It is the craziest thing.

The notion of vitamin D being easily and readily toxic has grabbed hold of many people, including my colleagues who were taught that vitamin D was toxic in medical school based on the skimpiest (and often misinterpreted) observations in a handful of unusual cases.

In my practice and in the Track Your Plaque program, we routinely use doses of 2000-10,000 units per day, occasionally more. We are guided by blood levels of 25(OH) vitamin D3. I have personally never witnessed vitamin D toxicity.

Here's an interesting graph from Dr. Reinhold Vieth. Those of you familiar with the vitamin D argument know that Dr. Vieth is among the few genuine gurus in the vitamin D world.

From Vieth R. Vitamin D supplementation, 25-hydroxyvitamin D concentrations, and safety. Am J Clin Nutr 1999;69:842-856. (Full text is available without charge.)

In the graph, the X's represent toxicity; circles fall within the non-toxic range. (Toxicity is generally defined as a level sufficient to raise blood calcium levels, "hypercalcemia.") Note that the 25(OH) vitamin D3 levels are given in nmol/L; to convert to ng/ml units that are customary in the U.S., divide the nmol/L value by a factor of 2.5.

You will notice that toxicity is virtually unheard of until the dose exceeds 10,000 units per day. Beyond 10,000 units per day, the curve heads upward sharply and toxicity does become a possibility, though not an absolute (since there are circles above 10,000 units).

You may also notice that the curve is relatively flat from vitamin D doses between 200 units and 10,000 units (log scale on x axis; arithmetic scale on y), the range of most common doses for vitamin D supplementation.

Another perspective on vitamin D blood levels is to examine the blood levels of people who are young and obtain plentiful sun exposure. Lifeguards, for instance, have blood levels of 84 ng/ml (210 nmol/L) without ill-effect. (Sun exposure cannot generate vitamin D toxicity, because of a feedback safety mechanism in skin.) While this may not represent an ideal level since they represent an extreme, it does provide reassurance that such levels are non-toxic. I also point out these levels occur in the youthful since most people lose 75% or more of vitamin D activating capacity in the skin by their 70s. Most of us over 40 are kidding ourselves if we think that a suntan provides sufficient vitamin D.

Keep in mind that it is not necessarily the dose of vitamin D that is toxic, but the blood level it generates. I take 10,000 units of vitamin D as a gelcap per day to maintain my blood level between 50-60 ng/ml (125-150 nmol/L). This strategy helps me keep my HDL in the 70-80 mg/dl range, my blood sugar around 90 mg/dl, my blood pressure <120/80, and I no longer experience colds nor winter "blues."

Copyright 2008 William Davis, MD

For reasons unknown to me, I received a solicitation to invest in a company called Prescient Medical, with a slogan that caught my eye:

Detect and treat heart attacks before they occur.

The glossy brochure details their technology development strategy:

Predict(TM) Optical Catheter System--A catheter introduced into the coronary artery during a catheterization procedure to determine whether a specific plaque or vessel area is "vulnerable," i.e., prone to rupture in future.

Protect(TM) Luminal Shield--A stent-like metal device deployed into the coronary artery at the region of vulnerable plaque to prevent future plaque rupture.

The company anticipates FDA approval for their systems by 2009 and sales to begin by 2010. They predict sales of $7 billion.

Let's stop and think about this for a moment. It seems to me that, rather than pursuing the market of another stent for a "severe blockage," this company is going after the untapped procedural market of vulnerable plaque. In other words, their technology (an optical sensor technology that emits and analyzes light wavelengths to map specific plaque characteristics) identifies plaque that may rupture in months or years, followed by implantation of stent(s) that presumably prevent plaque rupture.

Thus, conceivably, many 20%, 30%, 40% etc. "blockages", atherosclerotic plaques that do not block flow and thereby pose no need for a conventional stent, will end up with this new type of stent. One patient could therefore receive multiple "Luminal Shields" in a single procedure.

When would these devices be employed? One pathway I could conceive of that my colleagues will be sure to exploit is 1) identify plaque by CT angiography, then 2) bring patient to the catheterization laboratory and perform this procedure for whatever hot, vulnerable plaques are identified. In other words, symptoms are no longer necessary. Reduced blood flow is no longer necessary. An abnormal stress test is no longer necessary. All that is required is that you have plaque. If the plaque is then determined to be vulnerable, then it is stented.

What bothers me about all this is the emerging effort to exploit this untapped market--a big one--of early heart disease as identified by coronary atherosclerotic plaque. As heart scans have demonstrated, there is an enormous amount of hidden heart disease in this world. This company has discovered a way to turn plaque into a profit opportunity, much as the statin drug industry found a way to "turn cholesterol into money."

The conventional stent market has plateaued and now has been, to some degree, battered by the drug-coated stent argument. Prescient has found a new and significant market for procedures and stents.

Is this really necessary? Why does plaque have to become a procedural disease? Doesn't it make more sense that, if vulnerable plaque is identified, that clinical trials are then designed to develop treatment strategies that modify vulnerable characteristics? Shockingly, this has not been done to any significant extent. Instead, the easiest path to a profit opportunity is to implant a "Luminal Shield."

You and I are able to inactivate, disempower, and essentially shut down plaque, while others are working furiously to convert it into a procedural profit opportunity. I personally find this so distasteful that I would sooner endorse a high-dose statin strategy than this approach.

You can view a video of my colleague, Dr. Martin Leon, on the Prescient Medical website, (or click here to go directly to the video), talking about how this technology will "change the treatment paradigm of the interventionalist from reactive to proactive." Scary stuff. Dr. Leon has made millions of dollars (probably more like tens of millions of dollars) from his support of technology companies for the interventional coronary device market.

My hope is that word of the sorts of techniques we use in the Track Your Plaque program disseminate before this sort of luminal coating idiocy gets off the ground.

(In actuality, a different version of this approach has been available for years using intravascular ultrasound (IVUS), another procedure that involves threading a catheter down each coronary artery during a catheterization procedure. IVUS can also cross-sectionally map a plaque's anatomy and identify "vulnerable" features, like a thin cap overlying a collection of semi-liquid fat ("lipid pool"). There has been some discussion of using this approach to identify vulnerable plaque followed by stent implantation, but it has never gotten off the ground and has certainly not found validation in any clinical study. By the way, any stent prevents plaque rupture, since by their very nature, the plaque contents are compressed, modified, and excluded to the exterior of the stent. Plaque rupture within a stent is very rare in its few millimeters of length. It may therefore not require some new technology to prevent plaque rupture.)

Evan's first heart scan score in November, 2006 yielded a high score for a 56-year old male: 542.

So he put up little fuss when his doctor prescribed simvastatin at a high dose.

Evan's LDL cholesterol before simvastatin: 158 mg/dl

Evan's LDL cholesterol on simvastatin: 72 mg/dl.

By conventional standards, Evan has had an excellent response. The rest of his lipid (cholesterol) panel was unrevealing: HDL 62 mg/dl, triglycerides 78 mg/dl. Evan doesn't smoke, has a normal blood pressure, and he is not diabetic. That should do it, right?

So his doctor thought. So Evan asked if another heart scan was in order. In December, 2007, after one year of simvastatin, his second heart scan score: 705--a 30% increase over one year.

Recall that, with no effort at prevention whatsoever, the natural progression of heart scan scores is a 30% per year increase. Did simvastatin do nothing?

This is quite typical of people who do nothing more than take a statin drug. While some people do slow plaque growth (we say "decelerate") modestly on a statin drug, Evan's experience is not unusual: plaque continues to grow despite high-dose statin drug and an apparently favorable cholesterol panel.

In fact, I can count the number of people who reduced their heart scan scores taking a statin drug alone on one finger.

Statins do not represent a cure for heart disease. They cannot be used as sole therapy to reduce risk for heart attack. In fact, given sufficient time, the majority of people who do nothing more than follow this standard line of treatment (along with the equally lame low-fat diet, etc.) will have done nothing more than postpone their heart attack. Elimination of risk? Nope.

This is among the reasons we developed the Track Your Plaque approach. While not foolproof, I know of no better approach to seize control over plaque growth.

Additional conversations on clinical studies which, as with Evan's experience, demonstrated how statin drugs fail to slow plaque growth can be found in previous Heart Scan Blog posts:

Don't be satisfied with "deceleration"

Study review: Yet another Lipitor study

Copyright 2008 William Davis, MD

Triglycerides are a potent trigger for coronary plaque growth.

Triglycerides in and of themselves probably do not cause plaque growth. Instead, triglycerides contribute to the formation of abnormal lipoproteins in the blood that, in turn, trigger coronary plaque, like VLDL, intermediate-density lipoprotein (IDL), and small LDL. Excess triglycerides also modify HDL structure and cause you to lose HDL in the urine.

I see plenty of people who begin with triglycerides of 200 mg/dl, 300, 700, even over 1000 mg/dl. It doesn't take long before you learn what works, what doesn't to reduce triglycerides. This is especially true in the Track Your Plaque approach, in which our target for triglycerides is 60 mg/dl or less.

Here's a list of things to consider if you are trying to gain control of your triglycerides:

--Fish oil--A mainstay of treatment. The omega-3 fatty acids from fish oil are the number one most potent treatment for high triglycerides.

--Reduction of high-glycemic index foods--Most notably wheat. Everybody knows that we shouldn't eat Snickers bars or bags of licorice. But many people eat plenty of wheat-containing breads, pastas, pretzels, crackers, breakfast cereals, etc., all in the name of increasing whole grains and fiber. In reality, they are causing triglycerides to skyrocket, dropping HDL, forming small LDL, increaaing blood sugar and blood pressure, and increasing obesity.

--Eliminating fructose and high-fructose corn syrup--This ubiquitous sweetener is now consumed in enormous quantities by the average American, nearly 80 lbs per year per person. You'll find it in soft drinks, ketchup, beer, breads, breakfast cereals, and many other processed foods. You'll find none in green peppers, cucumbers, and raw nuts. Fructose causes large rises in triglycerides, as well as diabetic patterns. Don't let "fat-free" claims fool you. Take a look at the ingredients in Kraft Fat-Free Caesar Italian salad dressing, for instance:

Kraft Fat-Free Caesar Italian

Ingredients:
Water, Vinegar, High Fructose Corn Syrup, Corn Syrup, Salt, Parmesan Cheese, Part-Skim Milk, Cheese Culture, Salt, Enzymes, Contains less than 2% of Garlic, Whey, Onion Juice, Autolyzed Yeast Extract, Phosphoric Acid, Worcestershire Sauce, Vinegar, Molasses, Corn Syrup, Water, Salt, Caramel Color, Dried Garlic, Sugar ,Spices, Tamarind, Natural Flavors, Hydrolyzed Soy Protein, Xanthan Gum, Potassium Sorbate and Calcium Disodium EDTA as Preservatives, Dried Garlic, Buttermilk, Spice, Dried Parsley, Caramel Color, Sodium Phosphate, Oleoresin Paprika.

--Alcohol--While a couple of drinks a day raises HDL, exerts anti-inflammatory effects, and reduces blood pressure, more than this begins to raise triglycerides. Although I've come across no formal studies on this question, my gut sense is that beer, in particular, raises triglycerides more than wine or other alcoholic beverages. Could it be the wheat source of beer? Or its high-fructose corn syrup? I don't know, but beer is the least desirable form of alcohol of the choices we have.

Following these simple steps, it is unusual in my experience that you cannot achieve a triglyceride level <60 mg/dl. Rarely do we need to add fibrate drugs or other prescription agents to reduce triglycerides.

Copyright 2008 William Davis, MD

Lipoprotein(a), or Lp(a), is a problem area in coronary plaque reversal.

While our current Track Your Plaque record holder for largest percentage reduction in heart scan score has Lp(a), it remains among the more troublesome lipoprotein patterns.

One unique treatment for Lp(a) is high-dose omega-3 fatty acids from fish oil. While the data are relatively meager, there is one solid study from Lp(a) expert, Dr. Santica Marcovina of the University of Washington, called "The Lugalawa Study."

In this unique set of observations, 1300 members of a Bantu tribe living in Tanzania were studied. What made this population unusual is the fact that two groups of Bantus lived under different circumstances. One group lived on Nyasa Lake (3rd largest lake in Africa and reputed to have the greatest number of species of fish of any lake in the world) and ate large quantities of freshwater fish providing up to 500 mg of omega-3s, EPA and DHA, per day. Another Bantu group lived away from the lake as farmers, eating a pure vegetarian diet without fish.

Nyasa Lake

This situation among genetically similar stock provided a unique learning opportunity, a chance to assess whether different diets influenced Lp(a) levels.

The results: The fish-eating Bantus had an average Lp(a) level of 14.0 mg/dl. The farming, non-fish eating Bantus had an average Lp(a) of 27.0--a 48% difference. Curiously, a comparison of the apo(a) component of Lp(a) between the groups also showed that the fisherman expressed fewer dangerous small apo(a) forms, despite equal potential to express both.

The Lugalawa Study opens the question of whether similar results can be obtained not by moving to Tanzania and fishing Nyasa Lake, but by mimicking their experience by supplementing high doses of omega-3 fatty acids.

It's an intriguing question. In the Track Your Plaque program, we have no specific experience with this strategy, but it is certainly worth exploring further.

Watch for two upcoming Special Reports on the Track Your Plaque website in which we will be detailing 1)unique strategies for Lp(a) reduction, and 2) the usefulness of high-dose fish oil for coronary plaque reversal.

Interesting enough for a Virtual Clinical Trial?

Image courtesy Wikipedia.

Copyright 2008 William Davis, MD

Pam has an LDL cholesterol of 144 mg/dl.

To most people, this means that she has a mildly elevated LDL value. Many people would respond by cutting the saturated fat in their diet. Most physicians would concur and talk about prescribing a statin drug.

Let me tell you what an LDL cholesterol of 144 mg/dl means to me:

1) It could mean an LDL of all large particles (which is good) or an LDL of all small particles (which is very bad). Or, perhaps it's some combination of big and small. I can't tell which just by knowing that LDL is 144.

Small LDL responds to a diet reduced in processed carbohydrates and wheat flour; large LDL does not. Small LDL responds in an exagerrated way to niacin; large LDL does not. It makes a difference.

2) It could mean that, hidden within LDL, is lipoprotein(a), or Lp(a). Recall that Lp(a) is a high-risk genetic pattern that can provide the false appearance of high LDL cholesterol. If Pam were prescribed a statin drug, it would have little effect and little benefit. (See Red flags for Lipoprotein(a).)

Knowing that Pam has Lp(a) can point us in an entirely different direction than just LDL cholesterol. It might mean high-dose fish oil, a more serious approach to niacin, hormonal treatments like DHEA or testosterone. It might mean more attention to warning your children about the possibility that they, too, might share this genetic trait.

3) It could mean both small LDL and Lp(a) are present simultaneously, an especially dangerous combined pattern that is among the highest risks for heart disease known.

4) Because Pam's LDL of 144 mg/dl was not measured, but calculated, it means that it is subject to tremendous inaccuracy.

In my office, calculated LDL cholesterols can be inaccurate by 50 or 100 mg/dl--commonly. So Pam's LDL of 144 mg/dl could really be 70 mg/dl, or it could be 244 mg/dl. Once again, it's a big difference.

Just like The Three Faces of Eve, the 1957 film in which Joanne Woodward played the three wildly different sides of Eve's personality--the daytime Eve White, the fun-loving and daring Eve Black, and Jane--so can LDL assume several different faces, all with different personalities, different implications.

Accepting LDL cholesterol as LDL cholesterol is a fool's game. It is only a starting point, nothing more. Accepting a statin drug based on LDL is, likewise, a trap fraught with uncertainty, the potential for limited or ineffective results, the price being your heart and health.

Don had an angioplasty 6 months ago. When asked about the symptoms that prompted him to go to the hospital, he explained:

"I remember feeling really tired for about a week before I went. I'd read that fatigue can sometimes be a sign of heart disease. But then I had some trouble breathing. You know, like not being able to get a deep breath."

"My wife and I were planning on going on vacation. So I wanted to be certain something wasn't going on in my heart. That's when my wife insisted that she take me to the hospital.

"I kind of remember going there and arriving in the emergency room, but then I don't remember anything. Next thing I know, I'm waking up in a hospital bed. My wife and kids were there, looking all concerned. They said that I just got two stents and that the doctor just barely saved my life."

Happy story, happy ending? Not quite.

I reviewed the angiograms made during Don's hospital stay. They did, indeed, show some plaque, but not anywhere close to the amount necessary to account for symptoms like fatigue or breathlessness. For symptoms like this to occur without physical exertion, say, at your desk or relaxing at home, a critical >90% blockage would be required.

The worst "blockage" Don had was 50% at most. The leap was made to connect his relatively vague symptoms with these "blockages," leading to the implantation of two stents.

This is not as uncommon as you think. Yes, the practice of cardiology can be a life of acute procedures, urgent situations, and crises. Unfortunately, some people with questionable need for these procedures also get swept up in the wave. Sometimes it's due simply to the doctor's need to do "something," nervous family waiting in the wings. Sometiems it's intellectual laziness: putting in two stents seems to satisfy many patients' needs to have something "fixed," even when symptoms like fatigue could be due to anemia, sleep deprivation, a thyroid disorder, or any other myriad conditions that require a diagnostic effort (otherwise known as thinking). And sometimes it's simply done with financial motives, since angiplasty and related procedures pay well.

I call this "drive-by angioplasty," the impulsive, poorly considered coronary procedure that really should never have happened. How often does this happen? What percentage of heart procedures fall into this category? There are no clear-cut estimates. There are crude attempts by independent agencies that have put the number of unnecessary heart catheterizations up to 20% of the total number performed. The proportion of angioplasty procedures, stents, etc. that are not necessary is a tougher number to pinpoint, given the uncertainties surrounding the indications for these procedures, physician judgment that factors into the decision-making process, and the fact that many decisions are made on a qualitative basis, not precise quantification.

In real life, I would put the proportion of flagrant drive-by procedures at no more than 10%. However, that is 10% of an enormous number. The annual cardiovascular healthcare bill is $400 billion. 10% of that is $40 billion--an unimaginable sum. It also adds up to tens of thousands of people per year needlessly subjected to procedures. Consider that 10,000 heart procedures were performed today alone.

Should we push for legislation to control how and when heart procedures are performed? I don't think so. Despite my criticisms of the status quo in heart care, I still favor the freedom and rapid development of a free-market approach. However, you as a healthcare consumer need to be armed with information. You don't go to the car dealer unarmed with information on prices and comparative performance of the car you want. You should do the same with health. Information is your weapon, your defense against becoming the victim of the next drive-by heart procedure.

"Bankers believe liquidation has run its course and advise purchases."

New York Times headline, Oct 30, 1929, at the start of the Great Depression.

"I did not have sexual relations with that woman, Ms Lewinsky."

Former President Bill Clinton at a Washington Press Conference, 1998.

"The third quarter is going to be great."

Enron CEO, Ken Lay, just before the company reported a $638 million third-quarter loss, triggering the company's collapse.

Should we add the following to the list?

Heart Healthy Bisquick

Heart Healthy snacks according to the National Heart, Lung, and Blood Institute:

Animal crackers, devil's food cookies, fig and other fruit bars, ginger snaps, graham crackers, vanilla or lemon wafers

Angel food cake or other lowfat cakes

Low fat frozen yogurt, ice milk, fruit ices, sorbet, sherbet

Pudding (make it with fat free or 1% milk), gelatin desserts

Popcorn without butter or oil; pretzels, baked tortilla chips

67% digestible carbohydrates/sugars from corn syrup, sugar, raisins, and honey. Oh, yes . . . and it contains plant sterols.

"Heartzels are a healthy snack alternative for anyone wanting to control fat intake and add fiber to their diet," said Tracy LaRosiliere, a Frito-Lay vice president of marketing. "What better time for Frito-Lay to launch its first heart-healthy snack than during American Heart Month and just in time for Valentine's Day."

The relationship with the American Heart Association and the launch of Rold Gold Heartzels Pretzels is the latest move by Frito-Lay to continue its commitment to offering a wide variety of low-fat and better-for-you snacks nationally, which like the company's assortment of regular chips can be enjoyed as part of a healthy diet and lifestyle.

Imagine that I'm planning to build a wall of bricks. I start by throwing cement at a pile of bricks, hoping that it forms a nice, orderly brick wall.

Fat chance, you say.

I believe that is what appears to be emerging as the situation with calcium supplementation.

A recent study from New Zealand reported an experience with 1,471 postmenopausal women, mean age of 74 years, who were randomized to treatment with either calcium supplements or placebo. Calcium was supplied as calcium citrate (Citrical) to provide 1000 mg of (elemental) calcium per day (400 mg morning, 600 mg evening).

(Bolland MJ, Barber PA, Doughty RN et al. Vascular events in healthy older women receiving calcium supplementation: randomised controlled trial. Brit Med J BMJ, doi:10.1136/bmj.39440.525752.BE; published 15 January 2008)

Over 5 years, women taking calcium had twice the risk of having a heart attack compared with women taking the placebo; women taking calcium had a 47 percent higher risk of having any one of three "events" (heart attack, stroke or sudden death) than women in the placebo group.

The findings of this study run counter to what we've been telling people all these years: Calcium supplementation, usually taken to halt deteriorating bone health and osteoporosis, modestly reduces blood pressure, reduces LDL and raises HDL cholesterol. At first blush, we might thereby presume that it also reduces cardiovascular events.

This study suggests that calcium supplementation does not result in reduction of cardiovascular events, perhaps even increases risk.

Certainly, this new finding will serve to confuse the public even more than it is already, particularly when it comes to strategies that modify risk for heart attack. However, this may make more sense once we stop and think for a moment.

Calcium supplementation inarguably slows, occasionally halts, calcium resorption from bone (through suppression of parathyroid hormone). Calcium also accumulates as part of atherosclerotic plaque in coronary and other arteries.

How does oral calcium know where to go--bones, not arteries or kidneys, in addition to serving all its other crucial functions?

Keep in mind that, in many roles, calcium is passive, something that responds to control exerted by some other factor. Vitamin D is that factor. Vitamin D controls the absorption of calcium in the intestinal tract (calcium aborption quadruples when vitamin D is restored to normal), it controls whether calcium is deposited in bone or extracted from arteries. It is the master control over the fate of calcium. Calcium just goes along for the ride.

Bone and arterial health do indeed intersect via calcium, but not through calcium supplementation. Instead, the control exerted by vitamin D (and vitamin K2, another conversation) connects the seemingly unrelated processes.

At what calcium dose threshold do the benefits stop and the adverse effects begin? That remains unanswered, particularly in light of this new study. However, this study calls into serious question the wisdom of supplementing calcium at a dose of 1000 mg, particularly when taken without normalization of vitamin D.

Calcium is therefore emerging as an important player in artery health. But just taking calcium makes no more sense than our brick wall and cement analogy. You might regard vitamin D as the mason that skillfully lays down both brick and cement in a neat, orderly way.

Lorenzo is an 81-year old retired manufacturing engineer whose intial heart scan score in late 2006 was an alarming 1102.

Recall that, despite feeling well and having a normal stress test, Lorenzo was facing a heart attack and death risk that was as high as 25% per year without preventive action.

Lorenzo was moderately interested in the Track Your Plaque concepts. While not exactly the most highly motivated, he did see the rationale in our approach. But he came to us mostly because his primary care doctor told him to.

Nonetheless, one year later, he underwent another heart scan. His score: 588--a 46.6% drop in score, nearly cutting his plaque in half. While Lorenzo didn't set any new records in terms of percentage drop in score, he has reduced his score in real numbers more than anybody else before: a 514 point drop in score.

Lorenzo joins the ranks of our current record holders, Amy, with a 63% drop in heart scan score, and Neal with a 51% drop in score. Both of these Track Your Plaque record holders, while achieving larger percentage reductions in score, achieved less when viewed on an absolute number basis.

Now, breaking records is not necessary to succeed in the Track Your Plaque program or at heart disease reversal. Even 1% reversal is still a big success, certainly more than is achieved in conventional practice.

No special commitment was necessary in Lorenzo's case. All he required was a little of the right kind of information. I can tell what he didn't do: Lorenzo did not follow a low-fat American Heart Association diet, he did not take high-dose statin drug, he did not deprive himself of food, he did not exercise to extremes. He just applied some simple strategies from the Track Your Plaque program.

I play these sorts of games just to make a point and to show just what is possible. While the world of hospital procedures and emergency management of coronary disease marches on, we are quietly reversing the disease. Sometimes, we achieve results that even surprise ourselves.

Lorenzo's full story will be detailed in the February 2008 Track Your Plaque newsletter. If you are not yet a subscriber, you can sign up (without cost)here.

Copyright 2008 William Davis, MD

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.

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.

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.

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.

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?

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

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.

Vitamin D toxicity

Turning plaque into profit

Statin mono-failure

Triglyceride traps

High-dose fish oil for Lp(a)

The many faces of LDL

Drive-by angioplasty

"Heart Healthy" and other lies

Calcium chaos

Another big Track Your Plaque success story

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