All posts by william-davis

Firefighters are twice as likely to die from a heart attack in the line of duty than are policemen, and three times more likely than EMTs.

That's among the headlines run today because of a report in the New England Journal of Medicine documenting a dramatically higher risk for heart attack for fire fighters putting out fires. The above headline is from an excellent report run on NPR radio. You can listen to the webcast at http://www.npr.org/templates/story/story.php?storyId=9047656.

The story sparked comments from experts insisting that all fire fighters should have physicals, should be in better physical condition, should be covered by health insurance (the NPR report said that 1 out of 4 fire fighters lack health insurance). Judging from the indisputable risk firefighters encounter, these are all good ideas.

But if you've been following my blog or the Track Your Plaque program, you know that physicals alone are hopeless exercises for identifying hidden heart disease. Among the solutions: identify whether or not heart disease is present in the first place--do a CT heart scan.

In fact, several local fire companies in my area have done just that: insisting that all firefighters undergo a heart scan. When groups of people like firefighters arrange for heart scans, they gain the advantage of doing so en masse, thereby allowing many scan centers to offer a dramatically reduced price to the city, town, or village that is paying for them. I've even seen many firefighters scanned at no cost.

It would also help to have health insurance, be physically fit, and have a stress test (an exception to my view that stress tests are also useless to screen asymptomatic people for heart disease). But a CT heart scan would settle the question quickly, easily, undeniably, and inexpensively.

This question comes up around once a week:

My CT heart scan score is ____. Wouldn't I be better off just getting a bypass (or stent, etc.) and getting it over with? If I know that heart attack is in my future, why not just get it over with?

The most recent source of this question was the wife of a patient. Jack had a heart scan score of 92 in 2005. He made very little effort to correct his causes, permitting pre-diabetic patterns to persist, failed to correct vitamin D, etc. and a repeat heart scan score showed a dramatic rise to 264.

Jack's wife asked whether he should just have a bypass.

There are several problems with this line of reasoning:

1) Bypass surgery does not reduce the long term risk for heart attack.

2) The risk of bypass surgery often outweighs the risk of an asymptomatic heart scan score.

3) Bypass surgery is a temporary "fix," a fancy Band Aid for a disease that progresses after the procedure. One bypass typically prompts another, and another...

4) Bypassing arteries that have vigorous blood flow often causes the bypass graft to not "take" and close within the first few days.

Thankfully, nobody in his right mind has proposed that we perform prophylactic bypass operations.

Of course, hospitals and surgeons would jump at the chance to perform procedures in anybody with some threshhold heart scan score. It would double or triple their business overnight. At $70,000 or more per procedure, they would dance in glee. Of course, you and I would pay for their new burst of wealth by a sharp increase in our health insurance premiums. Not only that, the people who underwent the procedure would not benefit.

I'm seeing more and more people taking 80 mg of Lipitor per day. For the most part, these are people who come in for another opinion after a stent or heart attack and are prescribed the drug during their hospitalization.

This practice is based on the results of the PROVE IT-TIMI 22 (PRavastatin Or atorVastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction) trial, and the Reversal of Atherosclerosis with Aggressive Lipid Lowering (REVERSAL) trial, both reported in 2005. In the PROVE IT Trial, 4,000 people experiencing heart attacks were treated with Lipitor (atorvastatin), 80 mg, or Pravachol (pravastatin), 40 mg. There was a reduction in events like recurrent heart attack from 13.1% in the Pravachol group to 9.6% in the Lipitor group. In the REVERSAL Trial, the Lipitor group also showed no plaque growth compared to the Pravachol group, which did progress, with disease tracked by intracoronary ultrasound.

I believe that many of my colleagues took the bait. In a half-hearted effort to reduce events and trend towards better coronary plaque control, writing a prescription for 80 mg rather than a lower dose has become increasingly popular.

Some problems: Despite the favorable tolerance to high dose Lipitor in these trials, I don't know anybody who can tolerate 80 mg per day for more than a few months in real life. In my experience, people inevitably end up with intolerable muscle aches.

Also, I believe it is folly to believe that we can regress coronary plaque on a broad scale by just using one drug that addresses only a single cause (i.e., LDL cholesterol). Yes, drug companies would argue that the statin drugs are so wonderful because of their so-called "pleiotropic", or non-lipid, effects like reducing inflammation. I have seen regression of plaque once using Lipitor alone. We struggle to reduce coronary plaque using a multi-faceted approach. It is highly unlikely that Lipitor alone at a 80 mg dose will be sufficient in most people to regress plaque. How about lipoprotein(a)? Or vitamin D deficiency? Lipitor has no effect on these patterns and people do not regress just by taking statin agents.

In early February, the FDA approved orlistat, formerly known as prescription Xenical, for over-the-counter sale. Orlistat is a blocker of fat absorption.

The new OTC version will be called "Alli" (pronounced like "ally") and will come at a dose of 60 mg to be taken three times a day with meals. Prescription Xenical came as a 120 mg tablet. However, the company claims that the reduced dose sacrifices only 5% in reduced fat absorption, dropping from 30% with Xenical to 25% with Alli. It will cost in the neighborhood of $1 to $2 per day, or $30-60 per month, far less expensive than the $110-150 for the prescription form.

Does it work? Is it worth the money? Clinical trials document around 5-10 lbs lost over a 3 to 6 month period, 50% greater than using diet and exercise alone.

Our experience is that it works, though inconsistently. Results depend heavily on how reliant you are on fat calories. If you were to follow a low-fat diet while on the drug, you likely will lose little or no weight, since there's little fat absorption to block. However, I have witnessed more substantial weight loss of 10-20 lbs. in people who follow a higher fat intake in their diet, e.g., a traditional American diet. However, these people gain the weight back immediately because they've made no effort to modify food choices.

It is messy. Even though the clinical trials claims modest inconvenient effects like gas and greasy stools, I have found that it is, without fail, a very annoying product that results in crampiness and frequent messy stools in nearly everybody.

The company has created a glitzy website that you can view at www.myalli.com and promises to provide a personalized program and support for registrants when it is up and running by summer 2007.

I think that's a good idea, since the drug itself is no more than a temporary fix unless it's combined with long-term diet changes. However, the website, I believe, oversells the value of the drug with a drug company's usual over-the-top hints and innuendoes without actually coming out with straight pitches of the truth.

Beware of the vitamin D-blocking effect of Orlistat. The period of time you take it may be a time to resort to some modest sun exposure (10-15 minutes; be careful not to burn), rather than than oil-based vitamin D capsules, in order to avoid the inevitable vitamin D plunge in blood level.

I am not a fan of orlistat, having seen it tried many times with minimal success. However, it is another option for those who are really struggling. Personally, I would try fasting or some of the other strategies we've detailed on the www.cureality.com website before I resorted to orlistat.

There's a $22 billion industry based on treating LDL cholesterol, a fictitious number.

LDL cholesterol is calculated from the following equation:

LDL cholesterol = Total cholesterol - HDL cholesterol - triglycerides/5

So when your doctor tells you that your LDL cholesterol is X, 99% of the time it has been calculated. This is based on the empiric calculation developed by Dr. Friedwald in the 1960s. Back then, it was a reasonable solution, just like bacon and eggs was a reasonable breakfast and a '62 Rambler was a reasonable automobile.

One of the problems with Dr. Friedewald's calculation is that the lower HDL cholesterol, the less accurate LDL cholesterol becomes. If it were just a few points, so what? But what if it were commonly 50 to 100 mg/dl inaccurate? In other words, your doctor tells you that your LDL is 120 mg/dl, but the real number is somewhere between 170 and 220 mg/dl. Does this happen?

You bet it does. In my experience, it is an everyday event. In fact, I'm actually surprised when the Friedewald calculated LDL closely approximates true LDL--it's the exception.

Dr. Friedewald would likely have explained that, when applied to a large population of, say, 10,000 people, calculated LDL is a good representation of true LDL. However, just like saying that the average weight for an American woman is 176 lbs (that's true, by the way), does that mean if you weigh 125 lbs that you are "off" by 41 lbs? No, but it shows how you cannot apply the statistical observations made in large populations to a single individual.

The lower HDL goes, the more inaccurate LDL becomes. This would be acceptable if most HDLs still permitted reasonable estimation of LDL--but it does not. LDL begins to become significantly inaccurate with HDL below 60 mg/dl.

How to get around this antiquated formula? In order of most accurate to least accurate:

--LDL particle number (NMR)--the most accurate by far.

--Apoprotein B--available in most laboratories.

--"Direct" LDL

--Non-HDL--i.e., the calculation of total cholesterol minus HDL. But it's still a calculated with built-in flaws.

--LDL by Friedewald calculation.

My personal view: you need to get an NMR if you want to know what your LDL truly is. A month of Lipitor costs around $80-120. A basic NMR costs less than $90. It's a relative bargain.

Faye was clearly frustrated.

At age 52, she was having chest pains every day. A CT heart scan showed a score of zero. A CT coronary angiogram showed no plaque whatsoever.

"Everything went downhill when my menopause started. I gained weight, I started to have chest pains, my blood pressure went up, my cholesterol shot up."

She saw three physicians, none of whom shed much light on the situation. They ran through the predictable sequence of (horse, not human) estrogens, anti-depressants, suggestions for psychological counseling.

But we checked Faye for lipoprotein(a), which she proved to have at a high level of 182 nmol/l. This explained a lot.

A curious and predictable set of phenomenon occur to females with Lp(a) proceeding through the menopause. As estrogen recedes:

--Lp(a) levels rise dramatically.

--Blood pressure goes up, sometimes creating severe hypertension by mid- to late-50s.

--Chest pain can develop, presumably due to "endothelial dysfunction" or "microvascular angina", both representing abnormal coronary artery constriction facilitated by worsening expression of Lp(a).

All too often, these phenomena get dismissed as simply part of the menopausal package, when they are, in fact, important facets of this very important genetic pattern that confers high risk for heart disease.

If any of this rings familiar for you or a loved one, think Lp(a). Though Faye hadn't yet developed any measurable coronary plaque by her CT heart scan score, it was likely on its way, given the surge in Lp(a) expression as menopause unfolded--unless its recognized and appropriate preventive action taken.

I've talked about this before, but I need to periodically remind everybody:
Vitamin D must be an oil-based capsule, a gel-cap, not a tablet.

Lisa is one of early success stories: a heart scan score of 447 in her early 40's, modest reduction of CT heart scan score three years ago.

However, Lisa had a difficult time locating oil-based vitamin D. There has, in fact, been a national run on vitamin D and I'm told that even manufacturers are scrambling to keep up with the booming demand. So, she bought tablets instead and was taking 3000 units per day.

She came in for a routine check. Lisa's 25-OH-vitamin D3: 17 ng/ml, signifying severe deficiency, the same as if she were taking nothing at all. (Recall that we aim for 50 ng/ml.)

In other words, vitamin D tablets do not work. It is shameful. I see numerous women taking calcium tablets with D--the vitamin D does not work. I've actually seen blood levels of zero on these preparations.

You may have to look, but if you want to enjoy the extraordinary benefits of vitamin D replacement, it must be an oil-based capsule. Carlson's and Vitamin Shoppe have excellent prepartions. They raise blood levels substantially and consistently, and they're inexpensive. We pay $5.99 for a bottle of 120 capsules.

What if vitamin D cost $200 rather than $2?

In other words, what if cholecalciferol, or vitamin D3, was a patent-protectable agent that would sell for an extravagant price, just like a drug?

Vitamin D would be the hot topic. There would be TV ads run during Oprah, slick magazine two-page spreads with experts touting its outsized benefits, insurance companies would battle over how much your copay should be.

The manufacturer would host large fancy symposia to educate physicians on how wonderful vitamin D is for treatment of numerous conditions, complete with dinner, a show, and gifts. They would hire expert speakers to speak, scientists to have articles ghost-written, give out knick knacks with the brand label inscribed--just like Lipitor, Actos, Vytorin, ReoPro, Plavix . . .

After all, what other "drug" substantially increases bone density (up to 20% in adult females), enhances insulin responses 30% (equivalent to the TZD drugs, Actos and Avandia), and slashes colon cancer risk?

But it's not a drug. That is both vitamin D's strength and its weakness. It's a strong point because it's natural, phenomenally helpful across a variety of conditions, and inexpensive. It is also a weakness because, at $2 a month, no one is raking in the $12 billion annually that Pfizer makes for Lipitor that allows it to fund an enormous marketing campaign.

Vitamin D is a "discovery" of huge importance for health, including making reductions of CT heart scan scores far more likely for more people. And it comes without a prescription.

Fanatic Cook has posted an excellent summary on the recent negative attention cast on garlic preparations, at least for LDL cholesterol reduction.

Go to http://fanaticcook.blogspot.com to view.

I think Fanatic Cook is right--despite the lack of LDL reducing effects, it doesn't necessarily mean no benefit whatsoever. Anti-coagulation and anti-inflammatory effects, in particular, are well proven.

I do think, however, that it argues more in favor of sticking to whole cloves, rather than supplements. The benefits are also likely small. I would view garlic as a soft advantage for your plaque control program. You can do fine without it. You might do slightly better with it.

Most hospitals maintain the "Saint _____" in their names, despite many having little or nothing to do with the church.

Out of 15 hospitals in my area, 13 are named after saints.

In my view, a more honest name would be something like "ABC Medical Enterprises, Inc." The profit motive, aggressive marketing tactics, and high CEO salaries would make better sense then. The trend to convert practicing physicians from professionals acting on behalf of patient welfare into paid employees would also be clearer.

Imagine Walmart were to change its name to "St. Mary's Emporium" Would it modify your perception of their business? I think it would. It would cause many people to believe that maybe their work was, at least in part, charitable and being done for the public welfare. But Walmart makes such pretense--they are in business for profit, just like all businesses.

It's time for the pretense to be dropped. Hospitals are cut-throat profit-seeking operations, operating under the guise of charitable, tax-free institutions. It's the farthest thing from the truth.

Like many scams, this one follows a predictable formula.

It is a formula widely practiced among food manufacturers, ever since food products began to jockey for position based on nutritional composition and purported health benefits.

First, identify a component of food, such as wheat fiber or oat bran, that confers a health benefit. Then, validate the healthy effect in clinical studies. Wheat fiber, for instance, promotes bowel regularity and reduces the likelihood of colon cancer. Oat bran reduces blood cholesterol levels.

Second, commercialize food products that contain the purported healthy ingredient. Wheat bran becomes Shredded Wheat, Fiber One, and Raisin Bran cereals and an endless choice of “healthy” breads. Oat bran becomes Honey Bunches of Oats, Quaker’s Instant Oatmeal, and granola bars. Even if many unhealthy components are added, as long as the original healthy product is included, the manufacturer continues to lay claim to healthy effects.

Third, as long as the original healthy ingredient remains, get an agency like the American Heart Association to provide an endorsement: “American Heart Association Tested and Approved.”

The last step is the easiest: just pay for it, provided the product meets a set of requirements, no matter how lax.

You will find the American Heart Association certification on Quaker Instant Oatmeal Crunch Apples and Cinnamon. Each serving contains 39 grams carbohydrate, 16 grams sugar (approximately 4 teaspoons), and 2.5 grams fat of which 0.5 grams are saturated. Ingredients include sugar, corn syrup, flaked corn, and partially hydrogenated cottonseed oil. Curiously, of the 4 grams of fiber per serving, only 1 gram is the soluble variety, the sort that reduces cholesterol blood levels. (This relatively trivial quantity of soluble fiber is unlikely to impact significantly on cholesterol levels, since a minimum 3 grams of soluble fiber is the quantity required, as demonstrated in a number of clinical studies.) Nonetheless, this sugar product proudly wears the AHA endorsement.

Thus, a simple component of food that provides genuine benefit mushrooms into a cornucopia of new products with added ingredients: sugar, high fructose corn syrup, corn starch, carageenan, raisins, wheat flour, preservatives, hydrogenated oils, etc. What may have begun as a health benefit can quickly deteriorate into something that is patently unhealthy.

There’s a clever variation on this formula. Rather than developing products that include a healthy component, create products that simply lack an unhealthy ingredient, such as saturated or trans fats or sodium.

Thus, a ¾-cup serving of Cocoa Puffs cereal contains 120 calories, no fiber, 14 grams (3 ½ teaspoons) of sugar—but is low in fat and contains no saturated fat. Proudly displayed on the box front is an American Heart Association stamp of approval. It earned this stamp of approval because Cocoa Puffs was low in saturated, trans, and total fat and sodium. Likewise, Cookie Crisp cereal, featuring Chip the Wolf, a cartoon wolf in a red sweater (“The great taste of chocolate chip cookies and milk!”), has 160 calories, 26 grams carbohydrate and 19 grams (4½ teaspoons) of sugar per cup, and 0 grams fiber—but only 1.0 gram fat, none saturated, thus the AHA check mark. (Promise margarine, made with hydrogenated vegetable oil and therefore containing significant quantities of trans fats, was originally on the list, as well, but removed when the trans fat threshold was added to the AHA criteria.)

It is this phenomenon, the sleight of hand of taking a healthy component and tacking on a list of ingredients manageable only by food scientists, or asserting that a product is healthy just because it lacks a specific undesirable ingredient, that is a major factor in the extraordinary and unprecedented boom in obesity in the U.S. Imagine the chemical industry were permitted such latitude: “Our pesticide is deemed safe by the USDA because it contains no PCBs.” Such is the ill-conceived logic of the AHA Heart-Check program the "Heart Healthy" claims.

It’s best we keep in mind the observations of New York University nutritionist and author of the book, Food Politics, Marion Nestle, that “food companies—just like companies that sell cigarettes, pharmaceuticals, or any other commodity—routinely place the needs of stock holders over considerations of public health. Food companies will make and market any product that sells, regardless of its nutritional value or its effect on health. In this regard, food companies hardly differ from cigarette companies. They lobby Congress to eliminate regulations perceived as unfavorable; they press federal regulatory agencies not to enforce such regulations; and when they don’t like regulatory decisions, they file lawsuits. Like cigarette companies, food companies co-opt food and nutrition experts by supporting professional organizations and research, and they expand sales by marketing directly to children, members of minority groups, and people in develop countries—whether or not the products are likely to improve people’s diets.”

Qualms over just how heart-healthy their products are? Doubtful.

Once upon a time, the tobacco industry was guilty of conducting a widespread, systematic, highly organized campaign to deliver their product to as much of the unsuspecting public as possible.

As clinical data mounted linking smoking and health problems like cancer and heart disease, tobacco producers labored fiercely to counter these claims despite darkening public sentiment. When individual company executives were questioned on why they continued to perpetuate the industry’s scandalous practices, the invariable justification offered was “Well, I had to pay my mortgage.” That tidy ends-justifies-the-means rationalization has a familiar ring when you examine the behavior of those in the heart "industry."

Things are not what they seem. The hospital, once an institution to serve the sick, a place for clergy, volunteers, and other altruists, has evolved into a business serving a thriving bottom line. You are the “product” they seek. The cardiologist, ostensibly in the service of alleviating heart disease, instead seeks to grow his checkbook by performing procedures that have nothing to do with lessening the burden of heart disease. He dives into the water to save drowning victim after drowning victim, but fails to simply toss in the life preserver that has been close at hand all along.

The woeful family practitioner, who is expected to bear undue responsibility for the broad spectrum of health, ignorantly permits heart disease to grow under his or her nose and, by default, allows heart disease to become the exclusive province of the proceduralist. Worse, the family practitioner or internist in the employ of the hospital (a situation that has quietly grown to encompass 80% of all primary care physicians) labors to fatten hospital business by directing patients into hospital services. The comparative lowly incomes of the primary care physician are substantially supplemented by participating in this huge revenue-generating machine called heart care.

The astounding grasp of the system has caused one of every 10 adults in the U.S. to have undergone a heart procedure. The lemming-like procession to the hospital creates a crowd mentality among some sectors of the frightened public. “My friends and neighbors have all had bypass operations. Sooner or later I guess it’s going to be my turn.”

Tragically, the system has grown through the exploitation of trust. The faith we have in doctors, hospitals, and the institutions and people associated with healthcare has been subverted into the service of profit. Many practitioners and institutions choose to operate under the guise of doing good, but instead capitalize on the public’s willingness to accept as fact the need for major heart procedures and all its associated costly trappings.

"When banks compete, you win.”

The TV ad opens with a 60-something man sitting in his living room, talking to a three-piece suit-clad, 30-something banker. The older man is explaining to the dismayed younger man why he’s going to use Lending Tree loan service for a home loan.

“But Dad, I’m you’re son!” the younger whines.

Many of Lending Tree’s clients have collaborated in filing a multi-million dollar class action suit against the company, claiming “bait and switch” tactics. They claim that home buyers are lured by low interest rates or low closing costs on a home loan. Once the buyer concludes the hassle of filling out numerous forms, the suit accuses Lending Tree of making a switch to a costlier loan.

Bait and switch is among the oldest con games around. If you’ve ever bought a car from a car dealer, chances are you’ve had your own little brush with this deception. The ad promises the SUV you’ve wanted for only $299 per month. Only, once you get there, the salesman informs you that only a limited number of special deals were available and they’ve run out. But he’s still got a really good deal right over here!

Most of us recognize that we’ve been hookwinked. Yet we still go along and buy a car from the dealer.

What if it’s not a sleazy salesman behind the pitch, but a physician. If it’s hard to resist the sales pitch at the car dealership, it can be near impossible to ignore the advice of your doctor. But the truth is often loud and clear: in many instances, it is a genuine, bona fide, and fully-certified scam.

Among the most common bait-and-switch heart scams: Your cholesterol is high. The sequence of subsequent testing is well-rehearsed. “Gee, Bob, I’m worried about your risk for heart disease. Let’s schedule you for a nuclear stress test.”

The stress test, like 20% or more of them, is “falsely positive,” meaning abnormal even though there’s nothing wrong with you. Another 30% are equivocal, not clearly abnormal but also not clearly normal. Now up to 50% of people tested “need” a heart catheterization in the hospital to clarify this frightening uncertainty. You might end up with a stent or two, even bypass surgery. Your simple $20 cholesterol panel has metamorphosed into $100,000 in hospital procedures.

That familiar sequence is followed thousands of times, seven days a week, 365 days a year.

Congestive heart failure is among the most common diagnoses in the hospital nowadays.

Congestive heart failure is the result of injury to the heart muscle such as that occurring during heart attack, viral infections of the heart (myocarditis), poorly controlled high blood pressure, and a smattering of other rare causes. Eight million Americans with congestive heart failure account for over one million hospital admissions annually (AHA Update, 2007). It has become so common, in fact, that it has ranked as number one cause for hospital admission for the last several years.

Heart failure is a frightening condition causing the sufferer to gasp for breath. Excess fluid accumulates in the lungs, amplifying the work of breathing and imparting a feeling of unease. Some heart failure sufferers struggle to the point of blacking out or requiring mechanical ventilation on a respirator.

There are a number of standard treatments for heart failure that usually rapidly rescue the patient from the brink of respiratory failure. These generally consist of intravenous diuretics that force the kidney to clear excess water rapidly, medications to increase heart muscle strength, and other treatments. It’s not uncommon for a heart failure patient to drop 10–20 lbs. in water weight with treatment. The treatments are quite effective for the majority of patients with rapid relief of the breathlessness generally obtained within hours.

However, the problem with congestive heart failure is not generally the rapidity or effectiveness of acutely providing relief, it is the chronic recurring nature of the disease. Someone can come to the hospital, obtain prompt treatment with relief of the breathlessness within 48–72 hours, only to return to the hospital in several weeks with a recurrence of the same process.

As common as congestive heart is in hospitals, it has also presented the perennial problem: how to convert this frequent reason for hospitalization into a profit opportunity. Some people who experience heart failure will undergo the usual sequence of heart procedures of heart catheterization, stents, bypass surgery, valve surgery, etc. But, because heart failure tends to be a repeatedly recurring event, even patients tire of the “need” for heart procedures. Then how can more heart failure occurrences be converted into profitable events?

A unique principle operates in the medical device market: If a disease lacks a procedure . . . create one.

Several problems are solved by such a principle. First, procedures are much more generously reimbursed by insurers than standard medical care without procedures. Two, the physician is provided an opportunity to also bill at a higher level. Third, patients often love the more dramatic, heroic nature of procedures, whether or not there is true benefit.

To the rescue of the poorly reimbursed area of congestive heart failure walks a Minnesota company called CHF Solutions, Inc., manufacturers of the Aquadex device.

Cost? $14,500 plus $900 per filter every time a patient gets one treatment. The Aquadex works by a decades-old process called ultrafiltration, used for many years but used principally for kidney failure not severe enough to require regular dialysis. New York cardiologist Howard Levin simply adapted the process, using smaller catheters inserted into the arm veins, in 2000. As in conventional ultrafiltration, blood is taken from the body from a catheter, passed through a filter that removes excess water, then returned to the body.

This is a serious effort. Dr. Levin raised $51 million in venture backing on top of $12 million seed capital. The device sailed through the Food & Drug Administration in June 2002, since it was labeled a newer form of ultrafiltration, thereby obtaining approval through the FDA’s 501k rule, a minor modification of existing technology. (Many truly technologically unique devices do come to market and therefore require the full process of FDA approval, a generally lengthy and costly process for devices. However, there’s another way: bill a device as “substantially equivalent” to an existing technology and the approval process is relatively quick and easy.)

In an industry publication, Cath Lab Digest, Dr. Levin was interviewed in February, 2003, and proclaimed, “We can treat many of the symptoms of heart failure, but we’re a long ways off from a cure. That’s why new technologies are so exciting, such as LVADs for the very sickest heart failure patients; biventricular pacing for the small subset of patients who seem to benefit from it; and simplified ultrafiltration such as the System 100 that can be applied to a broad range of congestive heart failure patients with fluid overload. “

What does this have to do with heart scans and heart disease reversal? Nothing-directly. I highlight this phenomenon because it caricatures how things work in medicine and health care in general, more so in cardiovascular diseases in which the profit motive is especially deeply ingrained. Focus on a need, then generate a profitable treatment for it. Profits are what drive growth, marketing, sales, and expansion into new revenue-generating niches.

Sadly, the reverse principle does not work: Replace profitable procedures with unprofitable strategies, regardless of their effectiveness. Replacing coronary angioplasty and coronary stent implantation, or bypass surgery, with intensive prevention efforts is no easy matter. Just witness the enormous resistance to the concept of early heart disease detection achieved with heart scans. A day doesn’t go by without a major media outlet bashing heart scans, or confusing them with CT coronary angiograms with claims of excessive radiation.

But the mounting volume of criticisms against heart scans also means that they are gaining some traction in mainstream thinking. But will there be a day when they replace the need for profitable procedures? I believe they will, when coupled with a powerful program of prevention, but don’t hold your breath.

A friend of mine is a Type I, or childhood onset, diabetic. He's had it for nearly 50 years, since age 6. He's also in the health industry and is a good observer of detail.

He made the following interesting comments to me recently when talking about the effects of various foods on blood sugar:

"When I eat normally, like some vegetables or salad and meat, I dose up to 10 units of insulin to control my blood sugar.

"If I eat a turkey sandwich on two slices of whole wheat, I usually dose 15 units. The bread makes my blood sugar go to 300 if I don't.

"If I eat a Cousins's Sub [a local submarine sandwich chain], I dose 15 units. The bread really makes my blood sugar go up.

"I can only eat a Quarter Pound from McDonald's once a year, because it make my blood sugar go nuts. I dose 15-20 units before having it, and I feel like crap for two days afterwards.

"If I eat Mexican food, I have to dose 15-20 units. For some reason, it's gotten worse over the years, and I need to dose higher and higher.

"Chinese food is the absolute worst. I dose 20-25 units before eating Chinese. I'll often have to dose more afterwards, because my blood sugar goes so berserk."

Nothing beats the real-world observations on the impact of various foods on blood sugar than the observations of people with Type I diabetes. All the insulin they get is in a syringe. Dosing needs to match intake.

Personally, though I love the taste of Americanized Chinese food, I've always been suspicious of what exactly goes into these dishes. But I was unaware of the blood sugar implications.

The impact of Mexican I believe can be attributed to the cornstarch used in the tacos and tortillas, though I also wonder if there are other starches being snuck in, as well.

Image courtesy of apc33.

Japan provides a useful "laboratory" for studying the effect of a culture that relies heavily on eating fish.

The JELIS Trial, the topic of a previous Heart Scan Blog post, showed that supplementation with the single omega-3 fatty acid, EPA, 1800 mg per day (the equivalent of 10 capsules of 'standard' fish oil that contains 180 mg per day of EPA, 120 mg of DHA) significantly reduced heart attack in a Japanese population. Interestingly, this benefit was additive to the already substantial intake of omega-3 fatty acids among the general Japanese population, a population with a fraction of the heart attacks found in western populations like the U.S. (approximately 3% over 5 years in Japanese compared to several-fold higher in a comparable American group).

While there may be genetic and other cultural and lifestyle reasons behind the dramatically reduced cardiovascular risk in Japanese, it is undeniably at least partially due to the increased intake of omega-3 fatty acids from fish. Incidentally, the purported benefits of omega-3 fatty acids provide a vigorous counter-argument to the idea that all humans should be vegetarians.

Anyway, if we were to take some lessons from the Japanese and their greater habitual intake of omega-3 fatty acids from fish, they might include:

--Rural and coastal Japanese are the sub-populations with the highest reliance on fish, about a quarter-pound a day. (Gives new meaning to the idea of a "Quarter Pounder," doesn't it?) This is at least five-times greater than the intake of an average American.

--Likewise, the blood level of omega-3s in the blood of Japanese is 5-fold higher than in Americans.

--The average intake of omega-3s (EPA + DHA) among a broadly-selected population of Japanese is 850 mg per day (320 mg EPA; 520 mg DHA). Intake ranges from 300 mg per day all the way up to 3100 mg per day.

--Greater omega-3 intake (EPA + DHA) is associated with lesser carotid intimal-medial thickness, an index of body-wide atherosclerosis.

--Japanese have far less heart attack and stroke despite greater prevalence of smoking (nearly half of Japanese) and drinking.

--Total fat intake (percent of calories) is nearly identical between Americans and Japanese. It's the proportion of fat calories from omega-3 that is greater, the proportion of omega-6 that is less in Japanese.

The Japanese eat their fish in ways that we do not: As sashimi (raw, as with sushi in its various forms like Nigiri and Chirashi); fried in tempura; shaved, dried fish sprinkled on about anything you can imagine (it's not as bad as it sounds); as a snack, as in dried cuttlefish (which you can purchase in packages as a portable, sweetened fish that you eat on-the-run--I know it sounds awful, but don't poke fun at it until you've tried it); in "soups" with soba noodles. Fish is commonly consumed with rice and soy sauce, as well as other soy-based foods, such as tofu, miso (soy bean paste), or natto.

I believe that there are some lessons to take from the Japanese and their fish-consuming habits:

1) An omega-3 fatty acid intake of at least 1000 mg per day yields measurable cardiovascular benefits.

2) Despite the fears over mercury and pesticide residues in fish, this seems to not have played out to be a real-life effect in the Japanese, who consume five-fold greater quantities of fish.

3) My mother was right after all when she encouraged us to eat more fish.

Drs. Iris Shai and colleagues released results of a new Israeli study, the Dietary Intervention Randomized Controlled Trial (DIRECT) Trial, that compared three different diet strategies. Of those tested, a low-carbohydrate diet was most successful at achieving weight loss.

You can find the full-text of the study on the New England Journal of Medicine website.

322 participants followed one of three diets over two year period. Compared head-to-head, the (mean) weight loss in each group was:

• 2.9 kg (6.4 lbs) for the low-fat group
• 4.4 kg (9.7 lbs) for the Mediterranean-diet group
• 4.7 kg (10.3 lbs) for the low-carbohydrate group

(Average age 52 years at start; average body-mass index, or BMI, 31.)

The conclusion was that the low-carb diet performed the best, with 60% greater weight loss, with the Mediterranean diet a close second.

The diets

The low-fat diet was based on the American Heart Association diet, with 30% of calories from fat (10% from saturated fat) and food choices weighted towards low-fat grains, vegetables, fruits, and legumes and limited additional fats, sweets, and high-fat snacks; calorie intake of 1500 kcal per day for women and 1800 kcal per day for men was encouraged.

The Mediterranean diet was a moderate-fat diet rich in vegetables, with reduced red meat, and poultry and fish replacing beef and lamb. Total calories from fat of 35% per day or less was the goal, with most fat calories from olive oil and a handful of nuts. Like the low-fat program, calories were limited to 1500 kcal per day for women, 1800 kcal per day for men.

The low-carbohydrate diet was patterned after the popular Atkins’ program, with 8% participants achieving the ketosis that Dr. Atkins’ advocated as evidence that a fat-burning metabolism was activated, rather than sugar-burning as fuel. For the 2-month “induction phase,” 20 grams of carbohydrates per day was set as the goal, followed by 120 grams per day once the weight goal was achieved. Unlike the other two diets, calories, protein and fat were unlimited.

Weight loss, lipids, inflammation

You can see from the weight loss graph that the low-carb approach exerted the most dramatic initial weight loss. Interestingly, much of the weight-loss benefit was lost as the carbohydrate intake increased, by study design, back to 120 mg per day. However, the other two diet approaches showed similar phenomena of “giving back” some of the initial weight loss.

The low-carbohydrate diet exerted the greatest change in cholesterol, or lipid, panels: increased HDL 8.4 mg/dl vs. 6.3 mg/dl on low-fat; the triglyceride response was the most dramatic, with a reduction of 23.7 mg/dl vs. 3.7 mg/dl on low-fat. Interestingly, the LDL cholesterol-reducing effect of all three diets was modest, with the most reduction achieved by the Mediteranean diet.

The inflammatory measure, C-reactive protein (CRP), was reduced most effectively by the low-carb and Mediterranean diets, least by the low-fat diet. HbA1c, a measure of long-term blood sugar, dropped significantly more on the low-carb diet.

When the final dietary composition was examined, interestingly, there really were only modest differences among the three diets, with 8% less calories from carbs, 8% greater calories from fat, comparing low-carb to low-fat, with Mediterranean intermediate.

Taken at face value, this useful exercise quite clearly shows that, from the perspective of weight loss and correction of metabolic parameters like triglycerides, HDL,CRP, and blood sugar, low-carbohydrate wins hands down, with Mediterranean diet a close second.

It also suggests that a return to a carbohydrate intake of 120 mg/day allows a partial return of initial weight lost, as well as deterioration of metabolic parameters after the initial positive changes.

Although the study has already received some criticism for such potential flaws as the modest number of Atkins’ followers achieving ketosis (8%), suggesting lax adherence, and the reintroduction of the 120 mg/day carbohydrate advice, I can suspect that these may have been compromises drawn to satisfy some Institutional Review Board. (Whenever a study is going to be conducted involving human subjects, a study needs to pass through the review of an Institutional Review Board, or IRB. IRB’s, while charged to protect human subjects from experimental abuses, also tend to be painfully conservative and will block a study or demand changes even if they are not dangerous, but just veer too far off the mainstream.)

However, several unanswered questions remain:

1) How would the diets have compared if the carbohydrate restriction were continued for a longer period, or even indefinitely? (The divergences would likely have been dramatic.)
2) Will low-carb exert the same cardiovascular event reduction that the Mediterranean approach has shown in the Lyon study and others?
3) Are there effects on health outside of the measures followed that differ among the three diets, such as cancer? (I doubt it, especially given the modest real differences over time. But this will be the objection raised by various "official" organizations.)

I would further propose that:

Low-fat diets are dead

The AHA will cling to their version of low-fat diet, based on difficulty in changing course for any large, consensus-driven organization, not to mention the substantial ($100’s of millions) revenues derived from endorsing low-fat manufactured products. The AHA will also point to the lack of difference in LDL cholesterol among the three, since they cannot get beyond the fact that there’s more to coronary risk—a lot more—than LDL.

Off-the-shelf diets achieve off-the-shelf results

If you just need a T-shirt, a medium might fit fine. But if you’d like a nicely fitting suit or dress, then tailoring to your individual proportions is needed. When aiming towards maximizing benefits on lipoproteins and coronary risk, none of these diets achieve the kinds of changes we often need for coronary plaque reversal, as in the Track Your Plaque program. That requires making dietary changes that exert maximal effects on lipoprotein patterns.

I came across a criticism of the Track Your Plaque program recently that suggested that it was nothing more than a program to sell CT heart scans.

Huh?

I suppose if you say that the Track Your Plaque program is nothing more than a way to sell heart disease prevention, omega-3 fatty acids from fish oil, vitamin D, better nutrition, and better identification of causes of heart disease . . . well, I believe that would be true.

But is the program a "front" to sell heart scans?

No, it is not, nor has it ever been.

I've heard about these peculiar suspicions about the program before. Though I've never taken them seriously, let me clear up any lingering uncertainty:

--I have no relationship with any heart scan center, scanning facility, or hospital other than to interpret heart scans.

I do not own a scanner, I have no financial interest in a scanner or scanning center, nor have I ever had any interest. I also have no plans to do so in the future. Let business people in the imaging business do that. I want no part of it. I have seen what these people go through and, frankly, I want no part of it, nor do I want the appearance that I am advocating scans to make money. I'm accused of trying to make money from scans even when I do not have any financial interest!

--I do not sell heart scans or imaging packages, nor have I ever done so.

You can't buy a scan through Track Your Plaque, The Heart Scan Blog, or through me. To me, heart scans are simply a measuring tool to identify the extent of coronary plaque, as well as a tracking tool to follow its course. Without it, there would be no Track Your Plaque. But there is also no alternative. The closest alternative would be carotid intimal-medial thickness, a technique, while useful, is a distant second choice to indirectly gauge coronary plaque by examining the thickness of the carotid lining (not carotid plaque). Perhaps in 10 years, a better measure to gauge and track coronary plaque will emerge that has superior aspects over CT heart scanning. If reasonable, safe, accessible, and quantitative, then Track Your Plaque may adopt that technology as its measuring tool.

Track Your Plaque is not about heart scanning; Track Your Plaque is about measuring and tracking plaque that, in 2008, is still best accomplished with CT heart scans.

--I make loads of money from heart scans and Track Your Plaque.

Yeah, right.

Track Your Plaque is a volunteer venture for my team; none of us get paid a penny for doing all we do, including me. We charge a membership fee on the website (somewhere around $6-7 a month) to pay our expenses, such as code writing for our proprietary software (much of it remains under development), printing costs, modest legal costs, the costs of doing business (e.g., accountant). Despite the fact that Track Your Plaque and the Heart Scan Blog occupies a substantial part of the day of the Track Your Plaque team, none of us are reimbursed for our time. I do believe, however, that this concept is so enormously powerful that it will, someday, pay us all enough to allow us to devote more time and effort to it.

Personally, I can't wait to devote more time and effort to this concept that is simple, logical, and effective. More research is needed, more development is needed, more discussion is needed. Right now, it is all accomplished outside of our busy schedules, including my full-time cardiology practice. I continue to have 7 am procedures, middle-of-the-night calls, weekend hospital rounds and emergencies (though virtually none of these are the patients involved in prevention, but the "other" people: atrial fibrillation, elderly heart failure patients, rhythm disorders, cardiomyopathies, pulmonary hypertension, peripheral vascular disease, the non-compliant).

--The book, Track Your Plaque, is a gimmick to sell you a heart scan.

No, it's a program that relies on this technology. But there's no special deal, no discounts, no steering to heart scan centers that I have a special arrangement with. No such thing exists, nor has there ever been such an arrangement.

I've heard it all. Early on, when I was helping my friend, Steve Burlingame and his wife, Nancy, set up Milwaukee Heart Scan, I helped by providing medical oversite, education of physicians and public, and interpreting heart scans. After all, in the "early days," nobody knew anything about heart scans. It was a long, hard climb against ignorance, habit, entrenched thinking, stubbornness, and stupidity. I've been paid next to nothing for all this. I told Steve long ago that, given the extraordinary expenses of maintaining an independent scanning center, that he should first pay his expenses, pay his technologists, receptionists, and nurse, pay himself, then pay me for reading scans if he had any money left over. Most of the time, Steve had nothing left over and I was paid nothing.

So, while some of my colleagues were assuming that I was rolling in money from "promoting" heart scans, the reality was that I was doing nearly everything for free. (It certainly wasn't the high life I was living; I don't drive a Mercedes, take fancy vacations, none of that. In fact, I work about 51 weeks a year.)

Why do I do this if it doesn't yield a big flow of money? Because I believe in it as a superior path to the conventional. If I were simply interested in making more money--I wouldn't do it. I would simply do what all my cardiology colleagues are doing: more heart catheterizations, more angioplasties and stents, learning how to do carotid stents, iliac stents, peripheral angioplasty, renal stents, acquiring the skills to put in defibrillators, new device insertion like umbrellas in the interatrial septum, etc. There's plenty more money in that. It's also not that hard. I know, because that is my background: high-risk cardiac interventions. That's what I was trained to do, that's what I did from a number years, until I started to see that this was nothing more than "putting out fires" in people who became increasingly ill and reliant on bail-out procedures. It makes lots of money, but it is also fundamentally wrong.

So, no, I do not sell heart scans, nor is the Track Your Plaque program or The Heart Scan Blog meant to promote heart scans except as a tool for tracking this disease.

That's it, pure and simple.

Which is more important: cholesterol or coronary plaque?

Ask what Dr. Michael Eades' calls "statinators," and you will likely receive a befuddled look. Or, you might receive comments like "Measuring plaque has never been shown to reduce mortality."

While risk factors for heart disease are important, no doubt (my office practice is about half lipid consultation and complex hyperlipidemia management), for many they have become an end in themselves. In other words, LDL cholesterol in particular dominates thinking so much that it has caused many to exclude the fact that plaque---coronary atherosclerotic plaque---is the disease itself.

Dozens of studies, from the St. Francis Heart Study to the 25,000-participant UCLA registry, to the recently-released MESA database (ethic differences, women, as well as superiority to carotid measures) have repeatedly shown that heart scan scores (coronary artery calcium scores) are superior to conventional risk factors (usually via the Framingham risk score) for predicting future heart attack and other events. And the differences are not minor incremental differences. The predictive power of plaque measurement via heart scanning is multiples better: 4 times, 10 times, 20 times or more in various subgroups.

Much of what we do in medicine is not based on long-term studies of outcome, pitting some diagnostic measure or treatment against placebo. It is already standard practice to measure plaque via heart catheterization, crudely via stress testing, and increasingly popular CT coronary angiography. None of these methods have been subjected to studies comparing testing vs. not testing in a large population, followed by some program of prevention to assess differences in mortality, heart attack, and other events.

Why should heart scan be held to such a standard?

Dr. Scott Grundy, lipid guru and one of the experts who sat on the Adult Treatment Panel-II for lipid management guidelines, recently stated [emphasis added]:

"Imaging has at least 3 virtues. It individualizes risk assessment beyond use of age, which is a less reliable surrogate for atherosclerosis burden; it provides an integrated assessment of the lifetime exposure to risk factors; and it identifies individuals who are susceptible to developing atherosclerosis beyond established risk factors. Also of importance, in the absence of detectable atherosclerosis, short-term risk appears to be very low."

Well said, and from a vocal statinator, to boot.

Sadly, Dr. Grundy goes on to say how plaque imaging can serve to better determine who will benefit from statin drug use.

Of course, you and I know that there is far more to reduction of cardiovascular risk applied to a framework of serial plaque quantification ("tracking plaque"!) than statin drugs. I doubt that a man as intelligent as Dr. Grundy truly believes this. I suspect that he is simply stating what he knows what will be published without resistance in the standard medical literature, trying to achieve a modest incremental success just by raising consciousness about heart scanning and plaque imaging: first things first.

Maybe next will be a plaque-tracking, or even a plaque-reducing, mainstream conversation, just like the one we've been conducting for the past four years.

Joe was a Track Your Plaque Success Story. With a starting heart scan score of 278, he dropped it 12 months later to 264, a 5% reduction. Though not a huge reduction, Joe's risk for a heart attack or other coronary event was virtually zero. I was very proud of Joe.

Among the culprit lipoprotein patterns that caused Joe's plaque was lipoprotein(a), or Lp(a). Niacin was therefore crucial to his program. It was among the principal reasons he dropped his heart scan score and reduced his risk for heart attack so dramatically.

Since he retired, Joe has been freewheeling around the country, traveling and having a great time. He consequently stopped thinking about his heart disease and Lp(a). He also tired of the occasional hot flushes he'd experienced with niacin. Though the flushes were promptly aborted by drinking two glasses of water, he simply didn't want to be bothered.

So when Joe saw this interesting and tantalizing "flush-free niacin" on the store shelf, he grabbed it.

Joe came back to the office. His blood pressure was 190/94, so high that he was having occasional chest pains from it (which can happen when something called "left ventricular diastolic dysfunction" develops from hypertension). His lipoprotein patterns were terrible, including a big upward jump in Lp(a) and drop in HDL. So I asked him to have another heart scan right away: Score 371, a 40% increase. In other words, his program went down the toilet.

Why?

Simple: Flush-free niacin. I've said it before (No flush = No effect and No flush niacin kills) and I'll say it again:

Flush-free or No-flush niacin is a complete, unadulterated, completely ineffective SCAM.

Flush-free or no-flush niacin is not a substitute for niacin. Joe is yet another example of how dangerous this scam can be. It turned one of our great success stories into a failure.

Please, please, please do not fall for this misleading and potentially dangerous scam product. While the product itself is not intrinsically dangerous, it denies you the benefits of the real thing: niacin.

Thankfully, the mistake in Joe's program was caught before a heart attack or other catastrophe. He did manage to pass a stress test, though with a flagrantly out-of-control blood pressure response. We'll get him back on track--but with niacin, the real thing.

The Fanatic Cook has posted a stinging criticism of the American Heart Association (AHA):

American Heart Association My Fat Translator

Beyond the nonsensical nutritional recommendations (e.g., substitute small French fries for large French fries), she lists the major financial contributors to the AHA, a Who's Who in the pharmaceutical and processed food industry.

"For an organization that brought in close to a billion dollars last year, you'd think they could come up with something a little more pronounced. If I was more cynical I'd say the AHA had an interest in keeping Americans fat . . . or at least dependent on a highly-processed, fast food diet, requiring drugs to tweak lab values."

To be sure, the AHA does a great deal of good in funding research and educating the public about the prevalence of heart and vascular disease. But their fund raising interests have clearly subverted the honesty of their nutritional advice. Sadly, it is the AHA dietary advice that hospital dietitians use in counseling people with heart disease after their heart attack, stent, or bypass surgery. After my patients are discharged from the hospital for any reason, I tell them to please forget everything the nice hospital dietitian told them. It is not okay to eat the factory farm-raised hamburger on the sugar-equivalent enriched flour bun. Low-fat ice cream is not a healthy substitute for full-fat ice cream.

The AHA is no different than the USDA and the American Diabetes Association, "official" organizations that have, in effect, sold out to industry.

Sleep is a fascinating phenomenon.

Virtually all animals, certainly all mammals, sleep. While the form and shape of sleep can vary, sleeping is a universal phenomenon. Even fish sleep, though their eyes remain open.

Sleep disorders like sleep apnea ("apnea" = without breathing) are growing in prevalence nationwide as the country gets fatter and fatter. Our throats assume a smaller diameter, even our tongues get obese. This results in intermittent obstruction to the airway during sleep, causing snoring. It also results in sleep interruption, particularly during attempts to "descend" down to the deepest phases of sleep. Dire health and cardiac consequences can sometimes emerge, such as high blood pressure, higher blood sugar, abnormal heart rhythms, impaired heart muscle function, even sudden death.

We are all familiar with the perceptible effects of sleep deprivation: edginess, crabbiness, diminished attention span, slowed reaction time. I'm not talking about sleep apnea or sleep disorders, but just simple duration of sleep. Data are emerging that both sleep deprivation and sleep excess may trigger undesirable changes in lipids (cholesterol values):

Associations of usual sleep duration with serum lipid and lipoprotein levels.

Kaneita Y, Uchiyama M et al.

STUDY OBJECTIVES: We examined the individual association between sleep duration and a high serum triglyceride, low HDL cholesterol, or high LDL cholesterol level. DESIGN AND SETTING: The present study analyzed data from the National Health and Nutrition Survey that was conducted in November 2003 by the Japanese Ministry of Health, Labour and Welfare. This survey was conducted on residents in the districts selected randomly from all over Japan. PARTICIPANTS: The subjects included in the statistical analysis were 1,666 men and 2,329 women aged 20 years or older. INTERVENTION: N/A. MEASUREMENTS AND RESULTS: Among women, both short and long sleep durations are associated with a high serum triglyceride level or a low HDL cholesterol level. Compared with women sleeping 6 to 7 h, the relative risk of a high triglyceride level among women sleeping <5 h was 1.51 (95% CI, 0.96-2.35), and among women sleeping > or =8 h was 1.45 (95% CI, 1.00-2.11); the relative risk of a low HDL cholesterol level among women sleeping <5 h was 5.85 (95% CI, 2.29-14.94), and among women sleeping > or =8 h was 4.27 (95% CI, 1.88-9.72). On the other hand, it was observed that the risk of a high LDL cholesterol level was lower among men sleeping > or =8 h. These analyses were adjusted for the following items: age, blood pressure, body mass index, plasma glucose level, smoking habit, alcohol consumption, dietary habits, psychological stress, and taking cholesterol-lowering medications. CONCLUSIONS: Usual sleep duration is closely associated with serum lipid and lipoprotein levels.

Triglycerides go up with too little or too much sleep. Note especially the extraordinary association of low HDL cholesterol with sleeping <5 hours (nearly 6-fold increased risk) or sleeping >8 hours (more than 4-fold increased risk).

Why do these effects develop? Does sleep deprivation, for instance, trigger higher adrenaline levels, encourage carbohydrate cravings or binges, make us less likely to engage in physical activity? Cortisol is elevated; could this be a factor? I know that I am a different person when sleep-deprived: irritable, less clear-thinking, quicker to anger, more critical, and I develop carbohydrate cravings. It's curious that triglycerides increase when sleep excess is present; what might that represent?

Anyway, the data are growing: Sleep is an important facet of health, both for maintaining a bright outlook and to discourage development of low HDL and high triglycerides. Though not specifically examined in this study, we know that low HDL/high triglycerides are, as a rule, associated with the undesirable small LDL particle pattern.

As a practical matter, you may also find sleep and waking from sleep more satisfying and restful if you sleep in increments of 90 minutes, e.g., 7 1/2 hours (rather than 7 or 8 hours). This is because the full cycle of sleep, from phase 1 to REM (rapid-eye movement sleep), requires 90 minutes for completion. That doped feeling that sometimes develops when awaking will disappear if you sleep according to your sleep cycle, which is usually 90 minutes long.

There's no doubt that low thyroid function results in fatigue, weight gain, hair loss, along with rises in LDL cholesterol and other fractions of lipids. It can also result in increasing Lp(a), diabetes, and accelerated heart disease, even heart failure.

But how do we distinguish "normal" thryoid function from "low" thyroid function? This has proven a surprisingly knotty question that has generated a great deal of controversy.

Thyroid stimulating hormone, or TSH, is now the most commonly used index of the adequacy of thyroid gland function, having replaced a number of older measures. TSH is a pituitary gland hormone that goes up when the pituitary senses insufficient thyroid hormone, and a compensatory increase of thyroid hormone is triggered; if the pituitary senses adequate or excessive thyroid hormone, it is triggered to decrease release of TSH. Thus, TSH participates in a so-called "negative feedback loop:" If the thyroid is active, pituitary TSH is suppressed; if thyroid activity is low, pituitary TSH increases.

An active source of debate over the past 10 years has been what a normal TSH level is. In clinical practice, a TSH in the range of 0.4-5.0 mIU/L is considered normal. (Lower TSH is hyperthyroidism, or overactive thyroid; high TSH is hypothyroidism, or underactive thyroid.)

The data from a very fascinating and substantial observation called the HUNT Study, however, is likely to change these commonly-held thyroid "rules."

The association between TSH within the reference range and serum lipid concentrations in a population-based study. The HUNT Study

In this study, over 30,000 Norwegians without known thyroid disease were enrolled. TSH levels and lipid (cholesterol) levels were measured.

In this large and extraordinary observation, increasing TSH levels were associated with increasing levels of LDL cholesterol and triglycerides, and decreasing HDL. At what level of TSH did this relationship start? At TSH levels as low as 1.0!

In other words, there were perturbations in standard lipid measures even with TSH levels ordinarily regarded as "normal," even "perfect."

A subsequent observation from the HUNT Study was even more recently published:

Thyrotropin Levels and Risk of Fatal Coronary Heart Disease: The HUNT Study

Abstract:

Background Recent studies suggest that relatively low thyroid function within the clinical reference range is positively associated with risk factors for coronary heart disease (CHD), but the association with CHD mortality is not resolved.

Methods In a Norwegian population-based cohort study, we prospectively studied the association between thyrotropin levels and fatal CHD in 17 311 women and 8002 men without known thyroid or cardiovascular disease or diabetes mellitus at baseline.

Results During median follow-up of 8.3 years, 228 women and 182 men died of CHD. Of these, 192 women and 164 men had thyrotropin levels within the clinical reference range of 0.50 to 3.5 mIU/L. Overall, thyrotropin levels within the reference range were positively associated with CHD mortality (P for trend = .01); the trend was statistically significant in women (P for trend = .005) but not in men. Compared with women in the lower part of the reference range (thyrotropin level, 0.50-1.4 mIU/L), the hazard ratios for coronary death were 1.41 (95% confidence interval [CI], 1.02-1.96) and 1.69 (95% CI, 1.14-2.52) for women in the intermediate (thyrotropin level, 1.5-2.4 mIU/L) and higher (thyrotropin level, 2.5-3.5 mIU/L) categories, respectively.

Conclusions Thyrotropin levels within the reference range were positively and linearly associated with CHD mortality in women. The results indicate that relatively low but clinically normal thyroid function may increase the risk of fatal CHD.

In other words, the findings of this substantial observation suggest that the ranges of TSH usually regarded as normal contribute to coronary events, cardiac death, as well as lipid patterns. While several other studies have likewise shown a relationship of higher TSH/lower thyroid function with lipid abnormalities and overt heart disease, no previous study has plumbed the depth of TSH to this low level and to such a large scale.

I believe that these findings are enough cause to begin thinking seriously about monitoring thyroid function more seriously to uncover "borderline" TSH increases in the "normal" range. While higher TSH levels predict cardiovascular events, does thyroid replacement at these levels reduce it? Critics will say it's a big leap, but I think that it is worth at least considering.

Stay tuned for a lengthy Special Report followed by a full booklet on these issues on the www.cureality.com website.

Copyright 2008 Wiliam Davis, MD

Tne Philadelphia NBC affiliate's website carried this commentary from a colleague of mine:

Mark from the Lehigh Valley is curious about scans that can detect heart disease.

He asked, "I am in my early 50s. My father had a heart attack in his 40s. I am healthy with no symptoms of heart disease, should I consider a heart scan?"

"Well, Mark, occasionally family history needs to be considered more closely. If your father had coronary disease at a relatively young age at the absence of any known risk factor for heart disease for example diabetes, smoking, obesity, high blood pressure, than your level of risk should be considered more closely," Dr. Kevin Shinal, a cardiologist, said.

"There are a number of studies available to access [sic] your level of risk. One such study is a calcium score. A calcium score is a form of a CAT scan that access [sic] the calcium burden or presence of calcium in your coronary arteries. It assigns you a score and score is translated into a level of cardiovascular risk," Shinal said.

But the doctor warned because Mark doesn't have active symptoms, the scan probably wouldn't be covered by insurance.

Was there an understandable answer in there? I certainly couldn't find it.

Why pick on some yokel responding inarticulately to the local media's quest for content? Because this is, all too often, what the public hears: Ill-informed blather from someone who has little or no understanding of the issues. Maybe this doctor wanted his practice group to get some free publicity. "Doctor, could you just answer a few questions from viewers?"

Unfortunately, it's not just local media who are guilty of consulting with know-nothings with only passing knowledge of an issue. National media are guilty of it, too. The need to fill airtime with content is better filled with talking heads who present a compelling story, whether or not it is accurate or insightful, rather than an expert with deep insight into a topic who might not present as pretty a story. I've seen this countless times. A good portion of my day, in fact, is occupied responding to patient questions based on the misinformation presented in some media report.

My message of this brief rant: Be very careful of the messages delivered by the media, even if provided by some supposed "expert." In fact, I regard "experts" in health about as believable as politicians. Sure, sometimes they provide accurate information. But they often do not, or provide information with limited understanding. Or, worse, information intended to serve some hidden agenda.

Were the media to ask me to respond to the question, however, I would say:

"Yes, you should absolutely have a heart scan--yesterday! With your family history, there is no other way to accurately, easily, and inexpensively quantify the amount of coronary atherosclerosis in your heart's arteries. A stress test only uncovers advanced disease. A heart catheterization is overkill and absolutely not indicated in an asymptomatic man. Judging the presence of heart disease from cholesterol values is folly.

"What's left? A CT heart scan. So, yes, you need a CT heart scan ASAP with no doubt whatsoever."

But they didn't ask.

Although Dr. John Cannell's most recent Vitamin D Newsletter concerns the connection between autism and vitamin D, and has nothing to do with coronary plaque reversal, this fascinating discussion between a mother of an autistic boy and Dr. Cannell is so enlightening that I thought that it was still worth passing on.

I also feel very deeply for parents with autistic children, who I see struggle with the developmental difficulties their children encounter. (I even have several patients who are parents of 2 or 3 autistic children.)

As always, Dr. Cannell is at the cutting-edge of converting hard scientific information into practical use. You will note several points or questions raised:

1) Dr. Cannell advocates a powdered capsule form of vitamin D. In my experience, most powdered or tablet forms do not work. But some do. He apparently has success with the brand he specifies.

2) Are there vitamin D-receptor (VDR) genotypes that respond differently? Should there be different 25 (OH) vitamin D blood level targets for different VDR genotypes? Nobody knows yet, but it will be an important question to explore in the future.

3) Is heavy metal toxicity, at least in its milder forms, a surrogate for vitamin D deficiency? (Are chelationists unwittingly treating vitamin D deficiency?)

4) If this is a genuine association, and vitamin D replenishment exerts profound neurologic effects in autistic children, does a similar, though less marked effect, hold in non-autistic children? Will children perform better, learn more effectively, etc. with vitamin D supplementation to normal levels?

5) Vitamin A--Is vitamin A with vitamin D good or bad? This one I do not have an answer to. Reading the literature Dr. Cannell cites didn't help much. (Dr. BG--Any comments? Dr. BG is a vitamin A advocate.)

Perhaps, should the association between autism and vitamin D hold, it raises more questions than it settles. But, true to my experience with vitamin D, every day I stumble on some unique, fascinating effect, all beneficial. We continue to learn new lessons about vitamin D and Dr. Cannell's insights as a practicing psychiatrist deeply concerned with vitamin D issues have helped enormously.

(Sorry, but I did not copy the links to the literature Dr. Cannell cites. To obtain the links, go to the original Vitamin D Newsletter.)

The Vitamin D Newsletter
June 2008

This month we feature a remarkable series of letters from a mother of an autistic son who treated her child with vitamin D. It is the first case report in the medical literature suggesting vitamin D has a treatment effect in autism.

First, a brief case report and then a more detailed exchange of emails between the mother and me.

Case Report:

John is a seven-year old boy living in the northeastern U.S. with a long-standing diagnosis of autism. Symptoms include temper tantrums, repetitive self-stimulatory behavior, impaired language, mood swings, fear of being alone, toileting problems, dysbacteriosis, and impaired muscle strength. John spends a lot of time outdoors starting in the spring and his mother noticed a distinct seasonal variation in his symptoms in that he improved in the summer and regressed in the winter. A 25-hydroxy-vitamin D in April of 2008 was 25 ng/ml and obtained after John had begun to play outside. Due to the seasonality of John's symptoms the mother consulted me. I advised the mother to stop all products containing vitamin A including cod liver oil and begin John on 5,000 IU of vitamin D3 per day for two weeks followed by 2,000 IU per day in the form of powdered vitamin D dissolved in juice. Within a week of starting the vitamin D, John's language began to return and he was no longer as fearful of being alone. At the end of two weeks his language showed further improvement, he began to toilet himself, counted to 10 and knew the spelling of his name. After three weeks language continued to improve and some improvements were noted in his dysbacteriosis. After four weeks of vitamin D treatment, the mother noted improvements in muscle strength as well as continued improvements in language. A repeat 25-hydroxy-vitamin D is pending while John continues taking 2,000 IU of vitamin D per day.

Before you read the series of emails between the mother and me, I'd like to caution that this is only a case report of sorts and does not prove a treatment effect. Spontaneous remissions, while rare in autism, have been reported, thus the supplemental vitamin D may have had nothing to do with his improvement. If the response is due to vitamin D, there is no assurance it will prove lasting. I think it unlikely that older autistic children or individuals with severe autism will show these sorts of apparent improvements. Furthermore, autism is a multifactorial disease with strong genetic roots and it is highly unlikely that treatment of vitamin D deficiency in all autistic children will result in similar improvements. Finally, I did not examine this child, and I am relying on the child's mother to report both his condition and his apparent response to vitamin D treatment. However, the mother agreed to speak with the press about her son and allow for independent confirmation of the apparent treatment response.

Below are the emails, edited for brevity, clarity, and confidentiality.

Dear Dr. Cannell:

I am writing because I believe my son John is strongly affected by vitamin D and I need some advice. John is seven and autistic and weighs 50 pounds. We live in the northeastern part of the United States . He starts spending lots of time outside in May and continues until September. Every year, like clockwork, he has the same patterns of behavior and ability. After about six weeks of sun exposure, every July, he begins feeling much better, seems to be comfortable in his skin, does not have as much self-stimulatory behavior, can eat a variety of foods and has language. This past summer, he was using 14-word sentences. By the end of November, he can't even ask you for a cup of juice. He becomes more exclusive, has emotional highs and lows, has tantrums and is easily frustrated.

His 25(OH)D level on April 15th was 25 ng/ml but he had already been going out in the sun so his level must have been lower in the winter. I have had his genetics tested (Nutrigenomic) and he has mutations in his vitamin D receptors:

VDR Bsm/Taq ++
VDR Fok --
VDR Taq ++

My first question, does it sound like the changes in his behaviors and abilities could be caused by lack of vitamin D? Could you elaborate on the time it would take to get adequate amounts of vitamin D to start seeing positive results? For example, even if he starts going out in the sun in May, it's usually not until July that I see positive changes. Then would it take a month or two to go back to being deficient, thus explaining his 'regression' by the time November comes around. Secondly, I am looking at different forms of vitamin D therapy: a vitamin D lamp, vitamin D3 cream, or oral vitamin D. Can you tell me what might be the best form during the winter months?

Thank you very much for your time and attention.

Jane, Boston MA

Dear Jane:

Yes, it is possible your son's autism is related to vitamin D. Such seasonality has been reported before in autism, both in an individual and in autistic children at a summer camp. Although suggestive, such seasonality does not prove a vitamin D connection. Sun exposure, unless it is full body, takes several months to get vitamin D levels up. If sunblock or clothes are worn sun exposure will not get 25(OH)D levels much above 30 ng/ml. As far as the "mutations" you list, they are actually vitamin D receptor (VDR) polymorphisms and not referred to as mutations although all such changes occurred through mutations at some time in the past. VDR polymorphisms are simply the different structures of the vitamin D receptor that different people have and they are widely distributed. A pilot study of actual VDR receptor mutations did not detect VDR mutations in 24 autistic individuals but they did not assess for VDR polymorphisms. However, a highly significant association exists between one VDR polymorphism and larger head size. Mean head circumference is larger in autism.

Yan J, et al. Vitamin D receptor variants in 192 patients with schizophrenia and other psychiatric diseases. Neurosci Lett 2005;380(1-2):37-41.

Handoko HY, et al. Polymorphisms in the vitamin D receptor and their associations with risk of schizophrenia and selected anthropometric measures. Am J Hum Biol 2006;18(3):415-7.

Lainhart JE, et al. Head circumference and height in autism: a study by the Collaborative Program of Excellence in Autism. Am J Med Genet A 2006;140(21):2257-74.

Lainhart JE, et al. Macrocephaly in children and adults with autism. J Am Acad Child Adolesc Psychiatry 1997;36(2):282-90.

I emailed the world's foremost expert on VDR polymorphisms asking him about your son's polymorphisms and his reply, quite technical, is below.

Dear John:

I apologize for the delay in getting back to you regarding VDR polymorphisms. Initial studies by Eisman and coworkers many years ago suggested that several of the polymorphs identified above in the VDR gene (Bsm/Tag) correlated strongly with osteoporosis. Despite the hoopla, subsequent analyses by many different investigators did not really confirm these results, i.e. only a very modest (3%) correlation. This spawned multiple studies searching for correlations between VDR polymorph's and cancer, autoimmune disease and so forth. It is fair to say from all of these studies that the correlation is at best weak, and in most cases non-existent. Part of this may be due to the fact that the Bsm and Taq polymorphs are located in VDR gene introns and as a first approximation cannot affect the VDR protein's function. This is not an absolute statement, however, as our work is now showing that regulatory regions that control the VDR's expression are located within introns as well as upstream. Therefore the possibility exists that these polymorphs could affect expression, although we have not found these regions to contain enhancers yet. This is clearly where gene and disease studies are going. The only polymorph that could affect function is the Fok1 site, which we identified many years ago following our initial cloning and structural analysis of the human VDR gene. The presence of this site leads to the expression of a shorter VDR protein (424 aa) that is purported to have a slight increase in transcriptional activity (10%?) vs the large protein (427 aa). The above analysis suggests that this polymorph is absent, leading to production of the larger perhaps less active protein. On a single patient basis, it is really difficult to conclude anything regarding this finding. Indeed, despite large numbers of patients, the VDR polymorph have not really revealed any significant insight. Given the summer correlations, it is probably more likely that the individual is low in vitamin D3 in winter.

Sincerely,

Professor John Doe

Thus, one of your son's polymorphisms may have less functionality but that should be easily overcome by higher vitamin D levels. The first thing to do is stop all vitamin A, multivitamins containing vitamin A, or cod liver oil and start vitamin D. As you will see below, vitamin A antagonizes the action of vitamin D and he should have plenty of vitamin A if he eats colorful vegetables, colorful fruit, eggs and fortified oatmeal. As far as vitamin D, I think the easiest way to give vitamin D is powdered capsules, not a cream. You can open the capsule and put the powder in about anything, such as juice. To buy the capsules, go toBio Tech Pharmacal and buy both a bottle of the 5,000 and the 1,000 IU capsules. He should take one 5,000 IU capsule a day for two weeks then take 2,000 IU per day. After a month, go to the doctor and have another 25-hydroxy-vitamin D blood test. Do not let your doctor order a 1,25-dihydroxy-vitamin D as it will give you and your doctor false information about your son's vitamin D status. The other option is buying a Sperti vitamin D light. Daily use of the light on both sides of his trunk will raise levels fairly quickly but he should still have a 25(OH)D blood test every month to assure his levels rise to the mid level of normal ranges, about 70 ng/ml. Vitamin D is very safe. Your son would have to take more than 10,000 IU a day for more than a year to have any risk of toxicity. If he improves and his level is 50 ng/ml, the next question is would he improve even more if his level was 70 ng/ml? Some lifeguards have levels of 80-100 ng/ml; normal ranges in the labs in the USA are 30 -100 ng/ml (ideal ranges are 50 -100 ng/ml.) If you have any more questions, let me know. I certainly want to know how he is doing.

Sincerely,

John Cannell

Dear Dr. Cannell:

It has been one week on 5,000 IUs of vitamin D3 daily and already we're getting some language back! We haven't had original language since probably around the end of November. The only language we have had in the past five months has been verbal scripting. Today John has already told me "turn off the TV" and "clean up the water". This is all very exciting. Will it last? I will continue to keep you updated on progress and change in behavior. One more thing, all winter long he was afraid to be by himself anywhere. Now he is starting to be able to be in another room or outside by himself.

Thanks so much,

Jane

Dear Jane:

I can't tell you how happy I am for you. I suspect John will continue to improve. Do you have any parent rating scales or does his treating pediatrician have any objective rating scales? If you have before and after rating scales or his treating doctor does then it becomes important to track his progress on an objective measure. Jane, if you are a member of any autism discussion groups, you should post about this, including doses used. If your son's case is typical, then hundreds of thousands of autistic children may be helped with vitamin D.

John Cannell

Dear Dr. Cannell:

It has been two weeks on 5,000 IU per day and I want to inform you that we are having continued success with language. Continued in the sense that it is consistent, it wasn't just a one day fluke. In addition, he is taking himself to the bathroom; this is another thing that goes away in winter months. I usually have to catch him holding it in and then suggest he go, but now he is going completely by himself. In therapy last week, he started drawing again. He drew a bee and then ran around the room buzzing. His toileting is consistent with his therapists, not just mommy. Last night, I asked him to count to 10 for me and he did - quite enthusiastically. Then I said what does J-O-H-N spell? It took him a bit but then he said "John."

Unfortunately, the last scale taken was when he was 3 when he had his first developmental evaluation. But we do track behavior and language on a weekly basis. The forms we fill out give a good indication as to how he is doing.

I belong to a parent forum. It was created by a doctor named Amy Yasko. She's a PhD, a researcher, not a medical doctor. It was through her that I got John's genetics tested. She advocates vitamin D as being very crucial. I will post something on her forum for the parents there. However, if the parents on the forum are following her recommendations, they should be taking it already - 2000 IUs in winter and 1000 IUs in summer is her recommendation. I will post something on the forum to really emphasize how important vitamin D is.

Jane

Dear Jane:

I'm glad the improvements are continuing. I see Dr. Yasko recommends 10,000 IU of vitamin A/day as well as cod liver oil. I strongly disagree. Make sure your son is taking neither vitamin A nor cod liver oil. Rather, make sure he eats colored fruits and vegetables as well as fortified oatmeal. Vitamin A interferes with vitamin D's function, especially at the doses Dr. Yasko recommends.

Vitamin A antagonizes the action of vitamin D. In humans, even the vitamin A in a single serving of liver impairs vitamin D’s rapid intestinal calcium response. Furthermore, the consumption of preformed retinols, even in amounts consumed by many Americans in both multivitamins and cod liver oil appears to be causing low-grade, but widespread, bone toxicity, perhaps through its antagonism of vitamin D. In a recent dietary intake study, Kyungwon et al found high retinol intake completely thwarted vitamin D’s otherwise protective effect on distal colorectal adenoma and they found a clear relationship between vitamin D and vitamin A intakes as the women in the highest quintile of vitamin D intake also ingested almost 10,000 IU of retinols/day. As early as 1933, Hess et al warned about vitamin A consumption, concluding, “as to a requirement of thousands of units of vitamin A daily, the unquestionable answer is that this constitutes therapeutic absurdity, which, happily, will prove to be only a passing fad.”

Rohde CM, Deluca HF. All-trans retinoic acid antagonizes the action of calciferol and its active metabolite, 1,25-dihydroxycholecalciferol, in rats. J Nutr. 2005;135(7):1647-1652.

Johansson S, Melhus H. Vitamin A antagonizes calcium response to vitamin D in man. J Bone Miner Res. 2001;16(10):1899-1905.

Penniston KL, Tanumihardjo SA. The acute and chronic toxic effects of vitamin A. Am J Clin Nutr. 2006;83(2):191-201.

Oh K, Willett WC, Wu K, Fuchs CS, Giovannucci EL. Calcium and vitamin D intakes in relation to risk of distal colorectal adenoma in women. Am J Epidemiol. 2007;165(10):1178-1186.

Hess AF, Lewis JM, Barenberg LH. Does our dietary require vitamin A supplement? JAMA. 1933;101:657-663.

Unfortunately, Hess’s prophecy of a passing fad proved premature and many Americans continue to consume “absurd” and dangerous quantities of vitamin A. For example, multivitamins, until recently, had small amounts of vitamin D (200 to 400 IU) but high amounts of preformed retinols (5,000 to 10,000 IU). This pales in comparison to a tablespoon of modern cod liver oil, which contains sub-physiological amounts of vitamin D (400 to 1200 IU) but supra-physiological amounts of completely preformed retinols (5,000 to 15,000 IU or in some cases 30,000 IU).

John Cannell

Dear Dr. Cannell:

It has been three weeks and he went from 5,000 IU of vitamin D per day to 2,000 IU per day a week ago. His language is increasing. He's now back to saying the things he wants with some prompting. He also has gut dysbiosis and I'm sure the D is helping with microbes in his gut. He has a lot of problems with his immune system and bacteria and viruses. Also, doesn't vitamin D aid in the production of glutathione? I feel that could be a big part of his increased language.

Jane

Dear Jane:

Yes, abnormal immune responses are associated with both autism and vitamin D deficiency. For example, autistic individuals have immune abnormalities that show a striking similarity to the immune functions affected by vitamin D. Animal evidence indicates some vitamin D deficiency induced brain damage may be malleable, that is, vitamin D may partially reverse the brain damage, if given early enough. These studies offer hope that sunlight or oral vitamin D, especially in young autistic children, may have a treatment effect.

Ashwood P, et al. The immune response in autism: a new frontier for autism research. J Leukoc Biol 2006;80(1):1-15.

Cantorna MT, et al. Vitamin D status, 1,25-dihydroxyvitamin D3, and the immune system. Am J Clin Nutr 2004;80(6 Suppl):1717S-20S.

Burne TH, et al. Combined prenatal and chronic postnatal vitamin D deficiency in rats impairs prepulse inhibition of acoustic startle. Physiol Behav 2004;81(4):651-5.

Both the brain and the blood of autistic individuals show evidence of ongoing chronic inflammation and oxidative stress. That is, the disease process is probably increasingly destructive. Further hope for a treatment effect rests in activated vitamin D's powerful anti-inflammatory properties. Its administration reduces production of inflammatory cytokines in the brain, which have consistently been associated with cognitive impairment. Furthermore, activated vitamin D is remarkably neuroprotective by stimulating neurotropin release, reducing toxic cellular calcium levels in the brain, inhibiting the production of nitrous oxide, and by its immunomodulating properties, especially in reducing inflammatory cytokines and by increasing brain glutathione.

Moore ME, Piazza A, McCartney Y, Lynch MA. Evidence that vitamin D3 reverses age-related inflammatory changes in the rat hippocampus. Biochem Soc Trans 2005;33(Pt 4):573-7.

Cohen-Lahav M, Shany S, Tobvin D, Chaimovitz C, Douvdevani A. Vitamin D decreases NFkappaB activity by increasing IkappaBalpha levels. Nephrol Dial Transplant 2006;21(4):889-97

Kalueff AV, Eremin KO, Tuohimaa P. Mechanisms of neuroprotective action of vitamin d(3). Biochemistry (Mosc) 2004;69(7):738-41.

This last function of vitamin D, increasing cellular levels of glutathione, may explain the purported link between heavy metals, oxidative stress, and autism. For example, activated vitamin D reduces iron-induced and zinc-induced oxidative injuries in rat brain. The primary route for the neurotoxicity of most heavy metals is through depletion of glutathione and subsequent generation of reactive oxygen and nitrogen species. Besides its function as a master antioxidant, glutathione acts as a chelating (binding) agent to remove heavy metals. Several studies indicate autistic individuals have difficulty excreting heavy metals, especially mercury. If vitamin D deficient brains are unable to utilize glutathione properly, and thus unable to remove heavy metals, they may be oxidatively damaged by heavy metal loads normal children easily excrete. The amount of activated vitamin D in the brain directly depends on how much vitamin D is made in the skin or put in the mouth.

Garcion E, Wion-Barbot N, Montero-Menei CN, Berger F, Wion D. New clues about vitamin D functions in the nervous system. Trends Endocrinol Metab 2002;13(3):100-5.

Chen KB, Lin AM, Chiu TH. Systemic vitamin D3 attenuated oxidative injuries in the locus coeruleus of rat brain. Ann N Y Acad Sci 2003;993:313-24.

Lin AM, Chen KB, Chao PL. Antioxidative effect of vitamin D3 on zinc-induced oxidative stress in CNS. Ann N Y Acad Sci 2005;1053:319-29.

Valko M, Morris H, Cronin MT. Metals, toxicity and oxidative stress. Curr Med Chem 2005;12(10):1161-208

Kern JK, Jones AM. Evidence of toxicity, oxidative stress, and neuronal insult in autism. J Toxicol Environ Health B Crit Rev 2006;9(6):485-99.

Sincerely,

John Cannell

Dear Dr. Cannell:

It has been a month now and John's Improvements are continuing. In the last week, he has been using his muscles more, he goes on the swing outside and lifts his legs and bends in ways that take core muscle strength. This is yet another skill or interest that left and is returning. I will report more next week.
Jane

Conclusion:

It is too early to say vitamin D has a treatment effect in autism. However, a simple risk/benefit analysis suggests that autistic children should be diagnosed and aggressively treated for vitamin D deficiency. If readers want to learn more about vitamin D and autism, they can obtain the entire paper on the link below. Unfortunately, Elsevier charges $31.50 to download it. You can read a similar document for free on the website, where we first published the theory a year ago.

Cannell JJ. Autism and vitamin D. Med Hypotheses. 2008;70(4):750-9.

http://vitamindcouncil.org/newsletter/2007-may.shtml

In summation, autistic children should be given enough vitamin D to get their 25(OH)D levels up to the mid to high range of normals, that is, 70 ng/ml (175 nmol/L in countries that use the metric system). In the absence of sun exposure, this usually requires long-term administration of about 1,000 IU/day per 20 pounds of body weight with a loading dose of 2,000 IU of vitamin D/day for every 20 pounds of body weight for the first two weeks. As individual variation in response is very high, they should have 25(OH)D blood tests every month until their level has stabilized around 70 ng/ml. They should stop all products containing preformed retinols (vitamin A), especially cod liver oil.

John Cannell, MD
The Vitamin D Council

This is a periodic newsletter from the Vitamin D Council, a non-profit trying to end the epidemic of vitamin D deficiency. If you don't want to get the newsletter, please hit reply and let us know. As we are a 501(3)(c) non-profit corporation, dedicated to ending vitamin D deficiency and not making money, the Vitamin D Council does not copyright this newsletter. Please reproduce it and post it on Internet sites. If this newsletter proves useful to a child you know with autism, the Vitamin D Council asks for a donation as we have not been able to secure a grant and our bank account balance is again below $5,000. Send your tax-deductible contributions to:

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

Rather than the headline New Study Could Change Heart Disease Diagnosis And Treatment being run in Utah TV and newspapers, instead it should read:

Make big money fast with CT scans!

Is your bottom line shrinking? Have you fallen on hard economic times? Is competition from other hospitals and providers threatening your financial health?

Then we have a solution: Do a CT coronary angiogram on everybody! Look for disease in people with no symptoms, scare the heck out of them, and voila! Instant need for bypass surgery!

Ka-ching!! That'll be $100,000, please.

Do it again, and again, and again, and your hospital will be quickly in the black in no time!

And, for the savvy marketer, tell the newspapers that you're going to conduct a study to see if this approach works--even before the study gets started! Even if the study pans, you'll come out a winner because you did it in the name of "research"!

Apparently a group of cardiologists at the Intermountain Medical Center and LDS Hospital in Salt Lake City, with the financial assistance of Siemens, a manufacturer of CT scanners, is funding a 1000-patient study of diabetics, all without symptoms of heart disease, half of whom will undergo "screening" CT coronary angiograms (not heart scans) followed by bypass surgery, if "needed". The other half will receive conventional, "aggressive" medical therapy. "Aggressive" means cholesterol treatment, blood pressure control, and blood sugar control (no kidding).

The outcomes of the two groups will be compared after two years.

To understand the absurdity of this study, note that they are proposing what amounts to "prophylactic" bypass surgery, since the participants are without symptoms. Since there are no stress tests, a measurement of flow or functional capacity (exercise tolerance) cannot be factored in. Decisions will be made on the basis of severity of "blockages" in asymptomatic people, a hazardous notion that has never been shown to provide benefit. No doubt: Some diabetics with extensive disease may obtain benefit from screening, but many more will undergo what amounts to unnecessary bypass that provides no benefit. We already know from studies dating back over 20 years to the days of the original CASS (Coronary Artery Surgery Study) that putting asymptomatic people through bypass surgery willy-nilly does not reduce mortality.

Of course, the "aggressive" preventive treatment they propose is more like the least common denominator level of treatment. In fact, I would characterize the "aggressive" preventive treatment as ridiculous. Doing less would be malpractice. Much more could be done, but doing a lot more would pose a real challenge to the bypass arm of the trial.

But the smell of money drives such efforts: More CT angiograms, more hospitalization for bypass surgery. The payoff to the hospitals from this effort is likely to exceed $5 to $10 million, all money that they might not have otherwise seen. The ill-informed people in the local media gush with enthusiasm, the hospital acts like they are at the cutting edge of medical technology, the doctors pose as saviors.

All this time, real preventive efforts go unmentioned. No fish oil (28% reduction in heart attack, 45% reduction in sudden death from heart attack), no genuine diet efforts (i.e., not the diabetes-promoting American Diabetes Association diet), no effort to identify sources of coronary risk beyond LDL cholesterol (low HDL,small LDL,and postprandial or after-eating abnormalities, for instance, are prominent sources of risk in diabetics), no vitamin D. In my view, the preventive arm of the study amounts to doing virtually nothing beyond prescribing statin drugs.

Don't fall for it.

The Fountain of Youth, Louis Cranach the Younger (1546)

In the Track Your Plaque program, we sometimes use the adrenal hormone, DHEA. It is a fascinating and--surprisingly--an over-the-counter hormone that can be useful and safe when used properly.

DHEA can be useful for:

--Reduction of Lp(a)--Though more effective in females, it can also be useful in males. In the women, DHEA often reduces Lp(a) 15-18%, somewhat less in males. The lower the starting DHEA, the greater the Lp(a) reduction.

--Improved libido--in both men and women. The effect is modest. It's magnified when used with other strategies. Although this is not specifically a goal in the program, it sure helps to get side-benefits like this, rather than unwanted side-effects.

--Increased energy and mood--The boost in mood is, for many, the most perceptible effect: More ambition, more stamina, greater staying power in work and exercise.

--Reduction in abdominal (visceral) fat--A modest effect, but one that, over a long period of use (>6 months) can yield improved insulin responses.

Most commonly, I will suggest DHEA supplementation when blood levels allow. Some people, however, Google "DHEA" and come back horrified that I would suggest such a dangerous supplement.

"I read that it makes women grow mustaches and makes their voices deeper!"

And it does--if you take a lot.

10-15 years ago, when the benefits of DHEA became apparent, some people wanted to believe that DHEA was the fountain of youth. People interested in the anti-aging potential for DHEA figured that, if 50 mg per day made you feel energized and vigorous, what would be the effect of 1000 mg, 2000 mg, or 3000 mg per day? A number of clinical trials were conducted using these doses and, interestingly, depression can lift, men and women increase muscle mass, there is a slight increase in bone density, even pain symptoms from rheumatoid arthritis and lupus may improve. But . . . women grow mustaches, become sexually aggressive, and develop deep voices. Men can become hyperaggressive or overly emotional.

No wonder: Any hormone taken in extraordinary, supraphysiologic doses will exert wacky effects. Imagine taking testosterone or estrogen at 50 times the usual dose.

The doses we use for the above benefits, including Lp(a) reduction, range from 25-100 mg per day; most people do fine with 50 mg. We also adjust doses to starting blood levels. In this dose range, I have never seen any of the above side-effects.

The only side-effects I see at these doses are 1) excessive assertiveness or crabbiness, and 2) insomnia if taken at bedtime.

In my experience, DHEA is a benign hormone, provided it is taken in limited doses and not abused. An occasional female younger than 55 years old will be able to tolerate only 10-20 mg per day before developing the edgy side-effects, but I've never witnessed masculinizing side-effects at these low doses, nor have I ever seen excessive increases in testosterone in men or women. (Women can raise testosterone levels slightly, but almost never enough to exert much effect beyond modestly increased libido.)

Copyright 2008 William Davis, MD

Here is detailed comment from a reader who figured out the wheat (and dairy) issue on her own with impressive results.

Though it seems an unpardonable over-simplification of diet, this concept of eliminating wheat-based products (along with obvious unhealthy foods like candy and soda) yields unexpectedly large results, as our reader relates.

Hi Dr. Davis,

Several years ago, chronic untreated asthma infections hospitalized me. I thought it was recurring bronchitis as I'd never had asthma in my life. Killed much of the alveoli... took awhile to de-crap the lungs and regrow the alveoli. Got assigned a cardiologist sort-of by accident while in the hospital for that (couple days of constant heated steroid, stress, a pain + situation combined, elevated my heart rate to 298 for a brief time). When I went to see him, he wrote me a prescription for the Eades' PPLP [Protein Power LifePlan] book.

It's taken awhile, since it's required radical gradual changes in most aspects of my overly Type-A life, but I'm now about 140 lbs lighter, and hopefully much more in the future.

Miraculously, after 10 days on a hard meat-eggs-cheese-veggie-berry approach (which I sadly confess was mostly pepperoni & mozz nuked... I was busy! ;-)), all my medical symptoms disappeared too. Acid reflux, acne, brain-fog, rashes, 'severe asthma', allergies, etc. etc. By trial and error I realized I wrongly attributed that to lowcarbing when it was getting off gluten that actually did it for me. Which since I'm lowcarb also means all the crap my celiac boyfriend can eat, I can't. Lowcarb does many great things for me (just dropping all the bloating and increasing the energy level are awesome), but getting off wheat was critical.

I've since found that a single tablespoon of "milk" in the morning, or something with wheat (say a tortilla), will make me ravenous *specifically for milk and wheat* all day. Conversely, I can be eating lowcarb and then eat total junk--but something without gluten--and not have it bother me much at all. But one pumpernickel slice at Outback and I am DOOMED. It doesn't always happen that instant; will-power has some sway; but the odds of my making a 'poor decision that leads to cascade failure and totally abandoning my eating plan' in the next 48 hours is astronomically higher if milk or wheat were involved. Oddly, cheese does not seem to affect me this way.

When I was younger (I'm 42 now) I had to stop drinking milk. If I drank some I wanted more. If I drank more I needed more. If I drank more, that was it: I'd be stumbling to the kitchen in the dark at 3am, drinking out of the carton, falling gasping against the refrigerator after several long gulps, like a heroin addict who just got a fix. I finally realized that since I'd lived on a ton of milk my whole life, maybe this was a milk problem; so I usually stayed away from it. So then it turned out wheat/gluten were an issue too. Which made me realize how much of my life was filled with not-eating most of the time (very busy, workaholic, but very sedentary), but when I did eat, ingesting amazing amounts of wheat products. I'm astounded that my whole life I mostly ate things I am apparently intolerant to "or something." Sometimes I wonder how much different even my brain would be if it'd been different.

This might contribute to my ending up weighing 500# at one point. The only amazing thing is that I didn't get a disease. (Well I did--obesity--but I mean any others.) I'm from a family of people who are mostly fat, mostly alcoholic, and mostly dead of cancer. I'm just fat, worse than the others but otherwise seemingly ok. Now I'm starting to think that maybe my whole family may have some 'issue' with the primary foods of our culture.

I tell friends that my horrible chronic acid reflux was solved merely by getting off gluten. They nearly all say, "I could never give up bread!" (Isn't it funny, you never hear people say, "Oh man, I could never give up broccoli!") I tried to convince one young friend to try it; her doctor told her eating more protein and fat was unhealthy, and gave her a prescription (this is lifetime--it doesn't cure it, merely treats the symptom) to a drug to help with acid reflux. I said you're kidding me, you think taking a drug the rest of your life is healthier than trading your pasta for a steak?? Go figure.

I still haven't figured out the milk connection (or why I seem ok with cheese for some reason; maybe there is a dosage-difference, or the sugar combined with it has some effect), but I think it's pretty clear that dropping milk and wheat has very radically changed my life for the better. I may actually live, which being a single mom to an awesome 11 year old girl, is a good thing.

Best,
P.

Given the confusion over what constitutes the "ideal" diet, a discussion that has been hotly debated for decades, some people become very angry that we still don't agree on what is truly healthy.

"Why should I even try if the experts don't agree? They say something is bad one day, then say it's okay the next!"

But that's a short-sighted half-truth born of frustration. We have certainly zigzagged in our understanding of diet over the years. The grand national experiment in low-fat eating, for instance, clearly failed to improve our health. In fact, the opposite occurred: The largest epidemic of obesity and diabetes in world history. You could get angry from this failed experiment . . . or you could learn from it, take what lessons we can and improve on it.

Step back for a moment and consider: In what other age could we even have this discussion?

If we lived in a world where you were hungry, your children were hungry, and you didn't know where the day's food was to be found, we would have no need whatsoever for this conversation: You would take whatever you could find, kill, or steal.

Say you woke up this morning and your cabinets and refrigerator were empty. The stores were far away or non-existent. You and your family would have to improvise, to forage or hunt your day's food. It would require hours. You wouldn't fuss about glycemic index, or saturated fat, or whether or not sugar or wheat was present. You would just eat whatever you could get your hands on. When caloric deprivation threatens, we take what is available.

But we live in a world of plenty--of enormous excess--that allows us choices. It is a world that encourages eating more than is required for existence, a world tailored more to indulgence than to simple satiety or sustenance. That's when distinctions among food types and quality make a difference. But it is a dilemma born of riches.

Starvation and caloric deprivation would settle the argument for us very quickly. It doesn't mean that we shouldn't continue to debate the finer points of diet. But don't do it with anger or frustration. Do it GRATEFULLY, recognizing that we are lucky to be able to have such a conversation in the first place.

Image courtesy Food and Agriculture Organization of the United Nations.

I frequently peruse conventional health websites to keep track of their message. One painfully conventional (read "drug company-supported") website that echoes the standard advice on heart disease and heart health is Everyday Health .

Since I subscribe to the newsletters for many conventional sites, I received an e-mail that took me to this Q & A about HDL cholesterol:

Q: I'm 36 years old and my good cholesterol is too low. What can I do?
– Nilsa, Florida

Dr. Lori Mosca of New York-Presbyterian Hospital responds:

A: A woman's HDL goal should be greater than 50 mg/dL (greater than 40 mg/dL in men). You can raise your HDL levels by eating a diet low in saturated fat and trans fat but high in monounsaturated fats. Lose weight if you need to and get at least 30 minutes of moderate-intensity exercise on a minimum of four days per week. If you smoke, quit. Despite positive lifestyle changes, though, some individuals may still be candidates for HDL-raising drug therapy because they are at increased risk for cardiovascular disease. Discuss your options with your health care provider.

Are you satisified with that answer? I certainly am not.

First of all, is this something you've never heard before? "Eat right, exercise, cut your unhealthy fats." Then why do people who follow this sort of conventional advice often still fail? Is the next step always medication?

Here's the part that Dr. Mosca and other conventional, drug-minded "authorities" have left out:

To raise HDL powerfully--not to 40 mg/dl for males or 50 mg/dl for females, but to 60, 70 or 80 mg/dl--think about the following strategies:

--Eliminate wheat and cornstarch products. I have droned on endlessly about this concept, but it is enormously effective. While the weight loss that inevitably follows elimination of these foods adds to the HDL-raising effect, there is also an independent effect, as well.

--Fish oil--The omega-3 fatty acids in fish oil reduce triglycerides. Triglycerides accelerate the destruction of HDL. Remove triglycerides, HDL goes up. (Though krill oil may share, even surpass this effect, we need more data than the single manufacturer-sponsored study.) Of course, this requires real doses, not the namby-pamby doses you often read about.

--Vitamin D--Achieving normal levels of 25(OH) vitamin D raises HDL with power I have never witnessed from any other strategy before, barring weight loss of 30+ lbs. Readers of the Heart Scan Blog know that just taking vitamin D is not enough. Verification with blood levels is an absolute necessity, particularly if raising HDL maximally is among your goals.

--Adding back saturated fat. I say "adding back" since most of us (including myself) went too far down the "saturated fat is bad" path over the past few years. While I do not advocate a carte blanche approach to saturated fat, I believe that adding back eggs (preferably free-range and/or omega-3 rich), lean meats, and hard cheeses is a good idea. The saturated fat in these foods raise HDL 5 or more mg/dl.

--Dark chocolate--Or other cocoa prepartions. What a cool way to raise HDL! Reach for the lowest-sugar, highest cocoa preparations.

--Alcoholic beverages--I am partial to the red wine/flavonoid-rich concept, being a wine drinker. Although all alcoholic beverages raise HDL due to the ethanol content, for benefits beyond alcohol (as well as to avoid wheat-based drinks like beer), I do believe that the bulk of data argue for flavonoid-rich red wines from southern France, Italy, and California.

--Achieve ideal weight--The toughest of all. But eliminating wheat and cornstarch makes it far easier.

Follow the conventional advice of those like Dr. Lori Mosca, and the majority of people will fail. ("It just so happens that I have a prescription drug just for that purpose!")

Buck the conventional advice, adopt strategies that won't be found in the drug ads, nor be provided by the conventionally-thinking, and you can succeed to heights you never thought possible.

Copyright 2008 William Davis, MD

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