Cureality | Real People Seeking Real Cures

I dare you: Ask your doctor whether coronary heart disease can be reversed.

My prediction is that the answer will be a flat "NO." Or, something like "rarely, in extraordinary cases," kind of like spontaneous cure of cancer.

There are indeed discussions that have developed over the years in the conventional scientific and medical literature about reversal of heart disease, like Dean Ornish's Lifestyle Heart Trial, the REVERSAL Trial of atorvastatin (Lipitor) and the ASTEROID Trial of rosuvastatin (Crestor). Reversal of atherosclerotic plaque in these trials tends to be small in scale and sporadic.

Of course, the medical literature is swamped with studies that have nothing to do with reversal, like what stent is best, what platelet-inhibiting intravenous drug is best, when should angioplasty or stents be used and when, do implantable defibrillators save lives, improvements in coronary bypass techniques, etc. There are tens of thousands of these studies for every study that focuses on the question of atherosclerotic plaque reversal.

The concept of reversal of heart disease has simply not gained a foothold in the lexicon nor in the thinking of practicing physicians. Heart disease is a relentlessly, unavoidably, and helplessly progressive disease in their way of thinking. Perhaps we can reduce the likelihood of cardiovascular events like heart attack and death with statin drugs and beta blockers. But reverse heart disease ? In your dreams!

We need to change this mentality. Heart disease is a reversible phenomenon. Atherosclerosis in other territories like the carotid arteries is also a reversible pheneomenon. Rather than throwing medicines and (ineffective) diets at you (like the ridiculous American Heart Association program), what if your doctor set out from the start not just to reduce events, but to purposefully reduce your heart's plaque? While it might not succeed in everyone, it would certainly change the focus dramatically.

After all, isn't this the theme followed in cancer treatment? If you had a tumor, isn't cure the goal? Would we accept an oncologist's advice to simply reduce the likelihood of death from cancer but ignore the idea of ridding yourself completely of the disease? I don't think so.

Then why accept "event reduction" as a goal in heart disease? We shouldn't have to. Heart disease reversal--elimination--should be the goal.

Once upon a time, remember how medical information was mysterious, hospitals were places where frightening, inscrutable things happened, diseases were strange maladies that struck without reason, and obtaining information about health was like hunting for buried treasure? The full extent of many peoples' understanding of health came through relatively anemic sources like Readers' Digest. (Remember "I am Joe's Colon"?)

Compare this to what we have now. If I wanted to obtain information about ankylosing spondylitis (a rare genetic disease of the spine), a Google search yields 1.46 million citations. Not all the information, of course, is helpful or relevant, but there's certain to be a bounty of information that far exceeds what you could have uncovered 40 years ago.

Suppose you enter the search phrase "antithrombin III" into your Google search. Citations: over 900,000. (The number of search citations, in fact, exceeds the number of Americans with a deficiency of this blood clotting protein!)

The same is true with heart disease. There was a time, not more than 30-40 years ago, when information about the heart and heart disease was hard to come by. The most you would find were superficial discussions about heart attacks, what chest pain means, descriptions of bypass surgery. Ask your doctor, you'd likely receive a brief, cursory response about how you probably shouldn't worry it.

Even during medical school in the 1980s, I remember struggling to get answers to my questions from faculty during medical school and medical training. It was as if providing too much information would eliminate the advantage superiors wielded over trainees.

The same selfish sentiment, the "I know something you don't know" mentality reminiscent of a schoolboy's "naa na na naa naa!" unfortunately persists. But it is rapidly disintegrating. Soon it will join the junk heap of medical mis-information accumulated over the years (a big pile, to be sure). The internet and, I'll admit (grudgingly), the media, have been responsible for demystifying the formerly mysterious and indecipherable world of health.

You now have, at a moment's disposal, access to an extraordinary array and breadth of health information that was inconceivable just a few years ago.

Times are changing. Doctors no longer hold the monopoly over health information. The public--YOU--are rapidly becoming the arbiters of health, the informed consumers of a soon-to-be retail product called health care, and the increasingly savvy judges of what should join the mainstream path of health. It is all part of this wave of change that I've been advocating: the emerging concept of self-empowerment in healthcare.

Added to the junk heap of health-mistakes-of-years-past will be medical protectionism over health information, heart procedures, drug industry excesses, nutritional mis-information, among others. The demystification of health information will open the floodgates of individual insight into health. It delivers control over your own health destiny straight into your own lap.

Walking the supermarket aisles, you may have lately noticed that numerous new products are appearing sporting "omega-3s" on the label.

Some products simply contain alpha-linolenic acid, a tiny amount of which is converted to the biologically active omega-3s, EPA and DHA. Natural Ovens' Brainy Bagel, for instance, carries a claim of "620 omega-3."

I find this confusing and misleading, since people will often interpret such a claim to mean that it contains 620 of EPA and DHA, similar to two capsules of standard fish oil (1000 mg capsules). Of course, it does NOT. I find this especially troublesome when people will actually stop or reduce their fish oil, since they've been misled into thinking that products like this bread contain active omega-3 fatty acids that yield all the benefits of the "real stuff."

Other products actually contain the omega-3, DHA, though usually in small quantities. Breyer's Smart with DHA is an example, with 32 mg DHA per container.

I find products with actual DHA (from algae) a more credible claim. However, the Center for Science in the Public Interest (CSPI) has looked at the actual contents of DHA in some of these products and found some discrepancies, including amounts of DHA less than the labeled amount and claims of omega-3 wihtout specifying DHA vs. linolenic acid. (It's probably linolenic acid, if it's not specified.)

All in all, the addition of DHA to food products is a nice way to boost your intake of this healthy omega-3. However, keep in mind that these are processed, often highly processed, foods and you will likely pay a premium for the little boost. For now, stick to fish oil, the real thing.

For a brief summary of the CSPI report and a link to the Nutrition Action Newsletter, see Omega-3 Madness: Fish Oil or Snake Oil.

I'm sitting at dinner with two colleagues. One is a cardiology colleague, another an internist who, in addition to practicing general internal medicine, also takes heart disease prevention very seriously. He has, in fact, participated in the Track Your Plaque program and dropped his heart scan score substantially.

"Why don't we see you in the cath lab much?" my cardiology colleague asked me. He was puzzled, since he knew my background in cath lab work from years before, spending day and night doing procedure after procedure. He spends virtually all his days there.

"Well, my patients simply don't have events any more. Heart attacks and angina among people in my program are just about non-existent. They don't have symptoms and they don't have to go to the hospital. I can't remember the last time that I was woken up in the middle of the night for an urgent procedure for one of my patients."

The internist across the table smiled and expressed his agreement. "That's the same thing I'm seeing: No heart attacks, very few if any referrals to cardiologists for procedures. I remember when it was a several times a week thing. Now, almost never. "

Looking at my cardiology colleague, I saw the usual cardiologist reaction: Eyes searching left and right and behind us for something more interesting. Certainly, talking about a virtual cure for coronary heart disease was just too damn dull.

Such is the attitude of 98% of my colleagues: If it doesn't generate a revenue-producing procedure, why bother? Prevention is for general practitioners, the line of thinking goes. "And anyway, I'm too busy doing procedures! I don't ahve time to talk about prevention and health!" Of course, the poor general practitioner is already overloaded with caring for arthritis, flu, diabetes and all the new drugs for diabetes, headaches, vaccinations, diarrhea, and . . .oh, yes, heart disease prevention.

Are cardiologists the enemy? No, of course they are are not. But they often act like they are. Talking to cardiologists is like going to the car dealer with your checkbook out, pen in hand. The salesman gets to write the check himself and you just sign it. Talk to a cardiologist and more often than not you will end up with a heart procedure--whether or not you need it.

Unfortunately--tragically--they often forget what they are supposed to be doing: Taking care of a disease by preventing it. Putting in a defibrillator is not preventing a disease. Putting in three stents, laser angioplasty, and thrombectomy are not ways of preventing a disease.

I'm thankful for my internist friend who sees the light. Coronary heart disease is a an easily measurable, quantifiable, preventable, and REVERSIBLE process for many, if not most, people when provided the right tools. But don't ask your neighborhood cardiologists to give you those tools.

Was torcetrapib’s crash and burn fatal for this class of drug?

At the 2007 American Heart Association meetings in Orlando, Florida, Dr. Philip Barter of Sydney, Australia, presented an update of the ILLUMINATE drug trial for the once-promising drug, torcetrapib, the billion-dollar bet that Pfizer made on its first entry into the new drug class.

You may recall that the crash and burn of Pfizer’s torcetrapib in December 2006 made headlines and prompted enormous disappointment for many patients and doctors who had hoped for a new drug choice to raise HDL cholesterol. Pfizer executives (heads flew!) and investors were also disappointed, anticipating release of a drug that might have become the number one biggest selling drug in the world—ever, surpassing even Lipitor's® $13 billion annual sales.

Torcetrapib is the first among the “cholesteryl-ester transfer protein inhibitors,” or CETP-inhibitors, drugs that block the exchange of cholesterol and triglycerides between HDL and VLDL particles and prevent formation of the unwanted small LDL particles. Preliminary efforts suggested that effects were positively enormous.

However, the 15,000-participant trial was abruptly terminated after 550 days when an excess of deaths were identified among the group taking the experimental drug: 59 deaths in control group; 93 deaths in the torcetrapib group.

In addition, cardiovascular events were 24% greater in the torcetrapib group, numbering 373 compared to 464 in the no-torcetrapib group, including a substantially greater number of heart attacks and hospitalizations. Another surprise came in the way of cause of death among some of the torcetrapib patients, with an excess of deaths due to cancers (twice as many in the torcetrapib group), strokes, and infections.

Why the divergence: enormous improvements in cholesterol values, yet increase in adverse effects including more heart attack? Deeper digging by the principal investigators uncovered unexpected distortions of electrolytes like sodium and potassium. They then re-analyzed blood samples from participants on both sides of the trial and discovered that participants taking torcetrapib experienced significant rise in the blood pressure hormone, aldosterone. This, they surmised, also likely accounted for the 4 mmHg average rise in blood pressure among those taking the experimental drug. (This is the same pathway blocked by blood pressure drugs like ACE inhibitors lisinopril and enalapril, ARBs like losartan.)

Simultaneously (what a coincidence!) with the torcetrapib data, investigators at competing drug manufacturer, Merck, reported encouraging data with their version of CETP inhibitor, anacetrapib. In a phase II FDA trial of 589 patients, anacetrapib reduced LDL-C levels by up to 40% and increased HDL-C up to 139%.

Spokesman Daniel Bloomfield, M.D., of Merck Research Laboratories reported that "The favorable lipid effects seen in this study with multiple doses of anacetrapib were significant, and confirm the continued evaluation of the clinical benefits of CETP inhibitors in the treatment of dyslipidemia." Quick to distinguish this drug from torcetrapib’s track record of dangerous effects on blood pressure, he added that "the decreased LDL-C concentrations, increased HDL-C concentrations and no demonstrable increase in blood pressure seen with anacetrapib are particularly encouraging results of this study."

However, the data reported only an 8 week expereince. Given the experience with torcetrapib, longer term data will obviously be required to assess safety. After Pfizer spent over $1 billion and sacrificed lives to obtain this experience, Merck will need to tread carefully.

It will clearly be many years before we have a confident answer on whether the CETP-inhibitor class of drugs will be a safe choice for correction of cholesterol abnormalities, especially low HDL. Are we helpless until then?

Though CETP inhibitors offer the potential for a one-stop opportunity to raise HDL substantially, there are still many strategies available to raise HDL.

Strategies that raise HDL and are available today include:
• Weight loss—to your ideal weight. A very effective strategy.
• Reduction in processed carbohydrates—like breads, pasta, cookies, pretzels, etc. Note that very low-fat diets reduce HDL. Often a huge effect.
• Fish oil—A small effect, more dramatic when triglycerides are high.
• Niacin—Vitamin B3, the best we have at present. Doses of 500-1500 mg per day raise HDL 20–50%; work with your doctor if you are contemplating niacin. We use this agent everyday and have had great success; good hydration is key to minimize the annoying “hot-flush” effect.
• Dark chocolate—40 grams, or about 2 inches square, a delicious way to squeeze out a little rise in HDL.
• Alcoholic beverages—Red wines are almost certainly the preferred route, rich in flavonoids.
• Exercise—HDL-raising effects vary, but can sometimes be as much as 10–20 mg.
• Other drugs—Though not commonly used for this effect, drugs like pioglitazone (for diabetes and pre-diabetes); fibrates (Tricor® or fenofibrate; Lopid® or gemfibrozil); and Pletal® or cilostazol are occasionally prescribed.
• Vitamin D—You won’t find validation of this effect in any scientific study, but our emerging experience in our heart disease reversal program is suggesting that this neglected nutrient can exert powerful HDL-raising effects. In fact, supplementing vitamin D has made my life much easier.

And, last I checked, none of these HDL-raising strategies are ever fatal.

Joe, a machinist, was frightened and frustrated.

With a heart scan score of 1644 at age 61, his eyes bulged when I advised him that, if preventive efforts weren't instituted right away, his risk for heart attack was a high as 25% per year. Joe had "passed" a stress test, thus suggesting that, while coronary plaque was present--oodles of it, in fact--coronary blood flow was normal. Thus, there would be no benefit to inserting three stents, say, or a bypass operation.

(Illustration courtesy Wikipedia)

"I don't get it, doc. Why can't you just take it out? You know, like Roto-Rooter it out? Or give me something to dissolve it!"

Of course, if there were such a thing, I'd give it to him. But, of course, there is not. It doesn't mean that there haven't been efforts in this direction over the years. Among the various attempts made to "Roto-Rooter" atherosclerotic plaque have included:

Coronary endarterectomy
This is a drastic procedure rarely performed anymore but enjoyed some popularity in the 1980s and 1990s. Coronary endarterectomy was performed during coronary bypass surgery, but few thoracic surgeons performed it. Milwaukee's Dr. Dudley Johnson was the foremost practitioner of this procedure (retired a few years ago after his own bypass operation) with a mortality in excess of 25%. A very dangerous procedure, indeed. The technical hurdle, beyond the tedium and length of time required to remove plaque that had a tendency to fragment, was blood clot formation after tissue was exposed upon plaque removal. I saw many lengthy hospital stays and deaths following this procedure.

Coronary atherectomy
This is an angioplasty-type procedure that has gone through several variations over the years.

In the early 1990s, transluminal extraction atherectomy (TEC) was a technique involving low-rpm drill bits with a suction apparatus that was used to clear soft debris, usually from large coronary arteries or, more commonly, bypass grafts. Then came direction atherectomy, in which a steel housing contained a sharp drill bit that captured atherosclerotic plaque in an aperture along the housing length and stuffed it into a nosecone, retrieved once the device was removed.

Then came high-speed rotational atherectomy in which a diamond-tipped drill bit rotated up to 200,000 rpm and essentially pulverized plaque to flow downstream and, presumably, eventually captured by the liver for disposal. Rotational atherectomy is still in use on occasion. Laser angioplasty, usually using the excimer wavelength, vaporizes plaque. I did plenty of all of these back in the early and mid-1990s.

While all atherectomy procedures sound clever, they are all plagued by the same problem: vigorous return of plaque. Remove plaque, it grows back. There are few instances today in which atherectomy is still performed.

Chelation
This involves a metal-binding, or "chelating," agent like EDTA normally used in conventional practice for lead poisoning. Usually administered IV, some have also advocated oral use. People who use chelation also tend to believe in faith healing and other practices based on faith, not science. There is an international trial that is nearing completion that should provide the final word on whether there is any role to intravenous chelation.

There are numerous other oral treatments that claim a Roto-Rooter-like effect. Nattokinase, for example--an outright, unadulterated, and unqualified scam.

Unfortunately, the helpless, ignorant, and gullible are many. When frightened by the specter of heart disease, there are plenty of people who will willingly pay for the hope provided by clever ads, fast-talking salespeople, and unscrupulous practitioners.

So, Joe, there is no Roto-Rooter for coronary atherosclerotic plaque, at least one that is safe, doesn't involve a life-threatening effort, provides results that endure beyond a few months, and truly works.

The Track Your Plaque program may not be easy. There are obvious common hurdles to adhering to these concepts: obtaining lipoprotein testing, getting intelligent interepretation of the results, persuading your doctor to measure vitamin D blood levels, battling the onslaught of prevailing food propaganda that confuses and misleads. The Track Your Plaque program also requires time, at least a year.

But it's the best program there is. Do you know of anything better?

In our effort to expand the reach for the nationwide conversation on heart disease reversal, I'd like to welcome the newest contributor to the Track Your Plaque family, a new Member blogger, Heart Cipher.

We first came to appreciate the insights of Heart Cipher on our Member Forum. His curiousity and ability to cut through the bull--- have won over our hearts and minds. I think you will appreciate his unique perspective as someone who has experienced first hand the inadequacies of the present procedure-focused, drug-obsessed standard of medical care that dominates, yet has the intelligence and worldliness to recognize that there are better ways.

Read his post about meeting a new cardiologist for the first time and the reaction he receives when he describes the Track Your Plaque program here.

http://www.heartcipher.com/

For the last few years, most practicing physicians have followed a rough blueprint for cholesterol management provided by the Adult Treatment Panel-III “consensus” guidelines, or ATP-III, a lengthy document last released in 2001, updated in 2004.

For instance, ATP-III suggests reducing LDL cholesterol to 100 mg/dl or less for those deemed to be at high risk for future heart disease, arbitrarily defined as a risk of 20% over a 10-year period. It also suggests that a desirable triglyceride level is no more than 150 mg/dl. The ATP-III guidelines have been the topic of discussion in thousands of medical meetings, editorials, and reports. They have served as the basis for many dinners at nice restaurants, weeks in Vegas or Honolulu, many, many lunches catered by pharmaceutical representatives. For most internists, family doctors, cardiologists, and lipid clinics, ATP-III is the Bible for cholesterol management.

AT-III has also become the de facto standard that could conceivably held up as the prevailing "standard of care" in a court of law in cases of presumed negligence to treat cholesterol values. “Doctor, would you agree that the consensus guidelines issued by the National Institutes of Health and endorsed by the American Heart Association state that LDL cholesterol should be reduced to 100? You do? Then why was Mr. Jones’ LDL not addressed according to these guidelines?”

Who was on the ATP-III panel and on what scientific evidence were the guidelines based? Several problems:

1) Of the 9 physician members of the panel, 8 had ties to industry, some of them quite intimate.

2) The studies upon which the guidelines were based and figure prominently, such as the Heart Protection Study, PROVE IT, and 4S, were all funded by the pharmaceutical industry. Of course, it would be unreasonable to expect anyone other than the pharmaceutical industry to fund drug studies. But prominently neglected or understated in the guidelines are all the other insights and treatments for coronary atherosclerotic risk available that were NOT funded by industry.

Of course, there’s money to be made in reducing LDL cholesterol. Lots of it--$23 billion last year alone, in fact. Just keeping that fact in mind makes the ATP-III guidelines make far better sense.

ATP-III is really not a blueprint for heart disease prevention. It is a blueprint--by industry, for industry--on how and when to treat LDL cholesterol.

But what if ATP-III had been a map for navigating coronary plaque reversal instead? What if it were not obsessed with just reducing LDL cholesterol, but was focused on providing the corner internist, family doctor, or cardiologist a roadmap for navigating the highways and byways of reversal?

That would be interesting. Mainstream reversal. Imagine that.

Among the difficulties is that the path to reversal is not lined with deep pockets. Treat LDL and who gains? That's easy. Reverse heart disease and who gains? Beyond LDL reduction, very few (beyond you and me, of course).

That’s why the call for a new Age of Self-Empowerment in healthcare is necessary now more than ever. In my view, in the foreseeable future, we will not have an ATP-III-like blueprint for heart disease control or reversal, nor will we witness a boom of nationwide appreciation that coronary atherosclerosis is a reversible process.

It’s time to take the control back and put it in our own hands. Don't expect the American Heart Association to do it. Don't expect the pharmaceutical industry to do it. If there's anyone who's going to do it, it's YOU.

Greg slumped back in his chair.

"I'm sorry, doc. I feel like the world's biggest schlump!"

He was referring to the fact that he had gone wheat-free for two months--eliminated all breads, bagels, donuts, pasta, breakfast cereals, crackers, pretzels--and promptly lost 30 lbs. He felt great, discovered new levels of energy he thought he'd lost long ago.

Then some friends convinced him to have some cheeseburgers at a fast food restaurant.

"After that, it was downhill. I couldn't get enough. My wife made chile and I had to have four slices of bread with it. Then I'd have two more. I just couldn't stop."

Now, having regained the 30 lbs in the space of another two months, Greg was expressing his disgust.

And it's not the first time. Greg has struggled with his wheat-alholism for as long as I've known him. I've tried motivating him by showing him the flagrant lipoprotein patterns that his wheat habit and excess weight caused: markedly elevated LDL particle number, severe small LDL, low HDL, high triglycerides, high C-reactive protein, high blood sugar, high blood pressure. Greg has received a total of 7 stents over the past 5 years. His next stop is the operating room for a bypass if he can't bring his patterns and impulses under control.

But for some reason, Greg seems to always return to the wheat trough, gorging on breads, pretzels, cake, often in great quantities.

I'm not entirely sure what to do with someone with Greg's severe degree of wheat-aholism. I view wheat-aholism as similar to alcoholism. For some, it can be as addictive.

The only strategy that I know can work is to make a clean break and drop wheat products altogether. Just as an alcoholic cannot just satisfy him/herself with a drink or two a day, so a wheataholic can't be satified with just a couple of wheat crackers. It inevitably leads to the avalanche of wheat indulgences.

Perhaps we should form a new group: Wheataholics Anonymous. "Hi. My name is Greg and I'm a wheataholic."

The heart disease revenue pie is shrinking. So is the "serving size" being shared by competing hospitals.

In other words, as more hospitals open heart programs, there is more competition for the same heart patient. Throw into the mix the drop in "acute" presentations of disease, probably due to the now widespread prescribing of statin drugs. When I first started cardiology practice 15 years ago, for instance, days and nights spent taking care of heart attacks coming through the emergency room was a common event. It still happens, but far less frequently. (I don't mean to suggest that the actual prevalence of coronary heart disease has decreased, just the acute, catastrophic version of it.)

Throw into this mix the results of the COURAGE Trial that has put a damper on the value of stents and angioplasty vs. "optimal" medical therapy in people with stable anginal symptoms, since there was little advantage of procedures. Though it has not stopped the practice, it has reduced the enthusiasm for procedures. Though data are hard to come by, I've heard talk of 10% or greater drops in total procedural volume over the past year.

It's not uncommon for hospitals to have overbuilt heart facilities in anticipation of continued growth of this--until recently--growth industry called heart disease. However, factors are converging that may provide a new profit opportunity for hospitals.

One such opportunity is CT coronary angiography. The usual scenario: Man or woman without symptoms is persuaded somehow--an ad, primary care physician, next door neighbor with a scary event, Dr. Mehmet Oz gushing about this sexy new technology on yet another Oprah episode--to undergo a CT coronary angiogram. A "severe" blockage is found, despite the lack of symptoms, and voila! A stent patient or bypass patient is created out of nothing! Do this repeatedly and systematically, and a hospital can regain its former high-procedural volume glory.

Heart scans, though I believe deeply in them and they are the basis for the Track Your Plaque prevention and reversal program, can also be used and abused this way. Asymptomatic person has a score 150. Concerned, they go to their physician who orders a nuclear stress test. An "inferior perfusion defect" is seen, presumably representing poor flow through the right coronary artery (but often just means that the diaphragm overlaps the heart muscle and yields this apparition, a "false positive" or misleading result). "But--wink--we've got to find out if there's a severe blockage, don't we? You don't want to end up in an early grave!"

Thus, the battle for new patients with asymptomatic disease is getting underway in earnest. The scramble for cardiologists to learn how to use CT coronary angiograms is proceeding at breakneck speed, with new training courses being offered nationwide several times and places every month. CT coronary angiography is a useful test, but it is also subject to enormous abuse. It also provides the ticket for the unscrupulous physician and the revenue-hungry hospital eager to expand its patient volume.

Many people believe that this cannot happen commonly in 2007, given scrutiny of practices, litigiousness, and the expectation of a moral sense in medicine. However, I've witnessed such incidents several times this month alone. If you need graphic proof of just how far this can go before action is taken, read Coronary, Stephen Klaidman's chilling tale of a cardiologist and cardiothoracic surgeon in small-town northern California who built an enormous heart center based on fabricated heart disease diagnoses. You'll also find their story in Shannon Brownlee's recently released Overtreated: Why Too Much Medicine Is Making Us Sicker and Poorer.

Of course, the Track Your Plaque program is meant principally for people without symptoms, also. But we are advocating that asymptomatic disease is a reason for prevention, not procedures. There's a difference.

By the way, the two practitioners who engineered the escapade detailed in these books, cardiologist Chae Hyun Moon and cardiac surgeon Fidel Realyvasquez, walked away with a monetary fine and suspension of their California medical licenses. It is likely that many people died because of their abusive practices, but the state struggled to make a sufficiently persuasive case for reasons that I still don't understand.

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.

The manufacturers of krill oil claim that the phospholipid form of omega-3 fatty acids, EPA and DHA, enhance their absorption. There are indeed some data to that effect:

Here are some representative krill oil preparations available on the market:

MegaRed Krill Oil:
EPA 50 mg
DHA 24 mg
Total omega-3s (EPA + DHA + other forms) 90 mg
Price: $28.99 for 60 softgels

Source Naturals (a fine company otherwise, by the way):

EPA 150 mg
DHA 90 mg
Total omega-3 fatty acids 300 mg
Price: $24.99 for 60 softgels

Alright, let's do some simple math:

Average volume of blood in the human body (all components): 5000 cc
Percentage of red blood cells (RBCs) by volume: 45%
Total volume RBCs: 2250 cc
Percentage of total volume RBCs occupied by fatty acids:

In the conventional practice of early heart disease prevention, cholesterol testing takes center stage. Rarely does it go any further, aside from questions about family history and obvious sources of modifiable risk such as smoking and sedentary lifestyle.

So standard practice is to usually look at your LDL cholesterol, the value that is calculated, not measured, then--almost without fail--prescribe a statin drug. While there are indeed useful values in the standard cholesterol panel--HDL cholesterol and triglycerides--they are typically ignored or prompt no specific action.

But a genuine effort at heart disease prevention should go farther than an assessment of calculated LDL cholesterol, as there are many ways that humans develop coronary atherosclerosis. Among the tests to consider in order to craft a truly effect heart disease prevention program are:

--Lipoprotein testing--Rather than using the amount of cholesterol in the various fractions of blood as a crude surrogate for lipoproteins in the bloodstream, why not measure lipoproteins themselves? These techniques have been around for over 20 years, but are simply not part of standard practice.

Lipoprotein testing especially allows you to understand what proportion of LDL particles are the truly unhealthy small LDL particles (that are oxidation- and glycation-prone). It also identifies whether or not you have lipoprotein(a), the heritable factor that confers superior survival capacity in a wild environment ("The Perfect Carnivore"), but makes the holder of this genetic pattern the least tolerant to the modern diet dominated by grains and sugars, devoid of fat and organ meats.

--25-hydroxy vitamin D--The data documenting the health power of vitamin D restoration continue to grow, with benefits on blood sugar and insulin, blood pressure, bone density, protection from winter "blues" (seasonal affective disorder), decrease in falls and fractures, decrease in cancer, decrease in cardiovascular events. I aim to keep 25-hydroxy vitamin D at a level of 60 to 70 ng/ml. This generally requires 4000-8000 units per day in gelcap form, at least for the first 3 or so years, after which there is a decrease in need. Daily supplementation is better than weekly, monthly, or other less-frequent regimens. The D3 (cholecalciferol) form is superior to the non-human D2 (ergocalciferol) form.

--Hemoglobin A1c (HbA1c)--HbA1c represents glycated hemoglobin, i.e., hemoglobin molecules within red blood cells that are irreversibly modified by glucose, or blood sugar. It therefore provides an index of endogenous glycation of all proteins of the body: proteins in the lenses of the eyes that lead to cataracts; proteins in the cartilage of the knees and hips that lead to brittle cartilage and arthritis; proteins in kidney tissue leading to kidney dysfunction.

HbA1c provides an incredibly clear snapshot of health: It reflects the amount of glycation you have been exposed to over the past 90 or so days. We therefore aim for an ideal level: 5.0% or less, the amount of "ambient" glycation that occurs just with living life. We reject the notion that a HbA1c level of 6.0% is acceptable just because you don't "need" diabetes medication, the thinking that drives conventional medical practice.

--RBC Omega-3 Index--The average American consumes very little omega-3 fatty acids, EPA and DHA, such that a typical omega-3 RBC Index, i.e., the proportion of fatty acids in the red blood cell occupied by omega-3 fatty acids, is around 2-3%, a level associated with increased potential for sudden cardiac death (death!). Levels of 6% or greater are associated with reduced potential for sudden cardiac death; 10% or greater are associated with reduced other cardiovascular events.

Evidence therefore suggests that an RBC Omega-3 Index of 10% or greater is desirable, a level generally achieved by obtaining 3000-3600 mg EPA + DHA per day (more or less, depending on the form consumed, an issue for future discussion).

--Thyroid testing (TSH, free T3, free T4)--Even subtle degrees of thyroid dysfunction can double, triple, even quadruple cardiovascular risk. TSH values, for instance, within the previously presumed "normal" range, pose increased risk for cardiovascular death; a TSH level of 4.0 mIU, for instance, is associated with more than double the relative risk of a level of 1.0.

Sad fact: the endocrinology community, not keeping abreast of the concerning issues coming from the toxicological community regarding perchlorates, polyfluorooctanoic acid and other fluorinated hydrocarbons, polybrominated diphenyl ethers (PDBEs), and other thyroid-toxic compounds, tend to ignore these issues, while the public is increasingly exposed to the increased cardiovascular risk of even modest degrees of thyroid dysfunction. Don't commit the same crime of ignorance: Thyroid dysfunction in this age of endocrine disruption can be crucial to cardiovascular and overall health.

All in all, there are a number of common blood tests that are relevant--no, crucial--for achieving heart health. Last on the list: standard cholesterol testing.

Happy Thanksgiving 2012, everyone, from all the staff at Track Your Plaque!

Here’s a zesty version of traditional cranberry sauce, minus the sugar. The orange, cinnamon, and other spices, along with the crunch of walnuts, make this one of my favorite holiday side dishes.

There are 31.5 grams total “net” carbohydrates in this entire recipe, or 5.25 grams per serving (serves 6). To further reduce carbs, you can leave out the orange juice and, optionally, use more zest.

1 cup water
12 ounces fresh whole cranberries
Sweetener equivalent to 1 cup sugar (I used 6 tablespoons Truvía)
1 tablespoon orange zest + juice of half an orange
½ cup chopped walnuts
1 teaspoon ground cinnamon
½ teaspoon ground nutmeg
¼ teaspoon ground cloves

In small to medium saucepan, bring water to boil. Turn heat down and add cranberries. Cover and cook at low-heat for 10 minutes or until all cranberries have popped. Stir in sweetener. Remove from heat.

Stir in orange zest and juice, walnuts, cinnamon, nutmeg, and cloves.

Transfer mixture to bowl, cool, and serve.

Apple, cranberry, and cinnamon: the perfect combination of tastes and scents for winter holidays!

I took a bit of carbohydrate liberties with this recipe. The entire recipe yields a delicious cheesecake-like crumble with 59 “net” grams carbohydrates (total carbs – fiber); divided among 10 slices, that’s 5.9 grams net carbs per serving, a quantity most tolerate just fine. (To reduce carbohydrates, the molasses in the crumble is optional, reducing total carbohydrate by 11 grams.)

Other good choices for sweeteners include liquid stevia, stevia glycerite, powdered stevia (pure or inulin-based, not maltodextrin-based), Truvía, Swerve, and erythritol. And always taste your batter to test sweetness, since sweeteners vary in sweetness from brand to brand and your individual sensitivity to sweetness depends on how long you’ve been wheat-free. (The longer you’ve been wheat-free, the less sweetness you desire.)

Crust and crumble topping
3 cups almond meal
1 stick (8 tablespoons) butter, softened
1 cup xylitol (or other sweetener equivalent to 1 cup sugar)
1½ teaspoons ground cinnamon
1 tablespoon molasses
1½ teaspoons vanilla extract
Dash sea salt

Filling
16 ounces cream cheese, softened
2 large eggs
½ cup xylitol (or other sweetener equivalent to ½ cup sugar)
1 Granny Smith apple (or other variety)
1 teaspoon ground cinnamon
1 cup fresh cranberries

Preheat oven to 350° F.

In large bowl, combine almond meal, butter, sweetener, cinnamon, molasses, vanilla, and salt and mix.

Grease a 9½-inch tart or pie pan. Using approximately 1 cup of the almond meal mixture, form a thin bottom crust with your hands or spoon.

In another bowl, combine cream cheese, eggs, and sweetener and mix with spoon or mixer at low-speed. Pour into tart or pie pan.

Core apple and slice into very thin sections. Arrange in circles around the edge of the cream cheese mixture, working inwards. Distribute cranberries over top, then sprinkle cinnamon over entire mixture.

Gently layer remaining almond meal crumble evenly over top. Bake for 30 minutes or until topping lightly browned.

Biscuits and gravy: the ultimate comfort food . . . one you thought you’d never have again!

The familiar dish of breakfast and holiday meals is recreated here with a delicious gravy that you can pour over piping hot biscuits. Because it contains no wheat or other unhealthy thickeners like cornstarch made with “junk” carbohydrates, there should be no blood sugar or insulin problems with this dish, nor joint pain, edema, acid reflux, mind “fog,” or dandruff—life is good without wheat!

While the gravy is also dairy-free for those with dairy intolerances, the biscuits are not, as there are cheese and butter in the biscuits, both of which are optional, e.g., leave out the cheese and replace butter with coconut or other oil.

Makes 10 biscuits

Gravy:
2 tablespoons extra-virgin olive oil
1 pound loose sausage meat
2½ cups beef broth
¼ cup coconut flour
½ cup coconut milk (canned variety)
1 tablespoon onion powder
1 teaspoon garlic powder
½ teaspoon sea salt
Dash ground black pepper

Biscuits:
1 cup shredded cheddar (or other) cheese
2 cups almond meal/flour
¼ cup coconut flour
¾ teaspoon baking soda
½ teaspoon sea salt
2 large eggs
4 ounces butter, melted (or other oil, e.g., extra-light olive, coconut, walnut)

To make gravy:
In large skillet, heat oil over medium heat. Sauté sausage, breaking up as it browns. Cook until thoroughly cooked and no longer pink.

Turn heat up to medium to high and pour in beef broth. Heat just short of boiling, then turn down to low heat. Stir in coconut flour, little by little, over 3-5 minutes; stop adding when gravy obtains desired thickness. Pour in coconut milk and stir in well. Add onion powder, garlic powder, salt, and pepper and simmer over low heat for 5 minutes. Add additional salt and pepper to taste. Remove from heat and set aside.

To make biscuits:
Preheat oven to 325° F.

In food chopper or processor, pulse shredded cheese to finer, granular consistency.

Pour cheese into large bowl, then add almond meal, coconut flour, baking soda, and salt and mix thoroughly. Add the eggs and butter or oil and mix thoroughly to yield thick dough.

Spoon out dough into 10 or so ¾-inch thick mounds onto a parchment paper-lined baking pan. Bake for 20 minutes or until lightly browned and toothpick withdraws dry.

Ladle gravy onto biscuits just before serving.

People who carry the gene for lipoprotein(a), Lp(a), tend to be:

--Intelligent--The bell curve of IQ is shifted rightward by a substantial margin.
--Athletic--With unusual capacity for long-endurance effort, thus the many marathoners, triathletes, and long-distance bikers with Lp(a).
--Tolerant to dehydration
--Tolerant to starvation
--Resistant to tropical infections

In other words, people with Lp(a) have an evolutionary survival advantage. More than other people, they make clever, capable hunters who can run for hours to chase down prey, not requiring food or water, and less likely to succumb to the infections of the wild. In a primitive setting, people with Lp(a) are survivors. Evolution has likely served to select Lp(a) people for their superior survival characteristics.

But wait a minute: Isn't Lp(a) a risk for heart attack and stroke? Don't we call Lp(a) "the most aggressive known cause for heart disease and stroke that nobody gives a damn about"?

Yes. So what allows this evolutionary advantage for survival to become a survival disadvantage?

Carbohydrates, especially those from grains and sugars. Let me explain.

More so than other people, Lp(a) people express the small LDL pattern readily when they consume carbohydrates such as those from "healthy whole grains." Recall that the gene for Lp(a) is really the gene for apoprotein(a), the protein that, once produced by the liver and released into the bloodstream, binds to an available LDL particle to create the combination Lp(a) molecule. If the LDL particle component of Lp(a) is small, it confers greater atherogenicity (greater plaque-causing potential). Thus, carbohydrate consumption makes Lp(a) a more aggressive cause for atherosclerotic plaque. The situation can be made worse by exposure to vegetable oils, such as those from sunflower or corn, which increases production of apo(a).

Also, more than other people, Lp(a) people tend to show diabetic tendencies with consumption of carbohydrates. Eat "healthy whole grains," for instance, or if a marathoner carb-loads, he/she will show diabetic-range blood sugars. I have seen long-distance runners or triathletes, for instance, have a 6 ounce container of sugary yogurt and have blood sugars of 200 mg/dl or higher. The extreme exercise provides no protection from the diabetic potential.

Because carbohydrates are so destructive to the Lp(a) type, it means that people with this pattern do best by 1) absolutely minimizing exposure to carbohydrates and vegetable oils, ideally grain-free and sugar-free, and 2) rely on a diet rich in fats and proteins.

The perfect diet for the Lp(a) type? It would be a diet of feasting on the spoils of the hunt, devouring the wild boar captured and slaughtered and eating the snout, hindquarters, spleen, kidneys, heart, and bone marrow, then eating mushrooms, leaves, nuts, coconut, berries, small rodents, reptiles, fish, birds, and insects when the hunt is unproductive.

Capable hunter, survivor, consumer of muscle and organ meats: I call people with Lp(a) "The Perfect Carnivores."

The NPR Health Blog contacted me, as they were interested in learning more about health strategies and tools that are being used by individuals without their doctors. The Track Your Plaque website and program came up in their quest, as it is the only program available for self-empowerment in heart disease.

Several Track Your Plaque Members spoke up to add their insights. The full text of the article can be viewed here.

How's Your Cholesterol? The Crowd Wants To Know
Mainstream medicine isn't in favor of self-analysis, or seeking advice from non-professionals, of course. And anyone who does so is running a risk.

But there are folks who want to change the course of their heart health with a combination of professional and peer support. Some are bent on tackling the plaque that forms in arteries that can lead to heart disease. They gather online at Track Your Plaque, or "TYP" to the initiates.

"We test, test, test ... and basically experiment on ourselves and have through trial and error came up with the TYP program, which is tailored to the individual," Patrick Theut, a veteran of the site who tells Shots he has watched his plaque slow, stop and regress.

The site was created in 2004 by Bill Davis, a preventive cardiologist in Milwaukee, Wisc. Davis is also the author of Wheat Belly: Lose the Wheat, Lose the Weight and Find Your Path Back to Health, which argues that wheat is addictive and bad for most people's health. Davis recommends eliminating wheat from the diet to most new members of Track Your Plaque.

"The heart is one of the hardest things to self-manage but when you let people take the reins of control, you get far better results and far fewer catastrophes like heart attacks," Davis tells Shots.

Doctors typically give patients diagnosed with heart disease two options: take cholesterol-lowering statin drugs, or make lifestyle changes, like diet. It's usually far easier for both parties — the doctor and the patient — to go with the drugs than manage the much more difficult lifestyle changes, Davis says.

"Doctors say take the Lipitor, cut the fat and call me if you have chest pain," he explains. "But that's an awful way to manage care."

TYP has members submit their scores from heart CT scans, cholesterol values, lipoproteins and other heart health factors to a panel of doctors, nutritionists and exercise specialists. Then they receive advice in the form of an individualized plaque-control program. But the online forum, where users share their results with other members and exchange tips, is where most of the TYP action happens.

The community currently has about 2,400 members who pay $39.95 for a quarterly membership, or $89.75 for a yearly membership. Davis says all proceeds go towards maintaining the website.

Ilaine Upton is a 60-year-old bankruptcy lawyer from Fairfax, Va., and a TYP member. At a friend's suggestion, Upton decided to get a heart CT scan in July. Her score was higher than it should have been (22 instead of 0), so she decided to get her blood lipids and cholesterol tested, too, and sent a sample off to MyMedLabs.com.

She learned that her LDL particle count was over 2,000 ("crazy high," she says), and she posted her results on TYP. Davis advised her that a low-carb diet would reduce it, so she decided to try it.

Since July, she says she has had "excellent results" with the program, and her LDL counts are coming down.

"It would be nice to have a [personal] physician involved in this, but [my insurer] Blue Cross won't pay if you are not symptomatic, and I am trying to prevent becoming symptomatic," says Upton. "I feel very empowered by this knowledge and the ability to take better control of my health by getting feedback on the decisions I make."

This is about as decadent as it gets around here!

Here’s a recreation of an old-fashioned coffee cake, a version with a delicious chewy-crunchy streusel topping.

I’ve specified xylitol as the sweetener in the topping, as it is the most compatible sweetener for the streusel “crumb” effect and browning.

Variations are easy. For example, for an apple pecan coffee cake, add a layer of finely-chopped or sliced apples to the cake batter and topping.

Additional potential carbohydrate exposure comes from the garbanzo bean flour and molasses. However, distributed into 10 slices, each slice provides 7.2 grams “net” carbs (total carbs minus fiber), a perfectly tolerable amount. Be careful not to exceed two slices!

Yield 10 slices

Cake:
2½ cups almond flour
½ cup garbanzo bean flour
1 tablespoon ground cinnamon
1 teaspoon baking soda
Sweetener equivalent to ¾ cup sugar
Dash sea salt

3 eggs separated
3/8 teaspoon cream of tartar
1 tablespoon vanilla extract
4 ounces butter, melted
Juice of ½ lemon

Topping:
½ cup almond flour
¼ cup pecans, finely chopped
1 tablespoon ground cinnamon
½ cup xylitol
1 tablespoon molasses
6 ounces butter, cut into ½-inch widths, at room temperature

Preheat oven to 325º F. Grease bread pan.

In bowl, combine almond flour, garbanzo flour, cinnamon, baking soda, sweetener, salt, and mix.

In small bowl, whip egg whites and cream of tartar until stiff peaks form. At low speed, blend in egg yolks, vanilla, melted butter, and lemon juice.

Pour liquid mixture into almond mixture and mix thoroughly. Pour into microwave-safe bread pan and microwave on high for 3 minutes. Remove and set aside.

To make topping, combine almond flour, pecans, cinnamon, xylitol, and molasses in small bowl and mix. Mix in butter

Spread topping on cake. Bake for 20 minutes or until toothpick withdraws dry.

If you miss peanut butter and jelly sandwiches, you’re going to absolutely love these peanut butter and jelly macaroons!

Not everybody loves the taste or texture of coconut. This issue is solved by the first step: toasting shredded coconut, then reducing them down to a granular consistency. This yields a macaroon consistency without the dominant coconut taste, replaced instead with the flavors of PB & J.

I’ve specified liquid stevia as the sweetener, but this is easily replaced by your choice of sweetener. Note that, regardless of which sweetener used, they vary in sweetness from brand to brand and the quantity required to equal the ½ cup of sugar equivalent can vary. It always helps to taste your batter and adjust sweetness.

Also, I used Swerve in this recipe, the erythritol-inulin mix that enhances texture, but its use is optional.

As written, each macaroon contains just over 3 grams “net” carbohydrates (total carbs minus fiber), meaning you can have several before doing any damage!

Makes 24 macaroons

3 cups shredded unsweetened coconut
2 tablespoons vanilla extract
1 teaspoon almond extract
¼ cup coconut flour
¼ cup dried unsweetened cherries (or other unsweetened berries)
2 tablespoons coconut oil
¼ cup natural peanut butter, room temperature
2 egg whites
½ teaspoon liquid stevia or sweetener equivalent to ½ cup sugar
2 tablespoons Swerve

Preheat oven to 300° F.

In large bowl, combine coconut, vanilla and almond extracts, and mix.

Spread mixture on baking sheet and bake for 10 minutes, stirring occasionally, until very lightly browned. Be careful not to burn. Remove and cool. (Leave oven at 300° F.)

When cooled, using food chopper, food processor, or coffee grinder, pulse coconut mixture until coconut reduced to consistency of coffee grounds. Pour back into bowl. Stir in coconut flour.

Place cherries or other berries in food chopper, food processor, or coffee grinder and pulse until reduced to small granules or paste. Remove with spatula and add to coconut mixture. Set aside.

Place egg whites in bowl and whip until frothy and stiff peaks form.

In small microwave-safe bowl, combine coconut oil and peanut butter and microwave in 10-second increments until warm (not hot) liquid. Stir in egg whites, followed by stevia and Swerve, and blend thoroughly.

Dispense dough onto a parchment paper-lined baking sheet using a 1 ½-inch cookie scooper or spoons.

Bake for 15 minutes or until lightly browned.

Why would I say such a thing? Well, a number of reasons. People with lipoprotein(a), or Lp(a), are, with only occasional exceptions:

--Very intelligent. I know many people with this genetic pattern with IQs of 130, 140, even 160+.
--Good at math--This is true more for the male expression of the pattern, only occasionally female. It means that men with Lp(a) gravitate towards careers in math, accounting, financial analysis, physics, and engineering.
--Athletic--Many are marathon runners, triathletes, long-distance bicyclists, and other endurance athletes. I tell my patients that, if they want to meet other people with Lp(a), go to a triathlon.
--Poor at hydrating. People with Lp(a) have a defective thirst mechanism and often go for many hours without drinking water. This is why many Lp(a) people experience the pain of kidney stones: Prolonged and repeated dehydration causes crystals to form in the kidneys, leading to stone formation over time.
--Tolerant to dehydration--Related to the previous item, people with Lp(a) can go for extended periods without even thinking about water.
--Tolerant to periods of food deprivation or starvation--More so than other people, those with Lp(a) are uncommonly tolerant to days without food, as would occur in a wild setting.

In short, people with Lp(a) are intelligent, athletic, with many other favorable characteristics that provide a survival advantage . . . in a primitive world.

So when did Lp(a) become a problem? When an individual with Lp(a) is exposed to carbohydrates, especially those from grains. When an evolutionarily-advantaged Lp(a) individual is exposed to carbohydrates, more than other people they develop:

--Excess quantities of small LDL particles--Recall that Lp(a) is a two-part molecule. One part: an apo(a) made by the liver. 2nd part: an LDL particle. When the LDL particle within the Lp(a) molecule is small, its overall behavior is worse or more atherogenic (plaque-causing).
--Hyperglycemia/hyperinsulinemia--which then leads to diabetes. Unlike non-Lp(a) people, these phenomena can develop with far less visceral fat. A Lp(a) male, for instance, standing 5 ft 10 inches tall and weighing 150 pounds, can have as much insulin resistance/hyperglycemia as a non-Lp(a) male of similar height weighing 50+ pounds more.

Key to gaining control over Lp(a) is strict carbohydrate limitation. Another way to look at this is to say that Lp(a) people do best with unlimited fat and protein intake.

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