Increased blood calcium and vitamin D

Conventional advice tells us to supplement calcium, 1200 mg per day, to preserve bone health and reduce blood pressure.

Here's a curious observation I've now witnessed a number of times: Some people who supplement this dose of calcium while also supplementing vitamin D sufficient to increase 25-hydroxy vitamin D blood levels to 60-70 ng/ml develop abnormally high levels of blood calcium, hypercalcemia.

This makes sense when you realize that intestinal absorption of calcium doubles or quadruples when vitamin D approaches desirable levels. Full restoration of vitamin D therefore causes a large quantity of calcium to be absorbed, more than you may need. In addition, two studies from New Zealand suggest that 1200-1300 mg calcium with vitamin D per day doubles heart attack risk.

We have 20 years of clinical studies demonstrating the very small benefits of supplementing calcium to stop or slow the deterioration of bone density (osteopenia, osteoporosis). These studies were performed with no vitamin D or with trivial doses, too small to make a difference. I believe those data have been made irrelevant in the modern age in which we "normalize" vitamin D.

Should hypercalcemia develop, it is not good for you. Over long periods of time, abnormal calcium deposition can occur, leading to kidney stones, atherosclerosis, and arthritis.

Until we have clarification on this issue, I have been advising patients to take no more than 600 mg calcium supplements per day. I suspect, however, that the vast majority of us require no calcium at all, provided an overall healthy diet is followed, especially one that does not leach out bone calcium. This means no foods like those made with wheat or containing powerful acids, such as those in carbonated drinks.

Heart health consultation with Dr. Joe D. Goldstrich

Cardiologist, nutritionist, and lipidologist, Dr. Joe D. Goldstrich, is a frequent contributor to the Track Your Plaque Forum, where we discuss the full range of issues relevant to coronary health and coronary plaque reversal.

I have come to value Dr. Goldstrich's unique insights, especially in nutrition. Formerly National Director of Education and Community Programs for the American Heart Association and a physician at the Pritikin Center, his dietary philosophy has evolved away from low-fat and towards a low-carbohydrate focus, much as we use in Track Your Plaque. Like TYP, Dr. Goldstrich is always searching for better answers to gain control over coronary health. His unique blend of ideas and background has helped us craft new ideas and strategies. Dr. Goldstrich has proven especially adept at understanding how to incorporate new findings from clinical studies in our framework of coronary atherosclerotic plaque management strategies.

Dr. Goldstrich is offering to share his expertise with our online community. If you would like a one-on-one phone consultation with Dr. Goldstrich, you can arrange to speak with him at his HealthyHeartConsultant.com website.

Wheat aftermath

Following my 4 oz whole wheat misadventure that yielded the sky-high blood sugar of 167 mg/dl, compared to einkorn wheat's 110 mg/dl, I suffered through a 36-hour period of misery.

After I obtained the blood sugar of 167 mg/dl, I biked hard for one hour. This yielded a blood sugar back down in the 80s. I felt spacey in the ensuing few hours, as well as a little queasy. However, about 12 hours later, I awoke with overwhelming nausea along with that hypersalivating thing that happens just prior to vomiting. It did not come to that, but persisted all through the following day.

The next morning, I could barely concentrate. Trying to read a study (admittedly on the complex topic of agricultural genetics), I had to read each paragraph 4 or 5 times. Abdominal cramps and a bloated feeling also developed, though I was able to eat.

The 2nd night was filled with incredibly vivid dreams and intermittent sleeplessless. I awoke about 5 times through the night, but periods of sleep were filled with detailed, colorful dreams. I dreamt that a large corporation was secretly trying to gain control over the world's water supply, and I snuck onto a complex underwater vessel that was exploring and mapping the coastline of the Great Lakes in preparation. Weird.

I recognized these odd feelings as various facets of wheat intolerance, since they were all reminiscent of feelings I used to experience before I removed wheat from my diet. They were amplified and compressed, likely because I had been wheat-free for so long.

The odd thing is that, despite the modest blood sugar effect of my einkorn experience, none of the gastrointestinal or neurologic effects of wheat developed. So far, two other people with acute gastrointestinal wheat sensitivities have consumed our einkorn bread, also without reproduction of their usual symptoms.

Einkorn contains gluten, though the structure of the many gluten proteins of einkorn differs from that of the wheat bread I consumed, an example of modern Triticum aestivum. 14-chromosome einkorn carries what biologists call the "A" genome, while Triticum aestivum has the combines genomes of 3 plants, the combination of the A, B, and D genomes. It is the D genome that contains the genes coding for the most obnoxious, immunogenic forms of gluten.

So einkorn may not be entirely benign, but it is a good deal less obnoxious than modern Triticum aestivum.

I am awaiting the reports from a few other people on their experiences.

In search of wheat: Einkorn and blood sugar

There are three basic aspects of wheat's adverse health effects: immune activation (e.g., celiac disease), neurologic implications (e.g., schizophrenia and ADHD), and blood sugar effects.

Among the questions I'd like answered is whether ancient wheat, such as the einkorn grain I obtained from Eli Rogosa, triggers blood sugar like modern wheat.

So I conducted a simple experiment on myself. On an empty stomach, I ate 4 oz of einkorn bread. On another occasion I ate 4 oz of bread that dietitian, Margaret Pfeiffer, made with whole wheat flour bought at the grocery store. Both flours were finely ground and nothing was added beyond water, yeast, olive oil, and a touch of salt.

Here's what happened:

Einkorn wheat bread:

Blood sugar pre: 84 mg/dl
Blood sugar 1-hour post: 110 mg/dl

Conventional wheat bread
Blood sugar pre: 84 mg/dl
Blood sugar 1-hour post: 167 mg/dl

The difference shocked me. I expected a difference between the two, but not that much.

After the conventional wheat, I also felt weird: a little queasy, some acid in the back of my throat, a little spacey. I biked for an hour solid to reduce my blood sugar back to its starting level.

I'm awaiting the experiences of others, but I'm tantalized by the possibility that, while einkorn is still a source of carbohydrates, perhaps it is one of an entirely different variety than modern Triticum aestivum wheat. The striking difference in blood sugar effects make me wonder if einkorn eaten in small quantities can keep us below the Advanced Glycation End-Product threshold.
 

In search of wheat: We bake einkorn bread

With the assistance of dietitian and health educator, Margaret Pfeiffer,MS RD CD, author of Smart 4 Your Heart and very capable chef and breadmaker (previously, before she gave up wheat), we made a loaf of bread using Eli Rogosa's einkorn wheat. Recall that einkorn wheat is the primordial 14-chromosome wheat similar to the wild wheat harvested by Neolithic humans and eaten as porridge.

The essential question: Has wheat always been bad for humans or have the thousands of hybridization experiments of the last 50 years changed the structure of gluten and other proteins in Triticum aestivum and turned the "staff of life" into poison? I turn to einkorn wheat, the "original" wheat unaltered by human manipulations, to figure this out. While einkorn wheat is still a source of carbohydrates, is it something we might indulge in once in a while without triggering the adverse phenomena associated with modern wheat?   

Here's what we did:

This is the einkorn grain as we received it from Eli's farm. This was enough to make one loaf (approximately 3 cups).











The einkorn grain is a dark golden color. I tried chewing them. They taste slightly nutty. They soften as they sit in your mouth.





Here's Margaret putting the einkorn grain into the electric grinder.









We tried to grind the grain by hand with mortar and pestle, but this proved far more laborious than I anticipated. After about 15 minutes of grinding, this is what I got:



Barely 2 tablespoons. That's when Margaret fired up the electric grinder. (I can't imagine having to grind up enough flour by hand for an entire family. Perhaps that's why ancient cultures were thin despite eating wheat. They were just exhausted!)

We added water, salt, and yeast, then put the mix into an electric breadmaker to knead the dough and keep it warm.

We let the dough rise for 90 minutes, much longer than conventional dough. The einkorn dough "rose" very little. Margaret tells me that most dough made with conventional flour rises to double its size. The einkorn dough increased no more than 20-30%.

The einkorn dough also distinctly smelled like peanut butter.





After rising, we baked the dough at 350 degrees F for 30 minutes. This is the final product.

Because I want to gauge health effects, not taste, the bread we made had no added sugar or anything else to modify taste or physiologic effect.

On first tasting, the einkorn bread is mildly nutty and heavy. It had an unusual sour or astringent taste at the end, but overall tasted quite good.

Next: What happens when we eat it? I'm going to give the einkorn bread (I've got to make some more) to people who experience acute reactions to conventional wheat and see if the einkorn does the same. I will also assess blood sugar effects since, after all, hybridizations or no, it is still a carbohydrate.



Margaret Pfeiffer's book is available on Amazon:

Ezekiel said what?

Some people are reluctant to give up wheat because it is talked about in the Bible. But the wheat of the Bible is not the same as the wheat of today. (See In search of wheat and Emmer, einkorn and agribusiness.) Comparing einkorn to modern wheat, for example, means a difference of chromosome number (14 chromosomes in einkorn vs. 42 chromosomes in modern strains of Triticum aestivum), thousands of genes, and differing gluten content and structure.

How about Ezekiel bread, the sprouted wheat bread that is purported to be based on a "recipe" articulated in the Bible?

Despite the claims of lower glycemic index, we've had bad experiences with this product, with triggering of high blood sugars, small LDL, and triglycerides not much different from conventional bread.

David Rostollan of Health for Life sent me this interesting perspective on Ezekiel bread from an article he wrote about wheat and the Bible. David argues that the entire concept of Ezekiel bread is based on a flawed interpretation.

"I Want to Eat the Food in the Bible."


Are you sure about that?

Some people, still wanting to be faithful to the Bible, will discard the "no grain/wheat" message on the basis of biblical example. After all, God told Ezekiel to make bread, he gave the Israelites "bread from heaven," and then Jesus (who is called the "Bread of Life"!) multiplied bread, and even instituted the New Covenant with what? Bread and wine! If you're going to live the Bible, it seems that bread and/or wheat is going to play a part.

But this is unnecessary. Sure, the Bible can and does tell us how to live, but this doesn't mean that everything in the Bible is meant to be copied verbatim. Applying the Bible to our lives requires wisdom, not a Xerox machine.

The Bible was written in a historical context, and the setting happened to be an agricultural one. Because of this, the language used to describe blessing spoke of things like fields full of grain, or barns overflowing with wheat. Had the Bible been written in the context of a hunter-gatherer culture, the language describing blessing probably would have been about the abundance of wild game, or baskets full of vegetables. Whatever is most valuable in your time and in your culture is a blessing. God accommodated His message to the culture as it existed at the time. This is done throughout Scripture.

There is a danger, then, in merely copying what the Bible says, instead of extracting the principles by which to live. Take the above example of Ezekiel, for instance. There's a whole product line in health food stores called "Ezekiel Bread" that supposedly copies the recipe given in Ezekiel 4:9. This is from the website:

"Inspired by the Holy Scripture verse Ezekiel 4:9., 'Take also unto thee Wheat, and Barley, and beans, and lentils, and millet, and Spelt, and put them in one vessel, and make bread of it...'"

Believing that this "recipe" has some kind of special power just because it's in the Bible is ridiculous. How ridiculous is it? I'll tell you in a moment, but first let me say that this is why it's so important not to confuse descriptives with prescriptives. Is the Bible telling a story, or is it telling us to do something? We would be well-advised not to confuse the two.

In the case of the Ezekiel Bread, what is going on in the passage? There's a siege going on, with impending famine, and Ezekiel is consigned to eating what was considered back then to be some of the worst possible food. It was basically animal chow. But that's not the worst thing going on in this passage. Apparently, when the makers of Ezekiel Bread were gleaning their inspiration for the perfect recipe, they stopped short
of verse 12:

"And thou shalt eat it as barley cakes, and thou shalt bake it with dung that cometh out of man, in their sight."

Um...what? Well, there was a good reason for this. God was judging His people, and by polluting this really bad bread with dung (which was a violation of Mosaic law; Lev. 5:3), He was saying that they were no different from the unclean Gentiles.

So why would we take this story and extrapolate a bread recipe from it? Beats me. If you were going to be consistent, though, here's what you'd have to end up with:



Let that be a lesson to you. We don't just go and do everything that we see in the Bible.

Low-carb gynecologist

I met infertility specialist, Dr. Michael Fox, on Jimmy Moore's low-carb cruise just this past March.

Dr. Fox is quiet and unassuming, but had incredible things to say about his experience with carbohydrate restriction in female infertility and pregnancy. While readers of The Heart Scan Blog already know that I advocate a diet free of wheat, cornstarch, and sugar for heart health and correction of multiple lipoprotein abnormalities, it was fascinating to hear how a similar approach seems to yield extraordinary benefits in this entirely unrelated area of female health. Obviously, female infertility and pregnancy are unrelated to heart health, but the extraordinary benefits witnessed by Dr. Fox in this area suggest that some fundamental lessons in human physiology can be learned. The results are so incredible that we are all sure to hear more about this approach as experience grows.

So I tracked Dr. Fox down in his busy Jacksonville, Florida practice to fill us in on some details.

WD: Dr. Fox, could you tell us something about yourself and what led you to use carbohydrate restriction in your female patients?

MF: I have been in practice as a reproductive endocrinologist for 15 years. During that time, I have seen our specialty move from a broad based practice of reproductive endocrinology to a narrow IVF [in vitro fertilization] focus, with patients being pushed through IVF in a cookie-cutter fashion without any emphasis on non-medical therapy.

Our focus has been to remain as a broad practice where we individualize care and attempt in every case to achieve pregnancy short of IVF. Five years ago, this continued quest for better care led us into the insulin resistance, low-carbohydrate metabolic world that has transformed our practice, although our practice offers all aspects of reproductive endocrinology including sub-specialized minimally invasive surgery, and all available infertility options.


WD: I have been intrigued by your comments about improved fertility with the low-carb diet. Could you elaborate on this?

MF: Yes, five years ago, as more information regarding Polycystic Ovarian Disease or Syndrome (PCOD/S) and its relationship to insulin resistance (high insulin levels) was emerging, we had a simple realization. As we've known for some time, insulin stimulates excess male hormone levels in the ovary, which disrupts ovulation and fertility. Then our job was to lower or virtually eliminate high insulin levels. Again, in simple fashion, we looked at physiology and realized that insulin is released only in response to dietary carbohydrates. Thus, elimination of carbohydrates should resolve the problem. This, in fact, is the effect that we have seen.

In our previous approaches to PCOD, we utilized oral ovulation medicines generating pregnancy rates in the 40% range overall. Now, with the nutritional approach, for those patients that follow our recommendations, our pregnancy rates are over 90%! This has dramatically reduced the need for in vitro fertilization in these patients.

To extend this idea further, we first started with relative low-carbohydrate diets, such as the South Beach diet, but quickly realized this didn't produce a metabolic effect. Over time, it has borne out that only the very low-carbohydrate diet (VLCD) approach produces significant metabolic change. Our impression then was that the current U.S. nutritional exposure probably increases insulin levels and that this has a detrimental effect on fertility.

To counter this effect, we now recommend the VLCD to all fertility patients and their spouses. The pregnancy rates do seem much better overall, as well as seeing a reduction in miscarriage rates. For the first time at our national meeting last year, there were three articles that showed improved pregnancy rates in patients without PCOD or insulin resistance in IVF when Glucophage was used. This drug decreases insulin. This supports the idea that our entire population is subjected to fertility-reducing high-carbohydrate diet.

WD: Do you see any other changes in these patients on the diet?

MF: Yes. All metabolic parameters, as well as many common complaints, improve. Cholesterol and triglyceride levels improve, while "good" HDL cholesterol levels increase. Weight drops at a pace of 12 lbs per month very steadily and we have many many patients who have experienced 50lb wt loss. Blood pressure decreases steadily in these patients and we are often able to get them off of cholesterol and blood pressure medicines. Common symptoms such as anxiety, sleep disturbances, decreased energy, migraine headaches and depression all dramatically improve. Again we can often get patients off depression and migraine suppression medications. So this approach helps in a multitude of areas.



WD: I was also interested in hearing more about your experience with morning sickness and the effects of a low-carb diet. Could you tell us more about this? Also, any thoughts on why this happens?

MF: As we continued to expand our thoughts about VLCD and fertility/pregnancy, we began to extend the nutritional approach into pregnancy. We know that pregnancy hormones dramatically worsen insulin resistance that is responsible for the condition, gestational diabetes. If insulin resistance is worsened, then reactive hypoglycemia is worsened. One of the biggest symptoms of hypoglycemia is nausea. So, in response to this, we have counseled our patients on the diet in pregnancy and have found a dramatic reduction in nausea. We recommend snacking every two hours in pregnancy.

The other "traditional" issue in pregnancy are cravings. These also likely stem from hypoglycemia. I have had many husbands tell us later that their wives, in contrast to friends etc, were calm and not moody or anxious during their pregnancies. Hypoglycemia probably is a serious issue for the fetus as well and may be the "signal" that turns on the insulin-resistant gene. Many theorists feel this might be an activated gene during the pregnancy.


WD: Do you use any unique approaches to the low-carbohydrate approach, e.g., inclusion of dairy, meal frequency, "induction" strategies (i.e., induction to the diet, not of labor!), etc.?

MF: Yes. As I'm sure everyone who works in the VLCD world does, we also have some tricks to make this work better. My biggest push, although hard to get patients to agree, is to see a counselor along with our follow-up in order to deal with "addictive behaviors" and "stress eating" that so many of our patients relate to us. Good stress management and cognitive behavioral therapy go a long way in helping this become a permanent change.

We also really push frequent calorie intake or "snacking." I think again that hypoglycemia produces an inborn drive to "cure" or "fix" starvation and leads to dramatic overeating. We have a short list of snacks that we recommend. The concept of hunger is offered as a failure of the program. We aim to eliminate hunger, as it represents hypoglycemia. The analogy I use is, if you drove your car until you ran out of gas before you ever sought to find gas, your life would be miserable. So it is the same with your metabolic engine: If you let it run out, the measures your system takes to fix it are very detrimental to life and certainly to nutritional health.

Our other big push is fat. People can wrap themselves around protein and vegetables, but they totally miss the high-fat (animal fat) part of the conversation. We have to really push that aspect. In regards to dairy, we allow for non-processed cheeses and minimal milk. An alternative is to mix about 4 oz whole milk with 4 oz of heavy whipping and 4 oz of water to create a "milk" with less sugar. Similarly, shakes and smoothies can be made with heavy whipping cream with pure whey protein powder added to create a liquid meal for those who "don't have time" to cook.


WD: Thanks, Dr. Fox. We look forward to hearing more about your approach in future.

Contact information:

Michael D. Fox, MD
Jacksonville Center
Reproductive Medicine
www.JCRM.org
Phone 904-493-2229

Track Your Plaque reduces healthcare costs 35%

Allow me to wear my Track Your Plaque hat for this post.

Mr. Richard Rawle is CEO of Utah company, Tosh, Inc. Mr. Rawle has been an avid follower of the Track Your Plaque program and has introduced the program to company employees. Here's what he has to say about the experience:

“Our company has been utilizing the principles of TYP [Track Your Plaque] for over a year and has experienced great results that have positively impacted the lives of our employees and our health care costs.

Since we began our wellness program, we have presented the TYP diet and lifestyle guidelines to all of our employees and their families. Although the overwhelming majority of our employees do not have cardiovascular issues, the preventative nature of TYP is too important not to be utilized. The TYP principles along with our increased focus on healthy living have already changed our group’s blood chemistry. HDL levels in particular have increased significantly and resulted in a large percentage of our employees having HDL levels of 60 or higher. Vitamin D levels have substantially increased and LDL levels have significantly decreased in the majority of our employees. Subsequently, in the 12 months just ended, our health care costs are some 35% less than other groups of comparable size and age.

I believe the TYP program has been an integral part of the success of our company's vast improvement in employee health/wellness, resulting in significant health care cost reductions."

Richard Rawle
CEO Tosh Inc.


Track Your Plaque saves lives. Track Your Plaque also saves money . . . lots of it. Despite the upfront costs of some additional blood testing and a heart scan, the dramatic reduction in need for medications, reduced heart attack, diabetes, and many other chronic conditions add up to a huge cost savings, much as Tosh, Inc. employees have enjoyed.

The Federal government has been looking towards large hospital systems to lead the way in healthcare delivery, systems that employ their physicians and possess economies of scale. But I say the answer to reducing healthcare costs will NEVER be found in hospital systems. Healthcare cost savings will be realized by delivering truly effective health solutions directly to people themselves, much as we do in Track Your Plaque.

In search of wheat

Many people ask: "How can wheat be bad if it's in the Bible?"

Wheat is indeed mentioned many times in the Bible, sometimes literally as bread, sometimes metaphorically for times of plenty or freedom from starvation. Moses declared the Promised Land "a land of wheat, and barley, and vines, and fig trees, and pomegranates; a land of oil olive, and honey" (Deuteronomy 8:8).

Wheat is a fixture of religious ceremony: sacramental bread in the Eucharist of the Christian church, the host of the Holy Communion in the Catholic church, matzoh for Jewish Passover, barbari and sangak are often part of Muslim ritual. Wheat products have played such roles for millenia.

So how can wheat be bad?

What we call wheat today is quite different from the wheat of Biblical times. Emmer and einkorn wheat were the original grains harvested from wild growths, then cultivated. Triticum aestivum, the natural hybrid of emmer and goatgrass, also entered the picture, gradually replacing emmer and einkorn.

The 25,000+ wheat strains now populating the farmlands of the world are considerably different from the bread wheat of Egyptians, different in gluten content, different in gluten structure, different in dozens of other non-gluten proteins, different in carbohydrate content. Modern wheat has been hybridized, introgressed, and back-bred to increase yield, make a shorter stalk in order to hold up to greater seed yield, along with many other characteristics. Much of the genetic work to create modern wheat strains are well-intended to feed the world, as well as to provide patent-protected seeds for agribusiness.

What is not clear to me is whether original emmer, einkorn, and Triticum aestivum share the adverse health effects of modern wheat.

Make no mistake about it: Modern wheat underlies an incredible range of modern illnesses. But do these primitive wheats, especially the granddaddy of them all, einkorn, also share these effects or is it a safe alternative--if you can get it?

I've ordered 2 lb of einkorn grain, unground, from Massachusetts organic farmer, Eli Rogosa, who obtained einkorn seed from the Golan Heights in the Middle East. We will be hand-grinding the wheat and making einkorn bread. We will eat it and see what happens.

Super-carbohydrate

Wheat starches are composed of polymers (repeating chains) of the sugar, glucose. 75% of wheat carbohydrate is the chain of branching glucose units, amylopectin, and 25% is the linear chain of glucose units, amylose.

Both amylopectin and amylose are digested by the salivary and stomach enzyme, amylase, in the human gastrointestinal tract. Amylopectin is more efficiently digested to glucose, while amylose is less efficiently digested, some of it making its way to the colon undigested.

Amylopectin is therefore the “complex carbohydrate” in wheat that is most closely linked to its blood sugar-increasing effect. But not all amylopectin is created equal. The structure of amylopectin varies depending on its source, differing in its branching structure and thereby efficiency of amylase accessibility.

Legumes like kidney beans contain amylopectin C, the least digestible—hence the gas characteristic of beans, since undigested amylopectin fragments make their way to the colon, whereupon colonic bacteria feast on the undigested starches and generate gas, making the sugars unavailable for you to absorb.

Amylopectin B is the form found in bananas and potatoes and, while more digestible than bean amylopectin C, still resists digestion to some degree.

The most digestible is amylopectin A, the form found in wheat. Because it is the most readily digested by amylase, it is the form that most enthusiastically increases blood sugar. This explains why, gram for gram, wheat increases blood sugar to a much greater degree than, say, chickpeas.

The amylopectin A of wheat products, “complex” or no, might be regarded as a super-carbohydrate, a form of highly digestible carbohydrate that is more efficiently converted to blood sugar than nearly all other carbohydrate foods.

The Framingham Crap Shoot

The Framingham risk score is a risk-assessment tool that has become the basis for heart disease prediction used by practicing physicians.

The Framingham system determines that:

· 35% of the adult population in the U.S., or 70 million, is deemed “low-risk.” Low-risk is defined as the absence of standard risk factors for heart disease; low-risk persons have no more than a 1-in-20 chance (5%) of dying from heart disease in the next 10 years. Physicians are advised by the American Heart Association (AHA) and its experts that no specific effort at risk reduction is necessary.

· 25%, or approximately 50 million, U.S. adults are deemed “high-risk,” based on the presence of 2 or more risk factors. High-risk persons experience a 20%-30% likelihood of heart attack in the next 10 years. People at high-risk are candidates for preventive efforts according to the guidelines set by the Adult Treatment Panel-III (Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults; ATP-III) for cholesterol-reducing statin drug treatment and for “lifestyle-modifying” advice.

· The remaining 40% of the adult population, or 80 million people, are judged “intermediate-risk,” with the likelihood of heart attack between 5-20% over the next 10 years. This group should receive preventive advice and might be considered for statin drug treatment.


Let’s do some arithmetic. By the above scheme, the low-risk population will experience 3,500,000 heart attacks over the next decade, or 350,000 heart attacks per year.

The intermediate-risk population (without preventive treatment) will experience 8,000,000 heart attacks over the 10-year time period, or 800,000 per year.

The high-risk population, the group most likely to receive standard advice on diet, exercise, and be prescribed statin cholesterol drugs, will have their risk reduced by 35% by preventive efforts over the 10-year period. This means that heart attacks over 10 years will be reduced from 12,500,000 to 8,125,000 by standard prevention efforts, or reduced to 812,500 heart attacks per year.

These numbers are no secret. They are well known facts that have simply come to be accepted by the medical community. In other words, the standard approach to heart attack prediction makes the fact that two million people will succumb to cardiovascular events in the next year no mystery. This exercise in prediction is coldly accurate when applied to a large population.

The problem is that this approach cannot reliably distinguish which individuals will have a heart attack from those who will not.

From 100 people chosen at random, for instance, the numbers game played above will not confidently identify who among those 100 will have a heart attack, who will not, who will develop anginal chest pains and end up with stents or bypass surgery, or who will die. We just know that some of them will. Some people at high risk will have a heart attack, some people at intermediate risk will have a heart attack, some people at low risk will have a heart attack.

For any specific individual (like you or me), it’s a crap shoot.

That's why precise individual measurement of cardiovascular risk is required for real risk assessment, not applying broad statistical observations and forcing them to conform to the unique life of a specific individual, particularly risk calculators with as few risk parameters as the Framingham risk score.

At what score should a heart catheterization be performed?

That's easy: NONE.

(Although I've addressed this previously, the question has come up again many times and I thought it'd be worth repeating.)

In other words, no heart scan score--100, 500, 1000, 5000--should lead automatically to procedures in someone who underwent a heart scan but has no symptoms.

This question is a common point of confusion.

In other words, is there a specific cut-off that automatically triggers a need for catheterization?

In my view, there is no such score. We can't say, for instance, that everybody with a score above 1000 should have a catheterization. It is true that the higher your score, the greater the likelihood of a plaque blocking flow. A score of 1000 carries an approximately 25-30% likelihood of reduced blood flow sufficient to consider a stent or bypass. This can nearly always be settled with a stress test. Recall that, despite their pitfalls for uncovering hidden heart disease in the first place, stress tests are useful as gauges of coronary blood flow.

But even a score of 1000 carries a 70-75% likelihood that a procedure will not be necessary. This is too high to justify doing heart catheterizations willy-nilly.

Unfortunately, some of my colleagues will say that any heart scan score justifies a heart cath. I believe this is absolutely, unquestionably, and inexcusably wrong. More often than not, this attitude is borne out of ignorance, laziness, or a desire for profit.

Does every lump or bump justify surgery, radiation, and chemotherapy on the chance it could represent cancer? Of course not. There is indeed a time and place for these things, but judgment is involved.

In my view, no heart scan score should automatically prompt a major heart procedure like heart catheterization in a person without symptoms. If a stress test is normal, signifying normal coronary flow (and there are no other abnormal phenomena, such as abnormal left ventricular function), then there is no defensible rationale for heart procedures. Heart procedures like stents and bypass cannot prevent heart attacks in future; they can only restore flow when flow is poor, or stop the heart attack that is about to occur.

However, EVERY heart scan score above zero is a reason to engage in a program of prevention.

"It's genetic"

At 53, Sam had been through the wringer with heart disease. After his first heart attack at age 50, he'd undergone four heart catheterizations, 5 stents, and, most recently, a bypass operation. He came to us to see if there was a better solution.

After hearing Sam's story, I asked,"Did your doctors suggest to you why you had heart disease?"

"Well, they said it was genetic, since my father went through the same thing in his early 50s, though he died after his second heart attack at age 54. They said it was bad luck and nothing could be done about it."

Though Sam's case is more dramatic than most, I hear this argument every day: Risk for heart disease is genetic.

It's true: There are indeed multiple reasons for inheriting causes for coronary heart disease, genes that heighten inflammatory responses, oxidative responses, modify lipoprotein particles, increase blood pressure, etc. There has even been some excitement over developing chromosomal markers for heightened risk.

That's all well and fine, but what can we do about it today?

In practical life, many inherited genetic patterns can be expressed in ways that you and I can identify--and correct. They are not chromosomal markers, but end products of genetic patterns. (Although there are indeed identifiable chromosomal markers, they have not yet led to meaningful treatments to my knowledge.)

These readily identifiable patterns include:

--Lipoprotein(a)--Clearly genetically transmitted, passed from mother or father to each child with a 50% likelihood, then you onto your children if you have it.

--Small LDL--Although small LDL is amplified by high-carbohydrate diets and obesity, it can also occur in slender people who do not indulge in carbohydrates --i.e., a genetic tendency. Or, it can be a combination of poor lifestyle magnifying the genetic tendency for small LDL.

--Low HDL--Particularly the extremes of low HDL below 30 mg/dl. (Although, interestingly, I am seeing more of these people, though not all, respond to vitamin D replacement. Perhaps an important subgroup of low HDL people are really Vitamin D Receptor (VDR) variants.)

--ApoE--Two variants are relevant: ApoE2 and ApoE4. In my experience, it's the E2 that carries far greater significance, though the data are somewhat scanty. ApoE4 people are more sensitive to the fats in their diet (greater rises in LDL with fats; thus, some people advocate a tighter saturated fat restriction with this pattern, though I am not convinced that is the best solution), while ApoE2 people are exceptionally sensitive to carbohydrates, develop extravagant increases in triglycerides, and are very diabetes-prone with even the most minimal weight gain. If two "doses" of the E2 gene are present (homozygotic), then the tendencies are very exagerrated. E4 people are also subject to greater likelihood of Alzheimer's, though it is not a certain risk in a specific individual.

--Postprandial disorders--We use the fasting intermediate-density lipoprotein (IDL) as an easy, obtainable index of the ability to clear after-eating byproducts of meals from the blood. Increased IDL has been related to increased coronary, carotid, and aortic aneurysmal disease.

--Hypertriglyceridemia-i.e., increases in triglycerides, While not all forms of high triglycerides confer risk for atherosclerosis, many do, particularly if associated with IDL, small LDL, increased LDL particle number and/or apoB.


There are more, but you get the point. There are clear-cut genetically-transmitted reasons for greater risk for cardiovascular disease. Some, like lipoprotein(a), yield very high risk. Others, like increased triglycerides, yield mixed levels of risk.

Importantly, all of these patterns--ALL--are identifiable and are treatable. Treatment may not always be the easiest thing, but they are treatable nonetheless. While lipoprotein(a), for instance, is the most difficult pattern to correct in the above list, I remind everyone that our current "record holder" for reversal of plaque and heart scan scores--63% reduction--has lipoprotein(a) that we corrected.

If you've been told that your risk for cardiovascular disease or coronary plaque is "genetic" and thereby uncorrectable and hopeless, run the other direction as fast as you can. Get another opinion from someone willing to take the modest effort to tell you precisely why.

Tim Russert Revisited

A Heart Scan Blog reader brought this piece by Dr. MacDougall to my attention.

Dr. MacDougall created a fictitious posthumous conversation between himself and the late Tim Russert. MacDougall paints a picture of a hardworking, hard-living man who adhered to an overindulgent lifestyle of excessive eating. He concludes that a vegetarian, low-fat diet would have saved his life.

Beyond being disrespectful, I would differ with Dr. MacDougall’s assessment. In fact, I’ve heard an interview with Mr. Russert’s primary care physician in which the doctor claimed that Mr. Russert had been counseled on the need for a low-fat diet and, in fact, adhered to it quite seriously. Far from being an overindulgent, overeating gourmand, he followed the dictates of conventional dietary wisdom according to the American Heart Association. The low-fat diet articulated by Dr. MacDougall is simply a little more strict than that followed by Mr. Russert.

What exactly could Mr. Russert have done to prolong his life? Several basic strategies:

--Added fish oil. This simple strategy alone would have reduced the likelihood of dying suddenly by almost half.

--Eliminated wheat and cornstarch—Mr. Russert developed diabetes in the last few years of his life. By definition, diabetes is an inability to handle sugars and sugar-equivalents. Wheat and cornstarch yield immediate and substantial surges in blood sugar greater than table sugar; elimination causes weight to plummet, blood sugar to drop, and diabetes (at least in its early phases) can be eliminated in many people, particularly those beginning with substantial excess weight.

Just those two strategies alone would more than likely have avoided the tragic death that brought Mr. Russert’s wonderful life and career to an abrupt end.

Of course, he could have even taken his heart health program even further, as we do in the Track Your Plaque program. While the conversation has focused on how to avoid tragic events like sudden cardiac death, why not take it a step farther and ask, "How can coronary plaque be measured, tracked, and reversed?"

In that vein, Mr. Rusert could have restored vitamin D to normal levels; identified all hidden sources of heart disease using lipoprotein testing (though he had small LDL without a doubt, given his generous waist size, HDL of 36 mg/dl and high triglycerides); considered niacin. Simple, yet literally lifesaving efforts, that make reversal much more likely.

Those simple steps, in fact, would have tipped the scales heavily in Mr. Russert’s favor, making a heart attack and/or sudden death from heart disease exceptionally unlikely.

Water: Bottled vs. tap

The Fanatic Cook has a great post discussing the findings of the Environmental Working Group (EWG) on the quality of bottled water.

The full text of the study from the EWG can be viewed here.

They report that "the bottled water industry promotes an image of purity, but comprehensive testing by the Environmental Working Group (EWG) reveals a surprising array of chemical contaminants in every bottled water brand analyzed" . . . After analyzing 10 brands, they conclude that "tests strongly indicate that the purity of bottled water cannot be trusted. Given the industry's refusal to make available data to support their claims of superiority, consumer confidence in the purity of bottled water is simply not justified."

"EWG's study has revealed that bottled water can contain complex mixtures of industrial chemicals never tested for safety, and may be no cleaner than tap water. Given some bottled water company's failure to adhere to the industry's own purity standards, Americans cannot take the quality of bottled water for granted. Indeed, test results like those presented in this study may give many Americans reason enough to reconsider their habit of purchasing bottled water and turn back to the tap."


For these reasons, as well as environmental reasons (plastic bottles filling up dumpsites), I think it is becoming clearer and clearer that bottled water is something we should only use in a pinch, not habitually.

Can CRP be reduced?

The JUPITER study has sparked a lot of discussion about c-reactive protein, or CRP.

If we follow the line of reasoning that prompted this study, reducing CRP may correlate with reduction of cardiovascular events. Thus, in the JUPITER study, Crestor 20 mg per day reduced cardiovascular events by nearly half.

From a CRP perspective, starting values were 4.2 mg/dl in the Crestor group of the trial, 4.3 mg/dl in the placebo group. After 24 months, CRP in the Crestor group was 2.2 mg/dl, 3.5 mg/dl in the placebo group, representing a 37% reduction.

Now, in our Track Your Plaque program--an experience that has yielded the virtual ELIMINATION of cardiovascular events--we aim for a CRP level of 1.0 mg/dl or less, ideally 0.5 mg/dl or less. The majority of people achieve these ambitious levels. In fact, it is a rare person who does not.

How do we achieve dramatic reductions in CRP? We use:

--Weight loss through elimination of wheat and cornstarch--This yields impressive reductions.

--Vitamin D--I have no doubt whatsoever of vitamin D's capacity to exert potent anti-inflammatory effects. I am not entirely sure why this happens (enhanced sensitivity to insulin, reduced expression of tissue inflammatory proteins like matrix metalloproteinase and others, etc.), but the effect is profound.

--Elimination of junk foods--like candies, cookies, pretzels, rice cakes, potato chips, etc.

--Exercise--Amplifies the benefits of diet on CRP reduction.

--Not allowing saturated fats to dominate--Yes, yes, I know. The demonization of saturated fat conversation has been largely replaced by the Taubesian saturated fat has not been confidently linked to heart disease conversation. But controlled feeding studies, in which a single component of diet is manipulated (e.g., saturated vs. monounsaturated vs. polyunsaturated fat) have clearly shown that saturated fats do activate several factors in the inflammatory response.

--Fish oil--Though I am a firm believer in the huge benefits of omega-3 fatty acid supplementation/restoration, the anti-inflammatory effect is modest from a CRP perspective. However, there are anti-inflammatory benefits beyond that of simple CRP (via normalization of eicosanoid metabolism and other pathways).

--Weight loss--A BIG effect. Weight loss drops CRP like a stone. The CRP-reducing effect is especially large if achieved via carbohydrate reduction.

Of course, this is much more complicated than taking a pill. But it is effective to achieve health benefits outside of cardiovascular risk, is enormously useful as part of a weight loss effort, and doesn't cost $1400 per year like Crestor.

In short, if CRP reduction is the goal, it certainly does not have to involve Crestor.

CRP and Jupiter

What is C-reactive protein (CRP)?

It is a blood-borne protein that originates in the liver and serves as an index of the body's inflammatory state. It is triggered by yet another inflammatory signal molecule, interleukin-6.

What triggers this cascade of inflammatory markers? Any inflammatory stimulus, such as being overweight, lack of exercise, vitamin D deficiency, viral illness no matter how trivial, any inflammatory disease like arthritis, small LDL, high triglycerides, poor diet rich in processed foods, resistance to insulin, any injury, incipient diabetes, hidden cancer, lack of education (no kidding), etc.

In other words, many, many conditions, from trivial to serious, trigger increased inflammatory markers like CRP.

A recent analysis (Genetically elevated C-reactive protein and ischemic vascular disease of persons with genetically elevated levels of CRP) suggests that CRP does not, by itself, cause atherosclerotic disease. CRP is therefore simply a marker for conditions that heighten inflammatory responses.

The AstraZeneca people sponsored the enormous JUPITER study of the statin drug, Crestor, that has been causing a stir, mostly glowing pronouncements of how the world would be a better place if everyone took Crestor.

In JUPITER, nealry 18,000 people (men 50 years and over, women 60 years and over) took 20 mg per day Crestor for two years. Participants all had starting LDL cholesterols in the "normal" range of no higher than 130 mg/dl and elevated CRP of 2 mg/dl or greater.

Crestor treatment resulted in 44% reduction in nonfatal heart attack, nonfatal stroke, hospitalization for unstable angina, revascularization (bypass surgery, stents) and death from cardiovascular causes. The reduction in nonfatal heart attack was most marked at 55%.

Admittedly, these are impressive results. Benefits held true for both males and females. At the very least, JUPITER should put to rest some of the fringe arguments that statins do not reduce cardiovascular events. They do. There is no sense in arguing against that. While we might argue about the value of statins in various subsets of people, there is no doubt that they do indeed exert a significant effect.

However, contrary to the hype and broad pronouncements of my colleagues, my concerns are:

1) Rather than shotgun the inflammatory response with a statin drug regardless of cause, doesn't it make more sense to ask why a specific individual has an increased CRP in the first place? For instance, if the answer is vitamin D deficiency, doesn't correction of the deficiency make more sense? (Vitamin D by itself reduces CRP around 60%--more than statin drugs.) Not to mention you obtain all the extraordinary benefits of vitamin D restoration, such as reduced cancer risk, increased bone density, relief from winter "blues," rise in HDL, etc. How about junk foods, obesity, and unrelated inflammatory conditions? Would we therefore indirectly be treating obesity with Crestor?

2) Crestor 20 mg per day, contrary to the study and to many statin studies, will not be tolerated for long by the majority. Muscles aches are not common--they are inevitable, sometimes incapacitating. While JUPITER showed 15% of both treatment and placebo groups experienced muscle effects--no different--this is wildly contrary to real life.

3) While there was a 55% reduction in the number of heart attacks, there continued to be a substantial number of heart attacks in the Crestor treatment arm. Clearly, reduction of CRP with Crestor, while helpful, is not a cure.

I view studies like JUPITER as simply an interesting piece of semi-scientific evidence, tainted to an unknown degree by commercial interests (including those of Dr. Paul Ridker, one of the principal investigators). It is not a mandate to use Crestor carte blanche in people with elevations of CRP.

My interpretation of these data in a practical sense is that Crestor 20 mg per day as sole therapy is useful in a disinterested, non-compliant patient who is unwilling to make substantial changes in lifestyle and nutrition. Helpful? Yes, but hardly an invitation for the world to take Crestor.

I believe that doesn't include any of the readers of this blog.

Nutritional approaches: Large vs. small LDL














It is now a rare person who does not have at least some proportion of their LDL cholesterol as small particles. I estimate that, of the people who come to the office or report their data on the Track Your Plaque website, 90% have at least 40-50% small LDL particles. Some people have 100% small LDL particles. The sample NMR lipoprotein report shows the result for someone with a severe small LDL pattern (the tallest red bar labeled 1354 nmol/L, compared to the 74 nmol/L of the tiny red bar of large LDL.)

The nutritional approach for small vs. large LDL differs. Small LDL particles are most sensitive to carbohydrate intake; large LDL particles are more sensitive to saturated fats.

The conventional "heart healthy" diet that restricts saturated fat reduces large LDL but exerts no effect on small LDL. Thus, a diet that is restricted in saturated fat and weighed more heavily with "healthy whole grains" triggers small LDL particles. Followers of the conversations here recognize that small LDL particles are flagrant triggers for coronary plaque; they have, in fact, become the number one most common cause for heart disease in the U.S.

When you have lipoproteins tested, you can therefore gauge the likely result obtained when specific dietary changes are made. Follow the low saturated fat advice, large LDL will drop modestly, but small LDL skyrockets.













(Image courtesy Liposcience, Inc.)


Eliminate sugars, wheat, and cornstarch and you will see small LDL plummet (along with total LDL).

As an aside, my personal observation is that the "need" for statin cholesterol drugs can be reduced dramatically by paying attention to this important LDL size distinction.

Factory hospitals

Twenty years ago, the American farming industry experienced a dilemma: How to grow more soybeans, corn, or wheat from a limited amount of farmland, raise more cattle and hogs in a shorter period of time, fatter and ready for slaughter within months rather than years?













(Image courtesy Wikipedia)

The solution: Synthetically fertilize farmland for greater crop yield; “factory farms” for livestock in which chickens or pigs are crammed into tiny cages that leave no room to turn, cattle packed tightly into manure-filled paddocks. As author Michael Pollan put it in his candid look at American health and eating, The Omnivore’s Dilemma:


“To visit a modern Concentrated Animal Feeding Operation (CAFO) is to enter a world that for all its technological sophistication is still designed on seventeenth-century Cartesian principles: Animals are treated as machines—“production units”—incapable of feeling pain. Since no thinking person can possibly believe this anymore, industrial animal agriculture depends on a suspension of disbelief on the part of the people who operate it and a willingness to avert one’s eyes on the part of everyone else. . .”


Pollan goes on to argue that the cultural distance inserted between the brutal factory farm existence of livestock and your dinner table permits this to continue:


“. . .the life of the pig has moved out of view; when’s the last time you saw a pig in person? Meat comes from the grocery store, where it is cut and packaged to look as little like parts of animals as possible. The disappearance of animals from our lives has opened a space in which there’s no reality check on the sentiment or the brutality . . .”


The same disconnect has occurred in healthcare for the heart. The emotional distance thrust between the hospital-employed primary care physician, the procedure-driven cardiologist, the crammed-into-a-niche electrophysiologist (heart rhythm specialist) or cardiothoracic surgeon whose principal concerns are procedures—with an eye always towards litigation risk—mimics factory farms that now litter the landscape of the Midwest. The hospitals and doctors who deliver the process see us less as human beings and more as the next profit opportunity.

The “factory hospital” has allowed the subjugation of humans into the service of procedural volume, all in the name of fattening revenues. Never mind that people are not (usually) killed outright but subjected to a succession of life-disrupting procedures over many years. But whether livestock in a factory farm or humans in a factory hospital, the net result to the people controlling the process is identical: increased profits.

The system doesn’t grow to meet market demand, but to grow profits. The myth that allows this growth is perpetuated by the participants who stand to gain from that growth.

See hospitals for what they are: businesses. Despite most hospitals retaining "Saint" in their name, there is no longer anything saintly or charitable about these commercial operations. They are ever bit as profit-seeking as GE, Enron, or Mobil.

Medicare and The Law of Unintended Consequences

This post carries on the line of conversation begun in The Origins of Heart Catheterization: Part I and Part II.



While Dr. Sones labored in the relative obscurity of his catheterization laboratory, the American public was experiencing a crisis in healthcare availability, particularly among the over-65 age group. The population of elderly in the U.S. was growing rapidly. Between 1950 and 1963, their ranks grew from 12 million to 17.5 million. The cost of hospital care was also increasing 6.7% annually, several times the rate of increase in the cost of living of the time. From 1950 to the day of Dr. Sones’ discovery, the average cost for a day in the hospital jumped from $29 to $40. As a result, private health insurance carriers were forced to increase rates, driving premiums higher and farther out of reach for many. Half of all elderly were uninsured. Many feared that, while the sophistication of medical services advanced, healthcare was becoming increasingly unavailable to many, perhaps most, Americans.

The pivotal contribution that ignited wide dissemination of healthcare technology didn’t come from a physician, nor someone in healthcare. It was spurred by a nearly-forgotten bureaucrat. Without the behind-the-scenes laboring of this one man, the present healthcare system might be quite different.

It was largely the work of Nelson H. Cruikshank, an ordained Methodist minister with a Master of Divinity degree and veteran of battling for rights of the elderly and poor deprived of health care. For 10 years, Cruikshank served as director of the AFL-CIO's Social Security Department and had been instrumental in getting the Social Security Disability act passed. Working on the side of organized labor but maintaining the public demeanor of a church pastor, Cruikshank gained a reputation as a fighter for the working man, one who didn’t back down from a political brawl. In an interview regarding the question of corporate-retained earnings for capital investment, he blasted the practice, calling it "taxation by corporation without representation. Through prices paid for consumer goods, buyers are providing capital for industries over which they have no control and from which they receive no dividends” (Time Magazine, Dec. 20, 1948).

For years, Cruikshank lobbied tirelessly on behalf of American unions to bring the new national healthcare bill, known as Medicare, to a vote on the floor of Congress. Numerous efforts at a national program had languished for a decade before Medicare was drafted, and the Medicare legislation remained bottlenecked for years in committees. Cruikshank’s relentless and forceful persuasion was instrumental in finally bringing the bill to a vote. Among the most vocal opponents Cruikshank parried was the American Medical Association (AMA), terrified that the new program would lead to loss of control over healthcare delivery and reimbursement. The AMA labeled Medicare "the most deadly challenge ever faced by the medical profession."

Cruikshank proved how tough he was when he faced off with Dr Morris Fishbein, then president of the AMA, in a radio debate. Oscar R. Ewing, attorney and Democratic political organizer under the Truman administration, offered these reminiscences of the debate:

“Dr. Fishbein described the horrible confusion that existed in the [government-run] British Health Service that had recently been established in Britain. He told of the utter confusion that he found existed when he was in England a few weeks previously; that there were long queues in every doctor's office, that doctors were overburdened with paper work; that a mother who wanted an extra allowance of milk for her sick child had to get a doctor's prescription for it and then go to the Health Department for permission to buy the milk. Dr. Fishbein painted a picture of complete confusion.

“After Dr. Fishbein had described all these horrible details he found existing when in England a few weeks earlier, Mr. Cruikshank pulled out this particular diary [published in a nationally-syndicated column called “Dr. Fishbein's Diary” ] of Dr. Fishbein in which he described his last visit to London. He had arrived in London Friday morning and that afternoon had gone out to spend the weekend with Lord and Lady so-and-so at their country place; that he'd come back to London Monday morning, had stopped by the Health Department to pick up some papers, and had gone on to catch the noon plane for Paris. So the questioner then asked, "Well, is your appraisal of the British Health Service based on those few hours in London?" The question was a stinger and pretty much discredited Dr. Fishbein.”


(Interview by Mr. J.R. Fuchs, April 29, 1969; Harry S. Truman Library Archives)



Cruikshank went on to point out that Dr. Fishbein had indeed never visited the offices of British general practitioners and had spent his brief stay in the company of British aristocracy, attending the Olympics, then making the rounds of Parisian night clubs. Fishbein stumbled through the remainder of the interview, trying unsuccessfully to cover up his gaff. Dr. Fishbein was forced out of his post as AMA president by his peers shortly following the humiliating episode.

Largely due to the years of behind-the-scenes maneuvering by Mr. Cruikshank, on July 30, 1965, President Lyndon Johnson signed the Social Security Amendment that enacted the Medicare program. The legislation that survived into law included Medicare Part A, the portion of the program providing payment for hospital-based diagnostic and treatment services, and Medicare Part B, allowing payment for office-based services and outpatient diagnostic tests.

Finally, after decades of political battles, a national healthcare bill had been passed. Although benefits were restricted to only those eligible for Social Security benefits, it represented a start, a first step toward greater access to healthcare for the broader American public.

At first, the full implications of the Medicare program were not apparent. But as healthcare technology advanced, including that sparked by Sones’ innovation in coronary imaging, Medicare, much as engineered in large part by Nelson Cruikshank, proved a bonanza of payment for heart procedures. Medicare also set the pace for the payment for procedures by non-government, private health insurance.

Thus the stage was set. Thanks to Medicare, over the next 40 years cardiovascular healthcare services, yielding generous revenue for practitioners and hospitals, exploded on the scene, much to the surprise of many, including the AMA. When then president of the American College of Cardiology, Dr. Charles Fisch, was asked how the passage of Medicare affected cardiology, he replied, “It made cardiologists rich, as simple as that” (American Cardiology: The History of a Specialty and Its College, W. Bruce Fye, MD). Indeed, from its introduction in 1965 to 1980, Medicare payments for health claims ballooned 10-fold from $9.6 billion to $105.7 billion, a substantial portion of which went to pay for cardiology claims.

Little did Nelson Cruikshank, ministerial defender of the working man, anticipate that the Medicare he helped engineer would prove to be the catalyst for explosive growth of the modern cardiovascular healthcare system. Ironically, the program of healthcare-for-all that Cruikshank envisioned has, over the last 40 years, soured into a self-serving system that has been corrupted by the profit motive.

In too many instances, it’s a system that uses the working man as its victim, rather than its beneficiary.