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.

Quieting the insulin storm

The cycle of eating, satiety, and hunger is largely driven by insulin and blood sugar responses.

For instance, if I eat a bowl of Cheerios, my blood sugar will surge to 140 mg/dl or higher (how high depending on insulin sensitivity). The flood of sugar from this Frankenfood triggers the release of insulin; blood sugar then settles back down.

The decline in blood sugar back down to normal or below normal powerfully triggers hunger. Variable degrees of shakiness, mental fogginess, and irritability also commonly occur. Most people experience this to some extent; some experience an exagerrated version called "reactive hypoglycemmia" and can suffer peculiar personality changes, irrational and even violent behavior.

Foods made with wheat or cornstarch raise blood sugar higher and faster than table sugar. Accordingly, blood sugar and insulin swing more widely with these food: highs are higher, lows are lower. People who therefore follow the standard mantra of "eat plenty of healthy whole grains" therefore experience a 2-3 hour long cycle of eating, brief satiety, and recurrent hunger. Cravings for snacks, impulsive eating, and overeating all occur during the period when blood sugar has dropped and hunger is powerfully triggered.

Eliminating this up and down fluctuation is therefore key to regaining control over appetite, losing weight, reducing small LDL and triglycerides, reducing blood sugar, and putting out the fires of inflammatory responses.

You can accomplish this by:

1) Eliminating foods that trigger the exagerrated rises in blood sugar--Wheat, cornstarch, polished rices, white and red potatoes, and candy.

2) Adding a healthy oil to every meal--a strategy that prolongs satiety and helps suppress sugar-insulin fluctuations.


The ful nuts and bolts details of this diet will be released with the New Track Your Plaque Diet. Part I has already been released; part II is coming any day on the Track Your Plaque website.

Scare tactics

"You're a walking time bomb."

"I can't be responsible for what happens to you."

"Your blockage is in the artery called the 'widow-maker.'"




Familiar lines? These are the well-rehearsed warnings commonly used by cardiologists to persuade a patient to undergo a procedure (heart catheterization and all that follow).

Something happens when you hear these words about your health. Most people's resolve to explore alternatives, get another opinion, think it over, promptly crumbles when they hear these words. These particular warnings have been time-tested and are surprisingly effective.

Unlike many other conditions, heart disease does indeed result in catastrophic events without warning. Unlike, say, cancer, heart disease can wreak damage suddenly. That's all true.

What bothers me is the vigor with which the opportunity for hospital procedures is pursued.

The thinking is that hospitals procedures = saving a life. In the vast majority of people, this is nonsense. Procedures like heart catheterization, stents, bypass, do save lives if someone is in the throes of a catastrophe. The problem is that most people who undergo procedures are not in the midst of catastrophe and have every hope of avoiding it altogether with some simple efforts towards prevention.

Imagine this conversation: "Yes, Mr. Smith, you do have heart disease, Even though you have no symptoms and your stress test is normal, I believe that we should 1) identify the causes of your heart disease, then 2) correct them. Of course, if you don't want to engage in this prevention process, then there may be a point at which heart procedures may be necessary. But I believe that you have great hopes of avoiding them and avoiding heart attack."

Self-Directed Testing

In the last Heart Scan Blog post, I listed the poll results on success vs. failure in trying to obtain requested blood work through doctors. The results of that informal poll revealed that a substantial number of people encounter resistance to one degree or another in trying to obtain blood tests.

But the world of self-directed testing is growing. In addition to your ability to circumvent your doctor by getting your own blood work done, you can now:

--Obtain many imaging tests on your own--Heart scans can be obtained without your doctor's involvement, for instance. The ultrasound screening services, like that offered by Lifeline, mobile services that provide carotid, abdominal aorta, and osteoporosis screening services; full body scans, and others.
--Identify and treat some conditions--Internet information has gotten quite powerful to assist individuals in recognizing when a condition might be present. (However, this is also a landmine for trouble if not properly used.)
--Genetic testing--While just in its infancy, direct-to-consumer genetic testing is now offered by two outfits that I'm aware of.
--Unusual laboratory tests--e.g., heavy metals, omega-3 fatty acid content, cancer markers.

One drawback to the emerging world of self-directed testing: There is no insurance coverage. However, this will become less and less of an issue as time passes, since it is clear that most Americans will need to bear a greater portion of healthcare costs in future, since some conventional services may even be rationed for cost containment; higher copays and the emergence of medical savings accounts, providing the individual with more control over how healthcare dollars are spent; competition in self-directed healthcare services, which will reduce costs. Imagine, for instance, several more direct-to-consumer services to obtain blood tests appear. They will need to compete on price and service.

While my colleagues are terrified of the potential for abuse of such tests, my reaction is the opposite: I am enormously excited by the potential for individuals to seize more and more control over their health.

Of course, with greater freedom comes greater responsibility. But the long-term net result will be, in my view, a healthier, more satisfied healthcare consumer with reduced healthcare costs.

Self-testing

Here are the results of the latest Heart Scan Blog poll (84 respondents):


When you ask your doctor to perform a specific blood test, does he/she:


Do it without question?
38 (44%)


Do it but express reservations?
25 (29%)


Do it very grudgingly?
13 (15%)


Refuse outright?
9 (10%)



I was encouraged that 44% of respondents are/were able to obtain the blood work they requested without resistance. Sadly, however, the majority do either encounter reluctance or outright resistance.

Why would your doctor impose barriers to your ability to obtain laboratory tests? Well, several potential reasons:

1) He/she feels that they are charged with your health safety, and you might be led down a misleading, potentially dangerous path.

2) He/she feels that the tests are truly unnecessary and that you will be wasting the money of the "system."

3) He/she doesn't understand the tests, or is unfamiliar with them.

4) He/she feels that the doctor should be in complete control, not you. How dare you try to usurp the doctor-as-dictator of your health!


In reality, number 1 is understandable but rarely occurs. I have indeed have had requests, though rare, for outrageously inappropriate tests for the issue at hand, usually due to a misinterpretation of some information by the patient.

I'm not sure how often number 2 truly is. For instance, it is not uncommon for the doctor to have an ownership stake in the laboratory. There are several large primary care groups in Milwaukee who are notorious over-users of laboratory tests, with extraordinary batteries of dozens of tests every few months on the flimsiest reasons , clearly motivated by . . . money. On the other hand, there are physicians who do consciously try and order tests rationally and cost-effectively. I suspect that this is a minority.

I feel quite confident that number 3--your doctor's ignorance--is probably the most common reason he/she is reluctant or refuses to allow you access to a test. Most respondents I suspect are referring to many of the tests that I have been advocating, such as lipoprotein testing, lipoprotein(a), and vitamin D blood levels. I am uncertain how any of these could be construed to be dangerous. But ignorance of the value of these tests is rampant and resistance is nearly always based on not having explored these issues and having no appreciation for their importance. Of course, the beleaguered primary care physician is, no surprise, inundated by so much information across such a wide range that he/she has become expert at nothing, barely able to even deliver the full scope of genuine up-to-date primary services any longer. My colleagues, the cardiologists. . . well, you know my feelings about their attitudes: If it doesn't make money, then why should I bother? Devote months or years studying something that doesn't ring the cash register?

I see this dilemma as yet more evidence of the growing disenchantment with the doctor-as-gatekeeper model, the centuries old paternalistic "I will tell you what to do and you will do it." It worked when the doctor was educated and had access to knowledge you could never realistically obtain because you couldn't read, or you were too poor to afford books and education, or because medical information was made privy only to select people.

It's not that way anymore: The information you have access to is the same information my colleagues and I have access to: a level playing field. Along with the changing rules of the game, the game itself must eventually change.

I believe that people should have access to self-testing. Indeed, there is a growing industry of direct-to-consumer laboratory testing, such as that offered by Life Extension and LabSafe . For the most part, these offer tests without potential insurance reimbursement.

But the landscape is changing: We are just beginning a new age of self-empowerment, self-directed healthcare.

Whenever I say this, some people are angered that the majority of people will be too lazy, stupid, or poor to join the movement. What I am not saying is that we should agitate to make the system a patient-only directed process and completely remove the doctor. What I am saying is that the patient should and will play an increasingly important role in determining the content and direction of his/her care, especially as the patient becomes far more knowledgeable about issues relevant to his/her health.


The new tools of health measurement

If there were a new mantra of the new science of insight into health and long life, it would be “measure, measure, and measure.”

Never before in history have we had access to the analytical, laboratory, imaging, quantifying health tools that we have today. We can locate, scan, measure, all down as far as the level of basic codons of the genetic sequence.

The health-inquiring public has so far been permitted just a tip-of-the-tongue taste of these quantitative phenomena in such things as cholesterol values (“know your numbers!”) and blood pressure. Women now discuss their bone density scores over coffee, men their PSAs (prostate specific antigen).

But a curious irony has emerged: Like early 20th century males uncomfortable with women battling for suffrage, healthcare professionals, themselves comfortable with measurements and numbers, are distinctly uncomfortable when some of the same information falls into the hands of the healthcare consumer.

These phenomena play out in especially dramatic fashion in the world of heart health. The public now has broad access (many without a doctor’s order) to an extraordinary array of health measurement tools that can potentially yield enormous benefits for prevention of the most common conditions, information that can be applied by tracking over time.

Measures like heart scan scores, vitamin D blood levels, lipoprotein(a)--measures that most doctors have little or no interest in obtaining, yet they serve crucial roles in maintaining and tracking your health.

The new paradigm is emerging: the tools are getting better and better, they are becoming more accessible.

Increasing sales, growing the business

I continue my portrayal of the fictional hospital, St. Matthews. Though fictional, it is based on real facts, figures, and situations.

Despite their success, administrators at St. Matthews’s Hospital continually fret over how to further expand their enterprise.

Market share can be increased, of course, by competing effectively with other hospitals, but that can be a tough arena. After all, St. Matthews’ competitors deliver pretty much the same services, and draw areas for patients overlap. The last thing the hospital wants is the appearance that heart care is a “cookie cutter” process, the same everywhere. In fact, this trend has hospital administrators wringing their hands. Two competing hospital systems in town recently launched multi-million dollar ad campaigns employing some of the same aggressive tactics St. Matthews’ marketers used successfully in past.

If St. Matthews is going to grow, new markets will need to be explored. What other strategies can a hospital system use to continue climbing the growth curve?

St. Matthews’ hospital administrators have drawn a number of lessons from other businesses. How about squeezing more procedures out of the population you already take care of? That’s an age-old rule of business: your easiest sales come from repeat customers. A former stent patient is going to “need” annual nuclear stress testing ($4000), more stents (about $25,000–39,000 per hospitalization), CT angiogram ($1800–2400), bypass surgery ($84,000), and so on. “Check-up” catheterizations, though clearly of little or not benefit to patients, are silently encouraged, yet another example of the bonanza of repeat procedures possible.

The lesson that “once a heart patient, always a heart patient” has been honed to an art form in business practices at St. Matthews and other hospitals like it. If you enter the system through your primary care physician or cardiologist, there’s an excellent chance you’ll end up with several procedures, diagnostic and therapeutic, over the ensuing years. Accordingly, St. Matthews provides a very attentive after-discharge follow-up program, complete with access to friendly people, phone centers, “support groups,” and even an occasional festive get-together, all in an effort to ensure future return to the system.

All in all, the St. Matthews Hospital System is a hugely successful operation. It provides jobs for thousands of area residents and provides high-tech, high-quality healthcare. Like any business—and no doubt about it, St. Matthews is a business with all the trappings of a profit-seeking enterprise—it grows to serve its own interests. The tobacco industry didn’t grow to its gargantuan proportions by doing good, but by selling a product to an unsuspecting public. So, too, hospitals.

Curiously, hospitals like St. Matthews continue to operate under the sheltered guise of not-for-profit institution with the associated tax benefits, ostensibly serving the public good. This means that all end-of-year excess revenues are re-invested and not distributed to investors. But non-profit does not mean that individuals within the system can’t benefit, and benefit handsomely. Under St. Matthews’ non-profit umbrella, many businesses thrive: 35 pharmacies, extended care facilities to provide care after hospital discharge, drug and medical device distributors, even a venture capital arm to fund new operations. The financial advantage conferred by “non-profit” status has permitted the hospital to compete with other, for-profit businesses, at a considerable advantage. For this reason, attempts have been made over the years to strip them of what some believe is an unfair advantage; all have failed.

While profits may not fall to the bottom line, money does indeed get paid out to many people along the way. Executives, for instance, pay themselves generous salaries and consulting fees, often from several of the entities in this complex business empire. Physicians are brought in as “consultants” or are awarded “directorships” for hundreds of thousands of dollars per year—Director of Research, Director of Cardiovascular Services, etc. Don’t forget the $3.7 million dollar annual salary paid to the CEO.

Hospitals and doctors have a vested interest in preserving this financial house of cards. They will fiercely battle anyone or anything that threatens the stream of cash. During a recent meeting of important doctors at St. Matthews Hospital, one cardiologist bravely voiced his concern that bypass surgery was performed too freely on too many patients in the hospital. The doctor was promptly and quietly asked to remove himself from the meeting. Several days later, he received a letter announcing his dismissal from the committee.

The silent conspiracy conducted by hospitals and cardiologists serves their own purposes better than the good of the public. Under the guise of good works, hospitals continue to promote strategies which are, for the most part, outdated, inefficient, inaccurate, and expensive. But that’s the rub. Expensive to you and your insurance company means more money for the recipient: your hospital and cardiologist, and the powers that support them. All this occurs while the real solutions that are of benefit to the public continue to be overlooked, hidden in the shadows.

Top Doctor

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

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

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

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

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

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

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

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

True story, though names have been changed to protect the guilty.

Is Dr. Connors just an “outlier” among colleagues who toe a more conservative line? Or does his brand of commercial enterprise in hospital heart care represent the ideal that they seek, brazenly and ambitiously seeking to expand the procedural solution to heart disease to the exclusion of patient care and real human interaction?
All posts by william-davis

Heart Scan Blog Redux: Cheers to flavonoids

Because in Track Your Plaque we've been thinking a lot about anthocyanins, here's a rerun of a previous Heart Scan Blog post about red wine. (Anthocyanins are among the interesting flavonoids in red wine, along with resveratrol and quercetin.)


The case in favor of healthful flavonoids seems to grow bit by bit.

Flavonoids such as procyanadins in wine and chocolate, catechins in tea, and those in walnuts, pomegranates, and pycnogenol (pine bark extract) are suspected to block oxidation of LDL (preventing its entry into plaque), normalize abnormal endothelial constriction, and yield platelet-blocking effects (preventing blood clots).

Dr. Roger Corder is a prolific author of many scientific papers detailing his research into the flavonoids of foods, but wine in particular. He summarizes his findings in a recent book, The Red Wine Diet. Contrary to the obvious vying-for-prime-time title, Dr. Corder's compilation is probably the best mainstream discussion of flavonoids in foods and wines that I've come across. Although it would have been more entertaining if peppered with more wit and humans interest, given the topic, its straightfoward, semi-academic telling of the story makes his points effectively.

Among the important observations Corder makes is that regions of the world with the greatest longevity also correspond to regions with the highest procyanidin flavonoids in their wines.




Regarding the variable flavonoid content of wines, he states:

Although differences in the amount of procyanidins in red wine clearly occur because of the grape variety and the vineyard environment, the winemaker holds the key to what ends up in the bottle. The most important aspect of the winemaking process for ensuring high procyanidins in red wines is the contact time between the liquid and the grape seeds during fermentation when the alcohol concentration reaches about 6 percent. Depending on the fermentation temperature, it may be two to three days or more before this extraction process starts. Grape skins float and seeds sink, so the number of times they are pushed down and stirred into the fermenting wine also increases extraction of procyanidins. Even so, extraction is a slow process and, after fermentation is complete, many red wines are left to macerate with their seeds and skins for days or even weeks in order to extract all the color, flavor, and tannins. Wines that have a contact time of less than seven days will have a relatively low level of procyanidins. Wines with a contact time of ten to fourteen days have decent levels, and those with contact times of three weeks or more have the highest.

He points out that deeply-colored reds are more likely to be richer in procyanidins; mass-produced wines that are usually "house-grade" served at bars and restaurants tend to be low. Some are close to zero.

Wines rich in procyanidins provide several-fold more, such that a single glass can provide the same purported health benefit as several glasses of a procyanidin-poor wine.

So how do various wines stack up in procyanidin content? Here's an abbreviated list from his book:

Australian--tend to be low, except for Australian Cabernet Sauvignon which is moderate.

Chile--only Cabernet Sauvignon stands out, then only moderate in content.

France--Where to start? The French, of course, are the perennial masters of wine, and prolonged contact with skins and seeds is usually taken for granted in many varieties of wine. Each wine region (French wines are generally designated by region, not by variety of grape) can also vary widely in flavonoid content. Nonetheless, Bordeaux rate moderately; Burgundy low to moderate (except the village of Pommard); Languedoc-Roussillon moderate to high (and many great bargains in my experience, since these producers live in the shadow of its northern Bordeaux neighbors); Rhone (Cote du Rhone) moderate to high, though beware of their powerful "barnyard" character upon opening; decanting is wise.

Italy--Much red Italian wine is made from the Sangiovese grape and called variously Chianti, Valpolicella, and "super-Tuscan" when blended with other varietals. Corder rates the southern Italian wines from Sicily, Sardinia, and the mainland as high in procyanidins; most northern varieties are moderate.

Spain--Moderate in general.

United States--Though his comments are disappointingly scanty on the U.S., he points out that Cabernet Sauvignon is the standout for procyanidin content. He mentions only the Napa/Sonoma regions, unfortunately. (I'd like to know how the San Diego-Temecula and Virginian wines fare, for instance.)

The winner in procyanidin content is a variety grown in the Gers region of southwest France, a region with superior longevity of its residents. The wines here are made with the tannat grape within the Madiran appellation; wines labeled "Madiran" must contain 40% or more tannat to be so labeled (such is a quirk of French wine regulation). Among the producers Dr. Corder lists are Chateau de Sabazan, Chateau Saint-Go, Chateau du Bascou, Domaine Labranche Laffont, and Chateau d'Aydie. (A more complete list can be found in his book.)

How does this all figure into the Track Your Plaque program? Can you succeed without red wine? Of course you can. I doubt you could do it, however, without some attention to flavonoid-rich food sources, whether they come from spinach, tea, chocolate, beets, pomegranates, or red wine.

Though my wife and I love wine, I confess that I've never personally drank or even seen a French Madiran wine. Any wine afficionados with some advice?

Can wheat elimination cure ulcerative colitis?

Tammy is a 36-year old mother of three young children. Since age 20, she has suffered with the debilitating symptoms of ulcerative colitis: constant, gnawing abdominal pain; frequent diarrhea, often bloody.



Tammy has had to take several medications, some with significant side-effects, all of which provided only partial relief from the pain and diarrhea. Her gastroenterologist and surgeon were planning a colectomy (removal of the colon) with creation of an ileostomy (rerouting of the small intestine to the abdominal surface, which would require Tammy to wear an ileostomy bag under her clothes for the rest of her life).



Although Tammy had previously tested negative for celiac disease (an allergic sensitivity to the gluten in wheat products), I urged her to attempt a trial of a wheat-free diet. Having witnessed many people experience relief from irritable bowel syndrome, acid reflux, and other common gastrointestinal complaints, all while trying to reduce blood sugar and small LDL, I'd hoped that Tammy would obtain at least some small improvement in her terrible symptoms.



I therefore urged Tammy to try it. After all, what was there to lose? Tammy grudgingly agreed.



She returned 6 months later. Her report: She had lost 38 lbs, virtually all of it within the first 6-8 weeks. Her diarrhea and cramping were not better, but gone. She was down to a single medicine from her former list of drugs.



I am unsure what proportion of people with ulcerative colitis or other inflammatory bowel diseases like Crohn's will experience a result like Tammy's. Perhaps it's only a minority. But I take this another piece of evidence that this enormously destructive thing called wheat has no place in the human diet.



We have no facts or figures on the prevalence of various forms of wheat intolerance in the U.S. When I contacted the Celiac Disease Foundation, they had no figures on the number of fatalities per year in the U.S. from celiac disease. But if there are 2-3 million Americans with celiac disease, there are probably 100 times that many people with various forms of wheat intolerance.



Postprandial pile-up with fructose

Heart disease is likely caused in the after-eating, postprandial period. That's why the practice of grazing, eating many small meals throughout the day, can potentially increase heart disease risk. Eating often can lead to the phenomenon I call triglyceride and chylomicron "stacking," or the piling up of postprandial breakdown products in the blood stream.

Different fatty acid fractions generate different postprandial patterns. But so do different sugars. Fructose, in particular, is an especially potent agent that magnifies the postprandial patterns. (See Goodbye, fructose.)

Take a look at the graphs from the exhaustive University of California study by Stanhope et al, 2009:



From Stanhope KL et al, J Clin Invest 2009. Click on image to make larger.

The left graphs show the triglyceride effects of adding glucose-sweetened drinks (not sucrose) to the study participants' diets. The right graphs show the triglyceride effects of adding fructose-sweetened drinks.

Note that fructose causes enormous "stacking" of triglycerides, meaning that postprandial chylomicrons and VLDL particles are accumulating. (This study also showed a 4-fold greater increase in abdominal fat and 45% increase in small LDL particles with fructose.)

It means that low-fat salad dressings, sodas, ketchup, spaghetti sauce, and all the other foods made with high-fructose corn syrup not only make you fat, but also magnifies the severity of postprandial lipoprotein stacking, a phenomenon that leads to more atherosclerotic plaque.

Track Your Plaque: Safer at any score

Imagine two people.

Tom is a 50-year old man. Tom's initial heart scan score was 500--a concerning score that carries a 5% risk for heart attack per year.

Harry is also 50 years old. His heart scan score is 100--also a concerning score, but not to the same degree as Tom's much higher score.

Tom follows the Track Your Plaque program. He achieves the 60:60:60 lipid targets; chooses healthy foods, including elimination of wheat; takes fish oil at a therapeutic dose; increase his blood vitamin D level to 60-70 ng/ml, etc. One year later, Tom's heart scan score is 400, representing a 20% reduction from his starting score.

Harry, on the other hand, doesn't understand the implications of his score. Neither does his doctor. He's casually provided a prescription for a cholesterol drug by his doctor, a brief admonition to follow a low-fat diet, and little else. One year later, Harry's heart scan score is 200, a doubling (100% increase) of the original score.

At this point, we're left with Tom having a score of 400, Harry with a score of 200. That is, Tom has twice Harry's score, 200 points higher. Who's better off?

Tom with the score of 400 is better off. Even though he has a significantly higher score, Tom's plaque is regressing. Tom's plaque is therefore quiescent with active components being extracted, inflammation subsiding, the artery in a more relaxed state, etc.

Harry's plaque, in contrast, is active and growing: inflammatory cells are abundant and producing enzymes that degrade supportive tissue, constrictive factors are released that cause the artery to pinch partially closed, fatty materials accumulate and trigger a cascade of abnormal responses.

So it's not just the score--the quantity of atherosclerotic plaque present--but the state of activity of the plaque: Is it growing, is it being reduced? Is there escalating or subsiding inflammation? Is plaque filled with degradative enzymes or quiescent?

Following the Track Your Plaque program therefore leads us to the notion that it's not the score that's most important; the most important thing is what you're doing about it. We sometimes say that Track Your Plaque makes you safer at any score.

Triglyceride and chylomicron "stacking"

Continuing the comments started in Grazing is for cattle, here's an interesting study from the Oxford Center for Diabetes, Endocrinology and Metabolism.

Volunteers were fed a test meal breakfast of Rice Krispies, a banana, and a chocolate milkshake (76.4 grams carbohydrates, 51.9 grams fat, 12.2 grams protein). Lunch was served 5 hours later and consisted of a cheese sandwich and a second chocolate milkshake 43.4 grams carbohydrates, 49.6 grams fat, 24.0 grams protein). Frequent blood samples were then assessed over the day. (Don't try this at home: These are obviously very dangerous foods!)

Here's the pattern of triglycerides that was observed (1st dotted vertical line = breakfast, 2nd dotted vertical line = lunch):



Note that triglycerides only begin to decline 3-4 hours after breakfast, only to peak higher after lunch.


Here's the pattern observed for chylomicrons, the "granddaddy" of lipoproteins that derives from intestinal absorption of fatty acids:



Both graphs from Heath RB et al Am J Phyiol Endocrinol Metab 2006.


With chylomicrons, note a similar pattern to triglycerides: Chylomicrons begin to decline at 3-4 hours, only to peak higher after lunch.

This is the first study to examine the effect of sequential meals on such postprandial (after-eating) patterns. But it makes the graphic point that, if insufficient time is permitted between meals, both triglycerides and chylomicrons will "stack" themselves higher and higher. (Chylomicrons are subjected to processing by the enzyme, lipoprotein lipase, to form highly atherogenic, or plaque-causing, chylomicron remnants.)

While not examined in this study, my bet is that "grazing," i.e., eating small meals or snacks frequently, is an extreme instance of triglyceride, chylomicron, and chylomicron remnant stacking. That can only lead to one thing: accelerated heart and vascular plaque.

What is a healthy vitamin D blood level?

When measuring blood levels of vitamin D (as 25-hydroxy vitamin D), what constitutes a desirable level?

There's no study that directly examines this question, no study that enrolled thousands of people and assigned a placebo group and groups receiving escalating doses of vitamin D and/or achieved higher levels of vitamin D, then observed for development of cancer, diabetes, depression, heart disease, multiple sclerosis, osteoporosis, osteoarthritis, etc. Such a study would requires many thousands of participants (particularly to observe cancer and multiple sclerosis incidence), many years of observation, and many tens of millions of dollars. Nope, only a drug company could afford such costs.

So we have to piece together various observations and extrapolate what we believe to be the ideal level of vitamin D. Epidemiologic observations in several cancers (breast, colon, prostate, and bladder) suggest that a 25-hydroxy vitamin D level of 30 ng/ml or higher is desirable (with less cancer incidence above this level). Other data suggest a level of 52 ng/ml or greater is desirable. Unfortunately, much cancer research looked at intake of vitamin D from food and supplement sources, rather than actual blood levels. We also have to factor in the great individual variation in vitamin D metabolism, with a single dose yielding variable blood levels (as much as a 10-fold difference). There's also the variation introduced by vitamin D-receptor variation (genetic polymorphisms).

A new study using vitamin D administration helps chart the desirable levels of vitamin D.

Vitamin D supplementation reduces insulin resistance in South Asian women living in New Zealand who are insulin resistant and vitamin D deficient - a randomised, placebo-controlled trial.

In this New Zealand study, 42 women (23 to 68 years old) were given 4000 units vitamin D, 39 women given placebo. Median 25-hydroxy vitamin D levels increased from 21 nmol/L (8.4 ng/ml) to 75 nmol/L (30 ng/ml). Both HOMA (a measure of insulin sensitivity) and fasting insulin levels improved, with greatest improvement seen at 25-hydroxy vitamin D levels of 80-119 nmol/L (32-47.6 ng/ml) or greater.

We also know that a vacation on a Caribbean beach in a bathing suit will increase vitamin D blood levels to the 80-110 ng/ml range without ill-effect (at least in young people who maintain the capacity to activate vitamin D in the skin, a phenomenon that declines as we age).

So do we really know the truly ideal level of vitamin D to achieve? I believe that, given the above observations, it is reasonable to extrapolate that the ideal vitamin D blood level likely lies somewhere above 50 ng/ml. We also know that vitamin D toxicity (i.e., hypercalcemia) is virtually unheard of until vitamin D blood levels approach 150 ng/ml, and even then is inconsistent. The health benefits of vitamin D supplementation are so tremendous, that I am not willing to wait for the prospective data to explore this question fully. For now, I aim for a blood level of vitamin D of 60-70 ng/ml (150-175 nmol/L).

Grazing is for cattle

Many dietitians and nutritionists advise many people today to "graze," i.e., to eat small snacks every couple of hours. They argue that it blocks the drop in insulin and blood sugar that can trigger greater appetite and claim it can facilitate weight loss.



This is an absurd notion. Humans are not meant to graze. Humans are meant to find a wild boar or other animal, kill it, gorge on the meat, organs, and fat, then revert to berries, roots, leaves, and other foraged foods until the next kill. A human living in the wild does not have a cupboard or refrigerator full of ready-to-eat snacks to graze on.

The several hours after a meal is the most dangerous for creating coronary atherosclerotic plaque, i.e., the post-prandial period. In other words, eat dinner and, for the next 6-12 hours, your intestinal tract degrades the food; food byproducts are absorbed into the blood or lymph system. The blood is literally flooded with the byproducts of your meal.

Postprandial abnormalities are emerging to be a potent, and much underappreciated, means of causing heart disease and atherosclerosis in other vascular territories (especially carotid arteries and thoracic aorta).

Not eating--i.e., the fasting state--for extended periods is good for you. Encouraging people to graze amplifies atherosclerotic risk, since it creates an abnormal prolonged postprandial state.

The disastrous results of a low-fat diet

Rob was never that committed to following the program in the first place.

I met Rob because of a modest heart scan score and consultation for a cholesterol abnormality. Rob had been cycled through all the statin agents by his primary care physician, all of which resulted in terrible muscle aches that he found intolerable.

I started out, as usual, characterizing his cholesterol abnormality with lipoprotein testing (NMR):

LDL particle number 1489 nmol/L
LDL cholesterol (Friedewald calculation) 143 mg/dl
Small LDL 52% of total LDL
HDL 50 mg/dl
Triglycerides 82 mg/dl

(LDL particle number is the emerging gold standard for LDL quantification, superior to calculated or Friedewald LDL cholesterol for prediction of cardiovascular events.)

Rob is a busy guy. After only a couple of brief visits, life and work got in the way and Rob let his attentions drift away from heart health. Since the information I provided made little impact on his thinking, he reverted to the low-fat diet his primary care doctor had originally prescribed and that he read about in magazines and food packages. He also ran out of the basic supplements I had advised, including fish oil and vitamin D, and just never restarted them.

A couple of years passed and Rob decided that just poking around on his own might not cut it. So he came back to the office. We repeated his NMR lipoprotein analysis:

LDL particle number 2699 nmol/L
LDL cholesterol (Friedewald calculation) 229 mg/dl
Small LDL 81% of total LDL
HDL 53 mg/dl
Triglycerides 78 mg/dl


Two years of a low-fat diet had caused Rob's LDL particle number to skyrocket by 81%, nearly all due to an explosion of small LDL. Recall that small LDL is more susceptible to oxidation, more inflammation-provoking, more adhesive--the form of LDL particles most likely to cause heart disease.

Also, note that, despite the enormous increase in small LDL, HDL and triglycerides remained favorable. This counters the popular rule-of-thumb offered by some that small LDL is not present when HDL is "normal."

Low-fat diets as commonly practiced are enormously destructive. In Rob's case, a low-fat diet caused both calculated Friedewald LDL as well as LDL particle number to increase dramatically. In many other people, low-fat diets increase calculated Friedewald LDL modestly or not at all, but cause the more accurate LDL particle number to increase significantly, all due to small LDL.

I'm happy to say that, once Rob witnessed how far wrong he could go on the wrong program, he's back on Track. (Sorry, pun intended.) He has resumed his supplements and eliminated the food triggers of small LDL--wheat, cornstarch, and sugars.

Dr. David Grimes reminds us of vitamin D

In response to the Heart Scan Blog post, Fish oil makes you happy: Psychological distress and omega-3 index, Dr. David Grimes offered the following argument.

Dr. Grimes is a physician in northwest England at the Blackburn Royal Infirmary, Lancashire. He is author of the wonderfully cheeky 2006 Lancet editorial, Are statins analogues of vitamin D?, questioning whether the benefits of statin drugs simply work by way of increased vitamin D blood levels.


There is a fashionable interest in Omega-3 fatty acids, and these become equated with fish oil.

But fish oil is much more. Plankton synthesise the related squalene (shark oil) which, in turn, is converted into 7-dehydrocholesterol (7-DHC). The sun now comes into play and it converts 7-DHC into vitamin D (a physico-chemical process).

Small fish eat plankton, large fish eat small fish, and we eat large fish. So vitamin D passes through the food chain.

This has been a vital source of vitamin D for the the Inuits and also for the Scots and other dwellers of northwest Europe. (Edinburgh is on the same latitude as Hudson Bay and Alaska, further north than anywhere in China). In these locations there is not adequate sunlight energy to guarantee synthesis of adequate amounts of vitamin D, again by the action of sunlight on 7-DHC in the skin.

When the Scots moved from coastal fishing villages to industrial cities such as Glasgow, they became seriously deficient in vitamin D, and so the emergence of rickets. This was followed by a variety of other diseases resulting from vitamin D deficiency: tuberculosis, dental decay, coronary heart disease, and even multiple sclerosis and depression (the Glasgow syndrome).

And so it was with the Inuits. When their diet changed from fish for breakfast, fish for lunch, fish for dinner, they became deficient of vitamin D and they developed diseases characteristic of industrial cities, where there is indoor work for long hours, indoor activities, and atmospheric pollution.

It is the vitamin D component of fish and fish oils that is important.

I recently saw an elderly lady from Bangladesh living in northwest England. I would have expected her to have a very low blood level of vitamin D, as her exposure to the sun was minimal. However the blood level was 47ng/ml, not 4 as expected. She eats oily fish from Bangladesh every day, showing its value as a source of vitamin D with subsequent good health. I expect her blood levels of omega-3 fatty acids would also be high.

But it is unfashionable vitamin D that is important, not fashionable omega-3.

David Grimes
www.vitamindandcholesterol.com


Excellent point. The health effects of omega-3 and vitamin D are intimately intertwined when examining populations that consume fish.

In this study of Inuits, it is indeed impossible to dissect out how much psychological distress was due to reduced vitamin D, how much due to reduced omega-3s. My bet is that it's both. Thankfully, we also have data examining the use of pure omega-3 fatty acids in capsule (not intact fish) form, including studies like GISSI Prevenzione.

Nonetheless, Dr. Grimes reminds us that both vitamin D and omega-3 fatty acids from fish oil play crucial roles in mental health and other aspects of health, and that it's the combination that may account for the extravagant health effects previously ascribed only to omega-3s.

Why does fish oil reduce triglycerides?

Beyond its ability to slash risk for cardiovascular events, omega-3 fatty acids from fish oil also reduce triglycerides.

There's no remaining question that omega-3s do this quite effectively. After all, the FDA approved prescription fish oil, Lovaza, to treat a condition called familial hypertriglyceridemia, an inherited condition in which very high triglycerides in the 100s or 1000s of milligrams typically develop.

The omega-3 fraction of fatty acids are unique for their triglyceride-reducing property. No other fraction of fatty acids, such as omega-6 or saturated, can match the triglyceride-reducing effect of omega-3s.

But why does fish oil reduce triglycerides?

First of all, what are triglycerides? As their name suggests, triglycerides consist of three ("tri-") fatty acids lined up along a glycerol (sugar) "backbone." Triglycerides are the form in which most fatty acids occur in the bloodstream, liver, and other organs. (Fatty acids, like omega-3, omega-6, mono- or polyunsaturated, or saturated, rarely occur as free fatty acids unbound to glycerol.) In various lipoproteins in the blood, like LDL, VLDL, and HDL, fatty acids occur as triglycerides.

Of all lipoproteins, chylomicrons (the large particle formed through intestinal absorption of fatty acids and transported to the liver via the lymph system) and VLDL (very low-density lipoprotein, very low-density because they are mostly fat and little protein) particles are richest in triglycerides. Thus, we would expect that omega-3s exert their triglyceride-reducing effect via reductions in either chylomicrons or VLDL.

Indeed, that seems to be the case. The emerging evidence suggests that omega-3 fatty acids from fish oil reduce triglycerides through:

--Reduced VLDL production by the liver (Harris 1989)
--Accelerating chylomicron and VLDL elimination from the blood
--Activation of peroxisome proliferator-activated receptor gamma (PPAR-gamma)--Omega-3s ramp up the cellular equipment used to convert fatty acids to energy (oxidation) (Gani 2008)

Combine omega-3 fatty acids from fish oil with wheat elimination and you have an extremely potent means of reducing triglycerides. Read a previous Heart Scan Blog post here to read how a patient reduced triglycerides 93.5% from 3100 mg/dl to 210 mg/dl in just a few weeks using fish oil and wheat elimination.