I recently provided another interview for Livin' La Vida Low Carb's Jimmy Moore.

You may remember Jimmy as the irrepressible host of the Livin' La Vida Low Carb Show who lost around 200 lbs, dropping from 410 to 230 lbs on a low-carbohydrate diet.

In this hour-long interview, we discussed some of the dietary strategies that we use in the Track Your Plaque program.

Jimmy's website is definitely worth exploring. It's loaded with great interviews, including with Good Calories, Bad Calories author, Gary Taubes.

"Millions of needless deaths" is the title of an editorial by Life Extension Magazine's Bill Faloon.

". . . If vitamin D’s only benefit was to reduce coronary heart attack rates by 142%, the net savings (after deducting the cost of the vitamin D) if every American supplemented properly would be around $84 billion each year. That’s enough to put a major dent in the health care cost crisis that is forecast to bankrupt Medicare and many private insurance plans."

Although I don't agree with all the over-the-top commentary that issues from Mr. Faloon or Life Extension (although I sit on their Medical Advisory Board), I agree with virtually all of the issues he raises with vitamin D.

Despite the enormously compelling observations of vitamin D potential effects in populations, the medical community's reluctance comes from the lack of treatment data. In other words, what we lack are long-term data on vitamin D supplementation vs. placebo on rate of heart attack, vitamin D vs. placebo on risk of colon cancer, etc.

The data that exists connecting vitamin D levels with cardiovascular risk originate from three population observations:

1) The NHANES data in 16,000 participants showed 20% increased risk of cardiovascular events in those with vitamin D levels <20>20 ng/ml after factoring in all standard risk factors.

Another NHANES analysis showed the high prevalence of vitamin D deficiency in those with cardiovascular disease.

2) A German study of 2500 participants that showed showed the lowest quartile of vitamin D levels (<13.3>28.4 ng/ml.

3) The Health Professionals' Follow-Up Study of 18,000 males showed a 2.4-fold increase in cardiovascular events in those with vitamin D levels <15>30 ng/ml.

While we lack treatment data (vitamin D vs. placebo) in a large population, we do have data that Suzie Rockway, Mary Kwasny (both from Rush University, Chicago) and I generated on the effect of vitamin D as a part of a broader treatment program on coronary calcium scores:

Effect of a Combined Therapeutic Approach of Intensive Lipid Management, Omega-3 Fatty Acid Supplementation, and Increased Serum 25 (OH) Vitamin D on Coronary Calcium Scores in Asymptomatic Adults.
Davis W, Rockway S, Kwasny M. Amer J Ther 2008 (Dec 15).

The impact of intensive lipid management, omega-3 fatty acid, and vitamin D3 supplementation on atherosclerotic plaque was assessed through serial computed tomography coronary calcium scoring (CCS). Low-density lipoprotein cholesterol reduction with statin therapy has not been shown to reduce or slow progression of serial CCS in several recent studies, casting doubt on the usefulness of this approach for tracking atherosclerotic progression. In an open-label study, 45 male and female subjects with CCS of >/= 50 without symptoms of heart disease were treated with statin therapy, niacin, and omega-3 fatty acid supplementation to achieve low-density lipoprotein cholesterol and triglycerides /=60 mg/dL; and vitamin D3 supplementation to achieve serum levels of >/=50 ng/mL 25(OH) vitamin D, in addition to diet advice. Lipid profiles of subjects were significantly changed as follows: total cholesterol -24%, low-density lipoprotein -41%; triglycerides -42%, high-density lipoprotein +19%, and mean serum 25(OH) vitamin D levels +83%. After a mean of 18 months, 20 subjects experienced decrease in CCS with mean change of -14.5% (range 0% to -64%); 22 subjects experienced no change or slow annual rate of CCS increase of +12% (range 1%-29%). Only 3 subjects experienced annual CCS progression exceeding 29% (44%-71%). Despite wide variation in response, substantial reduction of CCS was achieved in 44% of subjects and slowed plaque growth in 49% of the subjects applying a broad treatment program.

I also summed up the data as of early 2008 in a Life Extension article:

Vitamin D's Crucial Role in Cardiovascular Protection

I do agree with Mr. Faloon: It's time to take the vitamin D issue very seriously. Personally, I think it is foolhardy to not correct vitamin D deficiency, even in the absence of long-term treatment data.

Should we subject people living in tropical climates with vitamin D blood levels of 90 ng/ml to long-term observation? Though that has not yet been done, it has been done--in effect--through observations on the prevalence of diabetes, heart disease, and various cancers by latitude: the farther away from the equator, the greater the prevalence of these diseases.

That's more than good enough for me.

Thiazide diuretics are a popular first-line treatment for hypertension among the primary care set.

This practice became especially well-established with the 2002 publication of the ALLHAT Study (Major Outcomes in High-Risk Hypertensive Patients Randomized to Angiotensin-Converting Enzyme Inhibitor or Calcium Channel Blocker vs Diuretic:The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT)).

ALLHAT showed that an inexpensive diuretic like chlorthalidone (a weak diuretic in the thiazide class, similar to hydrochlorothiazide) as first-line treatment for hypertension achieved equivalent reductions in cardiovascular events (cardiovasular death and heart attack) as non-thiazide antihypertensives, lisinopril (an ACE inhibitor) and amlodipine (a calcium channel blocker, better known as Norvasc).

After 7 years of treatment, there was 14% death or heart attack among all three groups--no difference.

This was interpreted to mean that inexpensive thiazide diuretics like chlorthalidone offer as much benefit as other blood pressure medications at reduced cost.

On the surface, that's great. Anything that detracts from the ubiquitous pharmaceutical industry propaganda of bigger, better, more expensive drugs to replace old, inexpensive, generic drugs is fine by me.

But you knew there'd be more to this issue! If we accept that thiazides are equivalent to other single-drug treatments for high blood pressure, what do we do with the following issues:

--Thiazides deplete body potassium-This effect can be profound. In fact, built into the ALLHAT mortality rate is an expected death rate from potassium depletion. When potassium in the body and blood go low, the heart becomes electrically unstable and dangerous rhythms develop.

--Thiazides deplete magnesium--Similar in implication to the potassium loss, magnesium loss also creates electrical instability in the heart, not to mention exaggeration of insulin resistance, rise in triglycerides, reduction in HDL.

--Thiazides reduce HDL cholesterol

--Thiazides increase triglycerides

--Thiazides increase small LDL particles--You know, the number one cause for heart disease in the U.S.

--Thiazides increase uric acid--Uric acid is increasingly looking like a coronary risk factor: The higher the uric acid blood level, the greater the risk for heart attack. Thiazides have long been known to increase uric acid, occasionally sufficient to trigger attacks of gout (uric acid crystals that precipitate in joints, like rock candy). (Fully detailed Special Report on uric acid coming this week on the Track Your Plaque website.)

What about the advice we commonly give people to hydrate themselves generously? Yet we give them diuretics? Which is it: More hydration or less hydration? You can't have both.

Do thiazides exert an apparent cardiovascular risk reduction in a society due to its flagrant sodium obsession?

Thus, there are a number of inconsistencies in the thinking surrounding thiazides. In my experience, I have seen more harm done than good using these agents. While I cannot fully reconcile the reported benefit seen in ALLHAT with what I see in real life, all too often I see people having to take another drug to make up for a side-effect of a thiazide diuretic (e.g., high-dose prescription potassium to replace lost potassium, allopurinol to reduce uric acid, etc.). I have seen many people get hospitalized, even suffer near-fatal or fatal events from extremely low potassium or magnesium levels.

My personal view: ALLHAT or no, avoid thiazide diuretics like the plague. Sure, it might save money on a population basis, but I suspect that the ALLHAT data are deeply misleading.

What's better than a thiazide, calcium blocker, or ACE inhibitor? How about vitamin D restoration, thyroid normalization, wheat elimination?

I stumbled on one of the growing number of local media stories on the power of vitamin D.

In one story, a purported "expert" was talking about the benefits of "high-dose" vitamin D, meaning up to 1000, even 2000 units per day.

I regard this as high-dose---for an infant.

Judging by my experiences, now numbering well over 1000 patients over three years time, I'd regard this dose range not as "high dose," nor moderate dose, perhaps not even low dose. I'd regard it as barely adequate.

Though needs vary widely, the majority of men require 6000 units per day, women 5000 units per day. Only then do most men and women achieve what I'd define as desirable: 60-70 ng/ml 25-hydroxy vitamin D blood level.

I base this target level by extrapolating from several simple observations:

--In epidemiologic studies, a blood level of 52 ng/ml seems to be an eerily consistent value: >52 ng/ml and cancer of the colon, breast, and prostate become far less common; <52 ng/ml and cancers are far more likely. I don't know about you, but I'd like to have a little larger margin of safety than just achieving 52.1 ng/ml.

--Young people (not older people >40 years old, who have lost most of the capacity to activate vitamin D in the skin) who obtain several days to weeks of tropical sun typically have 25-hydroxy vitamin D blood levels of 80-100 ng/ml without adverse effect.

More recently, having achieved this target blood level in many people, I can tell you confidently that achieving this blood level of vitamin D achieves:

--Virtual elimination of "winter blues" and seasonal affective disorder in the great majority
--Dramatic increases in HDL cholesterol (though full effect can require a year to develop)
--Reduction in triglycerides
--Modest reduction in blood pressure
--Dramatic reduction in c-reactive protein (far greater than achieved with Crestor, JUPITER trial or no)
--Increased bone density (improved osteoporosis/osteopenia)
--Halting or reversal of aortic valve disease

(I don't see enough cancer in my cardiology practice to gauge whether or not there has been an impact on cancer incidence.)

My colleagues who have bothered to participate in the vitamin D conversation have issued warnings about not going "overboard" with vitamin D, generally meaning a level of >30 ng/ml.

I know of no rational basis for these cautions. If hypercalcemia (increased blood calcium) is the concern, then calcium levels can be monitored. I can reassure them that calcium levels virtually never go up in people (without rare diseases like sarcoid or hyperparathyroidism). Then why any hesitation in recreating blood levels that are enjoyed by tropical inhabitants exposed to plentiful sun that achieve these extraordinary health effects?

For the present, I have applied the target level of 60-70 ng/ml without apparent ill-effect. In fact, I have witnessed nothing but hugely positive effects.

The ever-resourceful Dr. John Cannell of the Vitamin D Council has announced the availability of an at-home, self-ordered vitamin D test kit for $65. The Vitamin D Council newsletter is reprinted below.

(However, please note that, as wonderful as the advice Dr. Cannell provides, I don't agree on several small points, such as the lack of need for vitamin D if you use a tanning bed or obtain "sufficient" sun; I have seen many people with dark tans, virtually all over 40 years old, who are still severely deficient. I attribute this to the lost capacity for vitamin D activation as we age.)

I have not used this service. Should anyone choose to try it, please let us know how it goes.

The Vitamin D Newsletter
December 28, 2008

The Vitamin D Council is happy to announce that we have partnered with ZRT Laboratory to provide an inexpensive, $65.00, in-home, accurate, vitamin D [25(OH)D] test. The usual cost for this test is between $100.00 and $200.00.

If you read this newsletter, you know about our interest in accurate vitamin D testing. In the next few weeks, you may read about the Vitamin D Council's quest for accurate vitamin D blood tests in the national media. Before we partnered with ZRT, we verified, repeatedly, that ZRT provides accurate and reliable vitamin D tests and that their method corresponds very well to the gold standard of vitamin D blood tests, the DiaSorin RIA.

Our ZRT service is not just inexpensive, it means no more worrying about your doctor ordering the right test or interpreting it correctly. You buy the test kit on the internet or by phone, a few days later the kit comes in the mail, you or a nurse friend do a finger stick, collect a few drops of blood, and send the blotter paper back to ZRT in the postage paid envelope provided with the kit. A week later you get results back in the mail and know accurate 25-hydroxy-vitamin D levels of you and your family.

For every test you order, ZRT will donate $10.00 to the Vitamin D Council. Please read the new page hyperlinked below on our website as it both explains the procedure and how to order the test.

http://www.vitamindcouncil.org/health/deficiency/am-i-vitamin-d-deficient.shtml

Executive summary: keep your family's 25-hydroxy-vitamin D blood test above 50 ng/ml, year around. Most adults need at least 5,000 IU per day, especially this time of year. Most children need at least 1,000 IU per day per every 25 pounds of body weight. Bio Tech Pharmacal provides high quality and inexpensive vitamin D. Currently Bio Tech Pharmacal is providing vitamin D for numerous scientific studies. To see their prices and for ordering, click the hyperlink below.

http://www.bio-tech-pharm.com/catalog.aspx?cat_id=2

As a gift to our readers for the New Year, Thorne publications have provided a free download to a basic paper about vitamin D. I wrote it earlier this year for educated lay people as well as health care practitioners. Please read this paper carefully, your family's well-being, even lives, may depend on you understanding it.

http://www.thorne.com/altmedrev/.fulltext/13/1/6.pdf

Seasons Greetings
John Cannell, MD
vitamindcouncil.org

People pay about $90 per year to become Members on the Track Your Plaque website. This provide access to our in-depth Special Reports, guides, webinars, and our proprietary software data tracking tools. Members can also participate in online discussions, such as those in the Track Your Plaque Forum and chats.

Why is there a charge for membership in the program and where does the money go?

Money raised from membership fees goes towards:

1) The costs of doing business, e.g., server fees, software purchases, legal fees. Hosting webinars, for instance, costs us about $99 per month for the GoToWebinar software service.

2) Software development--Our most recent round of software data tracking tools, for instance, cost us nearly $30,000. That may not be a lot from big business standards, but it is onerous enough that obtaining membership dues really helps.

3) Graphics development--A website without graphics would be awfully dull, regardless of the quality of the textual content. Some of the newest tools on the Track Your Plaque website require photography and graphics work, which can add up very quickly.

Where membership fees do NOT go:

1) In our pockets--In fact, except for the various contractors who are paid for their services (e.g., software developers), NOBODY on the Track Your Plaque staff are paid: not me, nor any of the behind-the-scenes staff. Some of the staff overlap with my office staff, but they are paid purely out of the office revenues, not out of Track Your Plaque membership dues.

2) Towards overhead costs beyond those listed above--For example, membership fees do not pay for office lease, utilities, phones, etc.

We rely on membership fees because we have chosen to remain as free of commercial bias as possible. We host no advertising, we have no behind-the-scenes corporate or institutional agendas, we show no favoritism to any business or commercial operation. We believe this permits editorial freedom that few other health websites can enjoy. (In fact, I know of no other that is so free of commercial bias, outside of small blogs or narrow-interest websites.)

If you want to see what damage commercial bias can create, just go to a health website like WebMD. I challenge you to find information that is not flagrantly biased by commercial influence, namely that of the drug industry. (According to the WebMD SEC filings, in fact, the great majority--approximately 80%--of their $331 million revenues (2007) were derived directly or indirectly from the drug industry.) This commercial bias reaches into all of WebMD's related businesses, including MedicineNet.com, RxList.com, Medscape.com, and several others.

Preventing heart disease is not a money maker, sad to say. It is, from the perspective of conventional heart care, a big money loser. Undergo a heart catheterization, hospitalization, stent or bypass for anywhere from $14,000 to well over $100,000---or pay $90 for in-depth health information that dramatically reduces the potential need for the hospital and its procedures, minimizes need for prescription medication (statins alone, of course, are a $27 billion annual revenue phenomenon), and achieves all this by maximizing nutrition, self-purchased nutritional supplements, and inexpensive heart scans. Nobody is going to make a bundle off of this approach.

So that is why we charge a membership fee. I often get a laugh from some of the comments of people on this blog or even in my office who believe that we are rolling in money from the website from membership dues. The opposite is true: We don't pay ourselves. Virtually every penny is reinvested back into the website to better serve the Members.

Confusion often stems from the simplest of calculations: dose of fish oil.

Actually, you and I don't take fish oil for fish oil. We take fish oil for its content of omega-3 fatty acids, the dominant ones being EPA and DHA. The contents of fish oil outside of its EPA + DHA content likely exert little or no benefit (beyond that of other dietary oils).

To determine what you are currently taking, simply examine the back of your fish oil bottle and look for the EPA + DHA composition. This should be clearly and prominently labeled. If not, don't buy that brand again. Add up the EPA + DHA content per capsule, then multiply by the number of capsules you take per day. That yields your daily EPA + DHA intake.

The only other substantial source of omega-3 fatty acids is fish. Other food sources, such as non-fish meats, eggs, etc., contribute little or none. Processed foods that bear health claims of "contains heart healthy omega-3" often contain linolenic acid or flaxseed oil, which contributes very little to total EPA + DHA, or contain relatively trivial quantities of DHA. What are you doing eating processed foods, anyway?

What should the total daily dose of EPA + DHA dose be? That depends on what your goals are.

If your goal is to modestly reduce the risk of dying from heart attack, then just eating fish a couple of times per month will begin to exert an effect, or just taking a dose of 300 mg EPA + DHA per day from a low-potency capsule will do it. However, that's an awfully unambitious goal.

Our starting omega-3 dose in the Track Your Plaque program has, over the years, increased and now stands at 1800 mg EPA + DHA per day. However, the dose for 1) full reduction of triglycerides and/or triglyceride-containing abnormal lipoproteins, 2) reduction of Lp(a), and 3) the ideal dose for coronary and carotid plaque control are substantially higher.

But once you know your desired daily target of total EPA + DHA, you can easily determine the quantity of capsules to take by doing the above arithemetic, totaling the EPA + DHA per capsule. For example, if you have been instructed to take 6000 mg per day EPA + DHA, and your capsule contains 750 mg EPA + DHA, then you will need to take 8 capsules per day (6000/750).

When I go to the hospital, I am continually amazed at some of the hospital staff: 5 ft 4 inch nurses weighing over 200 lbs, etc.

But what I find particularly bothersome are some (not all) hospital dietitans--presumably experts at the day-to-day of healthy eating--who waddle through the halls, easily 40, 50, or more pounds overweight. It is, to say the least, credibility-challenging for an obese dietitian to be providing nutritional advice to men or women recovering after bypass or stent while clearly not in command of nutritional health herself.

What's behind this perverse situation? How can a person charged to dispense "healthy" nutritional information clearly display such clear-cut evidence of poor nutrition?

How would you view a success coach dressed in rags? Or a reading coach who can barely read a sentence?

Easy: She follows her own advice.

Hospital dietitians are essentially forced to adhere to nutritional guidelines of "official" organizations, such as the American Heart Association and the USDA. There is some reason behind this. Imagine a rogue dietitian decides to advocate some crazy diet that yields dangerous effects, e.g., high-potassium diets in people with kidney disease. There is a role for oversite on the information any hospital staff member dispenses.

The problem, of course, doesn't lie with the dietitian, but with the organizations drafting the guidelines. For years, the mantra of hospital diets was "low-fat." More recently, this dated message has begun--only begun--to falter, but now replaced with the "healthy, whole grain" mantra. And that is the advice the hapless dietitian follows herself, unwittingly indulging in foods that make us fat.

Sadly, the "healthy, whole grain" message also contributes to heart disease via drop in HDL, increased triglycerides, a huge surge in small LDL, rise in blood sugar, increased resistance to insulin, tummy fat, and diabetes. Yes, the diet provided to survivors of heart attack increases risk.

The "healthy, whole grain" message also enjoys apparent "validation" through the enormous proliferation of commercial products cleverly disguised as healthy: Cheerios, Raisin Bran, whole grain bread, whole wheat pasta, etc. The "healthy, whole grain" message, while a health disaster, is undoubtedly a commercial success.

I'll bet that our fat dietitian friend enjoys a breakfast of healthy, whole grains in skim milk, followed by a lunch of low-fat chicken breast on two slices of whole grain bread, and ends her day with a healthy meal of whole wheat pasta. She then ascribes her continually climbing weight and size 16 figure to slow metabolism, lack of exercise, or the once-a-week piece of chocolate.

Wheat has no role in the Track Your Plaque program for coronary plaque control and reversal. In fact, my personal view is that wheat has no role in the human diet whatsoever.

More on this concept can be found at:

What's worse than sugar?

The Wheat-Deficiency Syndrome

Nutritional approaches: Large vs. Small LDL

Are you wheat-free?

I sense a growing revolt against the intrusion of statin drugs into our lives.

No doubt, the statin drug industry is, at least from an economic perspective, a huge success: $27 billion annual revenues at last accounting. The latest big plug for more and more statins was the JUPITER trial that showed reduced cardiovascular events on Crestor in people with "normal" LDL cholesterol levels and increased c-reactive protein.

It seems that not one day passes that doesn't include some news story about the "benefits" of statin drugs: reduction in heart attack, stroke, colon cancer, osteoporosis, heart failure, etc.

Ironically, the overwhelming economic success of the statin drug industry also seems to be encouraging a grassroots revolt.

More and more people are coming to the office, more people commenting on the web over how they want to avoid statin drugs, stop a drug they are already taking, or at least reduce the dose of an ongoing drug.

My day-to-day experience with coronary plaque control and reversal is that, while statin drugs are helpful tools, they are not necessary tools for full benefit of a prevention program. "Need" for statin drugs can differ by the patterns measured, though not the usual patterns suggested by the drug industry. For instance, using C-reactive protein, a la JUPITER, as justification for statin prescription is, in my view, totally absurd and makes no sense whatsoever, since inflammatory responses can be effective reduced with plenty of other strategies besides statin drugs. Conventional LDL, likewise, is a fictitious number that often bear little or no resemblance to the true and genuine measured value (apoprotein B or LDL particle number).

So here are a number of strategies that can help reduce or eliminate the "need" for a statin drug:

--Elimination of wheat and cornstarch--This is no namby-pamby dietary strategy, as low-fat diets were. This is a powerful, enormously effective strategy, particularly if LDL is in the small category. Small LDL drops like a stone when these foods are eliminated. This means no breads, pasta, breakfast cereals, pretzels, crackers, chips, tacos, wraps, etc.
--Non-wheat fibers--Especially raw nuts, ground flaxseed, and oat bran.
--Vitamin D restoration
--Fish oil
--Weight loss
--Niacin

There are additional strategies that focus on specific subsets of LDL cholesterol (e.g., Lp(a) masquerading as LDL). But the above list can reduce LDL cholesterol substantially, reducing the apparent "need" for a statin drug.

You will notice that there are few money makers in the above list, compared to the billions of dollars reaped by the statin drug industry. There is therefore little incentive to allow a pretty sales rep to go to your doctor and pitch the use of over-the-counter vitamin D or make changes in diet.

Statin drugs in my view need to be shoved back into their more limited role as drugs to be used on occasion when necessary (e.g., heterozygous familial hypercholesterolemia with LDL cholesterol values of 250 mg/dl in a person with measurable coronary plaque). These should never have achieved the "celebrity" status they enjoy, complete with gushing endorsements by TV personalities, daily news stories, and back-to-back TV commercials.

Join the revolt!

Lovaza is GlaxoSmithKline's prescription fish oil, an ethyl ester modification to allow higher concentration of omega-3 fatty acids, EPA + DHA, per capsule. Each capsule contains 840 mg EPA + DHA.

It is FDA-approved for treatment of high triglycerides (>500 mg/dl). In their marketing, they claim "Unlike LOVAZA, dietary supplements are not FDA approved to treat any disease." They also highlight the "patented five-step" purification process that eliminates any concerns over mercury or pesticide residues.

What does Lovaza cost? In Milwaukee, it costs about $70 per capsule per month (PCPM). Most people are taking four capsules per day: $280 per month, or $3360 per year to obtain 3360 mg of EPA + DHA per day. (Funny coincidence with the numbers.)

Did you catch that? $3360 per year, just for one person to take Lovaza.

What if I instead went to Costco and bought their high-potency fish oil. This is also an ethyl ester form. It costs $14.99 for 180 capsules, or $2.50 PCPM; each capsule contains 684 mg EPA + DHA. I would therefore have to take five capsules per day to obtain the same 3360 mg EPA + DHA per day. This would cost me 5 x $2.50 = $12.50 per month, or $150 per year.

$3360 per year vs. $150 per year to obtain the same dose of omega-3 fatty acids, or a 22.4-fold difference.

Lovaza is FDA-approved for treatment of high triglycerides. But I am seeing more and more people take it for other reasons at this four-capsule-per-day dose. Regardless, this "drug" is adding $3360 per year costs to our healthcare. A school teacher, for instance, recently commented to me that she didn't care about the costs, since her insurance (in Milwaukee county, teachers have unbelievably generous healthcare coverage) covers Lovaza. I've heard this from others: insurance covers it, so they don't care how much it costs.

Guess who eventually has to pay the $3360 per year per person costs? Yup, you and me. We all bitch and moan about the costs of healthcare and health insurance, but many of us are more than willing to shift the costs to our friends and neighbors to save a few bucks. You think Lipitor makes a bundle of money for Pfizer at about $120 per month? Lovaza is making a bundle of money for GlaxoSmithKline, and all because people are cheap and willing to selfishly shift costs to other people.

Keep in mind that $3360 per year is just for fish oil. It's not for surgery, it's not for hospital care, it's just for stinking fish oil.

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.

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

The Vitamin D Newsletter

December, 2007

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

Vitamin D cuts colon cancer death risk

Study Finds No Connection Between Vitamin D And Overall Cancer Deaths

Vitamin D protects against colorectal cancer

Vitamin D May Not Cut Cancer Deaths

Vitamin D protects against colorectal cancer

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

Another option is to read the study yourself.

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

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

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

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

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

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

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

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

Cancer society calls for major vitamin D trial

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

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

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

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

Lake Woebegone Effect

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

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

Vitamin D may fight cancer

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

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

Maybe Vitamin D Isn't The Answer After All

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

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

John Cannell, MD

The Vitamin D Council

9100 San Gregorio Road

Atascadero, CA 93422

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

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The Vitamin D Council

9100 San Gregorio Road

Atascadero, CA 93422

A Heart Scan Blog reader recently posted this comment:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Can I eat foods with sugar in them?

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

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

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

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

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

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

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

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

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

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

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

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

You can always count on Dr. John Cannell for unique perspectives on vitamin D. I reprint here his unfailingly entertaining and informative Vitamin D Newsletter on whether vitamin D replacement enhances physical performance.

The whole vitamin D "discovery" sometimes worries me. Vitamin D has proven to be an unbelievable, remarkable, dramatic boon to health, including facilitation in dropping CT heart scan scores. Yet the answer was always right in front of us. It worries me that you and I might have the answer to important questions right within our grasp all along--but don't know it. What if the same were true, say, for cancer? That is, a profound answer is right there, but our eyes just pass right over it.

Anyway, we should all keep our eyes open and perhaps you and I will continue to identify the most powerful tools available that return control over heart disease to us and take it away from the perverse, procedural hospital formula that still reigns.

If you haven't done so already, be sure to visit Dr. Cannell's website, www.vitamindcouncil.com.

The Vitamin D Newsletter
March, 2007

Peak Athletic Performance and Vitamin D

"No way doc." I had just finished telling my patient about the benefits of vitamin D, telling him he should take 4,000 IU per day, using all the techniques I had learned in 30 years of medical practice to convince someone proper treatment is important. But, he knew the U.S. government said he only needed 200 IU per day, not 4,000. He also knew the official Upper Limit was 2,000 IU a day. "What are you trying to do doc, kill me?" I told him his 25(OH)-vitamin D blood test was low, only 13 ng/ml. He had read about that too, in a medical textbook, where it said normal levels are between 10 and 40 ng/ml. "I'm fine doc;" adding "Are you in the vitamin business?" I explained I was not; that the government used outdated values; that recent studies indicate ideal 25(OH)D levels are about 50 ng/ml; and that they indicated that he needed about 4,000 IU per day to get his level up to 50. "No thanks doc, I'm fine."

So I tried a different tact. I brought him copies of recent press articles. "Look," I said, "look at these." Science News called vitamin D the Antibiotic Vitamin. The Independent in England says vitamin D explains why people die from influenza in the winter, and not the summer. U.S. News and World Report says almost everyone needs more. Newsweek says it prevents cancer and helps fight infection. In four different recent reports, United Press International says that: it reduces falls in the elderly, many pregnant women are deficient , it reduces stress fractures, and that it helps heals wounds.

He glanced at the articles, showing a little interest in stress fractures. Then he told me what he was really thinking. "Look doc, all this stuff may be important to old guys like you. I'm 22. All I care about are girls and sports. When I get older, maybe I'll think about it. I'm too young to worry about it. I'm in great condition." I couldn't argue. He was in good health and a very good basketball player, playing several hours every day, always on indoor courts.

What could I do to open his eyes? As an African American, his risk of early death was very high, although the risk for blacks doesn't start to dramatically increase until their 40's and 50's. Like all young people, he saw himself as forever young. The U.S. government was no help, relying on a ten-year-old report from the Institute of Medicine that is full of misinformation.

I tired to tell him that the 200 IU per day the U.S. government recommends for 20-year-olds is to prevent bone disease, not to treat low vitamin D levels like his. I pointed out the U.S. government's official current Upper Limit of 2,000 IU/day is the same for a 300 pound adult as it is for a 25 pound toddler. That is, the government says it's safe for a one-year-old, 25-pound, child to take 2,000 IU per day but it's not safe for a 30-year old, 300-pound, adult to take 2,000 and one IU a day. I mean, whoever thought up these Upper Limits must have left their thinking caps at home. Nevertheless, nothing worked. My vitamin D deficient patient was not interested in taking any vitamin D.

What are young men interested in? I remembered that he had told me: "Sex and sports." Two years ago I had researched the medical literature looking for any evidence vitamin D enhanced sexual performance. Absolutely nothing. That would have been nice. Can you imagine the interest?

Then I remembered that several readers had written to ask me if vitamin D could possibly improve their athletic performance? They told me that after taking 2,000 to 5,000 IU per day for several months, they seemed just a little faster, a little stronger, maybe had a little better balance and timing. A pianist had written to tell me she even played a better piano, her fingers moved over the keys more effortlessly! Was vitamin D responsible for these subtle changes or was it a placebo effect? That is, did readers just think their athletic performance improved because they knew vitamin D was a steroid hormone precursor (hormone, from the Greek, meaning "to set in motion")?

The active form of vitamin D is a steroid (actually a seco-steroid) in the same way that testosterone is a steroid and vitamin D is a hormone in the same way that growth hormone is a hormone. Steroid hormones are substances made from cholesterol, which circulate in the body, and work at distant sites by "setting in motion" genetic protein transcription. That is, both vitamin D and testosterone regulate your genome, the stuff of life. While testosterone is a sex steroid hormone, vitamin D is a pleomorphic (multiple function) steroid hormone.

All of a sudden, it didn't seem so silly. Certainly steroids can improve athletic performance although they can be quite dangerous. In addition, few people are deficient in growth hormone or testosterone, so when athletes take sex steroids or growth hormone they are cheating, or doping. The case with vitamin D is quite different because natural vitamin D levels are about 50 ng/ml and, since almost no one has such levels, extra vitamin D is not doping, it's just good treatment. I decided to exhaustively research the medical literature on vitamin D and athletic performance. It took me over a year.

To my surprise, I discovered that there are five totally independent bodies of research that all converge on an inescapable conclusion: vitamin D will improve athletic performance in vitamin D deficient people (and that includes most people). Even more interesting is who published this literature, and when. Are you old enough to remember when the Germans and Russians won every Olympics in the 60's and 70's? Well, it turns out that the most convincing evidence that vitamin D improves athletic performance was published in old German and Russian medical literature.

With the help of my wife and mother-in-law, both of whom are Russian, and with the help of Marc Sorenson, whose book Solar Power is a must read, I finally was able to look at translations of much of the old Russian and German literature. When one combines that old literature with the modern English language literature on neuromuscular performance, the conclusion is inescapable. The readers who wrote me are right.

If you are vitamin D deficient, the medical literature indicates that the right amount of vitamin D will make you faster, stronger, improve your balance and timing, etc. How much it will improve your athletic ability depends on how deficient you are to begin with. How good an athlete you will be depends on your innate ability, training, and dedication. However, peak athletic performance also depends upon the neuromuscular cells in your body and brain having unfettered access to the steroid hormone, activated vitamin D. In addition, how much activated vitamin D is available to your brain, muscle, and nerves depends on having ideal levels of vitamin D in your blood - about 50 ng/ml, to be precise.

Why would I write about such a frivolous topic like peak athletic performance when cancer patients all across this land are dying vitamin D deficient? Like many vitamin D advocates, I have been disappointed that the medical profession and the public don't seem to care about vitamin D. Maybe people, like my young basketball player, will care if it makes better athletes. So, Hey! You jocks! Listen up! I'm talking speed, balance, choice reaction time, muscle mass, muscle strength, squats, reps, etc. Important stuff. Here's the Vitamin D Council's first ever sports quiz.

1. Vitamin D-producing UVB radiation improves athletic performance and may have been widely practiced by German and Russian Olympic athletes in the 1960's and 70's.

True. I found tantalizing evidence the Russians and especially the Germans were on to this during the 60's and 70's when those two nations took turns placing number one and number two in the Olympics every year?

For example, in 1938, Russian researchers reported that a course of ultraviolet irradiations improved speed in the 100-meter dash in college students compared to matched controls, both groups undergoing daily training. Average 100-meter dash times decreased from 13.51 seconds to 13.28 seconds in the non-irradiated controls, but from 13.63 seconds to 12.62 seconds in the irradiated students. Here we see training improved times but training and irradiation improved times much more. Obviously, irradiation or vitamin D would not render the same magnitude of improvements in world-class sprinters, but they would be happy with a few milliseconds.

Gorkin Z, Gorkin MJ, Teslenko NE. [The effect of ultraviolet irradiation upon training for 100m sprint.] The Journal of Physiology of the USSR [Fiziol, z. (RSSR)] 1938; 25: 695-701. (In Russian)

If you want to know what early German thinking was on this, read this summation of the German literature:

"It is a well-known fact that physical performance can be increased through ultra-violet irradiation. In 1927, a heated argument arose after the decision by the German Swimmers' Association to use the sunlamp as an artificial aid, constituting an athletic unfairness, doping, so to speak. In 1926, Rancken had already reported the improving effect of sunlamp irradiation on muscle work with the hand-dynamo-graph. Heib observed an improvement in swimming times after repeated irradiations. In thorough experiments, Backmund showed that a substantial increase in muscle activity happens after radiation of larger portions of the body with an artificial sunlamp; that this performance increase is not caused through local - direct or indirect - effects on the musculature, but through a general effect. This general effect, triggered by ultra-violet irradiation, is caused by a systemic effect on the nervous system." (p. 17)

Parade GW, Otto H. Die beeinflussung der leistungsfahigkeit durch Hohensonnenbestrahlung. Zeitschrift fur Klinische Medizin (Z Klin Med),1940;137:17-21 [In German]

In 1945, two Americans measured the cardiovascular fitness and muscular endurance of 11 male Illinois subjects undergoing training in an indoor physical education class, comparing them to 10 matched controls. Both groups underwent similar physical training. Treatment consisted of ultraviolet irradiation, given in the nude, up to two minutes per session, three times per week, for ten weeks in the late fall and winter. After ten weeks, the treatment group had a 19% standard score gain in cardiovascular fitness compare to a 2% improvement in the control students. To regular readers of this newsletter, it should come as no surprise that the un-irradiated control group reported twice as many viral respiratory infections as the treatment group.

Allen R, Cureton T. Effects of Ultraviolet Radiation on Physical Fitness. Arch Phys Med 1945: 10: 641-44.

In 1952, the German sports medicine researcher, Spellerberg, reported on the effects of wholesale irradiation of athletes studying and training at the Sports College of Cologne - including many elite athletes - with a "central sun lamp." He irradiated the athletes in their bathing suits, on both sides of their bodies, for up to ten minutes, twice a week, for 6 weeks. He reported a "convincing effect" on athletic performance and a 50% reduction in sports injuries. Results were particularly impressive for swimmers, soccer, handball, hockey, and tennis players, as well as for boxers and most track and field athletes. He reported that irradiation leading to burns, further irradiation of athletes having achieved peak performance, and irradiation within 24 hours of competition, all impaired athletic performance. Their results were so convincing, the Sports College of Cologne officially notified the "national German and International Olympic committee." (p. 570)

Spellerberg AE. [Increase of athletic effectiveness by systematic ultraviolet irradiation.] Strahlentherapie 1952; 88: 567-70. [In German]

In 1952, Ronge exposed 120 German schoolchildren to UV lights installed in classrooms and compared them to 120 un-irradiated control children. Over a two-year period - excluding summer vacations - he tested both groups with a series of six cardiovascular fitness tests using a bike ergometer. Un-irradiated children showed a distinct seasonality in fitness, with the highest values right after summer break and the lowest values in the spring. Treated children showed no seasonal differences in physical performance. Differences in work performance between the irradiated and un-irradiated children were most conspicuous in the spring with 56% difference between the two groups. In a final experiment, he gave 30 children in the control classrooms 6.25 mg (250,000 IU) of vitamin D as a single dose in February and found their performance had "increased considerably," one month later but did not report the actual numbers. He concluded that vitamin D, either as a supplement or induced via UV irradiation, improved physical performance.

Ronge HE. [Increase of physical effectiveness by systematic ultraviolet irradiation.] Strahlentherapie 1952; 88: 563-6. [In German]

In 1954, another researcher, at the Max-Planck Institute for Industrial Physiology in Dortmund, Germany, administered three different wavelengths of UV light over 8 weeks to university students. He found that ultraviolet light in the vitamin D-producing UVB range was consistently effective in reducing resting pulse, lowering the basal metabolic rate, and increasing athletic performance. UVA had no effect; interestingly, artificial UVC irradiation (the atmosphere normally completely filters out UVC radiation and thus it's not naturally present on earth) also gave some positive results.

Lehmann G. [Significance of certain wave lengths for increased efficacy of ultraviolet irradiation.] Strahlentherapie. 1954 Nov;95(3):447-53. [In German]

In 1956, Hettinger and Seidel irradiated seven subjects in two different experiments: athletic performance on bike-ergometers and forearm muscle strength. They found that UV radiation induced a significant improvement in both muscle strength and athletic performance.

Hettinger T, Seidl E. [Ultraviolet irradiation and trainability of musculature.] Internationale Zeitschrift für angewandte Physiologie, einschliesslich Arbeitsphysiologie 1956; 16: 177-83. [In German]

Another German researcher, at the Institute for Medical Physics and Biophysics at the University of Gottiingen, studied reaction times (the time needed to recognize a light and switch it off) during October and November in a series of controlled experiments on 16 children and an unspecified number of adults. He first controlled for practice effects (getting better by practicing) and then administered nine full-body UV radiation treatments over three weeks to the two treatment groups, using placebo radiation in the two control groups. UV radiation improved choice reaction time by 25% in children and 20% in adults while reaction time worsened in controls. The improvements in the irradiated groups peaked at the end of the three weeks of UV treatments and reverted to baseline levels three weeks later. In the two control groups, he found distinctly improved reaction times in the sunnier months.

Sigmund R. [Effect of ultraviolet rays on reaction time in man.] Strahlentherapie. 1956; 101: 623-9. [In German]

The next study threw me because it was very well conducted, meticulously designed, and completely negative. In 1963, Berven reported on the effects of ultraviolet irradiation and vitamin D supplementation in a group of 30 Stockholm schoolchildren, aged 10 -11, comparing them to appropriate controls. He found no seasonality of fitness in the control group and no effect from either irradiation or two different vitamin D supplementation protocols (1500 IU of cholecalciferol daily for two months and a single dose of 400,000 IU of ergocalciferol) on performance on a bike ergometer.

Berven H. The physical working capacity of healthy children; seasonal variations and effect of ultraviolet irradiation and vitamin-D supply. Acta paediatrica. Supplementum 1963; 148: 1-22.

However, two things were not right and got me thinking. One, Berven found no seasonality of physical fitness and was the only author who found no such seasonal variations in athletic performance. Second, he found no effect from irradiation, again, the only author. Then I realized he was working with Swedish children in the late 1950's. Supplementation of children with high doses of vitamin D - often as cod liver oil - was routine in Scandinavia in the past, particularly in children. For example, in neighboring Finland, the official recommended daily dose of vitamin D for children - including infants - was 4,000 IU per day until 1964, when authorities reduced it to 2,000 IU/day. (That's right, you read that correctly, 4,000 IU per day for infants, which is too much by the way.)

In 1975, Finnish authorities reduced it to 1,000 IU per day, and, in 1992, to 400 IU per day. I emailed Professor Elina Hypponen who confirmed that the Swedish recommendations were similar to the Finnish ones. Therefore, it seems highly unlikely that many of Berven's Swedish children, studied in 1958 and 1959, all from "families with a good standard of living," were vitamin D deficient. Therefore, this study showed that vitamin D will not improve athletic ability in vitamin D replete people. That's very important because it indicates more is not necessarily better. More is only better if you are not taking enough.

Hypponen E, et al. Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study. Lancet. 2001 Nov 3;358(9292):1500-3.

In the 1960's, three American researchers conducted experiments with university students. Rosentswieg studied the effects of a single six-minute dose of UV light on each side of the trunk in 23 college women, recording changes in various tests of muscle strength at one and five hours. He found a trend towards significance after five hours in white but not African American students. In 1968, Cheatum found that a six-minute administration of UV light, on each side of the trunk, increased the speed of 15 college women in the 30-yard dash. In 1969, Rosentswieg found a six-minute dose of UV light, on each side of the trunk, finding improved performance on a bicycle ergometer in college women. However, unlike the Germans and Russians, I could find no evidence that any of these American findings interested any American professionals involved in the care or training of athletes.

Rosentsweig J. The effect of a single suberythemic biodose of ultraviolet radiation upon the strength of college women. J Assoc Phys Ment Rehabil. 1967 Jul-Aug;21(4):131-3.

Cheatum BA. Effects of a single biodose of ultraviolet radiation upon the speed of college women. Res Q. 1968 Oct;39(3):482-5.

Rosentswieg J. The effect of a single suberythemic biodose of ultraviolet radiation upon the endurance of college women. J Sports Med Phys Fitness. 1969 Jun;9(2):104-6.

2. Athletic performance peaks in the summer when vitamin D levels peak, and is at its lowest in the winter when vitamin D levels are at their lowest.

A. True
B. False

True. The studies below - all I could find in the literature - show tests of physical performance peak in the summer, when vitamin D levels peak, start to decline in early autumn, as vitamin D levels decline, and athletic performance reaches its lowest point in late winter, when vitamin D levels bottom out. However, it is reasonable to assume that any associations between athletic performance and summer season may be due to "reverse causation." That is, improved athletic performance in the summer might be secondary to increased outdoor physical and recreational activity in the warmer weather with an indoor sedentary lifestyle during the colder months. Maybe people have better athletic ability in the summer because they exercise more. If that is true - and using the same logic - athletic performance should not begin to decline until late autumn, because at most temperate latitudes early fall weather is ideal for outdoor physical activities.

However, some of the studies below controlled for seasonal variations in time spent exercising. Furthermore, besides a consistent positive association of summer season with improved athletic performance, the below studies found an abrupt - and unexplained - reduction in athletic performance beginning in the early fall - when vitamin D levels decline - but when the weather is ideal for outdoor activities.

For example, in 1956, German researchers found a distinct seasonal variation in the trainability of musculature, studying wrist flexor strength in 21 German subjects undergoing daily training. They found highly significant seasonal differences with peak performance during the later part of the summer, nadirs in the winter, and an unexplained sharp autumn decline beginning in October.

Hettinger T, Muller EA. Seasonal course of trainability of musculature. Int Z Angew Physiol. 1956;16(2):90-4.

A study of Polish pilots and crew found physical fitness and tolerance to hypoxia were highest in the late summer with an unexplained sharp decline starting in September. The authors hypothesized that seasonal variations in an unidentified hormone best explained their results.

Kwarecki K, Golec L, Klossowski M, Zuzewicz K. Circannual rhythms of physical fitness and tolerance of hypoxic hypoxia. Acta Physiol Pol. 1981 Nov-Dec;32(6):629-36.

Cumulative work ability among 1,835 mainly sedentary Norwegian men during bicycle exercise tests showed an August peak, a sharp decline starting in the autumn, and a wintertime nadir. There were no seasonal changes in body weights, as might be expected if more caloric-demanding recreational activity during the sunnier months explained their results.

Erikssen J, Rodahl K. Seasonal variation in work performance and heart rate response to exercise. A study of 1,835 middle-aged men. Eur J Appl Physiol Occup Physiol. 1979 Oct;42(2):133-40.

Koch and Raschka reviewed the mostly German literature on the seasonality of physical performance, discussing studies indicating that muscle strength and stamina peak in the late summer. The authors then attempted to control for seasonal variations in the time spent exercising by instituting a controlled yearlong training regimen, beginning in December. The training regimen consisted of at least 20 push-ups per day and 2 or 3 long-distances races per week for the entire year. They found the both the number of push-ups and muscle strength peaked in late summer followed by a rapid decline in the fall, and a nadir in the winter, despite continued training. They concluded that seasonal variations in an unidentified hormone best explained their results. In addition, by now we all know that vitamin D is a seasonal hormone, and a steroid hormone precursor to boot.

Koch H, Raschka C. Circannual period of physical performance analysed by means of standard cosinor analysis: a case report. Rom J Physiol. 2000 Jan-Dec;37(1-4):51-8.

3. Vitamin D has direct muscle-building (anabolic) effects.

A. True
B. False

True, but only in vitamin D deficient subjects. Both animal and human studies have found that vitamin D directly affects muscle. That is, vitamin D increases muscle mass.

For example, Birge and Haddad found that vitamin D caused new protein synthesis in rat muscle.

Birge SJ, Haddad JG. 25-hydroxycholecalciferol stimulation of muscle metabolism. J Clin Invest. 1975 Nov;56(5):1100-7.

What about humans? In 1981, Young performed muscle biopsies on 12 severely vitamin D deficient patients before and after vitamin D treatment. They found type-II (fast-twitch) muscle fibers were small before treatment and significantly enlarged after treatment. Sorensen performed muscle biopsies on eleven older patients with osteoporosis before and after treatment with vitamin D. The percentage and area of fast twitch fibers increased significantly after treatment, despite the lack of any physical training.

Young A, Edwards R, Jones D, Brenton D. Quadriceps muscle strength and fibre size during treatment of osteomalacia. In: Stokes IAF (ed) Mechanical factors and the skeleton. 1981. pp 137-145.

Sorensen OH, Lund B, Saltin B, Lund B, Andersen RB, Hjorth L, Melsen F, Mosekilde L. Myopathy in bone loss of ageing: improvement by treatment with 1 alpha-hydroxycholecalciferol and calcium. Clin Sci (Lond). 1979 Feb;56(2):157-61.

Sato reported that two years of treatment with 1,000 IU of vitamin D per day significantly increased muscle strength, doubled the mean diameter, and tripled the percentage of fast-twitch muscle fibers, in the functional limbs of 48 severely vitamin D deficient elderly stroke patients. The placebo control group suffered declines in muscle strength, and in the size and percentage of fast-twitch muscle fibers.

Sato Y, Iwamoto J, Kanoko T, Satoh K. Low-Dose Vitamin D Prevents Muscular Atrophy and Reduces Falls and Hip Fractures in Women after Stroke: A Randomized Controlled Trial. Cerebrovasc Dis. 2005 Jul 27;20(3):187-192 [Epub ahead of print]

These studies clearly show that vitamin D when administered to vitamin D deficient people stimulates the growth and number of those muscle fibers critical to athletic ability, type-2, or "fast twitch," muscle fibers.

4. Many studies have found direct associations between physical performance and vitamin D levels. That is, the higher your vitamin D level, the better your athletic performance.

A. True
B. False

True. I found 13 positive studies of associations between vitamin D levels and various parameters of neuromuscular performance. However, they were all in old people. Of course, old people can be athletes too. Furthermore, age differences in physiology and pharmacology are quantitative, not qualitative. That is, what is true in old people will be true in young people, although the magnitude might be different. Higher vitamin D levels are associated with a wide variety of athletic performance but appear to have the strongest associations with balance, timing, and timed tests of physical performance.

The three largest studies had more than 7,000 elderly subjects. All found evidence of a vitamin D threshold of between 30 - 50 ng/ml, above which further improvements in athletic performance were not seen. Wicherts and her colleagues found a linear correlation between vitamin D and neuromuscular performance; scores were 78% better for those with vitamin D levels greater than 30 ng/ml compared to those with levels less than10 ng/ml.

Bischoff-Ferrari HA, Dietrich T, Orav EJ, Hu FB, Zhang Y, Karlson EW, Dawson-Hughes B. Higher 25-hydroxyvitamin D concentrations are associated with better lower-extremity function in both active and inactive persons aged > or =60 y. Am J Clin Nutr. 2004 Sep;80(3):752-8.

Gerdhem P, Ringsberg KA, Obrant KJ, Akesson K. Association between 25-hydroxy vitamin D levels, physical activity, muscle strength and fractures in the prospective population-based OPRA Study of Elderly Women. Osteoporos Int. 2005 Nov;16(11):1425-31.

Wicherts IS, et al. Vitamin D status predicts physical performance and its decline in older persons. J Clin Endocrinol Metab. 2007 Mar 6; [Epub ahead of print]

Professor Heike Bischoff-Ferrari, now in Switzerland, did the largest study. She and her colleagues found a strong positive correlation and suggestion of a U-shaped curve with athletic performance on one test peaking with vitamin D levels of 50 ng/ml but deteriorating at higher levels. It is interesting to speculate that levels around 50 ng/ml may be optimal for athletic performance as such levels are common in humans living in a "natural" state of sun-exposure, such as lifeguards or tropical farmers.

Bischoff HA, Stahelin HB, Urscheler N, Ehrsam R, Vonthein R, Perrig-Chiello P, Tyndall A, Theiler R. Muscle strength in the elderly: its relation to vitamin D metabolites. Arch Phys Med Rehabil. 1999 Jan;80(1):54-8.

Interestingly, all three studies that looked for an association between mental abilities and vitamin D levels found one. A fourth study, unrelated to athletic function, also found an association. The obvious explanation for these findings is that cognitively impaired patients do not go outdoors as often as higher functioning patients and thus have lower vitamin D levels. However, Dhesi found the association after excluding all but mildly demented patients, making such an explanation more difficult. Flicker and - more recently - Przybelski and Binkley, found the association after controlling for outdoor activities, raising the possibility that the association of vitamin D levels with cognitive abilities is casual. Both the vitamin D receptor and the enzyme necessary to activate vitamin D are present in a wide-variety of human brain tissue. If vitamin D deficiency impairs cognitive abilities, it is likely that such deficiencies will also impair the brain's ability to process the complex circuits needed for peak athletic performance.

Dhesi JK, Bearne LM, Moniz C, Hurley MV, Jackson SH, Swift CG, Allain TJ. Neuromuscular and psychomotor function in elderly subjects who fall and the relationship with vitamin D status. J Bone Miner Res. 2002 May;17(5):891-7.

Kenny AM, Biskup B, Robbins B, Marcella G, Burleson JA. Effects of vitamin D supplementation on strength, physical function, and health perception in older, community-dwelling men. J Am Geriatr Soc. 2003 Dec;51(12):1762-7.

Flicker L, Mead K, MacInnis RJ, Nowson C, Scherer S, Stein MS, Thomasx J, Hopper JL, Wark JD. Serum vitamin D and falls in older women in residential care in Australia. J Am Geriatr Soc. 2003 Nov;51(11):1533-8.

Przybelski RJ, Binkley NC. Is vitamin D important for preserving cognition? A positive correlation of serum 25-hydroxyvitamin D concentration with cognitive function. Arch Biochem Biophys. 2007 Jan 8;

There can be no doubt that higher vitamin D levels are associated with improved athletic performance in the elderly. From what we know of physiology and pharmacology, the same associations should hold true in young people, including young athletes.

5. Numerous studies have found that vitamin D improves physical performance.

A. True
B. False.

True, but, again, most all the studies are in old persons, not young ones, and none of the studies are in world-class athletes. However, there is no medical reason why vitamin D would improve the athletic performance of vitamin D deficient old people but not vitamin D deficient young ones. Eleven studies found vitamin D improved physical performance, mainly on measures of balance and reaction time. The one study of younger subjects showed dramatic physical performance effects in 55 severely vitamin D deficient women.

Sorensen OH, Lund B, Saltin B, Lund B, Andersen RB, Hjorth L, Melsen F, Mosekilde L. Myopathy in bone loss of ageing: improvement by treatment with 1 alpha-hydroxycholecalciferol and calcium. Clin Sci (Lond). 1979 Feb;56(2):157-61.

Gloth FM 3rd, Smith CE, Hollis BW, Tobin JD. Functional improvement with vitamin D replenishment in a cohort of frail, vitamin D-deficient older people. J Am Geriatr Soc. 1995 Nov;43(11):1269-71.

Glerup H, Mikkelsen K, Poulsen L, Hass E, Overbeck S, Andersen H, Charles P, Eriksen EF. Hypovitaminosis D myopathy without biochemical signs of osteomalacic bone involvement. Calcif Tissue Int. 2000 Jun;66(6):419-24.

Prabhala A, Garg R, Dandona P. Severe myopathy associated with vitamin D deficiency in western New York. Arch Intern Med. 2000 Apr 24;160(8):1199-203.

Verhaar HJ, Samson MM, Jansen PA, de Vreede PL, Manten JW, Duursma SA. Muscle strength, functional mobility and vitamin D in older women. Aging (Milano). 2000 Dec;12(6):455-60.

Pfeifer M, Begerow B, Minne HW, Abrams C, Nachtigall D, Hansen C. Effects of a short-term vitamin D and calcium supplementation on body sway and secondary hyperparathyroidism in elderly women. J Bone Miner Res. 2000 Jun;15(6):1113-8.

Bischoff HA, Stahelin HB, Dick W, Akos R, Knecht M, Salis C, Nebiker M, Theiler R, Pfeifer M, Begerow B, Lew RA, Conzelmann M. Effects of vitamin D and calcium supplementation on falls: a randomized controlled trial. J Bone Miner Res. 2003 Feb;18(2):343-51.

Dhesi JK, Jackson SH, Bearne LM, Moniz C, Hurley MV, Swift CG, Allain TJ. Vitamin D supplementation improves neuromuscular function in older people who fall. Age Ageing. 2004 Nov;33(6):589-95.

Sato Y, Iwamoto J, Kanoko T, Satoh K. Low-Dose Vitamin D Prevents Muscular Atrophy and Reduces Falls and Hip Fractures in Women after Stroke: A Randomized Controlled Trial. Cerebrovasc Dis. 2005 Jul 27;20(3):187-192 [Epub ahead of print]

In summary, five converging - but totally separate - lines of scientific evidence leave little doubt that vitamin D improves athletic performance. (I actually left out a sixth line of evidence, something a little more complicated, studies of muscle strength and vitamin D receptor polymorphisms; the two studies I could find were both positive.) Anyway, the scientific evidence that UVB radiation, either from the sun or from sunbeds, will improve athletic performance is overwhelming and the mechanism is almost certainly vitamin D production. Peak athletic performance will probably occur with 25(OH)D levels of about 50 ng/ml, whether from sun, sunbeds, or supplements.

All that is missing is a big-time professional or college team identifying and then treating their elite athletes who are vitamin D deficient. Can you imagine what such performance-enhancing effects would do for basketball players, most of who are African American and who practice and play indoors all winter? Or gymnasts? Or weight lifters?

However, a word of caution. The above studies suggest that taking too much vitamin D (more than 5,000 IU per day) may actually worsen athletic performance. Take the right amount, not all you can swallow. Take enough to keep your 25(OH)D levels around 50 ng/ml, year round. Easier yet, regularly use the sun in the summer and sunbeds in the winter - with care not to burn. Once a week should be about right.

When you think about it, none of this should surprise anyone. Every body builder knows that steroid hormones can improve athletic performance, certainly increase muscle mass. Barry Bonds knows they increase timing and power. Moreover, activated vitamin D is as potent a steroid hormone as exists in the human body. However, unlike other steroids, levels of activated vitamin D in muscle and nerve tissue are primarily regulated by sun exposure. That's right, the rate-limiting step for the cellular function (autocrine) of activated vitamin D is under your control. It depends on how much you put in your both or go into the sun. It's ironic that many athletes now avoid the sun, organized baseball is even promoting sun avoidance and sunblocks. The ancient Greeks knew better; they had there elite athletes train on the beach and in the nude.

The medical literature indicates vitamin D levels of about 50 ng/ml are associated with peak athletic performance. Of course, recent studies show such levels are ideal for preventing cancer, diabetes, hypertension, influenza, multiple sclerosis, major depression, cognitive impairments, etc. But who cares about all that disease stuff old people get, we're talking about something really important: speed, balance, reaction time, muscle mass, muscle strength, squats, reps, etc. And guess who's now taking 4,000 IU/day? Yes he is, and he tells me his timing is better, he can jump a little higher, run a little faster, and the ball feels "sweeter," whatever that means.

John Cannell, MD

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The reason why I've been blogging lightly these past few days is because, as a favor, I'm covering the practice for some colleagues who I'm (very) loosely affiliated with. The time demands have been great.

Nonetheless, it is a good reminder to me just how far wrong conventional cardiology remains. Judging by what I see around me, there is a startling lack of restraint in proceeding to the catheterization laboratory. Curiously, the internists and family practitioners have been brainwashed into accepting this path. I suppose that all it takes is an occasional real "save" for these physicians to develop a fear of ever missing real disease.

What I'm seeing is just how many people presenting with chest pain or similar symptoms end up going to the cath lab. I would crudely estimate 80%. That is, once you make it past the emergency room, there's a four out of five chance that you'll end up with a heart catheterization to "be sure your heart is okay", "make certain you're not going to die of heart disease", "see if there's a ticking time bomb in your chest". You've heard all the clever, scary phrases that get tossed around to scare the pants off you and justify putting catheters in your groin.

Despite the fact that tools for heart disease prevention have improved dramatically, the volume of heart catheterizations continues to grow nationwide.

I find it shocking and unacceptable. We're currently working behind the scenes to help change this situation through education of the public. Persuade a $1 million a year cardiologist that he is overdoing procedures? Unlikely in my experience. Educate the public about the shocking over-reliance on high-revenue procedures? Perhaps more practical.

Garlic May Not Lower Cholesterol
Study Shows No Improvement in Cholesterol Levels From Raw Garlic or Garlic Supplements

Lots of reports continue to hit the press about a small study that hoped to determine whether garlic as whole cloves (4 to 6), an aqueous extract of garlic called Kyolic, or an oil extract called Garlicin (high in allicin), or placebo. No differences in lipid numbers including LDL cholesterol were observed.

(Full text at WebMD at http://www.webmd.com/cholesterol-management/news/20070226/garlic-may-not-lower-cholesterol?ecd=wnl_chl_030507. You may be required to log in or register.)

I believe that the researchers were sincere in their effort to follow an honest, scientfically sound clinical trial design. I'm personally not that surprised. The effect in prior studies has been modest, sometimes none. Does that mean that we should ignore the other studies that suggest there may be modest blood-thinning, anti-inflammatory, blood pressure-reducing, and cancer-preventing properties? No, it does not. Dr. Matt Budoff at UCLA even published a very small study in about 20 people that suggested a slowing of plaque growth by using Kyolic in persons tracked by CT heart scans.

Nonetheless, garlic is, at best, probably no more than a source of small benefits. The biggest fallout from this kind of report, however, is not the neutral results from garlic, but from the open door the drug companies sense when this happens.

If you read the WebMD report, you'll notice all sorts of advertisements from drug companies for statin cholesterol drugs ("Cholesterol health center"; "Understanding Cholesterol Numbers"; "There are two sources of cholesterol: food and family"), Niaspan (which I used to support but have been discouraged by the Kos companies excessively profiteering methods and recent big Wall Street sellout).

It doesn't follow. The failure of one nutritional strategy to reduce LDL does nothave to trigger a run to the drugs. Don't fall for it. Drugs have their place. So do supplements and food choices, which can be very powerful. Drug manufacturers and their marketing people salivate when something like this comes along, an open invitation to say, "If garlic doesn't work, _____ sure does."

Jason came to the office because of chest pain. At 34 years old, he works as manager of a (non-fast food) restaurant, but indulges in lots of the odds and ends. Among his indulgences: Diet Coke.

Every time he'd have a diet Coke, he'd have chest pain. Not drinking diet Coke--no chest pain. If Jason drank coffee, no chest pain. Other foods, no chest pain. Anyway, just eliminating the diet Coke seemed to do the trick. (Aspartame?)

Anyway, that's not why I tell you Jason's story. In the midst of his evaluation, an echocardiogram showed a mildly enlarged aorta, measuring 4.0 cm in diameter. So we obtained lipoproteins. Jason showed lipoprotein(a) and small LDL particles, the dreaded duo. We talked about how to correct this pattern. Among the strategies we discussed was niacin.

But what bothered me was that neither of Jason's parents had a diagnosis of heart disease. Jason had to have gotten Lp(a) from either his mother or father, since you obtain the gene from one or the other parent. You cannot acquire Lp(a). So one of Jason's parents was sitting on a genetic time bomb of unrecognized Lp(a) and hidden heart disease.

Because Jason's paternal grandfather had a heart attack at age 62, only Jason's Dad had the heart scan (though I urged both to get one). Score: 1483. Recall that heart scan scores >1000 carry a risk of death or heart attack of 25% per year if no preventive action is taken. Now, of course, we have to persuade Jason's Dad that a program of prevention--intensive prevention is in order, including a measure of Lp(a).

So that's the curious story of how Diet Coke probably saved Jason's Dad's life. The lesson is that if you or someone you know has Lp(a), think about their children as well as their parents, each of whom carry a 50% chance of having the pattern.

There's a widely-known (among cardiologists) problem with nuclear stress tests. It's called the "false positive." (Nuclear stress tests are known as stress Cardiolites, stress thalliums, stress Myoviews, persantine stress tests, adenosine stress tests)

Stress tests, nuclear and otherwise, are helpful for identifying areas of poor blood flow. If an area of poor blood flow is detected and the area is substantial, then there may be greater risk of heart attack and other undesirable events in the relatively near future.

What "false positive" means is a stress test that shows an abnormality but it's not true--it is falsely abnormal. There are a number of reasons why this can happen. The problem is that this phenomenon is very common. Up to 20% of nuclear stress tests are false positives.

There are indeed situations where there may an abnormality and it is not clear whether it is true or false. This may lead to a justifiable heart catheterization or CT coronary angiogram. But, given the extraordinary number of false positives, there's a lot of gray in interpreting these tests. Hospital staff, in fact, call nuclear medicine "unclear" medicine. It's common knowledge that you can often see just about anything you want to see on a nuclear image of the heart. Abnormalities in the bottom of the heart, the "inferior" wall, are especially common due to the overlap of the diaphragm with the heart muscle, yielding the appearance of reduced blood flow. Defects in the front of the heart heart are common in females with large breasts for the same reasons.

The problem: The uncertainty inherent in nuclear stress tests opens the door to the unscrupulous or lazy practitioner. Any blip, tick, or imperfection on the nuclear images serve as carte blanche to drag you into the hospital for procedures.

This abusive practice is, in my experience, shockingly common for two reasons: 1) It pays better to do heart catheterizations, and 2) Defensive medicine.

What's the disincentive? Only doing the right thing and maintaining a clear conscience. Slim reasons for many of my colleagues--and a lot less money.

If you are without symptoms and feel fine, and a nuclear stress test is advised by your doctor, followed by a discussion of an abnormality, insist on a discussion of exactly what is abnormal, just how abnormal, and what the alternatives might be. If you receive unsatisfactory or incomplete answers despite your best effort, it's time for another opinion.

Magnesium is kind of boring. So most people don't pay too much attention to it.

Magnesium can be important, however. I saw an interesting phenomenon recently. A type I diabetic patient of mine (that is, an adult who developed diabetes as a child), Mitch, was experiencing wide swings in blood sugar: low low's and very high high's (300-400 mg/dl). Mitch's magnesium was only marginally low at 2.0 mEq/L. (Ranges for normal magnesium blood levels are usually 1.3–2.1 mEq/L or 0.65–1.05 mmol/L.) Note that Mitch's blood levels fall within "normal." I do not agree with these "normal" ranges. I shoot for 2.1 to 2.4 mEq/L, which I think is the truly normal range.

In addition to eating plenty of raw nuts and green vegetables, Mitch began supplementing magnesium with magnesium citrate, 200 mg twice a day (our preferred supplement form). He reported that the wide swings in blood sugar were nearly eliminated.

Mitch's dramatic benefit is just a great illustration of how magnesium can help control blood sugar metabolism. A type I diabetic is more sensitive to the effects, but anyone with type II (adult) diabetes, metabolic syndrome, or just a slightly high blood sugar could benefit from magnesium supplementation.

There's a number of ways to accomplish getting sufficient magnesium in your daily regimen. Track Your Plaque members, Be sure to read:

Your water may be killing you at
http://www.cureality.com/library/fl_03-002magnesium.asp

Magnesium: Water to the rescue! at http://www.cureality.com/library/fl_03-010magnesium2.asp

It struck me recently that, for many people, it's not the second but the third heart scan that more commonly shows a reduction in score.

I think this is because many people's reaction to their first heart scan is "This can't be. There's no way my arteries have that much plaque." They then follow a half-hearted program to correct their patterns.

When the second heart scan shows a significantly higher score, that really catches their attention. This is when they finally buckle down and give it their all.

Only the occasional person will, after the first heart scan, seize full control and take their program very seriously. These tend to be highly motivated people.

Don't feel too bad if your second heart scan score shows an increase. Look at it for what it represents: feedback on the adequacy of your program.

Peter started out at age 59 at 248 lbs, standing 6 ft tall (BMI = 33.6!).

Along with his weight, Peter had the entire panel of phenemena of the so-called "metabolic syndrome", or pre-diabetes:

--Triglycerides 238 mg/dl and associated with extremes of excess VLDL and IDL
--High blood pressure
--Blood sugar 115 mg/dl
--High c-reactive protein
--Small LDL particles 99% of total LDL

Interestingly, Peter's HDL was a surprisingly favorable 58 mg/dl (HDL is usually low in this syndrome). However, when broken down by size, he had nearly zero large, healthy HDL (sometimes called HDL2b). Though total HDL was favorable, most of it was simply ineffective.

Peter eliminated snacks and processed foods, particularly bread; increased his reliance on healthy oils and lean proteins; incorporated soy protein; increased vegetables. He added 30 minutes of a rapid walk on a treadmill every day. He added vitamin D to achieve a blood level of 50 ng/dml. He added a magnesium supplement.

Peter has lost 31 lbs. in the last year. Weight 207 lbs., BMI 28.1 (desirable <25). Blood sugar: 96 mg/dl; triglycerides: 56 mg/dl; HDL 71 mg/dl with 35% in the large fraction; small LDL 45% of total. Not perfect, but a damn site better.

Control of metabolic syndrome is an achievable goal for over 90% of people, just with these simple efforts. We haven't yet had a chance to assess the effect on the progression or regression of Peter's heart scan score, but he has, at the very least, spared himself a future of diabetes and all its complications.

This is a "slice" from a normal heart scan in a 58 year old woman. Heart scan score zero. Look at the lungs, the dark areas left and right of the heart in the center. The lungs are also normal. Black represents normal density, healthy lung tissue. The white streaking is just normal lung blood vessels. This person doesn't smoke.

This woman smokes a pack of cigarettes a day and has done so for 45 years ("45 pack-years"). She had a surprisingly low heart scan score (at age 64) of only 71, despite the smoking. However, look at this woman's lungs. It's a little tough to make out, since the computer graphics loses some of the resolution. But you can see the near absence of lung tissue on both sides. This is an advanced phase of the destructive lung disease, emphysema, from smoking. Even if she quit smoking today, the destroyed lung tissue never grows back. She literally has huge gaps or holes in her lungs where lung tissue used to be.

Smoking is among the most destructive, terrible things you can do to your body, short of swallowing strychnine or jumping off a building. Stay as far the heck away from cigarettes as you possibly can. If you are exposed to "secondary" smoke, insist that the person never smoke in your presence. It's not the smell that destroys your lungs or causes coronary plaque (though it is indeed foul), it's the actual smoke.

Do you need to become a vegetarian in order to reduce your heart scan score?

No. Plain and simple. We’ve had many non-vegetarians drop their scores.

That said, are there still advantages to following a vegetarian diet, or some variation on the vegetarian theme?

Yes, there are. Let’s put aside the moral or religious arguments in favor of not eating animals—the need to eliminate killing animals for food, elimination of suffering common in modern livestock practices, Kosher considerations, etc. (Not that there aren’t real arguments here. Our focus for this conversation is not, however, the moral dilemma, but the health argument.)

Some of the most unhealthy people I’ve ever met, mostly males, are proud carnivores who boast of their prodigious capacities to eat meat. Unfortunately, it’s hard to tease out the ill-effects of excessive meat eating, since these same men also tend to be substantially overweight, smoke, drink excessively, and fail to get exercise unless their job is physically demanding. You know the type.

What advantages does a vegetarian obtain? A number of studies have suggested that the reduced saturated fat, reduced exposure to parasites, as well as reduced exposure to the antibiotics and hormones now used routinely in livestock-raising practices, do indeed provide benefits to the vegetarian. Thus, vegetarians tend to be substantially thinner, experience less bowel cancer, have less diabetes and heart disease, and live longer.

(If you are interested in reading or seeing more about just how inhumane modern livestock practices are, take a look at the video, "Meet Your Meat" at meat.org. Be sure not to view this after dinner.)

Of course, some of the disadvantages of eating animal products diminish when free-range livestock are eaten, i.e., livestock not raised in the inhumane cramped, filthy conditions of livestock factories, but in the open, grazing or rooting freely. These animals tend to have different fat compositions and taste different.

The advantages of vegetarianism, however, have blurred in recent years, since many so-called vegetarians have failed to maintain the distinction between naturally-occurring foods and processed foods. So, Ritz Crackers, Oreo cookies, whole wheat bread, and Raisin Bran fit into a vegetarian program, but they’re awful for your health. I’ll occasionally meet a self-proclaimed vegetarian who looks every bit as unhealthy as a conventionally eating American, that is, overweight, pre-diabetic person with a developing heart scan score.

So it is not necessary to be vegetarian to reduce your score. You might consider vegetarianism for other reasons, such as moral considerations, or to reduce your risk for cancer. But it is not necessary to drop your heart scan score. A non-processed food diet? Now that's is worth giving serious consideration.

Dr. Colin Campbell caused a stir with publication of his 2005 book, The China Study. Dr. Campbell, after extensive animal and epidemiologic research conducted in China over 20 years, concluded that a diet high in animal protein, especially casein, was associated with increased cancer, osteoporosis, and heart disease risk.

Richard Nikoley of Free the Animal and Stephan Guyenet of Whole Health Source have been talking about an analysis of the China Study raw data performed by a young woman named Denise Minger.

Denise's analysis is nothing short of brilliant, absolutely "must" reading for anyone interested in nutrition.

Her comments on the relationship of wheat to heart disease:

Why does Campbell indict animal foods in cardiovascular disease (correlation of +1 for animal protein and -11 for fish protein), yet fail to mention that wheat flour has a correlation of +67 with heart attacks and coronary heart disease, and plant protein correlates at +25 with these conditions?

Speaking of wheat, why doesn’t Campbell also note the astronomical correlations wheat flour has with various diseases: +46 with cervix cancer, +54 with hypertensive heart disease, +47 with stroke, +41 with diseases of the blood and blood-forming organs, and the aforementioned +67 with myocardial infarction and coronary heart disease?

Carbohydrates in the diet trigger formation of small LDL particles. Because carbohydrates, such as products made from wheat, increase triglycerides and triglyceride-containing lipoproteins (chylomicrons, chylomicron remnants, VLDL, and IDL), LDL particles (NOT LDL cholesterol) become triglyceride-enriched. Triglyceride-enriched LDL particles are "remodeled" by the enzyme, hepatic lipase, into triglyceride-depleted, small LDL particles.

The list of reasons why small LDL particles are more atherogenic, i.e., plaque-causing, is long:

--Small LDL particles, being smaller, more readily penetrate the endothelial barrier of the arterial wall.
--Small LDL particles are more adherent to glycosaminoglycans in the artery wall.
--Small LDL particles are poorly taken up by the liver LDL receptor, but enthusiastically taken up by macrophage receptors of the sort in your artery walls.
--Because of their poor liver clearance, small LDL persists in the bloodstream far longer than large LDL.
--Small LDL particles are more oxidation-prone. Oxidized LDL are more likely to trigger inflammatory phenomena and be taken up by macrophages in the artery wall.

Let me add another reason why small LDL particles are more likely to cause plaque: They are more likely to undergo glycation. (More on glycation here.)

Glycation occurs when glucose (sugar) molecules in the blood or tissue modify proteins, usually irreversibly. Small LDL particles are uniquely glycation-prone. (This is likely due to a conformational change of the apoprotein B in the small LDL particle, exposing lysine residues along apo B that become glycated.)

Here's a great demonstration of this phenomenon by Younis et al:

"LDL3" is the small type. Note that small LDL particles are 4-5 times more glycated than large LDL. That's a big difference.

Once glycated, small LDL is especially resistant to being taken up by the liver. Like annoying in-laws, they hang around and hang around and . . . The longer they hang around, they more opportunity they have to contribute to plaque formation.

So, carbohydrates trigger formation of small LDL particles. Once formed, small LDL particles are glycated when blood sugar increases. While LDL can be glycated even when blood sugars are in the normal range (90 mg/dl or less), glycation goes berserk when blood sugars go higher, such as a blood sugar of 155 mg/dl after a bowl of steel-cut oatmeal.

We know that foods that trigger insulin lead to fat storage. Putting a stop to this process allows you to mobilize fat and lose weight. If you're starting out from scratch, rapid and dramatic weight loss can be experienced, as much as one pound per day.

So how can you stop triggering insulin?

The easiest way is to eliminate, or at least minimize, carbohydrates. My favorite method to restrict carbohydrates is to eliminate wheat and minimize exposure to other carbohydrates, such as oats, cornstarch, and sugars. All these foods, wheat products worst of all, cause blood sugar and insulin to skyrocket.

Another way is to check your blood sugar one hour after completing a meal and keep your after-eating, or "postprandial," blood sugar 100 mg/dl or less. Let's say you are going to eat stone ground oatmeal, for example. Blood sugar prior to eating is, say, 90 mg/dl. One hour after oatmeal it's 168 mg/dl--you know that this is going to trigger insulin and make you fat. Oatmeal should therefore be eliminated.

Keeping blood sugar to 100 mg/dl or less after eating teaches you how to avoid provocation of insulin. A shrinking tummy will follow.

To do this, you will need:

1) A glucose meter--My favorite is the One Touch Ultra Mini ($13.42 at Walmart). It's exceptionally easy to use and requires just a dot of blood. Drawback: Test strips are about $1 each. Accuchek Aviva is another good device. (We've had a lot of problems with Walgreen's brand device.)
2) Test strips--This is the costly part of the proposition. Purchased 25 or 50 at a time, they can cost from $0.50 to $1.00 a piece.
3) Lancets--These are the pins for the fingerstick device that comes with the glucose meter. A box should be just a few dollars.

No prescription is necessary, nor will insurance pay for your costs unless you're diabetic. To conserve test strips, use them only when a new, untested food or food combination is going to be consumed. If you had two scrambled eggs with green peppers, sundried tomatoes, and olive oil yesterday and had a one hour postprandial glucose of 97 mg/dl, no need to check blood sugar again if you are having the same meal again today.

As the iodine experience grows, I've made several unique observations.

Up to several times per day, I see people who are responding in some positive way to iodine supplementation. (See previous Heart Scan Blog posts about iodine: Iodine deficiency is REAL and The healthiest people are the most iodine deficient.)

Among the phenomena I've observed:

1) A free T4 thyroid hormone at the low end of normal, or even in the below normal range, along with a highish TSH (usually >1.5 mIU/L) are the most frequent patterns that signal iodine deficiency. Occasionally, a low free T3 value will also increase, though this is the least frequent development.

2) At a dose of 500 to 1000 mcg iodine per day, it requires anywhere from 3 to 6 months to obtain normalization of thyroid measures.

3) Reversal of small goiters also occurs over about 6 months.

4) Iodine intolerance is uncommon. If it occurs, using a low starting dose, e.g., 100-200 mcg per day, usually works. The dose can be increased gradually over the ensuing months.

5) Perceptible benefits of iodine occur only occasionally. The most common perceptible effects are increased energy and increased warmth, especially of the hands and feet.

6) Some people who have taken thyroid hormones for years will develop reduced need for their medication with iodine supplementation. In other words, their physician was inadvertently treating iodine deficiency with thyroid hormone replacement. Anyone already on any thyroid preparation(s), e.g., Synthroid, levothyroxine, Armour thyroid, Naturethroid, etc., should watch for signs of hyperthyroidism when iodine is added. But having your own thyroid gland make its own thyroid hormones is better and healthier than relying on the prescription agents. Just be sure to monitor your thyroid measures.

7) Iodine toxicity can occur--Two people in my clinic population developed iodine toxicity by taking 6000 mcg iodine per day for 6 or more months. (Both patients did it on their own based on something they read). Iodine toxicity is evidenced by shutting down your thyroid, i.e., marked increase in TSH, e.g., 15 mIU/L.

Most of the people in my clinic obtain their iodine from kelp tablets. Some use potassium iodine (KI) drops. A handful have used the high-potency Iodoral (12.5 mg or 12,500 mcg iodine per tablet); this was also the form that generated the toxic effects in the two females.

All in all, iodine deficiency is actually far more common than I ever suspected. Not everybody is iodine deficient. But a substantial minority of the Midwest population I see certainly are.

Lipoprotein(a), or Lp(a), is the combined product of a low-density lipoprotein (LDL) particle joined with the liver-produced protein, apoprotein(a).

Apoprotein(a)'s characteristics are genetically-determined: If your Mom gave the gene to you, you will have the same type of apoprotein(a) as she did. You will also share her risk for heart disease and stroke.

When apoprotein(a) joins with LDL, the combined Lp(a) particle is among the most aggressive known causes for coronary and carotid plaque. If apoprotein(a) joins with a small LDL, the Lp(a) particle that results is especially aggressive. This is the pattern I see, for instance, in people who have heart attacks or have high heart scan scores in their 40s or 50s.

Lp(a) is not rare. Estimates of incidence vary from population to population. In the population I see, who often come to me because they have positive heart scan scores or existing coronary disease (in other words, a "skewed" or "selected" population), approximately 30% express substantial blood levels of Lp(a).

Then why haven't you heard about Lp(a)? If it is an aggressive, perhaps the MOST aggressive known cause for heart disease and stroke, why isn't Lp(a)featured in news reports, Oprah, or The Health Channel?

Easy: Because the treatments are nutritional and inexpensive.

The expression of Lp(a), despite being a genetically-programmed characteristic, can be modified; it can be reduced. In fact, of the five people who have reduced their coronary calcium (heart scan) score the most in the Track Your Plaque program, four have Lp(a). While sometimes difficult to gain control over, people with Lp(a) represent some of the biggest success stories in the Track Your Plaque program.

Treatments for Lp(a) include (in order of my current preference):

1) High-dose fish oil--We currently use 6000 mg EPA + DHA per day
2) Niacin
3) DHEA
4) Thyroid normalization--especially T3

Hormonal strategies beyond DHEA can exert a small Lp(a)-reducing effect: testosterone for men, estrogens (human, no horse!) for women.

In other words, there is no high-ticket pharmaceutical treatment for Lp(a). All the treatments are either nutritional, like high-dose fish oil, or low-cost generic drugs, like liothyronine (T3) or Armour thyroid.

That is the sad state of affairs in healthcare today: If there is no money to be made by the pharmaceutical industry, then there are no sexy sales representatives to promote a new drug to the gullible practicing physician. Because most education for physicians is provided by the drug industry today, no drug marketing means no awareness of this aggressive cause for heart disease and stroke called Lp(a). (When a drug manufacturer finally releases a prescription agent effective for reducing Lp(a), such as eprotirome, then you'll see TV ads, magazine stories, and TV talk show discussions about the importance of Lp(a). That's how the world works.)

Now you know better.

If you would like to plan a heart attack in your future, here are some easy-to-follow steps to get you there in just a few short months or years:

1) Follow a low-fat diet.

2) Replace fat calories with "healthy whole grains" like whole wheat bread.

3) Eat "heart healthy" foods like heart healthy yogurt and breakfast cereals from the grocery store.

4) Use cholesterol-reducing plant sterols.

5) Take a multivitamin to obtain all the "necessary" nutrients.

6) Take the advice of your doctor who declares your heart "in great shape" based on your cholesterol values.

7) Take the advice of your cardiologist who declares your heart "like that of a 30-year old" based on a stress test.

8) Take a statin drug to reduce LDL and c-reactive protein while maintaining your low-fat diet.

9) Neglect sun exposure and vitamin D restoration.

10) Limit your salt intake while not supplementing iodine.

There you have it: An easy, 10-step process to do your part to help your local hospital add on its next $40 million heart care center.

If you would instead like to prevent a heart attack in your future, then you should consider not doing any of the above.

C-reactive protein, or CRP, is a protein produced by the liver in response to inflammatory signals its receives. Thus, CRP has emerged as a popular measure to gauge the underlying inflammatory status of your body. Higher CRP levels (e.g., 3.0 mg/L or greater) are associated with increased risk of heart attack and other cardiovascular events.

The drug cartel have jumped on this with the assistance of Harvard cardiologist, Dr. Paul Ridker. Most physicians now regard increased CRP as a mandate to institute statin therapy, preferably at high doses based on such studies as The JUPITER Trial, in which rosuvastatin (Crestor), 20 mg per day, reduced CRP 37%.

I see this differently. Two strategies drop CRP dramatically, nearly to zero with rare exception: Vitamin D restoration and wheat elimination. Not 37%, but something close to 100%.

Yes, I know it sounds wacky. But it works almost without fail, provided the rest of your life is conducted in reasonably healthy fashion, i.e., you don't live on Coca Cola, weigh 80 lbs over ideal weight, and smoke.

How can something so easily reduced like CRP mean you "need" medication? Easy: Increased CRP means there are fundamental deficiencies and/or inflammation provoking foods in your diet. Correct neither and there is an apparent benefit to taking a statin drug.

Why not just correct the underlying causes?

One of the most common reasons people come to my office is to correct high cholesterol values without Lipitor. (Substitute "Lipitor" with Crestor, simvastatin, Vytorin, or any of the other cholesterol drugs; it's much the same.)

In the world of conventional healthcare, in which you are instructed to follow a diet that increases risk for heart disease and not advised to correct nutrient deficiencies like vitamin D and omega-3 fatty acids, then a drug like Lipitor may indeed provide benefit.

But when you are provided genuinely effective information on diet, along with correction of nutrient deficiencies, then the "need" and apparent benefits of Lipitor largely dissolve. While there are occasional genetic anomalies that can improve with use of Lipitor and other statins, many, perhaps most, people taking these drugs really would not have to if they were just provided the right information.

Anyone following the discussions on these pages knows that wheat elimination is probably one of the most powerful overall health strategies available. Wheat elimination reduces real measured LDL quite dramatically. Provided you limit other carbohydrates, such as those from fruits, as well, LDL can drop like a stone. That's not what your doctor tells you. This approach works because elimination of wheat and limiting other carbohydrates reduces small LDL. Small LDL particles are triggered by carbohydrates, especially wheat; reducing carbohydrates reduces small LDL. Conventional LDL of the sort obtained in your doctor's office will not show this, since it is a calculated value that appears to increase with reduced carbohydrates, a misleading result.

Throw vitamin D normalization and iodine + thyroid normalization into the mix (both are exceptionally common), and you have two additional potent means to reduce (measured) LDL. Not restricting fat but increasing healthy fat intake, such as the fats in lots of raw nuts, olive oil, and flaxseed oil reduce LDL.

While I still prescribe statins now and then, a growing number of people are succeeding without them.

(Note that by "measured" LDL I am referring to the "gold standard," LDL particle number by NMR provided by Liposcience. A second best is measured Apoprotein B available through most conventional labs.)

While einkorn is a 14-chromosome ancient wheat (containing the so-called "A" genome), emmer is a 28-chromosome wheat (containing the "A" and "B" genomes, the "B" likely contributed by goat grass 9000 years ago).

Both einkorn and emmer originally grew wild in the Fertile Crescent, allowing Neolithic Natufians to harvest the wild grasses with stone sickles and grind the seeds into porridge.

Having tested einkorn with only a modest rise in blood sugar but without the gastrointestinal or neurological effects I experienced with conventional whole wheat bread, I next tested bread made with emmer grain.

The emmer grain was ground just like the other two grains, cardiac dietitian Margaret Pfeiffer doing all the work of grinding and baking. Margaret added nothing but water, yeast, and a little salt. The emmer rose a little more than einkorn, but not to the degree of conventional whole wheat.

I tested my blood sugar beforehand: 89 mg/dl. I then ate 4 oz of the emmer bread. It tasted very similar to conventional whole wheat, but not as nutty as einkorn. Also not as heavy as einkorn, only slightly heavier than conventional whole wheat.

One hour later, blood sugar: 147 mg/dl. I felt slightly queasy for about 2-3 hours, but that was the end of it. No abdominal cramps, no sleep disturbance or crazy dreams, no nausea, no change in ability to concentrate.

I asked four other wheat-sensitive people to try the emmer bread. Likewise, nobody reacted negatively (though nobody tested blood sugar).

So it seems to me, based on this small, unscientific experience, that ancient einkorn (A) and emmer (AB) wheat seem to act like carbohydrates, similar to, say, rice or quinoa, but lack many of the other adverse effects induced by conventional wheat.

Modern wheat , Triticum aestivum, contains variations on the "A," "B," and "D" genomes, the "D" contributed by hybridization with Triticum tauschii at about the same time that emmer wheat hybridization occurred. It is likely that proteins coded by the "D" genome are the source of most of the problems with wheat products: immune, neurologic, gastrointestinal destruction, airway inflammation (asthma), increase in appetite, etc. This is consistent with observations made in studies that attempt to pinpoint the gliadin proteins that trigger celiac, the area in which much of this research originates.

If I ever would like an indulgence of cookies or cupcakes, I think that I will order some more einkorn grain from Eli Rogosa.

Lisa is a trained dietitian. Unlike many of her colleagues, she has "seen the light" and realized that the conventional advice that most dietitians are forced to dispense through hospitals, clinics, and other facilities is just plain wrong.

I know Lisa personally and we've had some great conversations on diet and nutritional supplements. I told Lisa about my einkorn experience and how I witnessed a dramatic difference between bread made from einkorn wheat and that made from conventional whole wheat. So she decided to give it a try herself.

Here's Lisa's experience:

This past Friday, June 18th, I conducted my "Einkorn Wheat Experiment".

7 am
FBG [fasting blood glucose] 97 mg/dl

8 am-9 am
1 hour high-intensity aerobic workout

10:05 am
BG 99

10:05 am
I embarked upon the journey of choking down, I mean enjoying, the hefty piece of Einkorn bread. Wow, was that bread dense! It was a lot of work chewing.

10:50 am
(45 minutes after consumption, wanted to see what BG did a bit before the 1 hr mark) BG 153

11:05 am
1hr PP 120

11:35 am
90 mins PP [postprandial] 113

12:05 pm
2 hours PP 114 ... at this time I ate an egg & veggie omelet for lunch.

12:50 pm
BG 100

Before dinner 5:10 pm
BG 88

I was surprised with the BG of 153. However, it was good to see my insulin response is reactive and decreased BG 33 points in 15 minutes to end up with a BG of 120 1 hr after the bread.

So, it appears my response is similar. A slight elevation of BG at the 1 hour mark, but not to the degree of conventional whole grain wheat bread.

Of note, also, was the fact that I cannot remember the last time I ate a piece of wheat bread of this magnitude that did not make me bloated... not at all: No cramps, no brain fog, no headache and, did I mention not bloated?

I believe you are on to something with tolerance of Einkorn wheat for those of us with wheat sensitivities, in addition to its apparent lower glycemic response.

Along with Lisa, I asked four other people with various acute intolerances (all gastrointestinal) to conventional wheat, i.e., people who experience undesirable effects from wheat within minutes to several hours, to eat the einkorn bread. None experienced their usual reactions.

Obviously, this does not constitute a clinical trial. Nonetheless, I find this a compelling observation: People like myself who generally experience distinct undesirable reactions to wheat did not experience these reactions with einkorn.

Note, however, that einkorn behaves like a carbohydrate. No different, say, from brown rice or quinoa. However, unlike modern whole wheat flour from Triticum aestivum, in this little experience there were no immune reactions, no neurologic phenomena, no gastrointestinal distress--just the blood sugar consequences.

While this may not be true for all people consuming einkorn, it suggests that primordial einkorn wheat is quite different from modern conventional wheat for most people.

Another interview with Livin' La Vida Low Carb's Jimmy Moore

"Millions of needless deaths"

Thiazide diuretics: Treatment of choice for high blood pressure?

"High-dose" Vitamin D

Vitamin D Home Test

Where do Track Your Plaque membership revenues go?

Getting your dose of fish oil right

Flat tummy . . . or, Why your dietitian is fat

Statin drug revolt

Lovaza Rip-off

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

Dr. Cannell on vitamin D and cancer

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

Diabetes: controlled or . . . cured?

Study review: cerivastatin

John Cannell on Vitamin D

Watch your groin

Garlic and cholesterol--Does everyone now need Lipitor?

Diet Coke saves father's life

Beware the "false positive" stress test

Don't neglect your magnesium

Third heart scan a charm

Metabolic syndrome--cured

Heart Scan Curiosities #6

Should you become a vegetarian?

China fiction?

Carbohydrate-LDL double whammy

To lose weight, prick your finger

Iodine update

Why haven't you heard about lipoprotein(a)?

How to have a heart attack in 10 easy steps

Kick inflammation in the butt

Life without Lipitor

In search of wheat: Emmer

In search of wheat: Another einkorn experience