Calcium reflects total plaque





People frequently ask, "Why measure coronary artery calcium? My doctor said that calcium only tells you if there's hard plaque, and that hard plaque is stable. He/she says that calcium doesn't tell you anything about soft plaque."

Is that true? Is calcium only a reflection of "hard" plaque? Is hard plaque also more stable, less prone to rupture and causes heart attack?

Actually, calcium is a means of measuring total plaque, both soft and hard. That's because calcium comprises 20% of total plaque volume. Within plaque, there may be areas that are soft (labeled "lipid pool" in the diagram). There are also areas made of calcium (shown in white arcs within the plaque). Even though this is just a graphic, it's representative of what is seen when we perform intracoronary ultrasound of a live human being's coronary artery. In other words, this cross section contains both "soft" (lipid pool) as well as "hard" (calcium) elements.

Is this artery "soft" or "hard"? It's both, of course. The artery compostion can vary millimeter by millimeter, having more soft or hard elements. The artery can also change over time in either direction. Thus, "soft" plaque may indeed be soft today, only to be "hard" in 6 months, and vice versa.

The essential point is that measuring just "soft" plaque provides limited information. What the CT heart scan does is provide a gauge of total plaque, soft and hard, and it does so easily, safely, precisely. If your score increases, the lengthwise volume of total plaque has also grown. If your score decreases, the total amount of plaque has also decreased.

Don't mistake marketing for truth

We're all so inundated with marketing messages for food. Unfortunately, many people confuse the messages delivered through marketing with the truth.

For instance:

Pork: "The other white meat." Pork is a high-saturated fat food.

"Bananas: A great source of potassium." Bananas are a high glycemic index (rapid sugar release), low fiber food.

"Pretzels: A low-fat snack." A high glycemic index food made from white wheat flour. It makes you fat and skyrockets blood sugar.

Jif peanut butter: "Choosy moms choose Jif." Do they also choose hydrogenated fats?

Hi-C: Upbeat jingles like "Who put the straw in my Hi-C fruit drink, a new cool straw that wriggles and bends? Who put the straw in my Hi-C fruit drink, with Vitamin C for me and my friends? Who was that man, I'd like to shake his hand, he made my Hi-C cooler than before!" What about the 25 grams of sugar per 4 oz serving? And the high fructose corn syrup that creates an insatiable sweet tooth, raises triglycrides 30%, and exagerates pre-diabetes?


Marketing is not reliable, unbiased information. If Ford boasts that their cars are superior to GM, do you say "Well then, I need to buy a Ford?" Of course not. Take marketing for what it is: A method of persuading people to buy. It may or may not contain the truth. It's a big part of the reason Americans are the fattest people on earth and are experiencing an explosion of chronic diseases of excess.

Tattered Red Dress

"Are you taking your health to heart? Perhaps you understand the importance of eating a diet low in cholesterol or getting 30 minutes of exercise a day. But do you know your own risk of developing cardiovascular disease?


It’s time to take your heart health personally. Heart disease is the No. 1 killer of American women — and that means it is not “someone else’s problem.” As a woman, it’s your problem.

That’s where the Go Red Heart Checkup comes in. This comprehensive evaluation of your overall heart health can help you now and in the future. By knowing your numbers and assessing your risks now, you can work with your doctor to significantly reduce your chances of getting heart disease tomorrow, next year, or 30 years from now!"



So reads some of the materials promoted by the American Heart Association Red Dress campaign to increase awareness of heart disease in women. The effort is well-intended. There is no doubt that most women are unaware of just how common coronary disease is in females.

But I've got a problem with the solutions offered. "Know your numbers"? Eat healthy, don't be overweight, be active, don't smoke. That's the gist of the program's message--nothing new. In 2006, why would some sort of screening effort for detectin of heart disease not be part of the message? Why isn't there any message about the real, truly effective means to detect hidden heart disease in women--namely, heart scanning?

Does a 58-year old woman with normal blood pressure, LDL 144, HDL 51, 20 lbs overweight have hidden heart disease? I've said it before and I'll say it again: You can't tell from the numbers. She could die of a heart attack tomorrow without warning, or maybe she'll be dancing on our graves when she's 95 and never have experienced any manifestation of heart disease. The numbers will not tell you this.

I'm glad the American Heart Association has seen fit to invest its sponsors' money in a campaign to promote prevention. I wish they hadn't fallen so far short of a truly helpful message. Perhaps the sponsors (like Pfizer, maker of Lipitor) will benefit, anyway.

Panic in the streets

Several days ago, I wrote about a local prominent judge in my neighborhood who was unexpectedly found dead in bed of a heart attack at age 49.

As expected, I've received multiple calls from patients and physicians who want heart catheterizations. For instance, an internist I know called me in a panic. He asked that I perform a heart catheterization in a patient with a heart scan score of 768. I've been seeing this patient for about a year. He's without symptoms, even with strenuous exercise; stress tests (i.e., tests of coronary bloow flow) have been normal.

I remind patients and colleagues every day, day in day out: Having a heart scan score revealing some measure of coronary plaque is not a sufficient reason by itself to proceed with procedures. Fear of suffering a fate like the unfortunate judge is also not a reason to proceed with procedures.

Increased awareness of the gravity of heart disease is a good thing. Some good can come out of a needless tragedy like this. The lesson from the judge's unfortunate experience: he needed a CT heart scan. I'm told that the judge's doctor advised him that a heart scan was a waste of time. I hope that appropriate legal action for negligence is taken by the judge's family against this physician.

Not doing a heart scan is wrong. That's the lesson to learn. The lesson is not that everybody with coronary plaque needs a procedure. Had the judge undergone a simple heart scan, intensified prevention could have been instituted and he'd still be alive with his wife and children today.

The indications for procedures are unchanged by your heart scan. If a stress test is abnormal and indicates poor flow to a part of the heart, that would be a reason. If symptoms like chest discomfort or breathlessness appear, that's an indication. If there's evidence of poor heart muscle contraction, that's a reason to proceed with a procedure. But just having coronary plaque is not a sufficient reason.

Heart scan curiosities 1

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

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



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

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

Annual physical

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

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

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

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

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

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

A curious case of regression

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

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

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

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

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

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

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

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

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

Fortune teller

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

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

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

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


Let's take three typical examples:

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

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

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

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

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

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

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

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

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

Heart scan score drops like a stone

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

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

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

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

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

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

How's that for an early Christmas gift?

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

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

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

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

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

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

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







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

What to eat: Part I

I've spent a good number of Heart Scan Blog posts detailing what foods to limit or avoid.

The list of unquestionably bad foods to avoid include foods made of wheat, cornstarch, and sugars. Fructose is proving to be an exceptionally bad form of sugar, worse than any other. I've issued warnings about levels of carbohydrates that can be determined by postprandial testing.

In response to several requests to clarify what foods to eat, this post begins a series discussing what foods are good to eat.

I believe that a strong case can be made for eating vegetables in nearly all its varied forms, from cucumbers to peppers to leafy vegetables to eggplant to alliums like onions. The only form we avoid are red and white potatoes due to the blood sugar-increasing effects.

While this seems obvious, I am impressed how many people who follow low-carb diets find themselves following a high-animal product diet with vegetables as the sideline. It should be the other way around: A high vegetable diet with animal products as the sideline.

Vegetables are your principal source of:

1) Flavonoids and polyphenols--e.g., anthocyanins and catechins. All the recently appreciated effects of flavonoids and polyphenols highlight the wonderful effects of compounds originating in plant foods. This includes the anthocyanins and resveratrol in red wine; the catechins and epicatechins cocoa and green tea; the hydroxytyrosol, phenolic acid, and flavonoids of olive oil.

2) Fiber--Fiber is essentially a plant phenomenon, since there is virtually none in chicken, fish, and beef. The benefits of fiber are, I believe, undisputed. Neglecting fiber can, at the very least, lead to a nasty case of hemorrhoids. At the worst, it is related to various cancers, especially colon cancer.

3) Vitamin C--While vitamin C may be old and boring in light of new, exciting discoveries like flavonoids, neglect leads to bad things.

Vegetables are generally classified as carbohydrate foods, since they are low in protein and fat. But this is the source of carbohydrates you do not want to sacrifice in a low-carbohydrate diet. There's just too much good from vegetables.

Notice that I didn't say "fruits and vegetables." This is a fundamental mistake made by many: Oveconsumption of fruits. I've even seen people who follow an otherwise good diet develop diabetes--just from too much fruit.

Vegetables should be the cornerstone of the human diet. But I'll bet you knew that already.

Carbohydrates and LDL

There's a curious and powerful relationship between carbohydrates and LDL particles. Understanding this relationship is crucial to gaining control over heart disease risk.

(Note that I did not say "LDL cholesterol"--This is what confuses people, the notion that cholesterol is used as a surrogate marker to quantify various lipoproteins, including low-density lipoproteins, LDL. I'm NOT interested in the cholesterol; I'm interested in the behavior of the low-density lipoprotein particle. There's a difference.)

Carbohydrates:

1) Increase triglycerides and very low-density lipoprotein particles (VLDL)
2) Triglyceride-rich VLDL interact with LDL particles, making them smaller. (A process mediated by several enzymes, such as cholesteryl-ester transfer protein.)
3) Smaller LDL particles are more oxidizable--Oxidized LDL particles are the sort that are taken up by inflammatory white blood cells residing in the artery wall and atherosclerotic plaque.
4) Smaller LDL particles are more glycatable--Glycation of LDL is an important phenomenon that makes the LDL particle more atherogenic (plaque-causing). Glycated LDLs are not recognized by the LDL receptor, causing them to persist in the bloodstream longer than non-glcyated LDL. Glycated LDL is therefore taken up by inflammatory white blood cells in plaque.

Of course, carbohydrates also make you fat, further fueling the fire of this sequence.

The key is to break this chain: Cut out the carbohydrates. Cut carbohydrates and VLDL and triglycerides drop (dramatically), VLDL are unavailable to transform large LDL into small LDL, small LDL is no longer available to become oxidized and glycated, blood sugar is reduced to allow less glycation. Voila: Less atherosclerotic plaque growth.

Yet the USDA, American Heart Association, and the Surgeon General's office all advise you to eat more carbohydrates. The American Diabetes Association tells you to eat 70 grams or so carbohydrates per meal. (Yes: Diabetes, the condition that is MOST susceptible to these carbohydrate effects.) Follow their advice and you gain weight; triglycerides and VLDL go up; calculated (Friedewald) LDL may or may not go up, but true measured LDL (NMR LDL particle number or apoprotein B) goes way up; small LDL is triggered . . . You know the rest.

The dance between carbohydrates and LDL particles requires the participation of both. Allow one partner to drop out of the dance and LDL particles will sit this dance out.

Strange but true: Part II

Here's the second part of the Heart Scan Blog post I wrote a couple of years back describing the wacky origins of this thing that has so changed the face of heart care in the U.S., the cardiac catheterization.

Heart catheterization: Strange, but true

It's a couple of years old, but this post from March, 2008, remains relevant.

It details the curious origins of heart catheterization, the procedure that has saved some lives, but also been responsible for the proliferation of unnecessary heart procedures.



The modern era of heart disease care was born from an accident, quirky personalities, and even a little daring.

The notion of heart catheterization to visualize the human heart began rather ignominiously in 1929 at the Auguste-Viktoria Hospital in Eberswalde, Germany, a technological backwater of the day. Inspired by descriptions of a French physician who inserted a tube into the jugular vein of a horse and felt transmitted heart impulses outside the body, Dr. Werner Forssmann, an eager 25-year old physician-in-training, was intent on proving that access to the human heart could be safely gained through a surface blood vessel. No one knew if passing a catheter into the human heart would be safe, or whether it would become tangled in the heart’s chambers and cause it to stop beating. On voicing his intentions, Forssmann was ordered by superiors not to proceed. But he was determined to settle the question, especially since his ambitions captured the interest of nurse Gerda Ditzen, who willingly even offered to become the first human subject of his little experiment.

Secretly gathering the necessary supplies, he made his first attempt in private. After applying a local anesthetic, he used a scalpel to make an incision in his left elbow. He then inserted a hollow tube, a catheter intended for the bladder, into the vein exposed under the skin. After passing the catheter 14 inches into his arm, however, he experienced cold feet and pulled it out.



One week later, Forssman regained his resolve and repeated the process. Nurse Ditzen begged to be the subject, but Forssmann, in order to allow himself to be the first subject, tricked her into being strapped down and proceeded to work on himself while she helplessly watched. After stanching the oozing blood from the wound, he threaded the catheter slowly and painfully into the cephalic vein, up through the bicep, past the shoulder and subclavian vein, then down towards the heart. He knew that simply nudging the rubber catheter forward would be sufficient to direct it to the heart, since all veins of the body lead there. With the catheter buried 25 inches into his body, Forssmann untied the fuming Ditzen. Both then ran to the hospital’s basement x-ray department and injected x-ray dye into the catheter, yielding an image of the right side of his heart, the first made in a living human.

Thus, the very first catheterization of the heart was performed.

An x-ray image was made to document the accomplishment. Upon hearing of the experiment, Forssmann was promptly fired by superiors for his brazen act of self-experimentation. Deflated, Forssmann abandoned his experimentation and went on to practice urology. He became a member of the Nazi party in World War II Germany and served in the German army. Though condemned as crazy by some, physicians in Europe and the U.S., after hearing of his experience, furthered the effort and continued to explore the potential of the technique. Forssmann himself was never invited to speak of his experiences outside of Germany, as he had been labeled a Nazi.

Many years after his furtive experiments, the once intrepid Dr. Forssmann was living a quiet life practicing small town medicine. He received an unexpected phone call informing him that he was one of three physicians chosen to receive the 1956 Nobel Prize for Medicine for his pioneering work performing the world’s first heart catheterization, along with Drs. André Cournand and Dickinson W. Richards, both of whom had furthered Forssmann’s early work. Forssmann remarked to a reporter that he felt like a village pastor who was made a cardinal.

Strange, but true.

Rerun: To let low-carb right, you must check POSTPRANDIAL blood sugars

Checking postprandial (after-eating) blood sugars yields extraordinary advantage in creating better diets for many people.

This idea has proven so powerful that I am running a previous Heart Scan Blog post on this practice to bring any newcomers up-to-date on this powerful way to improve diet, lose weight, reduce small LDL, reduce triglycerides, and reduce blood pressure.



To get low-carb right, you need to check blood sugars

Reducing your carbohydrate exposure, particularly to wheat, cornstarch, and sucrose (table sugar), helps with weight loss; reduction of triglycerides, small LDL, and c-reactive protein; increases HDL; reduces blood pressure. There should be no remaining doubt on these effects.

However, I am going to propose that you cannot truly get your low-carb diet right without checking blood sugars. Let me explain.

Carbohydrates are the dominant driver of blood sugar (glucose) after eating. But it's clear that we also obtain some wonderfully healthy nutrients from carbohydrate sources: Think anthocyanins from blueberries and pomegranates, vitamin C from citrus, and soluble fiber from beans. There are many good things in carbohydrate foods.

How do we weigh the need to reduce carbohydrates with their benefits?

Blood sugar after eating ("postprandial") is the best index of carbohydrate metabolism we have (not fasting blood sugar). It also provides an indirect gauge of small LDL. Checking your blood sugar (glucose) has become an easy and relatively inexpensive tool that just about anybody can incorporate into health habits. More often than not, it can also provide you with some unexpected insights about your response to diet.

If you’re not a diabetic, why bother checking blood sugar? New studies have documented the increased likelihood of cardiovascular events with increased postprandial blood sugars well below the ranges regarded as diabetic. A blood sugar level of 140 mg/dl after a meal carries 30-60% increased (relative) risk for heart attack and other events. The increase in risk begins at even lower levels, perhaps 110 mg/dl or lower after-eating.

We use a one-hour after eating blood sugar to gauge the effects of a meal. If, for instance, your dinner of baked chicken, asparagus brushed with olive oil, sauteed mushrooms, mashed potatoes, and a piece of Italian bread yields a one-hour blood sugar of 155 mg/dl, you know that something is wrong. (This is far more common than most people think.)

Doing this myself, I have been shocked at the times I've had an unexpectedly high blood sugar from seemingly "safe' foods, or when a store- or restaurant-bought meal had some concealed source of sugar or carbohydrate. (I recently had a restaurant meal of a turkey burger with cheese, mixed salad with balsamic vinegar dressing, along with a few bites of my wife's veggie omelet. Blood sugar one hour later: 127 mg/dl. I believe sugar added to the salad dressing was the culprit.)

You can now purchase your own blood glucose monitor at stores like Walmart and Walgreens for $10-20. You will also need to purchase the fingerstick lancets and test strips; the test strips are the most costly part of the picture, usually running $0.50 to $1.00 per test strip. But since people without diabetes check their blood sugar only occasionally, the cost of the test strips is, over time, modest. I've had several devices over the years, but my current favorite for ease-of-use is the LifeScan OneTouch UltraMini that cost me $18.99 at Walgreens.

Checking after-meal blood sugars is, in my view, a powerful means of managing diet when reducing carbohydrate exposure is your goal. It provides immediate feedback on the carbohydrate aspect of your diet, allowing you to adjust and tweak carbohydrate intake to your individual metabolism.

LDL glycation

The proteins of the body are subject to the process of glycation, modification of protein structures by glucose (blood sugar). In the last Heart Scan Blog post, I discussed how glycated hemoglobin, available as a common test called HbA1c, can serve as a reflection of protein glycation (though it does not indicate actual Advanced Glycation End-products, or AGEs, just a surrogate indicator).

There is one very important protein that is subject to glycation: Apoprotein B.

Apoprotein B, or Apo B, is the principal protein of VLDL and LDL particles. Because there is one Apo B molecule per VLDL or LDL particle, Apo B can serve as a virtual VLDL/LDL particle count. The higher the Apo B, the greater the number of VLDL and LDL particles.

Because Apo B is a protein, it too is subject to the process of glycation. The interesting thing about the glycation of Apo B is that its "glycatability" depends on LDL particle size: The smaller the LDL particle, the more glycation-prone the Apo B contained within.

Younis et al have documented an extraordinary variation in glycatability between large and small LDL, with small LDL showing an 8-fold increased potential.

Think about it: Carbohydrates in the diet, such as wheat products and sugars, trigger formation of small LDL particles. Small LDL particles are then more glycation-prone by up to a factor of 8. Interestingly, HbA1c is tightly correlated with glycation of Apo B. Diabetics with high HbA1c, in particular, have the greatest quantity of glycated Apo B. They are also the group most likely to develop coronary atherosclerosis, as well as other consequences of excessive AGEs.

No matter how you spin it, the story of carbohydrates is getting uglier and uglier. Carbohydrates, such as those in your whole grain bagel, drive small LDL up, while making them prone to a glycating process that makes them more likely to contribute to formation of coronary atherosclerotic plaque.

High HbA1c: You're getting older . . . faster

Over the years, we all accumulate Advanced Glycation End-products, or AGEs.

AGEs are part of aging; they are part of human disease. AGEs are the result of modification of proteins by glucose. AGEs form the basis for many disease conditions.

Accumulated AGEs have been associated with aging, dementia, cataracts, osteoporosis, deafness, cancer, and atherosclerosis. Most of the complications of diabetes have been attributable to AGEs.

There's one readily available method to assess your recent AGE status: HbA1c.

Hemoglobin is the oxygen-carrying protein of red blood cells. Like other proteins, hemoglobin becomes glycated in the presence of glucose. Hemoglobin glycation increases linearly with glucose: The higher the serum or tissue glucose level, the more glycation of hemoglobin develops. Glycated hemoglobin is available as the common test, HbA1c.

Ideal HbA1c is 4.5% or less, i.e., 4.5% of hemoglobin molecules are glycated. Diabetics typically have HbA1c 7.0% or greater, not uncommonly greater than 10%.

In other words, repetitive and sustained high blood glucose leads to greater hemoglobin glycation, higher HbA1c, and indicates greater glycation of proteins in nerve cells, the lens of your eye, proteins lining arteries, and apoprotein B in LDL cholesterol particles.

If AGEs accumulate as a sign of aging, and high blood sugars lead to greater degrees of glycation, it only follows that higher HbA1c marks a tendency for accelerated aging and disease.

Indeed, that is what plays out in real life. People with diabetes, for instance, have kidney failure, heart disease, stroke, cataracts, etc. at a much higher rate than people without diabetes. People with pre-diabetes likewise.

The higher your HbA1c, the greater the degree of glycation of other proteins beyond hemoglobin, the faster you are aging and subject to all the phenomena that accompany aging. So that blood glucose of 175 mg/dl you experience after oatmeal is not a good idea. 

The lesson: Keep HbA1c really low. First, slash carbohydrates, the only foods that substantially increase blood glucose. Second, maintain ideal weight, since normal insulin responsiveness requires normal body weight. Third, stay physically active, since exercise and physical activity exerts a powerful glucose-reducing effect. Fourth, consider use of glucose-reducing supplements, an issue for another day.

While HbA1c cannot indicate cumulative AGE status, it can reflect your recent (preceding 60 to 90 days) exposure to this age-accelerating thing called glucose.

If your doctor refuses to accommodate your request for a HbA1c test, you can perform your own fingerstick test.

Slash carbs . . . What happens?

Cut the carbohydrates in your diet and what sorts of results can you expect?

Carbohydrate reduction results in:

Reduced small LDL--This effect is profound. Carbohydrates increase small LDL; reduction of carbohydrates reduce small LDL. People are often confused by this because the effect will not be evident in the crude, calculated (Friedewald) LDL that your doctor provides.

Increased HDL--The HDL-increasing effect of carbohydrate reduction may require 1-2 years. In fact, in the first 2 months, HDL will drop, only to be followed by a slow, gradual increase. This is the reason why, in a number of low-carb diet studies, HDL was shown to be reduced.--Had the timeline been longer, HDL would show a significant increase.

Decreased triglycerides--Like reduction of small LDL, the effect is substantial. Triglyceride reductions of several hundred milligrams are not at all uncommon. In people with familial hypertriglyceridemia with triglyceride levels in the thousands of milligrams per deciliter, triglyceride levels will plummet with carbohydrate restriction. (Ironically, conventional treatment for familial hypertriglyceridemia is fat restriction, a practice that can reduce triglycerides modestly in these people, but not anywhere near as effectively as carbohydrate restriction.) Triglyceride reduction is crucial, because triglycerides are required by the process to make small LDL--less triglycerides, less small LDL.

Decreased inflammation--This will be reflected in the crude surface marker, c-reactive protein--Yes, the test that the drug industry has tried to convince you to take statins drugs to reduce. In my view, it is an absurd notion that you need to take a drug like Crestor to reduce risk associated with increased CRP. If you want to reduce CRP to the floor, eliminate wheat and other junk carbohydrates. (You should also add vitamin D, another potent CRP-reducing strategy.)

Reduced blood pressure--Like HDL, blood pressure will respond over an extended period of months to years, not days or weeks. The blood pressure reduction will be proportion to the amount of reduction in your "wheat belly."

Reduced blood sugar--Whether you watch fasting blood sugar, postprandial (after-meal) blood sugars, or HbA1c, you will witness dramatic reductions by eliminating or reducing the foods that generate the high blood sugar responses in the first place. Diabetics, in particular, will see the biggest reductions, despite the fact that the American Diabetes Association persists in advising diabetics to eat all the carbohydrates they want. Reductions in postprandial (after-eating) blood sugars, in particular, will reduce the process of LDL glycation, the modification of LDL particles by glucose that makes them more plaque-causing.


You may notice that the above list corresponds to the list of common plagues targeted by the pharmaceutical industry: blood pressure, diabetes (diabetes being the growth industry of the 21st century), high cholesterol. In other words, high-carbohydrate, low-fat foods from the food industry create the list of problems; the pharmaceutical industry steps in to treat the consequences.

In the Track Your Plaque approach, we focus specifically on elimination of wheat, cornstarch, and sugars, the most offensive among the carbohydrates. The need to avoid other carbohydrates, e.g., barley, oats, quinoa, spelt, etc., depends on individual carbohydrate sensitivty, though I tend to suggest minimal exposure.

Normal fasting glucose with high HbA1c

Jonathan's fasting glucose: 85 mg/dl
His HbA1c: 6.7%

Jonathan's high HbA1c reflects blood glucose fluctuations over the preceding 60-90 days and can be used to calculate an estimated average glucose (eAG) with the following equation:

eAG = 28.7 X A1c – 46.7

(For glucose in mmol/L, the equation is eAG = 1.59 × A1C - 2.59)

Jonathan's HbA1c therefore equates to an eAG of 145.59 mg/dl--yet his fasting glucose value is 85 mg/dl. 

This is a common situation: Normal fasting glucose, high HbA1c. It comes from high postprandial glucose values, high values after meals. 

It suggests that, despite having normal glucose while fasting, Jonathan experiences high postprandial glucose values after many or most of his meals. After a breakfast of oatmeal, for instance, he likely has a blood glucose of 150 mg/dl or greater. After breakfast cereal, blood glucose likely exceeds 180 mg/dl. With two slices of whole wheat bread, glucose likewise likely runs 150-180 mg/dl. 

The best measure of all is a postprandial glucose one hour after the completion of a meal, a measure you can easily obtain yourself with a home glucose meter. Second best: fasting glucose with HbA1c.

Gain control over this phenomenon and you 1) reduce fasting blood sugar, 2) reduce expression of small LDL particles, and 3) lose weight.  

Can you handle fat?

No question: Low-carbohydrate diets generate improved postprandial lipoprotein responses.

Here's a graph from one of Jeff Volek's great studies:



Participants followed a low-carb diet of less than 50 g per day carbohydrate ("ketogenic") with 61% fat.   The curves were generated by administering a 123 g fat challenge with triglyceride levels assessed postprandially. The solid line represents the postprandial response at the start; dotted line after the 6-week low-carb effort.

Note that:

1) The postprandial triglyceride (area-under-the-curve) response was reduced by 29% in the low-carb diet.  That's a good thing.

2) The large fat challenge generated high triglycerides of greater than 160 mg/dl even in the low-carb group. That's a bad thing. 

In other words, low-carb improves postprandial responses substantially--but postprandial phenomena still occur. Postprandial triglycerides of 88 mg/dl or greater are associated with greater heart attack risk because they signify the presence of greater quantities of atherogenic (plaque-causing) postprandial lipoproteins.

A full discussion of these phenomena can be found in the Track Your Plaque Special Report, Postprandial Responses: The Storm After the Quiet!, part of a 3-part series on postprandial phenomena.
All posts by william-davis

Let's make it a lot easier

The American Heart Association just released a new set of consensus guidelines on heart disease prevention in women: Evidence-Based Guidelines for Cardiovascular Disease Prevention in Women: 2007 Update

For those of you following the Heart Scan Blog and the Track Your Plaque program, there will be little new in the guidelines. In fact, you'll wonder if the date on the front of the report should be 1987, rather than 2007. Did you know that you should exercise and eat healthy?

Take a look at the list of risk factors for coronary vascular disease (CVD) listed in the report:

Major risk factors for CVD, including:
Cigarette smoking
Poor diet
Physical inactivity
Obesity, especially central adiposity
Family history of premature CVD (CVD at <55>

Progress: You'll notice that buried inside the list is "Evidence of subclinical vascular disease (e.g., coronary calcification)". Just a few short years ago that wouldn't have even been included.

The Track Your Plaque contention is that, for the great majority of women, this list could be shortened to one item: coronary calcification. As time goes on, the people who argue and draft these guidelines will come to the realization that coronary calcification is the disease--it's not a risk for the disease, a predictor of the disease. Coronary calcification is the disease itself. The other items on the list recede way into the background when you know whether or not coronary atherosclerosis is present, i.e., you know your heart scan score (of coronary calcium).

The report goes to say such things as taking a little bit of fish oil is a good idea, maintaining a normal blood pressure is desirable. . . yada yada yada. You've heard this all before.

A major part of the treatment guidelines are devoted to LDL cholesterol reduction with statin agents. You shouldn't be surprised. It's amazing what $22 billion dollars in revenues will buy.

A closing paragraph reads:

'Population-wide strategies are necessary to combat the
pandemic of CVD in women, because individually tailored
interventions alone are likely insufficient to maximally prevent
and control CVD. Public policy as an intervention to
reduce gender-based disparities in CVD preventive care and
improve cardiovascular outcomes among women must become
an integral strategy to reduce the global burden of
CVD.'


Say that again? If you understood that bit of gobbledygook, you're a lot smarter than me.

Don't look to the American Heart Association report for any new ideas. It reminds me of the politician who reminds everybody of what a devoted family man he is: It has nothing to do with his policies. It just makes him look good. If compared to prior report, the 2007 report does indeed represent progress--but just oh so little.

No wonder nobody talks about real prevention

Take a look at this eye-opening statement taken from a well-written NY Times article about Dr. Arthur Agatston, the South Beach Diet and now South Beach Heart Program books:


'We have made major improvements in prevention,” Dr. Gregg W. Stone, the director of cardiovascular research at Columbia University, says. “But it’s difficult. It takes frequent visits, a close relationship between a physician and a patient and a very committed patient.'

Which is exactly the atmosphere Dr. Agatston’s practice tries to create. Nurses there give patients specific cholesterol goals to meet and help them deal with the side effects of the drugs they are taking. A nutritionist, Marie Almon, meets with patients frequently enough to discuss real-life issues like how to stick to a high-fiber Mediterranean diet even on a cruise or a business trip.

There is only one problem with this shining example of a medical practice: it is losing money.



From NY Times, January 24, 2007. What’s a Pound of Prevention Really Worth? (Find the full text at http://www.nytimes.com/2007/01/24/business/24leonhardt.html?ex=1172379600&en=4268a738e82857da&ei=5070.)

It gets at one of the fundamental reasons why your cardiologist will probably never talk to you about an intense approach to prevention: it doesn't pay. Because John Q. Cardiologist focuses, instead, on how to increase procedural volume, train how to put in the next best defibrillator, etc., there is little consciousness about preventive issues. Just the simple matter of taking fish oil causes their eyes to glaze over.

That's why the Track Your Plaque program exists: it is a portal for the kind of information you cannot get. Of course, you could read all the scientific studies, attempt years of trial and error, and try to gain a sense of how to do this yourself. Or you could follow this program. We are proud to not worry about generating procedural profits. We ar unbiased by drug or medical device money. We say exactly what we mean.

By the way, we are on a current push to really "beef-up" our online discussions via real-time chat. Long-term, we'd like to be able to offer chat with our staff many hours every day. Be patient. It will happen, but not today.

HDL and vitamin D

I know of no published reports on this question, but I've now seen numerous people experience significant jumps in HDL with raising blood vitamin D to 25-OH-vitamin D3.

Last week, for example, I had a man who had struggled with raising HDL from a starting level of 28 mg/dl. On niacin, exercise, weight loss, fish oil, red wine, and cilostazol (a prescription agent that I use occasionally that raises HDL), his HDL rose to 41 mg/dl--better, but hardly to our goal.

I added vitamin D, 4000 units, and raised his 25-OH-vitamin D3 level from 22 ng/ml to 53 ng/ml. Next HDL: 73 mg/dl! Small LDL improves along with a rise in HDL.

Not everybody's response is this dramatic. I see more typical rises of 5 to 10 mg/dl every day. I'm uncertain of why the response is inconsistent, though people who begin with lower vitamin D levels seem to experience a larger HDL increase. I wonder if the partial normalization of insulin and glucose responses is at work, or some anti-inflammatory effect.

Vitamin D provides so many other benefits, as well as HDL-raising. I hope you've gone to the effort to have your blood level checked to determine your replacement need. If not, now's the time. February represents your nadir (lowest point) for 25-OH-vitamin D3 blood levels.

Even more Michael Pollan

"Eat food. Not too much. Mostly plants.

That, more or less, is the short answer to the supposedly incredibly complicated and confusing question of what we humans should eat in order to be maximally healthy. I hate to give away the game right here at the beginning of a long essay, and I confess that I’m tempted to complicate matters in the interest of keeping things going for a few thousand more words. I’ll try to resist but will go ahead and add a couple more details to flesh out the advice. Like: A little meat won’t kill you, though it’s better approached as a side dish than as a main. And you’re much better off eating whole fresh foods than processed food products. That’s what I mean by the recommendation to eat “food.” Once, food was all you could eat, but today there are lots of other edible foodlike substances in the supermarket. These novel products of food science often come in packages festooned with health claims, which brings me to a related rule of thumb: if you’re concerned about your health, you should probably avoid food products that make health claims. Why? Because a health claim on a food product is a good indication that it’s not really food, and food is what you want to eat."


Michael Pollan, author of my latest favorite book, The Omnivore's Dilemma, wrote a wonderful piece for the New York Times entitled "Unhappy Meals". You can find the full text at http://www.nytimes.com/2007/01/28/magazine/28nutritionism.t.html?ex=1172120400&en=a78c20f4da0cdc7b&ei=5070. (Another favorite read of mine, The Fanatic Cook's Blog at , alerted me to Pollan's article. Incidentally, take a look at the Fanatic Cook's latest posts--very entertaining and informative. She's got incisive insight into foods as well as a great sense of humor.)

Pollan goes on to say that...

"...typical real food has more trouble competing under the rules of nutritionism, if only because something like a banana or an avocado can’t easily change its nutritional stripes (though rest assured the genetic engineers are hard at work on the problem). So far, at least, you can’t put oat bran in a banana. So depending on the reigning nutritional orthodoxy, the avocado might be either a high-fat food to be avoided (Old Think) or a food high in monounsaturated fat to be embraced (New Think). The fate of each whole food rises and falls with every change in the nutritional weather, while the processed foods are simply reformulated. That’s why when the Atkins mania hit the food industry, bread and pasta were given a quick redesign (dialing back the carbs; boosting the protein), while the poor unreconstructed potatoes and carrots were left out in the cold.

Of course it’s also a lot easier to slap a health claim on a box of sugary cereal than on a potato or carrot, with the perverse result that the most healthful foods in the supermarket sit there quietly in the produce section, silent as stroke victims, while a few aisles over, the Cocoa Puffs and Lucky Charms are screaming about their newfound whole-grain goodness."


Not everything Pollan says is new, but he says it so eloquently and cleverly that he's worth reading. If you haven't yet read Omnivore's Dilemma, or just want a condensed version of the book, the New York Times piece is a great piece of the world according to Michael Pollan.

My life is easy

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

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

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

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

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

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

My bread contains 900 mg omega-3

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

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

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

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

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

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

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

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

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

More Omnivore's Dilemma

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

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

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

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

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

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

Pollan's The Omnivore's Dilemma


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

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

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

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

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

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

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

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

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

The most frequently asked question of all

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

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

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

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

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

3) Correct all patterns.


But we don't.

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

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

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

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

Do stents kill?

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

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

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

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

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

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