Risks for coronary disease 2008

According to conventional thinking, there are identifiable risks for coronary disease and heart attack. These risk factors are:

* smoking
* high blood pressure
* high blood cholesterol and excessive saturated fat intake
* diabetes
* being overweight or obese
* physical inactivity

I'd agree with all the factors listed (though I would argue about the importance of high blood cholesterol and saturated fat; they are not as important as commonly made to be.)

Is the list complete?

From the unique perspectives gained in the Track Your Plaque program, I'd offer a significantly different list. Trying to stop or reduce coronary atherosclerotic plaque and heart scan scores makes you a whole lot smarter about what works and what doesn't work.

So, in addition to the risk factors listed above, I would add:

* Small LDL particles--Lots of small LDL particles is MORE important than high LDL.
* High blood pressure with exercise
* Excessive wheat intake and other processed carbohydrates--An issue of explosive importance today. Wheat creates large numbers of small LDL particles, among other adverse effects.
* Vitamin D deficiency--Among the most powerful risks I know of. It belongs at the top of the list.
* Vitamin K2 deficiency
* Low HDL cholesterol
* Blood sugar >100 mg/dl
* High triglycerides--While some argue about whether triglycerides are a risk that behaves independently of patterns like low HDL, they are neglecting the potent force of this risk. Sure, it occurs in tandem with low HDL (usually, though not always), but it is a factor that can leave you with risk even when HDL is raised to healthy levels.
* Lipoprotein(a)--It is eminently, positively crystal clear that lipoprotein(a) is a powerful risk for heart disease. The lack of a profitable treatment keeps it hidden in the shadows.
* Pessimism--Be happy, do better. Be a constantly angry, frustrated, complaining sourpuss and you are more likely to succumb to heart disease, cancer, or other undesirable fate.


These are the risk factors that we address through the Track Your Plaque program, a list that yields a far more powerful and comprehensive approach to control over coronary plaque/atherosclerosis, sufficient to achieve reversal in many (though not in all) instances.

I view the list of conventional risk factors as a "no brainer" list. Sure, smoking is a risk factor. But there are virtually no smokers in the Track Your Plaque program. If you smoke, you clearly don't care enough to engage in a high-intensity prevention program like this.

Saturated fat? Perhaps, but the battlefield of heart disease is riddled with the bodies of those who employed this as their sole strategy and failed catastrophically.

Diabetes, hypertension, and overweight all represent a continuum of risk; the solutions offered in the conventional scheme (i.e., low-fat diet, etc.) make these patterns worse, not better.

The conventional response to heart disease risk is trapped somewhere in 1973 and has not changed in over 30 years. Heart disease continues to be a growth industry for hospitals and the pharmaceutical and medical device industries. The "official" organizations continue to deliver an antiquated, outdated message.

If you want heart disease, follow the American Heart Association diet. If you want established heart disease to get worse, follow the American Heart Association diet. If you want diabetes or, if you already have diabetes or pre-diabetes, if you want it to worsen and develop organ damage (eyes, kidneys, nervous system, etc.), then follow the American Diabetes Association diet. USDA food pyramid? Loosen your belt!

The list of conventional risk factors for heart disease is woefully inadequate. If that is as far as your prevention program takes you, heart disease will not be controlled or prevented. At best, it might be slowed; at worst--and more likely--it might be accelerated.

Food sources of vitamin K2



Vitamin K2 is emerging as an exciting player in the control and possible regression of coronary atherosclerotic plaque. Only about 10% of dietary vitamin K intake is in the K2 form, the other 90% being the more common K1.

The ideal source of K2 is natto, the unpalatable, gooey, slimy mass of fermented soybeans that Japanese eat and has been held responsible for substantial decreases in osteoporosis and bone fractures of aging. Natto has an ammonia-like bouquet, in addition to its phlegmy consistency that makes it virtually inedible to anyone but native Japanese.

I say that the conversation on vitamin K2 is emerging because of a number of uncertainties: What form of vitamin K2 is best (so-called MK-4 vs. MK7 vs. MK-9, all of which vary in structure and duration of action in human blood)? What dose is required for bone benefits vs. other benefits outside of bone health? Why would humans have developed a need for a nutrient that is created through fermentation with only small quantities in meats and other non-fermented foods?

Much of the developing research on vit K2 is coming from the laboratories of Drs. Vermeer, Geleijnse, and Schurgers at the University of Maastricht in the Netherlands, along with several laboratories in Japan, the champions of K2.

MK-7 and MK-8,9,10 come from bacterial fermentation, whether in natto, cheese, or in your intestinal tract; MK-4 is naturally synthesized by animals from vitamin K1. While natto is the richest source of the MK-7 form, egg yolks and fermented cheeses are the richest sources of the MK-4 form.

Chicken contains about 8 mcg MK-4 per 3 1/2 oz serving; beef contains about 1 mcg. Egg yolks contain 31 mcg MK-4 per 3 1/2 oz serving (app. 6 raw yolks). Hard cheeses contain about 5 mcg MK-4 per 3 1/2 oz serving, about 70 mcg of MK-8,9; soft cheeses contain about 30% less. Natto contains about 1000 mcg of MK-7, 84 mcg MK-8, and no MK-4 per 3 1/2 oz serving.











Feta cheese

Thanks to the research efforts of the Dutch and Japanese groups, several phenomena surrounding vitamin K2 are clear, even well-established fact:

--Vitamin K2 supplementation (via frequent natto consumption or pharmaceutical doses of K2) substantially improves bone health. While K2 by itself exerts significant bone density/strength increasing properties in dozens of studies, when combined with other bone health-promoting agents (e.g., vitamin D3, prescription drugs like Fosamax and calcitonin), an exaggerated synergy of bone health-promoting effects develop.



--The MK-4 form of vitamin K2 is short-lived, lasting only 3-4 hours in the body. The MK-7 form, in contrast, the form in natto, lasts several days. MK-7 and MK-8-10 are extremely well absorbed, virtually complete.

--Bone health benefits have been shown for both the MK-7 and MK-4 forms.

--Coumadin (warfarin) blocks all forms of vitamin K.





Interestingly, farm-raised meats and eggs do not differ from factory farm-raised foods in K2 content. (But please do not regard this as an endorsement of factory farm foods.)

Another interesting fact: Since mammals synthesize a small quantity of Vit K2 forms from vitamin K1, then eating lots of green vegetables should provide substrate for some quantity of K2 conversion. However, work by Schurgers et al have shown that K1 absorption is poor, no more than 10%, but increases significantly when vegetables are eaten in the presence of oils. (Thus arguing that oils are meant to be part of the human diet. Does your olive oil or oil-based salad dressing represent fulfillment of some subconscious biologic imperative?)

If we believe the data of the Rotterdam Heart Study, then a threshold of 32.7 micrograms of K2 from cheese yields the reduction in cardiovascular events and aortic calcification.

It's all very, very interesting. My prediction is that abnormal (pathologic) calcium deposition will prove to be a basic process that parallels atherosclerotic plaque growth, and that manipulation of phenomena that impact on calcium depostion also impact on atherosclerotic plaque growth. Vitamins D3 and K2 provide potential potent means of at least partially normalizing these processes.

As the data matures, I am going to enjoy my gouda, Emmenthaler, Gruyere, and feta cheeses, along with a few egg yolks. I'm going to be certain to include healthy oils like olive and canola with my vegetables.


All images courtesy Wikipedia.

Copyright 2007 William Davis, MD

Track Your Plaque: Naughty or nice?



Among the many wonderful surprises we've had at Track Your Plaque this holiday season was a letter from Santa Claus himself!

It seems that Santa, like the rest of us, has been busy surfing the web for useful health information the last few months. He was struck with this curious discussion we've been having about "wheat belly" and all the unhealthy consequences of wheat products in our diet.

He writes:

"I wouldn't have believed it myself, except that my waist size has grown four inches in as many years. Sure, I'm known for my healthy girth, but now even Mrs. Claus calls me fat!

"I was open to new ideas when I came across this crazy discussion about eliminating wheat from your diet. So I said, "What have I got to lose?" Well, four weeks later and 12 lbs lighter, I'm convinced. Now comes the tough part: I've got to deliver all the toys and resist all those cookies the children put out for me. I wonder if wheat makes reindeer fat, too?

"Anyway, thanks to your program I'm back to my old weight again. Doc says my blood sugar and blood pressure are also back down to normal. Thanks, Track Your Plaque! (You'll find something extra special under the tree this year.)"

And so it goes. I'm tempted to put Santa's testimonial on our homepage, but I think that may be tooting our own horn a bit too much.

Have a wonderful holiday!

Vitamin D: Treatment for metabolic syndrome?

Metabolic syndrome is that increasingly common collection of low HDL cholesterol, high triglycerides, high blood sugar, and high pressure that now afflicts nearly 1 in 4 adults, rapidly gaining ground to 1 in 3. Beyond these surface factors, metabolic syndrome also creates small LDL particles, VLDL, intermediate-density lipoproteins (IDL), increased imperceptible inflammation measured as higher c-reactive protein, and greater blood clotting tendencies. Metabolic syndrome is usually, though not always, associated with a big tummy ("beer belly," though I call it "wheat belly").

In short, metabolic syndrome creates a metabolic mess that leads to dramatic increases in heart disease, vascular disease and stroke, and cancer. The medical community has been paying increasingly greater attention to this condition because of its booming prevalence and because of the big bucks invested in "education" by the manufacturers of the diabetes and pre-diabetes drugs, particularly makers of Actos and Avandia.

But here's a curious observation:

Replacement of vitamin D to healthy levels (we aim for 50-60 ng/ml, or 125-150 nmol/l) yields:

--Higher HDL
--Lower triglycerides
--Lower blood sugar
--Reduced c-reactive protein
--Reduced blood pressure
--Reduced small LDL
--Enhanced sensitivity to insulin

(Whether blood clotting and effects on IDL should be added to this list is uncertain.)

It's obvious: Vitamin D is proving to be a very important and powerful corrective influence on many of the facets of the metabolic syndrome. In fact, I would go as far as saying that, side by side, vitamin D yields nearly the same effect as prescription drugs Actos and Avandia--without the extravagant cost (nearly $200 per month), leg swelling, congestive heart failure and heightened heart attack risk (with Avandia), and average 8 lb weight gain. Of course, vitamin D also provides benefits beyond metabolic syndrome like facilitation of coronary plaque regression, increased bone density, reduced arthritis, and reduced risk of several cancers.

You'd think that agencies like the American Diabetes Association (ADA) would be all over vitamin D like white on rice. Yet they remain curiously quiet about the entire issue. (That should come as no surprise to anyone familiar with the behavior and politics of this organization, the same outfit that has widely propagated the ADA diet, a program that accelerates diabetes and its complications. In my view, the ADA is an embarassment.)



For a really great story and video on vitamin D that includes a terrific interview with vitamin D guru and Track Your Plaque friend, California psychiatrist Dr. John Cannell, go to What's the Real Story on Vitamin D?. While the video will yield little new to readers of The Heart Scan Blog or Track Your Plaque members, it just feels really good to see a well-made, high-class video production echoing many of the things we've been talking about these past two years.

Appetite stimulants

Ever have days when you just can't seem to get enough to eat, your stomach gnawing just a hour after a meal? We all get them, some more than others. Other days, you can be content with a few simple foods and hunger is subdued, temptation easy to control.

Why such contrasts on different days?

A major part of the reason can be the presence of appetite stimulants, factors that trigger appetite beyond rational control. The list of common appetite stimulants includes:

--Sleep deprivation--A very important factor. Lack of sleep drives tremendous appetite, and often for the wrong foods (processed carbohydrates). I personally have experienced my most shamefully indulgent days when sleep-deprived. The solution is obvious: Sleep. Another factor that is based purely on personal observation is that of waking mid-phase. In other words, waking up while you're still enjoying the deeper phases of sleep (e.g., phase 3,4, or REM). This can oddly disrupt your day and your impulse control. I usually try and time sleep to increments of 90 minutes to coincide with the average duration of the full cycle of sleep. For example, 7 1/2 hours is better than 8 hours, since the extra half hour puts your square into a deeper sleep cycle.

--Excessive caffeine--Caffeine stimulates stomach acid. This triggers the impulse to eat . . . and eat and eat.













Image courtesy Wikipedia

--Aspirin and other anti-inflammatory agents--If you take aspirin (as many of our Track Your Plaquers do), then beware of the gastritis that can develop. Like excessive caffeine, it also triggers the impulse to eat, likely a protective mechanism, since food sops up excess acid. I ask patients to take periodic breaks from aspirin, e.g., a week off every two or three months, to allow the stomach to heal. Alternatively, an occasional dose of acid-suppressing medication is a safe practice, e.g., Pepcid AC 10-20 mg; Prilosec 10-20 mg.

--Wheat-containing foods--Followers of The Heart Scan Blog know my feelings on this. Wheat is a potent appetite stimulant: Eat something containing wheat like a pretzel or whole wheat bagel, and you want more. You may want more immediately, or a little later when your blood sugar plunges after the wheat-driven insulin surge. Solution: Dump the wheat, one of the most unhealthy food groups around.

--Alcohol--Though perhaps not a direct appetite-stimulating effect, the loss of impulse-control with alcoholic drinks can lead to overindulgence, often in the worst foods. Just beware.

--Hanging around with heavy people. Remember peer pressure? It can be subliminal. People with poor eating habits provide the silent message that it's okay to yield to impulse, overeat, overindulge, and choose the wrong foods.

--Stress--Whether through cortisol stimulation or other means, stress triggers appetite in some people. If you experience this and must give in, reach for raw nuts or nuts, rather than wheat snacks or chips. The effect will be minimal, perhaps even beneficial, rather than the bloating, appetite-stimulating, fattening effect of crackers, chips, or pretzels. This may be the same phenomenon as taking prescription steroids like prednisone.

--Short dark days, long nights--In other words, winter. Though just an anecdotal observation, I am convinced that vitamin D supplementation is an effective antidote to this effect. The short, dark days just don't bother you as much, perhaps not at all, and there's no impulse for comfort foods.


How about appetite suppressants? In this list I would include 1) raw nuts--especially almonds, walnuts, pecans, and pistachios, the sort with a fibrous covering and rich in monounsaturates, 2) other sources of plentiful healthy oils, e.g, use more olive oil in your salad or add it to hummus for your veggie dip, 3) space-occupying fibers such as glucomannan, inulin (such as in Fiber Choice), and psyllium seed products. Counteracting the above appetite stimulants like sleep deprivation is, of course, important.

The coming wheat frenzy, otherwise known as the holidays, is an especially important time to be aware of these effects. Eat, drink, and be merry--but with rational impulse control not driven by subconscious appetite stimulants.

"Heart scans are experimental"

Let me warn you: This is a rant.

It is prompted by a 44-year old woman. She has a very serious lipoprotein disorder. Her family experiences heart attacks in their 40s and 50s. I asked for a heart scan. Her insurance companied denied it.

This is nothing new: heart scans, like mammograms, have not enjoyed reimbursement from most insurers despite the wealth of data and growing acceptance of this "mammogram" of the heart.

However, 10 minutes on the phone, and the "physician" (what well-meaning physician can do this kind of work for an insurance company is beyond me) advised me that, while CT heart scans for coronary calcium scoring are not covered, CT coronary angiograms are.

Now, I've been witnessing this trend ever since the big players in CT got involved in the game, namely Philips, Siemens, Toshiba, and GE. These are enormous companies with hundreds of billions of dollars in combined annual revenues. They, along with the lobbying power of cardiology organizations like the American College of Cardiology, have gotten behind CT coronary angiograms. This is most likely the explanation of why CT coronary angiograms have rather handily obtaining insurance reimbursement. Interestingly, the insurance company I was speaking to is known (notorious?) for very poor reimbursement practices.

A CT heart scan, when properly used, generates little revenue, a few hundred dollars to a scan center, barely enough to pay for a device that costs up to $2 million. However, CT coronary angiograms, in contrast, yield around $2000 per test. More importantly, they yield downstream revenues, since CT angiograms are performed as preludes to conventional heart catheterizations, angioplasty, stents, bypass surgery, etc. Now we're talking tens or hundreds of thousands of dollars revenue per test.

What puzzles me is that much of that increased cost comes out of the insurance company. Why would they support such tests if it exposes them to more costs? I'm not certain. It could be the greater pressures exerted by the big CT companies and powerful physician organizations. I seriously doubt that the insurance companies truly believe that heart scans for coronary calcium scoring are "experimental" while CT coronary angiograms are "proven." If all we did was compare the number of clinical studies that validate both tests, we'd find that the number of studies validating heart scans eclipses that of coronary angiograms several fold. Experimental? Hardly.

The smell of money by physicians eager to jump on the bandwagon of a new revenue-producing procedure is probably enough to have them lobby insurers successfully. In contrast, plain old heart scans just never garnered the kind of vigorous and vocal support, since nobody gets rich off of them.

If CT coronary angiograms are sufficiently revenue producing that my colleagues and the CT scanner manufacturers have managed to successfully lobby the health insurers, even one as financially "tight" as the one I spoke to today, well then I take that as testimony that money drives testing, as it does the behavior of hospitals, many of my colleagues, and can even force the hand of insurers.

When meat is not just meat


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







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


Beef hearts
Pork
Water
Corn syrup
Beef

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


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

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

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

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

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

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



Copyright 2007 William Davis, MD

Don't lament no OTC mevacor

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

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

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

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

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

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

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

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

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



Copyright 2007 William Davis, MD

Damage control

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

The campaign opens with:

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

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

Life Wide Open


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

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

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

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

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

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

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

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

Low expectations

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

Let's put it to the test:

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

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

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


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

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

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

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

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

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

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


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

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

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

Why an RDA for vitamin D?

The Food and Nutrition Board (FNB) of the Institute of Medicine is charged with setting the values for the Recommended Daily Allowances of various essential nutrients. However, when it comes to vitamin D, the FNB decided that "evidence is insufficient to develop an RDA and [an Adequate Intake, AI] is set at a level assumed to ensure nutritional adequacy."

The National Institutes of Health Office of Dietary Supplements lists the AI's for various groups of people:

14-18 years
Male 200 IU
Female 200 IU

19-50 years
Male 200 IU
Female 200 IU

51-70 years
Male 400 IU
Female 400 IU

71+ years
Male 600 IU
Female 600 IU


A reconsideration is apparently being planned in near-future that will (hopefully) incorporate the newest clinical data on vitamin D.

My question: Who cares what the FNB decides? Let me explain.

I monitor blood levels of 25-hydroxy vitamin D to assess the 1) starting level of vitamin D without supplementation, and 2) levels while on supplementation, preferably every 6 months (during sunny weather, during cold weather). I have done for the past 3 years in over 1000 people.

The requirement for vitamin D dose in adults, in my experience, ranges from as low as 1000 units per day to as high as 20,000 units per day, rarely more. The vast majority of women require 5000 units per day, males 6000 units per day to maintain a blood level in the desirable range. (I aim for 60-70 ng/ml.) A graph of the distribution of vitamin D needs in my area (Milwaukee, Wisconsin) is a bell curve, a curve more heavily weighted towards the upper vitamin D dose range.

Need for vitamin D to achieve the same blood level is influenced by age, sex, body size, race, presence or absence of a gallbladder, as well as other factors. But needs vary, even among similar people. For instance, a 50-year old woman weighing 140 lbs might need 4000 units per day to achieve a blood level of 25-hydroxy vitamin D of 65 ng/ml. Another 50-year old woman weighing 140 lbs might need 8000 units to achieve the same level, and 4000 units might increase her level to only 38 ng/ml. Two similar women, very different vitamin D needs. The differences can be striking.

Being a hormone--not a vitamin, as it was incorrectly labeled--vitamin D needs to be tightly regulated. We should have neither too little nor too much. I would liken it to thyroid hormones, which need to be tightly regulated for ideal health.

Now the FNB, in light of new data, wants to set new AI's, or even RDA's, for vitamin D for the U.S. This is an impossible--impossible--task. There is no way a broad policy can be crafted that serves everyone. It is impossible to state that all men or women, categorized by age, require X units vitamin D. This is pure folly and it is misleading.

The only rational answer for the FNB to provide is to declare that:

It is not possible to establish the precise need for vitamin D in a specific individual because of the multiplicity of factors, only some of which are known, that determine vitamin D needs. Individual need can only be determined by assessing the blood level of 25-hydroxy vitamin D prior to initiation of replacement and periodically following replacement to assess the adequacy of replacement dose. Continuing reassessment is recommended (e.g., every 6-12 months), as needs change with weight, lifestyle, and age.

Sure, it adds around $100-150 per year per person for lab testing to assess vitamin D levels. But the health gains made--reduced fractures, reduced incidence of diabetes, reduced colon, breast, and prostate cancer, less depression, reduced heart attack and heart procedures--will more than compensate.

Bargains for Armour Thyroid

We use Armour thyroid almost exclusively. I take it myself.

I am thoroughly convinced that, for at least 70% of people requiring thyroid replacement, the added T3 component makes a world of difference compared to isolated T4: More energy, greater alertness, better mental clarity, better weight loss, larger effects on lipoprotein(a).

However, there are substantial price disparities in different pharmacies.

For instance, in Milwaukee, a one month supply of 1 grain (60 mg) tablets costs:

Walgreen's: $36.00

Walmart: $9.54


That's a considerable price difference of nearly 400%. It therefore always pays to do a little bit of shopping.

Heart scan mis-information on WebMD

If you want information on how prescription drugs fit into your life, then go to WebMD.

But, if you are looking for information that cuts through the bullcrap, is untainted by the heavy-handed tactics of the drug industry, or doesn't support the "a heart catheterization for everyone" mentality, then don't go there.

A Heart Scan Blog reader turned up this gem on the WebMD site:

Should I have a coronary calcium scan to check for heart disease?

In their report, they list some reasons why a heart scan should not be obtained:

Most of the time, a physical exam and other tests can give your doctor enough information about your risk for heart disease.

You've got to be kidding me. What tests are they talking about?

EKG? An EKG is a crude test that tells us virtually nothing about the coronary arteries or risk for heart attack. It is helpful for heart rhythm disorders and other abnormalities, but virtually useless for coronary disease unless a heart attack is underway or has already occurred.

Cholesterol? What level of cholesterol tells you whether you have heart disease? Tim Russert, for instance, had the same cholesterol values 5 years before his death as on the day of his death. How would cholesterol have told his doctor that heart disease was present? Does an LDL cholesterol of 180 mg/dl tell you that someone has heart disease, while a value of 130 mg/dl does not?

Stress test? You mean like the normal stress test Bill Clinton had 3 months before his near-fatal collapse? Stress tests are a gauge of coronary flow, not of coronary atherosclerosis. Huge amounts of coronary plaque can be present while a stress test--flow--remains normal.

No, a physical exam does not uncover hidden heart disease. The annual physical is, in fact, a miserable failure for detection of hidden heart disease.


You already know that your risk for heart disease is low or high. The test works best in people who are at medium risk but have no symptoms.

This bit of fiction comes from a compromise statement in the American College of Cardiology and American Heart Association "consensus" document detailing the role of heart scans in heart disease detection. Because conventional thinkers don't like the idea of very early detection in seemingly "low risk" people, nor do they like the idea of diabetics and smokers getting a heart scan because it's "obvious" that they are already at high risk, the middle ground was taken: Scan only people at "intermediate risk."

What the heck is "intermediate risk"? Are you intermediate risk?

In real life, using standard criteria (e.g., Framingham scoring) to decide who is low-, intermediate-, or high-risk fails to identify over 1/3 of people with heart disease, while subjecting many without heart disease (plaque) to needless treatment (meaning statins, since that's the only real preventive treatment on most doc's armamentarium).

Another fact: Heart scans are quantitative, not just normal or abnormal. Your heart scan score could be 5, it could be 150, it could be 500, or 5000---it makes a world of difference. The risk of someone with a score of 5000 is at very different risk than someone with a score of 5. It also provides much greater precision in determining a specific individual's risk.



The test could give a high score even if your arteries aren't blocked. This might lead to extra tests that you don't need.

This is true--if you doctor has no idea what he's doing.

This is like saying that you should never take your car to the repair shop because all mechanics are crooks. If you have an unscrupulous cardiologist who tells you that your heart scan score of 25 means you are a "walking time bomb" and heart catheterization is necessary to determine whether you "need" a stent . . . well, this is no different than the shady mechanic who advises you that your car's engine needs to be rebuilt for $3000, when all you really needed was a few new spark plugs.

Coronary plaque is coronary plaque, and all coronary plaque has potential for rupture (heart attack)--even if it doesn't block flow. This is true at a score of 10, or 100, or 1000--all plaque is potentially rupture-prone, though the more plaque you have, the greater the likelihood.


Not all blocked arteries have calcium. So you could get a low calcium score and still be at risk.

They're missing the point: ANY calcium score carries risk, so a low score should not be interpreted as having no risk. But, just because a procedure like stenting or bypass surgery is not necessary to restore flow, it does not mean that risk for plaque rupture is not present--it is.

Any heart scan score should be taken seriously, meaning sufficient reason to engage in a program of heart disease prevention.

Although not perfect, coronary calcium scoring remains the easiest, most accessible, and least expensive means for identifying and quantifying coronary atherosclerosis--whether or not WebMD and drug industry money endorse them.

Heart disease prevention for the helpless, ignorant, or non-compliant

The media outlets are gushing with the "research"/marketing spinoff of the JUPITER trial, an analysis conducted by Dr. Erica Spatz of Yale University, that suggests that statin use should be expanded to many millions more Americans.

USA Today: Study: 11M more should get statins

MedPage: JUPITER Findings Could Boost Statin Use by 20%

Health Day: Millions More Americans Might Be Placed on Statins

WebMD: More May Benefit From Cholesterol Drugs: Study Shows More Would Qualify for Statin Treatment if Levels of C-Reactive Protein Are Considered


You may recall that the JUPITER trial (discussed previously in a Heart Scan Blog post) studied the cardiovascular event risk in people with "normal" LDL cholesterols (calculated, of course, not measured) of 130 mg/dl or less, along with increased c-reactive protein, a crude inflammatory measure, of 2.0 mg/dl or greater. A 54% (relative) reduction in cardiovascular events occured in the group taking Crestor 20 mg per day.

What I see is a confluence of events that have brought us to the "statin drugs are necessary for everybody" mentality:

--The low-fat diet advice of the last 40 years has increased non-fat or low-fat foods that increase LDL, since removing fat from the diet provokes small LDL particle production and increases the inflammatory measure, c-reactive protein (CRP).

--The proliferation of "healthy whole grains" in the diet have also caused an enormous boom in small LDL particles, which is interpreted to the uninformed as "high cholesterol." It has also provoked CRP substantially.

--The advice to reduce salt intake has brought a broad re-emergence of iodine deficiency. When thyroid hormone production flags due to lack of iodine, LDL cholesterol (both large and small) increase.

--Our lives, which are increasingly conducted indoors, have worsened the already substantial vitamin D deficiency. While deficiency of vitamin D primarily reduces HDL cholesterol and increases triglycerides, it can also cause an increase in small LDL and a large increase in CRP.


In other words, a collection of events have converged to provide the appearance of high LDL cholesterol and high CRP. This creates the appearance of a "need" for statin drugs. The JUPITER trial now exploits both the LDL-reducing and CRP-decreasing effects of statins.

I view the foisting of Crestor via the JUPITER argument on the public as taking full advantage of the helpless situation many Americans find themselves in: Reduce fat intake, eat more healthy whole grains and . . . cholesterol and CRP skyrocket! "You need Crestor! See, I told you it was genetic," says the doctor after attending the nice AstraZeneca-sponsored drug dinner.

The notion of using a drug like Crestor to suppress inflammatory patterns is absurd. There are far better, easier, cheaper ways to achieve this goal, along with dramatic reduction in cardiovascular risk. But, to the ignorant, the helpless, or non-compliant with real change in diet and lifestyle, then Crestor does serve a purpose.

I can only hope that the excessive pushing of statin drugs on the public will sooner or later trigger a revolt.

Dangerous mis-information on vitamin D


Please be aware of the ignorant propagating information they have no business talking about.

This is one such example, a newsletter from pop exercise guru, Denise Austin.

Although I'm sure she means well, I have a problem with people who have little to no experience acting as experts, often simply repeating something they heard or read somewhere else. This has become particular problem with the internet, in which bad information can get repeated thousands of times, gaining a veil of "truth" through its repetition. I don't mean to pick specifically on Ms. Austin, since she joins a growing rank of pseudo-experts on vitamin D and other topics, but she provides a good example of how far wrong mainstream information can be.



Simple Steps
Do Your D!


Calcium often gets all the glory when it comes to bone health. But calcium wouldn't benefit your bones much without its partner, vitamin D!

Why? Vitamin D helps your body absorb calcium and keeps your bones strong; without enough vitamin D, the bones become weak and brittle, a condition called rickets in children, and osteomalacia in adults. Adults from 19 to 50 need 200 IU (international units) per day, while those from 51 to 70 need 400 IU daily. Those over 70 need 600 IU per day.

Unfortunately, not too many foods contain vitamin D naturally. (Tuna and sardines canned in oil are exceptions.) The good news is that many foods are now regularly fortified with vitamin D, including milk, some yogurts, margarines, and cereals. You can check the Nutrition Facts panel on packages and containers to see which products contain vitamin D. It should be listed after vitamins A and C, along with the percentage of the Daily Value that a serving of the food contains. The Daily Value (a standardized amount) for vitamin D is 400 IU, so if your milk has 25 percent of the Daily Value, it provides 100 IU per serving.

Your skin can also make vitamin D using sunlight — you need about a half hour of exposure to the midday sun twice a week to make enough. However, because of the increasing incidence of skin cancer in recent years, many experts are wary about recommending sun exposure.

So take a closer look at milk, yogurt, cereal, and margarine selections when you're doing your weekly shopping, and stock up on brands that are fortified with vitamin D. Challenge yourself to consume one source of vitamin D at least three days in the coming week! If you cannot eat or do not like any foods that contain vitamin D or are fortified with it, talk with your health care provider ASAP about taking a supplement. Your bones will thank you for it!



Let me list the mistakes in this piece:

Adults from 19 to 50 need 200 IU (international units) per day, while those from 51 to 70 need 400 IU daily. Those over 70 need 600 IU per day.

This is the same non-information that was the advice originally offered by the Food and Nutrition Board based on a best guesstimate due to lack of data. It is clear from newer data that doses required for full restoration of vitamin D are in the thousands of units. (My personal dose for full restoration of vitamin judged by serum levels of 25-hydroxy vitamin D is 8000 units per day.)

The information coming from the Food and Nutrition Board is about as good as the information coming from the USDA (you know, that "government" agency meant to represent the interests of ConAgra, Cargill, and Big Farming) and the American Heart Association (that represents consensus opinion from data 20 years out of date and now arm-in-arm with Big Food like General Mills, Kraft, and Nabisco). These agencies and the advice they offer has, over the past few years, become increasingly irrelevant and outdated. It is the Information Age, in which ulterior motives are becoming more readily exposed, yet they still operate by the rules of the Industrial Age and deliver a message that serves their own purposes.

Ms. Austin fell for it.


The good news is that many foods are now regularly fortified with vitamin D, including milk, some yogurts, margarines, and cereals.

First of all, what is a "diet expert" doing advocating industrial foods? Cereals, in particular, are among the worst foods on the supermarket shelves, whether or not they are fortified. Candy bars can be fortified, too; that doesn't make them any better for you.

The vitamin D added to these foods is, more often than not, the ergocalcferol, or D2, form that is woefully ineffective. And the dose added is trivial, usually in the 100-200 unit range per serving. The same goes for the milk, an inadequate source that we don't even factor into total intakes because of the low quantity.


Your skin can also make vitamin D using sunlight — you need about a half hour of exposure to the midday sun twice a week.


Nope. This might be true for a young person below age 30 in a southern environment. It is NOT true for the majority of people in northern climates and anyone over age 30 or 40, since we lose most of the capacity to activate vitamin D in the skin as we age. A deep, dark Florida tan does not necessarily mean that vitamin D has been activated. See A tan does not equal vitamin D. Here in Wisconsin, where, despite this darn cold winter, does enjoy wonderfully warm and beautiful summers, the average vitamin D dose need ranges from 4000-8000 units per day in summer, slightly more in winter.

By the way, it is not calcium that is instrumental to bone health. It is vitamin D. Calcium is the passive bricks and mortar of bones, while vitamin D is the bricklayer, the determinant of calcium's fate, the master control of bone health. Calcium supplementation becomes almost immaterial when vitamin D is restored.

I praise Ms. Austin for her hard work, trying to help fat Americans lose weight. But please ignore her advice on vitamin D, along with the numbing repetition of this mis-information that will likely propagate from other exercise gurus, dietitians, and pseudoexperts.

A Tale of Two LDL's

Kurt, a 50-year old businessman with a heart scan score of 323, had a :

--Conventional (calculated) LDL of 128 mg/dl
--Real measured LDL 241 mg/dl.


Laurie, a 53-year old woman who underwent a coronary bypass operation last year (before I met her), had a:

--Conventional LDL of 142 mg/dl
--Real measured LDL was 85 mg/dl.


(By "real, measured" LDL, I'm referring to LDL particle number in units of nmol/L obtained through NMR lipoprotein testing and dividing by 10, or just dropping the last digit to convert the value to mg/dl. This technique was arrived at by comparing the population distributions of these two parameters, LDL particle number and calculated LDL. This is the gold standard in my view. Similar numbers can be obtained by measuring apoprotein B, direct LDL, or calculated non-HDL, with diminishing reliability from first to last.)

In other words, Kurt's conventional LDL underestimated real LDL by 88%. Laurie's conventional LDL overestimated real LDL by 40%.

Interestingly, Laurie's doctor had insisted she take Lipitor for a high LDL cholesterol. Her real LDL was, in fact, low to begin with and benefits of a statin drug would be little to none. (Remember, in our Track Your Plaque approach, multiple other treatments are included, such as omega-3 fatty acids from fish oil, vitamin D normalization, and wheat elimination, strategies that yield benefits that others expect to obtain with statins.) Laurie's real cause of her heart disease proved to have nothing to do with LDL cholesterol, but involved lipoprotein(a) and thyroid issues.

Kurt proved to have a severe preponderance of small LDL particles--the worst kind of LDL, while Laurie had none--a benign pattern.

Then how can anyone make sense of the conventional, calculated LDL cholesterol that is generally (95% of the time) provided? If accuracy can stretch to plus or minus 80% . . . you can't. Conventional LDL is a miserably inaccurate number. The problem is that obtaining a superior number requires a step or two more testing and insight, something most busy primary care doc's simply don't have in the midst of a day filled with arthritis, bronchitis, diarrhea, belly aches, and seborrhea.

Yet conventional--I call it "fictitious"--LDL serves as the basis for this $27 billion (annual revenues) industry selling statin drugs.

This is meant to be neither an argument in favor of nor against statin drugs. However, it is plain as day that any study designed to reduce LDL cholesterol will be hopelessly clouded by calculated LDL imprecision. A calculated LDL of, say, 143 mg/dl might really be 187 mg/dl, or it might be 74 mg/dl--you can't tell by looking just at LDL. Yet billions of dollars of research and billions of dollars of healthcare costs are based on the treatment of this number.

This reminds me of the mark-to-market accounting magic that helped topple Wall Street.

I don't think that the statin world is poised for such a huge downfall. But I do see this as a source of enormous dilution of the effects of statin drugs. People who barely stand to benefit get the drugs, while others who might truly benefit are treated inadequately. It provides fuel to the growing idea that reducing LDL cholesterol fails to truly provide benefit.

I am no lover of statin drugs nor drugs in general. But I am a fan of knowing the truth. Despite my bashing of the drug industry (and make no mistake: the drug industry is a cutthroat, profit-seeking, do-anything-to-increase-sales industry), I do believe that there is a role for statin drugs (though far smaller than $27 billion per year). But the usual method of selecting people for treatment is pure fiction. The ATP-III cholesterol treatment guidelines? An anemic attempt to apply structure to meaningless values.

You and I do not need to subscribe to this sort of non-quantitative nonsense.

Niacin scams

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

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


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

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

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

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

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


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

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

Deja vu all over again?

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

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

Some interesting comments:

Dr. Jay Cohn (University of Minnesota):

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

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

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



Wow. The idea may be starting to catch on.

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

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


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

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


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

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


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

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

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

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



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

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

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

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

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

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

Well, perhaps in time.

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

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

1) Identify a nutritional supplement that works.

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


2) Identify a medical indication for your product.

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


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

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


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

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


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


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

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

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

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

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

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

Who said you can't turn lead into gold?

Niacin vs. low-carb weight loss

Niacin:

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


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

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


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

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

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

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

Explosive plaque growth

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

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

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

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



Image courtesy Wikipedia and the United States Geological Survey.









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

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

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

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

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

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

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

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


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

Dr. Cannell on "How much vitamin D?"

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

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

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

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

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

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

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

Hollis BW, et al. Circulating vitamin D3 and 25-hydroxyvitamin D in humans: An important tool to define adequate nutritional vitamin D status. J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):631-634.

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

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

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



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

The Vitamin D Newsletter
January, 2008


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


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

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

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

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


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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


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


This is a periodic newsletter from the Vitamin D Council, a non-profit trying to end the epidemic of vitamin D deficiency. If you don't want to get the newsletter, please hit reply and let us know. This newsletter is not copyrighted. Please reproduce it and post it on Internet sites. Remember, we are a non-profit and rely on donations to publish our newsletter and maintain our website. Send your tax-deductible contributions to:

The Vitamin D Council
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Atascadero, CA 93422



PS: The Vitamin D Council lost our webmaster. If you want to donate your time to a good cause, know all about maintaining websites, are interesting in keeping up with the latest press about vitamin D, and are willing to do so for free, please hit reply and let me know. We currently have $405.52 in our bank account so we cannot pay you now but may be able to pay you in the future.

End-stage vitamin D deficiency

Let me paint a picture:

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


(Image courtesy of National Library of Medicine)

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

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

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

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

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

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

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

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

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

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

Can you wait?

"Instant" reversal with fasting?

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

So here is Don's story:


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

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

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

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

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


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

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

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

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

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

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

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

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

Yours truly,

Don P.
Honolulu, Hawaii



Isn't that great?

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

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

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

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

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


Copyright 2007 William Davis,MD

Study review: yet another Lipitor study

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

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

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

Other findings included:

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

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

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


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

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

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

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

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

Dr. Cannell on vitamin D and cancer

Here is Dr. John Cannell's Vitamin D Council Newsletter reprinted in its entirety. It answers some of the questions that came up on The Heart Scan Blog about the recent release of a study of vitamin D and cancer



The Vitamin D Newsletter

December, 2007

Does vitamin D prevent cancer? If it does, will doctors who ignore the research end up with blood on their hands? The press makes it easy for doctors to believe what they want to believe. Below are six stories about the same scientific study; read the six different headlines. According to your a priori beliefs, you can choose the story you want to believe and read that one. Don't feel bad, we all do it. As Walter Lippman once said, "We do not see and then believe, we believe and then we see."


Vitamin D cuts colon cancer death risk



Study Finds No Connection Between Vitamin D And Overall Cancer Deaths



Vitamin D protects against colorectal cancer



Vitamin D May Not Cut Cancer Deaths



Vitamin D protects against colorectal cancer



Scientists advise a vitamin D downgrade as there is no real proof ...




Another option is to read the study yourself.


Freedman DM, et al. Prospective Study of Serum Vitamin D and Cancer Mortality in the United States. J Natl Cancer Inst. 2007 Oct 30; [Epub ahead of print]




What Dr. Freedman actually discovered is that when you take a very large group of people (16,818), some as young as seventeen, measure their vitamin D levels, and then wait about ten years to see who dies from cancer, you find 536 die and that a vitamin D level from ten years earlier is not a good predictor of who will die from cancer. However, even a level drawn ten years earlier predicted that those with the lowest level were four times more likely to die from colon cancer, suggesting, as Ed Giovannucci has, that colon cancer may be exquisitely sensitive to vitamin D. Furthermore, 28 women got breast cancer, 20 in the group with the lowest vitamin D level but only 8 in the highest. The breast cancer findings were not statistically significant - even during a very long breast cancer awareness month - but can you imagine what critics at the American Cancer Society would be telling women if the numbers were reversed, if the 20 women who got breast cancer were in the high vitamin D group?



Another large epidemiological study appeared about breast cancer the very next day. This time, the press passed on the story and the American Cancer Society was mum, no editorials by Dr. Lichtenfeld, their spokesman, in spite of breast cancer awareness month.



Abbas S, et al. Serum 25-hydroxyvitamin D and risk of postmenopausal breast cancer - results of a large case-control study. Carcinogenesis. 2007 Oct 31; [Epub ahead of print]



In the above study, 1,394 women with breast cancer were case-controlled with a similar number of women without breast cancer. The women with breast cancer were three times more likely to have low vitamin D levels. That is a lot of women who may be dying during next year's breast cancer awareness month.



Both of the above studies were epidemiological, not randomized controlled trials. Of course a randomized controlled trial has already shown a 60% reduction in internal cancers in women taking even a modest 1,100 IU per day of vitamin D.



Lappe JM, et al. Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial. Am J Clin Nutr. 2007 Jun;85(6):1586-91.



What is interesting is the difference in the response of the Canadian Cancer Society and the American Cancer Society. The Canadian Cancer Society has advised all Canadians to take 1,000 IU per day - not enough but a good first step - and for immediate additional large scale clinical trials. The Canadians simply performed a risk/benefit analysis. What is the risk of treating vitamin D deficiency versus what are the potential benefits? They quote the American Food and Nutrition Board, which says 2,000 IU/day is safe for anyone over the age on one to take, on their own, without being under the care of a physician. If there is little or no risk, then the next question is what are the potential benefits of treating vitamin D deficiency? This is not quantum mechanics.



Cancer society calls for major vitamin D trial



The Canadians acted because the Canadian government knows it could save billions of dollars by treating vitamin D deficiency.



Vitamin D Deficiency Drains $9 billion From Canadian Health Care ...



If wide spread treatment of vitamin D deficiency became the rule, ask yourself, "Who would be helped and who would be hurt." First ask yourself that question about Canada and then about the USA. Remember, in Canada, the government directly pays for its citizen's health insurance; in the USA, private insurance is the norm. In Canada, the government is realizing they could save billions if vitamin D deficiencies were treated. In the USA, a large segment of the medical industry would be hurt, some anti-cancer drug manufacturers would have to close their doors, thousands of patents would become worthless, lucrative consulting contracts between industry and cancer researchers would dry up.

Both Canadians and Americans are shocked to think their doctors care about money, are in the illness business. In some ways people think of their doctors like they do their local public schools. They know medicine is a business and know doctors do things for money but they don't think their own doctors do. Likewise they think public schools are in bad shape but think their local schools are above average. They think their doctor is above average, like their "Lake Woebegone" kids.

Lake Woebegone Effect

The fact is that doctors, hospitals, regional cancer centers, and the cancer drug manufacturers are all in business to make money and all of these businesses make money off the sick, not off the well. Just a fact, but, as Aldous Huxley once observed, "Facts do not cease to exist because they are ignored."



Vitamin D will save the Canadian government enormous amounts of money but will cause widespread economic disruption in the USA. Do the physicians leading the American Cancer Society have strong economic ties to the cancer industry in the form of patents, stock options, and consulting fees? If so, what do you expect them to do? What would you do? It's simple. You would believe what you have to believe, what you need to believe, that is, anything with the word "vitamin" in it is simply the latest Laetrile. Look to Canada, not the USA, to lead the way.



Vitamin D may fight cancer


What about American physicians? They are apparently waiting for the American trial lawyers to smell a tort. After all, the case is quite simple. Doctor, did you advise Mrs. Jones to avoid the sun? Doctor, did you tell her the sun is the source of 90% of circulating stores of vitamin D? Doctor, did you prescribe vitamin D to make up for what the sun would not be making? Doctor, did you measure her vitamin D levels? So you had no way of knowing if your sun-avoidance advice resulted in vitamin D deficiency? Doctor, do you know our expert tested her vitamin D level and it was less than 20? Doctor, did you tell her about any of the studies indicating vitamin D deficiency causes cancer? Doctor, did you know Mrs. Jones has terminal breast cancer and will be leaving behind a loving husband and two young children?

And what about the American Cancer Society? Dr. Lichtenfeld, their spokesman, quickly gave his opinion; from what I can tell the first time he ever commented on a vitamin D study. That is, he has ignored the hundreds of positive epidemiological studies, ignored the incredible randomized controlled trial, but he jumped on this one:

Maybe Vitamin D Isn't The Answer After All

Dr. Lichtenfeld, implied the Canadian Cancer Society has acted precipitously in recommending that all Canadians take 1,000 IU of vitamin D daily. He implied that Americans should placidly wait until more randomized controlled trials, such as Lappe JM, et al (above), accumulate before they address their vitamin D deficiency. That is, nothing should be done until more randomized controlled trials prove vitamin D prevents cancer, one randomized controlled trial is not enough; epidemiological studies are not enough, animal studies are not enough, multiple anti-cancer mechanisms of action are not enough? If that is his position, I challenge him to point to one human randomized controlled trial that proves smoking is dangerous?

If he cannot, then he must admit that the American Cancer Society's position on smoking is entirely derived from epidemiological studies, animal studies, and a demonstrable mechanism of action, not on human randomized controlled trials? Vitamin D not only has hundreds of epidemiological studies, thousand of animal studies, and at least four anti-cancer mechanisms of action, vitamin D deficiency has something smoking does not have, it has a high quality randomized controlled trial. If future randomized controlled trials fail to show vitamin D prevents cancer - and Dr. Lichtenfeld better hope they do - he can have the satisfaction of saying "I told you so." If future randomized controlled trials confirm vitamin D prevents cancer, then he needs to look at his hands, the red he sees is the blood of needless cancer deaths.

John Cannell, MD

The Vitamin D Council

9100 San Gregorio Road

Atascadero, CA 93422



This is a periodic newsletter from the Vitamin D Council, a non-profit trying to end the epidemic of vitamin D deficiency. If you don't want to get the newsletter, please hit reply and let us know.

Remember, we are a non-profit and rely on donations to publish our newsletter and maintain our website. Send your tax-deductible contributions to:

The Vitamin D Council

9100 San Gregorio Road

Atascadero, CA 93422

"Yes, Johnnie, there really is an Easter bunny"

A Heart Scan Blog reader recently posted this comment:

You wouldn't believe the trouble I'm having trying to get someone to give me a CT Heart Scan without trying to talk me into a Coronary CTA [CT angiogram]. Every facility I've talked to keeps harping on the issue that calcium scoring only shows "hard" plaque...and not soft.

I also had a nurse today tell me that 30% of the people that end up needing a coronary catheterization had calcium scores of ZERO. That doesn't sound right to me. What determines whether or not someone needs a coronary catheterization anyway?



There was a time not long ago when I saw heart scan centers as the emerging champions of heart disease detection and prevention. Heart scans, after all, provided the only rational means to directly uncover hidden coronary plaque. They also offered a method of tracking progression--or regression--of coronary plaque. No other tool can do that. Carotid ultrasound (IMT)? Indirectly and imperfectly, since it measures thickening of the carotid artery lining, partially removed from the influences that create coronary atherosclerotic plaque. Cholesterol? A miserable failure for a whole host of reasons.

Then something happened. General Electric bought the developer and manufacturer of the electron-beam tomography CT scanner, Imatron. (Initial press releases were glowing: The Future of Electron Beam Tomography Looks Better than Ever.The new eSpeed C300 electron beam tomographic scanner features the industry’s fastest temporal resolution, and is now backed by the strength of GE Medical Systems. Imatron and GE have joined forces to provide comprehensive solutions for entrepreneurs and innovative medical practitioners.)

Within short order, GE scrapped the entire company and program, despite the development of an extraordinary device, the C-300, introduced in 2001, and the eSpeed, introduced in 2003, both yanked by GE. The C-300 and eSpeed were technological marvels, providing heart scans at incredible speed with minimal radiation.

Why would GE do such a thing, buy Imatron and its patent rights, along with the fabulous new eSpeed device, then dissolve the company that developed the technology and scrap the entire package?

Well, first of all they can afford to, whether or not the device represented a technological advancement. Second (and this is my reading-between-the-lines interpretation of the events), it was in their best financial interest. Not in the interest of the public's health, nor the technology of heart scanning, but they believed that focusing on the multi-detector technology to be more financially rewarding to GE.

GE, along with Toshiba, Siemens, and Philips, saw the dollar signs of big money with the innovations in multi-detector technology (MDCT). They began to envision a broader acceptance of these devices into mainstream practice with the technological improvements in CT angiography, a device (or several) in every hospital and major clinic.

Anyway, this represents a long and winding return to the original issue: How I once believed that heart scan centers would be champions of heart disease detection and reversal. This has, unfortunately, not proven to be true.

Yes, there are heart scan centers where you can obtain a heart scan and also connect with people and physicians who believe in prevention of this disease. I believe that Milwaukee Heart Scan is that way, as is Dr. Bill Blanchet's Front Range Preventive Imaging, Dr. Roger White's Holistica Hawaii, and Dr. John Rumberger's Princeton Longevity Center.

But the truth is that most heart scan centers have evolved into places that offer heart scans, but more as grudging lip service to the concept of early detection earned with sweat and tears by the early efforts of the heart scan centers. But the more financially rewarding offering of CT coronary angiograms, while a useful service when used properly, has corrupted the prevention and reversal equation. "Entry level" CT heart scans have been subverted in the quest for profit.

CT angiograms pay better: $1800-4000, compared to $100-500 for a heart scan (usually about $250). More importantly, who can resist the detection of a "suspicious" 50% blockage that might benefit from the "real" test, a heart catheterization? Can anyone honestly allow a 50% blockage to be without a stent?

CT angiograms not only yield more revenue, they also serve as an effective prelude to "downstream" revenue. By this equation, a CT angiogram easily becomes a $40,000 hospital procedure with a stent or two, or three, or occasionally a $100,000 bypass. Keep in mind that the majority of people who are persuaded that a simple heart scans are not good enough and would be better off with the "superior" test of CT angiography are asymptomatic--without symptoms of chest pain, breathelessness, etc. Thus, the argument is that people without symptoms, usually with normal stress tests, benefit from prophylactic revascularization procedures like stents and bypass.

There are no data whatsoever to support this practice. People who have no symptoms attributable to heart disease and have normal stress tests do NOT benefit from heart procedures like heart catheterization. They do, of course, benefit from asking why they have atherosclerotic plaque in the first place, followed by a preventive program to correct the causes.

So, beware: It is the heart scan I believe in, a technique involving low radiation and low revenue potential. CT angiograms are useful tests, but often offered for the wrong reasons. If we all keep in mind that the economics of testing more often than not determine what is being told to us, then it all makes sense. If you want a simple heart scan, just say so. No--insist on it.

Take trust out of the equation. Don't trust people in health care anymore than you'd trust the used car salesman with "a great deal."

Finally, in answer to the reader's last comment about 30% of people needing heart catheterizations having zero calcium scores, this is absolute unadulterated nonsense. I'm hoping that the nurse who said this was taken out of context. Her comments are, at best, misleading. That's why I conduct this Heart Scan Blog and our website, www.cureality.com. They are your unbiased sources of information on what is true, honest, and not tainted by the smell of lots of procedural revenue.

Diabetes: controlled or . . . cured?

Russ had a beer belly, a big protuberant, hanging-over-the belt-on-top-of-skinny-legs sort of beer belly. Except he didn't get it from beer (only). Yes, he did drink beer, up to 3 or 4 per day on weekends, rarely during the week.

Russ got his "beer belly" from snack foods, processed foods, and yes, wheat products.

He came to my office for consultation for unexplained breathlessness. His primary care physician was stumped and asked for an opinion.

So, part of Russ' evaluation included laboratory work. Russ proved to have a blood sugar (glucose) of 136 mg/dl, well into the diabetic range. His insulin level was 102 microunits/ml, way above the desirable range of <10. I interpreted this to mean that Russ had early diabetes but still maintained vigorous pancreatic function, since the pancreas is the abdominal organ responsible for insulin production. In pre-diabetes and early diabetes, insulin levels can be high, reflecting the revved up output of the pancreas. However, the pancreas eventually "burns out," unable to keep up with the demand to product enormous quantities of insulin. That's when blood sugar skyrockets.

Along with the blood sugar and insulin, Russ showed all the expected markers of this syndrome (the "metabolic syndrome"): low HDL of 34 mg/dl, high triglycerides of 257 mg/dl, severe small LDL (80% of total LDL), high c-reactive protein, and high blood pressure.

A heart scan showed a surprisingly small amount of coronary plaque with a score of only 4. Thus, Russ' symptoms were unlikely to represent a coronary issue ("ischemia"). Breathlessness was far more likely to be from 1) his obesity and protuberant abdomen, large enough to encroach on his chest and lung volume, and 2) high blood pressure (which can, in turn, lead to high heart pressure and breathlessness, often called "left ventricular diastolic dysfunction").

I persuaded Russ to eliminate his previously flagrant and abundant over-reliance on wheat products and snack foods. Two months later, 15 lbs lighter, and a modestly less protuberant beer belly, Russ' laboratory evealuation showed:

--Blood sugar 90 mg/dl--normal.

--Insulin 12 microunit/ml--darn near normal.

Blood pressure was down 20 points. Russ' breathlessness was now entirely gone. He has another 30-40 lbs to go, but he's off to a great start. He is now clearly, solidly, and confidently NON-diabetic.

I see experiences like this every day, as do committed diabetes fighters like Jenny at Diabetes Update.

Why isn't this common practice? If pre-diabetes and diabetes can be cured by such a simple approach, why isn't it more widely embraced? After all, what other devastating diseases can claim to have such a simple, straightforward way to achieve cure?

And why does the American Diabetes Association (ADA) actually condone the inclusion of abundant carbohydrates in diabetics? Their modified food pyramid shows the widest part of the pyramid filled with "breads, grains, and other starches."



How about this question taken from a Q&A on the ADA website:

Can I eat foods with sugar in them?

For almost every person with diabetes, the answer is yes! Eating a piece of cake made with sugar will raise your blood glucose level. So will eating corn on the cob, a tomato sandwich, or lima beans. The truth is that sugar has gotten a bad reputation. People with diabetes can and do eat sugar. In your body, it becomes glucose, but so do the other foods mentioned above. With sugary foods, the rule is moderation. Eat too much, and 1) you'll send your blood glucose level up higher than you expected; 2) you'll fill up but without the nutrients that come with vegetables and grains; and 3) you'll gain weight. So, don't pass up a slice of birthday cake. Instead, eat a little less bread or potato, and replace it with the cake. Taking a brisk walk to burn some calories is also always helpful.


The answer is simple. Just as the American Heart Association focuses on ways to deliver the message of palliation, so does the ADA. So ADA diet advice is designed to help diabetics maintain a stable blood sugar on their medication. It is definitely not intended to reverse or eliminate diabetes. My patient Russ would be deep into diabetes on the ADA diet, enjoying his rolls, whole wheat bread, breakfast cereals, and birthday cake.

Once again, another example of the growing irrelevance of the "official" arbiters of health information for those of us looking for reversal of disease.

Study review: cerivastatin

I'd like to start an occasional series of blog posts on The Heart Scan Blog in which I review studies relevant to the whole heart scan score reversal experience.

In a previous post, Don't be satisfied with "deceleration,"I discussed the BELLES Trial (Beyond Endorsed Lipid Lowering with EBT Scanning (BELLES)), in which either atorvastatin (Lipitor), 80 mg, or pravastatin (Pravachol),40 mg, was given to 615 women. Both groups showed an average of 15% annual plaque growth, regardless of which agent was taken and regardless of the amount of LDL cholesterol reduction.

I cited another study in which 471 participants received either Lipitor, 80 mg, or Lipitor, 10 mg. The rate of annual score increase was 25-27%, regardless of drug dose or LDL lowering.

Here's yet another study, a small German experience in 66 patients, with a curious design and using the now-defunct statin drug, cerivastatin (Bayccol, pulled in 2001, nearly simultaneous with the publication of this study, due to greater risk of muscle damage, particularly when used in combination with gemfibrozil). Achenbach et al in Influence of lipid-lowering therapy on the progression of coronary artery calcification: A prospective evaluation reported on this trial in which all participants underwent heart scanning to obtain a heart scan score; no treatment was initiated based on the score. A second scan was obtained after the no treatment period, followed by treatment with cerivastatin, 0.3 mg per day. A third scan was finally obtained.

In year one without treatment, the average increase in heart scan scores was 25%. In year two with cerivastatin, the average increase in heart scan score was 8.8%. In 32 participants who achieved LDL<100 mg/dl on the drug, there was an average modest reduction in heart scan scores of 3.7% (i.e., -3.7%).

Now, that was eye-opening. Why did this small study achieve such startlingly different results from the other two studies that showed relentless progression despite even high doses of Lipitor? That remains unanswered. Was cerivastatin unique among statins? Did the unique two-phase trial design somehow change the outcome by triggering participants to change lifestyle habits after their first scan (since most exhibited an increase in score; they were not "blinded" to their scores). Those questions will remain unanswered, since the drug has been made unavailable. This smal l study had actually been intended to be larger, but was prematurely terminated because of cerivastatin's withdrawal.

This experience is unique, as you can see, compared to the two other studies. But it was also smaller. The results are also different than what I have seen in day-to-day practice when I've seen people treated with statin drugs alone (not cerivastatin, of course): rarely do heart scan scores stop increasing. While slowing does usually occur (18-24% per year rates of annual score increase are very common in people who do nothing but take a statin drug and make modest lifestyle changes), I have personally seen only two people stop their score with this strategy alone. Nobody has ever dropped their score taking a statin alone, in my experience.

You can also see the nature of clinical studies: single or limited interventions instituted in order to control for unexpected or complex effects. If three different treatments are used, then what desirable or undesirable effects, or lack of an effect, is due to which treatment agent?

My experience is that no single treatment stops or reduces heart scan scores. It requires a more rational effort that includes 1) identification of all causes of coronary plaque (e.g., low HDL, high triglycerides, Lp(a), small LDL, deficiency of vitamin D, etc, none of which are substantially affected by statin drugs), and 2) correction of all causes. That simple concept has served us well.