Cureality | Real People Seeking Real Cures

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.

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

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!

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.

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.

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.

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

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

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?"

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.

Here's a trick I learned after years of fussing over people's small LDL.

To gain better control over small LDL, follow blood sugars (blood glucose).

When you think about it, all the foods that trigger increases in blood sugar also trigger small LDL. Carbohydrates, in general, are the most potent triggers of small LDL. The most offensive among the carbohydrates: foods made with wheat. After wheat, there's foods made with cornstarch, sucrose (table sugar), and the broad categories of "other" carbohydrates, such as oats, barley, quinoa, sorghum, bulghur, etc.

Assessing small LDL requires a full lipoprotein assessment in which small LDL particles are measured (NMR, VAP, GGE). Not the easiest thing to do in the comfort of your kitchen.

However, you can easily and now cheaply check your blood sugar. Because blood sugar parallels small LDL, checking blood sugar can provide insight into how you respond to various foods and know whether glucose/small LDL have been triggered.

Here's how I suggest patients to do it:

1) Purchase an inexpensive blood glucose monitor at a discounter like Walmart or Walgreen's. You can buy them now for about $10. They're even sometimes free with promotional offers. You will also need to purchase lancets and test strips.

2) With a meal in question, check a blood sugar just prior to the meal, then again 60 minutes after finishing the meal. Say, for example, your pre-meal blood sugar is 102 mg/dl. You eat your meal, check it 60 minutes after finishing. Ideally, the postprandial (after-meal) blood sugar is no more than 102 mg/dl, i.e., no higher than pre-meal.

Perhaps you're skeptical that oatmeal in skim milk with walnuts and raisins will do any damage. So you perform this routine with your breakfast. Blood sugar beforehand: 100 mg/dl. Blood sugar 1 hour post: 163 mg/dl--Uh oh, not good for you. And small LDL will be triggered.

This approach is not perfect. It will not, for example, identify "stealth" triggers of blood sugar and small LDL like pasta, for the same reasons that pasta has a misleadingly low glycemic index: sugars are released slowly and not fully evident with the one-hour blood sugar.

Nonetheless, for most foods and meals, tracking your one-hour postprandial blood sugar can provide important insight into your individual susceptibility to sugar and small LDL-triggering effects.

C-reactive protein (CRP) is the liver product of inflammatory responses anywhere in the body. If there's an inflamed left knee, CRP will be increased. If viral bronchitis is making you cough, then CRP will be increased.

The argument put forward by the drug industry is that, because CRP indicates underlying inflammation, very low-grade levels that can be measured in the absence of overt inflammation like the sore knee or bronchitis is associated with increased risk for cardiovascular events. There are now many studies that conclusively demonstrate that, the higher the CRP, the greater the cardiovascular risk.

Naturally, any marker of risk is followed by the inevitable study: Do statin drugs reduce the excess cardiovascular risk of excessive CRP?

And, yes, indeed they do. My statin-crazed colleagues rave about the so-called "pleiotropic," or non-lipid, effects of statins. CRP reduction and the reduction of risk associated with CRP result with statin treatment.

But is life really statin vs. placebo, as most statin trials are constructed? Are there strategies that can outdo statins like Crestor for reduction of CRP?

A quick quiz:

How much omega-3 fatty acids, EPA + DHA, are in each capsule of fish oil with the composition shown on the label below:

If you said 1340 mg (894 mg + 446 mg), sorry, but you're wrong. There are 670 mg EPA + DHA per capsule.

Did you notice that the composition, or "Supplement Facts," lists the contents of two capsules? Rather than the usual one capsule contents, this product label lists two capsules.

I don't know why some manufacturers or distributors do this. However, I have seen many people tripped up by this kind of labeling, taking half the omega-3 fatty acids they thought they were taking. This can be important when you are trying to obtain a specific dose of EPA + DHA to reduce triglycerides, reduce Lp(a), control abnormal heart rhythms, reduce bipolar mood swings, or other important effects.

I liken this to pulling up to a gas station where the sign says gasoline for $1.25. Wow! Can't beat that! You then find out that it's really $1.25 for a half-gallon, or $2.50 a gallon.

In truth, the labeling is accurate; it's just very easy to not notice the two capsule composition.

Imagine this:

What is OLAVA?

Olava is prescription olive oil. It is the purest, highest concentration of olive oil available.

Why Do I Need a Prescription for OLAVA?

Studies show that olive oil contains essential fatty acids, "good" fats that:

--Contain natural compounds your body needs for good health but can't produce on its own.

--Has antioxidants that may provide protection from heart disease.

So, it is common for people to ask why they need a prescription for OLAVA if it is made from a natural ingredient--olive oil. It's time to get the facts about OLAVA. Learn why OLAVA is different from olive oil you can buy at a store.

OLAVA Is an FDA-Approved Medication

OLAVA is the only FDA-approved medicine made from olive oil that's proven, along with diet, to reduce risk for heart disease

The FDA enforces standards to make sure that prescription medications like OLAVA are safe, effective, and quality controlled.

The way OLAVA is manufactured is reviewed and approved by the FDA.

OLAVA uses a 10-step purification process that helps remove lead and other environmental toxins that can be present in olive oil.

Each 1-gram capsule of OLAVA contains 1000 mg of pure olive oil.

The FDA-approved dose of OLAVA is 4 capsules per day. It could take up to 2 tablespoons per day of regular olive oil to provide the same amount of active ingredients proven to lower heart disease risk.

What Else You Should Know About Olive Oil

Regular olive oil has not been approved by the FDA to treat any specific disease like heart disease.

Olive oil doesn't have specific dosing information; it has a food label.

Olive oil does not go through an FDA-approved manufacturing process.

Talk to Your Doctor About OLAVA

If you have very heart disease, you may need a prescription medicine, along with diet, to treat your condition. Talk to your doctor about OLAVA. Print a trial offer to use on your first prescription of OLAVA.

Let me tell you about my low-fat experience from 20 years ago.

At the time, I was living in Cleveland, Ohio, and served on the faculty at a large metropolitan university-affiliated hospital, supervising fellows-in-training and developing high-tech cath lab procedures like directional athererectomy and excimer laser coronary angioplasty. (Yes, another life.)

I was concerned about personal heart disease risk, though I knew next to nothing about lipids and coronary risk prediction outside of the little I learned in training and what the drug industry promoted.

I heard Dr. Dean Ornish talk while attending the American College of Cardiology meetings in Atlanta. Dr. Ornish spoke persuasively about the dangers of fat in the diet and how he "reversed" coronary disease using a low-fat, no added oils, no meat, vegetarian diet that included plenty of whole grains. So I thought I'd give it a try.

I eliminated all oils; I removed all meat, eggs, and fish from my diet. I shunned all nuts. I ate only low-fat products like low-fat yogurt and cottage cheese; and focused on vegetables, fruit, and whole grains. Beans and brown or wild rice were a frequent staple. I loved oatmeal cookies--low-fat, of course!

After one year of this low-fat program, I had gained a total of 31 lbs, going from 155 lbs to 186 lbs. I reassessed some basic labs:

HDL 28 mg/dl
Triglycerides 336 mg/dl
Blood sugar 151 mg/dl (fasting)

I became a diabetic. All through this time, I was also jogging. I ran on the beautiful paths along the Chagrin River in suburban Cleveland for miles north and south. I ran 5 miles per day most days of the week.

It was diabetes that hit me alongside the head: I was eating low-fat meticulously, exercising more than 90% of the population, yet I got fat and diabetic!

I have since changed course in diet. Last time I checked, my lipid values on NO statin agent:

HDL 67 mg/dl
Triglycerides 57 mg/dl
Blood sugar 91 mg/dl

That was my lesson that fat restriction is a destructive, misguided notion. The data since then have confirmed that restricting total fat is unnecessary, even undesirable, when fat calories are replaced by carbohydrate calories.

Here's just a smattering of the studies performed over the past 30 years on the psychological effects of wheat consumption.

Oddly, this never makes the popular press. But wheat underlies schizophrenia, bipolar illness, behavioral outbursts in autism, Huntington's disease, and attention deficit hyperactivity disorder (ADHD).

The relationship is especially compelling with schizophrenia:

Opioid peptides derived from food proteins: The exorphins.
Zioudrou C et al 1979
"Wheat gluten has been implicated by Dohan and his colleagues in the etiology of schizophrenia and supporting evidence has been provided by others. Our experiments provide a plausible biochemical mechanism for such a role, in the demonstration of the conversion of gluten into peptides with potential central nerovus system actions."

Wheat gluten as a pathogenic factor in schizophrenia
Singh MM et al 1976
"Schizophrenics maintained on a cereal grain-free and milk-free diet and receiving optimal treatment with neuropleptics showed an interruption or reversal of their therapeutic progress during a period of "blind" wheat gluten challenge. The exacerbation of the disease process was not due to variations in neuroleptic doses. After termination of the gluten challenge, the course of improvement was reinstated. The observed effects seemed to be due to a primary schizophrenia-promoting effect of wheat gluten."

Demonstration of high opioid-like activity in isolated peptides from wheat gluten hydrolysates
Huebner FR et al 1984

Is schizophrenia rare if grain is rare?
Dohan FC et al 1984
"Epidemiologic studies demonstrated a strong, dose-dependent relationship between grain intake and the occurrence of schizophrenia."

Measuring the number of small LDL particles is the best index of carbohydrate intake I know of, better than even blood sugar and triglycerides.

In other words, increase carbohydrate intake and small LDL particles increase. Decrease carbohydrates and small LDL particles decrease.

Why?

Carbohydrates increase small LDL via a multistep process:

First step: Increased fatty acid and apoprotein B production in the liver, which leads to increased VLDL production. (Apoprotein B is the principal protein of VLDL and LDL)

Second step: Greater VLDL availability causes triglyceride-rich VLDL to interact with other particles, namely LDL and HDL, enriching them in triglycerides (via the action of cholesteryl-ester transfer protein, or CETP). Much VLDL is converted to LDL.

Third step: Triglyceride-rich LDL is "remodeled" by enzymes like hepatic lipase, which create small LDL.

Carbohydrates, especially if they contain fructose, also prolong the period of time that triglyceride-rich VLDL particles persist in the blood, allowing more time for VLDL to interact with LDL.

Many people are confused by this. "You mean to tell me that reducing carbohydrates reduces LDL cholesterol?" Yes, absolutely. While the world talks about cutting saturated fats and taking statin drugs, cutting carbohydrates, especially wheat (the most offensive of all), cornstarch, and sugars, is the real key to dropping LDL.

However, the effect will not be fully evident if you just look at the crude conventional calculated (Friedewald) LDL cholesterol. This is because restricting carbohydrates not only reduces small LDL, it also increases LDL particle size. This make the calculated Friedewald go up, or it blunts its decrease. Conventional calculated LDL will therefore either underestimate or even conceal the real LDL-reducing effect.

The reduction in LDL is readily apparent if you look at the superior measures, LDL particle number (by NMR) or apoprotein B. Dramatic reductions will be apparent with a reduction in carbohydrates.

Small LDL therefore serves as a sensitive index of carbohydrate intake, one that responds literally within hours of a change in food choices. Anyone following the crude Friedewald calculated LDL will likely not see this. This includes the thousands of clinical studies that rely on this unreliable measure and come to the conclusion that a low-fat diet reduces LDL cholesterol.

Here's a great study from the prolific laboratory of Dr. Jeff Volek from the University of Connecticut. (Full text here.)

http://jn.nutrition.org/cgi/content/full/134/4/880

Dr. Davis is available for personal

one-on-one video teleconferencing

to discuss your heart health issues.

You can obtain Dr. Davis' expertise on issues important to your health, including:

Lipoprotein assessment

Heart scans and coronary calcium scores

Diet and nutrition

Weight loss

Vitamin D supplementation for optimal health

Proper use of omega-3 fatty acids/fish oil

Each personalized session is 30 minutes long and by appointment only. To arrange for a Video Teleconference, go to our Contact Page and specify Video Teleconference in your e-mail. We will contact you as soon as possible on how to arrange the teleconference.

The cost for each 30-minute session is $375, payable in advance. 30-minute follow-up sessions are $275.

(Track Your Plaque Members: Our Member cost is $300 for a 30-minute session; 30-minute follow-up sessions are $200.)

After the completion of your Video Teleconference session, a summary of the important issues discussed will be sent to you.

The Video Teleconference is not meant to replace the opinion of your doctor, nor diagnose or treat any condition. It is simply meant to provide additional discussion about your health issues that should be discussed further with your healthcare provider. Prescriptions cannot be provided.

Note: For an optimal experience, you will need a computer equipped with a microphone and video camera. (Video camera is optional; you will be able to see Dr. Davis, but he will not be able to see you if you lack a camera.)

We use Skype for video teleconferencing. If you do not have Skype or are unfamiliar with this service, our staff will walk you through the few steps required.

Of all the various factors we correct in the Track Your Plaque program in the name of achieving reversal of coronary plaque, there are two factors that are proving to be our greatest challenges:

1) Genetic small LDL

2) Lipoprotein(a)

More and more people are enjoying at least marked slowing, if not zero change or reduction, in heart scan scores following the Track Your Plaque program. We achieve this by correcting a number of factors. Some factors, like vitamin D deficiency, are easily corrected to perfection--supplement sufficient vitamin D to achieve a blood level of 25-hydroxy vitamin D of 60-70 ng/ml. Correcting standard lipid values--LDL cholesterol, HDL cholesterol, and triglycerides--child's play, even to our strict targets of 60-60-60.

However, what I call "genetic small LDL" and a subset of lipoprotein(a) are proving to be the most resistant of all.

Let's first consider genetic small LDL. Small LDL is generally the pattern of the carbohydrate-ingesting, overweight person. It has exploded in severity over the past decade due to overconsumption of carbohydrates due to the ridiculous low-fat notion. Reduce or eliminate carbohydrates, especially wheat, which permits weight loss, and small LDL drops like a stone. But there is a unique subset of people who express the small LDL pattern who start at or near ideal weight. Take Chad, for instance. At 6' 2" and 152 lbs and BMI of 19.6, there's no way excess weight could be triggering his small LDL. Yet he starts with 100% small LDL particles. All efforts to reduce small LDL, such as wheat, cornstarch, and sugar elimination; niacin; vitamin D normalization; thyroid normalization; and several supplements that yield variable effects, such as phosphatidylcholine, all leave Chad with more than 90% small LDL.

Lipoprotein(a) is a bit different. Over the past 5 years, our choices in ways to reduce Lp(a) expression have improved dramatically. Beyond niacin, we now have high-dose EPA + DHA, thyroid normalization that includes use of T3, and hormonal manipulation. In the Track Your Plaque experience, approximately 70% of people with Lp(a) respond with a reduction in Lp(a). (In fact, the 4 out of the 5 record holders for reduction of heart scan scores have Lp(a) that was successfully treated.) But about 30% of people with Lp(a) prove resistant to all these treatments--they begin with a Lp(a) of, say, 260 nmol/L and, despite niacin, high-dose EPA + DHA, and various hormones, stay at 260 nmol/L. It can be frustrating and frightening.

So these are the two true problem areas for the Track Your Plaque program, genetic small LDL and a subset of Lp(a).

We are actively searching for better options for these two problem areas. Given the collective exploration and wisdom that develops from such collaborative efforts as the Track Your Plaque Forum, I am optimistic that we will have better answers for these two stumbling blocks to plaque reversal in the future.

Rose is a 75-year old woman, mother of four, grandmother of many more.

Rose's story started after a heart attack 18 months ago that resulted in two stents. She was advised to follow an American Heart Association diet and take Lipitor. However, some months later, after her fourth stent, she became disilluioned in the conventional approach to heart disease and sought alternative therapies to help reduce or reverse her heart disease.

She found an alternative health practitioner who advised chelation, antioxidant vitamins for "excessive oxidation," and several homeopathic preparations.

Nothing was said about diet or exercise. Nothing was said about the baked flour products and pastries that occupied at least two meals every day. Nothing was said about the candies she indulged in several times per day, nor the soft drinks. Nothing was said about the wildly fluctuating blood sugars, poorly controlled by an oral diabetes agent. Thirty pounds of weight gain over the past 5 years with no exercise or physical activity? No comment here, too.

In short, Rose was the "graduate" of the conventional approach, as typically offered nationwide thousands of times a week. She was also the recipient of the insight of at least one alternative health practitioner, eager to reject conventional notions of how to achieve heart health.

So I then met her. She was experiencing chest pains every day, several times per day. Blood pressure over 200. At 5 ft, 3 inches, weight: 186 lbs.

Initial laboratory results:

HDL cholesterol 42 mg/dl
LDL 132 mg/dl
Triglycerides 263 mg/dl
Blood sugar 173 mg/dl

You can fill in the rest. In short, Rose was a disaster. Despite the attentions of several professionals from both the conventional as well as alternative camps, she was careening rapidly towards failure. She'd been given various crutches, Band-Aids, and salves, none of which resulted in any possibility of long-term relief from her aggressive disease.

My point: As I've said previously, all we want is truth. We want effective, rational approaches that yield real benefit. A stent? All that provides is temporary restoration of blood flow. Statin agents? They do indeed reduce LDL cholesterol. But what if Rose has 8, 9, or 10 other causes of heart disease unaffected by the statin drug? It will do little or nothing.

Nobody had addressed many of the root causes of Rose's disease: insulin resistance, high triglycerides, inactivity, obesity, hypertension (and identifying the reasons why her blood pressure was so high), vitamin D deficiency (virtually guarantted to be severe), junk foods including the ones known as "whole grains."

My message: Success in heart disease, as well as all aspects of health for that matter, doesn't necessarily have to come from an "alternative" approach, nor a "conventional" approach. It comes from applying what is truly effective, regardless of what label someone applied to it.

I would no sooner trust my health and life to an alternative health practitioner hawking unusual herbs and remedies than I would submit to a heart catheterization, three stents, followed by a statin drug. There's small benefit in both approaches, but none are the best. You've got to look elsewhere for that.

Copyright 2008 William Davis, MD

The Japan eicosapentaenoic acid (EPA) Lipid Intervention Study (JELIS) is a clinical trial that all Track Your Plaquers should know about.

This enormous trial followed a simple design:

Japanese men, between 40-75 years, and Japanese postmenopausal women aged <75 years with total cholesterol 250 mg/dl or greater were enrolled. A total of 18,645 subjects (mean age, 61 years; 31% male) participated: 36% had hypertension, 15% had diabetes, and 20% had coronary disease (history of heart attack or heart procedure). Average starting total cholesterol 275 mg/dl; LDL 180 mg/dl. All participants were treated with pravastatin 10 mg/day or simvastatin 5 mg/day; approximately half also received the omega-3, EPA, 1800 mg/day, in addition to one of the statin drugs.

Treatment resulted in an average LDL reduction of 26% in all participants; the group taking EPA experienced an additional 10% reduction in triglycerides. All major cardiovascular events were tracked and tabulated, including sudden cardiac death, fatal or nonfatal myocardial infarction (MI), unstable angina pectoris, coronary artery bypass surgery, and coronary angioplasty.

After nearly five years, 3.5% of statin-only participants experienced an event; 2.8% of statin + EPA experienced an event. The (often misleading and frequently abused value) "relative reduction" was therefore 19%.

There are several features that make the JELIS trial interesting:

--There were an unusually low number of cardiovascular events in the entire group, lower than nearly all American and European trials of similar design. This likely points to the greater burden of atherosclerotic heart disease in the U.S. compared to Japan. Rates in comparable U.S.-based trials usually range from 6-14%, sometimes more.

--Both the participants without identified heart disease at enrollment and those with heart disease at enrollment obtained a similar magnitude of beneficial reduction in cardiovascular events.

--There was an unusual preponderance of women--69%--unlike most other trials of cardiovascular events. We might therefore argue that JELIS most conclusively showed that benefits of EPA are most confidently demonstrated for females.

--A fish oil preparation containing only EPA was used, rather than the usual EPA + DHA. There are discussions from some corners that argue that DHA is more important than EPA, e.g., algae sources. However, JELIS would argue that EPA does play a role. Is EPA with DHA better, worse, or no different? Unfortunately, there are insufficient data--large, randomized data like JELIS--to help us. Recall that GISSI Prevenzione used a combination of EPA and DHA, as have virtually all other trials examining the effects of fish oil. Also, keep in mind that the epidemiologic observations of the cardiovascular benefits of eating fish suggest that the naturally-sourced omega-3s--a combination of EPA and DHA--are associated with benefit.

--It's surprising that any difference at all was demonstrated, given the high intake of fish in the Japanese. In fact, blood levels of EPA in participants before taking EPA was five-fold higher than in western populations.

One potential difficulty: The study was funded by the manufacturer of the EPA preparation used, Mochida Pharmaceutical Company. We all know what that can do to results.

Nonetheless, the JELIS trial is a study that adds to the emerging wisdom in fish oil.

Copyright 2008 William Davis, MD

Despite my rants in this blog and elsewhere, at least once a day I'll have a patient say, "I cut back (or eliminated) my fish oil because I get my omega-3s from _______ (insert your choice of flaxseed oil, walnuts, yogurt, mayonnaise, bread, etc.)."

(See prior Heart Scan Blog post: Everything has omega-3.)

When I point out to them that the "omega-3s" in these products are not the same as the EPA and DHA from fish oil, they invariably declare, "But it says so here on the label: 'Contains 200 mg of omega-3 fatty acids'!"

Apparently, some of my colleagues have even endorsed this concept of replacing the omega-3s from fish oil with these "alternatives."

It's simply not true. The linolenic acid that is being labeled as omega-3, while it may indeed provide health benefits of its own, cannot replace the EPA and DHA that fish oil provides.

The most graphic example of the differences between the two classes of oils is in people with a condition called familial hypertriglyceridemia. People with this condition have triglyceride levels of 400, 600, even thousands of mg/dl--very high. Fish oil, usually providing EPA and DHA doses of 1800 mg per day and higher, reduce triglycerides dramatically. A person with a starting triglyceride level of, say, 900 mg/dl, may take 2400 mg of EPA and DHA from fish oil and triglycerides plummet to 150 mg/dl. This person then decides to replace fish oil with a linolenic acid source like flaxseed oil. Triglycerides? 900 mg/dl--no effect whatsoever.

Familial hypertriglyceridemia represents an exagerrated example of the differences between the two oils. Even if you don't have this genetic condition, the differences between the oils still apply.

EPA and DHA are activators of the enzyme, lipoprotein lipase, that accelerates clearance of triglycerides from the blood. Linolenic acid from flaxseed oil, walnuts, and other food sources does not. EPA and DHA block after-eating (post-prandial) accumulation of food by-products that can contribute to coronary and carotid plaque. Linolenic acid does not. EPA and DHA block platelets, reduce fibrinogen, and exert other healthy blood clot-inhibiting effects. Linolenic does not.

The 11,000-participant GISSI-Prevenzione Trial that showed 28% reduction in heart attack, 45% reduction in cardiovascular death with omega-3s used . . . fish oil.

The 18,000 participant JELIS trial that showed 19% reduction in cardiovascular events when omega-3s were added to statin therapy used . . . fish oil. (Actually, in JELIS, they used only EPA wtihout DHA.)

Linolenic acid is not a waste, however. It may exert anti-inflammatory benefits of its own, for instance. But it exerts none of the triglyceride-modifying effects of EPA or DHA.

EPA and DHA from fish oil and linolenic acid from foods each provide benefits in their own way. Ideally, you include both forms of oils--fish oil and linolenic acid sources--in your daily diet and obtain full benefit from each separate class. But they are not interchangeable.

Copyright 2008 William Davis, MD

Several studies over the years have demonstrated a curious paradox:

People with more osteoporosis (thin bones) tend to be more likely to have coronary disease (heart attacks). They also tend to have higher heart scan scores (more coronary calcification as an index of atherosclerotic plaque).

People with more coronary disease and higher heart scan scores tend to have more osteoporosis.

In other words, regardless of which way you tackle the question--osteoporosis first or heart disease first--it leads to the same conclusion: Both conditions are somehow related.

I realize I harp an awful lot on this whole vitamin D issue. But, even after correcting the vitamin D blood levels of many hundreds of people, I remain enthusiastic as ever about the untapped potential of this fascinating factor.

So I couldn't resist showing this amazing comparison of how the long-term effect can be quite graphic.

The first scan is from a 46-year old man and shows normal coronary arteries without calcium and normal density of the vertebra (a common and reliable place to measure bone density).

The second image is from a 79-year old man with both severe coronary calcification (and therefore severe coronary disease) and severe osteoporosis.

It makes you wonder if the disordered metabolism of calcium through vitamin D deficiency allows transport of calcium away from bone and into coronaries. This has, however, been shown to not be the case. Instead, they are separate processes, each under local control, but sharing a common pathophysiology (causative factors).

An intriguing question: Would the 79-year old still look like the 46-year old had he begun increasing his vitamin D intake at, say, age 30?

Just a brief word about my responses to reader comments:

I appreciate the many often insightful and interesting reader comments I receive to the Heart Scan Blog. However, managing them and responding to them has simply become impossible, due to time demands.

I'm afraid that I am unable to answer questions seeking medical advice; this is for your doctor, who knows you and can diagnose and prescribe. I cannot.

I'm also unable to engage in lengthy debates; I've had commenters become very angry when I was unable to engage in lengthy conversations on some topic. Nor am I able to do Google or literature searches for commenters, or review studies, papers, or other materials.

I would urge any readers who wish to engage in in-depth discussions about these issues, talk about lipoproteins, heart disease reversal, etc. to do so on the Track Your Plaque Forums. Yes, it is a fee-for-membership website, a model that has become necessary to pay for the services we provide (not pay me).

I wish that I could answer all the concerns and questions that come my way, but it's simply physically impossible doing so while maintaining a full-time very busy cardiology practice, developing the Track Your Plaque website (which is becoming an enormous responsibility), publishing scientific data, maintaining hospital responsibilities, and spending time with my wife and family. We're all busy and I'm no different. I'm afraid that it's my responses to blog comments that I will have to sacrifice.

I invite commenters to continue to comment on these posts, as I've learned many new things by reading them and find them helpful feedback. And I do read them. Should an especially helpful comment be made, I will feature it in a new blog post, rather than respond directly.

I received this wonderful response to The Heart Scan Blog post Hammers and Nails:

I am 65 years old. I had a stent inserted in the "widow-maker" artery (80% blockage) a year ago. I had passed out a couple of times (heart rate dangerously low - 30s). I rode to the hospital in an ambulance. Tests revealed short LBBB episodes; mild mitral regurgitation, mild tricuspid regurgitation. Catherization showed 3 vessel CAD. I was told that a medicated stent was absolutely necessary given the situation; regardless, I have to accept that. A pacemaker was installed to prevent bradycardia and keeps heart rate from dropping below 60. I have 20% L distal main blockage and 90% lesion of the high first obtuse marginal at the takeoff. The right coronary had 60% posterior lateral branch stenosis.

Since then I have reduced TG from 360 to 60, LDL from 89 to 82 (although a few months ago it was in the mid-70s), and increased HDL from 30 to 46. I went from 265lbs to 190lbs and hope to eventually get to 180lb this Spring. I did it by progressing from walking to trotting (slow run) and dietstyle changes (low-GI veggies, fruits, etc.) .

On a recent visit the cardiologist said the the LDL needs to be 70 or below to "freeze" the 90% blockage and gave me a prescription for Lipitor. I asked if there were alternatives, like diet, supplements, etc. He admitted that he did not know about those alternative but did know Lipitor. When the only tool you have is a hammer then everything is a nail. I understand that the 90% blockage is important but will not take the Lipitor to achieve the 12 points reduction. Seems like an overkill.

I asked him if there was a way to evaluate my current condition. I was told there was no way. Basically, if I have no symptoms, good. If I have symptoms then it will have to be evaluated. Death could be the only symptom. I swear he was about to say bypass surgery ($$$$$$!) was inevitable. Something is wrong with this "fly-in-the-fog-and-hope-you-don't- hit-a-mountain" approach. Hope is not a strategy!

I am confident that I can reduce LDL to below 70 based on eliminating wheat-products in my diet plus increasing oat bran in my diet. I also take fish oil daily (EPA/DHA-2g). I am looking for a new cardiologist. I just recently purchased your book and find it very instructive. In the meantime I have an appointment with my primary care physician to discuss implementing the Track Your Plaque program. I realize that the one stent will skew the scan numbers but can be used as a baseline number.

Phenomenal weight loss! That alone has likely cut this man's risk in half. But is that it? Is the cardiologist correct--take Lipitor and hope for the best?

Of course not. There are many additional strategies to employ. Eliminating wheat from the diet is an excellent idea: HDL will skyrocket, triglycerides drop even further, small LDL will drop like a stone, blood sugar and blood pressure will drop. He will have more energy, get rid of afternoon energy slumps, sleep better.

He has already added fish oil. If his cardiologist did not mention this, I would say he was guilty of malpractice. The data supporting the addition of fish oil to the treatment program of anyone with heart disease is overhwelming. GISSI Prevenzione: 11,000 participants--28% reduction in heart attack, 45% reduction in death from heart attack. The Japanese JELIS trial of 18,645 participants--19% reduction in dangerous heart events. It's also clear that omega-3 fatty acids from fish oil also compound the benefits of statin agents, should this man choose to begin Lipitor.

Vitamin D brought to normal blood levels is his next "secret weapon" that will further boost his lipids and lipoproteins further into not just "normal" territory, but beyond belief. Even though we aim for 60-60-60 for LDL-HDL-triglycerides in the Track Your Plaque program, adding vitamin D can yield numbers you've never seen before. It's not uncommon, for instance, to see a 10 or 20 mg/dl jump in HDL.

Identify all other hidden causes of coronary plaque. If all the causes have not been fully identified, how can anyone hope to gain full control over coronary plaque growth?

Re: LDL cholesterol of 89 mg/dl at the start. Of course, this is a calculated value, not measured. Because HDL was low and triglycerides high at the start of his program, this means that true LDL--if actually measured--was probably more like 180 to 250 mg/dl, and it was probably nearly all small. So his cardiologist might have advised a helpful treatment, though for the wrong reasons.

Our reader has gone a long way on his own in creating his own prevention program. But there's yet more to do, particularly if the goal is reversal. It is shocking to me that a man like our reader, clearly articulate and motivated, gets virtually no advice beyond "take Lipitor" after all the procedural benefits have been reaped.

Even though one artery can no longer be "scored" due to the presence of the metallic stent, a heart scan would still be invaluable for long-term tracking purposes, just as we advocate in the Track Your Plaque program.

Copyright 2008 William Davis, MD

HeartWire, the news service of www.theheart.org, posted the following report:

Pfizer pulls Lipitor ads featuring Dr Robert Jarvik in HeartWire

New York, NY - After a series of questions and attacks over its choice of Dr Robert Jarvik to endorse Lipitor in a series of TV commercials, Pfizer has announced that it is withdrawing the ads. As previously reported by heartwire, Jarvik invented the first artificial heart, but he is not a cardiologist, nor does he hold a medical license—factors that drew criticism from detractors and made him and Pfizer a target of a US House Committee on Energy and Commerce investigation into celebrity endorsements in direct-to-consumer advertisements.

In a January 2008 statement, committee chair Rep John D Dingell (D-MI) observed: "Dr Jarvik's appearance in the ads could influence consumers into taking the medical advice of someone who may not be licensed to practice medicine in the United States. Americans with heart disease should make medical decisions based on consultations with their doctors, not on paid advertisements during a commercial break."

Complaints about Jarvik went up a notch this month when the latest ad in the series depicted the inventor rowing a racing scull across a lake, despite the fact that Jarvik himself does not row and the commercial used a body double.

This is typical pharmaceutical industry sleight-of-hand, now you see it, now you don't, that has come to define their policies. And this is just the stuff that comes to light because of some obvious blunders. We can only begin to imagine what sorts of other shenanigans have been swept under the rug, especially adverse effects of drugs that never made it to the light of publication.

Is this just another example of how direct-to-consumer advertising has backfired? I now have patient after patient tell me that they have been so overwhelmed and fed up with TV and magazine ads for drugs that they

Other media outlets have reported that Jarvik was guaranteed $1.35 million for the ads and that Pfizer spent $258 million on Lipitor advertisements between January 2006 and September 2007.

I'm sure you've heard the old saying that,

To a man with a hammer, everything looks like a nail.

It couldn't be truer than in heart procedures (the man with the hammer) and heart disease (the nail).

What does it take in 2008 to become an interventional cardiologist trained in all the techniques of angioplasty, stenting, intracoronary ultrasound, etc.? Start with your undergraduate degree (4 years), then medical school (another 4 years), then training in internal medicine (3 years), then general cardiology taining (3 years), then an additional year in interventional cardiology. Each step along the way also involves competing for these spaces, a process that requires much time, money, and sweat.

The total time investment is 15 years after high school. Many if not most college students graduate with debt. Pile on the substantial cost of medical school. Training after medical school pays a modest salary, enough for a single person. Many trainees by then have spouses and a family, would like to buy a house, have bills to pay. (I managed to buy my first house for $69,000 in Columbus, Ohio and paid my mortgage by sleeping only every other night and moonlighting on my off nights.)

By the time the interventional cardiologist-in-training finishes his/her 15 years, they are hungry for a hefty increase in income. After such a time and money investment, I do believe that there is at least some justification for generous income for the years of work involved.

Back to our hammer and nail metaphor. Not only do we now have a man or woman with a hammer, but a really expensive hammer that required a substantial amount of effort to obtain. Now, our hapless hammer-bearer is desperate to see everything in sight as a nail.

You're seen in consultation by this fresh interventional cardiologist in practice for only a few years. Guess what he/she advises? Go straight to the catheterization laboratory, of course. Throw in the fact that insurance reimbursement is most generous for heart procedures, far more than for consulting in the office, doing a stress test, or other simpler, non-invasive tests, and the incentives are clear.

The system, you see, is set up to follow such a path. The path to the cath lab is heavily incentivized, paths in the other direction discouraged, disparaged, or just ignored.

My message: Don't get nailed.

What is abnormal?

You'd think that the answer would be easy and straightforward.

However, consider these instances of medical findings that I have witnessed fall repeatedly into the "normal" category:

Diameter of the thoracic aorta: 4.5 cm

Mild coronary plaque by heart catheterization

Carotid plaque of 30-50%

Why isn't a thoracic aorta (the big artery in your chest) of 4.5 cm normal? Because it can be expected to increase in diameter by about 2.5 mm (0.25 cm) per year. All posts by william-davis

When meat is not just meat

18. December 2007 William Davis (7)

Don't lament no OTC mevacor

17. December 2007 William Davis (4)

Damage control

15. December 2007 William Davis (5)

Low expectations

12. December 2007 William Davis (6)

Niacin vs. low-carb weight loss

10. December 2007 William Davis (28)

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

10. December 2007 William Davis (3)

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?"

6. December 2007 William Davis (14)

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
9100 San Gregorio Road
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

6. December 2007 William Davis (7)

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?

3. December 2007 William Davis (17)

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

3. December 2007 William Davis (6)

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.

Risks for coronary disease 2008

Food sources of vitamin K2

Track Your Plaque: Naughty or nice?

Vitamin D: Treatment for metabolic syndrome?

Appetite stimulants

"Heart scans are experimental"

When meat is not just meat

Don't lament no OTC mevacor

Damage control

Low expectations

To track small LDL, track blood sugar

C-reactive protein: Fiction from the drug industry?

Watch your fish oil labels

Why do I need a prescription for Olava?

Overweight, hungry, diabetic, and fat-free

This is your brain on wheat

Small LDL: Perfect index of carbohydrate intake

Fat "conditioning"

Video Teleconference with Dr. William Davis

Track Your Plaque challenges

Conventional therapy vs. alternative therapy

The JELIS Trial

Omega-3 MUST be from fish oil

Osteoporosis and coronary calcium

About comment responses and moderation

"Flying in the fog"

Goodbye, Dr. Jarvik

Hammers and nails

What is abnormal?

When meat is not just meat

Don't lament no OTC mevacor

Damage control

Low expectations

Niacin vs. low-carb weight loss

Explosive plaque growth

Dr. Cannell on "How much vitamin D?"

End-stage vitamin D deficiency

"Instant" reversal with fasting?

Study review: yet another Lipitor study