“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.

There are times when these heart tests are valuable and provide meaningful answers. Then there's the other half of the time when they provide murky information that can be used for a practitioner's economic advantage.

Copyright 2008 William Davis, MD

Dr. Robert Connors is the hospital’s most prized cardiologist.

Practically a fixture in the cath lab, he generates more revenues for the hospital than any of his colleagues. Last year alone, he performed over 1500 procedures, bringing in $18 million dollars to the cath lab, $27 million to the hospital. Dr. Connors is very good at what he does: 55-years old, he has been involved in high-tech heart care since the “early days,” 25 years ago, when hospital procedures really began to take off.

Over his career, he has personally performed over 25,000 heart procedures and has built a reputation as a skilled operator of complex coronary procedures. Because of his skills, he enjoys a vigorous flow of referrals for procedures from dozens of primary care physicians. His skill has also earned him referrals from cardiologist colleagues who seek his abilities for difficult cases.

On any day, Dr. Connors typically schedules up to 12 procedures. His entire day is spent in the cath lab, usually from 7 am until 6 pm. He meets many patients for the first time on the catheterization laboratory table as staff shave their groin, preparing for the procedure. Much of the procedure itself is not even performed by Dr. Connors, but by one or another cardiologists-in-training, a “fellow,” or member of the fellowship the hospital proudly maintains as a clinical teaching institution. Nor will Dr. Connors talk to most patients at the close of the procedure. He leaves that to either the fellow or a nurse. Dr. Connors views himself as a procedural specialist, not someone who has to take care of patients. He gave up seeing patients in his office over 10 years ago.

Dr. Connors’ procedural enthusiasm gained him the attention of drug and medical device manufacturers. Because Dr. Connors lectures widely and advises colleagues, his comments can dramatically alter perceptions of the value of a technology. He has, on many occasions, catapulted an unpopular device to most-asked-for among colleagues, bringing millions of dollars in revenues to the manufacturer. One particularly lucrative arrangement he made around 10 years ago involved a “closure” device, a $400 single-use plug used to close the access site made during heart catheterizations. By swaying his colleagues at _______ Hospital, 50 orders per day (one per procedure) tallied $20,000 every day, $7.1 million dollars per year for the manufacturer. Although he’d used other devices on the market, the 5,000 shares of stock he was offered encouraged him to issue glowing comments to colleagues on the superiority of this specific brand of closure device. Now over 90% of all catheterizations at _______ Hospital conclude with the device manufactured by the company in which Dr. Connors maintains partial ownership.

Negative comments, on the other hand, topple other products when Dr. Connors sees fit to pan them. For this reason, device and drug manufacturers run straight to Dr. Connors to gain his good graces as soon as possible after a product is released into the market. Because the competition is just as likely to do the same, it has often come down to a bidding war, the company providing the most lucrative arrangement most likely to win.

Thus, Dr. Connors proudly boasts of how many times he has flown to Hawaii, Europe, and other exotic locations at industry expense. He also boasts of how, for $100,000 paid to him for a “consulting fee,” he can overturn the choice of products lining hospital shelves. As the hospital’s annual budget for coronary devices will top $84,000,000 this year, device manufacturers regard the sum paid Connors as a profitable investment.

Despite his lofty status in the hospital, Dr. Connors has long expressed a love-hate relationship with ________ Hospital. While he enjoys his work and has made a more than comfortable income, he has long felt that the hospital administration didn’t truly appreciate his contributions. Five years ago, he therefore demanded that he be made “Director of Research.” After all, he had hired a nurse to help him coordinate enrollment of patients into several device trials brought to him by medical device manufacturers. When he encountered an initial lukewarm response from hospital administrators, he threatened to take his “business” elsewhere to a competing hospital. Hospital administrators gave in. They provided him with the title he wanted, along with $100,000 annual “stipend.”

Just fiction? Make no bones about it: Cardiac care is business, big business. And there's money to be made, lots of it.

Copyright 2008 William Davis, MD

Imagine you catch pneumonia.

You have a fever of 103, you’re coughing up thick, yellow sputum. Breathing is getting difficult. You hobble to the doctor, who then fails to prescribe you antibiotics. You get some kind of explanation about unnecessary exposure to antibiotics to avoid creating resistant organisms, yadda yadda. So you make do with some Tylenol®, cough syrup, and resign yourself to a few lousy days of suffering.

Five days into your illness, you’ve not shown up for work, you’re having trouble breathing, and you’re getting delirious. An emergency trip to the hospital follows, where a bronchoscopy is performed (an imaging scope threaded down your airway) and organisms recovered for diagnosis. You’re put on a ventilator through a tube in your throat to support your breathing and treated with intravenous antibiotics. Delayed treatment permits infection to escape into the fluid around your lungs, creating an “empyema,” an extension of the infection that requires insertion of a tube into your chest through an incision to drain the infection. You require feeding through a tube in your nose, since the ventilator prevents you from eating through your mouth. After 10 days, several healing incisions, and a hospital bill totaling $75,000, you’re discharged only to be face eights weeks of rehabilitation because of the extreme toll your illness extracted. Your doctor also advises you that, given the damage incurred to your lungs and airways, you will be prone to more lung infections in the future, and similar situations could recur whenever a cold or virus comes long.

A disease treatable by taking a 10-day, $20 course of oral antibiotics at home was converted into a lengthy hospital stay that generated extravagant professional fees, testing, and costly supportive care. You’ve lost several weeks of income. You’re weak and demoralized, frightened that the next flu or virus could mean another trip to the hospital. You are susceptible to repeated bouts of such episodes in future.

Such a scenario would be unimaginable with a common infection like pneumonia, or it would be grounds for filing a malpractice lawsuit. But, as horrific as it sounds in another sphere of health care, it is, in effect, analogous to how heart disease is managed in current medical practice.

First, you’re permitted to develop the condition. It may require years of ignoring telltale signs, it may require your unwitting participation in unhealthy lifestyle practices, like low-fat diets, "eat more whole grains," and "know your numbers."

It then eventuates in some catastrophe like heart attack or similar unstable heart situation, at which point you no longer have a choice but to submit to major heart procedures. That’s when you receive your heart catheterization, coronary stents, bypass, defibrillators, etc.

Of course, none of these procedural treatments cures the disease, no more than a Band Aid® heals the gash in your leg. The conditions that were present that created heart disease continue, allowing a progressive disease to worsen. At some point, you will need to return to the hospital for yet more procedures when trouble recurs, which it inevitably does.

A coronary bypass operation costs, on average $67,823. That includes the cost for the heart catheterization performed by a cardiologist to provide the surgical roadmap of your coronary arteries, the surgeon’s fees, the hospital charges. If there are any complications of your procedure, then your hospital bill may total a substantially higher figure.

$67,823 is just the upfront financial pay-off. Over the long run, your life is actually worth far more to the cardiovascular health care system because no heart procedure yields a permanent fix. In fact, repeated reliance on the system is the rule.

In fact, over 90% of people who enter the American cardiovascular health care system do so through a revolving door of multiple procedures over several years. It is truly a rare person, for instance, who undergoes a coronary bypass operation, never to be seen again the wards of the hospital because he remains healthy and free of catastrophe. A much more familiar scenario is the man or woman who undergoes two or three heart catheterizations, receives 3,4, or 6 stents, followed a few years later by a heart bypass, pacemaker, defibrillator, as well as the tests performed for catastrophe management, such as nuclear stress test, echocardiogram, laboratory blood analysis, and consultation with several specialists. The total revenue opportunity is many-fold higher than the initial 60-some thousand dollars, but instead totals hundreds of thousands of dollars per person.

A heart attack alone is a $100,000 revenue opportunity (Agency for Healthcare Research and Quality, 2004).

Of all coronary bypass procedures performed, 25% are “re-do’s”, or bypasses in people who’ve had a previous one, two, or three bypass procedures.

Perhaps it's excessively cynical to label it "disease engineering." But, whether from benign neglect or purposeful failure to diagnose, the fact remains: Heart disease is, all too often by the standard path, undiagnosed and neglected for years until the procedural payoff strikes.

Copyright 2008 William Davis, MD

Of the three major highways that lace the city of Milwaukee, there are at least five, and sometimes as many as ten, billboards that prominently feature one hospital heart program or another.

The passing of former First Lady, Ladybird Johnson in July, 2007, reminds us that, just 30 years ago, billboards were a far more common feature (many called them eyesores), proliferating like a dense forest of trees competing for a sliver of sunlight. Ladybird Johnson played a pivotal role in helping to dramatically reduce the number of billboards permissible on the nation’s highways. Of the relative few that remain today, a premium must be paid to post an advertisement. It costs several thousands dollars every month to maintain these highway commercials. But it’s not just an expense; it’s an investment.

The tens of thousands of eyes that view these billboards every day are potential customers, insured Milwaukeeans who carry health insurance and represent a major heart procedure just waiting to happen. They “need” to be directed to the right place. The billboards don’t feature health and wellness, heart disease prevention, or nutritional advice. They feature surgeons proudly wearing scrubs and masks, nurses, and declarations of the advantages of each hospital program. In effect, they invite you to have your heart attack, heart catheterization, bypass surgery, or other major heart procedure at their hospital. High-tech, high-ticket hospital heart care has become the subject of mainstream marketing, the stuff of flyers, brochures, and billboards.

The excesses of “big heart disease” have created a system that makes procedural heart disease “repair” far more profitable than heart disease prevention. Unfortunately, “repair” has disastrous financial, physical, and emotional consequences for everyone save the “repairman.”

While great good has been achieved by the American health care system, this gargantuan and inefficient system has also cultivated a culture of excess that has made many of its participants—physicians, hospitals, drug and device manufacturers—rich. And at our expense.

This approach was, to a degree, justifiable at a time when nothing better was available. But that's no longer true.

Copyright 2008 William Davis, MD

Gwen was miserable and defeated.

No wonder. After a bypass operation failed just 12 months earlier with closure of 3 out of 4 bypass grafts, she has since undergone 9 heart catheterization procedures and received umpteen stents. She presented to me for an opinion on why she had such aggressive coronary disease (despite Lipitor).

No surprise, several new causes of heart disease were identified, including a very severe small LDL pattern: 100% of LDL particles were small.

Given her stormy procedural history, I urged Gwen to immediately drop all processed carbohydrates from her diet, including any food made from wheat or corn starch. (She and her husband were shocked by this, by the way, since she'd been urged repeatedly to increase her whole grains by the hospital dietitians.) I also urged her to begin to lose the 30 lbs of weight that she'd gained following the hospital dietitians' advice. She also added fish oil at a higher-than-usual dose.

I asked her to add niacin, among our most effective agents for reduction of small LDL particles, not to mention reduction of the likelihood of future cardiovascular events.

Although I instructed Gwen on where and how to obtain niacin, she went to a health food store and bought "no-flush niacin," or inositol hexaniacinate. She was curious why she experienced none of the hot flush I told her about.

When she came back to the office some weeks later to review her treatment program, she told me that chest pains had returned. On questioning her about what she had changed specifically, the problem became clear: She'd been taking no-flush niacin, rather than the Slo-Niacin I had recommended.

What is no-flush niacin? It is inositol hexaniacinate, a molecule that indeed carries six niacin molecules attached to an inositol backbone. Unfortunately, it exerts virtually no effect in humans. It is a scam. Though I love nutritional supplements in general, it pains me to know that supplement distributors and health food stores persist in selling this outright scam product that not only fails to exert any of the benefits of real niacin, it also puts people like Gwen in real danger because of its failure to provide the effects she needed.

So, if niacin saves lives, no-flush niacin in effect could kill you. Avoid this scam like the plague.

No-flush niacin does not work. Period.

Disclosure: I have no financial or other relationship with Upsher Smith, the manufacturer of Slo-Niacin.

Copyright 2008 William Davis, MD

I received some wonderful comments to the What's for breakfast blog post.

Even though comments are viewable by clicking on them, I wanted to be sure these were readily visible, since they were so helpful and augmented the few suggestions I made. I'm impressed with the variety of foods people are willing to introduce into breakfast, particularly foods not traditionally thought to be part of standard American breakfast choices.

I normally eat a handful of almonds, some raw cashews, and occasionally an orange for breakfast. I used to eat cheese with breakfast also, but found once I began eating cheese it was hard for me to stop at one or two pieces.

Anonymous

My favorite breakfast is often left over Thai curry. I omit the rice. I also like making a thai omelet which is simply 2 eggs and some fish sauce and water and serving it with Sirachi sauce or Thai peanut sauce. It is street vendor food in Thailand I hear. Here's a recipe.

I find left over dinners are quite wonderful for breakfast. You just have to get past this notion that you have to eat certain foods at certain times in the day. Where'd that idea come from anyway?

Zute

I’ve tried eating oatmeal throughout my life, really wanting to like it. Until now the mere taste or smell of it made my stomach queasy. The key for me was toasting the oatmeal. Here’s what I generally do:

For Steel-cut oatmeal with the taste and texture of rice pudding-

In a frypan:
Toss 1 TBS of butter or so into a hot pan.
Add 1 cup of steel-cut oatmeal until toasted.
--few minutes
In a saucepan:
Boil 2-1/2 cups water
Add 1 cinnamon stick (or equivalent)
Add toasted Steel-cut oatmeal and cook for 15-20 minutes or so

Add 1-1/2 cups of low-fat milk, yogurt, or some combination, etc…
-Optional- Wisk an egg yolk into the milk.
-Optional- Add ¼ tsp salt.
-Optional- 2 TBS honey or Brown sugar. I use one 1 TBS of each.
Add some lemon or orange zest

Return to a boil for 10-15 minutes and then chill before eating. The oatmeal will congeal, resembling rice pudding.
Sprinkle more cinnamon/sugar on top
Add what you like: raisins, nuts, etc...

Use the cinnamon stick if you can, it really makes the difference. I’m constantly refining this recipe.

Anonymous

Once I decided to give up my (former) love affair with breakfast cereals, I was in a quandary about what to do for breakfast. I don't have much time in the morning to get creative and don't have the inclination at that time of the day to do so either.

I've settled on a routine of 2 hard-boiled (organic free-range) eggs (I boil them up a week in advance and leave them, shells-on, in the fridge), and a home-made protein-berry smoothie (frozen organic unsweetened berries, water-based).

This 8 am combo is easy, fast and tasty (I vary the berries and sometimes add natural flavour extracts for variety). It keeps my blood sugar flat and me full until my 1pm lunchtime. And I don't miss the cereals one bit!

Anonymous

I met an out-of-town friend for breakfast the other morning at a French-style bakery cafe. I ordered the goat cheese and herb omelet, but said I didn't want the potatoes or bread with it. They offered extra fruit or a salad instead. I chose the salad, with olive oil and vinegar. My friend wondered how I could eat a salad so early. Why not?

At home I usually eat 2 or 3 eggs over easy cooked in butter for breakfast most mornings and I am comfortably hungry for lunch about 3-4 hours later. But after my nicely filling cheese omelet and generous romaine salad (with a tiny bit of fruit - I ate the berries/melon and left the super-sweet pineapple), I wasn't hungry again until very late in the afternoon so had a small snack (cheese and half an apple) to hold me off and ate my next meal at dinner time. And it was a slow-developing comfortable hunger, not the powerful, "gotta eat something, anything" hunger that follows carb-heavy food.

Breakfast food, indeed!

Anna

You are absolutely right - breakfast is the most difficult meal to change. When I gave up wheat, I started using brown rice or potatoes mixed with anything interesting - nuts or meat or veges. I have now learned that these carbs make my blood glucose skyrocket. I have dropped the rice and potatoes and my BG has dropped nicely.

My favorite breakfast is sauteed veggies with some leftover meat or even an omelette. Soups are great in the AM. Nuts are for the days I am in a hurry.

Would be a little easier if I were not dairy intolerant.

Anne

Here in South India,it is 'Idli' - steam-cooked Lentil-rice (predominantly lentil) droppings, and 'Dosa' - lentil-rice pancakes. We have altered it a bit by increasing lentil ratio and dropping the rice to a minimum. Tastes good and fills you nice, for 4-5 hours.

Neelesh

I have two or three eggs, usually scrambled, but sunny-side-up and over-easy get thrown in for variety. I cook them using butter made from grass-fed cows. I also make my scrambled eggs using whipping cream instead of the more typical water or milk. I'll put a spoonful of fresh-made salsa over the top for some zing, some sliced cheese on the side and a cup of whole, organic milk to drink.

I'm completely sold on the "high-fat, moderate-protein, low-carb" diet and especially the admonition to start the day with a strong breakfast. My overall energy levels are fantastic, running performance is as good as high-school, and my belly hasn't looked this tight in decades.

Ross

Breakfast, for some reason, seems to be the toughest meal of the day for many people.

I think it's because the quest for sweet has dominated the American breakfast for so long, with its half-century legacy of cartoon character-festooned breakfast cereals; baked flour products like pancakes, waffles, and English muffins; more recently, "healthy" alternatives like bran muffins and oat waffles.

This breakfast lifestyle has also contributed to the obesity and diabetes ("diabesity") epidemic. Breakfasts of wheat- or corn-based cereals, even those labeled "heart healthy," fruit, and whole grain breads are guaranteed paths to low HDL cholesterol, high triglycerides, flagrant small LDL, increased inflammatory responses, high blood pressure, and higher blood sugar. Such foods also make you tired, make your abdominal fat grow (wheat belly), and increase appetite so that you want more.

So what can you eat for breakfast that doesn't provoke these patterns?

I will never pretend to be terribly clever in creating meal menus, but I can tell you what has worked for me and many of my patients. Be warned: It may require you to suspend your previous notions of what "should" be included in a list of breakfast foods.

Here are some examples that you may find helpful:

--Raw nuts--one or several handfuls of raw almonds, walnuts, pecans, pistachios
--Cheeses--the real, traditional sorts like gouda, goat, Swiss, edam, etc. (not Velveeta, Cheez Whiz, etc.)
--Eggs, Egg Beaters--and "spice" them up with sun-dried tomatoes, salsa, olives, tapenades, olive oil, onions, green peppers, etc.
--Yogurt (real, of course), cottage cheese
--Ground flaxseed, oat bran--as hot cereals or added to yogurt, cottage, or other foods. Esp. helpful for reducing both total LDL and the proportion of small LDL.
--Oatmeal--slow-cooked, not the instant nonsense.
--Soups--great for winter.
--Dinner foods--chicken, beef, fish, green beans, asparagus, tomatoes, etc., most easily added by saving left-overs from dinner. You'll be surprised how filling dinner foods eaten at breakfast can be.

It's really not that tough. It just means selecting from an entirely different list of foods than you might be accustomed to.

Copyright 2008 William Davis, MD

The closing arguments in actor John Ritter's wrongful death lawsuit are over and the two doctors charged with negligence cleared, five years after his death from a dissection (tear of the inner lining) of the thoracic aorta. The family sought $67 million in damages, claiming that the aortic dissection was misdiagnosed as a heart attack and that the enlarged aorta should have been reported to Mr. Ritter two years earlier during a full body scan.

The AP story can be viewed at http://ap.google.com/article/ALeqM5gmv6HnJJPBee2gWgEYResT5m6YkAD8VDF9CO0

Well, perhaps this is the start of a trend. Up until now, it has been commonplace for doctors to ignore many of the important findings on heart scans, full body scans, and similar direct-to-the-public imaging services. For instance, similar to John Ritter's case, enlarged thoracic aortas are commonly ignored. I'd even say that as a rule they are ignored. I have seen many patients in consultation who have had large aortas identified on heart scans, yet nothing--not a thing--was done about it. While the doctors escaped a lawsuit this time, it might not happen a second time.

I truly hope that Mr. Ritter's unfortunate experience and the consequent lawsuit do not trigger the usual defensive medicine response of resorting to major procedural "solutions."

A better response would be to 1) identify the problem--enlarged aorta in this case, 2) identify the causes, then 3) correct the causes. It does not necessarily mean that a major procedure like replacing the aorta (a horrendous surgery, by the way) needs to be pursued each and every time.

It is possible that Mr. Ritter's lawsuit is just the first. Over the next several years, it could trigger an avalanche of lawsuits for all the neglected findings on tests like heart scans, body scans, and other imaging methods that are gaining expanded direct-to-consumer access.

Images courtesy Wikipedia.

On the afternoon of October 30th, 1958, nearly 30 years after Werner Forssmann’s fumbling attempts, Dr. Mason Sones, a 5 foot 5 inch, plain-talking, cuss-every-few-words, cigarette-wielding radiologist at the Cleveland Clinic, was performing a routine angiogram of a patient’s aorta (the large vessel emerging from the heart) in a dark basement laboratory. (In Sones’ day, imaging methods remained primitive, disease diagnosis relying more than anything else on the physician’s powers of observation and crude diagnostic procedures. Abdominal pain was assessed with exploratory laparotomy, headaches with air injected into the brain and nervous system (“pneumoencephalography”), an excruciatingly painful ordeal. Being able to track the course of x-ray dye injected into specific internal organs, whether liver, biliary tree, aorta, lungs, or coronary arteries, represented a huge advance in diagnostic tools for human disease.)

In 1958, no one had yet injected dye directly into the coronary artery of a living human.

Just as the dye injector was triggered, Dr. Sones’ eyes widened in horror when the black and white monitor showed that the catheter had inadvertently jumped into the right coronary artery. The injection pump, already triggered to release its load, proceeded to pump 30 cc of X-ray dye straight into the artery. (Modern techniques usually require only 5–10 cc of dye.) Dr. Sones recounts the incident:

“It was late in the day and we were tired. I hit the switch to rev up the x-ray generator so I could see. As the picture came on, I could see that the damn catheter was in the guy’s right coronary artery. And there I was, down in the hole [a recess to shield him from radiation]. I yelled, “Pull it out! Pull it out!”*? By that time, about 30 cc of the dye had gone into the coronary artery. I climbed out of the hole and I grabbed a knife. I thought that his heart would fibrillate and I would have to open his chest and shock his heart. [In Sones’ day, modern CPR hadn’t yet been developed as a method of resuscitation.] But he didn’t fibrillate—his heart stopped. I demanded he cough. He coughed three times and his heart began to beat again. I knew at once that if the heart could tolerate 30 cc of dye, we would be able to safely inject small amounts directly into the coronary artery. I knew that night that we would have a tool to define the anatomic nature of coronary disease.”

*An observer, Dr. Julio Sosa, reported that Dr. Sones, in his shock, also blurted, “We’ve killed him!” After all, conventional wisdom of that era, based on observations from dye injections into the coronary arteries of dogs, was that injecting x-ray dye into human coronary arteries would result in immediate death from the electrical imbalance provoked in heart muscle momentarily deprived of oxygen-carrying blood.

Thus it was established that it was indeed possible to directly inject x-ray dye into human coronary arteries and reveal its internal contours. That’s not to say that the x-ray dyes of 1958 were innocuous. Far from it. In addition to briefly interrupting heart rhythm, as happened with Sones’ first accidental attempt, the dyes used then typically caused dizziness and the sudden urge to vomit. During the first 30 years of direct coronary catheterizations, it was common for hospital staff to run to the patient’s side, bucket in hand to catch the inevitable vomit, once the heart was jump-started by coughing.

Not surprisingly, Dr. Sones’ discovery set off both an avalanche of criticism and bold predictions of how the new technique might change the course of diagnosis in heart disease.

Over the subsequent weeks and months, Dr. Sones proceeded to purposefully insert catheters into coronary arteries and create angiograms that revealed the extent of coronary atherosclerosis. He learned how to fashion new catheter shapes to facilitate access to the arteries. Sones developed an impressive experience in the new technique. For the first time, clear images of the coronary arteries were routinely obtainable for the confident diagnosis of coronary atherosclerosis before death. Dr. Sones became an unlikely celebrity in Cleveland, entertaining physicians from around the world eager to learn about his methods, politicians and celebrities, even Middle Eastern nobility complete with bodyguards and food testers.

Dr. Sones continued to work in Cleveland, furthering the techniques of heart catheterization after his fortuitous error. He died of lung cancer in 1985, 17 years after his discovery.

Thus was born the modern age of heart catheterization.

Today, over 10,000 heart procedures are performed in the U.S. every day, 365 days a year, the vast majority of which involve heart catheterization or begin with a heart catheterization. Dr. Sones' fortuitous blunder was followed by 30 years of productive refinement and development before the blatant excesses of this technique really began to be exploited.

Copyright 2008 William Davis, MD

The modern era of heart disease care was born from an accident, quirky personalities, and even a little daring.

The notion of heart catheterization to visualize the human heart began rather ignominiously in 1929 at the Auguste-Viktoria Hospital in Eberswalde, Germany, a technological backwater of the day. Inspired by descriptions of a French physician who inserted a tube into the jugular vein of a horse and felt transmitted heart impulses outside the body, Dr. Werner Forssmann, an eager 25-year old physician-in-training, was intent on proving that access to the human heart could be safely gained through a surface blood vessel. No one knew if passing a catheter into the human heart would be safe, or whether it would become tangled in the heart’s chambers and cause it to stop beating. On voicing his intentions, Forssmann was ordered by superiors not to proceed. But he was determined to settle the question, especially since his ambitions captured the interest of nurse Gerda Ditzen, who willingly even offered to become the first human subject of his little experiment.

Secretly gathering the necessary supplies, he made his first attempt in private. After applying a local anesthetic, he used a scalpel to make an incision in his left elbow. He then inserted a hollow tube, a catheter intended for the bladder, into the vein exposed under the skin. After passing the catheter 14 inches into his arm, however, he experienced cold feet and pulled it out.

One week later, Forssman regained his resolve and repeated the process. Nurse Ditzen begged to be the subject, but Forssmann, in order to allow himself to be the first subject, tricked her into being strapped down and proceeded to work on himself while she helplessly watched. After stanching the oozing blood from the wound, he threaded the catheter slowly and painfully into the cephalic vein, up through the bicep, past the shoulder and subclavian vein, then down towards the heart. He knew that simply nudging the rubber catheter forward would be sufficient to direct it to the heart, since all veins of the body lead there. With the catheter buried 25 inches into his body, Forssmann untied the fuming Ditzen. Both then ran to the hospital’s basement x-ray department and injected x-ray dye into the catheter, yielding an image of the right side of his heart, the first made in a living human.

Thus, the very first catheterization of the heart was performed.

An x-ray image was made to document the accomplishment. Upon hearing of the experiment, Forssmann was promptly fired by superiors for his brazen act of self-experimentation. Deflated, Forssmann abandoned his experimentation and went on to practice urology. He became a member of the Nazi party in World War II Germany and served in the German army. Though condemned as crazy by some, physicians in Europe and the U.S., after hearing of his experience, furthered the effort and continued to explore the potential of the technique. Forssmann himself was never invited to speak of his experiences outside of Germany, as he had been labeled a Nazi.

Many years after his furtive experiments, the once intrepid Dr. Forssmann was living a quiet life practicing small town medicine. He received an unexpected phone call informing him that he was one of three physicians chosen to receive the 1956 Nobel Prize for Medicine for his pioneering work performing the world’s first heart catheterization, along with Drs. André Cournand and Dickinson W. Richards, both of whom had furthered Forssmann’s early work. Forssmann remarked to a reporter that he felt like a village pastor who was made a cardinal.

Strange, but true.

Copyright 2008 William Davis, MD

Our efforts to obtain prebiotic fibers/resistant starches, as discussed in the Cureality Digestive Health Track, to cultivate healthy bowel flora means recreating the eating behavior of primitive humans who dug in the dirt with sticks and bone fragments for underground roots and tubers, behaviors you can still observe in extant hunter-gatherer groups, such as the Hadza and Yanomamo. But, because this practice is inconvenient for us modern folk accustomed to sleek grocery stores, because many of us live in climates where the ground is frozen much of the year, and because we lack the wisdom passed from generation to generation that helps identify which roots and tubers are safe to eat and which are not, we rely on modern equivalents of primitive sources. Thus, green, unripe bananas, raw potatoes and other such fiber sources in the Cureality lifestyle.

There is therefore no need to purchase prebiotic fibers outside of your daily effort at including an unripe green banana, say, or inulin and fructooligosaccharides (FOS), or small servings of legumes as a means of cultivating healthy bowel flora. These are powerful strategies that change the number and species of bowel flora over time, thereby leading to beneficial health effects that include reduced blood sugar and blood pressure, reduction in triglycerides, reduced anxiety and improved sleep, and reduced colon cancer risk.

HOWEVER, convenience can be a struggle. Traveling by plane, for example, makes lugging around green bananas or raw potatoes inconvenient. Inulin and FOS already come as powders or capsules and they are among the options for a convenient, portable prebiotic fiber strategy. But there are others that can be purchased. This is a more costly way to get your prebiotic fibers and you do not need to purchase these products in order to succeed in your bowel flora management program. These products are therefore listed strictly as a strategy for convenience.

Most perspectives on the quality of human bowel flora composition suggest that diversity is an important feature, i.e., the greater the number of species, the better the health of the host. There may therefore be advantage in varying

60-year old man dies of high cholesterol

1. February 2012 William Davis (12)

Never saw a headline like this? Neither have I. That's because it doesn't happen.

Cholesterol doesn't harm, maim, or kill. It is simply used as a crude--very crude--marker. It is, in reality, a component of the body, of the cell wall, of lipoproteins (lipid-carrying proteins) in the bloodstream. It is used a an indirect gauge, a "dipstick," for lipoproteins in the blood to those who don't understand how to identify, characterize, and quantify actual lipoproteins in the blood.

Cholesterol itself never killed anybody, any more than a bad paint job on your car could cause a fatal car accident.

What kills people is rupture of atherosclerotic plaque in the coronary arteries. For all practical purposes, you must have atherosclerotic plaque in order for it to rupture (much like a volcano erupts and spews lava). It's not about cholesterol; it's about atherosclerotic plaque. Plaque might contain cholesterol, but cholesterol is not the thing itself that causes heart attack and death.

So why do most people obsess about cholesterol? Good question. It is, at best, a statistical marker for the possibility of having atherosclerotic plaque that ruptures. High cholesterol = higher risk for heart attack, low cholesterol = lower risk for heart attack. But the association is weak and flawed, such that people with high cholesterol can live a lifetime without heart attack, people with low cholesterol can die at age 43.The same holds true for LDL cholesterol, you know, the calculated value based on flawed assumptions about LDL's relationship to total cholesterol, HDL cholesterol, and VLDL cholesterol.

A crucial oversight in the world of cholesterol: There are many other factors that cause atherosclerotic plaque and its rupture, such as inflammatory phenomena, calcium deposition, artery spasm, hemorrhage within the plaque itself, degradative enzymes, etc., none of which are suggested by cholesterol measures.

But one observation has held up, time and again, over the past 40 years of observations on coronary disease: The greater the quantity of coronary atherosclerotic plaque, the greater the risk of atherosclerotic plaque rupture. An increasing burden of atherosclerotic plaque along the limited confines of coronary arteries, just a few millimeters in diameter and a few centimeters in length, is like a house of cards: It's bound to topple sooner or later, and the bigger it gets, the less stable it becomes.

If you are concerned about future potential for heart disease and heart attack, don't get a cholesterol panel. Get a measure of coronary atherosclerotic plaque.

Back to basics: Coronary calcium

30. January 2012 William Davis (42)

After having my attentions pulled a thousand different directions these past 6 months, with the release of Wheat Belly and all the wonderful media attention it has attracted, I've decided to pick up here with a series of discussions about the fundamental issues important to the Track Your Plaque program and prevention and reversal of coronary atherosclerotic plaque.

I fear the discussions at times have drifted off into the exotic. This is great because this is how we learn new lessons, but we can never lose sight of the basics, else we risk losing control over this disease.

Imagine you've got a beautiful new car. You wax it, gap the spark plugs, rotate the tires, etc. and it looks brand-new, just like it came off the dealer's lot. 50,000 miles pass, however, and you realize you've forgotten to change the oil. Ooops! In other words, no matter how meticulous the attention to transmission, tires, and paint job, neglect of the most basic responsibility can ruin the whole thing. We can't let that happen with heart health.

If we propose to reverse coronary atherosclerotic plaque, we've got to have something to measure. First, it tells us whether we have atherosclerotic plaque in the first place, the stuff that accumulates and blocks flow and causes anginal chest pains, and ruptures like a little volcano and causes heart attacks. Second, it gives us something to track over the years to know whether plaque has grown, stopped growing, or been reduced. Without such a measure, you will be driving without a speedometer or odometer, just guessing whether or not you've gotten to your destination.

Of course, the conventional approach to heart disease and heart attack is not to track atherosclerotic plaque in your coronary arteries, but to track some distant "risk factor" for atherosclerotic plaque, especially LDL cholesterol. But LDL cholesterol is flawed at several levels. First, it is calculated, not measured. The nearly 50-year old Friedewald equation used to calculate LDL cholesterol is based on several flawed assumptions, yielding a value that can be 20, 30, or 50% inaccurate as a rule, only occasionally generating a value close to the real value. (No point in publicizing this problem, of course: Why compromise a $27 billion annual cash cow?) It also ignores the effect of diet. (No, cutting fat does not reduce LDL for real, only the calculated value. Cutting carbohydrates, especially wheat--"healthy whole grains"--slashes measured LDL values like NMR LDL particle number and apoprotein B.)

But all risk factors are, at best, snapshots of the situation at that moment in time. They change from day to day, week to week, month to month, year to year. If you do something dramatic in health, like lose 50 pounds, you can substantially change your risk factors values, like LDL cholesterol and HDL cholesterol. But you may not modify the amount of atherosclerotic plaque in your heart's arteries.

Measuring the amount of atherosclerotic plaque in your heart's arteries is, in effect, a cumulative expression of the effects of risk factors up until the moment of measurement.

There are several stumbling blocks, however, in the concept of measuring coronary atherosclerotic plaque. We cannot measure all the unique components of plaque, such as fibrous tissue like collagen, or degradative enzymes like collagenases, or inflammatory proteins like matrix metalloproteinase, or the debris of hemorrhage and inflammation. We struggle to contemporaneously mix in measures of bloodborne inflammation, coagulation and viscosity, and physiological phenomena of the artery itself, like endothelial dysfunction, medial (muscle) tone, and adventitial fat.

So we are left with semi-static measures of total coronary atherosclerotic plaque like coronary calcium, obtainable via CT heart scans as a calcium "score." No, it is not perfect. It does not reflect that moment's blood viscosity, it does not reflect the inflammatory status of the one nasty plaque in the mid-left anterior descending, nor does it reflect the irritating sheer effects of a blood pressure of 150/95.

But it's the best we've got.

If anyone has something better, I invite you to speak up. Carotid ultrasound, c-reactive protein, ankle-brachial index, stress nuclear studies, myoglobin, skin cholesterol, KIF6 genotype . . . none of them approach the value, the insight, the trackability of actually measuring coronary atherosclerotic plaque. And the only method we've got to gauge coronary atherosclerotic plaque that is non-invasive and available in 2012? Yup, a good old CT heart scan calcium score.

Myocardial infraction

15. January 2012 William Davis (45)

I've seen a few heart attacks this past year . . . but none in the people who follow this program.

I saw a heart attack in a priest, a wonderful man who was unable to say "no" to his parishioners who insisted on bringing pies, cakes, and cookies every day.

I saw an impending heart attack in a 74-year old man, a football coach who thought the whole wheat-free, low-carb thing was some wacko trend. Four stents later, he's changed his mind.

A 69-year old woman had to be hospitalized for heart failure due to partial closure of an artery. She repeatedly told me that she simply could not follow the diet because it was "too restrictive."

There were a few others. Interestingly, all felt they were eating healthy, minimizing junk foods and avoiding fatty foods. None were wheat-free nor restricted carbohydrates.

In other words, in the people who follow the basic advice of the Track Your Plaque program to do such simple things as eliminate wheat, don't indulge in junk carbohydrates, normalize vitamin D status, supplement omega-3 fatty acids, supplement iodine and correct any thyroid dysfunction . . . well, they have no heart attacks.

Diet is superior to drugs

7. January 2012 William Davis (27)

Might-o’chondri-AL left this wonderful record of his lipoprotein experience in the comments to the last Heart Scan Blog post. It is a great example of what is achievable with diet and a few supplements . . . without drugs.

(A) Jan. 2011 1st ever NMR lipo-protein analysis was done after 4 months of consistent home food prep of pretty low fat (only olive oil and 1 tablespoon coconut oil daily) but plenty of whole wheat and half potatoes:
* LDL # of particles (P) = 1,676 in nmol/L————being a LDL cholesterol (C) reading of 139 mg/dL
* small LDL # P = 1,021 nmol/L —————yikes! you advise smLDL be less than 117 nmol/L
* HDL # of particles = 28.8 umol/L ————–being a HDL C reading of 45 mg/dL
* Triglycerides = 90 mg/dL ————– true, I never struggled with my weight

(B) May 2011 2nd NMR after another 4 months but added in more fat (1 teaspoon highly concentrated fish oil daily, 90% chocolate, handfulls of nuts, more olive oil and kept coconut oil at 1 tablespoon daily for a controlled experiment), added 500 mg Niacin 3 times a day (in stages up to1,500 mg. total daily), 6000 IU daily vitamin D, deliberately cut out all grains except for social politeness and substituted in daily Koji fermented brown rice (rustic Amazake):
** LDL # P……………= 976 nmol/L ——————————– being LDL C of 100 mg/dL
** small LDL # P …. = 96 nmol/L ——————————– nice surprise
** HDL # P ………… = 27.3 umol/L ——————————being an increase to HDL C of 64 mg/dL
** Triglycerides …… = 42 mg/dL ——————————– despite daily carbs over 150 gr. daily

(C) Dec. 2011 3rd NMR after another 7 more months thinking Doc’s advice is worthwhile I added in yet more fat (mainly daily 2 tablespoons of coconut oil, more 90% chocolate), bumped Niacin up to 1,000 mg twice a day (2,000 mg. total daily), cut out the Amazake, kept up the vitamin D adding daily vitamin K & daily ate main mid-day meal out as lunch on spicy Thai & Chinese fish/shrimp/soup/rice meals (my next control):
*** LDL # P ………. = 764 nmol/L ————— being LDL C of 107 mg/dL ( 2x coconut’s saturated fat)
***small LDL # P… = less than 90 nmol/L ——–surprised me NMR can’t count lower
***HDL # P ……… = 41.4 umol/L ——————– being an increase to HDL C of 88 mg/dL
*** Triglycerides ….= 43 mg/dL ——————- daily carbs below ~ 120 gr. & lost too much weight

Isn't that great? Spectacular job, Might!

MIght achieved values that are superior to that achievable with, say, a high-dose statin strategy. Statins only reduce total LDL particles, reducing small LDL in a non-selective way. And, of course, this diet does not cause muscle aches, memory loss, nor liver problems.

Something to consider: As the diet has become so effective, we can reduce our reliance on niacin. In fact, the benefits of niacin diminish substantially, as small LDL is reduced, HDL increased, triglycerides decreased, and postprandial lipoproteins subdued with the diet only.

Low-carb is heart healthy

4. January 2012 William Davis (88)

Anybody following the discussions in these pages know that: Limiting carbohydrate intake reduces risk for coronary heart disease and heart attack.

First of all, why do conventional diets advocate restricting saturated and total fat? From the standpoint of surrogate markers of cardiovascular risk, cutting saturated and total fat reduces total cholesterol; reduces calculated LDL cholesterol; and may reduce c-reactive protein modestly (an index of inflammation). It also increases blood sugar and HbA1c (reflecting the prior 60 days blood sugars), increases glycation of the proteins of the body leading to cataracts, arthritis, and hypertension.

Problem: Total cholesterol is a combination of HDL cholesterol, an estimate of VLDL cholesterol (triglycerides), and LDL cholesterol. It is a composite of both "good" things (HDL) and "bad" things (LDL and VLDL). Cutting saturated and total fat results in reduced HDL, increased VLDL/triglycerides, and a reduction in calculated LDL. Pretty weak stuff. The last item, i.e., reduction in calculated LDL, is not even a real phenomenon. In fact, the net effect in most genotypes (genetic types) may be negative: increased heart disease risk.

In contrast, what is the effect of reducing carbohydrate without restricting fat? (In the approach I use, we start with elimination of the most destructive of carbohydrates, wheat, followed by reducing exposure to other carbohydrates, especially cornstarch and corn products, sugar, and oats.) If, say, we cut carbohydrate intake into the range of a truly low-carbohydrate diet of 10-15 grams per meal ("net" carbs, or total carbohydrates minus fiber), then we witness a number of metabolic transformations:

Reduced fasting triglycerides and VLDL
Reduced postprandial (after-eating) triglycerides, chylomicrons, and chylomicron remnants
Increased HDL and shift towards large HDL particles (presumably more protective)
Reduced small LDL particles
Reduced glycation and oxidation of small LDL particles
Reduced hemoglobin A1c
Reduced c-reactive protein and other inflammatory markers
Reduced blood pressure

By slashing carbohydrates, we also witness weight loss from visceral fat, reversal of pre-diabetes and diabetes, and reduced phenomena of glycation. And, if the wheat-free part of low-carb is maintained, you can also see marked improvement in gastrointestinal health, relief from joint pains, relief from leg edema, relief from migraine headaches, improved behavior and ability to concentrate in children with impaired learning, ADHD, and autism, better mood, deeper sleep. You will see multiple inflammatory and autoimmune diseases improve or completely relieved, such as rheumatoid arthritis and ulcerative colitis.

Having personally gone down the diabetic path and back by cutting the fat in my diet, now maintaining a HbA1c of 4.8% with fasting glucose 84 mg/d; (without medications), there should be no remaining doubt: Low-carb diets, especially if wheat-free, dramatically reduce the factors leading to heart disease; low-fat diets worsen the factors leading to heart disease.

Mocha Walnut Brownies

1. January 2012 William Davis (11)

Richer than a cookie, heavier than a muffin, brownies are ordinarily an indulgence that leaves you ashamed of your lack of restraint. Have one . . . or two or three, and you will surely pack on a pound of belly fat.

But these mocha walnut brownies, as with other recipes I provide, will not pack on the pounds. With no wheat to trigger appetite, nor any readily-digestible carbohydrate to generate blood sugar highs and lows, you can have a nice brownie or two or three and nothing bad happens: You don’t send blood sugar sky-high, don’t trigger formation of small LDL particles and triglycerides, you don’t trigger appetite, you don’t gain a pound of belly fat. You simply have your brownie(s) and enjoy them.

Serve these brownies plain or topped with cream cheese, natural peanut or almond butter, or dipped in coffee.

Ingredients:
8 ounces unsweetened baking chocolate (100% chocolate)
4 tablespoons coconut oil or butter, melted
2 large eggs, separated
½ cup coconut milk (or sour cream)
2 teaspoons vanilla extract
2 cups ground almonds
2 tablespoons coconut flour
1 cup chopped walnuts
¼ cup unsweetened cocoa powder
2 teaspoons instant espresso
Sweetener equivalent to 1 cup sugar or to taste (e.g., liquid stevia, Truvía, erythritol)

Preheat oven to 350º F.

Melt chocolate using double boiler method or in 15-second increments in microwave. Stir in melted coconut oil or butter.

In small bowl, beat egg whites until frothy. Add egg whites, egg yolks, coconut milk, and vanilla extract to chocolate mixture and mix thoroughly by hand.

In separate bowl, combine ground almonds, coconut flour, walnuts, cocoa powder, espresso, and sweetener. Mix thoroughly.

Add dry mix to chocolate mix and mix together thoroughly. If dough is too stiff, add additional coconut milk, one tablespoon at a time.

Place mixture in 9-inch baking pan and bake for 25 -30 minutes or until toothpick withdraws dry.

Are you hungry?

6. December 2011 William Davis (43)

Eliminate modern high-yield semi-dwarf Triticum aestivum . . . and what is the effect on appetite?

A reduction in appetite is among the most common and profound experiences resulting from wheat elimination. I know that I have personally felt it: Wake up in the morning, little interest in breakfast for several hours. Lunch? Maybe I'll have a few bites of something. Dinner . . . well, I'd like to exercise first.

The wheatless report that:

--Appetite diminishes to the point where you can't remember whether you've eaten or not. It is not uncommon to miss a meal, perfectly content. Calorie intake drops by 400 calories per day, on average, calories you otherwise would not have needed but all went to . . . you know where.
--Hunger feels different: It's not the gnawing, rumbling hunger that plagues you every 2 hours. In its place, you will find that hunger feels like a soft reminder that, gee, maybe it's time to have something to eat because you haven't had anything in--what?--4 to 6 hours. And it's a subtle reminder, not a desperate hunt that makes you knock people aside at the food bar, steal coworkers' lunches stored in the refrigerator, salivating at the mere thought of food.
--The simplest foods satisfy--It no longer requires an all-you-can-eat buffet to satisfy, but a few small pieces of healthy food. (Yeah, but what happens to revenues at Kraft, Nabisco, and Kelloggs, not to mention the revenues at agribusiness giants ADM and Monsanto? Slash consumption by, say, 30%, you likewise slash revenues by 30%. What would shareholders say?)
--Even prolonged periods of not eating, i.e., fasting, is endured with ease.

Hunger and the relentless search for something to eat disappear for most people. By eliminating the appetite-stimulating properties of wheat, we return to a natural state of eating for sustenance, to satisfy physiologic need. We are no longer victims of this incredibly powerful appetite-stimulant called gliadin from wheat.

This is why many diets fail: They fail to remove this powerful appetite stimulant. You might eat only lean meats, limit your calories, and exercise 90 minutes per day, but as long as the gliadin protein is pushing your appetite button, you will want to eat more or you will have to mount monumental willpower to resist it. You can lose 20 pounds on phase 1 of the South Beach diet, for instance, only to regain it in phases 2 and 3 when "healthy whole grains" are added back.

So the key is to remove the gliadin protein from your life, i.e., eliminate all things wheat.

Chocolate . . . for adults only

30. November 2011 William Davis (22)

If you've got a serious chocolate addiction and you'd like to make it as healthy as possible, give this X-rated dark chocolate a try.

I call it X-rated because it is certain to not satisfy young, sugar-craving palates, but is appropriate for only the most serious chocolate craver. This is a way to obtain the rich flavors and textures of cocoa, the health benefits (e.g., blood pressure reduction, antioxidation) of cocoa flavonoids, while obtaining none of the sugars/carbohydrates . . . and certainly no wheat!

It is easy to make, requiring just a few ingredients, a few steps, and a few minutes. Set aside and save for an indulgence, e.g., dip into natural peanut or almond butter.

Ingredients:
8 ounces 100% unsweetened cocoa
5 tablespoons coconut oil, melted
1/2 cup dry roasted pistachios
1/4 cup whole flaxseeds or chia seeds
Truvia or other non-aqueous sweetener

Using double-boiler method, melt cocoa. Alternatively, melt cocoa in microwave in 15-20 second increments. Stir in coconut oil, pistachios, and flaxseeds or chia seeds. Stir in sweetener, mixing thoroughly. (Note that the sweetener must be non-aqueous, as water-based sweeteners will separate in the oils.)

Lay a sheet of parchment paper out on a large baking pan. Pour chocolate mixture slowly onto paper, tilting pan carefully to spread evenly until thickness of thick cardboard obtained. Place pan in refrigerator or freezer for 20 minutes.

Remove chocolate and break by hand into pieces of desired size.

"Friday is my bad day"

19. November 2011 William Davis (29)

At the start, Ted had a ton of small LDL particles. His starting (NMR) lipoprotien values:

LDL particle number: 2644 nmol/L

Small LDL: 2301 nmol/L

In other words, approximately 85% of all LDL particles were abnormally small. I showed Ted how to use diet to markedly reduce small LDL particles, including elimination of wheat, limiting other carbohydrates, and even counting carbohydrates to keep the quantity no higher than 15 grams per meal ("net" carbs).

Ted comes back 6 months later, having lost 14 pounds in the process (and now with weight stabilized). Another round of lipoproteins show:

LDL particle number: 1532 nmol/L

Small LDL: 799 nmol/L

Better, but not perfect. small LDL persists, representing nearly 50% of total LDL particle number.

So I quiz Ted about his diet. "Gee, I really stick to this diet. I have nothing made of wheat, no sugars. I count my carbs and I almost never go higher . . . except on Fridays."

"What happens on Friday?" I asked.

"That's when I'm bad. Not really bad. Maybe just a couple of slices of pizza. Or I'll go out for a big custard cone or something. That wouldn't do it, would it?"

That's the explanation. Your liver is well-equipped to recognize normal, large LDL particles. Large LDL particles therefore "live" for only a couple of days in the bloodstream. But the human liver does not recognize the peculiar configuration of small LDL particles, so it lets them pass--over and over and over again. The result: Once triggered by, say two slices of pizza, small LDL particles persist for 5 days, sometimes longer.

So Ted's one "bad" day per week is enough to allow a substantial quantity of small LDL particles to persist. While a fat indulgence (if there is such a thing) pushes large LDL up, the effect is relatively short-lived. Have a carbohydrate indulgence, on the other hand, and small LDL particles persist for up to a week. It means that Ted's one "bad" day per week is enough to allow his small LDL particles to persist at this level, preventing him from gaining full control over coronary plaque.

It also means that, if you have blood drawn for lipoprotein analysis but had a carbohydrate goodie within the previous week, small LDL particles may be exaggeratedly high.

HDL 80 mg/dl

14. November 2011 William Davis (73)

More and more people in my clinic are showing HDL cholesterol values of 80 mg/dl or higher, males included.

Think about it: Nationwide, average HDL for males is 42 mg/dl and for females 52 mg/dl. Even though these average values are generally regarded as favorable, HDL cholesterol values at these levels are nearly always associated with higher levels of triglycerides, postprandial (after-eating) lipoprotein abnormalities, and excessive quantities of small LDL particles.

HDL particles are, of course, protective and are powerfully anti-oxidative. Higher levels of HDL have been associated with reduced potential for cancer, as well as reduced risk for heart disease.

Following the simple regimen that we follow to gain control over coronary plaque has therefore increased levels of HDL to heights that are uncommon in the rest of the population, levels that readily top 80, 90, or 100 mg/dl. That regimen includes:

1) Elimination of all wheat--Yes, consumption of "healthy whole grains" sets you up to have lower HDL levels; elimination of wheat increases HDL.
2) Limited carbohydrate consumption--While eliminating wheat is a powerful nutritional strategy to increase HDL, non-wheat carbohydrates like quinoa, millet, beans, rice, and fruit can still cause high triglycerides that lead to reduced levels of HDL. Limited exposure helps keep HDL at higher levels.
3) Omega-3 fatty acid supplementation--Because omega-3 fatty acids reduce both triglycerides and blunt the postprandial rise in lipoproteins that can cause HDL degradation, HDL rises with omega-3s from fish oil.
4) Vitamin D supplementation--The effect is slow, but it is BIG. HDL just goes up and up and up over about 2 years of supplementation. Before vitamin D, HDL levels of 60 mg/dl were the best I could hope for in most people. Now 80 mg/dl is an everyday occurrence.

Other factors can also be used to increase HDL levels, such as weight loss, red wine and alcohol, exercise, cocoa flavonoids, green tea, and niacin. But following the regimen above sends HDL through the roof in the majority.

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Older posts

Lipoprotein(a), Lp(a), can be a tough nut to crack.

Having struggled and wrestled with this genetic pattern for the last 12 years or so in hundreds of patients, I have gained great respect for this difficult to control pattern.

I regard lipoprotein(a) as the number one most aggressive cause for heart disease and coronary plaque known. It can account for heart attacks in men in their 40s, women in their 50s. It can cause heart disease and heart attacks in even the ultra-fit like marathon runners. It accounts for both excessive coronary risk and misleading cholesterol values in slender, healthy-appearing people.

Niacin is the number one treatment choice for Lp(a), followed by testosterone for men, estrogens (preferably human, not horse or other non-human mammal) for women. I then often resort to DHEA, along with adjunctive nutritional agents like raw almonds, ground flaxseed, and others.

Our most recent addition to the Lp(a) treatment list is high-dose fish oil, which appears to exert a significant effect in about 40% of people with Lp(a).

Even with this multi-agent approach, not everybody gains control over Lp(a).

That makes me wonder if someone has Lp(a) at a substantial level of, say, 200 nmol/L or 70 mg/dl (values can differ tremendously, depending on the method of measurement), should we throw everything but the kitchen sink at Lp(a) from the start? Right now, by adding an agent one at a time, it often takes two years to gain control over Lp(a) (if we are going to get it at all).

While many people might find this unpalatable and overwhelming from the starting gate of their program, I do believe it may be a strategy we should consider adopting for full and more immediate plaque control in the Track Your Plaque program. Something to chew on.

Clearly, we need better answers for Lp(a). A "kitchen sink," full-frontal assault might be a way to gain faster control, though not necessarily a superior approach with regards to efficacy and potency.

There are a number of unique, potentially effective therapies for Lp(a) that are worth examining. Given the difficulty of performing clinical trials with non-drug agents (largely a lack of financial support, since nobody gets a financial return with non-patent-protectable agents), I am anxious to put these potential treatments to a test in the Track Your Plaque program Virtual Clinical Trail (VCT). The VCT gives us a quick and relatively easy method to test various potential treatments, with feedback generated in months, rather than years.

Any suggestions on promising agents to test? Of course, they must be widely available nutritional agents, not drugs.

Colleen started with the usual discrepancy between conventional calculated LDL cholesterol of 121 mg/dl and the far more accurate LDL particle number (NMR) of 1927 nmol/L.

Those of you following this conversation or our many conversations on the Track Your Plaque Forum know that a useful and highly reliable rule-of-thumb for converting NMR LDL particle number to LDL is to drop the last digit: 1927 nmol/L becomes 192 mg/dl. (This is, admitttedly, arrived at empirically, not by design. However, it has held up through thousands of NMR analyses and plays out reasonably when you compare distributions of Friedewald LDL and LDL particle number on a population basis.)

In other words, by this simple manipulation, Colleen's Friedewald calculated LDL is off by 58%. This is very common, a phenomenon I witness several times every day.

By LDL particle size, 75% of all Colleen's LDL particle were abnormally small (small LDL particle number 1440 nmol/L). This is a moderately severe small LDL tendency.

So we took all the steps for reduction of small LDL/LDL, including elimination of wheat and cornstarch, exercise, weight loss (which happens inevitably when wheat and cornstarch are eliminated), fish oil, vitamin D, etc.

Another NMR lipoprotein panel showed an LDL particle number of 882 nmol/L and a Friedewald calculated LDL of 87 mg/dl. Using our rule-of-thumb, LDL by particle number is virtually the same as the calculated LDL. This time, small LDL numbered only 237 nmol/L, or 26.8% of the total, a marked reduction.

Isn't that interesting? As small LDL is corrected, the crude Friedwald calculated LDL approximates the more accurate LDL particle number.

It assumes that accuracy of the Friedewald calculation may be more likely to occur as LDL size approaches normal. However, when LDL size is abnormally small--a condition shared by at least 70% of people with coronary heart disease--then the Friedewald LDL becomes increasingly inaccurate.

The opposite can also happen: When all or nearly all LDL particles are large, Friedewald calculated LDL can markedly overestimate LDL particle number. Yesterday, for instance, a patient had a Friedewald calculated LDL of 183 mg/dl, but an NMR particle number of 1110 nmol/L--drop the zero . . . LDL 110 mg/dl. This woman was advised to take a statin drug by her primary care physician, based on the Friedewald LDL. Instead, she proved to have a far lower LDL. She would not have benefitted from taking a statin drug.

As I've warned many times before: Beware the Friedewald calculated LDL.

The last post on vitamin D raised a number of basic questions among readers. So let me discuss some of these questions one by one. All of them raise important issues surrounding the practical aspects of managing vitamin D in your health.

Anne said:

I think it is important to stress that vitamin D supplementation needs to be continued long term.

I have met too many people who have been prescribed 50,000 IU of D2 for 8-12 weeks and then told to stop because their 23(OH)D went over 30ng/ml. I know one person who's doctor stopped and started the D2 3 times.

Thanks for pointing that out, Anne. Excellent point. I also see doctors do this with statin drugs: start it, check a LDL level which is lower, then think that you're done and stop the drug. What the heck are they thinking?

If vitamin D is not being produced by sun exposure and not obtainable through diet, continued supplementation is necessary, essentially for life.

Twinb asked:

How often you think Vit. D levels should be tested after the initial test is done, especially if the levels are drastically low?

We have used every 6 months in the office. Ideally, levels are in mid-summer and mid- to-late winter in order to gauge the extremes of your seasonal fluctuations. While most adults over 40 fail to fluctuate more than 10 ng/ml in the Wisconsin climate (and this summer, after an initial rainy season early, has been flawlessly bright and sunny, in the high-70s and 80s every single day for months), an occasional person fluctuates more widely. The only way to judge is to check a blood level.

Rich said:

Vitamin D dosage effects appear to be quite idiosyncratic.

Yes, indeed it is. Despite using crude rules-of-thumb, like taking 1000 units of vitamin D per 10 ng/ml desired (a rule I learned from Dr. John Cannell, which he offered fully aware of its inaccuracy), many people will surprise you and have levels that make no sense. Testing is crucial to know your vitamin D level.

Richard asked: Where do we get enough vitamin D wihout worring about laboratory tests?

Well, the entire point of the post was that you absolutely, positively cannot just take vitamin D blindly at any dose and hope that your level is ideal, no more than you can blindly take a dose of thyroid and know you have achieved normal thyroid levels. In my view, vitamin D blood levels are an absolute.

Another simple issue: Don't be afraid of vitamin D. It is, in all practicality, no more dangerous than getting a dark tan. (But, as many of you realize, getting a tan is no assurance of raising vitamin D if you are over 40 years old.)

Wouldn't it be great if someone developed a do-it-yourself-at-home skin test for vitamin D? I know of no effort to develop this, but it would be a huge advantage for all of us.

It’s probably the number one most common question I get today:

“How much vitamin D should I take?”

Like asking for investing advice, there are no shortage of people willing to provide answers, most of them plain wrong.

The media are quick to offer advice like “Take the recommended daily allowance of 400 units per day,” or “Some experts say that intake of vitamin D should be higher, as high as 2000 units per day.” Or “Be sure to get your 15 minutes of midday sun.”

Utter nonsense.

The Food and Nutrition Board of the Institute of Medicine has been struggling with this question, also. They have an impossible job: Draft broad pronouncements on requirements for various nutrients by recommending Recommended Daily Allowances (RDA) for all Americans. The Food and Nutrition Board has tried to factor in individual variation by breaking vitamin D requirements down by age and sex, but what amounts to a one-size-fits-nearly-all approach.

Much of the uncertainty over dosing stems from the fact that vitamin D should not be called a “vitamin.” Vitamins are nutrients obtained from foods. But, outside of oily fish, you'll find very little naturally-occurring vitamin D in food. (Even in fish, there is generally no more than 400 units per 4 oz. serving.) Sure, there’s 20 units in an egg yolk and you can activate the vitamin D in a shiitake mushroom by exposing it to ultraviolet radiation. Dairy products like milk (usually) contain vitamin D because the USDA mandates it. But food sources hardly help at all unless you’re an infant or small child.

It all makes sense when vitamin D is viewed as a hormone, a steroid hormone, not a vitamin. Vitamin-no, steroid hormone-D exerts potent effects in tiny quantities with hormone-like action in cells, including activation of nuclear receptors.

It is the only hormone that is meant to be activated by sun exposure of the skin, not obtained through diet. But the ability to activate D is lost by the majority of us by age 40 and even a dark tan is no assurance that sufficient skin prohormone D activation has taken place.

As with any other hormone, such as thyroid, parathyroid, or growth hormones, dose needs to be individualized.

Imagine you developed a severely low thyroid condition that resulted in 30 lbs of weight gain, lose your hair, legs swell, and heart disease explodes. Would you accept that you should take the same dose of thyroid hormone as every other man or woman your age, regardless of your body size, proportion of body fat, metabolism, genetics, race, dietary habits, and other factors that influence thyroid hormone levels? Of course you wouldn’t.

Then why would anyone insist that vitamin D be applied in a one-size-fits-all fashion? (There’s another world in which a one-size-fits-all approach to hormone replacement has been widely applied, that of female estrogen replacement. In conventional practice, there’s no effort to identify need, estrogen-progesterone interactions, nor assess the adequacy of dose, not to mention the perverse non-human preparation used.)

With thyroid hormone, ideal replacement dose of hormone ranges widely from one person to another. Some people require 25 mcg per day of T4; others require 800% greater doses. Many require T3, but not everybody.

Likewise, vitamin D requirements can range widely. I have used anywhere from 1000 units per day, all the way up to 16,000 units per day before desirable blood levels were achieved.

Vitamin D dose needs to be individualized. Factors that influence vitamin D need include body size and percent body fat (both of which increase need substantially); sex (males require, on average, 1000 units per day more than females); age (older need more); skin color (darker-skinned races require more, fairer-skinned races less); and other factors that remain ill-defined.

But these are “rules” often broken. My office experience with vitamin D now numbers nearly 1000 patients. The average female dose is 4000-5000 units per day, average male dose 6000 units per day to achieve a blood level of 60-70 ng/ml, though there are frequent exceptions. I’ve had 98 lb women who require 12,000 units, 300 lb men who require 1000 units, 21-year olds who require 10,000 units. (Of course, this is a Wisconsin experience. However, regional differences in dosing needs diminish as we age, since less and less vitamin D activation occurs.)

Let me reiterate: Steroid hormone-vitamin D dose needs to be individualized.

There’s only one way to individualize your need for vitamin D and thereby determine your dose: Measure a blood level.

Nobody can gauge your vitamin D need by looking at you, by your skin color, size, or other simple measurement like weight or body fat. A vitamin D blood level needs to be measured specifically-period.

Unfortunately, many people balk at this, claiming either that it’s too much bother or that their doctor refused to measure it.

I would rank normalizing steroid hormone-vitamin D as among the most important things you can do for your health. It should never be too much bother. And if your doctor refuses to at least discuss why he/she won’t measure it, then it’s time for a new doctor.

If you’re worried about adding to rising healthcare costs by adding yet another blood test, think of the money saved by sparing you from a future of cancer, heart disease, osteoporosis, diabetes, etc. The cost of a vitamin D blood test is relatively trivial (around $40-50, a fraction of the cost of a one month supply of a drug for diabetes.)

So how much vitamin D should you take? Enough to raise your blood level of 25-hydroxy vitamin D to normal. (We aim for a normal level of 60-70 ng/ml.)

The results of the recent Heart Scan Blog survey in response to the question: MY DAILY DOSE OF EPA + DHA FROM FISH OIL IS revealed:

Zero--I don't take any
17 (7%) of respondents

Less than 1000 mg per day
24 (10%) of respondents

1000-2000 mg per day
91 (38%) of respondents

2000-3000 mg per day
44 (18%) of respondents

3000-4000 mg per day
40 (16%) of respondents

More than 4000 mg per day
20 (8%) of respondents

Based on the above results, I would say that only a minority of respondents are taking an ideal dose of omega-3 fatty acids. Nearly all of us should consider taking more.

Benefits of omega-3 fatty acids (EPA + DHA) from fish oil begin around a dose of 840 mg per day, according to the GISSI Prevenzione Trial of 1999, an 11,000-participant trial. This dose also corresponds to a quantity of omega-3s that have been shown to raise EPA + DHA blood levels and thereby reduce the notoriously high AA:EPA ratio of Americans.

But what dose is sufficient? What dose is ideal?

Well, the answer to a great degree depends on what you are taking the fish oil for. If being taken to reduce triglycerides and triglyceride-containing lipoproteins, like VLDL and the after-eating (postprandial) IDL, then a higher dose will be necessary. (Triglyceride reduction for the genetically-determined very high triglyceride level of familial hypertriglyceridemia is the FDA-approved indication for prescription Lovaza.)

If you are taking fish oil for treatment of ADHD, depression, or bipolar illness, very high doses are often necessary.

But how about maximal reduction of cardiovascular risk and for control or reversal of atherosclerotic plaque?

This conversation is still evolving. But we can learn some important lessons from three populations of the world that are vigorous consumers of fish:

--The Inuits (aka Eskimos) of Greenland and northern Canada
--The Japanese
--The Bantus of Tanzania who live along Nyasa Lake

All three indigenous populations have several-fold greater intakes of fish and omega-3 fatty acids, have higher blood levels of omega-3 fatty acids, and have enjoyed reduced cardiovascular events, reduced atherosclerotic plaque, or improvement in various surrogates of cardiovascular risk (e.g., Lp(a)).

The most recent addition to this conversation is the ERA JUMP Study, discussed in a previous Heart Scan Blog post. In ERA JUMP, despite being heavy smokers and having other markers for greater risk for heart disease, Japanese men living in Japan had markedly less carotid and coronary plaque, as compared to Caucasian men living in PIttsburgh or Hawaiian men of Japanese descent. The difference appeared to be attributable to serum levels of omega-3 fatty acids.

I believe that the trend is here is to increase the amount of omega-3 fatty acids that most of us take. In the Track Your Plaque program, we have been advocating a rock-bottom starting dose of EPA + DHA of 1200 mg per day. However, I believe that this is due for a change.

We will be increasing the minimum dose for plaque regression and control. Please attend our Webinar this evening for a full, in-depth discussion of the rationale behind this important change.

As always, let me remind you that I am not selling, nor ever have sold, fish oil supplements. If I advocate a specific dose, a higher dose, I do so based on my interpretation of the data and experience with patients, not because I am interested in selling brand X of fish oil.

Despite the paucity of scientific documentation of this phenomenon, I am continuing to witness extraordinary increases in HDL cholesterol levels with vitamin D supplementation.

I've touched on the interaction of vitamin D supplementation with HDL in The Heart Scan Blog previously:

Vitamin D: Treatment for metabolic syndrome?

HDL for Dummies

At first, I thought it was attributable to other factors. In real life, most people don't modify one factor at a time. They reduce
processed carbohydrates/eliminate wheat and cornstarch, lose weight, add or increase omega-3 fatty acids from fish oil, begin niacin, increase exercise and physical activity. All these efforts also impact on HDL.

Among the many things I do, I consult on complex lipid (cholesterol) disorders (complex hyperlipidemias) in my office. A substantial number of these people carry a diagnosis of hypoalphalipoproteinemia, a mouthful that simply means these people are unable to manufacture much apoprotein A1, the principal protein of HDL cholesterol particles. As a result, people with hypoalphalipoproteinemia have HDL cholesterol levels in the neighborhood of 20-30 mg/dl--very low. They are also at high risk for heart disease and stroke.

Encourage these people to exercise, attain ideal weight, eliminate wheat and cornstarch: HDL increases 5 mg/dl or so.

Add niacin, HDL increases another 5-10 mg/dl.

Perhaps we're now sitting somewhere around an HDL of 35-40 mg/dl--better, but hardly great.

Add vitamin D to achieve our target serum level . . . HDL jumps to 50, 60, 70, even 90 mg/dl.

The first few times this occurred, I thought it was an error or fluke. But now that I've witnessed this effect many dozens of time, I am convinced that it is real. Just today, I saw a 40-year old man whose starting HDL was 25 mg/dl increase to 87 mg/dl.

Responses like this are supposed to be impossible. Before vitamin D, I had never witnessed increases of this magnitude.

Not all therapies for raising HDL raise the important large (also known as HDL2b) fraction. With lipoprotein analyses, it appears that is principally the large fraction of HDL that rises with vitamin D supplementation.

Why? How?

That I can't tell you. But for those of you struggling with low HDL cholesterols despite your best efforts, vitamin D can make a world of difference.

An interesting corollary: If super-high HDL cholesterols are associated with extreme longevity, as they are with centenarians, does raising HDL to extraordinary levels with vitamin D lead to longer, healthier life, all the way up to age 110 years?

Again, no answers, but an interesting thought. And one I'd bet on. (And I'm not selling vitamin D.)

Here's another thought with regards to time issues with weight loss: reductions in blood pressure (BP).

The previous post talked about how triglycerides initially go up, sometimes way up, when weight drops, only to be followed months later by substantial drops. HDL initially drops in response to the triglyceride fluctuations, only to be followed by a rise.

Blood pressure also shows a curious pattern that is largely dependent on age.

Say someone in their 20s or 30s, for instance, loses 30 lbs (through elimination of wheat and cornstarch, say). BP usually drops within a few weeks, perhaps a month or two at most.

How about someone in their 70s? Say a substantial amount of weight is lost, say 50 lbs over 6 months. BP does indeed drop, but it may require 6 months or longer after weight plateaus for the full effects of BP-reduction to be fully expressed. But it will eventually drop.

Why the age-dependent difference?

It relates to the capacity of arteries to remain flexible and distensible. Over the years, cross-linking of collagen (a structural protein), glycation (glucose molecules attaching to proteins), loss of endothelial responsiveness to generate artery-dilating substances like nitric oxide, and arterial atherosclerotic plaque all all up to making older arteries less able to "relax" and BP to drop.

But given time and the proper effort, BP will eventually drop. Awareness of this time effect can help most people decide better when medications are necessary or if weight loss alone is sufficient to reach BP goals.

Brad needed to lose weight.

At 6 ft tall, he began the program at 291 lbs, easily 80 lbs overweight. He wore virtually all of it in his belly.

He had laboratory numbers to match: HDL 33 mg/dl, triglycerides 225 mg/dl, LDL (calculated) 144 mg/dl, blood sugar 122 mg/dl (fasting--clearly "pre-diabetic"), c-reactive protein 3.0 mg/dl. Among his lipoprotein abnormalities: small LDL representing 80% of all LDL (no surprise).

Readers of The Heart Scan Blog know that these are the patterns of the carbohydrate-indulgent. I asked Brad to eliminate all wheat flour products, all foods made with cornstarch, and follow a diet rich in healthy oils, raw nuts, vegetables, and lean meats.

Brad returned for a discussion about follow-up basic lipids (cholesterol) values four months later--31 lbs lighter, most of it clearly lost from his abdomen. He claimed he felt more energetic and clear-headed than he had in years.

His lipid panel: HDL 34 mg/dl, LDL 122 mg/dl, triglycerides 295 mg/dl. Brad's smile dissolved. "How could that happen? You said losing weight would make my HDL go up and my triglycerides go down!"

Yes, I had said that. But I was oversimplifying.

The truth is that, when there is weight loss, especially profound weight loss like Brad experienced eliminating wheat and cornstarch products, there is mobilization of fat stores. Fat is stored energy. Energy is stored as . . . triglycerides.

So when there is substantial weight loss, there is a flood of triglycerides in the blood, and triglyceride levels in the midst of weight loss can commonly jump up, not uncommonly to the 200-300+ mg/dl range. When triglycerides go up, there is also a drop in HDL (triglycerides interact with HDL particles, modify their structure and make them more readily destroyed, thereby dropping blood levels). Occasionally, substantial weight loss like Brad experienced will drop HDL really low, as low as the 20's.

Once weight stabilizes, this effect can last up to 2 months before correcting. Only then will triglycerides drop and HDL rise. The rise in HDL occurs even more slowly, requiring several more months to plateau.

In other words, weight loss like Brad's causes triglycerides to increase and HDL to decrease, to be followed later by a drop in triglycerides and a rise in HDL.

I know of no way to block this phenomenon. And perhaps we shouldn't, since this is how fat stores are mobilized and "burned off." Fish oil does blunt the triglyceride rise (perhaps through activation of lipoprotein lipase, an enzyme responsible for clearance of triglycerides), but doesn't eliminate it.

I call these changes "transitional" changes in lipids.

Patience pays. A few more months from now, Brad's numbers will be much happier, as will Brad.

The doctor-patient relationship has gone sour.

This probably comes as no surprise to most of you, particularly if you've been following conversations here in The Heart Scan Blog:

Who is your doctor? discussing the emergence of the physician-as-hospital-employee phenomenon that causes your doctor to become the de facto portal (seller?) of hospital services to you, a model fraught with conflicts of interest.

Exploitation of trust, my observation that the enormous gap in heart disease prevention between the woefully ignorant (by necessity) level of sophistication of the primary care physician and the procedure-obsessed cardiologist leads to an exploitation of humans-for-heart-procedures because of the failure to institute genuine preventive efforts.

Bait and switch , a description of how a minor test or symptom can reap a bonanza of medical testing; a $20 "screening" test yields $10's of thousands in hospital procedures. If it were entirely due to the imprecision of medical testing and detection of disease, that might be forgivable. But it often is not: It has become utterly distorted by the profit model.

Lest you think that I am a kook ranting off in some backwoods corner (Milwaukee), here are the comments of New York Times' Health Editor Tara Parker-Pope in a series called Doctor and Patient, Now at Odds:

Lately I've been hearing a lot from patients who are frustrated, angry, and distrustful of doctors. Their feelings speak to a growing disconnect between doctors and patients and worries that drug companies, insurance rules, and hospital cost-cutting are influencing the care and advice that doctors provide.

Research shows that even among patients who like their personal physicians, there is a simmering distrust of the medical system and the doctors who work inside it.

(There's also a series of candid video interviews with people who echo these sentiments.)

There are a number of reasons for this increasing "disconnect," some of them articulated by Ms. Parker-Pope, others detailed in my blog posts.

The solutions, however, will not be found by advancing technology: the newest robotic surgery, a better defibrillator, a new statin drug, the next best chemotherapeutic agent. It will not be found by adding a new wing to the hospital. It will not be found by the reorganization of healthcare delivery achieved by converting primary care and specialty practice into an arm of hospital care. It will not be improved by employing "hospitalists." It will not emerge from legislation controlling insurance company practices. It certainly will not come from increasing marketing dollars spent by drug companies (who make $4 for every $1 spent on direct-to-consumer marketing).

The solutions will come from shifting the idea of care from a paternalistic, "I'm the doctor and I'll tell you what to do" approach, to the doctor-as-advocate-and-supporter of the patient. The physician should act as someone with a particular sort of expertise that can advise a patient.

But a caveat: The patient MUST be informed.

Proper information will not originate with the doctor. It will originate with internet-based information portals and tools that help you understand the issues, often with far greater depth than your doctor could ever provide. The physician needs to accept this role, one of advocate, adviser, but not of being in charge, not of viewing the patient as profit-center, not as an opponent in a power struggle.

Sadly, the last few years in online information portals has been dominated by the drug company-dominated websites like WebMD, nothing more than a deliverer of the conventional wisdom with nothing whatsoever aimed towards empowering patients in a self-directed healthcare model.

Some people call the emerging new empowered and information-armed patient Medicine 2.0. Unfortunately, Medicine 2.0 will first benefit the intellectual upper crust of Americans, the web-savvy and motivated to engage in health issues. But, give it 10 years, and we will witness the effects on an unprecedented broad scale. Part of the Information Age is acceleration of information dissemination. Imagine your children, facile with a computer mouse, posting comments on FaceBook, doing homework with Google and Wikipedia, now turning their attentions to health.

It will be a startling change.

In the meantime, be wary. Be empowered. Think increasingly about self-direction in your health.

In a comment to the Bait and switch post, Jennytoo offered an insightful response:

You are getting to the essence of the problem, and it's not just cardiology that is rife with what is, at bottom, malpractice.

There is little incentive for the profession as a whole to know anything about or promote prevention, and many incentives from hospitals, drug and insurance companies to stick with the status quo or to change it in their corporate favor. The formulaic, conventional statements purporting to be guidelines for prevention that are put out by various interest groups and in such publications as hospital-sponsored newsletters ("eat a 'balanced diet', avoid stress, etc.") are useless sops to the concept of prevention.

It is, and I fear is going to remain, up to motivated individuals, both physicians and patients, to reshape the system, and it's going to be a long frustrating struggle.

It's my personal conviction that if just 4 things were promoted to the public, and people actually practiced them, we could change the health profiles of the majority of people in this country for the better within two years or less. They are:

(1) education on and promotion of a true low-carbohydrate, whole foods, diet,
(2) measurement and supplementation of Vitamin D3,
(3) supplementation with DHA/EPA (found in Fish Oils), and
(4) measurement and supplementation of intracellular magnesium.

I am not a health professional, and others may want to add to this list, but I don't think any strong case can be made against any of the items. The wonderful and hopeful thing is that each of us can implement them ON OUR OWN, and thereby take charge of our own well-being. (The Life Extension Foundation is one organization which provides access to lab tests you can request on your own.)

If you have a physician who is willing and capable of being your partner, you are richly blessed, and that is the ideal we all should hope for. But in the more likely event that you do not have such a physician, and if your physician demonstrates little potential for becoming one, think about firing the one you have and finding another.

Sometimes we are forced by circumstances, particularly urgent ones, to deal with physicians who are not ideal, but the main impetus for change will come from us, the patients, and the expectations we communicate to our individual doctors. In the meantime, we can be self-reliant in our own prevention practices.

Wow. A woman after my own heart.

This post just furthers this line of thinking out loud: How much fish oil is "enough"?

Observations over the last 30 years followed this path: If a little bit of omega-3 fatty acids from fish are beneficial in reducing cardiovascular events, and a moderate intake is even better, is even more better? When have we reached a plateau? When do adverse effects outweigh the benefits?

Some insight can be gained through studies that examined blood levels of omega-3s. Let's take a look at some data from 2002, a comparison of men dying from heart disease vs. controls in the Physicians' Health Study, Blood Levels of Long-Chain n–3 Fatty Acids and the Risk of Sudden Death.

This is a table that shows the blood levels of various fatty acids Group with sudden death vs Control Group:

Several observations jump out:

--The total omega-3 blood content differed significantly, 4.82 vs 5.24% ("Total long-chain n-3 polyunsaturated")
--Total omega-6 content did not differ
--Arachidonic acid (AA) content did not differ
--Linolenic acid content did not differ (i.e., plant sourced omega-3)

The fact that neither omega-6 nor arachidonic acid content differed counters the argument that Simopoulos has made that the omega-6 to omega-3 ratio (intake, not blood levels) is what counts. It also argues against the EPA to AA ratio (and similar manipulations) that some have argued is important. In this study, only the omega-3 level itself made a difference; no ratio was necessary to distinguish sudden death victims vs controls.

Further, quartiles of omega-3 blood levels showed graded reductions of risk:

An omega-3 blood level of 6.87% conferred greatest risk reduction. Depending on the model of statistical analysis, risk reductions of up to 81-90% were observed. Wow.

Taken at face value, this study would argue that:

--An omega-3 fatty acid blood level of 6.87% (or greater?) is ideal
--The omega-3 fatty acid blood level stands alone as a predictor without resorting to any further manipulation of numbers, such as relating EPA and/or DHA to AA levels.

Of course, this is just one study, though an important one. It is also not a study based on any intervention, just an observational effort. But it does add to our understanding.

We will develop these issues further in our upcoming Track Your Plaque Webinar on Wednesday, August 20th, 2008.

Bait and switch

A fictional tale of medical economics in heart disease

Disease engineering

Free checking, auto shows, low-cost hotel rooms, and bypass surgery

No-flush niacin kills

Breakfast comments

What's for breakfast?

The first lawsuit?

The origins of heart catheterization: Part II

The origins of heart catheterization: Part I

For the sake of convenience: Commercial sources of prebiotic fibers

60-year old man dies of high cholesterol

Back to basics: Coronary calcium

Myocardial infraction

Diet is superior to drugs

Low-carb is heart healthy

Mocha Walnut Brownies

Are you hungry?

Chocolate . . . for adults only

"Friday is my bad day"

HDL 80 mg/dl

Kitchen sink approach for Lp(a)

Making Dr. Friedewald an honest man

Some basic vitamin D issues

“How much vitamin D should I take?”

You probably don't take enough fish oil

Vitamin D and HDL

Weight loss and blood pressure

"I lost 30 lbs and my triglycerides went . . . up?"

Divorce court for the doctor-patient relationship?

How much fish oil is enough?