All posts by william-davis

Occasionally, someone will be unable to take fish oil due to the large capsule size, excessive fishy belching, or stomach upset. The easiest solution is usually just to try a different brand, e.g., Sam's Club (Makers' Mark brand) enteric-coated.

However, sometimes liquid fish oil preparations may be preferred. Here'a list of products we've used successfully. All cost more than plain old fish oil capsules, but fish oil is so crucial to your heart scan/coronary plaque control efforts, that it really pays to search out alternatives.

Liquid fish oil alternatives to capsules:

Liquid fish oil--e.g., Carlson's liquid fish oil.

Most liquid fish oil comes flavored either lemon or orange.

Frutol--A very clever re-formulation of fish oil that makes it water-soluble and non-oily. The Pharmax company has put their fish oil into a fruit flavored base that tastes pretty good and is not too expensive.

Go to www.pharmaxllx.com for more information. Unfortunately, I do not believe it's available in stores.

Coromega--another non-oily preparation, though available in some health food stores. Coromega comes in little single-serving foil dispensers. It tastes kind of fruity (though I personally like the Frutol better for taste and consistency). It's kind of pricey ($1.40 per day for two packets).

Regardless of what preparation you choose, you can determine the dose needed by adding up the EPA+DHA content. For the basic prevention effect, the starting dose for the Track Your Plaque program, you need a total of 1200 mg per day of EPA+DHA. Higher doses, e.g., 1800-2400 mg per day, may be required for correction of high triglyceres or postprandial (after-eating) abnormalities.

I continue to be dumbfounded that many doctors continue to pooh-pooh or ignore CT heart scans when people get them.

I can't count the number of people I've seen or talked to through the Track Your Plaque program who've been told to ignore their heart scan scores. The most extreme example was a man whose physician told him his heart scan score of nearly 4000 was nothing to worry about!

A real-life story of a retired public defense attorney whose heart scan score of 1200 was ignored, followed two years later by sudden unstable heart symptoms and urgent bypass prompted us to write this fictitious lawsuit. Though it's not real, it could easily become real. To our knowledge, no single act of ignorance about heart scans has yet prompted such a lawsuit, but it's bound to happen given the number of scans being performed every year and the continued stubbornness of many physicians to acknowledge their importance.

Major Malpractice Class Action Lawsuit Looms for Doctors Who Ignore Heart Scan Tests

It's been several years since new medical discoveries have debunked old theories regarding heart disease and heart attack and have verified the efficacy of CT heart scans for detecting both early and advanced heart disease. Doctors who fail to keep apprised of these finding or refuse to change their practice for financial reasons put themselves at risk for becoming defendants in a major malpractice class action lawsuit. The plaintiffs will be a growing class of persons who were debilitated by avoidable heart attacks and heart procedures and the heirs and estates of those who have died.
Milwaukee , WI (PRWEB) November 29, 2005 -- This press release outlines a template for a potential class action lawsuit that may be on the horizon for the medical industry. The class of plaintiffs for this theoretical action remains latent but is growing on a daily basis. However, it requires only one such plaintiff to find an attorney who recognizes the scale and magnitude of the potential damages and move forward on a contingency basis. In real terms, this class could include 80% of those who had a heart attack, underwent a heart procedure, or subsequently died. According to the latest American Heart Association statistics, this number is estimated to be a least 865,000 persons and the entire class could easily be 10 times that number. Using a conservative estimate of $500,000 in damages per class member, the total damages could exceed $400 billion.

The plaintiffs, defendants, third parties, and facts surrounding the following moot complaint represent an actual incident. The names, specific health information, and dates have been changed to protect potential litigants.

Plaintiff, through his attorneys, brings this action on behalf of himself and all others similarly situated, and on personal knowledge as to himself and his activities, and on information and belief as to all other matters, based on investigation conducted by counsel, hereby alleges as follows:

NATURE OF THE ACTION

1.Plaintiff brings this class action on behalf of himself and all other persons who suffered physical damages or mental distress as a result of receiving a medical diagnosis indicating they had no identifiable heart disease, elevated risk for heat attack, or who were prescribed medications not suited to treat their heart disease once detected.

2.Substantial and irrefutable medical evidence has established that cardiac stress testing is an ineffective method for detecting heart disease of the type that is the root cause in over 90% of all heart attacks and other complications of heart disease that result in death or debilitating injury. A readily available and well-publicized test known as “CT heart scanning” is capable of detecting virtually all heart disease of this nature. It has also been established that simple cholesterol testing often fails to detect persons like likely to develop serious heart disease and prevents them from receiving common treatments capable of reducing or eliminating the source of their undetected heart disease. Readily available blood testing techniques exist that are capable of detecting non-cholesterol related sources of heart disease.

3.The medical community has made significant investments in outdated methods of detecting and treating heart disease. They rely on the revenue streams generated by providing these treatments to persons whose heart disease has progressed to the stage that intervention is required to prevent death or debilitation. Any change in diagnostic or treatment methods resulting in the prevention of heart disease would require substantial investments in new technologies and would severely reduce the market for current treatments. Plaintiffs believe this is a motivating factor in the neglect and willful suppression of readily available technology capable of detecting and preventing heart disease and represents gross medical malpractice.

SUBSTANTIVE ALLEGATIONS

On January 23, 1999, Plaintiff underwent a CT Heart Scan which was interpreted by a cardiologist at the ABC Scan Center . Plaintiff received a report from the Scan Center cardiologist indicating that his “calcium score” placed him in the top 1% for heart attack risk among men in his age group. The report also included the comment “Patient has a high risk of having at least one major stenosis (50% or greater blockage) in his Left Anterior Descending (LAD) artery and is urged to consult with a physician regarding this finding.”

On March 3, 1999 Plaintiff presented Defendant with the results of the January 23, 1999 CT Heart Scan. Defendant told Plaintiff to disregard the CT Heart Scan Results and ordered a physical including a stress test and cholesterol blood test.

On April 1, 2005, Plaintiff had a heart attack and a subsequent coronary angiography that confirmed multiple obstructive coronary plaques in his LAD. Plaintiff received an emergency balloon angioplasty to relieve his acute condition. Substantial damage to plaintiff's heart was incurred before emergency angioplasty could be instituted.

On April 3, 2005, per Defendant's recommendation, Plaintiff underwent open heart surgery to insert three bypasses in his LAD to resolve substantial obstructive heart disease, the same artery identified as having likely obstructive heart disease over 5 years earlier via CT heart scan.

On July 7, 2005, Plaintiff independently obtained additional blood testing not ordered by Plaintiff and was found to have several additional blood abnormalities not discovered by Defendant that are known to contribute to the development of heart disease and were readily treatable using lifestyle changes, nutritional supplements, and prescription drugs.

As early as September, 1996, the American Heart Association (AHA) issued a “Scientific Statement” to health professionals acknowledging the strong link between heart attacks and high calcium scores in asymptomatic patients. Extensive studies and references have confirmed the ineffectiveness of stress testing to reveal early heart disease in asymptomatic patients.

Plaintiff alleges that Defendant failed to utilize readily available medical tests and protocols to identify, aggressively treat, and potentially delay, halt, or reverse advanced heart disease that later resulted in extensive physical and emotional trauma to the Defendant.

PRAYER FOR RELIEF

WHEREFORE, Plaintiff herein demands judgment:

A. Declaring this action to be a proper class action maintainable pursuant to Rule 23 of the Federal Rules of Civil Procedure and declaring Plaintiff to be a proper Class representative;

B. Awarding damages against each defendant, joint and severally, and in favor of Plaintiff and all other members of the Class, in an amount determined to have been sustained by them, awarding money damages as appropriate, plus pre-judgment interest;

C. Awarding Plaintiff and the Class the costs and other disbursements of this suit, including without limitation, reasonable fees for attorneys, accountants, experts; and

JURY DEMAND

Plaintiff hereby demands a trial by jury.

Father Bob, despite his calling as a priest and counselor, led a stressful life. His average day was packed tightly with commitments: counseling members of his congregation, visiting the hospital, more official priest and church duties.

At age 53, his heart scan score of 799 came as a complete surprise. Even more of a surprise, his stress test was dramatically abnormal showing poor flow in the front of his heart at a level of exercise that wouldn't challenge most 75 year olds. His blood pressure with exericse: 230/100. Bob was shocked.

A few stents to the LDL later, Bob was trying to turn a new leaf on lifestyle. His life prior to the diagnosis of heart disease was driven by convenience. Because his day was so filled with commitments, he simply grabbed what he could from hospital cafeterias, fast foods, etc.

But after his procedure, Bob committed to choosing healthier foods, walk every day, and resist the food temptations presented by convenience.

However, temptation defeated him twice in the first few weeks after his stents. On the first occasion, Bob gave into eating a cheeseburger. On the second, Bob was at a fish fry (this is Wisconsin, after all) and ate a large serving of deep-fried fish.

On both occasions, Bob started feeling awful within minutes after eating: foggy, bloated, gassy, and fatigued. He took his blood pressure after each incident: 210/90, even though his blood pressure had more recently been trending down towards 130/80.

What happened? Grotesquely unhealthy foods like the deep-fried fish and cheeseburger provoke an abnormal constrictive process body wide. Some call this "endothelial dysfunction". Regardless, it is a graphic and frightening demonstration of the power of these sorts of unhealthy foods to wreak immediate and dangerous effects. Father Bob's response was more exagerrated than most, but it happens to all of us.

Eat badly and your body will pay the price. Even that occasional hot chocolate sundae or Egg McMuffin will yield cumulative injury, among which will be a rise in your heart scan score.

Jim came to the office at the prompting of his wife.

At age 52, Jim was semi-retired, having to work only a few hours a week to maintain his business. He'd had a high cholesterol identified about 10 years earlier and had been taking one or another statin drug ever since.

However, Jim's wife was a pretty savvy girl and understood the inadequacies of the conventional approach to heart disease prevention. Nonetheless, when Jim came in, he declared, "I feel great. I don't know what I'm doing here!"

I persuaded Jim to undergo a heart scan. His score: 2211, in the 99th percentile (the worst 1% for men in his age group). However, it was worse than that. Any score above 1000 carries a heart attack risk of 25% per year unless prevention issues are fully addressed.

Indeed, Jim proved to have far more than a high LDL cholesterol. Among the patterns uncovered with his lipoprotein analysis were small LDL, the postprandial (after-eating) abnormality of intermediate-density lipoprotein (IDL), and high triglycerides and VLDL. All would require correction if Jim is to hope to gain control of his extensive coronary plaque.

The message: Trying to discern risk for heart disease from cholesterol is complete folly. This man was going to die or have an urgent major heart procedure within the next year or two, all while taking his statin drug.

Discard the silly notion that cholesterol tells you everything you need to know about heart attack risk. It does not. It helps a little but leaves vast voids in risk determination. Fill those gaps with a heart scan, plain and simple.

Kevin came to my office for another opinion.

A husband and father of two teenagers, Kevin had his first heart attack at age 39. Kevin received two stents to his right coronary artery. The entire process took place in a flurry with little explanation over 48 hours, start to finish.

He smoked a pack of cigarettes a day, but the only history of heart disease in his family was his father, who, also a smoker, had his heart disease uncovered in his late 70s.

His internist subsequently prescribed Zocor even though Kevin's LDL cholesterol was a relatively unimpressive 128 mg/dl.

Kevin subsequently asked his cardiologist, "Where did I get the heart disease from?"

"Cigarettes. And genetics. You can quit the first. There's nothing you can do about the second." End of explanation.

This left Kevin frightened and demoralized. If much of the cause of his heart disease couldn't be identified, why bother quitting smoking? Why not enjoy what time he had left?

Kevin was understandably shocked when I told him that genetic causes were 1)identifiable, 2)quantifiable, and 3) correctable.

Kevin's full lipoprotein analysis subsequently showed the most dire combination that commonly accounts for coronary disease in young people: Lp(a) with small LDL particles. This, along with smoking, fully accounted for this young father of two's heart disease.

Along with starting Kevin on a new program for correction of his patterns, I also persuaded him to get a heart scan. What usefulness is a heart scan after the fact? Plenty. Even though Kevin's right coronary was no longer "scorable" because the steel in the stent obscured our measurements, the two remaining unstented arteries would still yield a score. This provides a baseline for future comparison. Even after a stent, Kevin could "track his plaque".

There’s lot of confusion about butter, margarines, and their substitutes. Butter/margarine substitutes that avoid the negative aspects and provide modest health benefits are available, but I find that people confuse what's what. So here’s a brief primer.

Butter--Avoid it. Plain and simple. Butter is a rich source of saturated fat. Of 11.5 grams total fat per tablespoon, 7.3 grams are saturated. It is not better than margarine, contrary to simple-minded reports from some media sources. Butter raises LDL cholesterol, raises blood pressure, and has been related to various cancers.

Margarine--Not better than butter, arguably worse. Some argue that the trans-fatty acids, or hydrogenated oils, used to solidify vegetable oils to make margarine solid are worse than butter. In addition to the ill-effects of butter, margarine reduces HDL and raises cancer risk, perhaps even more than saturated fats. Hydrogenation yields a very unnatural structure that modifies cellular behavior of the sort that may promote the appearance of cancer cells. More recently, however, some of the major manufacturers, like Blue Bonnet, have produced soft spread products without hydrogenation. These are reasonable substitutes when used sparingly.

Smart Balance--This is a product made with canola oil, a source of monounsaturates (the best oil source after omega-3s), but manufactured without hydrogenation and therefore has no trans-fats. It does have, in my view, a bit too much saturated fat (1.5 gm per tbsp. in the 37% Light Spread; 2.5 gm per tbsp in the 67% regular spread). This is a reasonable product to use in small quantities.

There is also a Smart Balance Omega PLUS product that contains added flaxseed oil and sterol esters. I do not recommend this product because of the sterol content (see below). I also object to the manufacturers who label their products “rich in omega-3s” when they mean linolenic acid (in flaxseed), which is converted to a trivial quantity of omega-3s. Linolenic acid may pose unique benefits of its own, but it should not be listed as an omega-3 source.

Benecol--This is a butter substitute that contains stanol esters, a substance that reduces total and LDL cholesterol. Two tablespoons a day reduces LDL around 20 mg/dl, more or less depending on your starting cholesterol.

There’s a light and regular spread. The light contains 20 calories less per tablespoon but somewhat less monounsaturates, but the same LDL-reducing stanol esters. The manufacturer does hydrogenate the oils, yielding 0.5 mg trans-fats per tablespoon--a small drawback.

Take Control--Similar to Benecol, but made with sterol esters. Take Control also reduces LDL cholesterol. However, data from several high-quality studies from Finland suggest that sterol esters may, in some people, be absorbed into the blood. This is potentially concerning. There is a rare disease called sitosterolemia that results in coronary disease in teenagers and young adults in their 20s from increased absorption of sterol esters. While you can’t acquire this genetic disease, some people have the capacity to absorb sterol esters from their intestines very efficiently. I find it very disturbing and I suggest that you stay away this product and other sterol-containing products like HeartWise orange juice and Smart Balance Omega PLUS until the issue is clarified and safety assured.

Brummel and Brown--A blend of vegetable oils (soybean and partially hydrogenated soybean) with calories and fats reduced by blending in yogurt. This is an okay product. The hydrogenation yields trans-fats below the FDA required declaration limit of 1.0 mg.

There’s also 1.0 mg each of saturated and monounsaturated fats. The calories are relatively low as a consequence of the added yogurt, only 45 calories per tablespoon. This makes the Brummel and Brown a reasonable choice.

Other products are making their way out to supermarkets. Look for the type of oil used. Canola, olive, and flaxseed are the best. Also look for trans-fats and saturated fat content; both should be low, preferably <1.0 mg per tablespoon, ideally none.

The best choice among the above products in my view is Benecol, though it’s also the most expensive. It will yield substantial drops in LDL cholesterol. All the products in our informal tastings taste a lot like butter, or at least as well as we can remember what butter tasted like! The key with all of these products is use in moderation, since they all provide between 45?80 calories per tablespoon.

In the 1960s, doctors struggled with the concept of cholesterol and its relationship to heart disease. It was becoming clear that higher levels of cholesterol were predictive of heart disease. It was also becoming clear that the low-density fraction of cholesterol, or LDL, was somewhat better than total cholesterol in predicting heart attack.

Cholesterol was easily measurable in the 1960s. LDL was not. So, Dr. Friedewald, a noted lipid researcher at the National Institutes of Health, proposed an easy method to calculate LDL cholesterol from total choleseterol, HDL, and triglycerides:

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

This simple manipulation would put LDL cholesterols into the hands of the practicing physician and the American public. Dr. Friedewald recognized that this calculation only represented an approximation of LDL cholesterol and that it was thrown off, sometimes substantially, by any abnormal rise in triglycerides or reduction in HDL. But it served its purpose at an age when most doctors hadn’t even heard of cholesterol and the public was still sold on whole milk and “farm-fresh” butter, and Chesterfields were the cigarette choice of most doctors.

The world has since changed. Most doctors have heard about cholesterol and, along with the public, have been drowned in drug company marketing for cholesterol-reducing drugs. Most people with some level of common sense and health awareness no longer use butter or whole milk, and no longer believe that the brand of cigarette you choose can be healthy. But we’re still using Dr. Friedewald’s original calculation for LDL cholesterol. When you get an LDL cholesterol from your clinic, doctor, or hospital, >99% of the time it is obtained using Dr. Friedewald’s calculation.

Is it because there’s nothing better available? No, it’s not. There’s two reasons why your neighborhood primary care physician or cardiologist is still using this dinosaur of testing called LDL:

1) The lag in science to practice is 20 years. Accept that most primary care doctors are 20 years behind the times on many issues, LDL cholesterol included.

2) Insurance companies vigorously discourage testing beyond conventional lipids. The array of objections we get from insurance companies is mind-boggling. It would be funny if human life and finances weren’t at stake. These “new” tests are “experimental”, “unproven”, not endorsed by standard guidelines, not approved by some internal committee, or simply “We don’t know what this test is” ?we’ve heard them all.

What are the tests that are superior to Dr. Friendewald’s calculated LDL? There are several, listed here in order of best to worst:

1) LDL particle number--the value generated by NMR lipoprotein testing. This is the gold standard, most reliable test available, and the one I recommend.

2) Apoprotein B--More widely available even from conventional laboratories in hospitals. Not as accurate as NMR LDL particle number, but a pretty good choice. Apo B is the principal protein in LDL, VLDL, and IDL particles, and so it’s a better reflector of risk from all of these lipoprotein fractions, not just LDL.

3) “Direct” LDL--This is LDL that is actually measured. Unfortunately, it ignores the issues of LDL size and has some other pitfalls, but it’s still better than calculated LDL

4) Non-HDL cholesterol--So-called because it incorporates all undesirable cholesterol-containing lipids except good HDL, thus “non-HDL”. This is another calculation, though better than LDL (because it sums up the risk from other apoprotein B-containing lipoproteins). Non-HDL is calculated from Total cholesterol – HDL. It’s therefore available from any standard lipid panel. It’s little used in everyday practice, however, because most people and their physicians find it confusing.

5) Friedewald calculated LDL--You can see that calculated LDL is last on a list of choices. Yet this is the measure that doctors use day in, day out. It’s the measure that drug companies base billions of dollars of revenue and profits on.

It’s an everyday occurrence in my office that calculated LDL is 89 mg/dl, but the real value is somewhere between 160 and 200 mg/dl. That’s a big difference. Imagine your realtor tells you your house’s estimated value is $200,000 and that’s what you sell it for to an eager buyer. After closing, you find out your house was really worth $300,000. You’d be upset. But that’s what you’re often getting with LDL cholesterol?a bum deal.

It’s part of the reason people will say, “My doctor said my cholesterol was fine and that no cause for my heart disease can be found. He said it was genetic.” In reality, they could have sky-high LDL cholesterol revealed by LDL particle number or apoprotein B.

Use LDL cholesterol in a pinch when you’ve got nothing else. It’s also helpful to gauge any treatment effect of diet, functional foods, drugs, etc. But it is a seriously flawed tool to diagnose your initial level of risk.

I saw three people this past week, all of whom set off on an effort to lose substantial quantities of weight. And all seriously needed to.

All three started with at least 70 lbs. excess weight; all showed substantial weight-sensitive lipoprotein patterns like low HDL, small LDL, high triglycerides, VLDL, and pre-diabetic levels of blood sugar. They also all shared high blood pressure.

All three also had high heart scan scores. Kate’s score was just over 1200. Tom, a 58-year old real estate developer, had a score of nearly 600. Susan, the youngest of the three at 52, had a heart scan score of 377¾99th percentile at this age. Losing weight was an absolute requirement for their plaque control program. Because their lipoprotein abnormalities and pre-diabetic patterns were triggered by weight, weight loss would provide powerful correction. Each and every one of them would need to lose much of their excess weight¾at least 50 lbs¾if they hoped to halt the relentless progression of their heart scan scores.

All three of them returned after 6-8 weeks, and all had lost between 17-24 lbs: spectacular results.

There’s no secret to weight loss. Each of them achieved their weight loss in slightly different ways. But they also shared several critical ingredients in their weight-loss efforts:

1) All three dramatically slashed their intake of wheat flour-containing foods and other processed carbohydrates and did so consistently. All also avoided the usual high-fat, high caloric-density foods like butter, margarine, fried foods, greasy foods, nuts roasted in oil, etc. They concentrated on vegetables, salads, raw nuts, lean proteins (inc. turkey, chicken, fish, lean red meats, low-fat cottage cheese and yogurt).

2) They stopped using food as a reward or as a consolation tool.

3) Exercise for one hour a day at least 5 days a week. The exercise in 2 of 3 of these people was just walking. It wasn’t strenuous, it wasn’t expensive. The women both liked walking with friends or their spouse. Tom followed a more common male path of more strenuous work on his treadmill, elliptical, and biking at the fitness club. But they all did it religiously and missed rare sessions.

4) They refrained from any and all alcoholic beverages. Yes, there are some advantages to 1-2 glasses of wine per day, but it stalls weight loss efforts.

5) They didn’t allow themselves any major indiscretions. There were no binges, major pig-outs at weddings, barbecues, or all-you-can-eat buffets. They did allow themselves an occasional “treat” but did so in small portions.

That’s it. But for most people, that’s simply too much. Adhering to an effort to lose dramatic weight requires day-after-day consistency. Nobody can lose the equivalent of 70,000 calories (20 lbs.) just by skipping a meal, a 20-minute walk, skipping the mashed potatoes at dinner.

It can be done. You’ve just got to be consistent about it.

This question came up on our recent online chat session and comes up frequently in phone calls and e-mails.

If lipoprotein testing is the best way to uncover hidden causes of coronary heart disease, but your doctor is unable, unknowledgeable, or unwilling to help you, then what can you do?

There are several options:

1) Get the names of physicians who will obtain and interpret the test for you. Go to the websites for the three labs that actually perform the lipoprotein tests: www.liposcience.com (NMR); www.berkeleyheartlab.com (electropheresis or GGE); www.atherotech.com (VAP or centrifugation). None of them will provide you with the names of actual physicians. They will provide you with the name of a local representative who will know who the doctors in your area who are well-acquainted with their technology. I prefer this route to just having a representative identify a laboratory in your area where the blood sample can be drawn, because you will still need a physician to interpret the results¾this is crucial. The test is of no use to you unless someone interprets it intelligently and understands the range of treatment possibilities available. Don’t be persuaded by your doctor if he/she agrees to have the blood drawn but has never seen the test before. This will be a waste of your time. That’s like hoping the kid next door can fix your car just because he says he fixed his Mom’s car once. Interpretation of lipoproteins takes time, education, and experience.
2) Seek out a lipidologist. Lipidologists are the new breed of physician who has sought out additional training and certification in lipid and lipoprotein disorders. Sometimes they’re listed in the yellow pages, or you can search online in your area.
3) Contact us. I frankly don’t like doing this because I feel that I can only provide limited information through this method. I provide a written discussion of the implications and choices for treatment with the caveat to discuss them with your doctor, since I can’t provide medical advice without a formal medical relationship. We also charge $75 for the interpretation. But it’s a lot better than nothing.
4) Make do with basic testing. Basic lipids along with a lipoprotein(a), C-reactive protein, fibrinogen, and homocysteine would provide a reasonable facsimile of lipoprotein testing. You’ll still lack small LDL and postprandial (after-eating) information, but you can still do reasonably well if you try to achieve the Track Your Plaque targets of 60-60-60.

In 20 years, this will be a lot easier. But for now, you can still obtain reasonably good results choosing one of the above alternatives.

52-year old Jerry came in for a stress test. He displayed the usual apprehension: fidgeting while he sat on the bed, examining his surroundings, asking lots of questions.

“Your doctor asked you have have a stress test?” I asked.

“All the males in my family have had heart attacks by age 56, so my doctor suggested I have a stress test,” Jerry explained.

Jerry went on to tell me that he had exercised vigorously this morning for 45 minutes without symptoms. He had, in fact, gone surfing just several weeks earlier and described how aerobically challenging it was keeping up with the 20 year olds. “But I did it!” he proudly declared.

As he neared the end of his brisk walk on the treadmill, Jerry asked, “What do you think about those heart scans?”

Jerry had asked his primary care physician the same question. His doctor had apparently told him that they were just a gimmick. “We’ll get you a real test.”

Of course, Jerry’s stress test proved entirely normal. The likelihood of an abnormal stress test with his history of vigorous exercise was <2%. I explained to Jerry that not getting heart scan would be a mistake. In fact, a heart scan was the only easily obtainable test that would uncover hidden heart disease. In truth, the stress test was a waste of time—and an unneeded exposure to radiation.

If Jerry’s heart scan score turned out to be zero, great! He was probably spared the genes from the other males in his family, and his risk of heart attack in the next decade was nearly zero.

If his heart scan turned out be 1000, then an urgent scramble to uncover the causes and correct them to create a truly effective prevention program would be crucial for his long term health. Or, perhaps his score lies somewhere in between, but Jerry would then know how far along he stood on his way to heart disease.

Don’t be a victim of the ignorance of your doctor. Despite all the attention heart scans have received, the majority of doctors remain miserably, inexcusably in the dark. I say inexcusable because CT heart scans can uncover the number one killer of Americans, the number one cause of all deaths in any primary care physician’s practices, and it’s laughably easy. How can a physician not advise patients on the value of heart scans?

If given a choice and you’re without symptoms, a heart scan is far and away the superior test.

The sun is getting stronger and the days are getting longer, even here in Wisconsin.

Some people are coming to the office with nice tans obtained by sunning themselves for several hours. Others have come back from winter getaways to Florida, Arizona, or the tropics, also sporting nice, dark tans.

Several people, in fact, were so confident that sunning themselves provided sufficient vitamin D that they reduced their usual dose. Some even stopped their vitamin D altogether.

But, when blood levels of 25(OH) vitamin D were checked, they were virtually all low, sometimes as low as <20 ng/ml. Yet all had nice tans.

Why does this happen? Why would people with dark tans remain deficient in vitamin D?

One big factor is age: Anyone over 40 years old is fooling themselves if they think that a tan ensures raising vitamin D levels to a desirable range. Also, the more you tan, the more melanin skin pigment accumulates, and the more vitamin D activation in the skin is blocked.

Weight is another factor: Heavier people need more vitamin D, sometimes three- or four-fold more than slender people.

Why does aging result in inefficient skin activation of vitamin D? It seems that, once we are beyond our reproductively useful years, this ticking clock of aging gets triggered. The older we get, the less activation of vitamin D occurs in our skin, the less of the youth-maintaining, disease-preventing benefits of vitamin D we obtain with sun exposure.

The message: Don't rely on a tan to gauge the adequacy of vitamin D. Maybe that works when you're 16 years old, but not at age 50 or 60. There's only one way to know your vitamin D status: a blood level of 25(OH) vitamin D.

Copyright 2008 William Davis, MD

I admit it: In years past, I spoke for the drug industry.

In retrospect, I now regret it. In fact, I'm downright embarassed by it.

In the 1960s, you’d purchase a new car. If you changed the oil, adhered to the maintenance schedule—and were lucky—you might expect to get 100,000 miles out of your automobile. Only an occasional car made it beyond that odometer hurdle. Even if the engine made it past the 100,000 mile milestone, the automobile body would inevitably start to develop rusting decay at the edges of the fenders, signaling body rot that threatened to open gaping holes of metal.

Then along came Toyota and Honda, whose cars easily reached 100,000 miles and well beyond, reliably and with bodies intact. As this realization sunk into the American consciousness, many asked, “Why can’t American automakers accomplish the same sort of trouble-free longevity?” “Buy American” emerged as a mantra to preserve American jobs and prop up an economy vulnerable to the superior automotive products from Detroit’s competitors.

Of course, American automakers have since responded to the challenge posed by the Japanese auto industry and produced automobiles that essentially matched the reliability and longevity of Japanese cars. But, the great unanswered question remains: For years before the onslaught of Japanese competition, did Detroit quietly plot to maintain a policy of planned obsolescence that ensured Americans would have to scrap the old and buy a new car every few years whenever the odometer tipped over 100,000 miles?

We will never know. At worst, it may represent the behind-closed-doors, back-slapping sort of plotting that, for many years, maximized revenues, ensured shareholder returns, and secured executive paychecks. Or, perhaps it wasn’t some evil conspiracy but just complacency, a profitable position of comfort at that. There’s little incentive for industry insiders to reveal such self-incriminating information.

But the example set by the American auto industry presents an unusual learning opportunity for us, a chance to make some useful comparisons to the heart healthcare industry.

Is the American healthcare industry also guilty of practicing a policy of “planned obsolescence,” just like Detroit? The product that helplessly crumbles is, of course, not your rust-riddled automobile, but you.

When someone sees a primary care physician year after year, yet appears one morning in the emergency room, clutching his or her chest in agony from the closed coronary artery responsible for a life-threatening heart attack—prompting the flurry of activity that results in $100,000 in hospital procedures . . .

Perhaps “planned obsolescence” is not the perfect phrase to describe the situation, but the principle still applies: A failure to inform the patient that such an outcome was possible—no, probable—makes you wonder whether such an outcome was predictable and thereby preventable in the first place.

What should we do when planned obsolescence leads us down a path engineered by someone who has something, often substantial, to gain? Even if it's just complacency, or adhering to a beaten, ineffective status quo (can you say "low-fat diet?), it all points in the same direction.

You have a choice: Refuse to buy a 1962 Impala of health care, otherwise known as conventional heart disease management.

Melatonin is fascinating stuff.

In addition to its use as a sleep aid, melatonin exerts possible effects on cardiovascular parameters, including anti-oxidative action on LDL, reduction in sympathetic (adrenaline-driven) tone, and reduction in blood pressure.

Several studies document the blood pressure-reducing effect of melatonin:

Daily nighttime melatonin reduces blood pressure in male patients with essential hypertension.

Melatonin reduces night blood pressure in patients with nocturnal hypertension.

Prolonged melatonin administration decreases nocturnal blood pressure in women.

Blood pressure-lowering effect of melatonin in type 1 diabetes.

But blood pressure may be increased when melatonin is added to nifedipine, a calcium channel blocker:

Cardiovascular effects of melatonin in hypertensive patients well controlled by nifedipine: a 24-hour study.

Effects on BP tend to be modest, on the order of 5-8 mmHg reduction in systolic, half that in diastolic.

But don't pooh-pooh such small reductions, however, as small reductions exert mani-fold larger reductions in cardiovascular events like heart attack and stroke. NIH-sponsored NHANES data (see JNC VII), for example, document a doubling of risk for each increment of BP of 20/10. The Camelot Study demonstrated a reduction in cardiovascular events from 23% in placebo subjects to 16.7% in subjects taking amlodipine (Norvasc) with a 5 mm reduction in systolic pressure, 2 mmHg drop in diastolic pressure. Small changes, big benefits.

Many people take melatonin at bedtime and are disappointed with the effects. However, a much better way is to take melatonin several hours before bedtime, e.g., take at 7 pm to fall asleep at 10 pm. Don't think of melatonin as a sleeping pill; think of it as a sleep hormone, something that simply prepares your body for sleep by slowing heart rate, reducing body temperature, and reducing blood pressure. (You may need to modify the interval between taking melatonin and sleep, since individual responsiveness varies quite a bit.)

I also favor the sustained-release preparations, e.g., 5 mg sustained-release. Immediate-release, while it exerts a more rapid onset of sleep, allows you to wake up prematurely, The sustained-release preparations last longer and allow longer sleep.

The dose varies with age, with 1 mg effective in people younger than 40 years, higher doses of 3, 5, even 10 or 12 mg in older people. Sustained-release preparations also should be taken in slightly higher doses.

The only side-effect I've seen with melatonin is vivid, colorful dreams. Perhaps that's a plus!

Thinking about the programs for health care reform proposed by the three Presidential candidates highlights a distinct peculiarity of American style health care.

American health care is shaped to an unprecedented degree by five forces:

1) The drug industry

2) The health insurance industry

3) Hospitals

4) Fear of litigation

5) The uniquely American attitude of refusing compromise in access to health care services or products, regardless of the cost (for those who can afford health insurance)

All five of these unique forces have created this thing (monster?) we call health care. Remove or modify any one of these forces, and the health care landscape would look dramatically different.

The drug industry has recently been on the receiving end of plenty of negative press. This warms my bones. Decades of heavy-handed lobbying, sleazy marketing to physicians (all too willing to be wined and dined), and behind-the-scenes manipulation of clinical data are coming back to bite them. Sadly, the drug industry is so powerful that this bit of fuss is not likely to substantially change their ways.

I am thrilled that all three Presidential candidates agree that reimportation of drugs from outside the U.S. is a good idea. While the shrug of the shoulders federal and state attitude towards importation of drugs from Canada has not resulted in cost savings sufficient to impact on overall costs, it surely will lead to savings when practiced on a broad basis by pharmacies, distributors, and other bulk buyers of pharmaceuticals.

Senator Obama, in particular, has used strong language in his criticism of the health insurance industry, tough talk that is needed in an age in which insurance executives bring home salaries in the hundreds of millions of dollars and stock prices are climbing due to substantial profit gains within the industry, going against the grain of increasingly costly premiums. However, the Clinton experiment of federalizing health care during Bill Clinton's term that caused all the big boys to band together (most notably health insurance companies and drug industry) has tempered enthusiasm for attacking the insurance industry head-on. In both Democrats' health care reform proposals, the option of private insurance is preserved, as it is in the McCain proposal.

How about hospitals? Hospitals, though on a smaller scale than the nationwide reach of the drug and insurance industries, aim to maintain health service delivery in hospitals. For instance, the high-tech bypass service in the hospital gets plenty of local media coverage, as does the newest DaVinci robotic surgery, bariatric surgery, and other revenue-rich services. Many hospitals have forgotten that their mission is delivery of health, of which revenue creation and profiting from disease should only be part.

How big is fear of litigation? Estimates vary, but several have quoted numbers in the neighborhood of 20 to 30% of overall health care costs. At the street level from what I see, I'd say at least that much. Fear of litigation is rampant, often unrestrained, and sometimes leads to the craziest, illogical sequence of testing. Chest pain, for instance, no matter how trivial, will typically trigger around $5000 worth of testing (nuclear stress test, echocardiogram, laboratory work, etc.) Emergency room visit for a minor injury? CT scan of head, chest, abdomen. A formula to minimize this aspect of fear in health care delivery would generate enormous savings.

The last issue, the uncompromising nature of Americans in health--always wanting the latest new drug, new procedure, "best" surgeon--often simply causes the health care consumer to fall victim to marketing. If a hospital advertises the newest procedure, people want it regardless of whether it represents genuine improvement over the older procedure. The newest sleeping pill, antidepressant, antihypertensive, etc. replaces the old yet equivalent product, but at considerably greater cost.

I am optimistic that, regardless of which candidate gains the White House, that some reform is on the way. I do fear, however, that progress will be small and incremental, since major change of the sort that would slash hundreds of billions of dollars in costs would rouse the powers-that-be (drug industry, health insurers, etc.) to once again combine forces and combat the disruption of their franchise.

Until you and I see real change and cost savings coming through either legislation or free market advances, we need to continue to make full use of the self-empowering health information that we gain through venues like the web.

Copyright 2008 William Davis, MD

No doubt, our little informal poll asking readers whether they have lipoprotein(a), is skewed towards people inclined to respond because they have this genetic trait.

Nonetheless, the response is telling. Of 82 respondents:

--40 (48%) said they did have Lp(a)

--16 (19%) said that they did not have Lp(a)

--26 (31%) said that they did not know whether or not they had Lp(a)

Though admittedly an informal analysis, I'd draw several conclusions from this simple "experiment".

One, while the proportion of people responding that they have Lp(a) may not be accurate, it is a prevalent genetic risk factor that, according to formal studies, is present in 17% of people with coronary or vascular disease, 11% of the broader population. This number may be even higher if the newer particle number assays (measurements) are used (with results expressed in nmol/L), since an occasional person with a "normal" Lp(a) in mg/dl (weight-based) will prove to have increased Lp(a) by nmol/L (particle number-based). (The reason for this phenomenon is not clear. It may be consequent to variation in apo(a) size, with larger apo(a) varieties of Lp(a) occasionally escaping detection .) As our little poll shows, plenty of people have Lp(a).

Two, readers of this blog tend to be highly motivated, sophisticated, and knowledgeable about health and heart disease. Yet a substantial portion--31%--did not know whether they have this crucial risk factor. That shouldn't be. The unnecessary difficulty of getting this simple blood test performed has been driven home to me repeatedly when I identify this factor in someone and then suggest that their grown children and parents, each of whom have a 50% chance of having Lp(a), be tested. It's not uncommon for a 35-year old son, for instance, to say that his doctor refused, claiming it is an unproven risk marker, or to simply say that he/she doesn't know what it is.

No doubt, just knowing whether you have Lp(a) or not is not the end of the story. Reducing Lp(a) and its associated co-factors is no easy matter. With several hundred patients in my practice with Lp(a), it occupies much of my time and energy. Sometimes it leads to enormous successes , but it can also pose a real challenge.

There should no longer be any doubt that Lp(a) is associated with significantly increased risk of cardiovascular disease. This has been demonstrated conclusively across dozens of studies. Risk from Lp(a) is over and above that posed by other risk factors; it also amplifies the risk posed by other factors, e.g., small LDL, inflammatory phenemena, homocysteine, total LDL, low HDL.

In the world of Lp(a), our two most desperate needs for the future are:

1) Better education of physicians and the public, and

2) More effective treatment options.

Thus, our reasons to form The Lipoprotein(a) Research Foundation. Steps to gain tax-exempt status are being pursued as we speak.

I can't help but wonder whether, like vitamin D, a solution is right beneath our noses. An investment in research to fund the trials to better explore both basic science as well as practical treatment options might yield an answer more readily than we think. Wouldn't that be great?

Just a muse.

Endogenous substances are those that are already contained within our bodies. They are part of basic human equipment.

Exogenous substances are those that come from outside of our bodies. This includes various substances in foods, drugs (most, though not all), and pesticides.

I often mull over all of the tools we use in the Track Your Plaque program to achieve control over this thing called coronary plaque. It struck me that just about all the supplements we use that seem to provide outsized benefits are all endogenous substances themselves:

--Omega-3 fatty acids from fish oil
--Vitamin D
--l-arginine
--Niacin (vitamin B3)

Many of the other substances, though not directly relevant to our plaque-control efforts, but are among the most effective nutritional supplements, also supplement endogenous levels: calcium pyruvate, creatine, acetylcarnitine, DHEA, testosterone, progesterone, growth hormone, pregnenolone, phenylalanine, tyrosine, melatonin, etc.

Curiously, most drugs are not meant to directly supplement endogenous levels, but are designed either to enhance or block an enzyme (e.g., acetylcholinesterase inhibitors that block breakdown of acetylcholine; HMG CoA reductase inhibitors to block cholesterol synthesis; angiotensin converting enzyme inhibitors to reduce blood pressure), to exert toxic effects on an organism (antibiotics, antivirals), or to exert an entirely unique effect that does not ordinarily occur in the human body (some anti-cancer drugs, for instance). (This is an admitted, vast over-simplification.)

That's not to say that any endogenous substance is desirable or safe when supplemented. Cortisol, thyroid hormone, and estrogens are three examples of endogenous substances that have downsides when administered at slightly more than physiologic concentrations.

Nonetheless, it makes me wonder if the world of endogenous substance supplementation has not been fully explored. Are there other endogenous substances that are as potent and wonderful, for instance, as vitamin D but not yet fully appreciated? I'm sure there are.

Reprinted here is the unfailingly informative Vitamin D Newsletter from Dr. John Cannell. Although there's little here specifically about heart disease, there's so much great information about vitamin D that I thought most would still appreciate it.

The Vitamin D Newsletter

May, 2008

Yesterday's Washington Post article, Too-Good-To-Be-True Nutrient?, sums up the April 9th vitamin D symposium at UCSD in San Diego, which was nothing short of spectacular. Carole Baggerly outdid herself organizing it and explaining how she got involved. Make no mistake; Carole is both serious and energetic. She told about her efforts to introduce resolutions at upcoming meetings of various professional groups. Then she introduced the volunteers from the San Diego Black Nurses Association who made sure the conference went off without a hitch. Then Carole introduced the four speakers. The slides of each speaker are available at Grassroots Health.

Before I tell you the highlights of the conference, I'd like to tell you about another conference, this one in Germany, this May 17th and 18th. It is the Third International Symposium on Vitamin D Analogs in Cancer Prevention and Therapy. Readers know how I feel about giving analogs to vitamin D deficient patients instead of vitamin D but speakers include Michael Holick, Reinhold Veith, Bill Grant, Tai Chen, Heidi Cross, David Feldman, and Roger Bouillon, all of whom know the importance of the nutrient. Most of this conference is for scientists, not lay people. However, Michael Holick is the first speaker and if you have not heard his latest talk about vitamin D, it might be worth a trip to Germany.

The first San Diego speaker was Dr. William Grant. Since leaving NASA to begin a full-time career as a vitamin D researcher, Bill has published dozens of studies and has another dozen in the works. Using ecological studies (from Greek oikos, house + German -logie, study or studying your own house) of UVB irradiance and cancer, Bill reported that 15 cancers (colon, esophageal, gallbladder, gastric, pancreatic, rectal, small intestinal, bladder, kidney, prostate, breast, endometrial, ovarian, Hodgkin's lymphoma, and non-Hodgkin's lymphoma) are associated with lower UVB light. He concluded that 257,000 cancer deaths in 2007 in the USA were accounted for by inadequate vitamin D levels. Of course the problem with ecological studies is that it easy to be vitamin D deficient in Miami, all you have to do is listen to your doctor's advice and stay out of the sun. Recently, a group from the Arizona Cancer Center found almost 80% of Arizonians had levels below 30 ng/ml. So much for sunny spots.

Jacobs ET, et al. Vitamin D insufficiency in southern Arizona. Am J Clin Nutr. 2008 Mar;87(3):608-13.

The next speaker was Professor Cedric Garland. I found myself wondering how he did it. I became convinced that vitamin D prevents cancer five years ago. Cedric and his brother Frank and his colleague Ed Gorham knew it 30 years ago! I know what it is like to tell someone that vitamin D prevents cancer and see them think, "Here we go again, another miracle vitamin." I know what it is like to try and explain and watch people die unnecessarily. But I've only had that experience for five years. Cedric has dealt with that frustration for thirty years. Almost thirty years ago, Cedric and Frank Garland published evidence that vitamin D prevents cancer. In fact, it was Cedric's first publication. Thankfully, the paper was recently recognized as being so important that it was republished in 2006 by the International Journal of Epidemiology. You can read the entire paper for free by clicking on the second link below and then clicking on "free final text", courtesy of Oxford Journals.

Garland CF, Garland FC. Do sunlight and vitamin D reduce the likelihood of colon cancer? Int J Epidemiol. 1980 Sep;9(3):227-31.

Garland CF, Garland FC. Do sunlight and vitamin D reduce the likelihood of colon cancer? Int J Epidemiol. 2006 Apr;35(2):217-20.

Cedric began by showing the incidence of type-1 diabetes and multiple sclerosis by latitude. I had no idea that the latitudinal data was so strong for type 1 diabetes in children. This disease is almost nonexistent around the equator. Type-1 diabetes is but one of the three modern childhood epidemics caused by the sunlight-hating dermatologists, the other two, I think, are autism and asthma. Next he showed latitude and 25(OH)D levels, which reminded me to be suspicious of high levels, unless they use accurate methods of detecting 25(OH)D. Some methods used, even in this country, are over detecting vitamin D and telling patients their levels are above 50 ng/ml when they are, in reality, much lower. Cedric's data showed Thailand had mean levels of 70 ng/ml, which I doubt and suspect were due to inaccurate 25(OH)D tests. He then reviewed evidence of the 25(OH)D levels needed to prevent numerous cancers. The safest levels are somewhere above 50 ng/ml. Cedric spent most of his time presenting an entirely new theory of carcinogenesis, one dependent on vitamin D maintaining cellular junctions. I suspect this paper will also be reprinted in 20 years. The only disagreement I have is with his recommendation for cancer patients to start at fairly low doses. For reasons I recently explained, the risk benefit analysis indicates cancer patients should take 5,000 to 10,000 IU per day and they may have no time to lose. Why worry about the phantom of vitamin D toxicity if you may be dying of cancer? Just have your calcium checked along with frequent 25(OH)D levels. Get your levels up to 70-90 ng/ml if you have cancer.

Does vitamin D treat cancer?

The next speaker was Professor Bruce Hollis. He reviewed basic physiology of vitamin D and emphasized that the entire system is designed to deal with an excess not with an insufficiency of vitamin D. Numerous mechanisms are available in your body to prevent vitamin D toxicity but few are available to deal with insufficiency. Then he briefly mentioned one of the most important discoveries about vitamin D in the last few years, one where Professor Neil Binkley of the University of Wisconsin was senior author. (In the last four years, Professor Binkley has become a prolific vitamin D expert and I hope Carol Baggerly is able to get him to speak at some of the upcoming conferences she hopes to sponsor.) As I have pointed out before, Hollis and Binkley's crucial discovery was that the body doesn't start storing the parent compound, cholecalciferol, until 25(OH)D levels reach about 50 ng/ml. They showed, using basic steroid pharmacology, that 50 ng/ml should be considered the lower limit of adequate 25(OH)D levels.

Hollis BW, Wagner CL, Drezner MK, Binkley NC. Circulating vitamin D3 and 25-hydroxyvitamin D in humans: An important tool to define adequate nutritional vitamin D status. J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):631-4.

Bruce kept the audience enthralled with a review of all the disease states that indicate 25(OH)D levels need to be much higher than they are now, that is, the multiple biomarkers that suggest the lower limit of 25(OH)D levels should be above 40 ng/ml and closer to 50 ng/ml. Then Professor Hollis spoke of his ongoing study in pregnant women and how he got approval to use 4,000 IU of vitamin D per day back in 2003, quite an accomplishment. He also reviewed another one of his research projects, one that answered an age old question, why is breast milk a poor source of vitamin D? How were prehistoric infants supposed to get their vitamin D, by lying out in the sun where saber tooth tigers would eat them? No, they were hidden in caves and had to have another source or the human race would have died out long ago because rickets destroys a woman's and infant's chance to live through childbirth due to rachitic deformations of the mother's pelvis. Carol Wagner and Bruce Hollis, together with their colleagues, answered that age old question, human breast milk is a poor vitamin D source because virtually all modern mothers are vitamin D deficient. That is, when pregnant women keep their levels where we think prehistoric human levels were, about 50 ng/ml, breast milk becomes a rich source of vitamin D. First Carol and Bruce gave 2,000 IU per day, then 4,000 IU per day and finally 6400 IU of D3 per day to lactating women. Only at 6400 of D3/day did the women maintain both their own 25(OH)D levels and the levels of their breast feeding babies above 50 ng/ml. On 6400 IU/day, the vitamin D activity of the breast milk went from about 80 to 800 IU/L. Quite a discovery, and another reason for all of us to keep our levels above 50 ng/ml.

Wagner CL, Hulsey TC, Fanning D, Ebeling M, Hollis BW. High-dose vitamin D3 supplementation in a cohort of breastfeeding mothers and their infants: a 6-month follow-up pilot study. Breastfeed Med. 2006 Summer;1(2):59-70.

Professor Robert Heaney went last, discussing 74 slides. So much of what we know about vitamin D today is due to Robert's unceasing dedication to vitamin D, the most recent example being his and Joanne Lappe's randomized controlled trial showing that increasing baseline levels from 29 to 38 ng/ml reduced the risk of getting cancer by around 70%. He again pointed out that the body does not begin to consistently store much vitamin D until your levels get to around 50 ng/ml. He also went through multiple biomarkers of vitamin D. That is, what level or intakes do you have to have to reduce the incidence of multiple diseases? He covered calcium absorption, osteoporosis, risk of falling, muscle function, death and disability of the aged, TB, influenza, cardiovascular disease, hypertension, diabetes, cancer, multiple sclerosis, and gum disease. How can one vitamin be involved in so many diseases? Simple said Dr. Heaney, "vitamin D is the key that unlocks the DNA library." He then reviewed toxicity and concluded there is no evidence that it occurs at levels below 200 ng/ml or with intakes (total) below 30,000 IU per day. Of course, we have no reason to think anyone needs 30,000 IU per day or levels of 200 ng/ml, which would be irresponsible. But someone with a serious cancer should consider getting their level up to 70-90 ng/ml and that may take 10,000 IU per day or even more in some people. As a rule of thumb, 1,000 IU will raise 25(OH)D levels by about 10 ng/ml.

Then Professor Heaney addressed a public health question. How much would we have to give all Americans to get 98% of people above 32 ng/ml without causing toxicity in anybody? The answer: 2,000 IU per day. Of course 32 ng/ml is not adequate but it would be a great first step. Furthermore, of the people left out, a high percentage would be African Americans. In fact, Dr. Talwar recently reported that 40% of African American women fail to achieve a level of 30 ng/ml even after taking 2,000 IU/day for a year.

Talwar SA, Aloia JF, Pollack S, Yeh JK. Dose response to vitamin D supplementation among postmenopausal African American women. Am J Clin Nutr. 2007 Dec;86(6):1657-62.

He also discussed his recent study giving healthy adults 100,000 IU as a single dose. If you start with a baseline level of 28 ng/ml and take 100,000 IU as a single dose, mean levels will remain above 32 ng/ml for two months. If you rely on such stoss doses, but you start with a lower level, or want your levels above 50 ng/ml, how often do you need to take 100,000 IU? We don't know the answer to the last question but we know that Grey et al gave 50,000 IU per week for four weeks then 50,000 per month for a year to 21 patients with hyperparathyroidism. Blood levels rose from a mean of 11 ng/ml at baseline to 30 ng/ml at one year and levels did not continue to rise after six months. Remember, that means half the patients had levels lower than 30 ng/ml at the end of the year. Also remember that the metabolic clearance (how quickly you use it up) might be higher in certain disease states.

Grey A, et al. Vitamin D repletion in patients with primary hyperparathyroidism and coexistent vitamin D insufficiency. J Clin Endocrinol Metab. 2005 Apr;90(4):2122-6.

That last point, metabolic clearance, is only one of a number of reasons that patients vary in their response to vitamin D. Remember, a surprising number of patients will tell their physician they are taking vitamin D when they are not, some will be taking preparations that have less in it than the label says, some will not absorb it, and some people weigh more than others. As Dr. Heaney points out, even if you know patients took 100,000 IU, great variably exists in individual response. At the end of two months some will have shown a minimal response and other much more. This is a field where little is known. Do different disease states use up vitamin D quickly? The answer is probably yes. Furthermore, variability also exists in how one metabolizes and catabolizes (breaks down) vitamin D. Also, what is the interactive effect of drugs that use the same liver enzymes for catabolism? We just don't know and that is why vitamin D blood testing is crucial. Remember, the only test to have is a 25-hydroxy-vitamin D. Do not let anyone get a 1,25-dihydroxy-vitamin D; it will not tell you if you are vitamin D deficient and is usually only indicated in evaluating high blood calcium.

As far as 25(OH)D levels go, many of you have written complaining about the high cost of a 25(OH)D levels at some labs. I've got some good news. For the next month, Life Extension Foundation is having a sale on their 25(OH)D blood tests, only $32.25, including the fee for drawing the blood. (No, we don't get funding from Life Extension, I wish we did.) Life Extension uses LabCorp, which, in turn, uses an accurate method to determine 25(OH)D levels, the DiaSorin Laiason method. The only problem is that DiaSorin, LabCorp, and Life Extension all say that 30 ng/ml is acceptable. It is not. Take enough vitamin D or get enough UVB radiation to get your levels above 50 ng/ml. To order the test, call Life Extension at 800 208-3444. Unfortunately, this offer is not available in New York, New Jersey or Rhode Island.

Also, Dr. James Dowd has written a fine book about vitamin D, The Vitamin D Cure. Get this, he is board certified in internal medicine, adult rheumatology, and pediatric rheumatology, an associate professor at Michigan State University, and runs his own Arthritis Institute and the Michigan Arthritis Research Center. He gives a formula for how much vitamin D you need but stresses the importance of testing to know for sure. He uses the formula of 2000 IU for every 100 pounds of body weight, which is as accurate an estimation as one can make without knowing baseline levels. Of course it depends on so many things, as Dr. Dowd points out, such as percentage body fat, latitude, skin type, sun exposure and age. He gives case after case examples of how vitamin D not just prevents disease, but seems to have a treatment effect. He also stresses three other things I've written about before, acid base balance, magnesium and potassium. If you can't get eat enough fruits and green leafy vegetables to obtain your potassium and magnesium and to get rid of low-grade chronic metabolic acidosis, then you should consider magnesium supplements and potassium bicarbonate supplements.

With these four experts and with this month's vitamin D news articles about breast cancer, brain function, artery blockage in the legs, soft skulls in babies, peripheral neuropathy in diabetics, childhood type-1 diabetes, colon cancer, and stress fractures and with the increasing number of scientists around the world jumping on the vitamin D express, why doesn't the government do something? What will it take? Like Carole says it will take a grassroots effort.

The first thing to do is tell your family and friends about vitamin D. Tell your doctor. Get your family's 25(OH)D tested, including your children. Once people begin to see it works, they will get their family and friends to take it. They will feel better and then the word will spread. All the government can do is make vitamin D illegal or limit the amount in each pill. The first is unlikely but not the second. With 5,000 IU capsules widely available, many people give no thought to taking one a day. But if the government limits the sale of anything over 400 IU and people had to take 12 of the 400 IU tablets, instead of one of the 5,000 IU, they might balk at so many pills. Before our officials in Washington take such a step, let's hope they read the Washington Post.

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. This newsletter is not copyrighted. Please reproduce it and post it on Internet sites. We are a nonprofit tax-exempt educational organization and depend on your donations.

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

Judging by the conversations here, in the Track Your Plaque Forums, and elsewhere, it's clear that many people are searching for the perfect diet.

Should we reconsider the role of saturated fat? Are there fractions of fatty acids in saturated fat that are more or less harmful? How about the role of fats on cancer risk? How about the role of proteins like casein on cancer risk? Are there flavonoid sources, or combinations of flavonoids, that yield outsized health benefits? Is there a ceiling for omega-3 fatty acid supplementation? Is there a role for linolenic acid sources in cardiovascular disease prevention? And on and on.

All important issues, to be sure, ones that we've all zig-zagged through over the past 30 years.

I also see patients every day, however, who are not interested in micro-managing their diet. Their goals are less ambitious: lose 20 lbs, feel good, raise HDL, reduce triglycerides and small LDL, all while meeting all the other responsibilities in their lives, like children, spouses, maintaining a household and jobs.

So, if your interest is not to consider whether we should distinguish myristic acid sources from palmitic, or if epigallocatechin is better when combined with quercetin, then the biggest bang from your nutritional buck can come from one single strategy:

Eliminate wheat flour products

Secondarily, avoiding corn starch products and "goodies" (candy, fruit juices, fruit drinks, cookies, potato chips, etc.--you know what they are) is important, as well.

It means weighing your diet more heavily in favor of vegetables and fruits; lean meats; healthy oils; and raw nuts and seeds, all in unlimited quantities. Dairy products should be limited, however, because of sugar effects.

Of course, this advice clearly contradicts the pronouncements of the USDA Food Pyramid (6-8 servings of grains per day), the American Heart Association, and the diabetes-causing American Diabetes Association diabetic diets.

But, follow this approach, a diet strategy that appears too simple to be effective, and the majority of people lose dramatic amounts of weight, raise HDL, reduce triglycerides, reduce small LDL, reduce C-reactive protein and other inflammatory measures, reduce blood pressure, and raise self-esteem.

It's also a lot easier than it sounds (after habits are broken) because the appetite stimulating effect of wheat is removed. Many, if not most, people also experience increased energy, including elimination of the afternoon "slump," improved sleep, less mood swings, less intestinal problems.

It may not be perfect, but if your interest is to get the most with a modest amount of effort, it works like a charm for the majority of people.

Copyright 2008 William Davis, MD

You're going to hate this.

Dr. Romero-Corral and colleagues from the Mayo Clinic presented an analysis of the National Institutes of Health-funded National Health and Nutrition Examination Survey (NHANES-3) at the recent American College of Cardiology meetings. (Science Daily also has some coverage on this report.)

Their analysis identified 2127 adults from the NHANES database who had normal body-mass indexes (BMI) between 18.5 and 24.9 units), average age 41 years old. When broken down by percent body fat (measured with bioimpedance, meaning a small electrical current is passed through the body, much like what the store-bought Tanita devices do), with normal-weight obesity defined as >20% body fat in males, >30% body fat in females, 55% of participants met criteria for designation as normal-weight obesity.

Compared to people with similar BMI's but who fell below these body fat percentage cut-offs, the normal-weight obese men had increased ratios of Apo B to Apo A1; were much more likely to have increased blood sugars or be diabetic; have higher C-reactive protein (CRP); were several-fold more likely to meet other criteria for diagnosis of metabolic syndrome; had lower HDL cholesterols; and had higher blood pressure. Women with normal-weight obesity were four-fold more likely to have coronary disease.

While preliminary, this suggests that a substantial number of people with apparently favorable body weights and BMIs are, in actuality, overweight when judged by metabolic parameters. This then probably leads to increased risk for heart disease. We can then fairly readily extrapolate the argument that a reduction in weight to even lower BMIs likely reduces or corrects these patterns.

This argument is similar to that proposed by several others, arguing that BMI is a flawed measure, since it does not incorporate muscle mass or skeletal factors ("big- or small-boned"). Instead, they have argued that waist circumference is preferable.

The normal-weight obesity syndrome was originally identified by Dr. Antonio de Lorenzo and colleagues at the University of Tor Vergata, Rome, Italy, and reported in Normal weight obese (NWO) women: an evaluation of a candidate new syndrome. Their studies of women with this "syndrome" have suggested that heightened measures of inflammation are present despite apparently normal body weight and BMIs. One such report, Normal-weight obese syndrome: early inflammation?, is available in full-text.

Is there a lesson to be learned for the Track Your Plaque program? I believe there is. I believe it means that, if you have any weight-sensitive parameter, such as low HDL, small LDL, high triglycerides, high CRP, high blood sugar, high blood pressure, etc., then further weight loss might be considered, even if BMI is around 25. Obviously, there is a rational limit to how far you can push this concept. (Anorexia is not good for you either.)

I find this a useful concept. It provides yet another potential strategy to pursue when the above patterns are encountered. Perhaps it's also a way to cap reliance on niacin, whose effects closely mimic that of weight loss.

Now that's a lot more preferable to more and more statin drug, isn't it?

Copyright 2008 William Davis, MD

Alternatives to fish oil capsules

Ignoring your heart scan is medical negligence

Light the fuse of heart disease

"I don't know what I'm doing here"

I had a heart attack--and I don't know why!

Butter basics

Let Dr. Friedewald rest in peace

The key to losing weight

How can I get my lipoproteins tested?

What do you think about those heart scans?

A tan does not equal vitamin D

Confessions of a former drug company patsy

Planned obsolence

Melatonin for high blood pressure?

The forces that shape heatlh care

Lipoprotein(a): Surprising Poll Results

Are endogenous nutritional supplements better?

Vitamin D Newsletter reprinted

Biggest bang for your nutritional buck

Can skinny be fat?