All posts by william-davis

Another heated discussion is ongoing at The Heart.org, this one about Tim Russert's untimely death: Media mulls Russert's death as cardiologists weigh in

Although I posted a couple of brief comments there, I quickly lost patience with the tone of many of the other respondents. Should you choose to read the comments, you will see that many still cling to old notions like heart attack is inevitable, defibrillators should be more widely available, "vulnerable" plaques cannot be identified before heart attacks, etc.

I quickly lose patience with this sort of outdated rhetoric. However, our good friend, Dr. Bill Blanchet of Boulder, Colorado, has a far stronger stomach for this than I do.

Here, a sample of his wonderfully persuasive comments:

Heart disease cannot be stopped but we can certainly do better!

Goals we must achieve if we hope to solve the Rube Goldberg of coronary disease:

1. Find something more reliable than Framingham risk factors to determine who is at risk. Framingham risk factors are wrong more often than they are right. If you are comfortable treating 40% of the patients destined to have heart attacks, continue to rely on “traditional” risk factors only.

2. Treat to new standards beyond NCEP/ATP-III. These accepted standards prevent at best 40% of heart attacks in patients treated. This is unacceptable, and arguably why Tim is dead today! Why prevention protocols emphasize LDL and more or less ignore HDL, triglycerides and underemphasize blood pressure eludes me.

3. Motivate patients to participate in coronary prevention. Saying “you need to get exercise and lose weight” is not adequate motivation, it hasn't worked to date and probably won't work tomorrow. If you are satisfied saying it is "the patient's fault for not listening to me" so be it, that excuse doesn't work for me!

Currently “good results” consist of being able to convince 50% of patients at risk by traditional risk factors to participate in prevention and hopefully 30% will be treated to goal. Of those treated to goal, 60% of the heart attacks will still happen anyway. Mathematically we can hope to prevent <10% of heart attacks with this approach!

I have personally found a solution to this dilemma. It goes like this:

1. EBT-CAC [electron-beam tomography coronary artery calcium] is the most reliable predictor of coronary events period, the end! Anyone who disagrees has not objectively read the literature. The only test more predictive than the initial calcium score is the follow up score 12 to 36 months later. EBT predicted Tim Russert’s event 10 years before it happened; passing his stress test gave him inappropriate reassurance 2 months before he died. If only Tim had the benefit of a second EBT sometime over the last 10 years he and his doctor would have known that what they were doing was insufficient and improvements could have been made.

2. I treat to the standard of stable calcified plaque by EBT (<15% annualized progression, preferably <1% annualized progression). This correlates with a very low incidence of coronary events. Even the ACC/AHA 2007 position paper agrees with this. This is accomplished with aspirin, omega-3 fatty acids, diet, exercise, weight control, smoking cessation, treatment of sleep apnea, stress reduction, control of HDL, triglycerides and LDL cholesterol and excellent control of BP and insulin resistance plus the recent addition of vit D-3. Meeting an LDL goal of 70 is easy but prevents only a minority of events, treating to the goal of stable CAC by EBT is a challenge but when achieved, the reward is near elimination of heart attacks and ischemic strokes. This has indeed been my personal experience!

3. A picture of plaque in the coronary artery is a monumental motivator for patients to get on board to make things better. The demonstration of progression of that plaque despite our initial therapies gets all but a few suicidal patients interested in doing a better job. I think that similar motivational results can be had with carotid imaging; the difference is that CAC by EBT is clinically validated as being a much stronger predictor of events with progression and non-events with stability than any ultrasound test including IVUS.

Wow! I couldn't have said it better.

Sadly, I doubt even Dr. Blanchet's persuasive words will do much to convince my colleagues on this forum. And the cardiologists on this forum are likely among the more inquisitive and open-minded. The ones stuck in the cath lab day and night, or implanting defibrillators, are even less inclined to entertain such conversations.

While I admire Dr. Blanchet's energy for continuing to argue with my colleagues, the lesson I take is: Take charge of health yourself. If you wait for your doctor to do it for you, you could be in the same situation as poor Tim Russert. This is an age when your physician should facilitate your success, not prevent it or leave you wallowing in ignorance.

Without a concerted effort at prevention, heart scan scores (coronary calcium scores) grow like weeds. The average rate of growth is 30% per year.

Keith is an illustrative case. At age 39, Keith's heart scan score was 29, in the 99th percentile due to his young age. (In other words, young people before age 40 have no business having plaque. If they do, it's bad.)

True to conventional practice, Keith's doctor prescribed a cholesterol drug (Zocor), asked him to take a baby aspirin, and prescribed a blood pressure medicine. He asked Keith to cut the fat in his diet. His doctor even exceeded conventional (ATP-III) LDL cholesterol treatment targets.

Keith, an intelligent and motivated businessman, happily complied with his doctor's instructions. Eighteen months later, a 2nd heart scan showed a score of 68, representing an increase of 135%, or 76% per year.

This is the very same approach that the late Mr. Tim Russert's doctors employed: treat (calculated) LDL cholesterol with a statin drug, treat high blood pressure, reduce saturated fat, take aspirin. It was a miserable failure in Keith, whose plaque continued to grow at a frightening rate of 76% per year. It was also an obvious failure in poor Tim Russert.

Further investigation in Keith uncovered:

--Severe small LDL--80% of all LDL was small (despite a favorable HDL of 58 mg/dl)
--Measured LDL particle number (NMR) showed that "true" LDL was actually about 60 mg/dl higher than suggested by the crude calculated LDL
--An after-eating (postprandial) disorder (IDL)
--A pre-diabetic blood sugar and insulin
--Severe vitamin D deficiency
--Very low testosterone

All these patterns were present despite the steps Keith and his doctor had instituted. It's no wonder his plaque was undergoing explosive growth.

The conventional approach to coronary disease prevention is inadequate, more often than not a mindless adherence to one-size-fits-all template crafted to a great degree by drug industry interests and "experts" who often stand at arm's length from real live patients.

Keith's "residual" abnormalities are all readily correctable. He has since made dramatic improvements in all parameters. Among the strategies used is a wheat- and cornstarch-free diet that resulted in 12 lbs lost within the first few weeks of effort.

If you are on the "Russert Protocol," have a serious conversation with your doctor about the continued advisability of remaining on this half-assed approach to heart disease. Or, consider finding another doctor.

A petition to the National Institutes of Health (NIH) is being circulated in response to the mis-statement made in an NIH-sponsored study, ACCORD.

The ACCORD Trial included over 10,000 type II diabetics and compared an intensive, multiple-medication group to achieve a target HbA1c of <6.0%, with a less intensively treated group with a target HbA1c of 7-7.9%. (HBA1c is a long-term measure of glucose, averaging approximately the last 3 months glucose levels.) To the lead investigators' surprise, the intensively treated group experienced more death and heart attack than the less intensive group. The conclusion suggested that intensive management of diabetes may not be a desirable endpoint and may result in greater risk for adverse events.

The petitioners argue that the problem was not with intensive glucose control per se, but the use of multiple side-effect-generating medications. Unfortunately, the ACCORD conclusions give the impression that loose control over blood sugar may be desirable.

The petition originates from the Nutrition and Metabolism Society, a non-profit organization seeking to promote carbohydrate restriction.

The petition reads:

National Institute of Health re: the ACCORD Diabetes Study: "Intensively targeting blood sugar to near-normal levels ... increases risk of death. "

This statement is untrue. This study lowered blood glucose levels only by aggressive drug treatment.

Preventative measures and proven non-drug treatments are being ignored by the NIH, ADA and many other governing agencies.

There is abundant scientific evidence proving a carbohydrate restricted diet can be as effective as drugs in lowering blood glucose levels safely. Many times diet is more effective than medication in controlling diabetes - all without side effects or increased risk of death.

I ask that the NIH publicly retract the above statement. It is misleading the public.

I also request that the NIH acknowledge the existing science and fund more research by the experts who have experience with carbohydrate restriction as a means of treatment for diabetes.

For more info, or to help people with diabetes, please e-mail info@nmsociety.org .

Thank you.

I added my comment:

In my preventive cardiology practice, I have been employing strict carbohydrate restriction in both diabetics and non-diabetics. This results in dramatic improvement in lipids and lipoprotein abnormalities, substantial weight loss, and improved insulin sensitivity. This experience has been entirely different from the heart disease-causing and diabetes-causing low-fat diets that I used for years.

I have a substantial number of diabetics who have been to reduce their reliance on prescription medication for diabetes or even eliminate them. In my experience, the power of carbohydrate-restricted diets is profound.

However, better clinical data to further validate this approach is needed, particularly as diabetes and pre-diabetes is surging in prevalence. I ask that more funding to further explore and validate this research be made available if we are to have greater success on a broader basis.

If you are interested in adding your voice, you can also electronically sign the petition. It is optional, but you can also add your own comments regarding your own views or experiences.

It happens in the hospital every so often: A clean-cut, law-abiding person is hospitalized for, say, pneumonia, kidney stones, knee surgery, etc.

Everything's fine until . . . they're running down the hospital hallway stark naked, screaming about snakes on the wall, accusing nurses of trying to kill him, all while yanking out IV's and monitor patches.

It's called alcohol withdrawal. Alcohol withdrawal can range from tremulousness and sweatiness, all the way to delirium tremens, the full-blown form that leads to disorientation, seizures, fever, even death. Withdrawal can also be associated with a number of chronically used agents, such as sedatives/sleeping pills, pain medication/opiates, among others.

How about wheat?

I wouldn't have believed it, but after witnessing this effect countless times, I am convinced there is such a phenomenon: Wheat withdrawal.

You'll recognize it in someone who previously ate bread and other wheat flour-containing products freely, then eliminates them. This is followed by extreme cravings, usually for bread, cookies, or cake; profound fatigue; shakiness; mental fogginess; blue moods. The syndrome can last for up to one week.

Then, bam! Sufferers of wheat withdrawal report mental clarity superior to their wheat-crazed days, improved energy, decreased appetite and cravings, heightened mood, and, of course, fantastic drops in weight.

Why would removal of wheat from the diet trigger a withdrawal phenomenon? I can only speculate, but I believe that at least part of this response is due to a physical conversion from a glycogen (sugar)-burning metabolism to that of a fatty acid (fat mobilizing) metabolism. People who lived in the up-and-down cycle of craving and eating wheat constantly fed the sugar furnace for years and are enzymatically impaired in fat burning; they've been growing fat stores. Eliminating wheat deprives the body of this easy source of glycogen, forcing it to mobilize fatty acids in the fatty tissues. Sluggish at first, people feel fatigue, mental fogginess, etc. Once the enzymatic capacity for fat mobilization revs up, then these feelings dissipate.

Could it also relate to the opioid sequences apparently present in wheat? I wasn't even aware of this fact until a reader of The Heart Scan Blog, Anne, left this comment:

Wheat protein contains a number of opiod peptides which can be released during digestion. Some of these are thought to affect the central and peripheral nervous systems.

When I gave up gluten, I felt much worse for a few days. This is a very common reaction in those who stop eating gluten cold turkey.

Dr. BG provides a fascinating commentary on the addictive/opioid aspect of wheat addictions in her Animal Pharm Blog.

Whatever the mechanism, I believe it is a real phenomenon. It can, at times, be so overwhelming that about 20% of people who try to eliminate wheat find they are simply unable to do it without being incapacitated. Of course, that might be a lesson in itself: If withdrawal is so profound, it hints that there must be something very peculiar going on in the first place.

Some colleagues of mine brought this scary phenomenon to my attention last evening.

As insurance and Medicare reimbursement to doctors and hospitals fall (Medicare is enacting a series of substantial cuts, which will be followed by the private health insurers), you would expect the use of hospital procedures to drop. Makes sense, right? Less money paid per procedure, less incentive to do them.

Unfortunately, that's not how it's playing out in the real world. Your neighborhood interventional cardiologist or cardiothoracic surgeon is accustomed to a level of income and lifestyle. That lifestyle is now threatened by shrinking reimbursement. True to the Law of Unintended Consequences, rather than reducing use of procedures, diminishing procedural fees are prompting a good number of practitioners to do more.

In other words, if each heart catheterization pays less, why not do more of them, along with more stents, pacemakers, defibrillators, and the like? If four heart catheterizations per day pays less, why not do five to make up the difference?

Voila! Income protected. Of course, it comes at the cost of more work. But I will give one thing to my colleageus: They are a generally hard-working bunch who rarely balk at 12-16 hours days in the hospital.

How do you do more procedures? Easy. Just lower the bar on who to do a procedure on. Use more aggressive criteria for pacemaker implantation. Interpret the always-fuzzy nuclear stress tests weighed more towards abnormal. Use scare tactics: "You never know--that chest pain could be the last warning you're going to have!" Because the criteria for performing procedures is "soft" in the real world, it is easy to bend the criteria any way you want.

It's too early to measure the full impact of this unintended consequence of reduced reimbursement. But don't allow yourself to become a casualty in the reimbursement war. Remain vigilant. Recognize that, despite the fuzziness at the edges, there are still rational reasons for performing heart procedures. Always be armed with information and the right questions. Never submit unquestioningly or without satisfactory answers to your questions.

Despite the media blathering over how Mr. Russert's tragic death from heart attack could not have been predicted, it turns out that he had undergone a heart scan several years ago.

A New York Times article, A Search for Answers in Russert’s Death, reported:

Given the great strides that have been made in preventing and treating heart disease, what explains Tim Russert’s sudden death last week at 58 from a heart attack?

The answer, at least in part, is that although doctors knew that Mr. Russert, the longtime moderator of “Meet the Press” on NBC, had coronary artery disease and were treating him for it, they did not realize how severe the disease was because he did not have chest pain or other telltale symptoms that would have justified the kind of invasive tests needed to make a definitive diagnosis. In that sense, his case was sadly typical: more than 50 percent of all men who die of coronary heart disease have no previous symptoms, the American Heart Association says.

It is not clear whether Mr. Russert’s death could have been prevented. He was doing nearly all he could to lower his risk. He took blood pressure pills and a statin drug to control his cholesterol, he worked out every day on an exercise bike, and he was trying to lose weight, his doctors said on Monday. And still it was not enough.

“What is surprising,” Dr. Newman said, “is that the severity of the anatomical findings would not be predicted from his clinical situation, the absence of symptoms and his performing at a very high level of exercise.”

Buried deeper in this article, the fact that Mr. Russert had a heart scan score of 210 in 1998 is revealed.

That bit of information is damning. Readers of The Heart Scan Blog know that heart scan scores are expected to grow at a rate of 30% per year. This would put Mr. Russert's heart scan score at 2895 in 2008. But the two doctors providing care for Mr. Russert were advising the conventional treatments: prescribing cholesterol drugs, blood pressure medication, managing blood sugar, and doing periodic stress tests.

Conventional efforts usually slow the progression of heart scan scores to 14-24% per year. Let's assume the rate of increase was only 14% per year. That would put Mr. Russert's 2008 score at 779.

A simple calculation from known information in 1998 clearly, obviously, and inarguably predicted his death. Recall that heart scan scores of 1000 or greater are associated with annual--ANNUAL--risk for heart attack and death of 20-25% if no preventive action is taken. The meager prevention efforts taken by Mr. Russert's doctors did indeed reduce risk modestly, but it did not eliminate risk.

We know that growing plaque is active plaque. Active plaque means rupture-prone plaque. Rupture prone plaque means continuing risk for heart attack and death. Heart attack and death means the approach used in Mr. Russert was a miserable failure.

While the press blathers on about how heart disease is a tragedy, as Mr. Russert's doctors squirm under the fear of criticism, the answers have been right here all alone. It sometimes takes a reminder like Mr. Russert's tragic passing to remind us that tracking plaque is a enormously useful, potentially lifesaving approach to coronary heart disease.

Who needs to go next? Matt Lauer, Oprah, Jay Leno, some other media personality? Someone close to you? Can this all happen right beneath the nose of your doctor, even your cardiologist?

I don't need to remind readers of The Heart Scan Blog that heart disease is 1) measurable, 2) trackable, 3) predictable. Mr. Russert's future was clear as long ago as 1998. Every year that passed, his future became clearer and clearer, yet his doctors fumbled miserably.

Copyright 2008 William Davis, MD

Though Tim Russert was widely known and respected for his political commentary, he will likely be better remembered as an example of the gross shortcomings of the conventional approach to heart disease.

Let's face it:

Standard heart disease prevention efforts are a miserable failure.

A Track Your Plaque member brought this interview of Mr. Russert's doctor to my attention.

It appears that his doctor did all the correct conventional things. You know what became of it. In the eyes of the public and of any attorney, or even of my colleagues, no wrong was committed. The blame does not lie with Mr. Russert's hapless doctor. The blame lies on the system that endorses procedures, prescription medications, the blind adherence to dogma dictated by the pharmaceutical industry and FDA, along with a prevailing philosophy of preferring the management of catastrophes to preventing them. Dr. Newman's idea of a solution: Making an automatic defibrillator (AED) more widely available (!!!).

How long does this sort of idiocy have to go on? How many people have to die before the system uses the tools that are already available, tools that could have prevented this tragedy and many more like it?

If you and your doctor subscribe to the program that the unfortunate Mr. Russert was prescribed and the brainwashing, unthinking nonsense that his doctor follows, you are a fool. Shame on you. You therefore likely subscribe to the same variety of marketing BS that issues from food manufacturers about Cheerios, whole grains, and low-fat diets.

Get with the program. Sadly, Mr. Russert is not the first, he's not the last. The tragedies of conventional advice that line the pockets of drug and food manufacturers number in the millions. We're not talking about some obscure, rare disease. We're talking about the number one cause of death in both males and females nationwide.

I deeply wish this message could have reached Mr. Russert before his untimely death. We could all look forward to another Sunday morning with his usual incisive, unforgiving probing of the day's political figures.

The sudden passing of news giant, Tim Russert, yesterday of sudden cardiac death struck a blow to American consciousness.

Perhaps his hard-hitting interviewing style, while making guests squirm, made him seem invincible. But, of course, none of us is invincible. We are all vulnerable to this disease.

We should not allow Mr. Russert's tragic death to occur without taking some lessons. The media have already resorted to interviewing prominent doctors for their opinion.

Douglas Zipes, M.D., former President of the American College of Cardiology,was quoted in the media:

"An automated external defibrillator (AED) could have been a life-saver. AEDs should be as common as fire extinguishers."

This is typical sleight-of-hand, medicine-is-too-complex-for-the-public-to-understand sort of rhetoric that is surely to issue from the conventionally-thinking medical people and the press. Instead, let's cut the BS and learn the real lessons from Mr. Russert's needless death.

It is virtually certain that:

--Mr. Russert ruptured an existing coronary atherosclerotic plaque, prompting rhythm instability, or ventricular fibrillation.

--Making automatic external defibrillators (AED) available might have Band-Aided the ventricular fibrillation, but it would not have stopped the heart attack that triggered it.

--Though full details of Mr. Russert's health program have not been made available, it is quite likely that he was prescribed the usual half-witted and barely effective panoply of "prevention": aspirin, statin drug, anti-hypertensive medication. Readers of The Heart Scan Blog and members of Track Your Plaque know that this conventional approach is as effective as aspirin for a fractured hip.

--It is highly unlikely that all causes of Mr. Russert's heart disease had been identified--did he have small LDL (it's certain he did, given his body habitus of generous tummy), Lp(a), low HDL, pre-diabetic patterns, inflammatory abnormalities, vitamin D deficiency, etc.? You can be sure little or none of this had been addressed. Was he even taking simple fish oil that reduces the likelihood of sudden cardiac death by 45%?

--Far more could have been done to have prevented Mr. Russert's needless death. And I don't mean the idiocy of making AED's available in office buildings. I'm talking about preventing the rupture of atherosclerotic plaque in the first place.

Far more can be done to prevent future similar deaths among all of us.

Our jobs are to use the tragic death of Mr. Russert to help those around us learn that heart disease is identifiable and preventable. Though Mr. Russert did not stand for BS in his political commentary, he sadly probably received it in his health advice. Don't let this happen to you or those around you.

There's no doubt about it: The majority of people with heart disease are overweight. They may not be grotesquely overweight, just a few pounds over. But weight plays a crucial role in activating numerous factors that heighten risk for heart disease.

Excess weight reduces HDL cholesterol, raises triglycerides, increases small LDL (enormously), fans the fires of inflammatory responses (CRP, IL-6, TNF-alpha, etc.) raises blood pressure, increases resistance to insulin and raises blood sugar. Overweight people tend to be less physically active, may develop diseases of obesity like sleep apnea, and on and on. You've heard this all before.

But why do slender people develop heart disease? If we can't blame weight, what is to blame? By slender, I mean body mass index (BMI) of <25. (Yes, I know there are other ways, better ways, to gauge healthy weight. But, for simplicity, I'll use BMI.) Let's put aside the two obvious causes of heart disease, cigarette smoking and Type I diabetes. (I'd be shocked if any cigarette smokers read this blog.)

Slender people develop heart disease because:

1) They have lipoprotein(a)--The big, big neglected risk factor. In fact, the Lp(a) genotype is, in my casual observation, associated with a slender phenotype (genotypic expression). The prototypical example that makes headlines is the marathon runner--slender and superbly fit, but develops heart disease anyway. People wax on about the uncertainties of exercise and fitness when they hear about Jim Fixx and Alberto Salazar. But one factor would explain it all: Lp(a).

2) The murky category of the normal weight obesity. These people are generally recognizable by their flaccid tummies despite falling into a favorable BMI <25. Small LDL is the standout red flag in these people.

3) They were previously overweight but lost it.

4) They were former smokers.

5) Vitamin D deficiency--Deficiency of vitamin D is important for everyone's health. But there appears to be some people for whom it is the dominant risk. I believe that one of our great Track Your Plaque success stories, Neal, falls into this group. Some people who are vitamin D deficient develop colon cancer, others develop diabetes, others develop osteoporosis or multiple sclerosis, while others develop coronary heart disease and plaque. The likely reason for the varied expression is variation in vitamin D receptor genotypes (VDR genotypes).

6) The murkiest of all: Hypertension genotypic variants. This is a poorly sorted-out category, and one principally based on my observations along with scattered observations in such things as variations in the angiotensin converting enzyme genotypes. But I am convinced that there is a small percentage of slender people who show variation in some genetic type that predisposes to hypertension and heart disease. They also show a propensity towards enlargement of the thoracic aorta. This group is also among the most difficult to control in the Track Your Plaque approach, i.e., they have difficulty slowing or stopping the growth of heart scan scores. While blood pressure control in this group is important, it does not seem to remove the excess source of risk.

So, yes, being slender does put you into a lower risk for heart disease category. But it does not mean you are immune.

You can also be an overweight person who still harbors some of the features of the slender--you're an overweight slender person. The above list can still therefore apply.

Okay, so it's a shameless knockoff of chef Anthony Bourdain's titillating Kitchen Confidential.

But the confidences that I've heard whispered in the corridors of health involve something more provocative than how your food was prepared. Any service for humans performed by other humans is subject to the idiosyncrasies and weaknesses of human behavior. That's just life.

In healthcare for your heart, the consequences can be more profound than eating three day old fish on Monday's dinner menu.

Over my 15 years practicing cardiology in a variety of settings in three different cities, I've witnessed just about everything from shocking to sublime. Some of it speaks to the extraordinary commitment of people in healthcare, the unexpected courage people show in the midst of illness, the devotion of family in difficult times. It can also speak of mewling, sobbing carryings-on over the most minor conditions, the meanness that emerges when people are frightened, the vultures circling just waiting for Grandpa to kick the bucket and leave his will declaring the spoils.

For the most part, my cardiology colleagues are a hard-working bunch committed to . . . Uh oh. I was going to say "Saving lives, preserving health." But that's not true. Once upon a time, it was true for many of my colleagues, often revealed over $2-a-pitcher beer-softened, "we're going to save people" conversations in medical school. Ahhh, medical school. I remember walking along the street alongside my medical school in St. Louis, bursting with pride and a sense of purpose.

But, for many of us, something sours our purpose through the years. Maybe it's the smell of money, maybe it's the series of distasteful experiences that show that healthcare providers are, in the midst of health crises, the innocent recipients of anger, frustration, disappointment.

Whatever the genesis, the stage is set for an imperfect scenario that pits healthcare provider against patient in a less-than-perfect system.

This would read as a mindless rant if it wasn't based on such pervasive and pravalent truths, tales of the flawed deliverers of healthcare driven by motives less lofty than "saving people."

Take Dr. S, a doctor who performs a large number of procedures on patients. I'm told he is very capable. He manages an extraordinary amount of heart work--in between jail time for wife beating and Medicare fraud.

Or Dr. C, well-known in the region for his procedural talents, also. Usually acerbic and freely-swearing, he opens up engagingly when drinking--which is most of the time. Paradoxically, as is true for some serious drinkers, he works more effectively while intoxicated.

Or Dr. ST, who proudly admitted to me one evening over dinner that he has accepted 6-figure payments from medical device companies on a number of occasions to use their products.

Or the manic ups and downs of Dr. J, who refers just about every patient he sees for emergency bypass surgery when in his down phase, mangles coronary arteries in daring angioplasties during his up phase.

How about 310-lb Dr. P, who hounds her patients about indulgent lifestyles? That would be excusable as innocent lack of self-insight if it weren't for her propensity to use heart procedures on patients as punishment. "I have no choice but to take you to the hospital."

Dr. M. manages to maintain the appearance of straight-and-narrow during the day, all the way to attending church twice a week with his children. His daytime persona effectively covers up his frequent visits to prostitutes.

We are ALL flawed. My colleagues are no different. But some circumstances cultivate the flaws, fertilize corruptibility, reward it. Such has become the state of affairs in healthcare for heart disease. Why? Is it the excessive potential for money-making that existed until recently? Is there something about the save-the-day mentality of heart disease that attracts imperfect personalities looking for the adrenaline-charged thrill but morphs over time into near-psychopathic lives?

It's not the end of the world. The fact that my colleagues' behavior has reached such extravagant lows signals a bottom: things are about to change.

In the meantime, let me tell you a few more secrets . . .

Copyright 2008 William Davis, MD

I've discussed this before: The coming wave of self-empowerment in health. Health that is driven by you, not a hospital, not a doctor, not by procedures, but by information and access to tools that are powerful and effective.

The seeds are being planted right now and won't take full root for many years or decades. But it's going to happen.

I previously cited several broad trends that are examples of this emerging wave:

--The nutritional supplement movement. Contrary to the media's ill-informed bashing, nutritional supplements are getting better: improved quality, better substantiation of when/how to use them, new agents that appear rapidly, since introduction is not slowed by the molasses of the FDA.

--Medications moving to over-the-counter status. Health insurers are driving this one. OTC means not paid for by insurance. That also means access to you.

--What I call "retail imaging", i.e. screening ultrasound, heart scans, full body scans, etc. that are available in most states without a doctor's order.

--The Internet. The mind-boggling rapidity and depth of information available on the Internet today is fueling the self-empowerment movement by providing sophisticated information to health care consumers. Information here is uneven at present. But, as consumer sophistication increases and the system of checks and balances evolves, internet-driven information will be often superior to what you get from a doctor or other health professional.

--High-deductible health insurance plans. If health care consumers bear more and more of the costs of health care, they will seize greater responsibility for early identification and prevention and minimize long-term costs.

This trend does not mean treating your own infection, taking out your own gall bladder, repairing your own broken leg. It means that conventional routes of health delivery will recede into providing only catastrophic care.

It means that you and your family will take a larger role in learning how to eat and exercise properly, use foods to maintain and promote health (the "designer food" and "nutraceutical" movement), take supplements that have real benefits, use medications for treatment of many everyday ailments.

It also means seizing control of diseases that previously were only treated in hospitals, like coronary heart disease. This, of course, is where our program, Track Your Plaque, is an example of how you can have a powerful and effective role in your heart health. Track Your Plaque goes so far beyond the "eat low-fat, exercise, and know your numbers" media mantra that it's like comparing a brand-new Mercedes to a rusted, run-down '87 Ford Escort. There truly is no comparison. (Sorry if you're an Escort driver!) But you get the idea.

For those of you who have been frustrated in trying to get your lipoprotein analysis performed, here's another option.

The Life Extension Foundation at www.lef.org provides access to the VAP test, or Vertical Auto Profiler. This is the lipoprotein test run by the Atherotech company in Birmingham, Alabama. The name refers to the method used, a form of centrifugation, or high-speed spinning of your blood (plasma) to separate the various components by density.

This is a fine technique that works well. Though our preferred method is NMR (www.Lipoprofile.com, Liposcience Inc.), the Atherotech VAP is a reasonable alternative.

If you go through the Life Extension process, they will direct you to blood draw sites in your area. They charge $185 for Life Extension members, $247 for non-members. (Membership in Life Extension costs $75.) Drawback: No billing for health insurance reimbursement.

A full description of the significance of lipoproteins can also be found in my article posted on-line at the www.lef.org website at http://www.lef.org/magazine/mag2006/may2006_report_heart_01.htm

Tom, an accountant, came into the office eager to know what his 2nd heart scan score showed.

A year ago, Tom's view of himself as a healthy, middle-aged man was shattered when he found out his heart scan score: 1236. Tom had severe coronary plaque with a heart attack risk of 25% per year (without intensive preventive action).

In the way of lipoprotein abnormalities, he had several: low HDL, deficient large HDL, small LDL, high triglycerides, IDL (the after-eating inability to clear dietary fats), and a high blood sugar in the pre-diabetic range. In addition, Tom was hypertensive, with blood pressure so high it even landed him in the emergency room last winter.

In addition to our approach to correct all these patterns, Tom was urged to lose a significant quantity of weight. Starting at 225 lb., at 5 ft 7 inches, Tom was clearly at least 40 lbs over his ideal weight.

I stressed to Tom that the entire spectrum of causes of coronary plaque were weight-related. I likened his patterns to throwing gasoline on a fire: As weight increased, his lipoprotein and other abnormalties flared dramatically.

But each time Tom came back to the office over the ensuing year, he'd gained another 3 to 6 lbs. And each time he had an explanation. "My daughter just got married. I couldn't turn down wedding cake, now could I?" Or, I just survived another tax season. I was working day and night--no time for exercise!" "It's getting too hot to walk anymore."

Well, despite multiple treatments, Tom's repeat heart scan showed a score of 1677, a 35% increase. That's a dangerous rate of growth that virtually guarantees that plaque is building up momentum to "rupture", which results in heart attack.

I therefore stressed to Tom that weight loss was crucial. Control of coronary plaque was simply not going to occur without weight loss to our target. Alternatively, we could add several new prescription medicines and hope that they could achieve the same effect, though at a price (side-effects, expense).

I tell Tom's story to highlight again just how important weight loss can be for a number of lipoprotein abnormalities.

What measures specifically are sensitive to weight? They are:

--HDL cholesterol
--Triglycerides
--Small LDL
--VLDL
--Blood pressure
--Blood sugar and insulin
--C-reactive protein
--LDL

Weight exerts profound influence on these patterns. In Tom and people like him, weight can be a "make it or break it" issue.

If you, like Tom, have any of the above patterns, consider weight loss as a potent tool you can use to gain control of coronary plaque.

For Track Your Plaque followers, you know we are very concerned about vitamin D blood levels. My prediction is that, in 10 years, vitamin D will be regarded as an important item on the list of coronary artery disease risk factors.

In our experience of trying to stop or reverse heart scan scores, restoration of vitamin D to a blood level of 50 ng/ml appears to have increased our success rate dramatically.

As we've talked about before, on the bell curve of vitamin D dosing in a northern climate, the majority of women require 2000 units per day, men require 3000 units per day to achieve a level of 50 ng. However, there are "outliers" on this bell curve, i.e., people who require much more or much less.

This week, I saw two people who were very instructive cases of extreme requirements on the high end of vitamin D dosing. Both started with unmeasurable blood levels, i.e., essentially zero ng/ml. On 5000 units of vitamin D per day, both raised their blood levels to around 17-18 ng/ml--in the range of severe deficiency (defined as <20 ng/ml). I advised both to increase their oral dose of vitamin D to 8000 units per day.

Notably, both people avoided sunlight and lived in Wisconsin, a terribly sun-deprived locale 10 months a year. Both were also substantially overweight (around 300 lbs each).

The vitamin D issue continues to be endlessly fascinating in all its nuances and twists.

Two men from my community just died of heart attacks. Both were in their 40s.

What bothers me most about these all too frequent stories is that it is so preventable. You can bet that both had little or no symptoms prior to their deaths. You can also bet that they've had cholesterol panels taken by their doctors.

Followers of the Track Your Plaque program know that these are sure-fire paths to failure. The absence of heart disease symptoms should provide no reassurance whatsoever. High cholesterol, in-between cholesterol, low cholesterol--none are confident indicators in a specific individual.

Stress test? How about the patient I saw today who, until I met him, had been undergoing stress test after stress test, every year--all while the quantity of coronary plaque tripled. False reassurances provided by his cardiologist led him to believe that all was well--while this stack of oily rags was just waiting for the spark to ignite.

Too little time, too much money, too far away--there's a hundred excuses for not getting a heart scan. Or, you've had a heart scan and no one can tell you what to do about it. If you're reading this, however, you've found the most intensive source of information available on how your heart scan can serve as the start of a program of heart attack prevention for a life free of dangers.

It's not that tough. But it won't just go away on its own. I just have to look around me in my own community, watch the local news, talk to friends, and I'll heart about all the people just in my neighborhood who should be learning these lessons. I rant and rave about this but some people need to hear it from a friend, colleague, neighbor, rather than some crazy doctor bucking the standard line.

You, too, should be telling anyone who will listen about how heart disease can be identified and controlled.

That was the disturbing headline on a report from MSNBC, also reported nationally on all the major news networks.

The story goes on:

"A pilot suffering a heart attack made an emergency landing on a highway, saving his three passengers shortly before he died...He landed the single-engine Cessna 185 on Utah 30 near Park Valley and was taken to Bear River Hospital in Tremonton, where he died."

We track these sorts of stories and it's frightening just how common they are. A school bus driver recently had a heart attack while driving 30 children; the bus crashed but no one was hurt. A 52-year old commercial bus driver suffered a heart attack while transporting 49 conference attendees; the bus plunged 400 feet down a ravine. Remarkably, 17 passengers suffered only minor injuries and there were no deaths.

There have even been incidents where the pilot of a jet liner suffered a heart attack in-flight. In 2000, the 53-year old pilot of a Northwest Airlines DC-10 died while in-flight from a heart attack while landing in Minneapolis. The 290 passengers were landed safely by co-pilot.

Most incidents where the driver or pilot has been incapacitated or died resulted in the deaths of only a handful of people. No major catastrophe has yet occured. But--mark my words--it will. These incidents just happen too frequently.

Virtually all of these and similar incidents could have been prevented. If the FAA, for instance, would insist that all pilots have a simple CT heart scan, it would become immediately obvious which pilots should be grounded and who should fly. Similar requirements could easily be applied to persons in charge of the welfare of many people, most notably school bus drivers.

It's not that tough! The FAA currently requires stress testing and cholesterol testing. Well, guess what? Followers of the Track Your Plaque program know that these tests do not effectively identify the person at risk for heart attack in the majority of individuals. Just ask former President Bill Clinton how helpful his stress tests (five in a row!) were. Or how valuable his cholesterol monitoring was--all prior to his emergency bypass surgery.

Oxford University has issued a press release announcing plans for a new clinical trial to raise HDL cholesterol and reduce heart attack risk. 20,000 participants will be enrolled in this substantial effort. The agent? Niacin.

How is that new? Well, this time niacin comes with a new spin.

Dr. Jane Armitage, formerly with the Heart Protection Study that showed that simvastatin (Zocor) reduced heart attack risk regardless of starting LDL, is lead investigator. She hopes to prove that niacin raises HDL cholesterol and thereby reduces heart attack risk. But, this time, niacin will be combined with an inhibitor of prostaglandins that blocks the notorious "flushing" effect of niacin.

The majority of Track Your Plaque participants hoping to control or reverse coronary plaque take niacin. Recall that niacin (vitamin B3)is an extremely effect agent that raises HDL, dramatically reduces small LDL, shifts HDL particles into the effective large fraction, reduces triglycerides and triglyceride-containing particles like IDL and VLDL. Several studies have shown that niacin dramatically reduces heart attack. The HATS Study showed that niacin combined with Zocor yielded an 85-90% reduction in heart attack risk and achieved regression of coronary plaque in many participants.

In our experience, approximately 1 in 20 people will really struggle using niacin. Flushes for these occasional people will be difficult or even intolerable. Should Dr. Armitage's study demonstrate that this new combination agent does provide advantages in minimizing the hot flush effect, that will be a boon for the occasional Track Your Plaque participant who finds conventional niacin intolerable.

But you already have access to niacin, an agent with an impressive track record even without this new study. And you have a reasonably effective prostaglandin inhibitor, as well: aspirin. Good old aspirin is very useful, particularly in the first few months of your niacin initiation to blunt the flush.

Although this study is likely to further popularize niacin and allow its broader use, it's also a method for the drug companies to profit from an agent they know works but is cheap and available.

You don't have to wait. You already have niacin and aspirin available to you.

"I just got a heart scan!" declared Eric to his doctor. He handed the report to him.

"Oh my. Your score is 154." The doctor paused, then looked at Eric with a serious look on his face. "If we're going to understand whether or not you're in danger, you'll need a heart catheterization."

I've seen this happen countless times. How can I say this diplomatically? THIS IS WRONG!! In my view, it's absolutely criminal for this to happen. Physician ignorance, profiteering, whatever--it is wrong.

There's very few reasons why someone who has no symptoms should go directly to the cath lab for a procedure. (A rare exception might be an exceptional quantity of plaque in the left mainstem artery, e.g., >100. This is highly unusual.)

Even a nuclear stress test (e.g., thallium) at this level of scoring is only 10-15% likely to be abnormal. That means 85-90% likelihood of being normal. There's rare reasons to perform a heart catheterization in a person with no symptoms and an entirely normal stress test. The vast majority of people like Eric do not need a heart catheterization to discern risk.

If Eric's doctor had been up-to-date on the published literature on the prognostic value of heart scans, he could have advised Eric what the risks were--without a catheterization. Many doctors simply don't want to be bothered. Or, they opt for the more profitable method--a hospital procedure.

Always discuss your heart scan with your doctor--but be armed with information in case your doctor is uninformed or unscrupulous. Unfortunately, that's not uncommon. The Track Your Plaque program is your advocate, a source for unbiased information.

Jake had an abdominal aneurysm identified--by accident.

While getting a CT scan of his abdomen for unexplained abdominal pain, a 4.4 cm aneurysm was discovered. Jake's abdominal pain eventually passed without explanation, but he was left with this aneurysm.

Jake's primary care doctor referred him to a surgeon. "It's too small to require surgery right now. Wait a few years and it'll probably get bigger. When it gets to around 5.5 cm, that'll be the time to operate. Let's schedule an abdominal ultrasound or CT scan every 6 months."

Jake then got himself a heart scan. His high score of 879 then led him to my office. Lipoprotein testing, a stress test, correction of his lipoprotein patterns, changes in lifestyle followed. One year later, Jake's heart scan score was unchanged.

How about his abdominal aneurysm? 4.2 cm--a modest quantity of regression. When Jake's surgeon learned of the change, he just shrugged. "Okay, we'll just watch it from here."

Shockingly, the conversation surrounding aneurysms is just like the one Jake received: Let's just watch it grow until you need surgery.

If you've every seen anyone have abdominal aneurysm surgery, you know it is an awful, painful, barbaric process with high risk for major complications like kidney failure and loss of the legs. Waiting for an aneurysm to grow is a lousy solution. Surgeons point out that, although surgery is imperfect, it's better than the alternative: rupture, which is catastrophic with a 50% chance of dying.

But what about stopping the growth of the aneurysm? Or even reversing, or shrinking, it?

Surgeons say it can't be done. Yet we've done it--many times. And it's not that difficult.

The steps to take are very similar to that in the Track Your Plaque program for coronary plaque regression, with a few different strategies. Suppression of inflammation, for instance, plays a more important role and blood pressure must be abolutely normal, even during exercise.

More to come on this important topic in the future, including an upcoming Special Report on the www.cureality.com membership website.

I saw two instances of dramatic coronary plaque regression today.

John, a 53-years old mechanical lift operator, dropped his heart scan score from 479 to 323--a 32% regression of coronary plaque volume!

Eric, a 50-year consulting engineer, dropped his heart scan score from 668 to 580--a 13% reduction.

Both men did nothing special beyond the principles advocated in the Track Your Plaque program. Recall that, without preventive efforts, your heart scan score is expected to increase by 30% per year. Both men are well on their way to freedom from risk of coronary "events".

Two less people to feed the revenue-hungry hospital procedure system! We need many more like them.

There is no longer any doubt that lipoprotein(a) is a major causal factor in heart disease:

Meta-analysis (combined re-analysis) of 27 prospective studies:
Danesh J et al. Lipoprotein(a) and Coronary Heart Disease: Meta-Analysis of Prospective Studies

Lp(a) and "subclinical" atherosclerosis
Brown SA et al. The relation of lipoprotein[a] concentrations and apolipoprotein[a] phenotypes with asymptomatic atherosclerosis in subjects of the Atherosclerosis Risk in Communities (ARIC) Study.

Lp(a) and oxidized LDL
Tsimikas S et al. Oxidized phospholipids, Lp(a) lipoprotein, and coronary artery disease.

Lp(a) predicts peripheral vascular disease
Valentine RJ et al. Lp(a) lipoprotein is an independent, discriminating risk factor for premature peripheral atherosclerosis among white men.

Peltier M et al.Elevated serum lipoprotein(a) level is an independent marker of severity of thoracic aortic atherosclerosis.

Lp(a) across various populations
Gambhir JK et al. Association between lipoprotein(a) levels, apo(a) isoforms and family history of premature CAD in young Asian Indians.

Weber M et al. Metabolic factors clustering, lipoprotein cholesterol, apolipoprotein B, lipoprotein (a) and apolipoprotein E phenotypes in premature coronary artery disease in French Canadians.

Lp(a) and stroke risk
Jurgens G et al. Lipoprotein(a) serum concentration and apolipoprotein(a) phenotype correlate with severity and presence of ischemic cerebrovascular disease.

Willeit J et al. Lipoprotein(a) and asymptomatic carotid artery disease. Evidence of a prominent role in the evolution of advanced carotid plaques: the Bruneck Study.

From just about any direction, Lp(a) has been conclusively associated with atherosclerotic disease. We have more than enough data proving association.

But there are two areas of desperate need:

1) Data on effective treatments.

2) Raising awareness of this widely unknown (among the public) and ignored (among health professionals) genetic condition.

Treatment remains a real struggle. In a recent detailed Track Your Plaque Special Report, Unique Treatment Strategies for Lipoprotein(a) Reduction, we summarized the treatment approaches that have some power to reduce Lp(a) and/or its potential for causing heart disease. But, even armed with an appreciation for the world's scientific literature on this genetic condition, full control remains difficult for many people.

Track Your Plaque's HeartHawk has Lp(a) and he has struggled with this pattern for the last several years. He details some of his thoughts in a recent blog post.

More research and clinical studies are required and we need it soon if we hope to gain better control over this genetic pattern that affects up to 20% of people with coronary or vascular disease. Much of the needed research is sophisticated, background work similar to that being done by Dr. Santico Marcovina at University of Washington, Dr. Angelo Scanu at the University of Chicago, and Dr. Sally McCormick in New Zealand.

However, much of the needed research also consists of brief clinical experiences that detail whether or not there is an effect of various potential agents. Larger experiences, for instance, with potential treatment agents such as various phospholipid fractions, acetylcysteine, antibiotic regimens, some hormonal treatments, etc. could be performed quickly and simply. These studies would not require the $20 or $30 million typically spent by a drug company for a study, nor the several hundred million dollars to gain FDA approval of a new agent. They would simply be examinations of existing agents. These studies still cost money, require expertise, staff, and equipment. But the cost is a tiny fraction of the drug industry's investment in research. But it also means that investment return is nil from a drug manufacturer's perspective. Yet there are literally dozens, perhaps hundreds, of agents that hold some promise but have not been thoroughly studied.

For instance, if a specific modification of the phosphatidylcholine molecule were to generate a substantial Lp(a) reducing effect, Merck, Pfizer, and AstraZeneca would yawn--it is non-patent protectable, cannot be protected from competitors through the costly FDA approval process, and therefore is simply not worth their investment--regardless of whether it works or not.

(This is yet another example of how the drug industry, as well as hospitals and many health professionals, have lost sight of their real mission: to alleviate disease, not to profit from sickness.)

HeartHawk and I have discussed on a number of occasions whether a Lipoprotein(a) Research Foundation should be formed, an organization that seeks to fund the smaller research efforts that may accelerate productive research in Lp(a) and perhaps yield useful strategies faster than hoping for somebody to simply stumble on a treatment, or wait for the drug industry to create a unique, patentable entity that returns billions.

I'd like to propose that our Track Your Plaque program begin to fund such an effort. But a lot more help will be needed, particularly to generate the money to fund genuine, high-quality research from high-quality researchers.

If any readers of the Heart Scan Blog have any thoughts or insights into this process of creating a foundation, we'd appreciate your input.

Since we are on the topic of the ASTEROID trial and rosuvastatin, I'd make one more point before I start to sound like I'm plugging this drug (which I definitely am not).

In an informative Roundtable Discussion (open to subscribers to the American Journal of Cardiology; sorry) amongst Dr. Steve Nissen, principal investigator behind ASTEROID; and Drs. Vincent Friedewald, Christie Ballantyne, P. Shah, and William Roberts, Dr. Nissen made some interesting comments:

Dr. Shah: In ASTEROID, was the magnitude of atheroma volume change seen across different levels of LDL-C and HDL-C?

Dr. Nissen: No. There was no plaque regression seen in the 17 persons with LDL-Cs >/= 100 mg/dl, and there was little change in persons with LDL-Cs of 70 to 100 mg/dl. Only in persons with LDLs less than or equal to 70 mg/dl was there significant regression. The study was not powered to look for an HDL-C(which increased by 14.7%)-raising effect.

Interesting. In other words, ASTEROID, in a fairly internally consistent way, suggests that the lower the LDL is reduced, the more likely plaque regression is obtained. This is consistent with the Track Your Plaque experience, in which we've advocated reducing (calculated) LDL cholesterol to 60 mg/dl for the past several years.

Unfortunately, the message that the ASTEROID Trial sponsors, AstraZeneca, as well as the roundtable discussion panel (later in the discussion) try to make is that there is something magical about Crestor, that it yields benefits superior to other statin agents or other means of reducing LDL.

I disagree with this message. In the Track Your Plaque experience, we do aim for a similar LDL target. But we also employ a number of other strategies. We have also succeeded in regressing plaque without use of any statin drugs (though, admittedly, many people do require statin drugs to obtain LDLs in this range). We also witness magnitudes of reversal that often far exceed that seen in ASTEROID.

The Rountable Discussion is unfortunately tainted, as is the ASTEROID Trial itself, with deep drug industry financial involvement of the Roundtable participants. In fact, the discussion begins with a listing of the financial disclosures of the participants, a listing that occupies a full column of a two-column page. The potential biases of the participants doesn't necessarily invalidate the arguments, but to me suggests that participants are more likely to argue in favor of the sponsor's drug, or that participants were chosen because of these biases.

Why bother to even mention the ASTEROID Trial in a venue (the Heart Scan Blog, that is) that purports to seek unvarnished, unbiased truth in coronary plaque reversal? Because useful information can sometimes be found in unlikely places. Just like the four-year old child who blurts out an unexpected pearl of wisdom, so it can happen with the gobbledy-gook that emerges from the drug industry.

Every once in a while, they are worth paying attention to.

The ASTEROID Trial reported in 2006 examined the effects of LDL cholesterol reduction using the statin drug, rosuvastatin (Crestor), with coronary atherosclerosis quantified and tracked with intracoronary ultrasound. The Track Your Plaque report, New study confirms: LDL of 60 mg reverses plaque, on the ASTEROID Trial provides commentary on the results.

Though I remain skeptical that a statin-only treatment strategy can reverse coronary plaque in the majority of people, I do believe that the AstraZeneca-sponsored ASTEROID Trial does add to the wisdom on heart disease management. More importantly, it has served to raise awareness among both the public and my physician colleagues that atherosclerosis is indeed a potentially reversible condition.

Specifically, the ASTEROID results confirm that, either directly or indirectly, LDL cholesterol reduction achieved with statin agents does correspond to increasing degrees of plaque reversal. The mean (calculated) LDL cholesterol achieved in ASTEROID was 60 mg/dl, the same as the Track Your Plaque suggested LDL target.

Though the ASTEROID Trial is not news, I stumbled on a chart posted on the ASTEROID Trial website that clearly highlights how a number of other studies beyond ASTEROID have fallen into this pattern:

The graph reveals a linear relationship: The greater the reduction in LDL cholesterol with statin drugs, the greater the plaque regression ("change in percent atheroma volume"). (Several other studies not included in the graph also cluster into the same linear relationship.)

I am no supporter of drug companies, nor a defender of their policies and practices. But I do believe that their data can serve to teach us a few lessons. For instance, here is an (cherry-picked, to be sure) example of intracoronary ultrasound cross-sectional images before and after two years of rosuvastatin, 40 mg daily:

The color-coded/outlined atherosclerotic coronary plaque is shown shrinking, while the "lumen," or the path for blood to flow, enlarges. The reduction in coronary plaque is irrefutable. (The small circle within the lumen with the white halo surrounding it is the ultrasound catheter.)

If you and I were to choose a single treatment approach to coronary disease reversal, then 40 mg of rosuvastatin is probably at the top of the list. However, in the Track Your Plaque program, we do not advocate a single treatment strategy. While the Crestor-only approach is relatively straightforward--one pill a day--few people, in my experience, can tolerate this dose for any length of time. Patients invariably have to stop the drug or reduce the dose severely due to muscle aches when I've had patients try it. Contrary to the ASTEROID results, in my experience the majority of people, perhaps all, eventually give up with this improbable "one-size-fits-all" scheme.

The Track Your Plaque approach, while more complicated and involves several nutritional supplements and strategies, in my view addresses more causes of coronary plaque, is better tolerated, and provides health benefits outside of just LDL cholesterol reduction. It also minimizes or eliminates the need for prescription medication.

Studies cited in graph:

1.Nissen S et al. N Engl J Med 2006;354:1253-1263.
2 Tardif J et al. Circulation 2004;110:3372-3377.
3 Nissen S et al. JAMA 2006;295 (13):1556-1565
4 Nissen S et al. JAMA 2004;292: 2217–2225.
5 Nissen S et al. JAMA 2004; 291:1071–1080

One ounce of raw almonds (about 23 nuts) contains:

6 grams protein

14 grams fat

6 grams carbohydrate

3.5 grams fiber

For a total of 163 calories per ounce.

(From the USDA Nutrient Database)

Calorie content of foods is determined by summing up the calories from each constituent: 1 gram of fat = 9 calories; 1 gram protein = 4 calories; 1 gram carbohydrate = 4 calories. Calorie content can also be directly measured using a device called a burn calorimeter, in which the amount of energy released from a specific food is measured by literally burning it and gauging precisely how much energy is released.

The problem with both of these methods is that it is assumed that all foods are digested with equal efficiency. That is, it assumes that a potato chip is as readily digested and absorbed as energy from table sugar, a pretzel, oatmeal, a piece of steak, or a handful of nuts. In real life, of course this is not true. Different foods are absorbed with varying efficiency.

For a long time I've suspected that some foods are very inefficiently absorbed. I've particularly suspected that raw nuts are relatively poorly absorbed and thus yield only a fraction of the calories ingested.

Among the studies recently reported at the Federation of the Association of Societies for Experimental Biology (FASEB) meetings I attended in San Diego this past week were several devoted to almonds.

One study, to my surprise, documented this phenomenon. In Manipulation of lipid bioaccessibility of almonds influences postprandial lipemia in healthy human subjects, it was determined that, of 100 calories ingested from the fat fraction of almonds, only about half was actually absorbed. The remaining half passed out in the stool. (They did this by collecting stool samples and comparing the fat composition after eating the different almonds prepartions. This is not discussed in the limited text of the abstract.) In addition, postprandial (after-eating) surges in triglycerides were much less with whole almonds compared to the oil separated from the nut (i.e., broken down into almond oil + defatted almond flour). The researchers attributed the difference to the inhibitory effects of the almond nut's "food matrix," or the structural properties of chewed foods.

Add to this the fact that, of 6 grams of carbohydrate per ounce of whole almonds, 3.5 grams are indigestible fibers. This means that 6 - 3.5 = 2.5 grams of digestible carbohydrates are present per ounce (assuming 100% release).

If we follow the reasoning that only about half the fat fraction of almonds are absorbed, and assume that the protein and carbohydrate (minus the indigestible fibers) are absorbed efficiently (100%), then we would re-calculate the calorie content of almonds to be 97 calories per ounce, or 40% less than calories calculated by composition or measured with a calorimeter.

If we were to assume that protein and carbohydrates were, like fats, inefficiently absorbed because of the effects of the food matrix, then one ounce of almonds yields 88 calories per ounce, or 46% less. This is, in fact, a likely scenario, since the food matrix is largely created by the cell wall and should impede digestive access to fat, protein, and carbohydrate equally.

My point? Almonds and other nuts at first appear to be calorically dense due to fat composition. However, this simplistic view of nuts is misleading because of the confounding effects of the food matrix. Stated differently: Whole foods yield less calories. And, judging by the postprandial triglyceride effects: Whole foods yield less undesirable effects, such as postprandial rises in triglycerides.

Some other observations with almonds included:

The effect of almonds on plasma lipids in persons with prediabetes This study confirmed the LDL-reducing and modest HDL-raising effects of almonds.

Almonds (Amygdalus communis L.) as a possible source of prebiotic functional food This curious observation suggests that almonds modify the bacterial flora of the intestinal tract in a positive way (like the cultures in yogurts).

Copyright 2008 William Davis, MD

An extraordinary thing happened about 2 1/2 years ago.

While we have been following the Track Your Plaque program for coronary plaque regression for nearly 10 years, about 2 1/2 years ago we witnessed an extraordinary surge in success--bigger, faster, and more frequent drops in heart scan scores.

Up until then, we did witness significant reversal of coronary plaque by heart scan scores. We were planning to publish the data to validate this approach, but then . . .

Heart scan scores starting dropping not just 2%, or 8% . . . but 24%, 30%, 50% and more. Why? I attribute the surge in success to the addition of vitamin D.

Unfortunately, it also meant that the preceding 8 or so years of data lacked experience with supplementing vitamin D. The hundreds of participants in the Track Your Plaque program had not, until then, included vitamin D in their program.

So I decided to start from scratch (from the standpoint of data collection, not for the participants). That also meant that the preceding years of experience went unreported, though even that data far exceeded the results of what is achieved in conventional heart disease prevention.

Thus, the data I presented at the Experimental Biology Proceedings (FASEB 2008) in San Diego this week included only experiences in the group of participants that included vitamin D in their program, with data collected until mid-2007. The number of experiences is therefore modest.

However, the Track Your Plaque experience, as reported, far exceeds any prior experience in coronary plaque regression.

The full abstract will be published in the Track Your Plaque website.

Copyright 2008 William Davis, MD

Many people complain about the size of fish oil capsules. Let's face it: They're usually big and kind of smelly.

Women in particular struggle with big capsules. This becomes a real problem when somebody requires high-dose fish oil for treatment of post-prandial (after-eating) abnormalities, high triglycerides, or lipoprotein(a), when 6 or more--occasionally up to the equivalent of 20--standard fish oil capsules are required.

I came across a small capsule alternative for people who struggle with the big capsules. It's a product called Learn from PharmaOmega, a source of super purified fish oil.

The Learn product is actually made for children, since omega-3 fatty acid supplementation has been linked with improved intellectual performance. But the small capsule size is convenient for women and other people who would like to avoid the big standard-sized capsules.

Each capsule is about 60% of the size of a standard fish oil capsule (the smaller capsule in the photo, next to a standard size fish oil capsule), yet contains 375 mg EPA + DHA per capsule, 25% more than standard capsules (which contain 300 mg per capsule). The ratio of of EPA:DHA is a little more heavily weighted towards EPA with a 5:2 ration, compared to 3:1 of standard capsules. The capsules are also faintly orange flavored and non-fishy.

Disclosure: I receive no compensation for discussing or promoting this product.

Copyright 2008 William Davis, MD

Jenny provided permission to reprint her very excellent introduction to low-carbohydrate eating for people with diabetes. You can also view the original version on her Diabetes 101 website.

Jenny is a stickler for monitoring the effects of blood sugar. We might take some lessons from her experiences for improving management of people with metabolic syndrome or borderline blood sugars. In other words, monitoring the blood sugar-raising effects of various foods and food portions can provide great feedback on what foods are preferable, what undesirable, given your physiology.

Even if you are not a diabetic, Jenny's discussion is must reading to gain a better understanding of food choices, particularly carbohydrates. Along with seizing control of health, she has also gained deep wisdom in how to best manage this disease and its physiology.

Introduction to low-carb nutrition for diabetics

It's carbohydrates that raise blood sugar.

Sugars and starches, not the fats that dietitians have been warning you about for so long. If you've been testing your blood sugar after meals, you've probably noticed that already and you are starting to understand why a healthy diabetes diet will have to be one that limits carbohydrates to an amount that doesn't push your blood sugar up over the level where you are damaging your body.

But if your previous experience with restricting carbohydrates involved doing a weight loss diet like Atkins or Protein Power, which worked well for you until you crashed off it entirely and gained back all the weight you'd lost, you may be hesitant to embark on another course of dieting that requires some carb restriction.

I've been there myself. I've done the extremely low carb diet Dr. Richard Bernstein recommends for months on end. I did Protein Power for 3 years. And I've gone on the "Eat all the carbs you didn't eat over the past three years all at once" diet, too. The following observations grew out of my 8 years of experience with learning how to make carb restriction work long-term.

Unlike much of what you've read before, there are no scholarly references for this section. It's based entirely on my own observations and the experience of many dozens of people who have participated in online discussion groups devoted to low carb dieting and diabetes.

Weight Loss Diets Usually Fail but Diabetes Diets Can't Afford To Fail

People who adopt a low carb diet to lose weight tend to start out with great enthusiasm, adapt extreme dieting strategies, swear they will never eat another piece of bread or french fry for the rest of their lives, lose some weight, stall out, burn out, and slink back to their old diets, where they gain back all the weight they lost and more.

This is not a surprise. People on any diet, including low calorie and low fat, do the same thing. The body is very resistant to weight loss and deeply buried instincts in our brains do everything they can to maintain our weights, no matter how unhealthy they might be.

But while this pattern of dieting may be tolerable for those who are dieting to shed a few pounds before their class reunion, it spells disaster for those who must change their diet in order to prevent the high blood sugars that result in amputation, blindness, kidney failure and heart attack death.

Low carbing for diabetes means low carbing for life, long after the thrill has worn off of eating that runny brie and steak. Despite the hype in the diet books, it is not easy, simple, and fun. I know only a handful of people who have been able to sustain a low carb lifestyle for more than five years. And that is after years of online participation in low carb groups.

What you'll find below is what I've found works for me. I used a low carb diet to control my blood sugar for more than five years and have gone through the whole cycle, from enthusiasm, to boredom, to burnout, to saying "To hell with it, we've all got to die some time!" to starting all over again determined to avoid the mistakes that sent me round the bend the first time.

How Many Grams of Carbs to Eat? As Many as Allow You to Reach Your Blood Sugar Targets

When people think about adopting a lower carb diet, their first question is almost always, "How many grams of carbs can I eat at each meal?" Most of the diet books will answer that question with a hard and fast number. Atkins, for example, tells you to start out with 20 grams a day. Protein Power starts you at 30 grams. And Dr. Bernstein suggests 6 grams for breakfast and snacks and 12 grams at lunch and dinner.

Adopting these very low carbohydrate limits will control your blood sugar very nicely. But over time, many people find that sticking to a diet this low in carbohydrate becomes impossible. That's why I'm going to ask you to throw away all those diet books and try a new approach to restricting carbs.

What you will do is to try the strategy used by the people from the alt.support-diabetes newsgroup who informally call themselves "The 5% Club" because their A1c test results fall in the 5% range which doctors consider normal: use your blood sugar meter after each meal to determine how many grams of carbs you can eat and still meet a healthy blood sugar target.

You will start out by measuring your blood sugar one and two hours after each meal. Write down what you ate and observe what it did to your blood sugar. If a meal allows you to reach your blood sugar targets, try eating it again on a different day and test it test again, possibly at a later time, to make sure that your good numbers weren't just a result of slow digestion.

If you end up too high after a meal, the next time you eat it, cut back on the portion size of the carbohydrate elements in the meal and test again. Do this until you can hit your targets, or flag the carbohydrate-containing foods in that meal as ones your body can't handle.

What you're doing here is creating what newsgroup activist Alan S. calls, "a low spike diet" rather than a low carb diet. He can achieve normal post meal blood sugars by eating as many as 30 or 40 grams of carbohydrates at a meal. Others will find that they need to eat a lot less than that amount to hit safe post-meal blood sugar targets.

Usually how much carbohydrate you can manage has something to do with your body size. The more you weigh, the less each gram of carbohydrate you eat will raise your blood sugar. Those of us whose weight is less than 150 lbs often find that we can eat between 12 and 20 grams of carbohydrate and still reach normal blood sugar targets without the help of medications, and that we can add perhaps another 10 or 20 grams more, with medications. People who are much heavier can often eat 30 or 40 grams per meal and still reach their blood sugar targets. In general, men can eat more carbohydrates and still reach their targets than can women, again, because of their larger body size.

How to Learn How Much Carbohydrate is in Your Food

To make this system work, it helps if you start to learn how many grams of carbohydrate are in the foods you eat. That way you won't have to test hundreds of foods once you've learned how a representative sample affect you.

The best way to learn how many grams of carbohydrates are in the different foods you eat is to read food labels carefully, invest in a nutritional guide like one of Connie Netzer's books of nutritional information, download nutrition software like LifeForm (http://www.lifeform.com) or use online calculators like Fit Day (http://www.fitday.com). Software and online sites will compute the amount of carbohydrates and other nutrients in your meal for you as long as you know the portion size.

Learn about Portion Sizes!
This brings up an important point: When you estimate how many grams of carbohydrate there are in a portion of food, it is very important to find out if the amount of food on your plate corresponds to the amount in the "one serving" listed on a label, in a book, or in your software.

The best way to do this is to invest in an electronic food scale and to weigh your foods for a few weeks until you get the hang of estimating portion size. You can get a good food scale at a gourmet kitchen shop for $25 to $40 dollars. This food scale may be the best nutritional investment you'll ever make.

Once you start using your scale, you will find that the muffin you bought at the coffee shop weighs 8 ounces, which is fully four times the 2 ounces that most food databases give as "one serving" of a muffin. When you read that a mythical 2 ounce portion of muffin contains 27 grams of carbohydrate you will realize why that 8 ounce coffee shop muffin with its 108 grams of carbohydrates sends your blood sugar into the psycho zone!

With ice cream, when you weigh your ice cream on a food scale, you'll quickly see that the "one portion" listed on the package turns out to be only a few teaspoons' worth. That bowl you've been considering as one portion of ice cream weighs in as four servings or 72 grams of carbohydrate and 600 calories, which may explain its damaging effect on both your blood sugar and your waistline.

This may sound like a lot of work, and when you first start, it is. But after you do it for a few weeks you'll find you have memorized the carbohydrate gram counts and the portion sizes for the foods you usually eat, and once you have tested your blood after eating these portion sizes, you won't have to test every time you eat a favorite meal, because you will know what it is going to do to your blood sugar.

Eating Away from Home

The biggest challenge you'll encounter as you start learning what you can eat will be eating away from home. You aren't going to be able to weigh restaurant foods nor can you look up the nutritional values of many restaurant offerings--though many of the common fast food outlets do provide nutritional information online--though often without listing portion sizes.

That makes it a very good idea to avoid starchy or sugary restaurant foods or, if you do eat them, to eat only a small portion of what you are offered. Measure your blood sugar an hour or two hours after eating if you aren't sure about how a restaurant food will affect you.

Fat and Carbs Eaten Together will Digest Slowly

Foods with a lot of fat in them take longer to digest than those without a lot of fat. This is why pizza and ice cream often give deceptively good readings on your meter. If you test a meal and see a reading that is too good to be true, be sure you test at 3 or four hours after eating.

The Truth About Pasta

Pasta was long recommended to people with diabetes as a food that would not raise blood sugar and you will still see it starring in many cookbooks and magazines intended for people with diabetes.

However, if you test pasta 4 or 5 hours after eating, you may get an unpleasant surprise. This is true with the so-called "low carb" pastas, too. These foods give you excellent readings at one and two hours because they are resistant to digestion so they don't turn into glucose right away. But five hours later, they do break down into glucose and when they do, the 52 grams of carbohydrates found in each 2 ounce serving of pasta will hit your blood stream with a nasty wallop. (Not to mention that you almost need a microscope to see a 2 ounce portion of pasta. Most people's idea of a portion of pasta is closer to 6 ounces--and 156 grams of carbohydrate!)

If you have pasta for dinner and don't see a peak 3 hours later, be sure to check your fasting blood sugar the next morning. You may see the blood sugar rise there, too.

Sugar Alcohol and "Sugar Free" Foods

The sugar alcohol used in so-called "sugar free" foods can also show up in your blood sugar an hour or two after you'd expect to see them, especially the maltitol used in "sugar-free" candy. At least half of the sugar in Maltitol does turn into glucose in your blood stream and it can raise your blood sugar, but the rise is delayed so you may miss it on testing. So if a "sugar free" food seems to be kind to your blood sugar, try testing it an hour or two after your first tests. Erythritol is the one sugar alcohol that usually does not show up in your blood sugar.

Dealing with Limited Blood Testing Supplies

In in ideal world, we'd all have all the testing supplies we needed to control our blood sugar, but in real life blood sugar test strips are very expensive and many insurers sharply limit the number of strips people with Type 2 diabetes can get each month.

Here are some strategies that can help you if your access to strips is limited.

If you only have 50 strips to get you through a month, plan out what you are going to test ahead of time. Pick one of your favorite meals, and test at 1 hour after eating the first time you eat it and 2 hours after eating the second. Do this with a couple different meals and see if there's a pattern as to when you see the highest reading--whether it is at one hour or two. Then choose another meal and test it at the time when you saw the highest reading in the earlier meal. If you ever get a surprisingly low reading, try testing an hour later or earlier, to make sure you aren't missing the peak.

Make the goal of your testing be learning how many grams of carbs you can tolerate in one meal. If you learn that 30 grams is your upper limit, use software and your scale to find portions of other foods that will also clock in at 30 grams or less. Test one or two of these, and if you see the result you expect, you don't have to test every time you eat these foods again.

Wal-mart sells a cheap and effective blood sugar meter with strips that cost one half as much as other vendors. Some drug stores also sell store brand meters with cheaper strips. If you need more strips, consider the $50 you pay for another 100 strips an investment in your health. It's far better to spend that $50 now, than to spend it on expensive doctor bills caused by complications you don't need to develop!

Keep the focus on Achieving your Blood Sugar Goals

By testing after meals, you'll learn how many grams of carbohydrate your own, unique, body can handle. And more importantly, you'll also be able to decide if you are going to be able to control through diet alone, of whether it is time to talk to your doctor about supplementing dietary control with drugs.

Many people are so excited to learn that they can achieve normal blood sugars by cutting way back on carbohydrates that they become zealots for low carb dieting. I've been there and I've done that. But it's important not to get too carried away with a "Carbs are Evil" mentality which makes it a matter of religious zeal never to let evil carbs cross your lips again. Like all conversions this one tends to fade out in time. And as we said at the start of this chapter, your ultimate goal is to maintain your blood sugar targets for the rest of your life. So the safest approach is to get the most blood sugar benefit you can out of restricting carbohydrates, but restrict them to a level you can maintain year in and year out.

Most importantly, I have learned it is best to treat carb restriction as a strategy, one of many, which used in combination with other strategies including medications if needed, can give you normal blood sugars, rather than the One and Only True Way. If you can be flexible and find more than one tool to help you meet your blood sugar targets, you are more likely to be able to maintain those excellent blood sugars for years to come.

Eliminate "Habit Carbs" and Concentrate on "Value Carbs"
When people think about restricting their carb intake they assume this means never eating any of their favorite foods again.

But for many of us, this doesn't have to be true. Why? Because a quick look at your daily carb intake will often reveal that the bulk of the carbohydrates you are eating are what I call "habit carbs." These are the carbs you eat without a second thought because they are there. Not because they taste good. Not because you couldn't live without them. Just because you're in the habit of eating them.

Here is a list of some prime "habit carbs."

Steam table mashed potatoes

Limp french fries

Squashy hamburger buns

Cardboard toast

Cold home fries

Stale boxed cookies

How many of these flavorless, starchy foods are you consuming everyday just because they're there? Probably more than you realize. So before you lift that fork-full to your mouth, ask yourself, "Is this food thrilling me?" If not, put it down. This should go a long way towards getting your carb intake down.

What I'd call "value carbs" are those carb-rich foods that really do mean something to you. I'm not going to lie to you. You are not going to be able to make them the mainstays of your diabetes diet. But by using the strategies describe below, you should be able to eat enough of these foods to keep yourself from feeling deprived--without destroying your health.

Don't Create "Forbidden Foods!"

If you are one of those people who could live happily on Purina People Chow, you can skip what follows. But if food has been important to you, and if you have hitherto had a long and emotionally satisfying relationship with food, or if, like me, baking from scratch was one of your favorite ways to show love and express creativity, restricting your carbohydrate input will mean that a whole lot of what you've been eating (and baking) up until now is suddenly, completely, off limits. I can't eat cake and get a healthy blood sugar level. Even with two different diabetes drugs in my system. I can't eat cake even with an insulin shot before I eat it. I love cake but there is no way I can eat more than a bite or two without seeing very high blood sugars and there is no way I can eat two bites of cake and be happy. The same goes for french fries and Thai noodles.

During the first enthusiastic weeks of exploring carb restriction most people deal with this kind of discovery by coming up with new recipes and finding new, delicious and healthy things they can substitute for old, high carb standards. They appreciate the way cutting way back on carbohydrates curbs their hunger and makes food much more manageable. This is good and it is why long term low carbing is possible. But our old favorite foods do not go away that easily.

If you decide that some food you have been eating and enjoying all your life will never again cross your lips, it is almost 100% guaranteed that you'll end up pigging out on that very same food at some time in the future, hating yourself, and even beginning a binge that can throw you completely off your diet for months.

It might not happen the first month you are restricting your carb intake or even the first year. It took me three years of low carbing to get to where I crashed off my stringent low carb diet. But eventually it happens, and because after almost a decade of counting my carbs I've learned that I will never lose my love for certain foods that don't love me, I've put a lot of time into finding a way of restricting my carbohydrate intake in a way that avoids the buildup those feelings of deprivation that eventually lead to long periods of unwise eating.

The key, for me, is to build safety valves into my diet. I don't call them "cheats" or "bad foods" for reasons I'll get into later. I call them "off plan" foods because they are not food I can make an ongoing part of my daily food plan. Because my goal is life-long blood sugar control, I accept that I will occasional eat "off plan" and that this is okay as long as I am meeting my blood sugar targets most of the time. "Good enough" control that I can adhere to year in and year out beats a few months of perfection followed by crashing off the diet entirely and ruining my health. Here is one way to approach doing this:

Do the Diet Straight for a Month or Two Before You Try Off-Plan Goodies

As you learn what foods raise your blood sugar and what foods don't, you will almost certainly find that there are a lot of foods you used to love that don't work for you anymore. Waffles for breakfast, coffee cake at coffee break, three slices of pizza with crust, a burger with a bun and a side of fries are just a few of the foods that it is almost certain will not allow you to meet your post-meal blood sugar targets.

As you keep using your meter to test what you eat, if you are like most people with diabetes you'll also learn that some of the so-called "low glycemic" foods and the supposedly "healthy" whole grains that nutritionists recommend for people with diabetes won't work either. Oatmeal and whole wheat bagels raise my blood sugar far too high, so does cracked whole wheat, whole wheat bread, and brown rice.

If the dietician tells you a food is good for you, but your meter tells you it is raising your blood sugar to a level that is high enough to cause complications, you will have to listen to your meter. Your meter will tell you what is safe to eat and for the first couple of months while you are learning how to get your blood sugar under control and how bring those high blood sugars down to normal levels you will have to accept that you can only eat those foods that don't cause spikes.

If you attempt to add in off-plan foods before you are solidly on-plan you may never really get into the swing of eating a diet that controls your blood sugars and you may not get to where your body learns to enjoy the lower carb foods that don't give you blood sugar swings.

But after you've gotten your blood sugar under control, nothing horrible will happen if you make room for a small portion of some high carb treat every now and then.

How to Add Off-Plan Foods to the Plan

If you've avoided bread for a couple months, the humble roll in that restaurant bread basket may start to call out to you with an irresistible siren song. If you give in and eat it, with each bite you may find yourself feeling as if you are doing something incredibly sinful--the way you might have felt if you had eaten a whole box of chocolates in the past.

That feeling is the sign that you're heading for trouble. You've created a "forbidden fruit" and sooner or later that forbidden fruit is going to get you. You may find yourself thinking about that roll, craving another, sneaking off to eat one where nobody knows you, or, alternatively, you may declare that you will never again eat a roll ever--and then ruin your Thanksgiving holiday when you go to Aunt Glenda's and refuse to eat even a single one of those wonderful rolls of hers you've eaten every year of your life which say, "This is the family Thanksgiving" to you.

It is far better to make a bit of room in your diet for high carb treats so that they don't build up a charge. If you do this, you'll find that they almost never taste as good as you remembered, and you'll be able to leave them behind without turning them into an object of obsession.

Just knowing that you can eat some specific off-plan food at some future time, when it is scheduled, makes it that much easier to say, "No thanks" to it, and maintain your healthy blood sugar the rest of the time.

How Often Can You Eat Off-Plan?
How often you have an off-plan food depends a lot on your dietary goals, how high your blood sugar is before you eat carbs, and whether you are willing to exercise after eating. It also depends greatly on what medications you are taking for your diabetes. Whatever I eat, I try to keep my blood sugar below 120 mg/dl (6.7 mmol/l) at 2 hours after any meal.

Forty minutes of cardiovascular exercise will burn off a lot of extra carbs, so if you exercise regularly, try to eat your high carb treat before you head for the gym.

If you're trying to lose weight, you may have to keep off plan treats few and far between. When I was actively losing weight on a low carb diet without medications I ate one off-plan meal about once every two weeks.

Once I reached my weight loss goal I loosened up a bit but I found it best to cycle between weeks of eating a strict very low carb diet, and then a week of eating slightly more carbs--but I tried very hard not to ever anything that would cause my blood sugar to be over 120 mg/dl (6.7 mmol/L) at 2 hours after a meal because doing so makes me feel rotten.

Throw Away the Vocabulary of Self-Destructive Dieting

When you eat something with carbs in it, don't think of it as a "cheat." Cheating is what you do when faced with an authority figure--your 9th grade math teacher or the IRS. But you are the one in control of what you eat. So when you eat something that is off-plan, you should stop thinking of it as "getting away with something" and treat it instead as something you've decided to do--for a reason that should be clear to you while you do it.

If you keep eating things that were not what you had intended, rather than beating yourself up, it's time to reconsider your food plan and figure out why it isn't working. Are you having trouble finding foods in restaurants that don't raise your blood sugar? Maybe it's time to bring your lunch along to work for a while, or to find new place to dine.

Are you bored with what you have been eating? Google for good low carb recipes you can try at home. There are thousands of them. If you use the Google Groups search and look for messages in alt.support.diet.low-carb that start with "REC" you'll find a treasure trove of ideas to try.

Keep the vocabulary of sin and guilt for the confessional. You're going to eat a lot of things in the years to come that will mess up your blood sugar. But if you are kind to yourself and dust yourself off after you mess up and keep on going, doing the best you can to hit your blood sugar targets, you may very well end up healthier than many people who do not have diabetes. The important thing is to keep at it, doing the best you can and forgiving yourself when the best you can do isn't as good as you wish it was.

Know Your Limits
I've learned the hard way I can't eat half a blueberry muffin, so I don't even try portion control for that particular food. I know blueberry muffins are trouble and I also know that I will eventually eat one. That's just how it is, so every blue moon or so I eat a blueberry muffin, experience the miserable high blood sugars that follow, and then remember why I don't eat muffins every day any more. What I don't do is fool myself that I can buy a muffin and only eat half. Everyone has a few foods that fall into this category. Treat them with caution!

Eat Off-Plan Foods Out of the House
I've learned the hard way that if a big box of something full of carbs is in the fridge, bad things are going to happen. So I try to eat my off-plan foods away from home. I eat my muffins or cookies at a coffee house. I have a slice of pizza at a pizzeria. I don't buy a box of muffins or a whole pizza and bring them home.

Getting this strategy to work requires that your whole family understand what's at stake. It took me a couple years of harping on what "complications" means, but by now, my family understands that if my blood sugar is too high, I'm damaging my body. They want to keep me around for a while, so they understand that there are some foods that shouldn't be brought into the house--ever.

When other family members want to have treats at home, they are kind enough to buy things I don't like. For example, if someone wants Ben & Jerry's they buy the Chunky Monkey flavor that I find revolting, not the New York Fudge. By the same token, when my kids lived at home, I didn't buy them the brands of cookies I can't resist. There are plenty of others cookies they liked that don't tempt me at all, and those were the ones in the cupboard.

Over the years the nondiabetic members of my family learned that no one is doing themselves a favor scarfing down 300 grams of fast acting carbohydrate every day--particularly not people with a family history of diabetes and heart disease!

Medications Can Help

I'm not a big fan of medications because I've learned the hard way that drug companies lie about side effects and some of these side effects are permanent and can ruin your life. But I learned the hard way, too, that some of us (like, say me) can't get normal blood sugars no matter how low our carb intake. For us, adding a diabetic drug or two to our daily regimen may be the only way we can get normal blood sugars without a life of tormenting self-denial.

Drugs I have found useful over the years include metformin, precose, and post-meal insulin shots. The new incretin drugs, Januvia and Byetta help some people make dramatic improvements in their blood sugar, but the way that they work makes it necessary to eat a slightly higher amount of carbohydrates with them because they only work when your blood sugar rises over a certain threshold. Even with these drugs (including Januvia) I've never been able to eat more than 120 grams of carbohydrates a day, but after many years of eating an extremely low carb diet--which was the only diet that would control my blood sugars--120 grams of carbs a day feels like a completely normal diet!

Be Aware of Rising Insulin Resistance

Some people may find that eating a low carb diet is not enough to control their blood sugar because they are very insulin resistant. Perhaps they have been diagnosed with PCOS, or have to take a drug, like Prednisone that increases insulin resistance. The book, Dr. Bernstein's Diabetes Solution by Dr. Richard K. Bernstein, the distinguished diabetes doctor, recommends Metformin as an appropriate drug for patients on a low carb diet whose blood sugars are still not completely controlled. It isn't a cure by any means, just one more tool you can use to keep blood sugars under control, and if you limit your insulin resistance you may solve both weight and hunger problems that otherwise can derail your diet.

You can read more about the different drugs available to help control blood sugars HERE. Just remember that all these diabetes drugs work best when you combine them with some level of carbohydrate restriction. How much restriction? Test your meals one and two hours after eating, and your blood sugar meter will tell you exactly how much.

Top Medical Journal Publishes Landmark Study Showing Very Low Carb Diet Most Effective and Safest for Lipids etc.

In case you are still being given out-of-date medical or nutritional advice by people who tell you that a low carb/high fat diet will give you a heart attack, take a look at this recently published study, which appeared in the Journal of the American Medical Association.

This study found that an Atkins style low carb diet not only caused double the weight loss of the low fat diet at the end of one year, but it did not adversely affect cholesterol levels.

This finding, added to the Women's Health Initiative finding (after $40 million dollars of research) that low fat dieting does NOT prevent heart disease, should lay to rest any last fears you might have about the impact of cutting carbs on your health.

The findings of this study, are not news to anyone who has tried a low carb diet and stuck with it for any period of time, but they appear to amaze the entire medical community who continue to cling to their to the "Fat is Bad" religious belief long no matter what evidenced-based medical studies might come up with.

Bottom line: You can cut your carbs way down, replace carbs with fat, and await the better health this kind of eating will provide.

Comparison of the Atkins, Zone, Ornish, and LEARN Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal Women: The A TO Z Weight Loss Study: A Randomized Trial.Christopher D. Gardner, PhD; Alexandre Kiazand, MD; Sofiya Alhassan, PhD; Soowon Kim, PhD; Randall S. Stafford, MD, PhD; Raymond R. Balise, PhD; Helena C. Kraemer, PhD; Abby C. King, PhD

Here's the summary of the WHI findings:

NIH News: News from the Women?s Health Initiative: Reducing Total Fat Intake May Have Small Effect on Risk of Breast Cancer, No Effect on Risk of Colorectal Cancer, Heart Disease, or Stroke

Here's a study that documents the effectiveness of lowering carbs and increasing fat and protein consumption for the control of blood sugar in the absense of weight loss:

Control of blood glucose in type 2 diabetes without weight loss by modification of diet composition. Nutrition & Metabolism 2006, 3:16.

To Get More Help with Making a Low Carbohydrate Diet Work

My "Low Carb Facts and Figures" site, which now shares this server, has more information I collected back in the days when I used a low carb diet for both weight loss and blood sugar control.

You'll find articles there that address a few of the issues people run into while eating a very low carb diet,which are not answered in a completely honest fashion by the people who sell diet books promising you can lose weight easily while gorging on all your favorite foods--which, sadly, is 99% of all authors writing diet books.

I stumbled onto Jenny Ruhl's Diabetes Update blog after I received several very insightful comments to this blog whenever I posted a discussion on diabetes or pre-diabetes/metabolic syndrome.

Who the heck was this commenter who clearly had deep insight into diabetic issues?

It turned out to be Jenny Ruhl, a woman who learned her lessons the hard way: by receiving a belated diagnosis of (an unusual form of) diabetes, then receiving plenty of mis-guided advice from physicians on diet and treatment. Reading her many blog posts and websites, you get the clear sense of how hard this individual worked to gain the depth of knowledge she's acquired, on a par or superior to most diabetes specialists.

And she minces no words in expressing her heartfelt and carefully considered opinions. But that's what I look for: people who are unafraid to voice opinions that may not be consistent with the flow of conventional thought, but ring true and prove effective.

Dr. Davis: From your blog and websites on diabetes, it is clear that you exceptionally knowledgeable in the world of diabetes, metabolic syndrome, and related disorders. Can you give us a little background on how you came to this quest?

Jenny: Though I was told I was a "classic type 2" [diabetic] by my doctors, nothing I read about diabetes corresponded to my own experience. I knew my diabetes had not been caused by obesity because I'd been a normal weight all my life until my blood sugars went out of control at which point I developed ravenous hunger and gained a lot of weight very quickly.

I also wondered at the huge gap between what Dr. Bernstein said was a normal blood sugar and what my doctors told me was a safe blood sugar for a person with diabetes. The people I met who followed Bernstein's very low carb diet had much better blood sugars and far fewer complications, but my doctors dismissed this as irrelevant. So I decided to do some research to find out who to believe. I plunged into the medical journal articles that had recently been made available on the web to see if I could answer two questions: What causes diabetes? and "What does science actually know about what blood sugar levels damage organs?"

The result was the information that became the basis for the Blood Sugar 101 site. Initially, I attempted to sell it as a book, but editors told me that though what I'd learned was "fascinating" it would be "over the head" of the typical health book buyer who wanted simple explanations and if possible, a simplistic slant towards "cure." Fortunately, the very strong response and high traffic volume to the web site proved that, as I had thought, there are a lot of people who do want more than an oversimplified overview and who, given the information they needed, were able to make huge positive changes in their health.

Dr. Davis: What do you think your life would be like if you hadn't pursued this unique course?

Jenny: Possibly a lot shorter.

People in my family die of heart attacks in their 50s, probably from undiagnosed high blood sugars. The pattern of the type of diabetes I have is to have a normal fasting blood sugar and an extremely high post-meal blood sugar after consuming very few grams of carbohydrate. When doctors diagnose using only the fasting blood test, they miss those highs, which research is now finding to be a primary cause of heart disease.

I also would have been a lot fatter. My doctors told me that I was packing on 20 lbs a year due to "normal menopausal changes" and that there was nothing I could do about it. Lowering my carbs significantly dropped all the weight I had gained and I still weigh a lot less now than I did in 1998.

Dr. Davis: You've been a keen observer of the diabetes scene for some years. Have you discerned any important trends in both the public's perception of diabetes as well as how diabetes is managed in the conventional world?

Jenny: The huge difference I see is that, over the last decade, the online diabetes community has learned the value of cutting back on carbohydrates and shooting for truly normal blood sugar levels. So people who put some time into researching diabetes online and talking with those of us who have succeeded in avoiding complications will learn that they do not have to settle for very high blood sugars and deterioration their doctors think inevitable.

Unfortunately, the media have put most of their energy into promoting the discredited idea that diabetes is caused by gluttony and sloth and to promoting the equally discredited idea that people with diabetes should eat a high carbohydrate diet and avoid fat.

So for now there is a huge divide in the quality of life of those people with diabetes who educated enough to go out on the web and educate themselves and those who get their diabetes information from doctors. Sadly most doctors still encourage patients to eat low fat/ high carb diets, and counter the very high blood sugars this diet produces with oral drugs of questionable efficacy, while assuring patients they will be safe if they maintain blood sugar levels that meet the American Diabetes Association's recommendations, though a mass of research shows these are high enough to produce every single diabetic complication possible.

Dr. Davis: I understand that you've released a new book, Blood Sugar 101. How is your book unique in the world of diabetes books? Who should read Blood Sugar 101?

Jenny: Blood Sugar 101: What They Don't Tell You About Diabetes differs from other books in that it gives the reader a much deeper understanding of what is really going on in their bodies as their blood sugar control breaks down and what sciences knows about how abnormal blood sugars cause complications. Then it gives the reader the tools they need to find what diet and/or drug regimen will brings their own, unique, blood sugars down to a truly safe level.

Unlike some books, this one does not present a one-size-fits-all solution, but recognizes that Type 2 diabetes is really a catch-all diagnosis that covers a lot of disorders that behave quite differently. That is why what works for one person with diabetes may not work for another.

Because this book provides details available nowhere else about the physiology of diabetes and the drugs available to treat it, readers will find the information they need to work with their doctors to craft a regimen that brings their blood sugar into the range that preserves and improves their health.

Dr. Davis: Before we close, tell us a little about yourself outside of your diabetes advocate role.

Jenny: I live in rural New England and am a passionate gardener. I've been online since 1980 when I was part of the team at IBM that developed the first commercial email program, PROFS. I got involved in online discussion groups in 1987 and have been messaging on bulletin boards ever since.

I was a professional singer/songwriter in Nashville in my youth and spent my middle years as a bestselling author of books about consulting. Right now a lot of my energy goes into managing the financial and software side of a family business that makes hand made pocket tools for collectors.

Dr. Davis: Thank you for your great insights, Jenny!

True to form, Dr. John Cannell has published yet another wonderfully insightful Vitamin D Newsletter.

One item caught my eye, a response to a question about the Marshall Protocol. I, like Dr. Cannell, was inundated with questions about this so-called protocol, which amounts to little more than the unfounded speculations of a non-physician, actually someone not even involved in health care.

In all honesty, I blew the whole issue off after I read Dr. Marshall's rants. They smack of pure quackery, though from somebody who clearly has a command of scientific lingo. To Dr. Cannell's credit, he took the time and effort to construct a rational response in the latest issue of the newsletter. I reproduce his response here:

Dear Dr. Cannell:

I understand Dr. Marshall conducted a study and found vitamin D is bad for you. What kind of study did he do?

Mary, Minneapolis, Minnesota

Dear Mary:

I have been inundated with letters asking about Professor Marshall's recent "discovery." Some have written that to say they have stopped their vitamin D and are going to avoid the sun in order to begin the "Marshall protocol." The immediate cause of this angst is two publications, a press article in Science Daily about Professor Marshall's "study" (which is no study but simply an opinion) in BioEssays. Dr. Trevor Marshall has two degrees, both in electrical engineering. Before I begin, I want to again remind you that I am a psychiatrist who works at a state mental hospital. In my duty to full disclosure, I must say that I have known a lot of psychiatrists in my life and a few electrical engineers. If I knew nothing else of a disagreement between two people but their professions, I would believe the electrical engineer, not the psychiatrist.

In reading his two articles, Dr. Marshall's main hypotheses are simple. (1) Vitamin D from sunlight is different than vitamin D from supplements. (2) Vitamin D is immunosuppressive and the low blood levels of vitamin D found in many chronic diseases are the result of the disease and not the cause. (3) Taking vitamin D will harm you, that is, vitamin D will make many diseases worse, not better. If you read his blog, you discover that the essence of the Marshall protocol is: "An angiotensin II receptor blocker medication, Benicar, is taken, and sunlight, bright lights and foods and supplements with vitamin D are diligently avoided. This enables the body's immune system, with the help of small doses of antibiotics, to destroy the intracellular bacteria. It can take approximately one to three years to destroy all the bacteria." That is, Dr. Marshall has his "patients" become very vitamin D deficient.

Again, Dr. Marshall conducted no experiment and published no study. He wrote an essay. He presented no evidence for his first hypothesis (sunlight's vitamin D is different than supplements). From all that we know, cholecalciferol is cholecalciferol, regardless if it is made in the skin or put in the mouth. His second hypothesis is certainly possible and that is why all scientists who do association studies warn readers that they don't know what is causing what. Certainly, when low levels of vitamin D are found in certain disease states, it is possible that the low levels are the result, and not the cause, of the disease. Take patients with severe dementia bedridden in a nursing home. At least some of their low 25(OH)D levels are likely the result of confinement and lack of outdoor activity. However, did dementia cause the low vitamin D levels or did low 25 (OH)D contribute to the dementia? One way to look at that question is to look at early dementia, before the patient is placed in a nursing home. On the first day an older patient walks into a neurology clinic, before being confined to a nursing home, what is the relationship between vitamin D levels and dementia? The answer is clear, the lower your 25(OH)D levels the worse your cognition.

Wilkins CH, Sheline YI, Roe CM, Birge SJ, Morris JC. Vitamin D deficiency is associated with low mood and worse cognitive performance in older adults. Am J Geriatr Psychiatry. 2006 Dec;14(12):1032-40.

Przybelski RJ, Binkley NC. Is vitamin D important for preserving cognition? A positive correlation of serum 25-hydroxyvitamin D concentration with cognitive function. Arch Biochem Biophys. 2007 Apr 15;460(2):202-5. Epub 2007 Jan 8.

These studies suggest that the low 25(OH)D levels are contributing to the dementia but do not prove it. Only a randomized controlled trial will definitively answer the question, a trial that has not been done. So you will have to decide if vitamin D is good for your brain or not. Dr. Marshall seems to be saying demented patients should lower their 25(OH)D levels. Keep in mind, an entire chapter in Feldman's textbook is devoted to the ill effects low vitamin D levels have on brain function.

Brachet P, et al. Vitamin D, a neuroactive hormone: from brain development to pathological disorders. In Feldman D., Pike JW, Glorieux FH, eds. Vitamin D. San Diego : Elsevier, 2005.

It is true that in some diseases, high doses of vitamin D may be harmful. For example, in the early part of last century, the AMA specifically excluded pulmonary TB from the list of TB infections that ultraviolet light helps. They did so because many of the early pioneers of solariums reported that acutely high doses of sunlight caused some patients with severe pulmonary TB to bleed to death. Thus, these pioneers developed very conservative sun exposure regimes for pulmonary TB patients in which small areas of the skin were progressively exposed to longer and longer periods of sunlight. Using this method, sunlight helped pulmonary TB, often to the point of a cure. Furthermore, it is well known that sunlight can cause high blood calcium in patients with sarcoidosis. In fact, sarcoidosis is one of several granulomatous diseases with vitamin D hypersensitivity where the body loses its ability to regulate activated vitamin D production, causing hypercalcemia.

Cronin CC, et al. Precipitation of hypercalcaemia in sarcoidosis by foreign sun holidays: report of four cases. Postgrad Med J. 1990 Apr;66(774):307-9.

Furthermore, although medical science is not yet convinced, some common autoimmune diseases may have an infectious etiology. I recently spoke at length with a rheumatologist who suffers from swollen and painful joints whenever he sunbathes or takes high doses of vitamin D. As long as he limits his vitamin D input his joints are better. To the extent vitamin D upregulates naturally occurring antibiotics of innate immunity, sunlight or vitamin D supplements may cause the battlefield (the joints) to become hot spots. I know of no evidence this is the case but it is certainly possible.

However, If Dr. Marshall's principal hypothesis is correct, that low vitamin D levels are the result of disease, then he is saying that cancer causes low vitamin D levels, not the other way around. The problem is that Professor Joanne Lappe directly disproved that theory in a randomized controlled trial when she found that baseline vitamin D levels were strong and independent predictors of who would get cancer in the future. The lower your levels, the higher the risk. Furthermore, increasing baseline levels from 31 to 38 ng/ml reduced incident cancers by more than 60% over a four year period. Therefore, advising patients to become vitamin D deficient, as the Marshall protocol clearly does, will cause some patients to die from cancer.

Lappe JM, Travers-Gustafson D, Davies KM, Recker RR, Heaney RP. Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial. Am J Clin Nutr. 2007 Jun;85(6):1586-91.

I will not write again about Dr. Marshall's theories. No one in the vitamin D field takes him seriously. Personally, I admire anyone willing to swim against the tide and raise alternative theories. I have done the same with influenza and autism. However, I agree with the New York Times, An Oldie Vies for Nutrient of the Decade and Jane Brody's conclusion, "In the end, you will have to decide for yourself how much of this vital nutrient to consume each and every day and how to obtain it." I agree. You will have to decide for yourself.

John Cannell, MD
The Vitamin D Council

The American Heart Association (AHA) was kind enough to send me an e-mail headlining the breaking news from the American College of Cardiology (ACC) meetings underway in Chicago:

ISAR-REACT 3
A Randomized, Double-Blind, Active-Controlled, Multi-Center Trial (ISAR-REACT 3) of Bivalirudin Versus Unfractionated Heparin in Troponin-Negative Patients Undergoing Percutaneous Coronary Interventions After Pre-Treatment With 600 mg of Clopidogrel

TRITON - TIMI 38 Stent Analysis
Prasugrel Compared to Clopidogrel in Patients With Acute Coronary Syndromes Undergoing PCI With Stenting: The TRITON - TIMI 38 Stent Analysis

Percutaneous Coronary Interventions in Facilities without On-Site Cardiac Surgery (NCDR)

(And four other similar reports)

Let's meld the ACC headlines with the financial headlines:

July 2, 2007
The Medicines Company announces reacquisition of all marketing rights to bivalirudin, anticoagulant growing in use for coronary angioplasty and related procedures. 2008 sales anticipated to be in the $15-20 million range, to grow to $90-110 million, a growth rate of 50% per year.

November 20, 2007
Drug manufacturing giant, Eli Lilly, vies for a portion of the $5 billion (annual revenues) oral anti-platelet market, now occupied by Plavix, with its newer, but questionably better, agent, prasugrel.

Growth of the coronary angioplasty (percutaneous coronary intervention, or PCI) doesn't ordinarily make headlines, but the performance of specific companies within the industry does. Angioplasty and cardiac device maker (inc. the drug-coated stent, Taxus), Boston Scientific, for instance, announced record sales of $8.537 billion for 2007, an increase of $536 million. How to grow this market? We could always hope for more people with heart attacks or other unstable symptoms. Or, we could . . . increase the number of hospitals capable of PCI! Brilliant.

The money behind this push for procedures is staggering. It drives enormous marketing efforts, pays Washington lobbyists, pays for many nice dinners and trips for doctors who engage in the system, and pays for very costly research.

And the AHA and ACC are kind enough to let us know about these great pieces of news.

I'm itching to say that face-to-face to anyone from the wheat industry--agribusiness, baking, retail distribution . . . anybody. Because it's obvious; it's written on the face . . . and belly, and brain, and knees, and hips. And I believe I will soon have the opportunity.

Taking such a controversial stand in my new book, Wheat Belly, i.e., that wheat products, whole or refined, have NO ROLE IN THE HUMAN DIET whatsoever, was bound to provoke criticism and counterattacks. The wheat world has already taken a blow to the chin with the growing popularity of the (misguided) gluten-free movement and they're going to have to get into the business of media damage control.

Take a look at this press release from the Grain Foods Foundation:

RIDGWAY, COLO. — The Grain Foods Foundation has unveiled plans to counter media publicity attracted by “Wheat Belly.”

“Mullen, working with key members of the Grain Foods Foundation’s scientific advisory board, is addressing ‘Wheat Belly’ through proactive media outreach and its ongoing rapid response program,” said Ashley Reynolds, a Mullen account executive. “In particular, the public relations team will be contacting health and nutrition reporters at print and on-line media outlets, as well as editors at major women’s magazines to influence any diet-related stories that may be published in the coming months.”

. . . Ms. Reynolds, a registered dietitian, noted the author relies on anecdotal observations rather than scientific studies; wheat elimination “means missing out on a wealth of essential nutrients;” six servings of grain-based foods are recommended daily in the Dietary Guidelines for Americans; healthy weight loss depends on energy balance rather than elimination of specific foods; and elimination of wheat products makes sense only for those with medical diagnoses such as celiac disease or gluten sensitivity.

She said the group will lean on its scientific advisory board members to “discredit the book and ensure our messages are backed by sound science. “

Here's some of their starting salvos on their Six Servings Blog.

This reminds me of the fight with Big Tobacco in the '70s: "No, sir, we in the tobacco industry know of no research demonstrating that smoking is bad for health," complete with shots of tobacco executives puffing away on cigarettes.

So brace yourself for a fight. These people are protecting a multi-billion dollar franchise, not to mention their livelihoods and incomes. It could get ugly.

Wheat Belly is finally available in Barnes and Noble and all major bookstores nationwide! Also available at Amazon. Electronic versions for Nook and Kindle, as well as an audio CD, will also be available.

The notion of Wheat Belly got its start right here on The Heart Scan Blog and the diet developed for the Track Your Plaque program to conquer heart disease and plaque.

Chapters in the book include:

Not Your Grandma's Muffins: The Creation of Modern Wheat
Whence and where did this familiar grain, 4 1/2-foot tall "amber waves of grain," become transformed into a 2-foot tall, high-yield genetically unique plant unfamiliar to humans? And why is this such a bad thing?

Cataracts, Wrinkles, and Dowager's Humps: Wheat and the Aging Process
If you thought that bagels and crackers are just about carbs, think again. Wheat consumption makes you age faster: cataracts, crow's feet, arthritis . . . you name it, wheat's been there, done that and brings you one step closer to the big nursing home in the sky with every bite.

My Particles are Bigger than Your Particles
Why consuming plenty of "healthy whole grains" is the path to heart disease and heart attack and why saying goodbye to them is among the most powerful strategies around for reduction or elimination of risk.

Hello, Intestine: It's Me, Wheat
No discussion of wheat is complete without talking about how celiac disease and other common intestinal ailments, like acid reflux and irritable bowel syndrome, fit into the broader concept of wheat elimination.

Here's a YouTube video introduction to the book and concept posted on the YouTube Wheat Belly Channel. Also, join the discussions on The Wheat Belly Blog and Facebook. Have that last bite of blueberry muffin, because I predict you won't be turning back!

No, this is not a discussion of monounsaturated versus hydroxgenated fat. This is about the relatively benign fat that accumulates on your hips, rear end, or arms--the "good"--versus the deep visceral fat that encircles your intestines, kidneys, liver, pancreas, and heart--the "bad."

And I'm not talking about what looks good or bad. We've all seen the unsightly flabby upper arms of an overweight woman or the cellulite on her bulging thighs. It might look awful but, metabolically speaking, it is benign.

It's that muffin top, love handle, or wheat belly that encircles the waist, a marker for underlying deep visceral fat, that:

--Increases release of inflammatory mediators/markers like tumor necrosis factor, leptin, interleukins, and c-reactive protein
--Is itself inflamed. When examined under a microscope, visceral fat is riddled with inflammatory white blood cells.
--Stops producing the protective hormone, adiponectin.
--Traffics in fatty acids that enter the bloodstream, resulting in greater resistance to insulin, fat deposition in the liver (fatty liver), and increases blood levels of triglycerides
--Predicts greater cardiovascular risk. A flood of recent studies (here's one) has demonstrated that larger quantities of pericardial fat (i.e., visceral fat encircling the heart, visible on a CT scan or echocardiogram) are associated with increased likelihood of coronary disease and cardiovascular risk.

You can even have excessive quantities of bad visceral fat without much in the way of fat elsewhere. You know the body shape: skinny face, skinny arms, skinny legs . . . protuberant, flaccid belly, the so-called "skinny obese" person.

Nobody knows why fat in visceral stores is so much more evil and disease-related than, say, wheat on your backside. While you may struggle to pull your spreading backside into your jeans, it's waist girth that is the problem. You need to lose it.

You could take vitamin D and achieve a desirable blood level of 25-hydroxy vitamin D (I aim for 60-70 ng/ml), or you could:

--Take Actos to mimic the enhanced insulin sensitivity generated by vitamin D
--Take lisinopril to mimic the angiotensin-converting enzyme blocking, antihypertensive effect of vitamin D
--Take Fosamax or Boniva to mimic the bone density-increasing effect of vitamin D
--Take Celexa or other SSRI antidepressants to mimic the mood-elevating and winter "blues"-relieving effect of vitamin D
---Take Niaspan to mimic the HDL-increasing, small LDL-reducing effect of vitamin D
--Take naproxen to mimic the pain-relieving effect of vitamin D

So, given a choice, what do most doctors choose? Of course, they choose from the menu as presented by the sexy sales representative sitting in the office waiting room. These medications, of course, are among the top sellers in the drug world, taken by millions of Americans and not just one at a time, but several per person.

The Food and Nutrition Board of the Institute of Medicine, the panel of volunteers charged with drafting a Recommended Daily Allowance for vitamin D, says that you are already getting enough vitamin D, so don't bother taking any supplements and continue to wear your sunscreen. Wonder whose side they're on?

I continue to be impressed that many of the conditions that plague modern people are little more than deficiencies peculiar to modern life, such as vitamin D deficiency, or the result of the excesses of modern life, such as consumption of sucrose, fructose, corn, and "healthy whole grains."

I take 8000 units of gelcap vitamin D and haven't felt better.

A few posts back, I talked about how more people are showing us zero lipoprotein(a) and zero small LDL. That was about 4 weeks ago. By then, I had seen 3 people with zero values on both.

Well, it's now up to 9 people: 9 people who have achieved zero lipoprotein(a) and zero small LDL. These are people who started with typical lipoprotein(a) values of 150-300 nmol/L and small LDL values of 1000-2000 nmol/L, both substantial.

I still don't know how many people or what percentage can expect to show such extravagant results. But the sharp increase over a relatively brief period of time is extremely encouraging!

Heart Scan Blog reader, Frustrated, posted this comment:

Dr. Davis,
I have spent the last 5 months eating a diet that completely eliminated all wheat products. It was very low carb, and consisted of relatively high protein (eggs, grass fed beef, grass fed raw cheese, oily fish, chicken), good level of olive oil, walnuts, fish oil (3 mg per day), raw vegetables, little bit of fruit. So I had good amount of monounsaturated fat as well as saturated fat from eggs and grass fed products.

My recent NMR showed:
LDL-p. 2,800
Small LDL particle 1700
Small HDL particle 20
HDL-C 40
LDL-C 114
Trigs. 224
Total chol 208

So I was disappointed. Where have I gone wrong? No wheat and sky-high LDL-p and 1700 small LDL particles.

This is indeed unusual. I see this perhaps 5 or 6 times over a year's time, while thousands of other people show the usual expected respone. I don't have Frustrated's lipoprotein panel prior to starting the diet, but I'll bet the starting panel was similar to this "after" panel.

The overwhelming majority of people who follow a diet like the one described--no wheat, limited carbohydrate, grass fed beef, fish, chicken, vegetables, limited fruit--obtain extravagant reductions in small LDL, increased HDL, and reduced triglycerides. So why did Frustrated end up with such disappointing results, values that potentially provide for high risk for heart disease?

There are several possibilities:

1) He/she is in the midst of substantial weight loss. When labs are drawn in the midst of weight loss, stored energy is being mobilized into the blood stream. This energy is mobilized as fatty acids and triglycerides which, upon entering the blood stream, cause increased triglycerides, reduced HDL, chaotic or unpredictable small LDL patterns, and increased blood sugar sufficient to be in the diabetic or pre-diabetic range. This all subsides and settles down to better values around 2 months after weight loss has plateaued.

2) Apo E4--If Frustrated has one or two apo E4 genes, then increased dietary fat will serve to exaggerate measures like small LDL despite the reduction in carbohydrates, LDL particle number, and triglycerides. This is a tough situation, since small LDL particles and high triglycerides signal carbohydrate sensitivity, while apo E4 makes this person, in effect, unable to deal with fats and dietary cholesterol. It gives me the creeps to talk about reducing fat intake, but this becomes necessary along with carbohydrate restriction, else statin drugs will come to the "rescue."

3) Apo E2 + Apo E4--It's possible that an apo E2 is present along with apo E4. Apo E2 makes this person extremely carbohydrate-sensitive and diabetes-prone with awful postprandial (after-meal) persistence of dietary byproducts, alongside the hyperabsorption of fats and dietary cholesterol from apo E4. This is a genuine nutritional rock and a hard place.

4) Other variants--There are probably a dozen or more other genetic variants, thankfully rare, such as apo B and apo C2 variants, that are not generally available for us to measure that could influence Frustrated's response.

5) The low-carb diet is not truly low-carb--Frustrated sounds like a pretty sharp cookie. But it's not uncommon for someone to overlook a substantial source of carbohydrate exposure that triggers these patterns. Fruit is a very common tripping point, since people generally regard unlimited fruit as a healthy thing. This does not seem to be Frustrated's problem. Others indulge in quinoa, sweet potatoes, millet or other carbohydrate sources that look and sound healthy but, in sufficient quantities, can still trigger this pattern.

6) Other--Hypothyroidism, kidney disease, nephrotic syndrome, hypercortisolism and some other relatively rare conditions are worth considering if none of the above apply.

Anyway, that's the list I use when this peculiar situation arises. If obvious weight loss is not the culprit, the next step is apo E testing. However, the wrong response is to reject the low-carbohydrate notion altogether and just limit fat, since this typically leads to uncontrolled small LDL, high triglycerides, and diabetes. It can often mean limiting carbohydrates while also limiting fats. Just as with the combination of apo E4 with Lipoprotein(a), I lump many of these patterns into the emerging world of genetic incompatibilities, genetic traits that code for incompatible metabolic phenomena.

A Heart Scan Blog reader posted the link to this very excellent presentation by Dr. David Diamond, a neuroscientist at the University of South Florida.

ATP-3, or Adult Treatment Panel-3, is the set of cholesterol treatment guidelines as established by the National Cholesterol Education Panel, the guidelines used by practicing physicians nationwide. They are also the metric by which the "quality" of care is being judged by agencies like Medicare, health insurers, and other parties interested in policing healthcare. Dr. Diamond ably recounts how we ended up in this mess, the conflagration of "cut your fat, reduce cholesterol, and take a statin drug."

I was very impressed that, in his closing comments, he briefly discusses the pivotal role of glycation in heart disease causation. You will see in coming conversations how important an understanding of glycation is to create a healthy diet and lifestyle.

Conventional thinking is that high LDL cholesterol causes heart disease. In this line of thinking, reducing cholesterol by cutting fat and taking statin drugs thereby reduces or eliminates risk for heart disease.

Here's an (extreme) example of just how far wrong this simpleminded way of thinking can take you. At age 63, Michael had been told for the last 20 years that he was in great health, including "perfect" cholesterol values of LDL 73 mg/dl, HDL 61 mg/dl, triglycerides 102 mg/dl, total cholesterol 144 mg/dl. "Your [total] cholesterol is way below 200. You're in great shape!" his doctor told him.

Being skeptical because of the heart disease in his family, had a CT heart scan. His coronary calcium score: 4390. Needless to say, this is high . . . extremely high.

Extremely high coronary calcium scores like this carry high likelihood of death and heart attack, as high as 15-20% per year. So Michael was on borrowed time. It was damn lucky he hadn't yet experienced any cardiovascular events.

That's when Michael found our Track Your Plaque program that showed him how to 1) identify the causes of the extensive coronary atherosclerosis signified by his high calcium score, then 2) correct the causes.

The solutions, Michael learned, are relatively simple:

--Omega-3 fatty acid supplementation at a dose sufficient to yield substantial reductions in heart attack.
--"Normalization" of vitamin D blood levels (We aim for a 25-hydroxy vitamin D level of 60-70 ng/ml)
--Iodine supplementation and thyroid normalization
--A diet in which all wheat products are eliminated--whole wheat, white, it makes no difference--followed by carbohydrate restriction.
--Identification and correction of all hidden causes of coronary plaque such as small LDL particles and lipoprotein(a)

Yes, indeed: The information and online tools for health can handily exceed the limited "wisdom" dispensed by John Q. Primary Care doctor.

Our new recipes, such as New York Style Cheesecake and Chocolate Coconut Bread, are wheat-free and low- or no-carbohydrate. They fit perfectly into the New Track Your Plaque Diet for gaining control over coronary atherosclerotic plaque, not to mention diabetes, pre-diabetes, hypertension, small LDL particles, high triglycerides, high inflammation (c-reactive protein) and other distortions of metabolism.

However, there's one compromise: We include use of non-nutritive sweeteners. It's therefore important to know that artificial sweeteners are not all created equal.

One common tripping point: maltodextrin.

Maltodextrin is composed of polymers (repeating subunits) of glucose, as few as 3 or as many as 20 or more glucose subunits. So maltodextrin is glucose sugar. While it lacks the especially destructive pentose sugar, fructose, maltodextrin is metabolized to glucose and thereby increases blood sugar substantially.

Many artificial sweeteners are bulked up with maltodextrin. For instance, granulated Splenda and Stevia in the Raw, two sweeteners billed as low-calorie and sugar-free that is used on a cup-for-cup basis like sugar, are primarily maltodextrin--with only a teensy bit of Splenda or stevia.

The best artificial sweeteners, i.e., the most benign without a load of maltodextrin, are:

Liquid stevia--Just the extract from stevia leaves and water. It can be a bit pricey, e.g., $10 for a 2 oz bottle, but a little goes a long way.

Truvia--While I'm not too fond of the manufacturer (Cargill), I believe that Truvia is among the better sweeteners around. It is a mixture of the natural sugar, erythritol, that generates little to no blood sugar effects and rebiana (rebaudioside), an isolate of stevia. Some people aren't too fond of the mild menthol-like cooling effect of the erythritol nor the slight aftertaste. I find it works pretty well in most recipes.

Be aware that, no matter which artificial sweetener you use, it has the potential to stimulate appetite. I therefore like to not eat foods sweetened with liquid stevia or Truvia in isolation but as part of a meal. That way, any appetite stimulation that results is substantially quelled by the proteins and fats ingested.

Former Men's Health editor, Jeff O'Connell, has just released his new book, Sugar Nation.

Back in 2009, Jeff contacted me to obtain some background insights into diabetes and its relationship with diet. He recently sent me a copy of his new book that contains some brief quotes from me.

Jeff is a writer, not a physician nor scientist. But I think that you will find his grasp of diabetes and the nutritional and lifestyle events that led him there far exceed the insights held by most practicing physicians. Like many of us, Jeff discovered how to find his way back from pre-diabetes through lessons he had to learn on his own, but not from his doctor.

Jeff tells this story as reporter, son of an estranged diabetic father with whom he reconnects as he approaches the end of his life, and as fellow sufferer of the pre-diabetic/diabetic mess that modern habits and "official" dietary advice have given us. Jeff's book is worth a read to see yet another dimension of the human stories that are emerging from this incredible nutritional tangle we find ourselves in.

Here's a unique YouTube video about Jeff's story.

Dr. Bill Blanchet: A ray of sunshine

The Russert Protocol at work

Petition to the National Institutes of Health

Wheat withdrawal

The Big Squeeze

Tim Russert's heart scan score 210. . .in 1998

Another failure of conventional cardiac care

Tribute to Tim Russert

Why do skinny people get heart disease?

Cardiology Confidential

Self-empowerment is coming!

Another option for lipoprotein testing

Weight and lipoproteins

Variation in vitamin D requirements

Heart attacks in your own backyard

Pilot lands safely after heart attack, then dies

Large new clinical study launched to study. . .niacin

The dark side of CT heart scans

The dirty little secret about aneurysms

Heart scan scores dropping like stones!!

Lipoprotein(a) Research Foundation

More on ASTEROID

LDL cholesterol, statins, and plaque regression

When is a calorie not a calorie?

Track Your Plaque data abstract

Small fish oil capsules

Low-carb eating for diabetes

Interview with an outspoken advocate of truth in diabetes

The Marshall Protocol and other fairy tales

Breaking news from the American College of Cardiology meetings

Do you eat wheat? I thought so.

Wheat Belly explodes on the scene!

Good fat, bad fat

You could take vitamin D or . . .

More lipoproteins zero!

Diet: One size does NOT fit all

Why ATP-3 is B--- S---

How far wrong can cholesterol be?

The best artificial sweeteners

Sugar Nation