You just THINK you're low-carb

Systematically checking postprandial (after-eating) blood sugars is providing some great insights into crafting a better diet for many people.

I last discussed the concept of postprandial glucose checks in To get low-carb right, you need to check blood sugars.

Here are some important lessons that many people--NON-diabetic people, most with normal blood glucoses or just mildly increased--are learning:

Oatmeal yields high blood sugars. Even if your fasting blood sugar is 90 mg/dl, a bowl of oatmeal with skim milk, walnuts, and some berries will yield blood sugars of 150-200 mg/dl in many people.

Cheerios yields shocking blood sugars. 200+ mg/dl is not uncommon in non-diabetics. (Diabetics have 250-350 mg/dl.)

Fruits like apples and bananas increase blood sugar to 130 mg/dl or higher.

Odd symptoms, such as mental "fog," fatigue, and a fullness in the head, are often attributable to high blood sugars.

A subset of people with lipoprotein(a) can have wildly increased blood sugars despite their slender build and high aerobic exercise habits.


Once you identify the high blood sugar problem, you can do something about it. The best place to start is to reduce or eliminate the sugar-provoking food.

The LDL-Fructose Disconnect

I believe that we can all agree that the commonly obtained Friedewald LDL cholesterol (what I call "fictitious" LDL cholesterol) is wildly inaccurate. 100%--yes, 100% inaccuracy--is not at all uncommon.

This flagrant inaccuracy, unacceptable in virtually every other discipline (imagine your airplane flight to New York lands in Pittsburgh--close enough, isn't it?), is highlighted in the University of California study by Stanhope et al I discussed previously.

32 participants consumed either a diet enriched with either fructose or glucose. Compared to the effect of glucose, after 10 weeks fructose:

Increased LDL cholesterol (calculated) by 7.6%

Increased Apoprotein B (a measure of the number of LDL particles) by 24%

Increased small dense LDL by 41%

Increased oxidized LDL by 12.6%



In other words, conventional calculated LDL substantially underestimates the undesirable effects of fructose. The divergence between calculated LDL and small LDL is especially dramatic. (By the way, this same divergence applies to the studies suggesting that calculated LDL cholesterol is reduced by low fat diets--While calculated LDL may indeed be reduced, small LDL goes way up, a striking divergence.)

This is yet another reason to not rely on this "fictitious" LDL cholesterol value that, inaccuracies notwithstanding, serves as the foundation for a $27 billion per year industry.

"I dream about bread"

Marion sat in my office, sobbing.

It had been 4 weeks since the last piece of bread, bagel, or bun had passed her lips.

"I can't do it! I just can't do it! I've tried to eliminate wheat, but it's making me crazy. I'm having dreams about bread!"

Yes, Timmy, such dark corners of human behavior are truly unveiled by removing wheat from the diet. (See the previous Heart Scan Blog post, Wheat withdrawal.)

This is a real phenomenon: Wheat is the crack cocaine of the masses. Maybe you don't exchange $100 bills in dark corners of an inner city crack house, but I'll bet you paid $3.99 for your latest fix of French bread.

Just in the last 2 weeks, people in my office who have eliminated wheat have experienced:

14 lbs weight loss in 14 days

Increased mental clarity, reduced moodiness, deeper sleep

70% reductions in small LDL

More than 300 mg/dl reductions in triglycerides

Relief from chronic scalp rash


I could go on.

All the while, the USDA, the American Heart Association, the American Diabetes Association, the American Dietetic Association, the Surgeon General's Office all advise you to eat more "healthy whole grains."

70% of people (NOT 100%, but the majority) will experience unexpected health benefits by eliminating this corrupt, unphysiologic product called wheat from their diet.

You won't know until you try.

Prototypical Lipoprotein(a)

Here's the prototypical male with lipoprotein(a):



Several features stand out in the majority of men with lipoprotein(a), Lp(a):

Slender--Sometimes absurdly so: BMIs of 21-23 are not uncommon. These are the people who claim they can't gain weight.

Intelligent--Above average to way above average intelligence is the rule.

Gravitate to technical work--Plenty of engineers, scientists, accountants, and other people who work with numbers and/or technical details are more likely to have Lp(a).

Enjoy high levels of aerobic performance--I tell my Lp(a) patients that, if they want to see a bunch of other people with Lp(a), go to a marathon or triathlon. They'll see plenty of people with the pattern among the aerobically-elite.

Are rabid fans of Star Trek.


Okay, I made the last one up. But the rest are uncannilly true, shared by the majority (though not all) men with Lp(a).

Why? I can only speculate that the gene(s) for Lp(a) are closely linked to gene(s) for intelligence of a quantitative kind and some factor that enhances aerobic performance or yields a desirable emotional state with exercise.

Oddly, the same patterns tend not to occur in women in Lp(a). I have yet to discern a personality or body configuration phenotype among the ladies.

Gastric emptying: When slower is better

When it comes to the Internet and Nascar, speed is good: The faster the better.

But when it comes to gastric emptying (the rate at which food passes from the stomach and into the duodenum and small intestine), slower can be better.

Slower transit time for foods passing through the stomach leads to lower blood sugar, lower blood glucose area under-the-curve (AUC), i.e., reduced blood glucose levels over time. Lower postprandial (after-eating) blood sugars can reduce cardiovascular risk. It can lead to a reduction in net calorie intake and weight loss.

Strategies that can slow gastric emptying include:

--Minimizing fluids during a meal--Drinking a lot of fluids, e.g., water, accelerates gastric emptying by approximately 20%.

--Cinnamon--While the full reason to explain Cassia cinnamon's blood glucose-reducing effect has not been completely worked out, part of the effect is likely to due slowed gastric emptying. Thus, a 1/4-2 teaspoons of cinnamon per day can reduce postprandial blood sugar peaks by 10-25 mg/dl.

--Vinegar--Two teaspoons of vinegar in its various forms slows gastric emptying. The effect is likely due to acetic acid, the compound shared by apple cider vinegar, white vinegar, red wine vinegar, Balsamic vinegar, and other varieties.

--Increased fat content--Fat is digested more slowly and slows gastric emptying time, compared to the rapid transit of carbohydrates.

Not everybody should slow gastric emptying. Diabetics with a condition called diabetic gastroparesis should not use these methods, as they can further slow the abnormal gastric emptying that develops as part of their disease, making a bad situation worse.

However, in the rest of us with normal gastric emptying time, a delay in gastric emptying can reduce blood sugar and induce satiety, effects that can work in your favor in reducing cardiovascular risk.

Genetic vs. lifestyle small LDL

Let me explain what I mean by "genetic small LDL." I think it helps to illustrate with two common examples.

Ollie is 50 years old, 5 ft 10 inches tall, and weighs 253 lbs. BMI = 36.4 (obese). Starting lipoproteins (NMR):

LDL particle number 2310 nmol/L
Small LDL: 1893 nmol/L
(1893/2310 = 81.9% of total, a severe small LDL pattern)


Stan is 50 years old, also, 5 ft 10 inches tall, and weighs 148 lbs. BMI = 21.3. Starting lipoproteins:

LDL particle number 1424 nmol/L
Small LDL 1288 nmol/L
(1288/1424 = 90.4% of total, also severe)


Both Ollie and Stan go on the New Track Your Plaque diet and eliminate wheat, cornstarch, and sugars, while increasing oils, meats and fish, unlimited raw nuts, and vegetables. They add fish oil and vitamin D and achieve perfect levels of both. Six months later, Ollie has lost 55 lbs, Stan has lost 4 lbs. A second round of lipoproteins:

Ollie:

LDL particle number 1810 nmol/L
Small LDL: 193 nmol/L
(193/1810 = 10.6% of total)


Stan:

LDL particle number 1113 nmol/L
Small LDL 729 nmool/L
(729/1113 = 65.4% of total)


Ollie has reduced, nearly eliminated, small LDL through elimination of wheat, cornstarch, and sugars, along with weight loss, fish oil, and vitamin D.

Stan, beginning at a much more favorable weight, reduced both total and small LDL with the same efforts, but retains a substantial proportion (65.4%) of small LDL.

Stan's pattern is what I call "genetic small LDL." Of course, this is a presumptive designation, since we've not identified the specific gene(s) that allow this (e.g., gene for variants of cholesteryl ester transfer protein, hepatic lipase, lipoprotein lipase, and others). But it is such a sharp distinction that I am convinced that people like Stan have this persistent pattern as a genetically-determined trait.

Carbohydrate sins of the past

Fifty years ago, diabetes was a relatively uncommon disease. Today, the latest estimates are that 50% of Americans are now diabetic or pre-diabetic.

There are some obvious explanations: excess weight, inactivity, the proliferation of fructose in our diets. It is also my firm belief that the diets advocated by official agencies, like the USDA, the American Heart Association, the American Dietetic Association, and the American Diabetes Association, have also contributed with their advice to eat more “healthy whole grains.”

When I was a kid, I ate Lucky Charms® or Cocoa Puffs® for breakfast, carried Hoho’s® and Scooter Pies® in my lunchbox, along with a peanut butter sandwich on white bread. We ate TV dinners, biscuits, instant mashed potatoes for dinner. Back then, it was a matter of novelty, convenience, and, yes, taste.

What did we do to our pancreases eating such insulin-stimulating foods through childhood, teenage years, and into early adulthood? Did our eating habits as children and young adults create diabetes many years later? Could sugary breakfast cereals, snacks, and candy in virtually unlimited quantities have impaired our pancreas’ ability to produce insulin, leading to pre-diabetes and diabetes many years later?

A phenomenon called glucose toxicity underlies the development of diabetes and pre-diabetes. Glucose toxicity refers to the damaging effect that high blood sugars (glucose) have on the delicate beta cells of the pancreas, the cells that produce insulin. This damage isirreversible: once it occurs, it cannot be undone, and the beta cells stop producing insulin and die. The destructive effect of high glucose levels on pancreatic beta cells likely occurs through oxidative damage, with injury from toxic oxidative compounds like superoxide anion and peroxide. The pancreas is uniquely ill-equipped to resist oxidative injury, lacking little more than rudimentary anti-oxidative protection mechanisms.

Glucose toxicity that occurs over many years eventually leaves you with a pancreas that retains only 50% or less of its original insulin producing capacity. That’s when diabetes develops, when impaired pancreatic insulin production can no longer keep up with the demands put on it.

(Interesting but unanswered question: If oxidative injury leads to beta cell dysfunction and destruction, can antioxidants prevent such injury? Studies in cell preparations and animals suggest that anti-oxidative agents, such as astaxanthin and acetylcysteine, may block beta cell oxidative injury. However, no human studies have yet been performed. This may prove to be a fascinating area for future.)

Now that 50% of American have diabetes or pre-diabetes, how much should we blame on eating habits when we were younger? I would wager that eating habits of youth play a large part in determining potential for diabetes or pre-diabetes as an adult.

The lesson: Don’t allow children to repeat our mistakes. Letting them indulge in a lifestyle of soft drinks, candy, pretzels, and other processed junk carbohydrates has the potential to cause diabetes 20 or 30 years later, shortening their life by 10 years. Kids are not impervious to the effects of high sugar, including the cumulative damaging effects of glucose toxicity.

Saturated fat and large LDL

Here's a half-truth I often encounter in low-carb discussions:

Saturated fat increases large LDL particles


For those of you unfamiliar with the argument, I advocate a low-carbohydrate approach, specifically elimination of all wheat, cornstarch, and sugars, to reduce expression of the small LDL pattern (not to mention reduction of triglycerides, relief from acid reflux and irritable bowel, weight loss, various rashes, diabetes, etc). Small LDL particles have become the most common cause for heart disease in the U.S., exploding on the scene ever since agencies like the USDA and American Heart Association have been advising the public to increase consumption of "healthy whole grains."

This has led some to make the pronouncement that saturated fat increases large LDL, thereby representing a benign effect.

Is this true?

It is true, but only partly. Let me explain.

There are two general categories of factors causing small LDL particles: lifestyle (overweight, excess carbohydrates) and genetics (e.g., variants of the gene coding for cholesteryl-ester transfer protein, or CETP).

If small LDL is purely driven by excess carbohydrates, then adding saturated fat will reduce small LDL and increase large LDL.

If, on the other hand, your small LDL is genetically programmed, then saturated fat will increase small LDL. In other words, saturated fat tends to increase the dominant or genetically-determined form of LDL. If your dominant genetically-determined form is small, then saturated fat increases small LDL particles.

So to say that saturated fat increases large LDL is an oversimplification, one that can have dire consequences in the wrong situation.

Is glycemic index irrelevant?



University of Toronto nutrition scientist, Dr. David Jenkins, was the first to quantify the phenomenon of "glycemic index," describing how much blood sugar increased over 90 minutes compared to glucose. The graph is from their 1981 study, The glycemic index of foods: a physiologic basis for carbohydrate exchange. The research originated with an effort to characterize carbohydrates for diabetics to gain better control over blood sugar.

Since Dr. Jenkins’ original work, thousands of clinical studies have been performed by others exploring this concept. The food industry has also devoted plenty of effort exploiting it (e.g., low-glycemic index noodles, low-glycemic index cereals, etc.).

Most Americans are now familiar with the concept of glycemic index. You likely know that table sugar has a high glycemic index (60), increasing blood sugar to a similar degree as white bread (glycemic index 71). Oatmeal (slow-cooked) has a lower glycemic index (48), since it increases blood sugar less than white bread.

A number of studies have shown that when low glycemic index foods replace high glycemic index foods (e.g., whole wheat bread in place of cupcakes), people are healthier: less diabetes, less heart attack, less high blood pressure. Books have been written about glycemic index, touting its benefits for health and weight control. Health-conscious people will try to substitute low-glycemic index foods for high-glycemic index foods.

So what’s not to like here?

There are several fundamental flaws with the notion that low-glycemic index foods are good for you:

1) Check your blood sugar after a low-glycemic index food like oatmeal. Most non-diabetic adults will show blood sugars in the 140 to 200 mg/dl range. The more central (visceral) fat you have, the higher the value will be. In other words, an apparently “healthy” whole grain food like oatmeal can generate extravagantly high blood sugars. Repeated high blood sugars of 125 mg/dl or greater after eating increase heart disease risk by 50%.

2) Foods like whole wheat pasta have a low glycemic index because the blood sugar effect over the usual 90 minutes is increased to a lesser degree. The problem is that it remains increased for an extended period of up to several hours. In other words, the blood sugar-increasing effect of pasta, even whole grain, is long and sustained.

3) Low-glycemic index foods trigger other abnormalities, such as small LDL particles, triglycerides, and c-reactive protein (a measure of inflammation). While they are not as bad as high-glycemic index foods, they are still quite potent triggers.

Low-glycemic index foods trigger the very same responses as high-glycemic index foods—they’re just less bad. But less bad does not equate to good. Low-glycemic index foods cause weight gain, trigger appetite, increase blood pressure, and lead to the patterns that cause heart disease.

High-glycemic index foods are bad for you. This includes foods made with white flour (bagels, white bread, pretzels). Low-glycemic foods (whole grain bread, whole wheat crackers, whole wheat pasta) are less bad for you—but they are not necessarily good.

Don’t be falsely reassured by foods because they are billed as “low-glycemic index.” View low-glycemic index foods as indulgences, something you might have once in a while, since a slice of whole grain bread is really not that different from a icing-covered cupcake.

Heart scan curiosities 1

Heart scans often reveal more than coronary plaque. From time to time, I'll show some curious findings that people have displayed during routine heart scans.

This 65-year old man had a relatively low heart scan score of 73, but showed an impressive quantity of calcification of his pericardium, the usually soft-tissue sack that encases the heart. The calcified pericardium is the white arcs that surround the heart in the center of the image.



Thankfully, because he's without any symptoms of breathlessness, excessive fatigue, or leg swelling, he won't need to have it surgically corrected. When the pericardium becomes rigid and encircles the heart, it can literally squeeze the heart, a condition called "constrictive pericarditis". The surgery is pretty awful.

This man's calcified pericardium likely resulted from one or more viral infections over his lifetime.

Annual physical

A judge who lives in my neighborhood was found dead in his bed this week from a heart attack. He was 49 years old. His teenage kids found him and performed CPR, but he was cold and long-gone by then.

A close friend of the judge told me that he'd passed an annual physical just weeks before.

This sort of tragedy shouldn't happen. It is easily--easily--preventable. Had this man undergone a heart scan, a score of at least 400 if not >1000 would have been uncovered, and appropriate preventive action could have been taken. The conversation could have centered around the strategies to correct the patterns that triggered his plaque and how he could reduce his score.

Of course, hospitals make use of stories like this to fuel fear that brings hordes to their wards for procedures. Would the judge have required a procedure to save his life, had his heart disease been diagnosed at his annual physical? Not necessarily. Hospitals and cardiologists would try to persuade you that procedures have an impact on mortality. This is simply not true. In fact, the mortality benefits of procedures are questionable except in the midst of acute illness (e.g., unstable chest pain symptoms or heart attack).

Don't be falsely reassured by passing a physical. A physical does nothing to screen you for heart disease. An EKG and stress test, if included, is a lame excuse for heart disease screening. Remember that a stress test is a test of coronary blood flow, not for the presence of coronary plaque. The unfortunate judge most likely had a 30% "blockage" that did not block flow, but ruptured and closed an artery off sometime in the night when he died. A stress test even on the day of his death would not have predicted this.

A CT heart scan would have uncovered it easily, unequivocally, safely.

A curious case of regression

Randi came to me at age 43. Before I'd met her, she'd undergone two heart scans about one year apart. The initial score was 57--not terribly high, but very high for a 41-year old, pre-menopausal female. Recall that rarely do women have any heart scan score above zero before age 50. Randi's 2nd scan had yielded a score of 72, a 27% increase.

Randi even had her lipoproteins assessed and she had the dreaded Lp(a). So when I met her, we discussed the possible choices in Lp(a) treatment: niacin and estrogens as primary treatment, along with LDL reduction to rock-bottom numbers, along with adjunctive DHEA, almonds, ground flaxseed, and fish oil. Sandi was okay with the adjunctive treatments and was already slender and active (BMI <25), and did not show Lp(a)'s evil partner, small LDL. But Randi had no interest in estrogens, even bio-identical preparations, because of the usual uncertainties associated with estrogen replacement. She also proved to be one of the people truly intolerant to anything but the most minute dose of niacin, experiencing prolonged flushing and abdominal cramps with any dose >250 mg.

Randi even attempted a trial of the Mathias Rath concoction of high-dose vitamin C, lysine, and proline as treatment for Lp(a), but we saw no effect on Lp(a).

Unfortunately, this left Randi's Lp(a) essentially uncorrected. Another scan one year later: 90, another 25% increase. 18 months after that, another scan: 120, a 30% increase.

Now 47-years old, Randi had resigned herself to not being able to control her plaque. We'd run out of options. At that point, I'd started to have everyone's vitamin D blood level assessed and then replaced with vitamin D. I did this with Randi, too.

A year after her last scan, she underwent another. The score: 92, a 23% reduction--substantial reversal following a course of unrelenting progression.

Randi and I, of course, both rejoiced with this unexpected success. But it raised some interesting questions: How important is Lp(a) when vitamin D is normalized and small LDL is not a part of the picture? How consistent with regression be with this strategy over time? Would normalization of vitamin D have stopped plaque from becoming established in the first place?

I hope these issues will clarify over time. For now, I'm thrilled with Randi's success. She remains on her present, "incomplete", though successful program.

Note: I would not ordinarily advise a young woman to undergo serial heart scanning with this frequency. Randi had unusual access to a scan center through a relationship with the staff. I am nonetheless grateful for the lessons her experience have taught us.

Fortune teller

Whenever your doctor uses your cholesterol values--total, LDL, HDL, triglycerides--to judge your heart disease risk, he/she is trying to act as your fortune teller.

In some states, fortune telling is illegal, a misdemeanor. The New York State lawbooks say:

A person is guilty of fortune telling when, for a fee or compensation which he directly or indirectly solicits or receives, he claims or pretends to tell fortunes, or holds himself out as being able, by claimed or pretended use of occult powers, to answer questions or give advice on personal matters or to exorcise, influence or affect evil spirits or curses; except that this section does not apply to a person who engages in the aforedescribed conduct as part of a show or exhibition solely for the purpose of entertainment or amusement.
(Source : Wikipedia)

Rather than occult powers, your physician claims to use "medical judgement" to tell your fortune. Except for that distinction, it might be construed as a misdemeanor.


Let's take three typical examples:

58-year old Laura has a high LDL of 195 mg/dl. Her HDL is 52 mg/dl, triglycerides 197 mg/dl. Does she have heart disease?

51-year old Jonathan has an LDL of 174 mg/dl, HDL 34 mg/dl, triglycerides 156 mg/dl. Does Jonathan have heart disease?

71-year old Marian has an LDL cholesterol of 135 mg/dl, HDL 84 mg/dl, triglycerides of 67 mg/dl.

None of the three have symptoms. They all feel well. Nobody is taking a statin cholesterol drug or other agent that would modify the numbers. Jonathan is around 30 lbs overweight. Nobody has an impressive family history of heart disease.

Can you tell who has heart disease and who doesn't? If you can, you're smarter than I am, because I certainly can't tell. But your doctor tries to divine your future by looking at these numbers.

Do they know something that we don't know? No. It's a crude odds game, a guessing game. A guessing game that frequently comes up on the losing end.

These are three real people. Laura, despite her high LDL, has no identifiable coronary heart disease. Jonathan has advanced coronary disease. These were his numbers just prior to his stent. Marian has a moderate quantity revealed by a CT heart scan score of 419.

Don't even try predicting your future from your cholesterol numbers--it simply can't be done. Every day, I see patients and physicians beating their heads over this dilemma. Telling your fortune using pretended occult powers is illegal. Telling your fortune using cholesterol numbers should be, too.

If you want to know if you have coronary plaque, that's the role of the CT heart scan. Plain and simple.

Heart scan score drops like a stone

Matt was dumbfounded when he found out about his heart scan score of 317 in the summer of 2005.

Earlier that year he'd unintentionally lost 20 lbs. in the space of two months and was feeling awful. He was diagnosed with diabetes and put on several medications. He told me that the heart scan score was just adding insult to injury.

As you'd expect in someone with diabetes, Matt had a low HDL, increased triglycerides, and small LDL. Blood pressure and inflammation (C-reactive protein) were issues as well.

Matt's primary care physician had put him on a statin cholesterol drug as soon as he heard about Matt's heart scan score, so we kept this going. What Matt's primary care physician didn't know was that his "true" LDL had been much higher than the conventional calculated LDL had suggested, so the statin agent was a reasonable solution. (Matt was also not terribly motivated to make dramatic changes in lifestyle or food choices. The statin drug was a compromise.)

We added fish oil and vitamin D to his regimen. Though recent data have cast doubt on the value of treating homocysteine levels of around 12.5, Matt's much higher value of 28 was treated with vitamins B6, B12, and folic acid, with a resultant homocysteine of 7.6.

17 months into the Track Your Plaque approach, and Matt's repeat heart scan score: 244, a 23% reduction.

How's that for an early Christmas gift?

"You don't have a uterus. You don't need progesterone"

I was talking with a hospital nurse recently who told me about her lack of energy, blue moods, and other assorted complaints. At age 49, she was exasperated. So I suggested that she ask her gynecologist about progesterone cream.

The gynecologist advised her, "You don't have a uterus. You don't need progesterone." He went on to explain that the only reason to take progesterone was to prevent uterine cancer caused by estrogen.

Then what about progesterone's weight loss benefits? It's effects on increased energy, improved mood, deeper sleep? These benefits, of course, have nothing to do with the uterus.

I've witnessed these benefits in women many times, both in the peri-menopausal period (which starts around your late 30's) and menopause.

Why talk about progesterone when our focus is heart disease and reduction of heart scan scores? Because if progesterone in a woman helps her feel better, more upbeat, and accelerates weight loss, she's more likely to succeed in her plaque-control program.

For additional comments on progesterone, read the Track Your Plaque interview with women's hormone expert, Dr. Nisha Jackson, Females, hormones, and weight control:
An interview with Dr. Nisha Jackson
found at http://www.cureality.com/library/fl_04-008njacksonhormones.asp. Dr. Jackson also has a book available called "The Hormone Survival Guide to Perimenopause".







Or, read Dr. John Lee's pioneering books, What Your Doctor May Not Tell You About Menopause: The Breakthrough Book on Natural Hormone Balance and What Your Doctor May Not Tell You About Premenopause: Balance Your Hormones and Your Life from Thirty to Fifty . (An edition that combines the two books is available, also.)

Take a niacin "vacation"

I've been seeing a curious niacin phenomenon that has not, to my knowledge, been reported anywhere in the medical literature.

People with lipoprotein(a), or Lp(a), are best treated with niacin, particularly given the relative lack of other effective therapies. I now have seen approximately 10 people with great initial responses to niacin, only to observe Lp(a) levels slowly drift back up to the starting level over a period of 2-3 years.

In other words, if starting Lp(a) is 200 nmol/l (approximately 80 mg/dl), drops to 70 nmol/l on niacin. Then, over 2-3 years of treatment, it drifts back to 200 nmol/l. Very frustrating.

Somehow, your body's Lp(a) manufacturing mechanism circumvents the niacin, sort of like antibiotic resistance (without the bacteria, of course).

My response to this, though untested, is to have people take an occasional "niacin vacation". I don't mean take a trip to the Bahamas while on niacin. I mean take 2 weeks off from niacin every three months or so. My hope is that the occasional vacation from niacin will allow the body to continue to respond and suppress "resistance". When resuming niacin, you may have to escalate the dose gradually to avoid re-provoking the "flush".

The same "resistance" seems to develop to testosterone in males: an initial drop followed by a gradual increase. Curiously, I've not seen this in females with estrogens, which seems to generate a durable Lp(a) suppressing effect. For this reason, an occasional testosterone "vacation" might also be considered.

So far, I've advised several people to try this. The long-term success or failure, however, is uncertain. I know of no other solutions, however.

If you have Lp(a) and are on long-term niacin, you should consider talking about this issue with your physician. Like many aspects of Lp(a), while fascinating in its complexity, much remains uncertain. Stay tuned.

When LDL is more than meets the eye

Jerry wanted to know what to do with his LDL cholesterol of 112 mg/dl. "My doctor said that it's not high but it could be better."

So I asked him what the other numbers on his lipid panel showed. He pulled out the results:

LDL cholesterol 112 mg/dl

HDL 32 mg/dl

Triglycerides 159 mg/dl


I pointed out to Jerry that, given the low HDL and high triglycerides, his calculated LDL of 112 was likely inaccurate. In fact, if measured, LDL was probably more like 140-180 mg/dl. LDL particles were also virtually guaranteed to be small, since low HDL and small LDL usually go hand-in-hand (though small LDL can still occur with a good HDL).

So Jerry's LDL is really much higher than it appears. To prove it, Jerry will require an additional test, preferably one in which LDL is measured, such as LDL particle number (NMR), apoprotein B, or "direct" LDL.

It's really quite simple. Jerry likely has a high number of LDL particles that are too small. This pattern confers a three- to six-fold increased risk for heart disease.

Treatment requires more than just reducing LDL. Small LDL--an important component of this pattern, responds, for instance, to a reduction in processed carbohydrates like wheat products (breads, breakfast cereals, pretzels, etc.), NOT to a low-fat diet. Weight loss to ideal weight, especially loss of abdominal fat, will yield huge improvements in these numbers. Niacin may be a necessary component of Jerry's treatment program, since it increases LDL size and raises HDL.

For more discussion on measures superior to LDL cholesterol, see my upcoming editorial, Let Dr. Friedewald Lie in Peace (an expansion of a previous Heart Scan Blog). It will be posted on the Cardiologist on Call column on the Track Your Plaque website within the next week.)

Oil-based vitamin D


As time passes, I gain greater and greater respect for the power of restoring vitamin D blood levels to normal, i.e. 50-70 ng/ml. Just yesterday, I saw several people with blood levels of <10 ng/ml--severe deficiency.

Vitamin D deficiency this severe poses long-term risk for osteoporosis, arthritis, colon cancer, prostate cancer, inflammatory diseases, diabetes, and heart disease. Vitamin D appears to make coronary plaque reversal--reduction of your heart scan score--easier and faster.

But it is important that you take the right kind of vitamin D. Several of the people I saw yesterday with vitamin D levels of somebody living in total darkness were taking vitamin D, but they were taking tablets. Tablets are the wrong form. Powder-based tablets, in my experience, yield little or no rise in blood levels. Some preparations generate a small rise but the dose required is huge.

If you're going to take vitamin D, take a preparation that yields genuine and substantial rises in blood levels. This requires an oil-based capsule. I commonly see blood levels of 25-OH-vitamin D3 rise from, say, 10 ng/dl to 60 ng/ml when oil-based capsules are taken.

The most common dose I prescribe to patients is 2000 units per day to females, 3000-4000 units per day to males in non-sun exposed months. Ideally, your dose is adjusted to blood levels.

The Vitamin Shoppe preparation pictured here is one I've used successfully and generates bona fide rises in blood levels. And it costs around $5. Just be sure the preparation you buy is oil-based.

For rapid success, try the "fast" track

Have you tried fasting?

Before your eyes glaze over, let me tell you what I mean. I don't mean a water-only fast for two weeks while you drool over all the temptations around you and you feel sorry for yourself.

I also don't mean the juice fasts that some people use that turn into fruit juice fasts of pure sugar.

Here's another way to do it. Usually, 48 hours of doing this will yield several benefits:

--Weight loss of 1 lb. You will likely experience an even greater weight loss of 2-4 lbs, but much of this will be water loss.

--If you're like me and share a heightened sensitivity to sugars and carbohydrates (like wheat), you may find out just how awful you feel when you eat certain foods. Many people tell me they feel absolutely wonderful when they fast--clearer thinking, increased energy, improved mood. Not the constant gnawing urge to eat they expected.

--After your fast is over, you look back and realize just what large portions of food you were eating. You'll be content with smaller quantities--and enjoy it more.


The "fast" I've used successfully includes two foods:

1) Vegetable juices--that you either juice yourself or purchase. V8 or its equivalent works pretty well. Though purchased V8 is not the best, it's better than nothing and does work reasonably well. If you juice your own vegetable juices, watch out for the diarrhea if you're unaccustomed to vegetable juices. Four 8 oz glasses per day works well.

2) Soy milk--for a source of protein and modest quantity of sugar and fat. I like the Light Silk Soymilk (Vanilla) which contains 80 calories, 2 g fat (0.5 g monounsaturated), 7 g sugar, 6 g protein per 8 oz glass. Four 8 oz glasses of soymilk also work well. In my neighborhood, 8th Continent is another good choice.


Sip both of these throughout the day. Of course, drink water in unrestricted amounts.

What can you expect in your coronary plaque control/heart scan score reversal program? When the fast is over, a rise in HDL, reduction in small LDL, reduction in triglycerides, reduction in blood sugar and insulin, and a smaller tummy. This strategy can be useful to kick-start weight loss efforts or as a periodic way to maintain control over weight and lipid/lipoprotein patterns.


Nutritional Composition Silk Soymilk--Vanilla

Nutrition Facts
Serving Size 1 cup (240mL)
Servings per container 8 H/G OR 4 QT

Amount per Serving

Calories 70
Calories from Fat 20

% Daily Value
Total Fat 2g 3%
Saturated Fat 0g 0%
Trans Fat 0g
Polyunsaturated Fat 1g
Monounsaturated Fat 0.5g

Cholesterol 0mg 0%
Sodium 120mg 5%
Potassium 300mg 8%
Total Carbohydrates 8g 3%
Dietary Fiber 1g 4%
Sugars 6g
Protein 6g
Vitamin A 10%
Vitamin C 0%
Calcium 30%
Iron 6%
Vitamin D 30%
Riboflavin 30%
Folate 6%
Vitamin B12 50%
Magnesium 10%
Zinc 4%
Selenium 8%

My life is easy

In the old days (the 1980s and 1990s), practicing cardiology was very physically and emotionally demanding. Since procedures dominated the practice and preventive strategies were limited, heart attacks were painfully common. It wasn't unusual to have to go to the hospital for a patient having a heart attack at 3 am several times a week.

Those were the old days. Nowadays, my life is easy. Heart attacks, for the most part, are a thing of the past in the group of people who follow the Track Your Plaque principles. I can't remember the last time I had a coronary emergency for someone following the program.

But I am reminded of what life used to be like for me when I occasionally have to live up to my hospital responsibilities and/or cover the practices of my colleagues. (Though I voice my views on prevention to my colleagues, the most I get is a odd look. When a colleague recently covered my practice for a weekend while I visited family out of town, he commented to me how quiet my practice was. I responded, "That's because my patients are essentially cured." "Oh, sure they are." He laughed. No registration that he had witnessed something that was genuine and different from his experience of day-to-day catastrophe among his own patients. None.)

I recently had to provide coverage for a colleague for a week while he took his family to Florida. During the 7 days, his patients experienced 4 heart attacks. That is, 4 heart attacks among patients under the care of a cardiologist.

If you want some proof of the power of prevention, watch your results and compare them to the "control" group of people around you: neighbors, colleagues, etc. Unfortunately, the word on prevention, particularly one as powerful as Track Your Plaque, is simply not as widespread as it should be. Instead, it's drowned out in the relentless flood of hospital marketing for glitzy hospital heart programs, the "ask your doctor about" ads for drugs like Plavix, which is little better than spit in preventing heart attacks (except in stented patients), and the media's fascinating with high-tech laser, transplant, robotic surgery, etc.

Prevention? That's not news. But it sure can make the slow but sure difference between life and death, having a heart attack or never having a heart attack.

My bread contains 900 mg omega-3

Phyllis is the survivor of a large heart attack (an "anterior" myocardial infarction involving the crucial front of the heart) several years ago. Excessive fatigue prompted a stress test, which showed poor blood flow in areas outside the heart attack zone. This prompted a heart catheterization, then a bypass operation one year ago.

FINALLY, Phyllis began to understand that her unhealthy lifestyle played a role in causing her heart disease. But lifestyle alone wasn't to blame. Along with being 70 lbs overweight and overindulging in unhealthy sweets every day, she also had lipoprotein(a), small LDL particles, and high triglycerides. The high triglycerides were also associated with its evil "friends," VLDL and IDL (post-prandial, or after-eating, particles).

When I met her, Phyllis' triglycerides typically ranged from 200-300 mg/dl . Fish oil was the first solution, since it is marvelously effective for reducing triglycerides, as well as VLDL and IDL. Her dose: 6000 mg of a standard 1000 mg capsule (6 capsules) to provide 1800 mg EPA + DHA, the effective omega-3 fatty acids.

But Phyllis is not terribly good at following advice. She likes to wander off and follow her own path. She noticed that the healthy bread sold at the grocery store and containing flaxseed boasted "900 mg of omega-3s per slice!". So she ate two slices of the flaxseed-containing bread per day and dropped the fish oil.

Guess what? Triglycerides promptly rebounded to 290 mg/dl, along with oodles of VLDL and IDL.

A more obvious example occurs in people with a disorder called "familial hypertriglyceridemia," or the inherited inability to clear triglycerides from the blood. These people have triglycerides of 800 mg/dl, 2000 mg/dl, or higher. Fish oil yields dramatic drops of hundreds, or even thousands of mg. Fish oil likely achieves this effect by activating the enzyme, lipoprotein lipase, that is responsible for clearing blood triglycerides. Flaxseed oil and other linolenic acid sources yield . . .nothing.

Don't get me wrong. Flaxseed is a great food. As the ground seed, it reduces LDL cholesterol, reduces blood sugar, provides fiber for colon health, and may even yield anti-cancer benefits. Flaxseed oil is a wonderful oil, rich in monounsaturates, low in saturates, and rich in linolenic acid, an oil fraction that may provides heart benefits a la Mediterranean diet.

But linolenic acid from flaxseed is not the same as EPA + DHA from fish oil. This is most graphically proven by the lack of any triglyceride-reducing effects of flaxseed preparations.

Enjoy your flaxseed oil and ground flaxseed--but don't stop your fish oil because of it. Heart disease and coronary plaque are serious business. You need serious tools to combat and control them. Fish oil is serious business for triglycerides. Flaxseed is not.

More Omnivore's Dilemma

Another irresistible quote from Michael Pollan’s book, The Omnivore’s Dilemma:

“In many ways breakfast cereal is the prototypical processed food: four cents’ worth of commodity corn (or some other equally cheap grain) transformed into four dollars’ worth of processed food. What an alchemy! Yet it is performed straightforwardly enough: by taking several of the output streams issuing from a wet mill (corn meal, corn starch, corn sweetener, as well as a handful of tinier chemical fractions) and then assembling them into an attractively novel form. Further value is added in the form of color and taste, then branding and packaging. Oh yes, and vitamins and minerals, which are added to give the product a sheen of healthfulness and to replace the nutrients that are lost whenever whole foods are processed. On the strength of this alchemy the cereals group generates higher profits for General Mills than any other division. Since the raw materials in processed foods are so abundant and cheap (ADM and Cargill will gladly sell them to all comers) protecting whatever is special about the value you add to them is imperative.”

A food manufacturer’s nightmare is when you and your family shop in the produce aisle in the grocery store. Produce is unmodified (aside from the pesticide and genetic-engineering issues), not added to, and therefore of no interest to the food manufacturer, since no additional profit can be squeezed out of it. If you pay 45 cents for a cucumber, there’s no room for a processor to multiply it’s return.

Vegetables and fruits have imperfections, no doubt, particularly pesticide residues and the “dumbing-down” of some foods to increase their desirability (e.g., green grapes, what I call “grape candy”). But vegetables and fruits are the closest you can get to foods that are essentially unmodified by a food manufacturer. Due to the absence of processing, they are not calorie-dense like a bag of chips; they include all the naturally-occurring healthy factors like flavonoids that food scientists have, thus far, struggled and failed to identify, quantify, and control; and they lack all the unhealthy additives that processed foods require for extended shelf life, palatability, and reconstitution (anti-separating agents, emulsifiers, sweeteners, etc.)

Vegetables, in particular, should be the cornerstone of your plaque control program. Not breakfast cereals, breads, bacon, sausage, mayonnaise, fruit drinks and soda, all the foods that worsen the causes of coronary plaque and raise your heart scan score.

If you would like to understand how the current perverted state of affairs in food have come about, Pollan’s book is must reading.

Pollan's The Omnivore's Dilemma


“ ‘You are what you eat’ is a truism hard to argue with, and yet it is, as a visit to a feedlot suggests, incomplete, for you are what what you eat eats, too. And what we are, or have become, is not just meat but number 2 corn and oil.”

Author Michael Pollan offers unique, enlightening, and entertaining insights into the food we eat in his new book, The Omnivore’s Dilemma: A natural history of four meals.

Pollan draws parallels between the dilemma of the primitive human living in the wild, having to stumble through the choices of animals and plants that could nourish or kill, and the ironically modern return of this phenomenon in present-day supermarkets. While the dangers of food choices aren’t as immediate as in the wild (eat the wrong mushroom or herb, for instance, and you die), they can nonetheless be life-threatening, or at least health-threatening. Hydrogenated oils, high-fructose corn syrup, carageenan, guar gum. . .“What is all this stuff anyway, and where in the world did it come from?”

Among the issues Pollan discusses is that of modern cattle raising practices: the rush to fatten a cow from an 80 lb calf to a 1200-pound, bloated cow over a period of 14 months. Nature created this animal to mature over a 4 to 5 year period through grazing, thus it’s beautifully “engineered” ruminant system that allows it to digest cellulose in grasses, a process that humans and other mammals are incapable of. The pressures to bring greater quantities of beef to market at a reduced price and make more money have resulted in a farming industry that encourages the incorporation of unnatural, often inhumane practices like corn feeding (rather than grass grazing), refeeding of bovine body parts (thus “mad cow disease”), and widespread and chronic administration of hormones and antibiotics.

(I can't help but think that the rapid and perverse fattening of cattle by industrial "farming" is paralleled by the fattening of the eating American. After all, we are the hapless recipients of this flood of cheap, unhealthy, plasticized food.)

The industrialization of food has de-personalized the act of eating. You no longer have any connection with the green pepper in your salad (unless you grew it yourself), nor do you have any appreciation for the suffering of the cow in your hamburger. Worse, the distortion of livestock raising practices has modified the food composition of meat. Range-fed animals, leaner and richer in omega-3 fatty acids, have been replaced by the marbled, saturated fat-rich modern grocery bought meats.

This is a theme that Pollan reiterates time and again: how food processing adds value to the manufacturer, often starting with a healthy ingredient but modifying it, adding ingredients, taking out others, until it’s something decidedly unhealthy. Yet the manufacturer will trumpet the fact that a healthy ingredient is included. Breakfast cereals are the most blatant example of this. What the heck are Cheerios but an over-processed attempt to make more money out of the simple oat?

Pollan’s eloquent and unique insights into food are definitely worth reading.

As always, per our Track Your Plaque policy, I recommend Mr. Pollan’s book strictly on its merits. We obtain no “cut”, commission, or other financial gain by recommending his book. Track Your Plaque members pay their modest membership fee for truth. They do not pay for us to advertise something that provides hidden advantage to us. We do not advertise, editorialize to steer you towards a specific product or service. What we say, we truly believe.

The most frequently asked question of all

The most frequently asked question on the Track Your Plaque website:

"Can you recommend a doctor in my area who can help me follow the Track Your Plaque program?"

This is a problem. Unfortunately, I wish I could tell everyone that we have hundreds or thousands of physicians nationwide who have been thoroughly educated and adhere to the principles I believe are crucial in heart disease:

1) Identify and quantify the amount of coronary atherosclerotic plaque present. In 2007, the best technique remains CT heart scans.

2) Identify all hidden causes of plaque. This includes Lp(a), post-prandial disorders, small LDL, and vitamin D deficiency.

3) Correct all patterns.


But we don't.

You'd think that this simple formula, as straightforward and rational as it sounds, would be easily followed by many if not most physicians. But Track Your Plaque followers know that it simply is not true. My colleagues, the cardiologists, are hell-bent on implanting the next new device, providing a lot more excitement to them as well as considerably more revenue.

The primary care physician is already swamped in a sea of new information, going from osteoporosis drugs, to arthritis, to gynecologic issues, to skin rashes and flu. Heart disease prevention? Oh yeah, that too. They can only dabble in heart disease prevention a la prescription for Lipitor. That's quick and easy.

Nonetheless, I believe we should work towards identifying the occasional physician who is indeed willing to help people follow a program like Track Your Plaque. As we grow, we will need to identify some mechanism of professional education and we will maintain a record of these practitioners. But right now, we're simply already stretched to the limit just doing what we are doing.

If you come across a physician who practices in this fashion and you've had a positive relationship, we'd like to hear about it.

Do stents kill?

There's apparently a lively conversation going on at the HeartHawk Blog (www.hearthawk.blogspot.com). Among the hot topics raised was just how bad it is to have a stent.

I think that my comments some time back may have started this controversy. I've lately noticed that having a stent screws up your heart scan scoring in the vicinity of the stent. I was referring to the fact that I've now seen several people in the Track Your Plaque program do everything right and then show what I call "regional reversal": unstented arteries show dramatic drops in score of 18-30%, but the artery with a stent shows significant increase in score.

This is consistent with what we observe in the world outside Track Your Plaque when stents are inserted. Someone will get a stent, for instance, in the left anterior descending artery. A year later, there will be a "new" plaque at the mouth of the stent or just beyond the far end. This is generally treated by inserting another stent. Use of a drug-coated stent seems to have no effect on this issue.

Now, my smart friends in the Track Your Plaque program would immediately ask, "Does this mean you continually end up chasing these plaques that arise as a result of stents? Do you create an endless loop of procedures?"

Thankfully, the majority of times you do not. Rarely, this does happen and can lead to need for bypass surgery to circumvent the response. But it is unusual. The tissue that grows above and below stents does seem to be unusually impervious to the preventive efforts we institute.

Perhaps there's some new supplement, medication, or other strategy that will address this curious new brand of plaque growth. Until then, you and I can only take advantage of what is known. If it's any consolation, the plaque that seems to grow because of a previously inserted stent seems to lack the plaque "rupture" capacity of "naturally-occuring" plaque. It is, indeed, somehow different. It is more benign, less likely to cause heart attack. It's always been my feeling that this tissue behaves more like the "scar" tissue that grows within stents, causing "re-stenosis", a more benign, less rupture-prone kind of tissue.

Dr. Reinhold Vieth on vitamin D

A Track Your Plaque member brough the following webcast to our attention:

Prospects for Vitamin D Nutrition
which can be found at http://tinyurl.com/f93vl

Despite the painfully dull title, the webcast is the best summary of data on the health benefits on vitamin D that I've seen. The presenter is Dr. Reinhold Vieth, who is among the handful of worldwide authorities on vitamin D. In 1999, Dr. Vieth authored the first review to concisely and persuasively argue that vitamin D nutrition was woefully neglected and that its potential for health was enormous.
(See Vieth R, Am J Clin Nutr 1999 May;69(5):842-856 at http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=10232622&query_hl=1&itool=pubmed_DocSum.)

I predict that, after viewing Dr. Vieth's hour-long discussion, you will be as convinced as I am that vitamin D is crucial for health. Unfortunately, Dr. Vieth doesn't delve into the conversation about the potential effects on heart disease, since his audience was primary interested in multiple sclerosis, a disease for which vitamin D replacement promises to have enormous possibilities. Even in 2007, the data suggesting that vitamin D has heart benefits is circumstantial. Nonetheless, from our experience, I am thoroughly convinced that, with replacement to blood levels of vitamin D to 50 ng/ml, heart scan scores drop more readily and faster.

If you view Dr. Vieth's wonderful webcast, keep in mind that when he discusses vitamin D blood levels, he's using units of nmol/l, rather than ng/ml. To convert nmol/l to ng/ml, divided by 2.5. For example, 125 nmol/l is the same as 50 ng/ml (125/2.5 = 50).

Vitamin D on Good Morning America


Positive comments about vitamin D made it to a discussion on Good Morning America today about the new and exciting developments in nutrition and "functional foods".

I'm thrilled that the media is conducting these conversations. It sure is making my job easier, not having to persuade patients that taking vitamin D is truly and hugely beneficial for health. I still have to struggle with my colleagues, who tell patients to stop the "poisonous" doses we use.

But I worry that many of the details behind vitamin D don't quite make it to the media conversation. These are crucial, make-it-or-break-it issues, such as:

--Vitamin D must be vitamin D3 or cholecalciferol, not D2 or ergocalciferol. D2 is virtually worthless. Little or none is converted to the active D3, despite the fact that D2 is the form often added to some foods.

--Vitamin D3 supplements must be oil-based capsules, or gelcaps. Tablets are so poorly or erratically absorbed that it's simply not worth the effort. (We get ours from the Vitamin Shoppe.)

--The dose should be sufficient to eliminate the phenemena of deficiency, which is around 50 ng/ml. I take 6000 units per day. Dr. John Cannell of www.vitamindcouncil.com takes 5000 units per day. I give my wife 2000 units per day (she's not as deficient as I was), each of my kids 1000 units per day, except for my 180 lb. 15 year old who takes 2000 units.

I fear that, when people hear that vitamin D packs fabulous effects for health, they will take a 400 unit tablet--nothing will happen. They will not obtain the benefits such as reduction of blood pressure and blood sugar; increased bone density, reduction of arthritis, dramatic reduction in risk for fractures; reduction in risk for colon, prostate, and breast cancer; reduction in risk for multiple sclerosis; reduction in inflammatory processes such as those evidenced by C-reactive protein; and facilitation of reduction of heart scan score.

Would you bet your life on chelation?


Hugh's heart scan score was 1751, an awful score. Recall that, at this level of scoring, Hugh's heart attack and death risk is 25% per year.

Obviously, serious efforts need to be taken. In this situation, much as I despise drug companies and what they represent and their heavy-handed ways, I'm more inclined to resort directly to prescription agents, as well as our nutritional supplements and other strategies. The price of dilly-dallying could be his death.

Hugh and his wife asked about chelation. Now, there are five studies I'm aware of that have tried to examine the value of chelation. None showed any measurable benefit, though all were rather weak in design and small in number of participants. One study, for instance, looked at whether anginal chest pains were provoked any later after chelation. Another looked at whether calf claudication, or calf cramping while walking due to artery blockages in the leg arteries, was delayed on treadmill testing after chelation. No benefit was observed: no delay in provocation of angina, no delay in provocation of claudication.

However, the adherents of chelation have been vehement enough that the NIH has funded a large, multi-center study to settle the question once and for all. Best I can tell, the study has not been contaminated by any drug company involvement. It is meant to be an unbiased, objective study of whether chelation has any value.

My personal experience in patients who underwent chelation is that, despite spending hundreds or thousands of dollars, plaque grew at the expected rate--no effect at all.

None of this constitutes proof of efficacy nor proof of lack of efficacy. We will need to await the NIH trial to have better information.

Should Hugh bet his life on chelation? I advised him strongly against it. At this point, the only reason I can see to pursue chelation would be faith--that is, expectation based not on fact, but on hope.

The powerful forces preserving the status quo


An interesting quote from the book, Critical Condition: How health care in American became big business--and bad medicine:


Politics and Profits

To protect its interests and expand its influence, the health care industrial complex has done what all successful special interests do: It's become a big donor and a high-powered lobby in Washington. In the last fifteen years, HMOs, insurers, pharmacuetical companies, hospital corporations, physicians, and other segments of the industry contributed $479 million to political campaigns--more than the energy industry ($315 million), commercial banks ($133 million), and big tobacco ($52 million). More telling is how much the health care industry spends on lobbying. It invests more than any other industry except one, according to the nonpartiisan Center for Responsive Politics. From 1997 to 2000, the most recent year for which complete data is available, the industry spent $734 million lobbying Congress and the executive branch. Only the finance, insurance, and real estate lobby exceeded that amount in the same period, with a ttoal of $823 million. In contrast, the defense industry spent $211 million--less than one-third of the health care expenditure.


These telling statistics indicate just how vigorously profit-seeking forces in heart care are trying to preserve the status quo. Hospitals want to protect their valuable procedure-driven enterprise, the pharmaceutical industry wants to protect its enormous though little-known niche of procedure-based medications (like $1200 a dose ReoPro), and the medical device industry wants to maintain the multi-billion dollar-generating machine aided and abetted by the FDA's 501k rule (that makes entry to market a breeze).

The current procedure based formula for heart disease profits so many and they are desperate to preserve it. Resistance to the deep-pocketed efforts of industry and hospitals will come from people like you and me, trying to propagate a better way.

Remember: hospital procedures for coronary disease represent the failure of prevention. They are not--any longer--successes in and of themselves.

Read a scathing insight into some of these practices by reading investigative journalists' Donald Barlett and James Steele's book, Critical Condition. I found their descriptions painfully accurate. (But don't get too angry! Remember: only optimists reverse their plaque! We need to turn the conversation in a positive direction, not just in this Blog or the Track Your Plaque website, but nationwide.)

One of the new missions for the www.cureality.com website is to help you understand just how powerful, insidious, shrewd, and pervasive the efforts to maintain the current system truly are.