Overweight, hungry, diabetic, and fat-free

Let me tell you about my low-fat experience from 20 years ago.

At the time, I was living in Cleveland, Ohio, and served on the faculty at a large metropolitan university-affiliated hospital, supervising fellows-in-training and developing high-tech cath lab procedures like directional athererectomy and excimer laser coronary angioplasty. (Yes, another life.)

I was concerned about personal heart disease risk, though I knew next to nothing about lipids and coronary risk prediction outside of the little I learned in training and what the drug industry promoted.

I heard Dr. Dean Ornish talk while attending the American College of Cardiology meetings in Atlanta. Dr. Ornish spoke persuasively about the dangers of fat in the diet and how he "reversed" coronary disease using a low-fat, no added oils, no meat, vegetarian diet that included plenty of whole grains. So I thought I'd give it a try.

I eliminated all oils; I removed all meat, eggs, and fish from my diet. I shunned all nuts. I ate only low-fat products like low-fat yogurt and cottage cheese; and focused on vegetables, fruit, and whole grains. Beans and brown or wild rice were a frequent staple. I loved oatmeal cookies--low-fat, of course!

After one year of this low-fat program, I had gained a total of 31 lbs, going from 155 lbs to 186 lbs. I reassessed some basic labs:

HDL 28 mg/dl
Triglycerides 336 mg/dl
Blood sugar 151 mg/dl (fasting)


I became a diabetic. All through this time, I was also jogging. I ran on the beautiful paths along the Chagrin River in suburban Cleveland for miles north and south. I ran 5 miles per day most days of the week.

It was diabetes that hit me alongside the head: I was eating low-fat meticulously, exercising more than 90% of the population, yet I got fat and diabetic!

I have since changed course in diet. Last time I checked, my lipid values on NO statin agent:

HDL 67 mg/dl
Triglycerides 57 mg/dl
Blood sugar 91 mg/dl

That was my lesson that fat restriction is a destructive, misguided notion. The data since then have confirmed that restricting total fat is unnecessary, even undesirable, when fat calories are replaced by carbohydrate calories.

This is your brain on wheat

Here's just a smattering of the studies performed over the past 30 years on the psychological effects of wheat consumption.

Oddly, this never makes the popular press. But wheat underlies schizophrenia, bipolar illness, behavioral outbursts in autism, Huntington's disease, and attention deficit hyperactivity disorder (ADHD).

The relationship is especially compelling with schizophrenia:

Opioid peptides derived from food proteins: The exorphins.
Zioudrou C et al 1979
"Wheat gluten has been implicated by Dohan and his colleagues in the etiology of schizophrenia and supporting evidence has been provided by others. Our experiments provide a plausible biochemical mechanism for such a role, in the demonstration of the conversion of gluten into peptides with potential central nerovus system actions."


Wheat gluten as a pathogenic factor in schizophrenia
Singh MM et al 1976
"Schizophrenics maintained on a cereal grain-free and milk-free diet and receiving optimal treatment with neuropleptics showed an interruption or reversal of their therapeutic progress during a period of "blind" wheat gluten challenge. The exacerbation of the disease process was not due to variations in neuroleptic doses. After termination of the gluten challenge, the course of improvement was reinstated. The observed effects seemed to be due to a primary schizophrenia-promoting effect of wheat gluten."


Demonstration of high opioid-like activity in isolated peptides from wheat gluten hydrolysates
Huebner FR et al 1984


Is schizophrenia rare if grain is rare?
Dohan FC et al 1984
"Epidemiologic studies demonstrated a strong, dose-dependent relationship between grain intake and the occurrence of schizophrenia."

Small LDL: Perfect index of carbohydrate intake

Measuring the number of small LDL particles is the best index of carbohydrate intake I know of, better than even blood sugar and triglycerides.

In other words, increase carbohydrate intake and small LDL particles increase. Decrease carbohydrates and small LDL particles decrease.

Why?

Carbohydrates increase small LDL via a multistep process:

First step: Increased fatty acid and apoprotein B production in the liver, which leads to increased VLDL production. (Apoprotein B is the principal protein of VLDL and LDL)

Second step: Greater VLDL availability causes triglyceride-rich VLDL to interact with other particles, namely LDL and HDL, enriching them in triglycerides (via the action of cholesteryl-ester transfer protein, or CETP). Much VLDL is converted to LDL.

Third step: Triglyceride-rich LDL is "remodeled" by enzymes like hepatic lipase, which create small LDL.


Carbohydrates, especially if they contain fructose, also prolong the period of time that triglyceride-rich VLDL particles persist in the blood, allowing more time for VLDL to interact with LDL.

Many people are confused by this. "You mean to tell me that reducing carbohydrates reduces LDL cholesterol?" Yes, absolutely. While the world talks about cutting saturated fats and taking statin drugs, cutting carbohydrates, especially wheat (the most offensive of all), cornstarch, and sugars, is the real key to dropping LDL.

However, the effect will not be fully evident if you just look at the crude conventional calculated (Friedewald) LDL cholesterol. This is because restricting carbohydrates not only reduces small LDL, it also increases LDL particle size. This make the calculated Friedewald go up, or it blunts its decrease. Conventional calculated LDL will therefore either underestimate or even conceal the real LDL-reducing effect.

The reduction in LDL is readily apparent if you look at the superior measures, LDL particle number (by NMR) or apoprotein B. Dramatic reductions will be apparent with a reduction in carbohydrates.

Small LDL therefore serves as a sensitive index of carbohydrate intake, one that responds literally within hours of a change in food choices. Anyone following the crude Friedewald calculated LDL will likely not see this. This includes the thousands of clinical studies that rely on this unreliable measure and come to the conclusion that a low-fat diet reduces LDL cholesterol.

Fat "conditioning"

Here's a great study from the prolific laboratory of Dr. Jeff Volek from the University of Connecticut. (Full text here.)


http://jn.nutrition.org/cgi/content/full/134/4/880

Video Teleconference with Dr. William Davis


Dr. Davis is available for personal
one-on-one video teleconferencing

to discuss your heart health issues.


You can obtain Dr. Davis' expertise on issues important to your health, including:

Lipoprotein assessment

Heart scans and coronary calcium scores

Diet and nutrition

Weight loss

Vitamin D supplementation for optimal health

Proper use of omega-3 fatty acids/fish oil



Each personalized session is 30 minutes long and by appointment only. To arrange for a Video Teleconference, go to our Contact Page and specify Video Teleconference in your e-mail. We will contact you as soon as possible on how to arrange the teleconference.


The cost for each 30-minute session is $375, payable in advance. 30-minute follow-up sessions are $275.

(Track Your Plaque Members: Our Member cost is $300 for a 30-minute session; 30-minute follow-up sessions are $200.)

After the completion of your Video Teleconference session, a summary of the important issues discussed will be sent to you.

The Video Teleconference is not meant to replace the opinion of your doctor, nor diagnose or treat any condition. It is simply meant to provide additional discussion about your health issues that should be discussed further with your healthcare provider. Prescriptions cannot be provided.

Note: For an optimal experience, you will need a computer equipped with a microphone and video camera. (Video camera is optional; you will be able to see Dr. Davis, but he will not be able to see you if you lack a camera.)

We use Skype for video teleconferencing. If you do not have Skype or are unfamiliar with this service, our staff will walk you through the few steps required.

Track Your Plaque challenges

Of all the various factors we correct in the Track Your Plaque program in the name of achieving reversal of coronary plaque, there are two factors that are proving to be our greatest challenges:

1) Genetic small LDL

2) Lipoprotein(a)

More and more people are enjoying at least marked slowing, if not zero change or reduction, in heart scan scores following the Track Your Plaque program. We achieve this by correcting a number of factors. Some factors, like vitamin D deficiency, are easily corrected to perfection--supplement sufficient vitamin D to achieve a blood level of 25-hydroxy vitamin D of 60-70 ng/ml. Correcting standard lipid values--LDL cholesterol, HDL cholesterol, and triglycerides--child's play, even to our strict targets of 60-60-60.

However, what I call "genetic small LDL" and a subset of lipoprotein(a) are proving to be the most resistant of all.

Let's first consider genetic small LDL. Small LDL is generally the pattern of the carbohydrate-ingesting, overweight person. It has exploded in severity over the past decade due to overconsumption of carbohydrates due to the ridiculous low-fat notion. Reduce or eliminate carbohydrates, especially wheat, which permits weight loss, and small LDL drops like a stone. But there is a unique subset of people who express the small LDL pattern who start at or near ideal weight. Take Chad, for instance. At 6' 2" and 152 lbs and BMI of 19.6, there's no way excess weight could be triggering his small LDL. Yet he starts with 100% small LDL particles. All efforts to reduce small LDL, such as wheat, cornstarch, and sugar elimination; niacin; vitamin D normalization; thyroid normalization; and several supplements that yield variable effects, such as phosphatidylcholine, all leave Chad with more than 90% small LDL.

Lipoprotein(a) is a bit different. Over the past 5 years, our choices in ways to reduce Lp(a) expression have improved dramatically. Beyond niacin, we now have high-dose EPA + DHA, thyroid normalization that includes use of T3, and hormonal manipulation. In the Track Your Plaque experience, approximately 70% of people with Lp(a) respond with a reduction in Lp(a). (In fact, the 4 out of the 5 record holders for reduction of heart scan scores have Lp(a) that was successfully treated.) But about 30% of people with Lp(a) prove resistant to all these treatments--they begin with a Lp(a) of, say, 260 nmol/L and, despite niacin, high-dose EPA + DHA, and various hormones, stay at 260 nmol/L. It can be frustrating and frightening.

So these are the two true problem areas for the Track Your Plaque program, genetic small LDL and a subset of Lp(a).

We are actively searching for better options for these two problem areas. Given the collective exploration and wisdom that develops from such collaborative efforts as the Track Your Plaque Forum, I am optimistic that we will have better answers for these two stumbling blocks to plaque reversal in the future.

I'll supply the tar if you supply the feathers

The results of the latest Heart Scan Blog poll are in.


DIRECT-TO-CONSUMER PHARMACEUTICAL ADVERTISING HAS:

Increased public awareness of medical conditions and their treatment
19 (11%)

Has had little overall effect on health and healthcare
29 (18%)

Needlessly increased healthcare costs
81 (50%)

Further empowered the revenue-obsessed pharmaceutical industry
130 (81%)


Clearly, there's a lot of negative sentiment against direct-to-consumer (DTC) drug advertising.

It looks as if a small minority believe that good has come from DTC advertising, judging by the meager 11% who voted for increased awareness. In fact, the poll results are heavily weighed towards the negative: 50% voted for "needlessly increased healthcare costs," while an astounding 81% voted for "empowered the revenue-obsessed pharmaceutical industry."

It is, indeed, an odd situation: Pharmaceutical agents available only by prescription being hyped directly to the consumer.

Personally, I would vote for choices 1,3, and 4. While awareness has increased, it has come with a hefty price, not all of it well spent. I believe the pharmaceutical industry still adheres to the rule that, for every $1 spent on advertising, $4 is made in revenue. They are, in effect, printing money.

What goes up can't come down

According to conventional wisdom, heart scan scores cannot be reduced.

In other words, say you begin with a heart scan score of 300. Conventional wisdom says you should take aspirin and a statin drug, eat a low-fat "heart healthy" diet, and take high blood pressure medications, if necessary.

If your heart scan score goes up in a year or two, especially at an annual rate of 20% or more, then you are at very high risk for heart attack. If the heart scan score stays the same, then your risk is much reduced. These observations are well-established.

But more than 99% of physicians will tell you that reducing your heart scan score is impossible. Don't even try: Heart scan scores can go up, but they can't go down.

Baloney. Heart scan scores can indeed go down. And they can go down dramatically.

It is true that, following conventional advice like taking a statin drug, following a low-fat diet, and taking aspirin will fail to reduce your heart scan score. A more rational approach that 1) identifies all causes of coronary plaque, 2) corrects all causes while including crucial strategies like omega-3 fatty acid supplementation, vitamin D supplementation, and thyroid function normalization, is far more likely to yield a halt or reduction in score.

While not everybody who undertakes the Track Your Plaque program will succeed in reducing their heart scan score, a growing number are enjoying success.

A small portion of our experience was documented this past summer. (I collected and analyzed the data with the help of Rush University nutrition scientist, Dr. Susie Rockway, and statistician, Dr. Mary Kwasny.)


Effect of a combined therapeutic approach of intensive lipid management, omega-3 fatty acid supplementation, and increased serum 25 (OH) vitamin D on coronary calcium scores in asymptomatic adults.

Davis W, Rockway S, Kwasny M.

The impact of intensive lipid management, omega-3 fatty acid, and vitamin D3 supplementation on atherosclerotic plaque was assessed through serial computed tomography coronary calcium scoring (CCS). Low-density lipoprotein cholesterol reduction with statin therapy has not been shown to reduce or slow progression of serial CCS in several recent studies, casting doubt on the usefulness of this approach for tracking atherosclerotic progression. In an open-label study, 45 male and female subjects with CCS of > or = 50 without symptoms of heart disease were treated with statin therapy, niacin, and omega-3 fatty acid supplementation to achieve low-density lipoprotein cholesterol and triglycerides < or = 60 mg/dL; high-density lipoprotein > or = 60 mg/dL; and vitamin D3 supplementation to achieve serum levels of > or = 50 ng/mL 25(OH) vitamin D, in addition to diet advice. Lipid profiles of subjects were significantly changed as follows: total cholesterol -24%, low-density lipoprotein -41%; triglycerides -42%, high-density lipoprotein +19%, and mean serum 25(OH) vitamin D levels +83%. After a mean of 18 months, 20 subjects experienced decrease in CCS with mean change of -14.5% (range 0% to -64%); 22 subjects experienced no change or slow annual rate of CCS increase of +12% (range 1%-29%). Only 3 subjects experienced annual CCS progression exceeding 29% (44%-71%). Despite wide variation in response, substantial reduction of CCS was achieved in 44% of subjects and slowed plaque growth in 49% of the subjects applying a broad treatment program.

Gretchen's postprandial diet experiment

Gretchen sent me the results of a little experiment she ran on herself. She measured blood glucose and triglycerides after 1) a low-fat diet and 2) a low-carb diet.









Gretchen describes her experience:

Several years ago I received a windfall of triglyceride strips that would expire in a week or so. I hated to waste them, so I decided to use them to test my triglyceride and BG responses to two different diets: low carb and low fat.

The first day I followed a low-fat diet. For breakfast I ate a lot of carbohydrate, including 1 oz of spaghetti cooked al dente and ¾ cup of white rice. For the rest of the day I ate less carbohydrate but continued to eat low fat.

The second day I followed a low-carb diet. For breakfast I ate a lot of fat, including a sausage, mushrooms fried in butter, 2 slices of bacon, and ¼ cup of the creamy topping of whole-milk yogurt. For the rest of the day I ate less fat, especially less saturated fat, but continued to eat low carb.

Both days I measured both BG and triglyceride levels every hour until I went to bed. On the low-carb day I had 3 meals. On the low-fat day, I was constantly hungry, had 4 meals, and kept snacking.

You can see the results in Figure 1. On the low-fat diet, after a “healthy” low-fat breakfast of low-glycemic pasta with low-fat sauce, my BG levels shot up to over 200 mg/dL and took more than 6 hours to come down. My triglycerides, however, remained low, and at first I thought perhaps the low-fat diet might be better overall. However, after about 6 hours, the triglyceride levels started to increase steadily, and by the next morning, they were higher than they had been the day before.
On the low-carb diet, my BG levels stayed low all day. However, after meals, the triglyceride levels skyrocketed. After meals they came down, and by the next morning they were lower than they had been the day before.

As I interpret these results, the high triglyceride levels after eating the high-fat meals represent chylomicrons, the lipoproteins that transport fat from your meals to the cells of your body. The high triglyceride levels the morning after eating the low-fat meals represent very low density lipoprotein, which takes the cholesterol your liver synthesizes when your intake of dietary cholesterol is low and distributes it to cells that need it, or again, to the fat for storage.

There are several interesting factors to consider here. First, when you have a lipid test done at the lab, it’s usually done fasting, which means first thing in the morning after not eating for 8 to 12 hours. It tells you nothing about what your triglyceride levels were all day.

Second, the low-carb diet resulted in lower fasting triglyceride levels, but much higher postprandial triglyceride levels. Which are more dangerous? I’m afraid I don’t know. You should also note that the high-fat, low-carb breakfast was extremely high in fat, including saturated fat. I don’t normally eat that much fat but wanted to test extremes.

Third, although the low-fat diet didn’t produce the very high postprandial triglyceride levels that the high-fat diet did, it produced extremely high BG levels that persisted for 6 hours. Some people think that it’s oxidized and glycated lipids that are the dangerous ones, so high BG levels and normal triglyceride levels might be more dangerous than very high triglyceride levels and normal BG levels. Note that high BG levels also contribute to oxidation rates.

Fourth, this shows the results of an experiment with a sample size of one. My physiology might not be typical. If you want to know how your own body’s lipids respond to different types of diets, you should get a lipid meter and test yourself. Unfortunately, your insurance is unlikely to want to pay for this, so it will be an expensive experiment.

The main point of this is that the results of different diets are complex. We have to eat. And what we eat can affect many different systems in our bodies. Finding the ideal diet that matches our own physiology and results in the best lipid levels as well as BG levels is a real challenge.



This was a lot of effort for one person. Thanks to Gretchen for sharing her interesting experience.

Gretchen makes a crucial point: Some of the effects of diet changes evolve over time, much as triglyceride levels changed substantially for her on the day following her experiment. Wouldn't it be interesting to see how postprandial patterns develop over time if levels were observed sequentially, day after day?

The stark contrast in blood sugars is impressive--Low-carb clearly has the advantage here. Are there manipulations in diet composition in low-carb meals that we can make to blunt the early (3-6 hour) postprandial lipoprotein (triglyceride) peak? That's a topic we will consider in future.

More of Gretchen's thoughts can be found at:

http://wildlyfluctuating.blogspot.com
http://www.healthcentral.com/diabetes/c/5068

After-eating effects: Carbohydrates vs. fats

In the ongoing debate over whether it's fat or carbohydrate restriction that leads to weight loss and health, here's another study from the Oxford group examining the postprandial (after-eating) effects of a low-fat vs. low-carbohydrate diet. (Roberts R et al, 2008; full-text here.)

High-carbohydrate was defined as 15% protein; 10% fat; 75% carbohydrate (by calories), with starch:sugar 70:30.

High-fat was defined as 15% protein; 40% fat; 45% carbohydrate, with starch:sugar 70:30. (Yes, I know. By our standards, the "high-fat" diet was moderate-fat, moderate-carbohydrate--too high in carbohydrates.)

Blood was drawn over 6 hours following the test meal.




Roberts R et al. Am J Clin Nutr 2008

The upper left graph is the one of interest. Note that, after the high-carbohydrate diet (solid circles), triglyceride levels are twice that occurring after the high-fat diet (open circles). Triglycerides are a surrogate for chylomicron and VLDL postprandial lipoproteins; thus, after the high-carbohydrate diet, postprandial particles are present at much higher levels than after the high-fat diet. (It would have been interesting to have seen a true low-carbohydrate diet for comparison.) Also note that, not only are triglyceride levels higher after high-carbohydrate intake, but they remain sustained at the 6-hour mark, unlike the sharper decline after high-fat.

It's counterintuitive: Postprandial lipoproteins, you'd think, would be plentiful after ingesting a large quantity of fat, since fat must be absorbed via chylomicrons into the bloodstream. But it's carbohydrates (and obesity, a huge effect; more on that in future) that figure most prominently in determining the pattern and magnitude of postprandial triglycerides and lipoproteins. Much of this effect develops by way of de novo lipogenesis, the generation of new lipoproteins like VLDL after carbohydrate ingestion.

We also see this in our Track Your Plaque experience. Rather than formal postprandial meal-testing, we use intermediate-density lipoprotein (IDL) as our surrogate for postprandial measures. A low-carbohydrate diet reduces IDL dramatically, as do omega-3 fatty acids from fish oil.
All posts by william-davis

Are happy people more likely to reduce heart scan scores?

I was talking to Darryl, a patient today: 71 years old with a heart scan score of 378, as well as an enlarged aorta (4.5 cm).

We had identified numerous lipoprotein abnormalities 12 months ago and advised him on a program for correction. His patterns included small LDL, high triglycerides, sky-high IDL (VERY important when you have an enlarged aorta), and lipoprotein(a). Blood pressure was also high, another crucial fact to correct when the aorta is enlarged.

Anyway, Darryl corrected lipoproteins to perfection: basic lipids were substantially better than 60-60-60; lipoprotein(a) was reduced well into the desirable range; IDL was eliminated; blood pressure was 108/64. Repeat heart scan score: 354.

There's nothing spectacular about Darryl's story, except that, despite these issues, Darryl was a happy man. He smiled throughout our conversation. He has told me on several occasions how grateful he is for the life he has.

Darryl is not wealthy. He retired around 4 years ago and fills his day with helping his wife, walking outdoors, helping out at his church, and contributing to the care of his grandchildren. Through all this Darryl is incurably, unfailingly, and irrepressibly happy.

It made me think back through all the other people who've also had great succes in their Track Your Plaque program. It struck me that, for the most part, they too were a happy bunch: generally optimistic, happy, not overly stressed nor prone to extremely stressful responses to stressful situations. All seem to also be grateful for the good in their lives, though most had no more money than the average person and had their share of difficulties in life. In fact, I can only recall one person who reversed coronary plaque who was an angry, pessimistic personality. Just one.

Could it be that happy, optimistic people are more likely to reverse coronary plaque? It would, after all, be consistent with all the other observations that type A personalities have more heart attack, etc.

Anyway, this is just an informal observation but one that seems very consistent. Track your plaque--and be happy!

Don't overdo the vitamin D

As time passes and I advise more and more people to supplement vitamin D, I gain increasing respect for this powerful "vitamin". I am convinced that vitamin D replacement is the reason for a recent surge in our success rates in dropping CT heart scan scores. I believe it is also explains the larger drops we've been witnessing lately--20-30%.

But vitamin D can be overdone, too. Too much of a good thing . . .

Despite being labeled a "vitamin", cholecalciferol is actually a hormone. Vitamins are obtained from food and you can thereby develop deficiencies because of poor intake. Deficiency of vitamin C, for instance, arises from a lack of vegetables and fruits.

Vitamin D, on the other hand, is nearly absent from food. The only naturally-occuring source is oily fish like salmon and sardines. Milk usually has a little (100 units per 8 oz) because milk producers have been required by law to put it there to reduce the incidence of childhood rickets.

A woman came to me with a heart scan score of nearly 3800, the highest score I've every seen in a woman. (Record for a male >8,000!) She was taking vitamin D by prescription from her family doctor but at a dose of 150,000 units per week, or approximately 21,000 units per day. This had gone on for about 3-4 years. This may explain her excessive coronary calcium score. Interestingly, she had virtually no lipoprotein abnormalities identified, which by itself is curious, since most people have some degree of abnormality like small LDL. Obviously, I asked her to stop the vitamin D.

Should you be afraid of vitamin D? Of course not. If your neighbor is an alcoholic and has advanced cirrhosis, does that mean you shouldn't have a glass or two of Merlot for health and enjoyment? It's a matter of quantity. Too little vitamin D and you encourage coronary plaque growth. Too much vitamin D and you trigger "pathologic calcification", or the deposition of calcium in inappropriate places and sometimes to extreme degrees, as in this unfortunate woman.

Ideally, you should have your doctor check your 25-OH-vitamin D3 blood levels twice a year in summar and in winter. We aim for a level of 50 ng/ml, the level at which the phenemena of deficiency dissipate.

"It must have been the statin"

After four years of trying, Randy finally reduced her heart scan score. It not only dropped, it plummeted. After four previous scans that showed 25% or more increases, she'd finally dropped her score 23%. (I Blogged about Randy's case a few weeks ago.)

Randy also works for a cardiologist. When she told him that she had reversed her coronary plaque and reduced her heart scan score by 23%, he said, "It must have been the statin agent."

Randy was indeed on a statin drug at a low dose. But she also had taken great efforts in exercise, food choices, fish oil, and vitamin D. In fact, her score had progressed dramatically while she was taking the drug. Put simply, it was not the statin.

But that is the mindset of the conventionally thinking cardiologist. Stent, bypass, or statin drug--what else is there? Even with crystal clear evidence for coronary plaque regression, they refuse to acknowledge that tools that are not in their everyday consciousness could have achieved so spectacular a result.

Given a choice, 9 out of 10 cardiologists would rather put a stent in and walk away $2000 richer for an hour of work. Don't allow them to have this choice. Take control now.

Statin Drugs May Help the Healthy:
Cholesterol-Lowering Statin Drugs May Benefit People Without Heart Disease


That's the headline on WebMD, reporting the findings of a recent study published in the Archives of Internal Medicine. In reality, it wasn't really a study at all, but a re-analysis of previously published data, a so-called meta-analysis.

Nonetheless, the University of Toronto group re-analyzed the results of several studies, pooling data on 28,000 people, none of whom had known coronary disease. The results were similar to the results of the studies that were reported individually: a 29% reduction in heart attack and other "events" in people taking statin drugs.

What's surprising to me is this notion that statins, or any other treatment for that matter, prevent heart attack in people without heart disease. This is idiotic. Of course they had coronary heart disease. You can't have a heart attack in the absence of coronary disease. (There are very rare exceptions, like cocaine users, who experience coronary spasm from the drug).

What the study shows is that people with unrecognized heart disease experienced a reduction in heart attack. What it also means is that many, many people truly without heart disease were unnecessarily treated. As you'd predict, the drug manufacturers love this sort of broad, untargeted use of their drugs. It's an approach that brings in billions of dollars of revenues. The article on WebMD, in fact, was accompanied by three ads for various cholesterol drugs on this single page story.

What if only people with heart disease, as identified by CT heart scan scores, were treated? You would indeed witness an even larger reduction in heart attack risk, because the group receiving treatment both has the disease and is thereby at greater risk. Treatment should yield even greater risk reduction than treating broad groups who superficially appear to not have heart disease.

Ignore this nonsense about statin drugs reducing heart attack risk in people without heart disease. If you don't look for it, you won't know you have it. Once again, you can be lots smarter than the media. Get a heart scan and find out if your risk is worth reducing.

Heart attack guaranteed

What if you knew for a fact that your risk for heart attack was 100% by, say, age 58? This is indeed true for many people, though at age 60, 65, 70--or 45.

In other words, unless something were done about the causes of heart disease, you would inevitably suffer a heart attack at 58.

What sort of action could you take at age 45?

Obviously, not smoking is an absolute requirement. Continue and you may as well start getting your affairs together.

How about exercising and eating a generally healthy diet? Will your risk be reduced to zero? No. It might be reduced 20-30%, depending on genetic factors.

How about a statin drug? Watch TV ads during Oprah, and you might think it's a cure. But in reality, while it is a financial bonanza for the drug manufacturers, it will reduce risk for heart attack by 30%.

(Note that risk reduction by following multiple strategies is not necessarily additive. In other words, if you have a healthy lifestyle and take a statin agent, is risk reduced 60% (30 + 30)? No, because the effects may overlap.)

So, eating healthy, exercising, and taking a statin drug might reduce risk 35-40%, maybe 50% in the best case scenario. Would you be satisfied? Most would not.

Add fish oil at a truly therapeutic dose. Risk reduction by itself: 28%.

Add niacin or other strategies for correction of your individual, specific causes of heart disease: Now we're up to 90% reduction.

Throw in a tracking process to prove whether or not atherosclerotic plaque has progressed or reversed. Now we're approaching 100% if plaque reverses. The only way I know how to track plaque is through CT heart scans. What other test is readily available to you with low radiation exposure, yet is relatively inexpensive and precise? It certainly is not stress testing, heart catheterization, CT angiograms, or other techniques. Cholesterol won't tell you. Besides CT heart scans, there's nothing else I know of.

Let's fact it: For many people, uncorrected risk for heart attack is truly 100% at some age. Take action while you can.

That, in a nutshell, is the Track Your Plaque program.

Heart scan curiosities 3



This is a sample image from the heart scan of a 54-year old, 212 lb, 5 ft 2 inch woman. The heart is the whitish-gray in the center; lungs are the dark (air-filled) areas on either side of the heart. Note the massive amount of surrounding gray tissues that encircles the heart and lungs. This is fat. At this weight, the diameter of total fat exceeds the combined diameter of the heart and lungs. If we were to show the abdomen, there would be even more fat. (The image shows the body not well centered because the technologist centers the heart, since this is, after all, a heart scan.)





This is a 55-year old, 151 lb, 5 ft 4 inch woman. Note the contrast in the quantity of fat tissue surrounding the chest, a much more normal appearance. Note that this woman is still around 25 lb over ideal weight, but not to the extreme degree of the woman above.

Another curious observation: Note the more whitish streaking in the heavier woman's lungs. Heart scans are performed while holding a deep inspiration (a deep breath inwards), mostly to eliminate lung respiratory motion during image acquisition. Nonetheless, the heavier woman's lungs are not as fully expanded as the more slender woman. In other words, the heavier woman cannot inflate her lungs as effectively as the thinner woman. Ever notice how breathless heavy people are? Some of this effect is just being out of shape. But there's also the added effect of the abdominal fat exerting upwards compression on the lung tissues, and the constrictive effect of the encircling fat mass. At the beginning of inspiration, the chest fat exerts the resistance of inertia to inspiration that is absent, or less, in a slender person. With each breath, the heavy woman must move 50 lbs or so of surrounding fat mass just to inhale.

The heavier woman is, in effect, suffocating herself in fat.

The distortions to the human body incurred by extreme weight gain are both fascinating and shocking. I hope you're breathing easily.

The shameful "standard of care"

John's initial heart scan four years ago showed a score of 329. His physician prescribed Zocor for a somewhat high LDL cholesterol.

One year later, John asked for another scan. His score: 385, a 17% increase. John exercised harder and cut his fat intake.

This past fall--3 years after his last scan--John had yet another heart scan. Score: 641, a 66% increase over the last scan, all the while on Zocor.

John sought an opinion from a reputable cardiologist. He concurred with the prescription of Zocor and advised annual stress tests. That's it.

Followers of the Track Your Plaque approach know that the expected uncorrected rate of increase in heart scan score is 30% per year. On Zocor or other cholesterol reducing statin agent, a common rate of growth is between 18-24% per year--better but not great. Plaque growth is certainly not stopped.

But that is the full extent of interest and responsibility of your cardiologist. Prescribe a statin drug, perform a stress test, and the full extent of his obligation has been fulfilled. In legal terms, your physician has met the prevailing
"standard of care". No more, no less.

In other words, the prevailing standard of care falls shamefully short of what is truly possible. For the majority of the motivated and interested, coronary plaque reversal--reduction of your heart scan score--should be the standard aimed for. It's not always achievable, but it is so vastly superior to the prescribe statin, wait for heart attack approach endorsed by most cardiologists.

Heart scan curiosities 2



This is an example of a so-called "hiatal hernia", meaning the stomach has migrated through the diaphragmatic hiatus into the chest--the stomach is literally in the chest. This example is an unusually large one. Hiatal hernias can cause chest pain, indigestion, and a variety of other gastrointestinal complaints. Heart scans are reasonably useful to screen for this disorder, though very small ones could escape detection by this method.

Sometimes, you can actually hear the gurgling of stomach contents (the common "growling" stomach) by listening to the chest. Large ones like this actually crowd your heart (the gray structure above the circled hernia), irritating it and even causing abnormal rhythm disorders. The dense dark material within the hernia represents lunch.

I would not advocate CT heart scans as a principal method to make a diagnosis, but sometimes it just pops up during a heart scan and we pass it on to the person scanned.

Vitamin D: New Miracle Drug

At the meetings of the American Society of Bone and Mineral Research, Dr. Bruce Troen of the University of Miami detailed his views on the extraordinary benefits of vitamin D replacement. He also talked about the enormous problem of unrecognized vitamin deficiency.

“There’s a huge epidemic of hypovitaminosis D, and the real key here is not just that it’ll benefit you from a bone and neuromuscular standpoint, but if you correct hypovitaminosis D and the corresponding secondary hyperparathyroidism, then you’re going to decrease prostate cancer, colon cancer—actually “up to 17 different cancers, breast cancer included.”

Unfortunately, Dr. Troen did not talk much about the heart benefits of vitamin D, likely since the data is scant, nearly non-existent. However, if the Track Your Plaque experience means anything, I predict that vitamin D replacement will become among the most powerful tools you can use to gain control over coronary plaque.

Read the text of a report from the Internal Medicine World Report to read more of Dr. Troen's comments.


http://www.imwr.com/article.php?s=IMWR/2006/11&p=40

Heart disease "reversal" by stress test


Here's an interesting example of a 71-year old man who achieved "reversal" of an abnormality by a nuclear stress test.

This man underwent bypass surgery around 10 years ago, two stents three years ago. A nuclear stress test in April, 2005 showed an area of poor blood flow in the front of the heart. On the images, normal blood flow is shown by the yellow/orange areas. poor or absent blood flow is shown by the blue/purple areas within the white outline.

Now, I can tell you that this man is no paragon of health. He's only accepted limited changes in his otherwise conventional program--in other words, someone who I'd be shocked achieved true reversal of his heart disease. (I didn't have him undergo any CT heart scans because of the difficulties in scoring someone who has undergone bypass surgery and stents, and because of limited motivation. True plaque reversal is for the motivated.)This patient did, however, accept adding fish oil and niacin to his program.

Nonetheless, stress testing can be helpful as a "safety check". Here's the follow-up stress test:
You'll notice that the blue/purple areas of poor blood flow have just about disappeared. This occurred without procedures.

Does this represent "reversal"? No, it does not. It does represent reversal of this phenomenon of poor flow. It does not represent reversal of the plaque lining the artery wall. That's because improvement of flow, as in this man, can be achieved with relatively easy efforts, e.g., improvement in diet, statin drugs, blood pressure control, etc. True reversal or reduction of coronary plaque, however, is tougher.

If blood flow is improved, who cares whether plaque shrinks? Does it still matter? It does. That's because the "event" that gets us in trouble is not progressive reduction in blood flow, but "rupture" of a plaque. A reduction in plaque--genuine reversal--is what slashes risk of plaque rupture.
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.