Coenzyme Q10 and statin drugs

Although drug manufacturers claim that muscle side effects from statin drugs occurs in only around 2% or people or less, my experience is very different.

I see muscle weakness and achiness develop in the majority of people taking Lipitor, Crestor, Zocor, Vytorin, etc. I'd estimate that nearly 90% of people get these feelings sooner or later.

Thankfully, the majority of the time these feelings are annoyances and do not lead to any impairment. Full-blown muscle destruction is truly rare--I've seen it once in over 10 years and thousands of patients.

The higher the dose of statin drug and the longer you take it, the more likely you're going to have muscle aches.

I experienced a strange phemomenon myself today. I worked outdoors for about 4 hours, pulling weeds, digging in the dirt, spreading topsoil. (I have an area of overgrowth in the front yard.) Admittedly, I worked pretty hard and it was a warm, humid day.

I was sore, as you'd expect at age 49. But, much more than that, I was exhausted--my muscles ached and I had barely enough strength to get up the stairs.

Hoping for some relief, I took an extra dose of coenzyme Q10. I usually take 50-100 mg per day. Today, when I felt this overwhelming muscle fatigue, I took an additional 200 mg. Within 10 minutes, I felt a surge of energy. It was, in fact, a perceptible, quite dramatic feeling.

I am thoroughly convinced, through my own experiences on Lipitor (I have a high LDL particle number despite a healthy lifestyle, among other abnormalities), and the experiences of many other people, that coenzyme Q10 can be an extremely useful tool to minimize the muscle aches and weakness of the statin drugs.

If you do indeed need to take one of these agents, coenzyme Q10 is worth knowing about. Supplementing coenzyme Q10 has, for me, been a real lifesaver. For many people, LDL reduction is a crucial part of their heart scan score control program. In my experience, many of them would not be able to take the drug without eozyme Q10.

Blast your LDL with oat bran and almonds

Nearly all of us can use an extra boost in reducing LDL cholesterol. We have a large number of people, in fact, who have reduced LDL into the Track Your Plaque range of 60 mg/dl or less without the use of statin cholesterol-reducing drugs.




Oat bran is among my favorite ways to reduce LDL. Three tablespoons per day is a really effective method to drop your LDL around 20 points. There's twice the beta glucan (soluble, or "viscous", fiber)in oat bran, as compared to the more popular oatmeal. Add oat bran to anything you can think of: yogurt, cottage cheese, vegetarian chili, oatmeal, top desserts with it, etc. Some people struggle to find oat bran in the grocery store. Most health food stores that sell bulk products will have oat bran, usually less than a $1 per pound. Many grocery stores will also have an oat bran hot cereal along with the Cream of Wheat and oatmeal. That's okay, provided the only ingredient is oat bran--no added sugars, etc.





Another dynamite method to reduce LDL 10-20 points is adding raw almonds to your daily food choices. One or two handfuls per day works great. We find it at Sam's Club for around $12.99 for a 3 lb. bag. The plentiful fibers and monounsaturates in almonds keep you full and satisified, take the edge off your sweet tooth, and even blunt the blood sugar rise caused by other foods.

Both these foods are also great ways to combat the metabolic syndrome. Since both fiber-rich oat bran and almonds slow the release of sugars into the blood, blood insulin level is also reduced. This results in a happy cascade of less small LDL, increased HDL, and a reduction in inflammation.

All these wonderful effects contribute to inching you closer to success: dropping your heart scan score.

Pre-diabetes with normal blood sugar

We pay special attention to pre-diabetes, in all its varied manifestations, in the Track Your Plaque program. This is because these factors are potent instigators of coronary plaque growth.

Early in the Track Your Plaque program we ignored these measures. After all, this is a program for heart disease risk reduction, not for mangement of diabetes. But we saw explosive rates of plaque growth when pre-diabetic factors were not controlled--even when cholesterol and related factors were under excellent control.

It became increasingly clear that factors associated with pre-diabetes needed to be managed, as well. This includes small LDL, increased blood sugar, high blood pressure, increased inflammation (as CRP).

Many people, however, have normal blood sugars (100 mg/dl or less) with a high blood insulin level (>10 microunits/ml). (This blood test is available in most laboratories.) This means that they have early resistance to insulin. The pancreas, the source of insulin, responds to the body's unresponsiveness to insulin by increasing insulin production.

Increased blood insulin with normal blood sugar will drive production of higher triglycerides, a drop in HDL, creation of small LDL, and inflammation--and coronary plaque growth, as evidenced by increasing CT heart scan score.

Blood insulin levels can be very effectively dropped by weight loss; exercise; reduction of processed carbohydrates like breads, pretzels, and breakfast cereals; and increased raw nuts and oat products; and vitamin D replacement to normal levels. Drug manufacturers are desperately trying to make this a mandate for drug treatment (Actos, Avandia), but are encountering resistance, since most people without overt diabetes don't want to take diabetic medication (rightly so!).

You and your doctor should consider insulin as a factor to track, especially if you have small LDL, low HSL, or high triglycerides, or any of the other manifestations listed above.

Sometimes small LDL is the only abnormality

Janet is a 58-year old schoolteacher. At 5 ft 3 inches and 104 lbs, she had barely an ounce of fat on her size-2 body. For years, Janet's primary care physician complimented her on her cholesterol numbers: LDL cholesterol values ranging from 100 to 130 mg/dl; HDL cholesterol of 50-53 mg/dl.

Yet she had coronary disease. Her heart scan score: 195.

Lipoprotein analysis uncovered a single cause: small LDL. 95% of all of Janet's LDL particles were in the small category. What was surprising was that this pattern occurred despite her slender build. Weight is a powerful influence on the small LDL pattern and the majority of people with it are overweight to some degree. But not Janet.

How did she get small LDL if she was already at or below her ideal weight? Genetics. Among the genetic patterns that can account for this pattern is a defect of an enzyme called cholesteryl-ester transfer protein, or CETP. This is the exact step, by the way, that is blocked by torcetrapib, the new agent slated for release sometime in future (The manufacturer, Pfizer, is apparently going to sell this agent only packaged in the same tablet as Lipitor. This has triggered an enormous amount of criticism against the company and they are, as a result discussing marketing torcetrapib separately.)

Also note that Janet had a severe excess of small LDL despite an HDL in the "favorable" range. (See my earlier conversation on this issue, The Myth of Small LDL at http://drprevention.blogspot.com/2006/06/myth-of-small-ldl.html.)

With Janet, weight loss to reduce small LDL was not an option. So we advised her to take fish oil, 4000 mg per day; niacin, 1000 mg per day; vitamin D, 2000 units per day; use abundant oat bran and raw almonds, both of which suppress small LDL. This regimen has--surprisingly--only partially suppressed her small LDL pattern by a repeat lipoprotein analysis we just performed. We're hoping this may do it, i.e., stop progression or reduce her heart scan score.

The lesson: Small LDL is a very potent pattern that can be responsible for heart disease, even if it occurs in isolation. And, contrary to conventional thinking, small LDL can occur as an independent abnormality, even when HDL is at favorable levels.

Report from Washington II

Today's discussions at the Society for Cardiovascular Computed Tomography (SCCT) focused on atherosclerotic "plaque characterization".

As CT scanners get better and better at imaging the various components of plaque, some fascinating issues emerge:

--CT heart scans provide insights into what exactly is contained in an individual's atherosclerotic plaque that are not often provided even during heart catheterization. In other words, CT heart scanning is, in many instances, superior to heart catheterization, since it provides images of the artery wall, not just the internal contents.

--Progression (i.e., increase) in heart scan score is a powerful predicter of heart attack risk. Dr. Matthew Budoff of UCLA argued persuasively that the annual rate of increase in score is probably the most accurate measure of risk available, superior to cholesterol and calculated measures like the Framingham risk score.

--Coronary calcium scoring remains the best method to gauge total plaque throughout the entire coronary tree. In a person free of symptoms, the risk of a cardiac "event" (heart attack, death, procedures) is low and additional imaging (like CT angiography) is generally unnecessary.


Dr. Budoff, among the true thought leaders in CT heart scanning, also recounted his perspective on the history of heart scans. He noted that the questions asked through the years have evolved:




1995-2000 Should we do coronary calcium scans?

2000-2002 Do high or low risk patients benefit from coronary calcium scoring?

2003-2004 What is the better scanner, EBT or MDCT?

2006 How often should we perform coronary calcium imaging?


I believe that Dr. Budoff summarizes wonderfully where the Track Your Plaque programs fits into the overall scheme of things: Serial (repeated)CT heart scans to gauge progression or reversal is the wave of the future. We shouldn't just be interested in identifying persons at risk for heart attack. We should also be interested in showing the person at risk exactly how to reduce or eliminate that risk.

Report from Washington





I'm presently attending the Society for Cardiovascular Computed Tomography meetings in Washington, DC, along with 500 of my colleagues. It's exciting to see how interest in CT scanning for heart disease has balloonned in the past couple of years.

Several trends are noticeable today, based on the content and tone of the discussions:

--CT scanning of the heart, and imaging in general, is just getting started. In other words, the capabilities for CT scanners and other devices to detect heart disease (coronary and otherwise) are where the gasoline engine was in the 19th century. Scanning is getting faster, easier, safer, and more precise. Just as few people in 1905 could have predicted that automobiles would be computer-enhanced, high-speed, ubiquitous devices with several per household, the potential for CT imaging for heart disease is truly in its infancy.

--CT coronary angiography (so-called "64-slice CT scans") are not screening tests for hidden coronary disease in people without symptoms. I was grateful that this point has been made and reiterated by several speakers, as this is consistent with our views. Simple CT heart scans for coronary calcium scoring, in contrast, are screening tests. When the radiation exposure of CT angiograms are reduced to tolerable levels, then they may be used as screening tests. We are probably 3-4 years away from this point.

--Both stress testing and heart catheterizations will be partially replaced by CT scanning. In particular, over the next decade, you will see a dramatic drop in unnecessary catheterizations, i.e,, far less people saying "I had a heart cath but they told me that it was normal."


There has been heavy focus on applications of CT scanning for acute settings, particularly the emergency room and hospitals.

What has surprised me is that there is virtually no conversation whatsoever about the preventive uses of CT heart scanning. So far, only Dr. Daniel Berman of UCLA has shown that he has "seen the light": CT scans are a crucial tool for identification of early coronary plaque, and this tells us whether prevention is necessary and with what intensity.

There has been, however, no discussion at all about quantification of plaque in a program of reversal. Perhaps that should come as no surprise, given the imaging-technology focus of this convention. For most of my colleagues, prevention is also not terribly interesting. Identification and treatment of acute disease like impending heart attack is.

Of course, applying the information from your CT heart scan to empower you in a program and reversal is what the Track Your Plaque program is all about. I hope you see the light. I admit that it's not always easy to follow what we are advocating here. Perhaps not too different than telling someone in his horse-drawn buggy that one day he'll be driving a sleek car with onboard computerized mapping, air-conditioning, and micro-chips to modulate engine performance. He's probably tell us we're nuts.

I'll continue to update if any news relevant to our interests crops up in these meetings.

What about the Track Your Plaque failures?

I’d love to tell you that the Track Your Plaque program track record is of 100% success. It’s not.

It is very successful. But we’ve had some people who have failed and failed BIG. These are the people who've undergone bypass surgery, received one or more stents, or had heart attacks. Lesser failures are the people who’ve had large, undesirable increases in heart scan scores of >30% in one year. (The expected rate of increase in your heart scan score without preventive efforts is 30% per year, on average.)

What can we learn from those failures? There were several characteristics that stand out among this small group:

· Non-compliance--meaning they just didn’t stick with it. They started out right but then rapidly lost interest in maintaining all the pieces of the program and neglected their fish oil, niacin, gain weight, etc. Matthew did this and ended up with three stents to his left anterior descending. His slow start was due to skepticism that the program worked and just plain forgetfulness.

· Extreme stress--One of our earliest failures was a 38-year old man whose heart scan score doubled in one year, despite doing everything right. But three family members, all close to him, died within the space of six months, including his mother and a brother. I regard this as one of those instances in which we were powerless, unfortunately, though it is a graphic example of the power of unresolved stress and grief.

· Having a “better way”--These are the couple of people who were convinced that they had a better way to control their heart scan score. David firmly believed that his two dozen supplements and exercise program would drop his score. Instead, they permitted a 42% increase. Lee relied exclusively on chelation, along with several supplements of his own design. Lee had three-vessel bypass surgery.

· Starting too late--Gerome started with a score of 1179, but also was having chest pressure with emotional stress. His stress test was abnormal, with the entire upper half of his heart not receiving blood with exercise on a stress nuclear study (“anterior ischemia”). Gerome received four bypass grafts. Unfortunately, Gerome never really had a chance to engage in the Track Your Plaque program, since his health and safety were in jeopardy as soon as he started.

Have we had any big failures of people who did everything right, were compliant, were not subject to extreme stress (more than just job stress, or financial worries), didn’t neglect the basic requirements of the Track Your Plaque program, and had sufficient time (at least 6 months to 1 year)? No, thankfully, we have not.

No one who has stuck to the program has had a big failure.

Be smarter than your cardiologist

“Do you need a stent?”

Sad to say, but that sentence condenses the wisdom of over 90% of practicing cardiologists.

Prevention of heart disease means take Lipitor or some other statin and cutting the saturated fat in your diet. That’s it. Maybe throw in exercise.

Regression of coronary plaque? That phrase has only entered the conversation since the AstraZeneca-supported trial of Crestor succeeded in achieving 8% regression of plaque (Track Your Plaque Members: See News) as demonstrated by intracoronary ultrasound.



In other words, in the minds of my colleagues, it can’t be true until a drug company tells them it’s true. It’s beyond me why this brainwashing of otherwise intelligent people has occurred, but it is blatantly evident in practice.

Fish oil is another example. The spectacular benefits of fish oil have been known for 20 years. But only recently has it become a “mainstream” practice to recommend fish oil, largely because a drug manufacturer has put a preparation through the rigors of FDA approval (Omacor) and is now marketing directly to physicians. All of a sudden, fish oil is a good thing? No, it’s just achieved legitimacy in the eyes of practitioners because it graces marketing literature.

If you’re reading this, you’re likely interested in coronary plaque regression using the only tool available for you to measure, track, and regress coronary plaque: CT heart scans. Intracoronary ultrasound will achieve the same goal, but it is an invasive procedure performed at heart catheterization, involves threading a wire and imaging probe all the way down the artery, involves real risk of tearing the inner lining of the artery, and is costly (around $14,000-$20,000 for the entire package). Do it every year? That’d be nuts.

If you’re thinking about coronary plaque regression, using fish oil, concerned about patterns like low HDL and small LDL, aware of the vitamin D deficiency issue as a coronary risk factor, etc., you are far more aware than the vast majority of practicing cardiologists. They are interested in what new brand of anti-coagulant to use during their heart catheterization (because the product representative gushes about the new agent—only $1200 a dose!). Or, they are interested in gaining the procedural skills to put in a new device like a biventricular pacemaker. Regress/reverse coronary plaque? What for?

You already know that a conversation about coronary plaque reversal will not be obtained in your cardiologist’s office. Your family practice doctor or internist? Fat chance! Knee arthritis, pap smears, pneumovax inoculations, sore throats, gout, back pain—they’re spread far too thin to know anything more than the most superficial amount about coronary plaque control. Most know nothing.

That’s where we come in. That’s our mission: Educate people about the extraordinary tools that you have available to you, all in the cause of control or reversal of coronary plaque.

Why am I here?

Frank came to the office for an opinion, sent by his (proactive) family physician.

"I really don't know why I'm here, to be honest."

Two years earlier, Frank had a heart attack, survived and received two stents to his circumflex coronary artery. He now took Zocor and his LDL cholesterol was a reasonably favorable 89 mg, total cholesterol 183 mg.

"I walk with my wife every other day. I've been avoiding fish fries. You'll never see me eat fast food."

Frank was correct: If we were going to engage in the conventional approach to coronary disease, Frank was on the right track. We would have postponed his next heart attack or procedure by a couple of years. Stroke, aneurysm, and other atherosclerotic manifestations would be set back, likewise, a few years.

Would Frank have profound control over his disease? Absolutely not. In fact, his disease had probably advanced a huge amount just in the two years since his stents were placed and he was on his "prevention" program. Without his current effort, his coronary plaque would be expected to grow 30% per year. On Zocor and his modest lifestyle efforts, plaque growth was probably in the 14-28% per year range.

So I explained the unique Track Your Plaque approach to Frank. First, we start with a CT heart scan to establish where he was starting. Although he had two stents in his circumflex artery, we still had two other arteries (LAD, right coronary) to score and track.

We then attempt to identify all hidden causes of his heart disease and then correct them.

Of course, Frank had multiple hidden causes:

--HDL too low at 38 mg/dl
--Small LDL-severe, in fact, with 95% of all LDL particles in the small category
--Triglycerides too high
--Excesses of several triglyceride-containing particles (VLDL, IDL)
--Pre-diabetes--Frank had both a borderline high blood sugar and a high insulin level. This is a sure-fire stimulus to coronary plaque growth.
--A severe deficiency of vitamin D (<20 ng/ml)
--An excessivelyhigh blood pressure during exercise--With a blood pressure of 190/102 on the treadmill.

There were others(!), but that was the bulk of the causes behind Frank's coronary disease.

Once Frank recognized that there was indeed a huge panel of hidden causes for heart disease, not just too much fat in his diet and LDL cholesterol, he jumped into the program head first.

The message: The conventional approach is absurdly oversimplified, a certain path to failure for the majority of people. Even if you don't have known coronary disease like Frank, but just have a heart scan score >zero, the same principles apply to you.

Catheterization to “define coronary anatomy”

Gary is an avid jogger. On an average day, he runs 5-6 miles at a good clip. On two occasions recently, however, Gary experienced an ache in his left shoulder at mile 4. It was a toothache-like feeling, but he kept on going without difficulty.

Gary also had a heart scan score of 370.

Upon hearing of Gary’s score and his shoulder sensation, the cardiologist who saw him advised a heart catheterization “to define coronary anatomy”. (This is a real incident.)


What exactly does that mean? Why would Gary’s cardiologist need to define it?

In my view, this is an absurd notion. No one needs to “define coronary anatomy”. This catch-all phrase is commonly used to justify heart procedures. I believe what the cardiologist is saying is that it’s the easiest (for the cardiologist) and perhaps most generously reimbursed method to determine whether Gary’s symptoms are warning of an impending heart attack or not.

The problem is that the question can also be answered quite well by doing a stress test. Though not perfect diagnostic tests, stress tests are useful when symptoms are present that are doubtful in nature. Gary’s left shoulder ache could have been related to his heart, but the likelihood was that it was not. A stress test would have answered the diagnostic question quite adequately.

Instead, this man was subjected to an invasive test that was likely unnecessary. This happens dozens, if not hundreds, of times per day just around here. Nationwide, it is an epidemic of malpractice.

There are, indeed, times when a person should proceed directly to a heart catheterization. This is commonly and appropriately performed when a person develops unstable heart symptoms, such as chest discomfort or breathlessness at rest while not doing anything physical, or if the frequency is increasing, or if a stress test shows an important abnormality. There is no question that heart procedures can be lifesaving at times.

The problem is that thousands of people every year are scared into these procedures inappropriately. Beware!
All posts by william-davis

Brainwashed!

At a social gathering this weekend, as we humans like to do, someone asked me what I did for a living. I told him I was a cardiologist.

"What hospital do you work at?" he asked.

This is invariably the response I get whenever I tell people what I do. I wouldn't make much of it except that it happens just about every time.

This indicates to me just how successful hospitals, my colleagues, cardiac device manufacturers, and others supporting the status quo in heart care, have been in persuading us that the place for heart disease is the hospital--period.

Tense families, drama, high-tech...It all takes place in the hospital.

Yet the people destined to be the fodder for hospital heart care are presently well, mostly unaware of what the future holds. Also unaware that heart disease is readily, easily, inexpensively, and accurately identifiable. Ask anyone in the Track Your Plaque program who's had a CT heart scan.

We all need to rid ourselves of the idea that the hospital is the place for heart disease. If the coronary plaque behind heart attack is easy to detect and controllable, there's little or no need for the hospital for the vast majority of us.

In the majority of instances of coronary disease, the hospital should be the place for the non-compliant and the ill-informed, and not for those of us sufficiently motivated to know and do better. The formula is simple: 1) Quantify plaque with a CT heart scan, 2) Identify the causes, then 3) Correct the causes.

The Fanatic Cook: A fabulous Blog about food and nutrition

I came across this Blog authored by a nutritionist when it was highlighted on Blogger as an interesting site:

The Fanatic Cook at http://fanaticcook.blogspot.com/

I was thoroughly impressed with the insightful and entertaining commentary. I'd highly recommend this site to you for reading on nutrition. In particular, her coenzyme Q10 column was exceptionally well written and clear.(http://fanaticcook.blogspot.com/2005/02/statins-and-not-well-publicized-side.html)

Also read her column, Super NonFoods at http://fanaticcook.blogspot.com/2005/07/super-nonfoods.html.

There's also oodles of recipes, all for the taking.

Eggs: Good, bad, or indifferent?

Eggs have been in the center of the cholesterol controversy almost from the very start.

The traditional argument against eggs went that eggs, high in cholesterol (210-275 mg per egg)and with some saturated fat (1.5-2.5 grams per egg), raised blood cholesterol (and LDL). Out went the daily fried, scrambled, poached eggs that many Americans indulged in most mornings. (We replaced it with more breakfast cereals and other carbohydrate conveniences, then got enormously overweight.)





A large Harvard epidemiologic study in 1999 called this observation into question. They tracked the fate of 117,000 thousand people and then compared the rate of heart attack, death, and other cardiovascular events among various people correlated to the "dose" of eggs they ate. Egg intake varied from none to 7 or more per week. Lo and behold, people who ate more eggs appeared to not suffer more events.

This study, large and well-conducted by an internationally respected group of investigators, seem to reopen the gates for more egg consumption, though most Americans still consume eggs cautiously.

Deeper down in this study, however, was another observation: People with diabetes who ate 1 egg per day had double the risk of heart attack. Because this study was observational, no specific conclusion as to why could be drawn.

A new study conducted by a Brazilian group may shed some light. Healthy (non-diabetic) men were fed an emulsion of several eggs. Inclusion of plentiful yolks caused a dramatic slowing of fat clearance from the blood. Specifically, "chylomicron remnants" were abnormally persistent in the blood. Chylomicron remnants are potent causes of coronary plaque. (Chylomicron remnants can be measured fairly well by intermediate-density lipoprotein and VLDL by NMR, or IDL by VAP.)

Diabetics are know to have substantial disorders of after-meal fat clearance, including an excess of chylomicron remnants. Could the Brazilian observation be the explanation for the increased event rate in diabetics in the Harvard study? Interesting to speculate.

We continue to tell our patients that eating eggs in moderation is probably safe. After all, there are good things in eggs: the high protein in the egg white, lecithin in the yolk. It is the yolk's contents that are in question, not the white. Thus, you and I can eat all the egg whites (e.g., Egg Beaters) we want. It's the safety of yolks that are uncertain.

The abnormal after-eating effect suggested by the Brazilians opens up some very interesting questions and confirms that we should still be cautious in our intake of egg yolks. One yolk per day is clearly too much. What is safe? The exisitng information would suggest that, if you have diabetes, pre-diabetes, or a postprandial disorder (IDL, VLDL), you should minimize your egg yolk use, perhaps no more than 3 or so per week, preferably not all at one but spaced out to avoid the after-eating effect.

Others without postprandial disorders may safely eat more, perhaps 5 per week, but also not all at one but spaced out.

Track Your Plaque Members: Be sure to read our upcoming Special Report on Postprandial Disorders. It contains lots of info on what this important pattern is all about. Postprandial disorders are largely unexplored territory that hold great promise for tools to inhibit coronary plaque growth and drop your heart scan score. The Brazilian study is just one of many future studies that are likely to be released in future about this very fascinating area.




Hu FB, Stampfer MJ, Rimm EB, Manson JE, Ascherio A, Colditz GA, Rosner BA, Spiegelman D, Speizer FE, Sacks FM, Hennekens CH, Willett WC.A prospective study of egg consumption and risk of cardiovascular disease in men and women. JAMA 1999 Apr 21;281(15):1387-94.

Cesar TB, Oliveira MR, Mesquita CH, Maranhao RC. High cholesterol intake modifies chylomicron metabolism in normolipidemic young men. J Nutr. 2006 Apr;136(4):971-6.

Diabetes is Track Your Plaque's Kryptonite!


If there's one thing I truly fear from a heart scan score reduction/coronary plaque regression standpoint, it's diabetes.

I saw a graphic illustration of this today. Roy came into the office after his 2nd heart scan. His first scan 14 months ago showed a score of 162. Roy started out weighing well over 300 lbs and with newly-diagnosed adult diabetes.

Roy put extraordinary effort into his program. He lost nearly 70 lbs by walking; cutting processed carbohydrates, greasy foods, and slashing overall calories. His lipoproteins, disastrous in the beginning, were falling into line, though HDL was still lagging in the low 40s, as Roy remains around 60 lbs overweight, even after the initial 70 lb loss.

Unfortunately, despite the huge loss in weight, Roy remains diabetic. On a drug called Actos, which enhances sensitivity to insulin, along with vitamin D to also enhance insulin response, his blood sugars remained in the overtly diabetic range.

Roy's repeat heart scan showed a score of 482--a tripling of his original score.

Obviously, major changes in Roy's program are going to be required to keep this rate of growth from continuing. But I tell Roy's story to illustrate the frightening power of diabetes to trigger coronary plaque growth.

Like Kryptonite to Superman (remember George Reeves crumbling and falling to his knees when the bad guys got a hold of some?), diabetes is the one thing I fear greatly when it comes to reducing your heart scan score. As you see with Roy's case, diabetes can be responsible for explosive plaque growth, more than anything else I know.

The best protection from diabetes is to never get it in the first place. (See my earlier Blog, "Diabetes is a choice you make".)

Boy, was I wrong!

Around 10 years ago, I was talking to a balloon and stent manufacturer's representative, who was raving about some new device that was due for release to the market. Back then, the sky seemed the limit to cardiac device manufacturers, who were falling over themselves scrambling to design and market the next new device.

The angioplasty market then had ballooned (no pun intended) from nothing to a multi-billion dollar industry. Stents were just getting underway but clearly had potential for being at least as large.

But this was a time when preventive therapies were also beginning to get quite powerful. We had just gotten started doing CT heart scans and were excited about the possibilities, statin drugs were gaining evidence through clinical trials, and the power of many nutritional supplements was finally achieving validation. We were even learning the error of our prior low-fat ways.

So I broadly pronounced to the enthusiastic product representative, "In 10 years, balloons, angioplasty, and stents will occupy this little corner of cardiac care because prevention will have become so powerful. We won't talk about heart procedures. We'll talk about coronary plaque regression!"

I even advised the representative that he should consider a career change in anticipation of the coming wave of preventive strategies.

Was I ever wrong. Despite the power of heart disease prevention--which is indeed true--cardiac device and procedure technology has boomed, both in popularity as well as in revenue success. Device manufacturing and sales are hugely successful. Implanting devices into people is a hugely profitable enterprise.

Since my ill-timed comments to the salesman, Boston Scientific, a major manufacturer of stents and other cardiac devices, reported revenues of $6.2 billiondollars in 2005, a 12% increase over the prior year. Medtronic reported 2005 revenues of $11.3 billion, growing at 15% per year. Clearly, cardiac procedures are still quite popular--and profitable.

My timing was off, but not for long. The huge crest of change in preventive therapies is upon us. That's the premise behind the Track Your Plaque concept: heart disease prevention can't be found in a hospital, is not supported by cardiac device manufacturers, and is not being advocated by most cardiologists or primary care physicians. Yet the tools are getting better and better every day.

Those of you who succeed in halting or reducing your heart scan score are extremely unlikely to add to Boston Scientific's or Medtronic's revenues. Help me spread the word.

Don't forget how dangerous heart disease can be

Sometimes it's easy to get smug when coronary plaque is a reversible process.

When you see people day in, day out, week in, week out, drop their heart scan scores, reversing what could be a dangerous disease, you can sometimes lose sight of just how dangerous coronary disease can be.

Whether I like it or not, I maintain a reasonably active role in hospitals out of necessity. I do need their services occasionally for people with advanced heart disease when I meet them (when regression is not the initial conversation for safety reasons), or valve disease is diagnosed, or someone shows up with congenital or heart muscle diseases. In other words, although we focus on coronary issues, there's more to heart disease than just coronary disease.

This unfortunate case just served to remind me how powerful coronary disease can be. Elizabeth, an active 67-year old, finally came to the hospital after suffering 6 months of chest pain and increasing breathlessness. She hated hospitals and hadn't seen a doctor in 30 years since she was successfully treated for cancer.

In those 30 years, she'd been quite active with family and a small business. But she also smoked 2 packs of cigarettes most of those years.

After she was admitted to the hospital, it became clear that Elizabeth had experienced one, if not several, heart attacks along the way. The entire front 2/3 of her heart was non-functional. If that wasn't bad enough, two of her heart valves were severely diseased and dysfunctional: Her aortic valve barely opened (aortic valve "stenosis", or stiffness) and the mitral valve leaked severely (mitral valve "insufficiency", or leakiness). All of this was confirmed with conventional testing in the hospital, including a heart catheterization.

Elizabeth ended up in emergency surgery--very unusual, by the way, for valve surgery of the sort she had--but died in the first few hours after her procedure. Her heart had simply been too damaged from her heart attacks, and the extraordinary stress of surgery that included two valves was too much. She died on the ventilator.

Coronary disease is a very serious matter. When I see cases like Elizabeth, it boosts my commitment to tell everyone that heart disease--when identified early enough--is a controllable, preventable, even reversible process. For poor Elizabeth, she was much too far down the path of severe, irreversible disease that control or reversal was simply not an option. She was in imminent danger of dying even upon arrival.

It's exciting yet sometimes frightening to know what you have in your hands: The means to control this monster called coronary disease. Use it wisely. But don't lose sight of what it can do it you permit it to grow, fester, and explode.

How many ways can you disguise sugar?

I came across this shockingly silly report on AOL, who obtained their info courtesy Health Magazine:

The Best New Healthy Foods for Busy People
from Health


The foods on their list:

Kettle Brand Bakes Hickory Honey BBQ--the healthy claim is based on the lack of trans-fatty acids and low-fat.










Post Healthy Classics Raisin Bran Cereal Bars, Cranberry--Likewise, low-fat, sweet, and addictive means healthy to these people.




Amy’s Mediterranean Pizza With Cornmeal Crust --Please!!



Horizon Organic Colby Cheese Sticks --Because it's made by cattle without use of growth hormone or antibiotics, they declare this healthy. I guess we can ignore the saturated fat content and high total fat content.

100% Whole Grain Chips Ahoy! Cookies --You mean we can add the bran back to wheat products and make it healthy?!


This kind of mass-market marketing trickery leaves me incredulous. Don't believe it for a moment. This is typical of the food industry: Take one aspect of nutrition that is truly healthy, such as high-fiber, or low-fat, or organic. Then add undesirable, unhealthy ingredients. The current fad is to add lots of sugar and or sugar-equivalents (usually flour and other wheat products). Because there's one healthy ingredient, they'll call the end-product healthy, too.

If you want to see what health looks like if you indulge in "healthy" products like this, just look up and down the grocery aisles at your neighborhood grocery store. You're likely to see the results: Gross obesity, diabetes, and arthritis.

You won't, of course, see the huge acceleration of growth in coronary plaque, but it's there, ticking away.

To remind us what ideal body weight is: Watch an old movie!

Jack was skeptical. At 273 lbs, 5 ft 11 inches, he felt that he was "just right".

"I feel fine. I don't see why you think I should lose weight," he declared. "In fact, when I lost 25 lbs a couple of years ago, everyone said I was too skinny!"

I showed Jack why: He had an HDL of 35 mg/dl, small LDL (over 90% of all LDL particles), an elevated blood sugar of 123 mg/dl (diabetes is officially 126 mg/dl or greater), high blood pressure, and increased inflammation (C-reactive protein). These were all manifestations that his body weight was too much for it to handle.




So I told Jack that we've all forgotten what ideal weight should look like. Our perception of "normal" has been so utterly and dramatically distorted by the appearance of our friends, family, co-workers, and other people around us that we've all lost a sense of what a desirable weight for health should be.




So I suggested to Jack that, if he wanted to rememember what ideal weight is and what people are supposed to look like, just watch old movies.

Old movies, like the 1942 production of Casablanca, or the 1952 production of Singin' in the Rain, show the body build that was prevalent in those days. Look at Humphrey Bogart or Gene Kelly--men with average builds, weighing 140-160 lbs--that's how humans were meant to look.

A report this morning on the Today Show showed the "after" photos of several people following bariatric (weight reduction) surgery. The "after" pictures, from the perspective of ideal weight and ideal health, remain hugely overweight.

We need to readjust our perceptions of weight. The average woman in the U.S. now weighs 172 lbs(!!!). Don't confuse average with desirable.

Diabetes is a choice you make

Tim had heart disease identified as a young man. He had his first heart attack followed by a quadruple bypass surgery at age 38. Recurrent anginal chest pain and another small heart attack led to several stents over three procedures in the first four years after bypass.

Tim finally came to us, interested in improving his prevention program. You name it, he had it: small LDL, low HDL (28 mg/dl), lipoprotein(a), etc. The problem was that Tim was also clearly pre-diabetic. At 5 ft 10 inches, he weighed 272 lbs--easily 80 or more pounds overweight.

Tim was willing to make the medication and nutritional supplement changes to gain control over his seeminglly relentless disease. He even turned up his exercise program and lost 28 lbs in the beginning. But as time passed and no symptoms recurred, he became lax.

Tim regained all the weight he'd lost and some more. Now Tim was diabetic.

"I don't get it. I eat good foods that shouldn't raise my insulin. I almost never eat sweets."

I stressed to Tim that diabetes and pre-diabetes, while provoked acutely by sugar-equivalent foods (wheat products, breads, breakfast cereals, crackers, etc.), is caused chronically by excess weight. If Tim wants to regain control over his heart disease, he needed to lost the weight.

Unlike, say, leukemia, an unfortunate disease that has little to do with lifestyle choices, diabetes is a choice you make over 90% of the time. In other words, if you become diabetic (adult variety, not children's variety) as an adult, that's because you've chosen to follow that path. You've neglected physical activity, or indulged in too many calories or poor food choices, or simply allowed weight to balloon out of control.

But diabetes is also a path most people can choose not to take. And it is a painfully common choice: Nearly two-thirds of the adults in my office have patterns of pre-diabetes or diabetes when I first meet them.

Let me stress this: For the vast majority of adults, diabetes is a choice, not an inevitability.

I'll call the doctor when I feel bad!

Max just had his heart scan. He sat down with the x-ray technologist at the work console while she pointed out the white areas in his coronary arteries that represented plaque.

"It looks like you're going to have a fairly high score," the technologist commented. "The final report will be available after one of our cardiologists reviews your images."

Max shrugged. "Well, I don't feel anything. I'm always running around with work, with my kids, stuff like that. That's better than any stress test. I guess I'll worry about it if it starts to bother me."


You'd be surprised how common this view remains: If it's not bothering you, then just forget about it. It's easy to do, since you have no symptoms, nothing to impair your physical activities. But what are the potential consequences of ignoring your heart scan? Here's a few:

--Prevention and plaque reversal efforts are most effective the earlier you start. From a heart scan score viewpoint, the lower your starting score, the easier it is to gain control over it. More people will succeed in reducing their score when the starting score is lower.

--The role of prevention of heart disease instantly crystallizes when you know your score. Your LDL cholesterol of 142 mg/dl or HDL of 41 mg/dl no longer seem like just numbers of borderline signficance. Instead, they become useful tools to gain control over plaque. They cast your numbers in a new and clear light.

--Knowing your heart scan score today gives you a basis for comparison in future. Your score of, say 250, today, can be 220 in one year. Without your preventive efforts, it will be 30% higher: 325. That's a big difference!

--Sudden death or heart attack--can occur in up to 35-40% of people with hidden heart disease--without warning.

Don't even bother getting a heart scan if you're going to ignore it. I've said it before and I'll say it again: A heart scan is the most important health test you can get--but only if you do something about it.
All posts by william-davis

High blood pressure vanquished

Heart Scan Blog reader, Eric, related his blood pressure success story to me:

I'm 34 and have been battling chronic hypertension (systolic 150-200, depending on my anxiety levels) even with multiple prescriptions for over a decade now. I've seen four different cardiologists, all stumped as to what is causing my hypertension. First, they suspected coarctation of my aorta [a constriction in the aorta], but an angiogram determined blood pressure readings were the same on both sides of the narrowing.

The second angiogram performed last year to determine if my coarct had worsened determined that it had not, but that my aorta had calcium build up. The cardiologist was stumped because he told me he hasn't seen calcium in a patient so young. Needless to say, this scared me to death, with my wife being pregnant with our first child. I asked if it could be reversed and he didn't know so he sent me to get a Berkeley lab.

The Berkeley came back with LDL 91, HDL 41, Triglycerides 73, CRP 4.1, vit D 26. The doctors weren't very knowledgeable about explaining to me what these meant and how I could correct the low vit D and high CRP. They told me to follow the low-fat diet recommended by Berkeley. Well I've already tried the DASH diet and didn't like how I felt or my energy levels, so I didn't transition.

I was at a loss until I encountered your blog and it was truly a gift. It was a refreshing feeling to meet a knowledgeable Dr. who knew what I was going through and seems to truly care about reversing calcium in the heart (something I never got from my any of my cardiologists). With your blog I have an appointment to get a heart scan here in CO and take that number along with my Berkeley results and join Track Your Plaque.

For the past 2 weeks I've been following your advice by taking a D3+K2 supplement with Omega3 Fish oil and avoiding all grain, wheat, sugar and I'm already down 4lbs to 223.5lbs at 6'5" tall and my blood pressure readings have been 128/54 and 129/60 the past 2 days! With your help I may not have the dark future my father had: dead at 48 with a massive heart attack.

Stay on the look out because I look forward to telling you how I'm one of your top calcium losers!

Eric, Colorado


Conventional medical care fails at so many levels for so many people. While Eric's doctors were busy contemplating the next angiogram, they were neglecting several crucial aspects of his health.

It's really not that tough. But it can mean doing the opposite of what conventional "wisdom" tell us.

DHEA and Lp(a)

DHEA supplementation is among my favorite ways to deal with the often-difficult lipoprotein(a), Lp(a).

DHEA is a testosterone-like adrenal hormone that declines with age, such that a typical 70-year old has blood levels around 10% that of a youthful person. DHEA is responsible for physical vigor, strength, libido, and stamina. It also keeps a lid on Lp(a).

While the effect is modest, DHEA is among the most consistent for obtaining reductions in Lp(a). A typical response would be a drop in Lp(a) from 200 nmol/L to 180 nmol/L, or 50 mg/dl to 42 mg/dl--not big responses, but very consistent responses. While there are plenty of non-responders to, say, testosterone (males), DHEA somehow escapes this inconsistency.

Rarely will DHEA be sufficient as a sole treatment for increased Lp(a), however. It is more helpful as an adjunct, e.g., to high-dose fish oil (now our number one strategy for Lp(a) control in the Track Your Plaque program), or niacin.

Because the "usual" 50 mg dose makes a lot of people bossy and aggressive, I now advise people to start with 10 mg. We then increase gradually over time to higher doses, provided the edginess and bossiness don't creep out.

The data documenting the Lp(a)-reducing effect of DHEA are limited, such as this University of Pennsylvania study, but in my real life experience in over 300 people with Lp(a), I can tell you it works.

And don't be scared by the horror stories of 10+ years ago when DHEA was thought to be a "fountain of youth," prompting some to take megadose DHEA of 1000-3000 mg per day. Like any hormone taken in supraphysiologic doses, weird stuff happens. In the case of DHEA, people become hyperaggressive, women grow mustaches and develop deep voices. DHEA doses used for Lp(a) are physiologic doses within the range ordinarily experienced by youthful humans.

No more cookies

Jeanne enjoyed her Christmas holidays. She especially liked sharing the cookies she made for her grandchildren, sneaking 2 or 3 every day over a couple of weeks. On top of this, she enjoyed the Christmas candy, egg nog, leftover stuffing and cranberry sauce, topped off with a night of nutritional debauchery on New Year's Eve.

Lipid panel in October:

Total cholesterol 146 mg/dl
LDL cholesterol 72 mg/dl
HDL cholesterol 64 mg/dl
Triglycerides 49 mg/dl

Lipid panel in early January:

Total cholesterol 229 mg/dl
LDL cholesterol 141 mg/dl
HDL cholesterol 59 mg/dl
Triglycerides 147 mg/dl


I call the holidays The Annual Wheat and Sugar Frenzy. It's the carbohydrates, especially those from products made of wheat and sucrose, that caused the marked shifts in Jeanne's lipid patterns. Let's take each parameter apart:

--Triglycerides go up due to de novo lipogenesis, liver conversion of carbohydrates into triglycerides. Triglycerides enter the bloodstream as VLDL particles which, in turn, interact with LDL and HDL.

--LDL goes up because carbohydrate exposure increases VLDL, followed by conversion to LDL. The triglyceride-rich LDL created is converted to small LDL particles. Had we measured small LDL changes in Jeanne, we likely would have measured something like an increase (by NMR) from 800 nmol/L to 1600 nmol/L, a carbohydrate effect.

--The increased VLDL also makes HDL triglyceride-rich, cause more rapid degradation of HDL particles. (It also makes them smaller, like LDL.) Given sufficient time (a few more months), HDL would drop into the 40's.

--Total cholesterol changes reflect the composite of the above numbers. (Total cholesterol = LDL cholesterol + HDL cholesterol + Trig/5) (Note that, as HDL drops, so will total cholesterol; that's why this value is worthless and should be ignored.)

So don't be surprised by the above distortions after a period of carbohydrate indulgence. Although your unwitting primary care doc will see such changes as opportunity for Lipitor, it is nothing more than the cascade of effects from a carbohydrate-driven distortion of lipoproteins.

How to become diabetic in 5 easy steps

If you would like to become diabetic in as short a time as possible, or if you have someone you don't like--ex-spouse, nasty neighbor, cranky mother-in-law--whose health you'd like to booby trap, then here's an easy-to-follow 5-step plan to make you or your target diabetic.


1) Cut your fat and eat healthy, whole grains--Yes, reduce satiety-inducing foods and replace the calories with appetite-increasing foods, such as whole grain bread, that skyrocket blood sugar higher than a candy bar.

2) Consume one or more servings of juice or soda per day--The fructose from the sucrose or high-fructose corn syrup will grow visceral fat and cultivate resistance to insulin.

3) Follow the Institute of Medicine's advice on vitamin D--Take no more than 600 units vitamin D per day. This will allow abnormal levels of insulin resistance to persist, driving up blood sugar, grow visceral fat, and allow abnormal inflammatory phenomena to persist.

4) Have a bowl of oatmeal or oat cereal every morning--Because oat products skyrocket blood sugar, the repeated high sugars will damage the pancreatic beta cells ("glucose toxicity"), eventually impairing pancreatic insulin production. (Entice your target even further: "Would you like a little honey with your oatmeal?") To make your diabetes-creating breakfast concoction even more effective, make the oatmeal using bottled water. Many popular bottled waters, like Coca Cola's Dasani or Pepsi's Aquafina, are filtered waters. This means they are devoid of magnesium, a mineral important for regulating insulin responses.

5) Take a diuretic (like hydrochlorothiazide, or HCTZ) or beta blocker (like metoprolol or atenolol) for blood pressure--Likelihood of diabetes increases 30% with these common blood pressure agents.

There you have it! Perhaps we should assemble a convenient do-it-yourself-at-home diabetes kit to help, complete with several servings of whole grain bread, a big bottle of cranberry juice, some 600 unit vitamin D tablets, a container of Irish oatmeal, and some nice bottled water.

Restaurant eating: A fructose landmine

There is no remaining question that fructose is among the worst possible things humans can consume.

Followers of the Heart Scan Blog already know this, from conversations like The LDL-Fructose Disconnect, Where do you find fructose?, and Goodbye, fructose.

But fructose, usually as either high-fructose corn syrup (44%, 55%, occasionally higher percentage fructose) or sucrose (50% fructose), is ubiquitous. I've seen it in the most improbable places, including cole slaw, mustard, and dill pickles.

It's reasonably straightforward to avoid or minimize fructose exposure while eating at home, provided you check labels and focus on foods that don't require labels (like green peppers, salmon, and olive oil, i.e., unprocessed foods). But when you choose to eat at a restaurant, then all hell can break loose and fructose exposure can explode.

So what are some common and unsuspected fructose sources when eating at a restaurant?

Salad dressings--Dressings in all stripes and flavors are now made with high-fructose corn syrup and/or sucrose. This is especially true of low-fat, non-fat, or "lite" dressings, meaning oils have been replaced by high-fructose corn syrup. It can also be true of traditional non-low-fat dressings, too, since high-fructose corn syrup is just plain cheap.

Olive oil and vinegar are still your safest bets. I will often use salsa as a dressing, which works well.

Sauces and gravies--Not only can sauces be thickened with cornstarch, many pre-mixed sauces are also made with high-fructose corn syrup or sweetened with sucrose. Barbecue sauce is a particular landmine, since it is now a rare barbecue sauce not made with high-fructose corn syrup as the first or second ingredient. Sauces for dipping are nearly always high-fructose corn syrup-based.

Ketchup--Yup. Good old ketchup even is now made with high-fructose corn syrup. In fact, you should be suspicious of any condiment.

Highball, Bloody Mary, Margarita, Daiquiri, beer--Even the before-dinner or dinner drink can have plenty of fructose, particularly if a mix is used to make it. While Blood Marys seem the most benign of all, adorned with celery, pickle, and olive, just take a look at the ingredient label on the mix used: high-fructose corn syrup.

Fructose is a stealth poison: It doesn't immediately increase blood sugar; it doesn't trigger any perceptible effect like increased energy or sleepiness. But it is responsible for an incredible amount of the health struggles in the U.S., from obesity, to diabetes, to hyperlipidemias and heart disease, to arthritis, to cataracts.

A glycation rock and a hard place

Advanced Glycation End-products, or AGEs, the stuff of aging that mucks up brains, kidneys, and arteries, develop via two different routes: endogenous (from within the body) and exogenous (from outside the body).

Endogenous AGEs develop via glycation. Glycation of proteins in the body occurs when there are glucose excursions above normal. For instance, a blood glucose of 150 mg/dl after your bowl of stone-ground oatmeal causes glycation of proteins left and right, from the proteins in the lens of your eyes (cataracts), to the proteins in your kidneys (proteinuria and kidney dysfunction), to skin cells (wrinkles), to cartilage (brittle cartilage followed by arthritis), to LDL particles, especially small LDL particles (atherosclerosis).

At what blood sugar level does glycation occur? It occurs even at "normal" glucose levels below 100 mg/dl (with measurable long-term cardiovascular effects as low as 83 mg/dl). In other words, some level of glycation proceeds even at blood glucose levels regarded as normal.

There's nothing we can do about the low-level of glycation that occurs at low blood sugar levels of, say, 90 mg/dl or less. However, we can indeed do a lot to not allow glycation to proceed more rapidly, as it inevitably will at blood sugar levels higher than 90 mg/dl.

How do you keep blood sugars below 90 mg/dl to prevent excessive glycation? Avoid or minimize the foods that cause such rises in blood sugar: carbohydrates.

What food increases blood sugar higher than nearly all other known foods? Wheat.

Is einkorn the answer?

People ask: "What if I would like a piece of bread or other baked product just once in a while? What is safe?"

Eli Rogosa, Director of The Heritage Wheat Conservancy, believes that a return to the wheat of our ancestors in the Fertile Crescent, circa 10,000 years ago, is the answer.

Former science teacher, now organic farmer, farm researcher, and advocate of sustainable agriculture, Eli has been reviving "heritage" crops farmed under organic conditions, some of her research USDA-funded.

In particular, Eli has been cultivating original 14-chromosome ("diploid") einkorn wheat. Although einkorn contains gluten (in lesser quantities despite the higher total protein content), the group of proteins that trigger the immune abnormalities of celiac disease and other immune phenomena, Eli tells me that she has witnessed many people with a variety of wheat intolerances, including celiac disease, tolerate foods made with einkorn wheat. (The variety of glutens in einkorn differ from the glutens of the dwarf mutant that now dominate supermarket shelves.)

Eli travels to Israel every year, returning with "heritage" seeds for wheat and other crops. She formerly worked in the Israel GenBank as Director of the Ancient Wheat Program. She has written a brochure that describes her einkorn wheat.

Eli sent me 2 lb of her einkorn grain that nutritionist, Margaret Pfeiffer, and I ground into bread. Our experience is detailed here. My subsequent blood sugar misadventure, comparing einkorn bread to conventional organic whole wheat bread is detailed here, followed by the odd neurologic effects I experienced here.

Anyone else wishing to try this little ancient wheat experiment with einkorn can also obtain either the unground grain or ground flour through Eli's website, www.growseed.org. Most recently, einkorn pasta is being retailed under the Jovial brand at Whole Foods Market.

If anyone else makes bread or any other food with Eli's einkorn wheat, please let me know:

1) Your blood sugar response (before and 1 hour after consumption)
2) Whether you experienced any evidence of wheat intolerance similar to what you experienced with conventional wheat, e.g., rash, acid reflux, gas and cramping, moodiness, asthma, etc.

But remember: Wheat effects or no, einkorn is still a grain. My belief is that humans do best with little or no grain. The einkorn experience is an effort to identify reasonable compromises so that you and I can have a piece of birthday cake once a year without getting sick.

Genetic incompatibility

Peter has lipoprotein(a), or Lp(a), a genetic pattern shared by 11% of Americans.

It means that Peter inherited a gene that codes for a protein, called apoprotein(a), that attaches to LDL particles, forming the combined particle Lp(a). It also means that his overall pattern responds well to a high-fat, high-protein, low-carbohydrate diet: The small LDL particles that accompany Lp(a) over 90% of the time are reduced, Lp(a) itself is modestly reduced, other abnormalities like high triglycerides (that facilitate Lp(a)'s adverse effects) are corrected. Small LDL particles are, by the way, part of the genetic "package" of Lp(a) in most carriers.

Peter also has another gene for Apo E4, another genetically-determined pattern shared by 19% of Americans. (Another 2% of Americans have two "doses" of Apo E4, i.e., they are homozygotes for E4.) This means that the Apo E protein, normally responsible for liver uptake and disposal of lipoproteins (especially VLDL), is defective. In people with Apo E4, the higher the fat intake, the more LDL particles accumulate. (The explanation for this effect is not entirely clear, but it may represent excessive defective Apo E-enriched VLDL that competes with LDL for liver uptake.) People with Apo E4 therefore drop LDL (and LDL particle number and apoprotein B) with reductions in fat intake.

This is a genetic rock-and-a-hard-place, or what I call a genetic incompatibility. If Peter increases fat and reduces carbohydrates to reduce Lp(a)/small LDL, then LDL measures like LDL particle number, apoprotein B, and LDL cholesterol will increase. Paradoxically, sometimes small LDL particles will even increase in some genetically predisposed people.

If Peter decreases fat and increases carbohydrates, LDL particle number, apoprotein B, and LDL cholesterol will decrease, but the proportion of small LDL will increase and Lp(a) may increase.

Thankfully, such "genetic incompatibilities" are uncommon. In my large practice, for instance, I have about 5 such people.

The message: If you witness paradoxic responses that don't make sense or follow the usual pattern, e.g., reductions in LDL particle number, apoprotein B, and small LDL with reductions in their dietary triggers (i.e., carbohydrates, especially wheat), then consider a competing genetic trait such as Apo E4.

The folly of an RDA for vitamin D

Tom is a 50-year old, 198-lb white male. At the start, his 25-hydroxy vitamin D level was 28.8 ng/ml in July. Tom supplements vitamin D, 2000 units per day, in gelcap form. Six months later in January (winter), Tom's 25-hydroxy vitamin D level: 67.4 ng/ml.

Jerry is another 50-year old white male with similar build and weight. Jerry's starting summer 25-hydroxy vitamin D level: 26.4 ng/ml. Jerry takes 12,000 units vitamin D per day, also in gelcap form. In winter, six months later, Jerry's 25-hydroxy vitamin D level: 63.2 ng/ml.

Two men, similar builds, similar body weight, both Caucasian, similar starting levels of 25-hydroxy vitamin D. Yet they have markedly different needs for vitamin D dose to achieve a similar level of 25-hydroxy vitamin D. Why?

It's unlikely to be due to variation in vitamin D supplement preparations, since I monitor vitamin D levels at least every 6 months and, even with changes in preparations, dose needs remain fairly constant.

The differences in this situation are likely genetically-determined. To my knowledge, however, the precise means by which genetic variation accounts for it has not been worked out.

This highlights the folly of specifying a one-size-fits-all Recommended Daily Allowance (RDA) for vitamin D. The variation in need can be incredible. While needs are partly determined by body size and proportion body fat (the bigger you are, the more you need), I've also seen 105 lb women require 14,000 units and 320-lb men require 1000 units to achieve the same level of 25-hydroxy vitamin D.

An RDA for everyone? Ridiculous. Vitamin D is an individual issue that must be addressed on a person-by-person basis.

Heart scan: Standard of care?

If coronary disease is easy to detect by measuring coronary calcium, shouldn't this represent the standard of care?

In other words, if you've been seeing your doctor and he/she has been monitoring cholesterol levels and, inevitably, talks about statin drugs, then you have a heart attack, unstable angina, or die--yet never knew you had heart disease--isn't this negligence?

Coronary calcium, and thereby coronary atherosclerotic plaque, are markers for the disease itself. Unlike cholesterol, high blood pressure, etc., that represent risk factors for coronary atherosclerotic plaque, coronary calcium is a measure of total plaque: "soft" elements like lipid collections, necrotic tissue, fibrous tissue, as well as "hard" elements like calcium. Because calcium occupies 20% of total atherosclerotic plaque volume, it can be used as an indirect "dipstick" for total plaque.

So why isn't an unexpected heart attack, hospitalization for unstable heart symptions, emergency bypass, etc., not regarded as potential malpractice? These are not benign events, but potentially life-threatening.