A tan does not equal vitamin D

The sun is getting stronger and the days are getting longer, even here in Wisconsin.

Some people are coming to the office with nice tans obtained by sunning themselves for several hours. Others have come back from winter getaways to Florida, Arizona, or the tropics, also sporting nice, dark tans.

Several people, in fact, were so confident that sunning themselves provided sufficient vitamin D that they reduced their usual dose. Some even stopped their vitamin D altogether.

But, when blood levels of 25(OH) vitamin D were checked, they were virtually all low, sometimes as low as <20 ng/ml. Yet all had nice tans.

Why does this happen? Why would people with dark tans remain deficient in vitamin D?

One big factor is age: Anyone over 40 years old is fooling themselves if they think that a tan ensures raising vitamin D levels to a desirable range. Also, the more you tan, the more melanin skin pigment accumulates, and the more vitamin D activation in the skin is blocked.

Weight is another factor: Heavier people need more vitamin D, sometimes three- or four-fold more than slender people.

Why does aging result in inefficient skin activation of vitamin D? It seems that, once we are beyond our reproductively useful years, this ticking clock of aging gets triggered. The older we get, the less activation of vitamin D occurs in our skin, the less of the youth-maintaining, disease-preventing benefits of vitamin D we obtain with sun exposure.

The message: Don't rely on a tan to gauge the adequacy of vitamin D. Maybe that works when you're 16 years old, but not at age 50 or 60. There's only one way to know your vitamin D status: a blood level of 25(OH) vitamin D.


Copyright 2008 William Davis, MD

Planned obsolence

In the 1960s, you’d purchase a new car. If you changed the oil, adhered to the maintenance schedule—and were lucky—you might expect to get 100,000 miles out of your automobile. Only an occasional car made it beyond that odometer hurdle. Even if the engine made it past the 100,000 mile milestone, the automobile body would inevitably start to develop rusting decay at the edges of the fenders, signaling body rot that threatened to open gaping holes of metal.



Then along came Toyota and Honda, whose cars easily reached 100,000 miles and well beyond, reliably and with bodies intact. As this realization sunk into the American consciousness, many asked, “Why can’t American automakers accomplish the same sort of trouble-free longevity?” “Buy American” emerged as a mantra to preserve American jobs and prop up an economy vulnerable to the superior automotive products from Detroit’s competitors.

Of course, American automakers have since responded to the challenge posed by the Japanese auto industry and produced automobiles that essentially matched the reliability and longevity of Japanese cars. But, the great unanswered question remains: For years before the onslaught of Japanese competition, did Detroit quietly plot to maintain a policy of planned obsolescence that ensured Americans would have to scrap the old and buy a new car every few years whenever the odometer tipped over 100,000 miles?

We will never know. At worst, it may represent the behind-closed-doors, back-slapping sort of plotting that, for many years, maximized revenues, ensured shareholder returns, and secured executive paychecks. Or, perhaps it wasn’t some evil conspiracy but just complacency, a profitable position of comfort at that. There’s little incentive for industry insiders to reveal such self-incriminating information.

But the example set by the American auto industry presents an unusual learning opportunity for us, a chance to make some useful comparisons to the heart healthcare industry.

Is the American healthcare industry also guilty of practicing a policy of “planned obsolescence,” just like Detroit? The product that helplessly crumbles is, of course, not your rust-riddled automobile, but you.

When someone sees a primary care physician year after year, yet appears one morning in the emergency room, clutching his or her chest in agony from the closed coronary artery responsible for a life-threatening heart attack—prompting the flurry of activity that results in $100,000 in hospital procedures . . .

Perhaps “planned obsolescence” is not the perfect phrase to describe the situation, but the principle still applies: A failure to inform the patient that such an outcome was possible—no, probable—makes you wonder whether such an outcome was predictable and thereby preventable in the first place.

What should we do when planned obsolescence leads us down a path engineered by someone who has something, often substantial, to gain? Even if it's just complacency, or adhering to a beaten, ineffective status quo (can you say "low-fat diet?), it all points in the same direction.

You have a choice: Refuse to buy a 1962 Impala of health care, otherwise known as conventional heart disease management.

Melatonin for high blood pressure?

Melatonin is fascinating stuff.

In addition to its use as a sleep aid, melatonin exerts possible effects on cardiovascular parameters, including anti-oxidative action on LDL, reduction in sympathetic (adrenaline-driven) tone, and reduction in blood pressure.

Several studies document the blood pressure-reducing effect of melatonin:

Daily nighttime melatonin reduces blood pressure in male patients with essential hypertension.

Melatonin reduces night blood pressure in patients with nocturnal hypertension.

Prolonged melatonin administration decreases nocturnal blood pressure in women.

Blood pressure-lowering effect of melatonin in type 1 diabetes.


But blood pressure may be increased when melatonin is added to nifedipine, a calcium channel blocker:

Cardiovascular effects of melatonin in hypertensive patients well controlled by nifedipine: a 24-hour study.


Effects on BP tend to be modest, on the order of 5-8 mmHg reduction in systolic, half that in diastolic.

But don't pooh-pooh such small reductions, however, as small reductions exert mani-fold larger reductions in cardiovascular events like heart attack and stroke. NIH-sponsored NHANES data (see JNC VII), for example, document a doubling of risk for each increment of BP of 20/10. The Camelot Study demonstrated a reduction in cardiovascular events from 23% in placebo subjects to 16.7% in subjects taking amlodipine (Norvasc) with a 5 mm reduction in systolic pressure, 2 mmHg drop in diastolic pressure. Small changes, big benefits.

Many people take melatonin at bedtime and are disappointed with the effects. However, a much better way is to take melatonin several hours before bedtime, e.g., take at 7 pm to fall asleep at 10 pm. Don't think of melatonin as a sleeping pill; think of it as a sleep hormone, something that simply prepares your body for sleep by slowing heart rate, reducing body temperature, and reducing blood pressure. (You may need to modify the interval between taking melatonin and sleep, since individual responsiveness varies quite a bit.)

I also favor the sustained-release preparations, e.g., 5 mg sustained-release. Immediate-release, while it exerts a more rapid onset of sleep, allows you to wake up prematurely, The sustained-release preparations last longer and allow longer sleep.

The dose varies with age, with 1 mg effective in people younger than 40 years, higher doses of 3, 5, even 10 or 12 mg in older people. Sustained-release preparations also should be taken in slightly higher doses.

The only side-effect I've seen with melatonin is vivid, colorful dreams. Perhaps that's a plus!

The forces that shape heatlh care

Thinking about the programs for health care reform proposed by the three Presidential candidates highlights a distinct peculiarity of American style health care.

American health care is shaped to an unprecedented degree by five forces:

1) The drug industry

2) The health insurance industry

3) Hospitals

4) Fear of litigation

5) The uniquely American attitude of refusing compromise in access to health care services or products, regardless of the cost (for those who can afford health insurance)


All five of these unique forces have created this thing (monster?) we call health care. Remove or modify any one of these forces, and the health care landscape would look dramatically different.

The drug industry has recently been on the receiving end of plenty of negative press. This warms my bones. Decades of heavy-handed lobbying, sleazy marketing to physicians (all too willing to be wined and dined), and behind-the-scenes manipulation of clinical data are coming back to bite them. Sadly, the drug industry is so powerful that this bit of fuss is not likely to substantially change their ways.

I am thrilled that all three Presidential candidates agree that reimportation of drugs from outside the U.S. is a good idea. While the shrug of the shoulders federal and state attitude towards importation of drugs from Canada has not resulted in cost savings sufficient to impact on overall costs, it surely will lead to savings when practiced on a broad basis by pharmacies, distributors, and other bulk buyers of pharmaceuticals.

Senator Obama, in particular, has used strong language in his criticism of the health insurance industry, tough talk that is needed in an age in which insurance executives bring home salaries in the hundreds of millions of dollars and stock prices are climbing due to substantial profit gains within the industry, going against the grain of increasingly costly premiums. However, the Clinton experiment of federalizing health care during Bill Clinton's term that caused all the big boys to band together (most notably health insurance companies and drug industry) has tempered enthusiasm for attacking the insurance industry head-on. In both Democrats' health care reform proposals, the option of private insurance is preserved, as it is in the McCain proposal.

How about hospitals? Hospitals, though on a smaller scale than the nationwide reach of the drug and insurance industries, aim to maintain health service delivery in hospitals. For instance, the high-tech bypass service in the hospital gets plenty of local media coverage, as does the newest DaVinci robotic surgery, bariatric surgery, and other revenue-rich services. Many hospitals have forgotten that their mission is delivery of health, of which revenue creation and profiting from disease should only be part.

How big is fear of litigation? Estimates vary, but several have quoted numbers in the neighborhood of 20 to 30% of overall health care costs. At the street level from what I see, I'd say at least that much. Fear of litigation is rampant, often unrestrained, and sometimes leads to the craziest, illogical sequence of testing. Chest pain, for instance, no matter how trivial, will typically trigger around $5000 worth of testing (nuclear stress test, echocardiogram, laboratory work, etc.) Emergency room visit for a minor injury? CT scan of head, chest, abdomen. A formula to minimize this aspect of fear in health care delivery would generate enormous savings.

The last issue, the uncompromising nature of Americans in health--always wanting the latest new drug, new procedure, "best" surgeon--often simply causes the health care consumer to fall victim to marketing. If a hospital advertises the newest procedure, people want it regardless of whether it represents genuine improvement over the older procedure. The newest sleeping pill, antidepressant, antihypertensive, etc. replaces the old yet equivalent product, but at considerably greater cost.

I am optimistic that, regardless of which candidate gains the White House, that some reform is on the way. I do fear, however, that progress will be small and incremental, since major change of the sort that would slash hundreds of billions of dollars in costs would rouse the powers-that-be (drug industry, health insurers, etc.) to once again combine forces and combat the disruption of their franchise.

Until you and I see real change and cost savings coming through either legislation or free market advances, we need to continue to make full use of the self-empowering health information that we gain through venues like the web.



Copyright 2008 William Davis, MD

Lipoprotein(a): Surprising Poll Results

No doubt, our little informal poll asking readers whether they have lipoprotein(a), is skewed towards people inclined to respond because they have this genetic trait.

Nonetheless, the response is telling. Of 82 respondents:

--40 (48%) said they did have Lp(a)

--16 (19%) said that they did not have Lp(a)

--26 (31%) said that they did not know whether or not they had Lp(a)


Though admittedly an informal analysis, I'd draw several conclusions from this simple "experiment".

One, while the proportion of people responding that they have Lp(a) may not be accurate, it is a prevalent genetic risk factor that, according to formal studies, is present in 17% of people with coronary or vascular disease, 11% of the broader population. This number may be even higher if the newer particle number assays (measurements) are used (with results expressed in nmol/L), since an occasional person with a "normal" Lp(a) in mg/dl (weight-based) will prove to have increased Lp(a) by nmol/L (particle number-based). (The reason for this phenomenon is not clear. It may be consequent to variation in apo(a) size, with larger apo(a) varieties of Lp(a) occasionally escaping detection .) As our little poll shows, plenty of people have Lp(a).

Two, readers of this blog tend to be highly motivated, sophisticated, and knowledgeable about health and heart disease. Yet a substantial portion--31%--did not know whether they have this crucial risk factor. That shouldn't be. The unnecessary difficulty of getting this simple blood test performed has been driven home to me repeatedly when I identify this factor in someone and then suggest that their grown children and parents, each of whom have a 50% chance of having Lp(a), be tested. It's not uncommon for a 35-year old son, for instance, to say that his doctor refused, claiming it is an unproven risk marker, or to simply say that he/she doesn't know what it is.

No doubt, just knowing whether you have Lp(a) or not is not the end of the story. Reducing Lp(a) and its associated co-factors is no easy matter. With several hundred patients in my practice with Lp(a), it occupies much of my time and energy. Sometimes it leads to enormous successes , but it can also pose a real challenge.

There should no longer be any doubt that Lp(a) is associated with significantly increased risk of cardiovascular disease. This has been demonstrated conclusively across dozens of studies. Risk from Lp(a) is over and above that posed by other risk factors; it also amplifies the risk posed by other factors, e.g., small LDL, inflammatory phenemena, homocysteine, total LDL, low HDL.

In the world of Lp(a), our two most desperate needs for the future are:

1) Better education of physicians and the public, and

2) More effective treatment options.

Thus, our reasons to form The Lipoprotein(a) Research Foundation. Steps to gain tax-exempt status are being pursued as we speak.

I can't help but wonder whether, like vitamin D, a solution is right beneath our noses. An investment in research to fund the trials to better explore both basic science as well as practical treatment options might yield an answer more readily than we think. Wouldn't that be great?

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
All posts by william-davis

Dr. Michael Eades on the Paleolithic diet

Dr. Michael Eades has posted an absolutely spectacular commentary on the Paleolithic diet concept:

Rapid health improvements with a Paleolithic diet

The post was prompted by publication of a study that tried to recreate a Paleolithic-like diet experience over a brief study period:

Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet.

Dr. Eades discussion is wonderfully insightful and comprehensive and there's little to say to improve on his discussion.

I'd make one small point: From what I see in my experience, the improvements in lipid patterns seen in the brief period of this study are very likely to have been primarily due to the removal of wheat. Followers of this blog know that wheat elimination is among the most powerful cholesterol-reducing strategies available.

What vitamin D form?

In response to questions regarding why don't vitamin D tablets work, here are my observations.

When I first started correcting vitamin D levels around 3 1/2 years ago, people would begin with starting 25-hydroxy vitamin D blood levels of around 20 ng/ml.

Taking, say, 6000 units vitamin D as tablets over 3 months yielded blood levels of 24-30 ng/ml. Taking 6000 units in an oil-based form, and blood levels would commonly be 60-70 ng/ml.

In other words, tablets are very poorly absorbed. I also saw very erratic absorption with tablets, with tremendous variation in blood levels.

I witnessed this effect many times. I finally began telling patients to avoid the tablets altogether. It's simply not worth it. Taking dose X of tablets, you cannot predict what the blood level of vitamin D will be.

Now, you can sometimes make the tablets get absorbed by either taking with a teaspoon of oil (e.g., olive, flaxseed) or taking with an oil-rich meal. However, I am uncertain just how consistent the absorption is under these circumstances, not having done this enough times to know.

Oil-filled gelcaps are no more expensive than tablets (or perhaps a dollar more). Health food store employees and pharmacists don't know this. I have had many patients come to the office claiming they changed to tablets because that's all their health food store or pharmacy carried and the person behind the counter assured them it was the same. Blood level of vitamin D to confirm: right back down to the starting level or near it--little or no absorption.

The only way to know whether a preparation is absorbed is to check a blood level. But, in my experience, having checked vitamin D blood levels thousands of times, gelcaps never fail; tablets fail over 80% of the time.

Vitamin D for the pharmaceutically challenged

Most Heart Scan Blog readers already know:

Your doctor has been brainwashed by the pharmaceutical industry.

Your doctor more than likely has spent the better part of his or her career in the Guantanamo Bay of healthcare, water-boarded by seductive sales representatives, enticed with promises of fame and riches, threatened with ostracism from the clubby internal halls of healthcare if--gasp!--he or she didn't subscribe to the "rule" that only drugs are good, anything else is bad.

The same FDA-approval-is-necessary-to-be-good brand of nonsense is gaining popularity among my colleagues who, having caught some mention (on the Today Show, Oprah, or similar source of medical information), hope to join the vitamin D hoopla.

People will proudly declare that they are taking a high dose of vitamin D: 50,000 units once per week.

No. They are taking a barely useful form: D2, ergocalciferol.

Studies examining the reliability of the D2 form differ:

There's the Heaney study suggesting that D2 is less effective than D3:
Vitamin D2 is much less effective than vitamin D3 in humans

Then there's the Holick study showing they are equivalent:
Vitamin D2 is as effective as vitamin D3 in maintaining circulating concentrations of 25-hydroxyvitamin D.

My experience is more in line with the Heaney study: Little or no real effect with D2.

One particularly illustrative case I witnessed was a woman who was mistakenly prescribed D2 at 50,000 units per day. She told me that she'd been taking it for a year. I fully expected to see clear-cut signs of toxicity (e.g., high blood calcium levels). Curiously, she showed no signs of toxicity. Nor did she show any vitamin D at all in her blood: 25-hydroxy D level of zero--literally zero.

I've witnessed similar phenomena several times: plenty of vitamin D2 . . . very little vitamin D in the blood.

All in all, I suppose that D2 is better than No-D at all. But you are far better off joining the ranks of the pharmaceutically challenged and go with the stuff that really works: D3.

D3, or cholecalciferol, yields confident increases in blood levels. It is inexpensive, safe, and an exact copy of the human form of vitamin D. (Of course, gelcap or drops only, NEVER tablets.)

There is absolute NO reason to take vitamin D2, the form that sometimes works, sometimes doesn't, the facsimile plant form issued by the drug industry.

Why don't stents prevent heart attack?



No study has ever documented that stents prevent future heart attack. But, in day-to-day practice, stents are frequently implanted for just this reason.

A little clarification. Stents do prevent heart attack--if the heart attack is already underway, either as an "acute myocardial infarction" or "unstable angina."

In other words, a plaque in a coronary artery can rupture just like a little volcano. Rather than spewing lava, the underlying plaque contents--fibrous tissue, inflammatory cells, cholesterol crystals, fatty material, debris--are exposed to flowing blood and trigger spasm of the artery and blood clot formation. A ruptured plaque is typically found in people who go to the emergency room with severe chest pain or have difficulty breathing.

A heart catheterization is performed, a severe (e.g., 90-100%--completely closed) is found. A stent in this situation is of clear-cut benefit.

What is not clearly beneficial is someone with no symptoms, symptoms only with physical activity that has been present for at least several months, or someone with a high heart scan score and no symptoms. In these circumstances, stent implantation does not reduce risk for future heart attack.

Why?



Take a look at this angiogram of a right coronary artery. You can seen plaque all along the artery (represented by areas that appear pinched off. There are at least 4 visible.)

Putting one 15 millimeter stent in the artery will only affect the area of artery stented. (Stents vary in length, but typically are 12-18 millimeters in length.) The right coronary artery is about 10 times or more this length. There are also two other arteries of similar length. A stent at one location will do nothing to affect the potential for rupture in any of the other plaque-laden areas.

Say a stent is implanted in the "worst" blockage in this right coronary artery, the plaque located at around 9 o'clock. What about all the other plaques? They can still rupture.

Why not put in many stents, say, 4 or 5, and stent all the visible plaques?

Two reasons: 1) Plaque you can't even see on an angiogram can still rupture, and 2) it is very costly (easily $30,000 at the very least), 3) incurs greater procedural risk, and 4) messes up the artery for future procedures, since a steel-lined artery that develops more disease in future will be more difficult to re-implant stents, bypass, or perform other procedural manipulations.

The point: Putting in stents does not reduce potential for plaque rupture in the entire artery.

What can prevent plaque rupture? That's the whole point of following an effective prevention program: prevent plaque rupture.

(Of course, this discussion cannot encompass the wide variety of potential situations that may cause your doctor to individualize your approach. Nonetheless, when advised to have an elective heart procedure, a healthy dose of skepticism and is clearly a good practice.)

Top image courtesy National Heart, Lung, and Blood Institute.

Low thyroid: What to do?

I've gotten a number of requests for solutions on how to solve the low thyroid issue if either 1) your doctor refuses to discuss the issue or denies it is present, or 2) there are government mandates against thyroid correction unless certain (outdated) targets are met.

Oh, boy.

While I'm not encouraging anyone to break the laws or regulations of their country (and it's impossible to generalize, with readers of this blog originating from over 30 countries), here are some simple steps to consider that might help you in your quest to correct hypothyroidism:

--Measure your body temperature--First thing in the morning either while lying in bed or go to the bathroom and measure your oral temp. Record it and, if it is consistently lower than 97.0 degrees (Fahrenheit), show it to your doctor. This may help persuade him/her.(You can still be hypothyroid with higher temperatures, but if low temperatures are present, it is simply more persuasive evidence in favor of treatment).

--Supplement with iodine 150 mcg per day to be sure you are not iodine deficient. This is becoming more common in the U.S. as people avoid iodized salt. It is quite common outside the U.S. An easy, inexpensive preparation is kelp tablets.

--Show your doctor a recent crucial study: The HUNT Study that suggests that cardiovascular mortality begins to increase at a TSH of only 1.5 or greater, not the 5.5 mIU usually used by laboratories and doctors.

--Ask people around you whether they are aware of a health practitioner who might be willing to work with you, or at least have an open mind (sadly, an uncommon commodity).

Also, see thyroid advocate and prolific author, Mary Shomon's advice on how to find a doctor willing to work with you. Yes, they are out there, but you may have to ask a lot of friends and acquaintances, or meet and fire a lot of docs. It shouldn't be this way, but it is. It will change through public pressure and education, but not by next week.

Another helpful discussion from Mary Shomon: The TSH Normal Range: Why is there still controversy? You will read that even the endocrinologists (a peculiarly contentious group) seethingly debate what constitutes normal vs. low thyroid function.

Also, you might remind a resistant health practitioner that guidelines are guidelines--they are not laws that restrain anyone. They are simply meant to represent broad population guidelines that do not take your personal health situation into consideration.

Which statin drug is best?

I re-post a Heart Scan Blog post from one year ago, answering the question: Which statin drug is best?

I still get this question from patients in the office and online, nearly always prompted by a TV commercial. So let me re-express my thoughts from a year ago, which have not changed on this issue.


The statin drugs can indeed play a role in a program of coronary plaque control and regression.

However, thanks to the overwhelming marketing (and lobbying and legislative) clout of the drug manufacturing industry, they play an undeserved, oversized role. I get reminded of this whenever I'm pressed to answer the question: "Which statin drug is best?"

In trying to answer this question, we encounter several difficulties:

1) The data nearly all use statins drugs by themselves, as so-called monotherapy. Other than the standard diet--you know, the American Heart Association diet, the one that causes heart disease--it is a statin drug alone that has been studied in the dozens of major trials "validating" statin drug use. The repeated failure of statin drugs to eliminate heart disease and associated events like heart attack keeps being answered by the "lower is better" argument, i.e., if 70% of heart attacks destined to occur still take place, then reduce LDL even further. This is an absurd argument that inevitably encounters a wall of limited effects.

2) The great bulk of clinical data examining both the incidence of cardiovascular events as well as plaque progression or regression have all been sponsored by the drug's manufacturer. It has been well-documnted that, when a drug manufacturer sponsors a trial, the outcome is highly likely to be in favor of that drug. Imagine Ford sponsors a $30 million study to prove that their cars are more reliable and safer. What is the likelihood that the outcome will be in favor of the competition? Very unlikely. Such is human nature.

If we were to accept the clinical trial data at face value and ignore the above issues, then I would come to the conclusion that we should be using Crestor at a dose of 40 mg per day, since that was the regimen used in the ASTEROID Trial that achieved modest reversal of coronary atherosclerotic plaque by intravascular ultrasound.

But I do not advocate such an ASTEROID-like approach for several reasons:

1) In my experience, nobody can tolerate 40 mg of Crestor for more than few weeks, a few months at most. Show me someone who can survive and tolerate Crestor 40 mg per day and I'll show you somebody who survived a 40 foot fall off his roof--sure, it happens, but it's a fluke.

2) The notion that only one drug is necessary to regress this disease is, in my view, absurd. It ignores issues like hypertension, metabolic syndrome, inflammatory phenomena, lipoprotein(a), post-prandial (after-eating) phenomena, LDL particle size, triglycerides, etc. You mean that Crestor 40 mg per day, or other high-intensity statin monotherapy should be enough to overcome all of these patterns and provide maximal potential for coronary plaque reversal? No way.

3) Plaque reversal can occur without a statin agent. While statin drugs may provide some advantage in the reduction of LDL, much of the benefit ends there. All of the other dozens of causes of coronary atherosclerotic plaque need to be addressed.

So which statin is best? This question is evidence of the brainwashing that has seized the public and my colleagues. The question is not which statin is best. The question should be: What steps do I take to maximize my chances of reversing coronary atherosclerotic plaque?

The answer may or may not involve a statin drug, regardless of the subtle differences among them.

Dr. Nancy Sniderman, heart scans on Today Show

While shaving this morning, I caught the report by NBC medical expert, Dr. Nancy Sniderman, about her coronary plaque and CT coronary angiogram.




Those of you in the Track Your Plaque program or who follow The Heart Scan Blog know that we should tell Dr. Sniderman and her doctor that:

She has done virtually nothing that will stop an increasing heart scan score! In fact, Dr. Sniderman is now following the "prevention program" that is eerily reminiscent of Tim Russert's program! We all know how that turned out.

It is pure folly to believe that a combination of Lipitor, exercise, and a "healthy diet" (usually meaning a low-fat diet--yes, the diet that promotes heart disease) will stop the otherwise relentless increase in heart scan score.

Dr. Sniderman, please consider:

1) Having the real causes of your coronary plaque identified. (It is highly unlikely to be just LDL cholesterol, though the drug industry is thrilled that you believe this.)

2) Ask yourself (or, if your doctor knew what she was doing, ask her): Why do I have heart disease? LDL cholesterol is insufficient reason--virtually nobody I know has high LDL cholesterol as the sole cause. LDL cholesterol is, at most, one reason among many others, but is insufficient as a sole cause.

3) What is your vitamin D status? Crucial!

4) What is your thyroid status?

5) Fish oil--a must!

6) Do you have lipoprotein(a)? Small LDL?

Just addressing the items on the above checklist would put you on a far more confident path to stop your heart scan score from increasing.

If you were to repeat your heart scan score, my prediction: Your score will be higher by 18-24% per year.

My personal experience with low thyroid

Something happened to me around October-November of last year.

I usually feel great. Ordinarily, my struggles are sleeping and relaxing. As with most people, I have too many projects on my schedule, though I find my activities stimulating and fascinating.

I blasted through a very demanding November, trying to meet the needs of a book publisher. This involved sleeping only a few hours a night for several days on end, all after a full day of office practice and hospital duties.

But it was getting tougher. My concentration was becoming more fragmented. Getting things done was proving an elusive goal. Exercise became a real chore.

Although I usually force myself to go to sleep, I was starting to fall asleep before my usual bedtime, and I was sleeping longer than usual.

It's been a tough winter in Wisconsin. Let's face it: It's Wisconsin. But it's been tough even for this region, with weeks of temperatures consistently below 10 degrees. Even so, I was having a heck of a time keeping warm. Extra shirts, socks, soaking my hands in hot water--none of it worked and I was freezing.

So I had my thyroid values checked:

Free T3: 2.6 pg/ml (Ref 2.3-4.2)
Free T4: 1.20 ng/dl (Ref 0.89-1.76)
TSH: 1.528 uUI/ml (Ref 0.350-5.500)


Normal by virtually all standards. I measured my first morning oral temperature: 96.1, 96.3, 95.9. Hmmmm.

My experience coincided with the Track Your Plaque and Heart Scan Blog conversations about low thyroid being enormously underappreciated, with the newest data on thyroid disease suggesting that a TSH for ideal health is probably 1.5 mIU or less. (More about that: Is normal TSH too high? and Thyroid perspective update .

Could this simply be a case of medical student-oma in which every beginning medical student believes he has every disease he learns about?

Despite the apparently "normal" thyroid blood tests, I took the leap and started taking Armour thyroid, beginning at 1/2 grain (30 mg), increasing to 1 grain (60 mg) after the first week.

Within 10 days, I experienced:

--Dramatic restoration of the ability to concentrate
--A boost in mood. (In fact, the last few blog posts before I replaced thyroid reflect my deepening crabbiness.)
--Large increase in energy, now restored to old levels
--Need for less sleep
--I'm warm again! (It's still <20 degrees, but I get easily stay warm while indoors.)

I am absolutely, positively convinced of the power of thyroid. I am further convinced from the clinical data, patient experiences, and now my own personal experience, that low levels of hypothyroidism are being dramatically underappreciated and underdiagnosed.

I shudder to think of what my life would have been like 6 months or a year from now without correction of thyroid hormone.

Now, the tough question: Why the heck is this happening to so many people?

Speaking availability

Just a quick announcement:

If you would like to hear more about the concepts articulated in The Heart Scan Blog or in the Track Your Plaque program, I am available to speak to your group.

Among the possible topics:

Return to the Wild: Natural Nutritional Supplements That Supercharge Health
Why this apparent "need" for fish oil and other heart-healthy supplements? I discuss why some nutritional supplements make perfect sense when we are viewed in the context of primitive humans living modern lives, while other supplements do little.


Shrink Your Tummy . . .or, Why Your Dietitian is Fat!
Weight loss doesn't have to involve calorie counting, deprivation, or hunger pangs. But the conventional "rules" for weight loss and health have to be broken.

The Politically Incorrect Guide to Extraordinary Heart Health
Heart health is something that you can seize control over, something identifiable, correctable, and . . . reversible. Much of this can be achieved with little or no medication, nor procedures. I detail all the enormously empowering lessons learned through the Track Your Plaque program.


I can also present in-depth yet entertaining discussions on the power of vitamin D, natural cholesterol control, screening for heart disease, and similar topics covered in the blog.

To learn more, just e-mail us at contact@trackyourplaque, or call my office at 414-456-1123.

Learn how to eat from Survivorman


Look no farther than Discovery Channel to learn how humans were meant to eat.

The Survivorman show documents the (self-filmed) 7-day adventures of Les Stroud, who is dropped into various remote corners of the world to survive on little but ingenuity and will to live. Starting without food or water, the Survivorman scrapes and scrambles in the wilderness for essentials to survive in habitats as far ranging as the Ecuadorian rainforest to sub-arctic Labrador.

What does Survivorman have to do with your nutrition habits?

Everything. The lessons we can learn by watching this TV show are plenty.

Survivorman plays out the life we are supposed to be living: slaughtering wild game with simple handmade tools and his bare hands, identifying plants and berries that are safe to eat, trapping fish, scavenging the kill of other predators. He's even resorted to eating bugs and caterpillars, particularly following several days of unsuccessful hunting and scavenging.

What is notable from the Survivorman experience is what is absent: In the steppe, desert, tundra, or jungle, you will not find bread, fruit drinks, or Cheerios. You won't find farm-fattened, corn-fed livestock with meat marbled with fat.

Imagine the result of such an experience for us, drawn out over 6 months. Even an obese, diabetic, gluttonous, XXX dress size 350-lb woman would return a lean 105 lbs, size 0, non-diabetic, fully able to run miles in the wild tracking game.

Survivorman's quiet desperation of living in the wild, preoccupied with worries over where his next meal might be found, is a stark contrast to the bloated, shelves stacked floor-to-ceiling supermarkets, and our modern society's all-you-can-eat several times per day lifestyle.

Am I advocating selling the car and house and chucking modern society for the "safety" of the jungles of Borneo?

No, of course not. I am advocating taking a lesson from the clever experiment conducted by Mr. Stroud, a return-to-the-wild experience that should teach us something about how perverse our modern nutritional lives have become.
All posts by william-davis

Indian buffet

I took my family to a local all-you-can-eat Indian buffet. It was delicious.

I confined my food choices mostly to vegetables and soups. Within about 30 minutes, I started to get that odd buzz in my head that usually signals a high blood sugar.

When I got home, my fingerstick blood glucose: 173 mg/dl. Darn it! Must have been cornstarch or other sugars in the sauces.

I got on my supine stationary bike and pedaled for 40 minutes at a moderate pace while I played Modern Warfare on XBox. (A great way, by the way, to fit in some low- to moderate-intensity exercise while occupying your brain. My wife often has to yell at me to get off, it's so much fun.)

Blood glucose at the conclusion of exercise: 93 mg/dl-- a nice 80 mg/dl drop.

This is a useful strategy to use in a pinch when you've either been inadvertently exposed to more carbohydrate than you can tolerate, or if you'd like to blunt the adverse glucose effects of a bowl of ice cream or other carbohydrate indulgence.

Should we explore the idea of a "morning-after" pill, or actually a "meal-after" pill, a supplement pill or liquid that blunts or eliminates the blood glucose rise after a meal? I've considered such an idea, but have been fearful that people would start to use it habitually. Thoughts?

American Heart Association diet makes a monkey out of you

Heart Scan Blog reader, Roger, brought this New York Times article to my attention.

In an effort to develop a better experimental model for obesity than mice, scientists have turned to monkeys and other primates. The emerging observations are eerily reminiscent of what you and I witness just by going to the local grocery store or fast food outlet:

"'It wasn’t until we added those carbs that we got all those other changes, including those changes in body fat,' said Anthony G. Comuzzie, who helped create an obese baboon colony at the Southwest National Primate Research Center in San Antonio."

"Fat Albert, one of her monkeys who she said was at one time the world’s heaviest rhesus, at 70 pounds, ate “nothing but American Heart Association-recommended diet,” she said."

Yes, indeed: The American Heart Association diet makes monkeys fat. Extrapolate this a little higher on the evolutionary ladder and guess what?

This is one of the many reasons why, when I have a patient who is counseled by the hospital dietitian on the American Heart Association diet, I advise them to 1) ignore everything the dietitian told them, and then 2) follow the wheat-free, cornstarch-free, sugar-free, whole food diet I advocate.

Not unexpectedly, much of this primate research is not being devoted to just manipulating diet to achieve weight loss and health, but to develop new drugs to "treat" obesity.

Would you like a banana?

Construct your glucose curve

In a previous Heart Scan Blog post, I discussed how to make use of postprandial (after-meal) blood sugars to reduce triglycerides, reduce small LDL, increase HDL, reduce blood pressure and inflammatory measures, and accelerate weight loss.

In that post, I suggested checking blood glucose one hour after finishing a meal. However, this is a bit of an oversimplification. Let me explain.

A number of factors influence the magnitude of blood glucose rise after a meal:

--Quantity of carbohydrates
--Digestibility of carbohydrates--The amylopectin A of wheat, for example, is among the most digestible of all, increasing blood sugar higher and faster.
--Fat and protein, both of which blunt the glucose rise (though only modestly).
--Inclusion of foods that slow gastric emptying, such as vinegar and fibers.
--Body weight, age, recent exercise

Just to name a few. Even if 10 people are fed identical meals, each person will have a somewhat different blood glucose pattern.

So it can be helpful to not just assume that 60 minutes will be your peak, but to establish your individual peak. It will vary from meal-to-meal, day-to-day, but you can get a pretty good sense of blood glucose behavior by constructing your own postprandial glucose curve.

Say I have a breakfast of oatmeal: slow-cooked, stoneground oatmeal with skim milk, a few walnuts, blueberries. Blood glucose prior: 95 mg/dl. Blood glucose one-hour postprandial: 160 mg/dl.

Rather than taking a one-hour blood glucose, let's instead take it every 15 minutes after you finish eating your oatmeal:


In this instance, the glucose peak occurred at 90-minutes after eating. 90-minute postprandial checks may therefore better reflect postprandial glucose peaks for this theoretical individual.

I previously picked 60-minutes postprandial to approximate the peak. You have the option of going a step better by, at least one time, performing your own every-15-minute glucose check to establish your own curve.

Why is type 1 diabetes on the rise?

Type 1 diabetes, also called "childhood" or "insulin-dependent" diabetes, is on the rise.

Type 2 diabetes, or "adult," diabetes, is also sharply escalating. But the causes for this are easy-to-identify: overconsumption of carbohydrates and resultant weight gain/obesity, inactivity, as well as genetic predisposition. A formerly rare disease is rapidly becoming the scourge of the century, expected to affect 1 in 3 adults within the next several decades.

Type 1 diabetes, on the other hand, generally occurs in young children, not uncommonly age 3 or 4. Type 1 diabetes also shares a genetic basis to some degree. But the genetic predisposition should be a constant. Obviously, lifestyle issues cannot be blamed in young children.
Then why would type 1 diabetes be on the rise?

For instance, this study by Vehik et al from the University of Colorado documents the approximate 3% per year increase in incidence in children with type 1 diabetes between 1978 and 2004:


(From Vehik 2007)

(For an excellent discussion of the increase in type 1 diabetes in the 20th century, see this review.)

This is no small matter. Just ask any parent of a child diagnosed with type 1 diabetes who, after recovering from hearing the devastating diagnosis, then has to stick her child's fingers to check glucose several times per day, mind carefully what he or she eats or doesn't eat, watch carefully for signs of life-threatening hypoglycemic episodes, not to mention worry about her child's long-term health. Type 1 diabetes is a life-changing diagnosis for both child and parents.

Various explanations have been offered to account for this disturbing trend. Some attribute it to the increase in breast feeding since 1980 (highly unlikely), exposure to some unidentified virus, or other exposures.

I'd like to offer another explanation: wheat.

Lest you accuse me of becoming obsessed with this issue, let me point out the four observations that lead me to even consider such an association:

1) Children diagnosed with celiac disease, i.e., the immune disease of wheat gluten exposure, have 10-fold greater likelihood of developing type 1 diabetes.

2) Children diagnosed with type 1 diabetes are 10-fold more likely to have abnormal levels of antibodies (e.g., transglutaminase antibodies) to wheat gluten.

3) Experimental models, such as in these mice genetically susceptible to type 1 diabetes, showed a reduction of type 1 diabetes from 64% to 15% with avoidance of wheat.

4) The increase in type 1 diabetes corresponds to the introduction of new strains of wheat that resulted from the extensive genetics research and hybridizations carried out on this plant in the 1960s. In particular, unique protein antigens (immune-provoking sequences) were introduced with the dwarf variant attributable to alterations in the "D" genome of modern Triticum aestivum.

Proving the point is tough: Would you enroll your newborn in a study of wheat-containing diet versus no wheat, then watch for 10 years to see which group develops more type 1 diabetes? It is a doable study, just a logistical nightmare. Perhaps the point will be settled as more and more people catch onto the fact that modern wheat--or this thing we are being sold called "wheat"--is a corrupt and destructive "foodstuff" and eliminate it from their lives and the lives of their young children from birth onwards. Then a comparison of wheat-consuming versus non-wheat-consuming populations could be made. But it will be many years before this crucial question is settled.

Yet again, however, the footprints in the sand seem to lead back to wheat as potentially underlying an incredible amount of human illness and suffering. Yes, the stuff our USDA puts at the bottom, widest part of the food pyramid.

Apo E4 and sterols: Lethal combination?

Phytosterols, or just "sterols" to its friends and neighbors, are a group of cholesterol-like compounds that are abundant in the plant world. Lately, however, sterols have proliferated in the processed food supply, thanks to the observation that sterols reduce LDL cholesterol when ingested by humans.

This must mean that sterols are good for you.

Uh oh. Wait a minute: There is a rare disease called sitosterolemia in which there is unimpeded intestinal absorption of all sterols ingested through diet. They must have really low LDL cholesterols! Nope. They develop coronary disease--heart attacks, angina, etc.--in their late teens and 20s. In other words, if sterols gain access to your bloodstream, they are bad. Very bad.

Conventional thinking is that only a modest quantity of dietary sterols gain access to the bloodstream. But there are two potentially fatal flaws in this overly simplistic line of thinking:

1) What happens when you load up your diet with "heart healthy" sterols, such as those in "heart healthy" margarines, mayonnaise, and yogurt, effectively increasing sterol intake 10-fold?

2) What happens in people with the genetic pattern, apo E4, that is carried by 25% of the general population that permits much greater intestinal absorption of sterols?

My prediction: Despite the fact that sterols reduce LDL, they may, in certain genetically-susceptible people, such as those with apo E4, increase risk for heart disease: heart unhealthy.

Here are two studies that suggest that greater sterol absorption in people without sitosterolemia are at higher risk for heart disease:

Alterations in cholesterol absorption/synthesis markers characterize Framingham offspring study participants with CHD

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

Glucomania

As I suggested in a previous Heart Scan Blog post, a glucose meter is your best tool to:

1) Lose weight
2) Cure diabetes
3) Reduce or eliminate small LDL particles
4) Achieve anti-aging or age-slowing effects


But it means getting hold of a glucose meter and applying it in a very different way.

Diabetics typically check fasting morning glucose and again several times during the day to assess medication effects. But you and I can measure blood glucose to assess the immediate effects of food choices--two very different approaches.

The concept is simple: Check a blood glucose just prior to a food or meal of interest, then one hour after finishing.

Let's take two hypothetical breakfasts. First, oatmeal, a so-called "low-glycemic index" food. Slow-cooked, stone ground oatmeal with skim milk, a handful of walnuts, just a few blueberries.

Blood glucose just prior: 95 mg/dl
Blood glucose one hour after finish: 175 mg/dl

I made those numbers up, but this is a fairly typical response for many adults. (This is why "low-glycemic index" is an absurd notion.) This kind of response causes 1) glycation, the adverse effects of glucose modification of proteins that leads to cataracts, kidney disease, cartilage damage and arthritis, atherosclerosis, skin wrinkles, etc., 2) high insulin response that cascades into fat deposition, especially visceral fat ("wheat belly"), and 3) glucotoxicity, i.e., direct damage to the pancreas that can, over years, lead to diabetes.

Next day, let's try a breakfast of 3-egg omelet made with green peppers, sundried tomatoes, and olive oil.

Blood glucose just prior: 95 mg/dl
Blood glucose one hour after finish: 93 mg/dl

This is a meal of virtually zero-glycemic index. This kind of response triggers none of the effects experienced following the oatmeal. Repeated over time and you fail to trigger glycation, you stop provoking insulin, and visceral fat mobilizes rather than accumulates: you lose weight, particularly around the middle.

We therefore aim to keep the one-hour blood glucose 100 mg/dl or less. If you start with a high fasting blood glucose of, say, 118 mg/dl, then we aim to keep the one-hour after-eating blood glucose no higher than the pre-meal.

It works. Plain and simple.

This makes the primary care docs crazy: "How dare you check your blood sugar! You're not diabetic." In truth, blood glucose meters are relatively simple devices to use. The test strips and lancets will cost a few bucks. (The meters themselves are either low-cost or free, just like Gillette sometimes sends you a beautiful new razor for free but expects you to buy the blades). These are direct-to-consumer products. While a prescription written by your doctor for a glucose meter and supplies helps insurance cover the costs, you can easily get these devices without a prescription. Some stores, like Target, keep their devices out on the shelves with the shampoo and bath soap.

Warning: Anyone taking diabetes drugs will have to consult with their doctors about the safety of such an approach. Because this approach can actually cure diabetes in some people, if you are taking some diabetes drugs, especially glyburide, glipidize, and glimepiride, you can experience dangerously low blood sugars, just as any non-diabetic taking these drugs would.

Diarrhea, runny noses, and rage: Poll results

Here are the results of the week-long poll asking the question:

Have you experienced a wheat re-exposure syndrome?
Yes, undesirable gastrointestinal effects 223 (41%)

Yes, asthma or sinus problems 51 (9%)

Yes, joint pains and/or swelling 85 (15%)

Yes, emotional or other nervous system effects 59 (10%)
No, nothing, nada  107 (19%)

No. Wheat is sacred and you're all nuts  13 (2%)


There are several interesting observations to make from this informal poll. First, as I have observed, the most common wheat re-exposure syndrome is gastrointestinal, usually involving cramps, diarrhea, and lame explanations to your dinner partner.

Second most common: joint pains and/or swelling.

Third: asthma or sinus congestion.

The incidence of emotional or nervous system effects surprised me a bit. I didn't expect 10% of people to share this effect. This is an effect I also experience personally, along with the gastrointestinal consequences.

To be sure, this is a skewed poll, since many people likely come to this blog in the first place because of such issues. But I was nonetheless impressed with the relatively modest proportion of people who did not share such a re-exposure syndrome: only 19%.

Beyond the interesting numbers provided by readers, a good many also provided some fascinating and graphic comments. Here's a sample:




Sassy said:

Reflux -- starts a day later and goes for up to a week. And Bloat:2-5 inches on my waistline in a day, lasting up to three. Miserable. And why, having experienced this once, have I done it often enough to verify the connection with certainty? I am working on that one.



Anonymous said:
Wheat increased hunger with even with only a small amount. Crackers in soup was enough to set it off.

Also, when I was trying to get off wheat, I noticed that 2 eggs and 2 bacon and I could go 5 hours before hunger, or 2 eggs and 2 bacon and toast was good for three hours before hunger. That was the final step to giving up wheat. Now three years and 59 Kg [130 lbs!] loss later, there is no doubt in my mind that wheat is evil, and I do not regard it as suitable for human food. I speculate that it increases ghrelin or cortisol.

Anna said:
For me, in the two years since I began eating Gluten-Free (Low Carb for 6 years), the few times I've had re-exposure to wheat, I've experienced fast onset and intense abdominal pain (known exposure during the daytime) and heartburn, indigestion, intense nausea, and disrupted sleep (exposures during evening meal not discovered until the next day).

My husband wants to think he's fine with wheat (though I know that he has at least one gene that predisposes to celiac), but IMO, he isn't. He eats no wheat at home because that's the default, and he's OK with that. But if he goes out to dinner at a restaurant that serves "good" artisan bread, he will indulge in a few bites (he does restrict his carb intake, so it's still a limited amount). More often than not, he will sleep fitfully on those nights, snore more, and wake in the night with indigestion. He wants to bury his head in the sand and will only acknowledge the discomfort being due to eating too many carbs, not the wheat itself. I notice he sleeps fine if he eats a small amount of potato or rice. Go figure.

Our 12 yo son has been eating GF for two years also. About 6 months into GF, he unknowingly ate wheat a number of times (licorice candy laces at a friend's house), which resulted in outbreaks of canker sores in his mouth each time. He also exhibits mood and behavior changes when he eats wheat, which is what prompted me to test him for gluten intolerance in the first place.

Mark said:
If I go for 3-4 days without wheat, grains or sugar and then go out and binge on a pizza and ice cream or something like that I become explosive within 20 minutes to an hour. It's like a wheat and sugar rage.(I'm not saying this is an excuse for rage, I'm saying it has happened to me and I believe partly do to re-exposure) It seems the combination of the wheat plus sugar can be the worst.

I get red rashes around my neck sometimes right away and sometimes up to a day or later and sometimes get bad diarrhea. 
I think it can be almost dangerous to cut things like gluten and sugar suddenly out of the diet without being very serious about keeping them out. I have found it very hard to cut out wheat without binging on it later after 4 or 5 days. I don't believe that my symptoms are just psychological either.

I was also diagnosed with ADHD as a young kid and then rediagnosed with adult ADHD by 3 different doctors. I also have bouts of mania at times too. I am considering trying to go completely gluten/refined carbohydrate free to see if it helps with the symptoms and gives me some relief.

I have never been tested for celiac or gluten intolerance but I would like to be. I think it would help explain to my girlfriend, family and friends why I can't go out and eat pizza or have a beer or ice cream. Right now they all think I'm a hypochondriac. At times I have experienced an intense fatigue the next day like I can't wake up and also sharp pains in my body and headaches.

Anonymous said:
I ditched wheat a year ago after my wife was diagnosed celiac. I immediately experienced a number of health improvements (blood lipids, sleep, allergies, etc.).

Fast forward: We all suffered some inadvertent wheat exposure yesterday via some chocolate covered Brazil nuts (of all things). This accidental A-B-A experimental design resulted in the following:

1. My celiac wife experienced what she calls "the flip" within an hour of exposure (i.e., intense GI distress).
2. My five-year old son went to bed with some wicked reflux.
3. I woke up with some twinges in my lower back and an ache in my football-weary left shoulder. I was also complaining to my wife about fuzzy-headedness that refused to respond to caffeine or hydration. I could only describe it as "carb flu"...

And then I read your post!

Anne said:
Depression, agitation and brain fog if I get glutened. Some times this comes with abdominal pain and a rash on my back - I think it is dose dependent. Cross contamination with wheat is a big issue when eating out. Needless to say, I eat out infrequently and then try to stick with the restaurants that are the most aware of gluten issues.

Terrence said:
Several weeks ago, I started Robb Wolf's 30 day challenge.

The first two weeks were brutal - calling it a withdrawal flu was a massive understatement. So, I thought I would try some wheat and see what happened (could not be worse, I thought). Well, it was.

I still felt extremely crappy, but I was now MASSIVELY GASSY - AMAZINGLY GASSY, for about 48 hours - flatulence on wheels, in spades. I did not go out at all in those 48 hours - when the gas came on, it went out, LONG, and QUICKLY and LOUDLY.

I am easing back into wheat and grain free. I am gluten free today and tomorrow (Sunday and Monday). I expect to try a small amount of wheat on Thursday, then maybe a little more the following Thursday.

Donald said:
I have limited wheat consumption severely over the last 8 months. I have lost 120 pounds, no longer have bouts of illness, asthma, depression, or low energy. I also take vitamin D and other supplements that have helped (many are from your blog recommendations).

Last week I ate a small piece of cake and dessert pizza. Shortly thereafter I started sneezing, had a scratchy throat, and runny nose. I called off sick the next day for fear of being contagious. My symptoms subsided quickly and I am now attributing them to the processed flour eaten at my work luncheon. I think it was an allergic reaction since I recall having much more severe symptoms fairly regularly in my wheat eating days. Those were attributed to an "allergy" of unknown origin back then.

John said:
I suffered from Ankylosing Spondylitis, Iritis, Plantar Fasciits, etc for a number of years. I restricted carbs, especially wheat and I've been symptom free for the past two years now.

Lori said:
I found wheat to be one of the worst things for giving me gas bloating and acid reflux, and I'd had sinus and nasal congestion my whole life. When I ate that cookie, it just re-introduced old problems. I can occasionally eat a gluten-free, grainy goody at my party place without any side effects. I also have a little sprouted rice protein powder every day.

Another odd thing about wheat: it was hard for me to stop eating it once I started. I could go through a whole box of cookies in one sitting, even though I wasn't a binge eater. But I can have a couple of gluten-free cookies and stop.

Paul said:
Except for one slip up this recently past holiday season, I've been sugar-grain-starch free since July 2008. Mental fog was the most noticable re-exposure symptom I had.

My mom has had the worst acid-reflux for 40-plus years. It had become so bad that she was on three medications just to deal with the symptoms. After much training and coaxing, I finally got across to her 
how to totally get off wheat. Not at all to my surprise, after being wheat free for a few weeks, she lost weight and her acid reflux was GONE!

But she had been addicted to wheat for so long, she relapsed, and the reflux fire soon returned. Wheat must be akin to heroin with some people. Even though they know it's very bad for them, they can't help themselves.

Onschedule said:
Re-exposure often leads to diarrhea for me, or such a heavy feeling of tiredness that all I can do is lay down and pass out. A local pizzeria makes a darn good pie, but since I started practicing wheat-avoidance, I can't keep my eyes open after eating there. I can't say for sure that it's the wheat causing it, but definitely something in the crust. Diarrhea, on the other hand, is definitely triggered by the wheat for me.

My mom complained of gastric reflux for years, but never filled the prescriptions that her doctors would give her. I suggested wheat-avoidance- gastric reflux disappeared within 3 days and hasn't returned (has been 6 months now). I've already commented elsewhere on this blog about how much weight and bloating she has lost...

Steve said:
Interesting that I should sit down, turn on my computer and find your poll. Having gone several weeks, maybe months, avoiding gluten, I took my daughter and her boyfriend out to eat because my wife has been working late at the office lately. Although I was thinking I would just eat my steak and chicken, I succumbed to the temptation of eating about a dozen greasy, breaded shrimp that my daughter and her boyfriend ordered. It's 1:39am and I still do not feel sleepy. My left nostril is completely blocked, my stomach feels bloated, really, really full and I've been burping. In your poll I checked sinus problems but could have chose gastrointestinal or nervous problems just as well. 


A few weeks ago my daughter brought home a pizza and, once again, despite my knowing that I shouldn't, I ate a couple of pieces. I was sick for two days. The pain in what I think was my transverse colon was so bad I thought I might have to go to ther emergency room. Before I ate the pizza I had never gone grain-free that long before. I did this after reading Robb Wolf's book. 


I AM CONVINCED. No more wheat for me! Please, Lord, give me strength.

LV said:
What don't I experience! I typically avoid wheat (and gluten for that matter) as I'm pretty sure it makes me sick, but when I slip (or someone else slips me some) I end up with massive amounts of joint swelling and tenderness, diarhea, cramping, gas, bloating and brain fog. I'm absolutely miserable. Just that alone is enough to keep me off gluten. I have RA, so if I have repeated exposures I'll have a flare which SUCKS!

The perfect Frankengrain

Pretend I'm a mad food scientist. I'd like to create a food that:

1) Wreaks gastrointestinal havoc and cause intractable diarrhea, cramps, and anemia.
2) Kills some people who consume it after a long, painful course of illness.
3) Damages the brain and nervous system such that some people wet their pants, lose balance, and lose the ability to feel their feet and legs.
4) Brings out the mania of bipolar illness.
5) Amplifies auditory hallucinations in people with paranoid schizophrenia.
6) Makes people diabetic by increasing blood sugars.
7) Worsens arthritis, such as osteoarthritis and rheumatoid arthritis.
8) Triggers addictive eating behavior.
9) Punishes you with a withdrawal process if you try to remove it from your diet.

I will develop a strain that is exceptionally hardy and tolerates diverse conditions so that it can grow in just about any climate. It should also be an exceptionally high yield crop, so that I can sell it cheaply to the masses.

Now, if my evil scheme goes as planned, I will then persuade the USDA that not only is my food harmless, but it is good for health. If they really take the bait, they might even endorse it, create a diet program around it.

Dag nabit! Such a plan has already been implemented. Another evil food scientist already beat me to the punch. The food is called wheat.

Diabetes: A study in aging

Diabetics experience long-term health difficulties, including atherosclerosis/heart attacks, peripheral vascular disease, hypertension, cataracts, kidney disease, neuropathies, male erectile dysfunction, osteoarthritis, and colorectal cancer. They also die, on average, 10 years earlier than non-diabetics.

In effect, diabetics compress their lives into a shorter period of time. They experience all the "complications" of aging at a younger age. People without diabetes, of course, can develop atherosclerosis, cataracts, kidney disease, etc., but they tend to do so later in life compared to diabetics.

One index of the rate of aging (but not chronologic age itself) is hemoglobin A1c, or HbA1c, a "moving average" of glycated hemoglobin, i.e., glucose-modified hemoglobin. Blood glucose glycates hemoglobin linearly and irreversibly; measuring HbA1c thereby provides an index of the last 60 or so days average blood glucose.

To put HbA1c values into perspective:

Average HbA1c of hunter-gatherers: 4.5%
Average HbA1c for Americans: 5.6%
American Diabetes Association definition of diabetes: 6.5% or greater
American Diabetes Association definition of adequate control of diabetes: 7.0% or less

Why do diabetics age faster? There are likely several reasons. One important reason is glycation, as indexed by HbA1c. Glycated proteins in the lens of the eye causes cataracts. Glycated proteins in cartilage leads to arthritis. Glycated LDL particles (apo B) leads to atherosclerosis. Glycated nerve cells causes neuropathy. And so on.

If glycation underlies many of the phenomena of aging, then we might surmise that:

1) The less you glycate, the slower you age.
2) The more you glycate, the faster you age.

Therefore, the higher the HbA1c, the faster you are aging.

What foods increase HbA1c? Carbohydrates. That bowl of slow-cooked, stone ground oatmeal? A one-hour after-eating blood sugar of 170 mg/dl is common. Your doctor says that's okay because it's below 200 mg/dl and you don't "need" medication yet.

How important is high blood pressure?


Control of blood pressure is crucial for coronary plaque control and stopping your heart scan score from increasing.

Dr. Mehmet Oz (of Oprah fame and a cardiac transplant surgeon at Columbia University) made graphic point of this on the ABC TV news show, 20/20, last evening on an episode called "Our Bodies: Myths, Lies, and Straight Talk". (See a summary on the ABC News 20/20 website at http://abcnews.go.com/2020/story?id=2109291&page=1)

Although I believe he somewhat overstated the case for hypertension (proclaiming "If you're going to remember one number, if you're going to focus and fixate on one number in your entire health profile, it better be your blood pressure"), he made the point that a blood pressure of 115/75 is what you should have for optimal health.

I couldn't agree more. Unfortunately, the old advice that desirable blood is 140/90 or less is absolutely wrong. At this level, we see flagrant increases in heart scan scores. We also progressive enlargement of the thoracic aorta, the large vessel that leaves the heart and branches to provide the major arteries of the body. Growth of the aorta to an aneurysm is also common at these formerly acceptable blood pressure. (The diameter of your aorta in the chest is an easily obtainable measure on your CT heart scan.)

The blood pressure you need for halting and reversing plaque growth on your heart scan is indeed 115/75 or less. (Not so low, however, that you're lightheaded.) This is the blood pressure that you were meant to have evolutionarily. It's also the blood pressure that helps tremendously in keeping your aorta from enlarging.

Watch for an upcoming exhaustive report on blood pressure and its plaque-raising effects and how to reduce it using nutritional strategies on the www.cureality.com membership website.

Is your doctor in cahoots with the hospital?

I got a call from a doctor about a patient we've seen in past.

"I've got Tricia in the office. She's been having some kind of chest and abdominal pain. I think it's esophageal reflux, but just to be safe I'm sending her to the hospital."

I advised this physician that, given Tricia's low heart scan score, she was unlikely to be having a coronary "event" like heart attack or unstable symptoms. It wasn't impossible, but just highly unlikely.

As the patient was without symptoms at the moment and had driven herself to his office, I offered to perform a stress test immediately. (Though stress tests are of limited usefulness in people without symptoms, they can be useful provocative maneuvers in people with symptoms of uncertain significance.)

The doctor declined. Tricia was, after all, in his office and he was responsible for any decisions despite any objections I voiced. Well, Tricia was directed by her doctor to go to a local hospital, though one with an especially notorious reputation for putting virtually anyone they can get their hands on through as many procedures as possible.

As you might guess, this doctor was closely associated with this hospital. He and his colleagues obtain incentives (or are penalized) if they do not generate revenue-producing procedures for the hospital.

So, guess what? Tricia ended up with several procedures, all of which yielded nothing--except $30,000 in revenues from Tricia's insurance company.

I harp on this deplorable state of affairs because it is utterly, painfully, and shamefully TRUE. Just look at the hospital and you'd better brace yourself for a series of tests that could cost you the equivalent of a nice 3 bedroom home. If they were truly necessary after the failure of preventive and other simple efforts, fine. But, all too often, they are driven by profit motives.

Could I have stopped this somehow from occurring? After all, Tricia was reasonably aware of the way we do things around here. I fear that even this failed to serve Tricia well. But I remain hopeful that, as we build broader awareness of these issues, that more and more people and physicians will stand up and refuse to tolerate the status quo.

Where is the Track Your Plaque program going?

I spend a lot of time worrying about how people can be helped to navigate through this program.

Take, for instance, the man in rural Texas who, while traveling in Dallas, got a heart scan on a whim. His score was 990. When he took the report back to his doctor, he got a smirk--and that's all. When he came to the Track Your Plaque program, he lacked a physician advocate to help him.

Or the woman from Florida who sought opinions from two reputable cardiologists for her heart scan score of 377. Both advised her that she needed a heart catheterization--despite her lack of symptoms, her 5-day-a-week exercise program, and normal stress test. She also lacks a physician advocate who acts on her behalf, helping her achieve success, rather than just churning her for money from hospital procedures.

For people like this and for others, I see the Track Your Plaque program evolving in several directions:

1) An online clinic--You enter and we take your "hand" and lead you step by step through the process, not only at the beginning, but over the months and years. This would help clear up some of the confusion and zigzags that some people experience trying to navigate through the program.

2) Develop physician and non-physician partners--The woman in Florida, for instance, could be referred to a doctor nearby who understands the program and is able to assist her. At present, this is virtually impossible because of the bias towards heart procedures, drugs as the sole treatment for heart disease risk, and the superficial physician-patient relationship. The majority of practicing physicians just don't understand the program despite the fact that it is based on sound clinical and experimental data. But it will in time.

Looking back, we've come a long way. I remember first having patients undergo heart scans 10 years ago. My colleagues laughed or called it "silly". The general public didn't know what they meant.

Now we're talking about how to broadcast the most powerful heart disease prevention program available in the world to a larger audience, but making it easier and more accessible. Mass media like Oprah's two hour-long spots helped, but we need to make the next leap. Not just identifying hidden heart disease to feed the hungry cardiovascular hospital procedure monster, but to educate/inform/empower the public on what to do with the scan once they've had it.

Who cares about triglycerides?

Walter's triglycerides were 231 mg. His LDL cholesterol was "favorable" at 111 mg, HDL likewise at 49 mg.

"Everything looks good," his doctor declared.

"Do you think the triglycerides are okay, too?" Walter asked.

"Well, the guidelines do say that triglycerides should be less than 150, but I believe you're close enough. Anyway, triglycerides don't really cause heart disease."


When I met Walter, I made several comments. First of all, in light of his heart scan score of 713, none of his numbers--HDL, LDL, or triglycerides-- were acceptable. But the triglycerides were glaringly and terribly too high.

Why? What exactly are triglycerides?

Triglycerides are a basic fat particle that, though they do not cause heart disease directly, trigger the formation of an array of abnormal lipoprotein particles in the blood that are among the most potent causes of heart disease known.

These abnormal lipoprotein particles include small LDL, VLDL, and IDL (intermediate-density lipoprotein--a really bad pattern). Excess triglycerides also cause HDL to drop. They also cause a distortion of HDL structure, causing the particles to become abnormally small. Small HDL is also useless HDL, unable to provide the protection that HDL is designed to do.

So Walter's elevated triglycerides are, in reality, a substantial red flag for an entire panel of abnormal particles that contribute to the growth of his coronary plaque.

So, if you get this kind of commentary on your triglycerides, ask for another opinion. (Track Your Plaque Members: Also see Triglycerides: Mother of meddlesome particles at http://www.cureality.com/library/fl_dp002triglycerides.asp.)

Total cholesterol and heart scans

Andy was fearful of heart disease in his life. At age 52, he'd already had four CT heart scans--one each year on or near his birthday.

Yet, when I looked at Andy's scans, his scores had been increasing 20-24% per year. Each and every score was greater by 20% or more over the previous.

So I asked Andy what steps he had taken to stop this relentless progression. "Well, I've always been real health conscious. But ever since my first scan, I really started sticking to a healthy diet, exercising nearly every day, and I take a bunch of supplements."

"What did your doctor advise?" I asked.

"Well, Dr. ---- said that nothing needed to be done, since my total cholesterol was always below 200."



Men's Health magazine's fabulous story about the folly of using total cholesterol to gauge heart disease risk.




Aaaauuuggghhh!! Wrong!

This man was, in fact, at rapidly escalating risk for heart attack. This rate of growth simply can't continue forever without igniting this bomb.

A total cholesterol below 200 is meaningless, as Andy's increasing coronary plaque proved. For instance, you can have a total cholesterol of 165 mg but with an HDL cholesterol of 27 mg. This would constitute very high risk for heart disease despite the low total cholesterol. The low HDL pattern is among the most common reasons for a misleading total cholesterol. Small LDL, high triglycerides, and lipoprotein (a) are other frequent reasons.

Andy, run the other way! Do not heed this doctor's advice! You need a solid answer to the question: Why exactly do I have coronary plaque in the first place?

Then, agree on a treatment program that corrects your specific causes.

Cardiologists out of touch

This weekend, I'm fulfilling some responsiblities I have every so often to some of the local hospitals. It gives me a chance to interact with many of my colleagues who are likewise "on call" for the weekend.

I tried to strike up several conversations with colleagues about how they were managing heart disease prevention. I received blank stares, puzzled looks, indifference. One colleague declared that 80 mg of Lipitor is all you need to know.

These same colleagues are the ones scrambling for the heart attack patients in the emergency room, climbing over one another for consultation in the hospital for patients with chest pain and heart failure. They're consumed with expanding the range of procedures they can perform.

Carotid stenting is hot. So is stenting of the leg arteries. Defibrillators have been a financial bonanza. Opportunities abound on how to add these procedures to a cardiologist's abilities.

But heart disease prevention? How about heart disease reversal?

Frankly, I'm embarassed by my colleagues' lack of interest. Imagine we had a cure for breast cancer--not a palliative therapy that just slows the disease down or prolongs life, but actually cures it once and for all. I would hope that all physicians and oncologists would learn how to accomplish this. What if instead they focused on learning new ways to remove breasts, administer new toxic chemotherapies, etc. but ignored the whole idea of cure?

This is what is happening with coronary plaque reversal. The answer is right in front of them, but the vast majority (99%) of cardiologists choose to ignore it. After all, prevention and reversal simply don't pay the bills.

That means that, in 2006, you simply cannot rely on your cardiologist to counsel you on how to achieve regression or reversal of coronary plaque. How about your internist, family physician, or primary care doctor? Well, they're busy doing pneumovax injections, Pap smears, managing knee and hip arthritis, low back pain, diarrhea, headaches, sinus infections and . . yes, dabbling in heart disease prevention.

And, for the most part, doing a miserable job of it. What you generally get echoes the drug manufacturers pitch: Take a statin drug, cut the fat in your diet.

Until the majority of doctors catch on, you're going to have to rely on sources like the Track Your Plaque program for better information.

What if your lipoproteins are perfect?



Sandy is a 56-year old woman--fit, slender, physically active, with no bad habits. A retired teacher, she has time to devote to her health. She bikes several days per week, mountain bikes, walks, and takes fitness classes. In short, she's the picture of perfect health.

Her heart scan score was not terribly impressive: 41. However, at her age, this modest score placed her in the 77th percentile. This suggested a heart attack risk of around 2-3% per year.

So we measured Sandy's lipoproteins. They were shockingly normal. In fact, Sandy is among the very rare person with absolutely no small LDL particles. All other patterns were just as favorable, including an HDL in the 80s.

This may seem like good news, but I find it disturbing. People are often initially upset by seeing multiple abnormal lipoprotein patterns. But lipoprotein abnormalities are the tools that we use to gain control over coronary plaque.

So what do we do when there are no abnormalities?

There are several issues to consider:

1) Your heart scan score reflects the sum total of your life up until that point. What if you were 20 lbs heavier 10 years earlier and your lipoproteins were abnormal during that period? Or you smoked until age 45 and quit? As helpful as they are, lipoproteins and related patterns are only a snapshot in time, unlike the heart scan score.

2) You have a vitamin D deficiency. This is unusual as a sole cause of coronary plaque. Much more commonly, it is a co-conspirator.

3) The heart scan is wrong--highly unlikely. Heart scans are actually quite easy, straightforward tests. (The only time this tends to happen is when scoring that appears in the circumflex coronary artery is actually in the nearby mitral valve. This really occurs only when there's very minimal calcium in the valve.)

4) There's a yet unidentified source of risk. Probably very rare but conceivable. For instance, there's an emerging sense that phopholipid patterns may prove to be coronary risks. One clinically available measure that we've not found very useful is phospholipase A2, known by the proprietary name "PLAC" test. (See http://www.plactest.com for more information from the manufacturer/distributor of the test.) But there's probably lots of others that may prove useful in future.

How often does it happen that someone fails to show any identifiable source for their coronary plaque? I can count the number of instances on two fingers--very unusual. (Thank goodness!)

Sandy's case is therefore quite unique. How should we approach her coronary plaque? In this unusual circumstance, lacking a cause, we tend to introduce therapies that may regress plaque independent of any measurable lipoprotein parameters. But that's a whole new conversation.

Fly to India for a bypass operation?


In the June 19, 2006 issue of People Magazine, there's an article called "The Doctor is in . . .INDIA". The report talks about how, with health care costs in the U.S. spiralling out of control, more and more Americans are leaving the country to have their procedure performed.

They tell the story of Mr. Carlo Gislimberti of New Mexico and cite these numbers:

Heart Surgery
Cost in U.S.: $200,000

Cost in India: $10,000


Mr. Gislimberti opted to have his coronary bypass operation in India for cost reasons.

But the People magazine report left out one other option: The Track Your Plaque program: $39.00

Do your part to save ballooning health care costs: Engage in a truly powerful program of heart disease prevention like the Track Your Plaque program. The cost difference is laughably huge. And you won't require a 12-inch chest incision.

Follow conventional guidelines and guess what? You're going to have a heart attack. Follow the American Heart Association diet and you'll have heart disease.

Cut to the chase. The only program that is able to detect, track, and control coronary plaque better than any other process I know of is this program.

Note: I am not proposing that a heart disease prevention program like Track Your Plaque can replace a procedure like coronary bypass when a dangerous situation has developed. The Track Your Plaque program is designed to be implemented in the years before heart surgery is required. That's when you have the greatest control over your fate.

Surprise: Heart scan score reversal

Gene is a jovial, fun-loving railroad worker who didn't take anything too seriously--including his heart scan score of 767.

This score placed Gene solidly in the 99th percentile (in the worst 1%). It came as no surprise to Gene. After all, his father died at age 36 of a heart attack and Gene's brother died at 60 of a heart attack. So Gene took life as it came and long ago decided not to fret about his fate.

But Gene's wife prodded him and prodded him to get the heart scan. That's when I met him.

Of course, Gene had been prescribed Lipitor by his doctor for a somewhat high LDL cholesterol. Our assessment uncovered several additional patterns including lipoprotein (a), small LDL, a pre-diabetic tendency, and a severe deficiency of vitamin D.

At 224 lb and 5 ft 6 inches in height, I felt that Gene was at least 40 lbs overweight.

One year later and with reasonable correction of all his patterns except weight loss and Gene's heart scan score was 590--a reduction of 23%!

Gene was thrilled, as was I. But, frankly, I was also surprised. Dramatic regression of coronary plaque tends to not occur so readily as long as pre-diabetic patterns persist and weight is not controlled.

The lesson: Often the only way to tell if you've achieved control or regression of coronary plaque is to have another heart scan. The tremendous variation in human responses never ceases to amaze me.

Call me when you're having chest pain


I met a patient, Anna, yesterday. She was quite frustrated and frightened.

At age 50, Anna suffered a heart attack and received a stent to her left anterior descending coronary artery. What she found upsetting is that, because several members of her family had suffered heart attacks in their 40s (Dad--heart attack at age 45, paternal uncle--heart attack age 40, and even another uncle with heart attack in his late 20s), she had repeatedly asked her doctor whether she was okay.

She received the usual array of false assurances: "You're feeling fine, right? Then don't worry about it." "Look. Your cholesterol is in the normal range. Even your cholesterol/HDL ratio is fine." "Women don't get heart disease until later in life."

All proved absolutely false. As we talked, Anna exclaimed, "I think what I've been told all along is that we'll take you seriously when you finally have a heart attack!"

She's exactly right. The vast majority of times, heart disease is discovered by accident, usually because of an "event" like heart attack. This is like changing the oil in your car when it finally breaks down--it's too late.

CT heart scan, followed by lipoprotein testing and associated values, then correction of your specific causes. It's that simple.
All posts by william-davis

Firefighters Face Added Risk of Fatal Heart Attack

Firefighters are twice as likely to die from a heart attack in the line of duty than are policemen, and three times more likely than EMTs.

That's among the headlines run today because of a report in the New England Journal of Medicine documenting a dramatically higher risk for heart attack for fire fighters putting out fires. The above headline is from an excellent report run on NPR radio. You can listen to the webcast at http://www.npr.org/templates/story/story.php?storyId=9047656.

The story sparked comments from experts insisting that all fire fighters should have physicals, should be in better physical condition, should be covered by health insurance (the NPR report said that 1 out of 4 fire fighters lack health insurance). Judging from the indisputable risk firefighters encounter, these are all good ideas.

But if you've been following my blog or the Track Your Plaque program, you know that physicals alone are hopeless exercises for identifying hidden heart disease. Among the solutions: identify whether or not heart disease is present in the first place--do a CT heart scan.

In fact, several local fire companies in my area have done just that: insisting that all firefighters undergo a heart scan. When groups of people like firefighters arrange for heart scans, they gain the advantage of doing so en masse, thereby allowing many scan centers to offer a dramatically reduced price to the city, town, or village that is paying for them. I've even seen many firefighters scanned at no cost.

It would also help to have health insurance, be physically fit, and have a stress test (an exception to my view that stress tests are also useless to screen asymptomatic people for heart disease). But a CT heart scan would settle the question quickly, easily, undeniably, and inexpensively.

Prophylactic bypass surgery?

This question comes up around once a week:

My CT heart scan score is ____. Wouldn't I be better off just getting a bypass (or stent, etc.) and getting it over with? If I know that heart attack is in my future, why not just get it over with?

The most recent source of this question was the wife of a patient. Jack had a heart scan score of 92 in 2005. He made very little effort to correct his causes, permitting pre-diabetic patterns to persist, failed to correct vitamin D, etc. and a repeat heart scan score showed a dramatic rise to 264.

Jack's wife asked whether he should just have a bypass.

There are several problems with this line of reasoning:

1) Bypass surgery does not reduce the long term risk for heart attack.

2) The risk of bypass surgery often outweighs the risk of an asymptomatic heart scan score.

3) Bypass surgery is a temporary "fix," a fancy Band Aid for a disease that progresses after the procedure. One bypass typically prompts another, and another...

4) Bypassing arteries that have vigorous blood flow often causes the bypass graft to not "take" and close within the first few days.


Thankfully, nobody in his right mind has proposed that we perform prophylactic bypass operations.

Of course, hospitals and surgeons would jump at the chance to perform procedures in anybody with some threshhold heart scan score. It would double or triple their business overnight. At $70,000 or more per procedure, they would dance in glee. Of course, you and I would pay for their new burst of wealth by a sharp increase in our health insurance premiums. Not only that, the people who underwent the procedure would not benefit.

Lipitor 80 mg

I'm seeing more and more people taking 80 mg of Lipitor per day. For the most part, these are people who come in for another opinion after a stent or heart attack and are prescribed the drug during their hospitalization.

This practice is based on the results of the PROVE IT-TIMI 22 (PRavastatin Or atorVastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction) trial, and the Reversal of Atherosclerosis with Aggressive Lipid Lowering (REVERSAL) trial, both reported in 2005. In the PROVE IT Trial, 4,000 people experiencing heart attacks were treated with Lipitor (atorvastatin), 80 mg, or Pravachol (pravastatin), 40 mg. There was a reduction in events like recurrent heart attack from 13.1% in the Pravachol group to 9.6% in the Lipitor group. In the REVERSAL Trial, the Lipitor group also showed no plaque growth compared to the Pravachol group, which did progress, with disease tracked by intracoronary ultrasound.

I believe that many of my colleagues took the bait. In a half-hearted effort to reduce events and trend towards better coronary plaque control, writing a prescription for 80 mg rather than a lower dose has become increasingly popular.

Some problems: Despite the favorable tolerance to high dose Lipitor in these trials, I don't know anybody who can tolerate 80 mg per day for more than a few months in real life. In my experience, people inevitably end up with intolerable muscle aches.

Also, I believe it is folly to believe that we can regress coronary plaque on a broad scale by just using one drug that addresses only a single cause (i.e., LDL cholesterol). Yes, drug companies would argue that the statin drugs are so wonderful because of their so-called "pleiotropic", or non-lipid, effects like reducing inflammation. I have seen regression of plaque once using Lipitor alone. We struggle to reduce coronary plaque using a multi-faceted approach. It is highly unlikely that Lipitor alone at a 80 mg dose will be sufficient in most people to regress plaque. How about lipoprotein(a)? Or vitamin D deficiency? Lipitor has no effect on these patterns and people do not regress just by taking statin agents.

Orlistat for weight loss

In early February, the FDA approved orlistat, formerly known as prescription Xenical, for over-the-counter sale. Orlistat is a blocker of fat absorption.

The new OTC version will be called "Alli" (pronounced like "ally") and will come at a dose of 60 mg to be taken three times a day with meals. Prescription Xenical came as a 120 mg tablet. However, the company claims that the reduced dose sacrifices only 5% in reduced fat absorption, dropping from 30% with Xenical to 25% with Alli. It will cost in the neighborhood of $1 to $2 per day, or $30-60 per month, far less expensive than the $110-150 for the prescription form.

Does it work? Is it worth the money? Clinical trials document around 5-10 lbs lost over a 3 to 6 month period, 50% greater than using diet and exercise alone.

Our experience is that it works, though inconsistently. Results depend heavily on how reliant you are on fat calories. If you were to follow a low-fat diet while on the drug, you likely will lose little or no weight, since there's little fat absorption to block. However, I have witnessed more substantial weight loss of 10-20 lbs. in people who follow a higher fat intake in their diet, e.g., a traditional American diet. However, these people gain the weight back immediately because they've made no effort to modify food choices.

It is messy. Even though the clinical trials claims modest inconvenient effects like gas and greasy stools, I have found that it is, without fail, a very annoying product that results in crampiness and frequent messy stools in nearly everybody.

The company has created a glitzy website that you can view at www.myalli.com and promises to provide a personalized program and support for registrants when it is up and running by summer 2007.
I think that's a good idea, since the drug itself is no more than a temporary fix unless it's combined with long-term diet changes. However, the website, I believe, oversells the value of the drug with a drug company's usual over-the-top hints and innuendoes without actually coming out with straight pitches of the truth.

Beware of the vitamin D-blocking effect of Orlistat. The period of time you take it may be a time to resort to some modest sun exposure (10-15 minutes; be careful not to burn), rather than than oil-based vitamin D capsules, in order to avoid the inevitable vitamin D plunge in blood level.

I am not a fan of orlistat, having seen it tried many times with minimal success. However, it is another option for those who are really struggling. Personally, I would try fasting or some of the other strategies we've detailed on the www.cureality.com website before I resorted to orlistat.

Low HDL makes Dr. Friedewald a liar

There's a $22 billion industry based on treating LDL cholesterol, a fictitious number.

LDL cholesterol is calculated from the following equation:

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

So when your doctor tells you that your LDL cholesterol is X, 99% of the time it has been calculated. This is based on the empiric calculation developed by Dr. Friedwald in the 1960s. Back then, it was a reasonable solution, just like bacon and eggs was a reasonable breakfast and a '62 Rambler was a reasonable automobile.

One of the problems with Dr. Friedewald's calculation is that the lower HDL cholesterol, the less accurate LDL cholesterol becomes. If it were just a few points, so what? But what if it were commonly 50 to 100 mg/dl inaccurate? In other words, your doctor tells you that your LDL is 120 mg/dl, but the real number is somewhere between 170 and 220 mg/dl. Does this happen?

You bet it does. In my experience, it is an everyday event. In fact, I'm actually surprised when the Friedewald calculated LDL closely approximates true LDL--it's the exception.

Dr. Friedewald would likely have explained that, when applied to a large population of, say, 10,000 people, calculated LDL is a good representation of true LDL. However, just like saying that the average weight for an American woman is 176 lbs (that's true, by the way), does that mean if you weigh 125 lbs that you are "off" by 41 lbs? No, but it shows how you cannot apply the statistical observations made in large populations to a single individual.

The lower HDL goes, the more inaccurate LDL becomes. This would be acceptable if most HDLs still permitted reasonable estimation of LDL--but it does not. LDL begins to become significantly inaccurate with HDL below 60 mg/dl.

How to get around this antiquated formula? In order of most accurate to least accurate:

--LDL particle number (NMR)--the most accurate by far.

--Apoprotein B--available in most laboratories.

--"Direct" LDL

--Non-HDL--i.e., the calculation of total cholesterol minus HDL. But it's still a calculated with built-in flaws.

--LDL by Friedewald calculation.

My personal view: you need to get an NMR if you want to know what your LDL truly is. A month of Lipitor costs around $80-120. A basic NMR costs less than $90. It's a relative bargain.

Menopause unleashes lipoprotein(a)

Faye was clearly frustrated.

At age 52, she was having chest pains every day. A CT heart scan showed a score of zero. A CT coronary angiogram showed no plaque whatsoever.

"Everything went downhill when my menopause started. I gained weight, I started to have chest pains, my blood pressure went up, my cholesterol shot up."

She saw three physicians, none of whom shed much light on the situation. They ran through the predictable sequence of (horse, not human) estrogens, anti-depressants, suggestions for psychological counseling.

But we checked Faye for lipoprotein(a), which she proved to have at a high level of 182 nmol/l. This explained a lot.

A curious and predictable set of phenomenon occur to females with Lp(a) proceeding through the menopause. As estrogen recedes:

--Lp(a) levels rise dramatically.

--Blood pressure goes up, sometimes creating severe hypertension by mid- to late-50s.

--Chest pain can develop, presumably due to "endothelial dysfunction" or "microvascular angina", both representing abnormal coronary artery constriction facilitated by worsening expression of Lp(a).

All too often, these phenomena get dismissed as simply part of the menopausal package, when they are, in fact, important facets of this very important genetic pattern that confers high risk for heart disease.

If any of this rings familiar for you or a loved one, think Lp(a). Though Faye hadn't yet developed any measurable coronary plaque by her CT heart scan score, it was likely on its way, given the surge in Lp(a) expression as menopause unfolded--unless its recognized and appropriate preventive action taken.

Vitamin D must be oil-based

I've talked about this before, but I need to periodically remind everybody:
Vitamin D must be an oil-based capsule, a gel-cap, not a tablet.

Lisa is one of early success stories: a heart scan score of 447 in her early 40's, modest reduction of CT heart scan score three years ago.

However, Lisa had a difficult time locating oil-based vitamin D. There has, in fact, been a national run on vitamin D and I'm told that even manufacturers are scrambling to keep up with the booming demand. So, she bought tablets instead and was taking 3000 units per day.

She came in for a routine check. Lisa's 25-OH-vitamin D3: 17 ng/ml, signifying severe deficiency, the same as if she were taking nothing at all. (Recall that we aim for 50 ng/ml.)

In other words, vitamin D tablets do not work. It is shameful. I see numerous women taking calcium tablets with D--the vitamin D does not work. I've actually seen blood levels of zero on these preparations.

You may have to look, but if you want to enjoy the extraordinary benefits of vitamin D replacement, it must be an oil-based capsule. Carlson's and Vitamin Shoppe have excellent prepartions. They raise blood levels substantially and consistently, and they're inexpensive. We pay $5.99 for a bottle of 120 capsules.

Vitamin D for $200?

What if vitamin D cost $200 rather than $2?

In other words, what if cholecalciferol, or vitamin D3, was a patent-protectable agent that would sell for an extravagant price, just like a drug?

Vitamin D would be the hot topic. There would be TV ads run during Oprah, slick magazine two-page spreads with experts touting its outsized benefits, insurance companies would battle over how much your copay should be.

The manufacturer would host large fancy symposia to educate physicians on how wonderful vitamin D is for treatment of numerous conditions, complete with dinner, a show, and gifts. They would hire expert speakers to speak, scientists to have articles ghost-written, give out knick knacks with the brand label inscribed--just like Lipitor, Actos, Vytorin, ReoPro, Plavix . . .

After all, what other "drug" substantially increases bone density (up to 20% in adult females), enhances insulin responses 30% (equivalent to the TZD drugs, Actos and Avandia), and slashes colon cancer risk?

But it's not a drug. That is both vitamin D's strength and its weakness. It's a strong point because it's natural, phenomenally helpful across a variety of conditions, and inexpensive. It is also a weakness because, at $2 a month, no one is raking in the $12 billion annually that Pfizer makes for Lipitor that allows it to fund an enormous marketing campaign.

Vitamin D is a "discovery" of huge importance for health, including making reductions of CT heart scan scores far more likely for more people. And it comes without a prescription.

What's up with garlic?


Fanatic Cook has posted an excellent summary on the recent negative attention cast on garlic preparations, at least for LDL cholesterol reduction.

Go to http://fanaticcook.blogspot.com to view.

I think Fanatic Cook is right--despite the lack of LDL reducing effects, it doesn't necessarily mean no benefit whatsoever. Anti-coagulation and anti-inflammatory effects, in particular, are well proven.

I do think, however, that it argues more in favor of sticking to whole cloves, rather than supplements. The benefits are also likely small. I would view garlic as a soft advantage for your plaque control program. You can do fine without it. You might do slightly better with it.

Drop the pretense

Most hospitals maintain the "Saint _____" in their names, despite many having little or nothing to do with the church.

Out of 15 hospitals in my area, 13 are named after saints.

In my view, a more honest name would be something like "ABC Medical Enterprises, Inc." The profit motive, aggressive marketing tactics, and high CEO salaries would make better sense then. The trend to convert practicing physicians from professionals acting on behalf of patient welfare into paid employees would also be clearer.

Imagine Walmart were to change its name to "St. Mary's Emporium" Would it modify your perception of their business? I think it would. It would cause many people to believe that maybe their work was, at least in part, charitable and being done for the public welfare. But Walmart makes such pretense--they are in business for profit, just like all businesses.

It's time for the pretense to be dropped. Hospitals are cut-throat profit-seeking operations, operating under the guise of charitable, tax-free institutions. It's the farthest thing from the truth.