to think the answers to all the above questions were the same. Like anyone else, people with cancer should be screened for vitamin D deficiency and be treated if deficiency is present. Simple. However, it's not that simple. The real questions are, What are reasonable 25-hydroxy-vitamin D [25(OH)D] levels for someone with a life-threatening cancer? How much vitamin D do they need to take to obtain such levels? Is there any evidence, of any kind, that vitamin D will help treat cancer? The risk/benefit analysis of taking vitamin D is quite different if you are in perfect health than if your life, or your child's life, is on the line.

Remember, unlike cancer prevention, not one human randomized controlled trial exists showing vitamin D has a treatment effect on cancer. By treatment effect, I mean prolongs the lives of cancer patients. However, as I cited in my last newsletter, Dr. Philippe Autier of the International Agency for Research on Cancer, and Dr. Sara Gandini of the European Institute of Oncology, performed a meta-analysis of 14 randomized controlled trials showing even low doses of vitamin D extend life but they looked at all-cause mortality, not just cancer (Arch Intern Med. 2007;167(16):1730-1737). However, some epidemiological studies indirectly address the treatment issue and are quite remarkable. The first are a series of discoveries by Professor Johan Moan, Department of Physics at the University of Oslo, with Dr. Alina Porojnicu as the lead author on most of the papers.

Moan J, et al. Colon cancer: Prognosis for different latitudes, age groups and seasons in Norway. J Photochem Photobiol B. 2007 Sep 19

Lagunova Z, et al. Prostate cancer survival is dependent on season of diagnosis. Prostate. 2007 Sep 1;67(12):1362-70.

Porojnicu AC, et al. Changes in risk of death from breast cancer with season and latitude: sun exposure and breast cancer survival in Norway. Breast Cancer Res Treat. 2007 May;102(3):323-8.

Porojnicu A, et al. Season of diagnosis is a predictor of cancer survival. Sun-induced vitamin D may be involved: a possible role of sun-induced Vitamin D. J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):675-8.

Porojnicu AC, et al. Season of diagnosis is a prognostic factor in Hodgkin's lymphoma: a possible role of sun-induced vitamin D. Br J Cancer. 2005 Sep 5;93(5):571-4.

Porojnicu AC, et al. Seasonal and geographical variations in lung cancer prognosis in Norway. Does Vitamin D from the sun play a role? Lung Cancer. 2007 Mar;55(3):263-70.

What Professor Moan's group discovered, repeatedly, is quite simple, whether it be cancer of the breast, colon, prostate, lung, or a lymphoma. You live longer if your cancer is diagnosed in the summer. And it is not just Moan's group who has found this. A huge English study recently confirmed Moan's discovery.

Lim HS, et al. Cancer survival is dependent on season of diagnosis and sunlight exposure. Int J Cancer. 2006 Oct 1;119(7):1530-6.

What do these studies mean? Something about summer has a treatment effect on cancer. Whatever it is, you live longer if you are diagnosed in the summer but die sooner if you are diagnosed in the winter. What could it be about summer? Exercise? Fresh air? Melatonin? Sunlight? Pretty girls? Remember, these patients already had cancer. Whatever it is about summer, it is not a preventative effect that Professor Moan discovered, it is a treatment effect. Something about summer prolongs the life of cancer patients.

Dr. Ying Zhou, a research fellow, working with Professor David Christiani at the Harvard School of Public Health, went one step further. The stuffy Harvard researchers assumed summer worked its magic, not by pretty girls, but by summer sunlight making vitamin D. So they looked at total vitamin D input, from both sun and diet, to see if high vitamin D input improved the survival of cancer patients. Yes, indeed, remarkably. They found that early stage lung cancer patients with the highest vitamin D input (from summer season and high intake from diet) lived almost three times longer than patients with the lowest input (winter season and low intake from diet). Three times longer is a huge treatment effect, a treatment effect that most conventional cancer treatment methods would die for.

Zhou W, Vitamin D is associated with improved survival in early-stage non-small cell lung cancer patients. Cancer Epidemiol Biomarkers Prev. 2005 Oct;14(10):2303-9.

And that's not all, Marianne Berwick and her colleagues, at the New Mexico Cancer Institute, found malignant melanoma patients with evidence of continued sun exposure had a 60% mortality reduction compared to patients who did not. That implies a robust treatment effect from sunlight.

Berwick M, et al. Sun exposure and mortality from melanoma. J Natl Cancer Inst. 2005 Feb 2;97(3):195-9.

I will not list the thousands of animal studies that indicate vitamin D has a treatment effect on cancer as almost all of them studied activated vitamin D or its analogs, drugs that bypass normal regulatory mechanisms, cannot get autocrine quantities of the hormone into the cell, and that often cause hypercalcemia. However, Michael Holick's group found that simple vitamin D deficiency made cancers grow faster in mice. That is, vitamin D has a cancer treatment effect in vitamin D deficient mice. Professor Gary Schwartz, at Wake Forest, recently reviewed the reasons to think that vitamin D may have a treatment effect in cancer.

Tangpricha V, et al. Vitamin D deficiency enhances the growth of MC-26 colon cancer xenografts in Balb/c mice. J Nutr. 2005 Oct;135(10):2350-4.

Schwartz GG, Skinner HG. Vitamin D status and cancer: new insights. Curr Opin Clin Nutr Metab Care. 2007 Jan;10(1):6-11.

Finally, one human interventional study exists. In 2005, in an open trial, Professor Reinhold Vieth and his colleagues found just 2,000 IU of vitamin D per day had a positive effect on PSA levels in men with prostate cancer.

Woo TC, et al. Pilot study: potential role of vitamin D (Cholecalciferol) in patients with PSA relapse after definitive therapy. Nutr Cancer. 2005;51(1):32-6.

So we come back to the crucial question. If you have cancer, how much vitamin D should you take, or, more precisely, what 25(OH)D level should you maintain? We don't know. You can correctly say that definitive studies have not been done and, incorrectly, conclude physicians treating cancer patients should do nothing. I say incorrectly because standards of medical practice have always demanded that doctors make reasonable decisions based on what is currently known, doing a risk/benefit analysis along the way to decide what is best for their patients based on what is known today. If a patient has a potentially fatal cancer, the doctor cannot dismiss a relatively benign potential treatment modality just because definitive studies have not been done, and passively watch his patient die. Standards of care require doctors consider what is known now, using information currently available, perform a risk/benefit analysis, and then act in the best interest of their patient.

Luckily, such doctors recently obtained some guidance. In the first study of its kind, Professor Bruce Hollis of the Medical University of South Carolina gave all of us something to think about. He asked and answered a simple question: How much vitamin D do you have to take to normalize the metabolism of vitamin D?

Remember, unlike other steroid hormones, vitamin D has very unusual metabolism in most modern humans, called first-order, mass action, kinetics. All this means is that the more vitamin D you take, the higher the 25(OH)D level in your blood, and the higher the 25(OH)D level in your blood, the higher the levels of activated vitamin D in your tissues. No other steroid hormone in the body behaves like this. Think about it, would you like your estrogen level to be dependent on how much cholesterol you ate? Or your cortisol level? (I'd ask the same about testosterone levels but I know men well enough not to ask.) No, the body must tightly regulate powerful steroid hormones through substrate inhibition, that is, if an enzyme turns A into B, when the body has enough B, B inhibits the enzyme and so limits its own production.

Not so with vitamin D, at least at modern human vitamin D levels. Professor Reinhold Vieth was the first to write about this and Vieth's Chapter 61 in Feldman, Pike, and Glorieux's wonderful textbook, Vitamin D (Elsevier, 2005, second edition), is a great reason to buy the textbook or have your library do so. [ I'm glad to see Amazon is out of stock of the new ones (someone must be reading about vitamin D) but you can still buy used editions.)

Why would the kinetics of vitamin D be different from all other steroids? Maybe they are not, Hollis reasoned, like Vieth before him. Maybe vitamin D levels are so low in modern humans that its metabolic system is on full blast all the time in an attempt to give the body all the vitamin D metabolites it craves. So Hollis asked, Is vitamin D's metabolism different in populations in the upper end of 25(OH)D levels (a population of sun-exposed people and a group of women prescribed 7,000 IU per day)? Note, the Hollis study is free on Medline, you can download the entire paper on the right hand of the PubMed page below.

Hollis BW, et al. 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.

If you look at the two graphs, Figures 1 and 2 of Hollis' paper, you find vitamin D's kinetics can be normalized, made just like all other steroid hormones in the body, but you have to get enough sunshine or take enough vitamin D to get your 25(OH)D level above 50 ng/ml, and 60 ng/ml would be better. Then your body starts to store cholecalciferol in the body without much further increase in 25(OH)D levels. The reaction becomes saturable. This is a remarkable discovery and it implies levels of 30 and 40 ng/ml are usually not sufficient. It also implies actual vitamin D levels (cholecalciferol levels), not just 25(OH)D levels, may be useful in diagnosing and treating deficiency. Note, that not all of the sun-exposed individuals or women prescribed 7,000 IU/day achieved such levels. That's because the sun-exposed individuals were tested after an Hawaiian winter and because prescribing and taking are two different things.

So my answer to "How much should I take if I have cancer?" is "Take enough to get your 25(OH)D level above 60 ng/ml, summer and winter." In doing so, you will have normalized the kinetics of vitamin D and stored the parent compound, cholecalciferol, in your tissues. In the absence of sunshine, you need to take about 1,000 IU/day per 30 pounds of body weight to do this. A 150 pound cancer patient may need to take 5,000 IU per day, a 210 pound cancer patient about 7,000 IU per day, all this in the absence of sunlight. And this may not be enough; cancer patients may use it up faster (increased metabolic clearance) and children may do the same due to their young and vital enzymes. Or you may need less, because you get more sun than you think, more from your diet, or because you are taking a modern medicine that interferes with the metabolism of vitamin D. An even easier way to do it is go to a sun tanning booth every day and obtain and keep a dark, full-body, tan. Then you don't have to worry about blood levels but I'd get one anyway, just to be sure it was above 60 ng/ml.

Given what Hollis discovered, given the well-known potent anti-cancer properties of activated vitamin D, given epidemiological evidence that summer extends the life of cancer patients, given a meta-analysis of randomized controlled trials showed that vitamin D prolongs life, given animal data that simple vitamin D has a treatment effect on cancer, and given a patient with a life-threatening cancer, what would a reasonable physician do? Simply let their patient die while muttering something about the lack of randomized controlled trials?

No, they would simply check a 25(OH)D level every month and advise cancer patients to take enough vitamin D or frequent sun tanning parlors enough to keep their level above 60 ng/ml. Toxicity does not start until levels reach 150 ng/ml but if you take more than 2,000 IU per day have your doctor order a blood calcium every month or two along with the 25(OH)D. Both you and he will feel better and because if you have cancer, you are probably taking lots of other drugs and little is known about how modern drugs interact with vitamin D metabolism. By getting your level above 60 ng/ml, all you are doing is getting your level to where most lifeguards' levels are at the end of summer, to levels our ancestors had when they lived in the sun, to levels regular users of sun-tan parlors levels achieve, and most importantly, to levels where vitamin D's pharmacokinetics are normalized.

In the end, if you have cancer and your physician won't do a risk/benefit analysis, do it yourself. The risk side of that equation is easy. Both Quest Diagnostics and Lab-Corp, the two largest reference labs in the USA, report the upper limit of 25(OH)D normal is 100 ng/ml and toxic is above 150 ng/ml, so 60 ng/ml is well below both. The reason levels up to 100 ng/ml are published normals is because there is no credible evidence in the literature that levels of 100 ng/ml do any harm and because sun worshipers often have such levels. (If you don't believe me, go to the beach in the summer for one month, sunbath every day for 30 minutes on each side in your bathing suit, and go home and have a 25(OH)D level.) By getting your level above 60 ng/ml, all you are doing is getting your levels into the mid to upper range of laboratory reference normals. Little or no risk.

What are the potential benefits? It probably depends on a number of things. Did your cancer cells retain the enzyme that activates vitamin D? Many do. Did your cancer cells retain the vitamin D receptor? Many do. If your cancer cells get more substrate [25(OH)D], will that substrate induce the cancer cells to make more vitamin D receptors or more of the activating enzyme? Some cancer cells do both. In practical terms, vitamin D is theoretically more likely to help your cancer the earlier you start taking it. However, no one knows. Certainly there is no reason, other than bad medicine, for cancer patients to die vitamin D deficient. Unfortunately, most do.

Tangpricha V, et al. Prevalence of vitamin D deficiency in patients attending an outpatient cancer care clinic in Boston. Endocr Pract. 2004 May-Jun;10(3):292-3.

Plant AS, Tisman G. Frequency of combined deficiencies of vitamin D and holotranscobalamin in cancer patients. Nutr Cancer. 2006;56(2):143-8.

It is very important that readers understand I am not suggesting vitamin D cures cancer or that it replace standard cancer treatment. Oncologists perform miracles every day. Do what they say. The only exception is vitamin D. If your oncologist tells you not to take vitamin D, ask him three questions. 1) How do you convert ng/mls to nmol/Ls? How many IU in a nonogram? 3) How do you spell "cholecalciferol?" If he doesn't know how to measure it, weigh it, or spell it, chances are he doesn't know much about it.

All of the epidemiological and animal studies in the literature suggest cancer patients will prolong their lives if they take vitamin D. I can't find any studies that indicate otherwise. However, none of the suggestive studies are randomized controlled interventional trials; they are all epidemiological or animal studies, or, in the case of Vieth's, an open human study. However, if you have cancer, or your child does, do you want to wait the decades it will take for the American Cancer Society to fund randomized controlled trials using the proper dose of vitamin D? Chances are you, or your child, will not be around to see the results.


John Cannell, MD
The Vitamin D Council
9100 San Gregorio Road
Atascadero, CA 93422


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End-stage vitamin D deficiency

Let me paint a picture:

A 78-year old woman, tired and bent. She's lost an inch and a half of her original height because of collapse of several vertebra in her spine over the years, leaving her with a "dowager's hump," a stooped position that many older women assume with advanced osteoporosis. It's also left her with chronic back pain.


(Image courtesy of National Library of Medicine)

This poor woman also has arthritis in her knees, hips, and spine. All three locations add to her pain.

She also has hypertension, a high blood sugar approaching diabetes, and distortions of cholesterol values, including a low HDL and high triglycerides.

Look inside: On a simple x-ray, we see that the bones of her body are unusually transparent, with just a thin rim of bone at the outer edges, depleted of calcium. Weight-bearing bones like the spine, hips, and knees have eroded and collapsed.

On an echocardiogram of her heart (ultrasound), she has dense calcium surrounding her mitral valve ("mitral anular calcium"), a finding that rarely impairs the valve itself but is a marker for heightened potential for heart attack and other adverse events. Her aortic valve, another of the four heart valves, is also loaded with calcium. In the aortic valve, unlike the mitral valve, the collection of calcium makes the valve struggle to open, causing a murmur. The valve is rigid and can barely open to less than half of its original opening width.

If a heart scan were performed, we'd see the coronary calcification, along with calcification of the aorta, and the mitral and aortic valves.

Obviously, it's not a pretty picture. It is, however, a typical snapshot of an average 78-year old woman, or any other elderly man or woman, for that matter.

This collection of arthritis, osteoporosis, coronary and valve calcification, high blood pressure, abnormal cholesterol patterns, and pain is not unusual by any stretch. Perhaps you even recognize someone you know in this description. Perhaps it's you.

Look at this list again. Does it seem familiar? I'd say that the common factor that ties these seemingly unrelated conditions together is chronic and severe deficiency of vitamin D. Vitamin D deficiency leads to arthritis, osteoporosis, coronary and valve calcification, high blood pressure, abnormal cholesterol patterns, and pain.

Should we go so far as to proclaim that aging, or at least many of the undesirable phenomena of aging, are really just manifestations of vitamin D deficiency? I would propose that much of aging is really deficiency of vitamin D, chronic and severe, in its end stages.

My colleagues might propose a 30- or 40-year long randomized trial, one designed to test whether vitamin D or placebo makes any difference.

Can you wait?

"Instant" reversal with fasting?

Here's a fascinating e-mail we received recently. It came from a man in Hawaii who dropped his heart scan score a modest amount, but did it in two months using fasting. He also has the advantage of access to the Holistica Hawaii scan center with our friend, Dr. Roger White. His experience is so fascinating that we asked for his permission to reprint his story which he did enthusiastically.

So here is Don's story:


I am a 61 year old male with a history of heart disease in my family. My maternal grandfather, for instance, died at age 39 of a
heart attack and my mother died of a stroke. There are other instances in my family as well.

I, personally, before going to Holistica had had three heart procedures; one radio catheter ablation for WPW Syndrome, and two radio catheter ablations for atrial fibrilations. After suffering with WPW for over 30 years and A-Fibs for about a year, those issues seem to be behind me fortunately.

Three or four months back, however, I was suffering from shortness of breath and slight chest pains when doing the uphill part of a 5 mile walk that I do almost every day. My wife had had a coronary heart scan several years back at Holistica so that's how I knew about it.

I had a scan done on October 4th this year. The scan did show fairly
advanced plaque build up; my total coronary plague burden was
312.9. The day following the scan I felt absolutely terrible; lightheaded, weak, much like feeling you were at death's door.

I had read a book a number of years back about therapeutic fasting
(water only) called "Fasting and Eating for Health" by Dr. Joel
Furhman.


According to his book, one on the areas where he consistently has dramatic and quick results with fasting is with reducing arterial plaque. Based on how badly I was feeling at the time, I decided to start an immediate fast. Within just the first 24 hours, the relief was dramatic and amazing. I continued the water only fast for 3 weeks.

Yesterday, December 1st I went in for another cardio scan instead of the coronary angiogram that I had previously been scheduled for. I could tell they were a little confused why I was doing that but went ahead and did another coronary EBT scan.

When I went in for the doctor consultation, Dr. McGriff said, "OK, exactly what is it you've done since last time." In less than two months, my coronary plaque burden had dropped to 296.2. That's a 6% reduction in less than 2 months. Had I gone back in for the second scan right after my 3 week fast then it probably would have a 6%
reduction in less than a month.

Frankly, based on how good I've been feeling (I'm even thinking of
getting back into jogging instead of walking), I was surprised it was
only 6%. Based on the common experience, however, that it sometimes
takes a year or two to just stabilize your plaque increase, much less
actually start losing it, the doctor was truly startled and
surprised. He said he had never seen such a sudden reduction as that
before!

We are still going to proceed with the coronary angiogram and I
intend to apply what I find in your book but I thought you might be interested in these results since I've never heard or read of anyone actually measuring the effectiveness of a fast with before and after EBT Scans.

I admire your direction and work focusing on prevention instead of catastrophic management like most doctors. Dr. Fuhrman is very much the same with the greatest attention on prevention so if you haven't heard of his book you might be interested. Especially interesting regarding this particular issue is Chapter 5 entitled, "The Road Back to a Healthy Heart-the Natural Way."

I can personally verify everything he has said about the fasting procedure itself from start to finish. I consider his book the Bible about fasting. As I mentioned, given your similar direction in medicine, I thought I would bring my personal experience on the matter to your attention for your consideration. Maybe in a future edition of your book, you might want to include some information on fasting.

Anyhow, I hope you will find this helpful. Any other questions,
don't hesitate to e-mail back. Please keep up your good work and
thanks for what your doing!

Yours truly,

Don P.
Honolulu, Hawaii



Isn't that great?

Now, in all honesty, a change of 6% could conceivably be within the margin of error for heart scanning. (Although several studies from a number of years ago suggested that variation in heart scan scoring was about 10%, sometimes more, in my experience, on EBT devices like the one Don used, variation is <5% at this score range.) Genuine regression would probably be better documented by yet another scan down the road. If the trend is consistent, then it is probably real.

Nonetheless, Don's story may support we've been saying for some time: Fasting is a rapid method to gain control over plaque--but I didn't know it might be that quick! Perhaps Don is a living example of what I've called "instant" heart disease reversal.

Don is potentially off to a good start. But, unless he can periodically repeat his fast, he will still have to engage in a program that allows continuing control over coronary plaque in between fasts. Also, fasting cannot address issues like vitamin D deficiency, lipoprotein(a), and any residual lipid/lipoprotein issues. But I am continually impressed with the power of fasting to "jump start" a program of heart disease reversal.

It would be a fascinating study to perform, with serial heart scans within brief periods of weeks or months to gauge rapid response. However, we need to keep in mind that as wonderful as heart scans are, they do involve modest radiation exposure.

It might be interesting in future to add a fasting "arm" to the virtual clinical trial. That might yield some great insights.


Copyright 2007 William Davis,MD

Study review: yet another Lipitor study

This continues a series I've begun recently that discusses studies that have emerged over the past 10 years relevant to heart scan scoring and reversal of coronary atherosclerotic plaque.

The St. Francis Heart Study from St. Francis Hospital, Roslyn, New York, was released in 2005. This was yet another study that set out to determine whether Lipitor exerted a slowing effect on coronary calcium scores. This time, Lipitor (atorvastatin), 20 mg per day, was combined with vitamin C 1 g daily, and vitamin E (alpha-tocopherol) 1,000 U daily, vs. placebo. A total of 1,005 asymptomatic men and women, age 50 to 70 years, with coronary calcium scores 80th percentile or higher for age and gender
participated in the study.

After four years, heart scan scores in the placebo group increased 73%, compared to 81% in the treatment group. Statistically, the cocktail of drug, vitamins C and E had no effect on heart scan scores.

Other findings included:

--Participants experiencing heart attack and other events during the study showed greater progression of scores than those not experiencing heart attack: score increase of 256 vs. increase of 120.

--While treatment did not reduce the number of heart attacks and events overall, participants with starting heart scan scores >400 did show a benefit: 8.7% with events on treatment (20 of 229) vs. 15.0% with placebo (36 of 240).

(Note what is missing from the treatment regimen: efforts to raise HDL (starting average HDL 51 mg/dl); reduce triglycerides (starting average 140 mg/dl); identify those whose LDL was false elevated by lipoprotein(a); omega-3 fatty acids from fish oil; correction of other factors like vitamin D deficiency.)


Are we pretty in agreement that just taking Lipitor and following an American Heart Association low-fat diet is an unsatisfactory answer to gain control over coronary plaque growth? No slowing of heart scan score growth seen in the St. Francis Heart Study and similar studies is consistent with the 25-30% reductions in heart attack witnessed in large clinical trials. Yes, heart attack and related events are reduced, but not eliminated--not even close.

And when you think about it, it should come as no surprise that the simple strategy studied in the St. Francis Heart Study failed to completely control plaque growth. Lipitor and statin drugs exert no effect on small LDL particles, barely raise HDL cholesterol at all, and have no effect on Lp(a), factors that increase heart scan scores substantially.

Though these discussions have frightened some people because of the suggestion that increasing heart scan scores are inevitable and unavoidable, they shouldn't. It really should not be at all shocking to learn that taking one drug all by itself should cure coronary heart disease.

Instead, findings like those of the St. Francis study should cause us to ask: What could be done better? How can we better impact on heart scan scores and how can we further reduce heart attack, particularly in people with higher heart scan scores?

My answer has been the Track Your Plaque program, a comprehensive effort to 1) address all causes of coronary plaque, and then 2) correct all the causes.