All posts by william-davis

To track small LDL, track blood sugar

24. December 2009 William Davis (28)

Here's a trick I learned after years of fussing over people's small LDL.

To gain better control over small LDL, follow blood sugars (blood glucose).

When you think about it, all the foods that trigger increases in blood sugar also trigger small LDL. Carbohydrates, in general, are the most potent triggers of small LDL. The most offensive among the carbohydrates: foods made with wheat. After wheat, there's foods made with cornstarch, sucrose (table sugar), and the broad categories of "other" carbohydrates, such as oats, barley, quinoa, sorghum, bulghur, etc.

Assessing small LDL requires a full lipoprotein assessment in which small LDL particles are measured (NMR, VAP, GGE). Not the easiest thing to do in the comfort of your kitchen.

However, you can easily and now cheaply check your blood sugar. Because blood sugar parallels small LDL, checking blood sugar can provide insight into how you respond to various foods and know whether glucose/small LDL have been triggered.

Here's how I suggest patients to do it:

1) Purchase an inexpensive blood glucose monitor at a discounter like Walmart or Walgreen's. You can buy them now for about $10. They're even sometimes free with promotional offers. You will also need to purchase lancets and test strips.

2) With a meal in question, check a blood sugar just prior to the meal, then again 60 minutes after finishing the meal. Say, for example, your pre-meal blood sugar is 102 mg/dl. You eat your meal, check it 60 minutes after finishing. Ideally, the postprandial (after-meal) blood sugar is no more than 102 mg/dl, i.e., no higher than pre-meal.

Perhaps you're skeptical that oatmeal in skim milk with walnuts and raisins will do any damage. So you perform this routine with your breakfast. Blood sugar beforehand: 100 mg/dl. Blood sugar 1 hour post: 163 mg/dl--Uh oh, not good for you. And small LDL will be triggered.

This approach is not perfect. It will not, for example, identify "stealth" triggers of blood sugar and small LDL like pasta, for the same reasons that pasta has a misleadingly low glycemic index: sugars are released slowly and not fully evident with the one-hour blood sugar.

Nonetheless, for most foods and meals, tracking your one-hour postprandial blood sugar can provide important insight into your individual susceptibility to sugar and small LDL-triggering effects.

C-reactive protein: Fiction from the drug industry?

21. December 2009 William Davis (0)

C-reactive protein (CRP) is the liver product of inflammatory responses anywhere in the body. If there's an inflamed left knee, CRP will be increased. If viral bronchitis is making you cough, then CRP will be increased.

The argument put forward by the drug industry is that, because CRP indicates underlying inflammation, very low-grade levels that can be measured in the absence of overt inflammation like the sore knee or bronchitis is associated with increased risk for cardiovascular events. There are now many studies that conclusively demonstrate that, the higher the CRP, the greater the cardiovascular risk.

Naturally, any marker of risk is followed by the inevitable study: Do statin drugs reduce the excess cardiovascular risk of excessive CRP?

And, yes, indeed they do. My statin-crazed colleagues rave about the so-called "pleiotropic," or non-lipid, effects of statins. CRP reduction and the reduction of risk associated with CRP result with statin treatment.

But is life really statin vs. placebo, as most statin trials are constructed? Are there strategies that can outdo statins like Crestor for reduction of CRP?

Watch your fish oil labels

17. December 2009 William Davis (36)

A quick quiz:

How much omega-3 fatty acids, EPA + DHA, are in each capsule of fish oil with the composition shown on the label below:

If you said 1340 mg (894 mg + 446 mg), sorry, but you're wrong. There are 670 mg EPA + DHA per capsule.

Did you notice that the composition, or "Supplement Facts," lists the contents of two capsules? Rather than the usual one capsule contents, this product label lists two capsules.

I don't know why some manufacturers or distributors do this. However, I have seen many people tripped up by this kind of labeling, taking half the omega-3 fatty acids they thought they were taking. This can be important when you are trying to obtain a specific dose of EPA + DHA to reduce triglycerides, reduce Lp(a), control abnormal heart rhythms, reduce bipolar mood swings, or other important effects.

I liken this to pulling up to a gas station where the sign says gasoline for $1.25. Wow! Can't beat that! You then find out that it's really $1.25 for a half-gallon, or $2.50 a gallon.

In truth, the labeling is accurate; it's just very easy to not notice the two capsule composition.

Why do I need a prescription for Olava?

16. December 2009 William Davis (0)

Imagine this:

What is OLAVA?

Olava is prescription olive oil. It is the purest, highest concentration of olive oil available.

Why Do I Need a Prescription for OLAVA?

Studies show that olive oil contains essential fatty acids, "good" fats that:

--Contain natural compounds your body needs for good health but can't produce on its own.

--Has antioxidants that may provide protection from heart disease.

So, it is common for people to ask why they need a prescription for OLAVA if it is made from a natural ingredient--olive oil. It's time to get the facts about OLAVA. Learn why OLAVA is different from olive oil you can buy at a store.

OLAVA Is an FDA-Approved Medication

OLAVA is the only FDA-approved medicine made from olive oil that's proven, along with diet, to reduce risk for heart disease

The FDA enforces standards to make sure that prescription medications like OLAVA are safe, effective, and quality controlled.

The way OLAVA is manufactured is reviewed and approved by the FDA.

OLAVA uses a 10-step purification process that helps remove lead and other environmental toxins that can be present in olive oil.

Each 1-gram capsule of OLAVA contains 1000 mg of pure olive oil.

The FDA-approved dose of OLAVA is 4 capsules per day. It could take up to 2 tablespoons per day of regular olive oil to provide the same amount of active ingredients proven to lower heart disease risk.

What Else You Should Know About Olive Oil

Regular olive oil has not been approved by the FDA to treat any specific disease like heart disease.

Olive oil doesn't have specific dosing information; it has a food label.

Olive oil does not go through an FDA-approved manufacturing process.

Talk to Your Doctor About OLAVA

If you have very heart disease, you may need a prescription medicine, along with diet, to treat your condition. Talk to your doctor about OLAVA. Print a trial offer to use on your first prescription of OLAVA.

Overweight, hungry, diabetic, and fat-free

15. December 2009 William Davis (52)

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

10. December 2009 William Davis (32)

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

8. December 2009 William Davis (15)

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"

4. December 2009 William Davis (0)

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

2. December 2009 William Davis (0)

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

1. December 2009 William Davis (31)

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.

Pre-diabetes: An explanation for explosive coronary plaque growth

1. June 2006 William Davis (0)

Art's first CT heart scan in March, 2006 yielded a concerning score of 1336. He felt fine--no chest discomfort, no breathlessness, etc.

Art agreed to take the statin cholesterol drug his primary care doctor prescribed. He also agreed to take the fish oil, niacin, and some of the nutritional supplements that we advised. But Art just couldn't bring himself to make the commitment to lose weight.

At the start of his program, Art--at 5 ft. 8 inches--was 40 lbs overweight (212 lb). This was important since his blood sugar wavered in the pre-diabetic range, going as high as 130 mg. (The American Diabetes Assn. defines diabetes as a blood glucose of 126 mg or greater.)

One year later, Art's lipid and lipoprotein values were corrected to perfection. But he still weighed in at a hefty 209 lbs--essentially no change. His blood sugar likewise hovered in the 120's.

I felt Art need to be prodded, so I asked him to undergo another heart scan. His score: 1935--a 600 point increase, or 45%!

Only now has Art begun to comprehend to power of diabetes and pre-diabetes to fan the flames of plaque growth. Recent published data, in fact, show that the majority of recently diagnosed diabetics already have well-established coronary artery disease.

Don't let this happen to you. Do not dismiss diabetic patterns as they will catch up to you. If Art can lose the 30-40 lbs in the abdominal weight that is creating the diabetic pattern, he will likely succeed in stopping plaque growth. Otherwise, it's just a matter of time before his heart attack, stent, or bypass.

Who cares if you're pre-diabetic?

31. May 2006 William Davis (0)

Marta is a smart lady. She's worked in hospital laboratories for the last 23 years and knows many of the ins and outs of lab tests and their implications.

After years of being told that her cholesterol was acceptable, she needed to undergo urgent bypass surgery after experiencing severe breathlessness that proved to be a small warning heart attack at age 57. But this made Marta skeptical of relying on cholesterol to identify heart disease risk.

I met Marta two years after her bypass surgery when she was seeking better answers. And, indeed, she proved to have several concealed sources of heart disease: small LDL particles, Lipoprotein(a), intermediate-density lipoprotein (IDL--a very important abnormality that means she is unable to clear dietary fats from her blood), among others. But she was also mildly diabetic with a blood sugar of 131 mg (normal < or = 100 mg). This had not been previously recognized.

As I'm a cardiologist and our program focuses on reversal and control of coronary plaque, I asked Marta to return to her primary care doctor to continue the conversation about diabetes. She was a bit frightened but followed through.

"Well, you're not urinating excessively. And your long-term measure of blood sugar, hemoglobin A1C, is still normal. I wouldn't worry about it. We'll just watch it."

I guess I should know better. What the poor primary care doctor doesn't know is that pre-diabetes and mild diabetes are potent risks for heart disease. In fact, some of the most explosive rates of plaque growth occur when these patterns are present. It's well established that risk for heart attack in a diabetic is the same as that of someone who's already suffered a prior heart attack--very high risk, in other words.

Marta's primary care doctor's advice would be like inquiring about cancer and the doctor says "Let's just wait until it's metastatic--then we'll start to worry." Of course, this is insane.

Pre-diabetes and mild diabetes should not be ignored or just "watched". Even though the blood sugar itself may not be high enough to endanger you, the hidden patterns underlying your body's unresponsiveness to insulin creates a torrent of hidden coronary risk.

For better answers, Track Your Plaque members can read "Shutting Off Metabolic Syndrome" at http://www.cureality.com/library/fl_dp001metabolic.asp on the www.cureality.com website. ("Metabolic syndrome" is the name commonly given to the constellation of abnormalities associated with pre-diabetes and diabetes.)

Don't get smug!

31. May 2006 William Davis (2)

It may sound silly, but after someone succeeds in stopping their heart scan score from increasing or reduces their score, I warn them to not get smug. Let me explain.

I'll tell you about Jack. I met Jack a few years ago after he had a heart scan at age 39. His score: 1441! A score this high at his age obviously puts him in the 99th percentile. Also recall that a score >1000 carries a 25% annual risk for heart attack.

This captured Jack's attention. At the start, his lipoproteins were disastrous with numerous abnormal patterns. Jack committed to the program. After one year, his lipoproteins were around 80-90% corrected towards perfection. He'd lost 27 lbs, was exercising six days a week, and felt great.

Jack's repeat score one year later: 1107--over a 300 point drop! A huge success. He was ecstatic.

Unfortunately, work and life in general distracted him. Jack allowed himself to drift back to old habits, indulging in fast food 2 or 3 times a week, slacking on exercise such that it became sporadic, half-hearted efforts, and regained 15 lbs. He even failed to show up for appointments and we lost contact for two years.

One day, Jack simply decided to see where he stood, so he got himself another heart scan. The score: 2473--over a doubling from his reduced score.

The message: Long-term consistency is key, even after you've achieved control over your score. Stick with your program--and don't get smug!

Holidays are dangerous!

29. May 2006 William Davis (0)

If you're on holiday from work today, make sure you're not on holiday from your health, too.

Too often, people come back to the office telling me that the holidays simply got out of hand--cookouts, picnics, family gatherings, etc.--and they simply couldn't avoid overeating, overdrinking, sitting around--and gaining 3-5 lbs in a weekend. (Our record is 10 lbs in a weekend!)

I don't want to harp on this issue and ruin your holiday, but I can't stress how important it is that you don't allow this to happen to you. Weight gained in a brief space of time has exceptionally destructive effects. Ever see the movie "Super Size Me"? It's an entertaining and well-done yet graphic portrayal of the damaging effects of rapid weight gain.

Enjoy your time off. Relax, enjoy your family and friends--but continue to pay attention to choosing the right foods, don't overeat, take time out to do something (or several things) physical. It'll pay off hugely in the long run.

More on carotid plaque...

29. May 2006 William Davis (1)

Although not a perfect test, carotid ultrasound is an exceptionally easy and accessible test. Using high-frequency sound, clear images are available for most people.

I say it's not perfect because the way it's done in 2006 makes it a non-quantitative test. It is a qualitative test. In other words, you may find out that there's a 30% blockage ("stenosis"), at the far end of the common carotid artery on the right side. Unfortunately, this gives you an isolated measure of diameter of the plaque compared to the artery. What it does not tell you is what the volume of the entire plaque is. That's a far more accurate measure (and one that is incorporated into your heart scan score, by the way).

Nonetheless, carotid ultrasound is easy, very safe, and available in most hospitals and many clinics. One difficulty: most insurance companies will not allow you to go through a carotid ultrasound scan as a "screening" procedure, i.e., a test just to see if you have a carotid plaque. They will generally pay if you're having symptoms of a stroke or "mini-stroke" (transient ischemic attack, or "TIA"), have an abnormal sound in your carotid ultrasound detected by your doctor (a carotid "bruit"), or some other unusual indications. Sometimes, a resourceful physician will muster up a diagnosis based on something in your history (e.g., left arm numbness, a common and often benign complaint that can also signal stroke).

Another option are the mobile scanners or some hospital services that offer carotid screening, usually for a very modest price. Drawback: Sporadic availability, difficulty in obtaining serial scans, and imprecise reporting since it's viewed as a screening test. But it's better than nothing.

My hope is that, as screening services using safe imaging techniques like ultrasound propagate and increase in direct availability to the public, you'll be able to circumvent the obstacles imposed by your insurance company and even, sometimes, your doctor. But try your doctor first.

Carotid plaque can be shrunk

28. May 2006 William Davis (1)

Rose, a 64-year old woman, just had a 70% carotid blockage identified by a screening ultrasound. When the result was given to her doctor, he prescribed Lipitor and told Rose that an ultrasound would be required every year. She would need carotid surgery, an "endarterectomy", if the blockage worsened.

"Can't I reduce the amount of blockage I have?" asked Rose.

"No. Once you've got it, it doesn't get any better."

Is this true? Once you've got carotid plaque, you can only expect it to get worse and it can't be reduced?

This is absolutely not true. In fact, compared to coronary plaque, carotid plaque is easier to reduce!

Of course, the Track Your Plaque program is designed to help you control or reduce coronary plaque. But, in our experience, people who have both coronary and carotid plaque will show far greater and faster reduction of carotid plaque. Dramatic reductions are sometimes seen. I've personally seen 50-70% blockages reduced to <30% on many occasions.

The requirements to achieve reduction of carotid plaque are very similar to the approach we use to reduce coronary plaque. One difference is that hypertension may play a more important role with carotid plaque and needs to be reduced confidently to the normal range before carotid plaque is controlled.

I find it shocking that the attitude like the one provided by this physician continue to prevail. Unlike coronary plaque, which has a relatively small body of scientific literature documenting how it can be reduced, carotid plaque actually enjoys a substantial clinical literature. Part of the reason is that the carotids are more easily imaged using ultrasound. (Heart structures can be seen with ultrasound, but not the coronary arteries.)

Numerous agents have been shown to contribute to reduction of carotid plaque: statin drugs, niacin, fish oil, the anti-diabetic "TZD" drugs (Actos, Avandia), several anti-hypertensive drugs, vitamin E, pomegranate juice, and several others.

It outrages me to hear stories like this. Rose is not the only one.

Don't accept the flip dismissals or the over-enthusiastic referral for carotid procedures. Insist on a conversation about plaque regression.

Note: Although I am a vigorous advocate of atherosclerotic plaque regression, this does not mean that if you have a severe (70% blockage or greater), or if there are symptoms from your carotid disease, that you should engage in a program of reversal. You must always take the advice of your doctor if your safety is in question.

Vitamin D--A coronary risk factor

27. May 2006 William Davis (1)

Look up "coronary risk factors" in any text and you'll find high cholesterol, smoking, diabetes, and high blood pressure listed. You won't find deficiency of vitamin D listed.

Ask 99% of physicians if a deficiency of vitamin D is a coronary risk factor and you'll get rolling eyes and a sigh.

Yet, in the Track Your Plaque experience, vitamin D is emerging as a very important factor in coronary plaque development. We have observed that there are a substantial number of people whose lipids and lipoproteins are not abnormal enough to fully explain their heart scan score. In other words, there seems to be something else necessary to satisfactorily explain the magnitude of coronary plaque.

I believe that severe vitamin D deficiency is at least one of the most important factors. We've seen many people with blood levels of vitamin in the range of severe deficiency (<20 ng/ml of 25-OH-Vitamin D3) yet bland lipids and lipoproteins.

Correcting vitamin D blood levels to 50 ng/ml also seems to be among the required factors in stopping coronary plaque growth, or stopping your heart scan score from increasing.

Keep your eye on this extremely important and exciting issue. Sadly, it won't be propelled into the media like the conversation about cholesterol or high-tech procedures, since no company stands to profit from it. But you and I don't have to play that game.

Cholesterol is dead!

26. May 2006 William Davis (0)

I saw a patient in the office yesterday. He came to me for an opinion regarding his high heart scan score of 525, putting him in the 90th percentile (5% annual risk of heart attack).

His doctor had been puzzled because his LDL cholesterols had ranged from 110 to 131 mg--actually below average. (The average LDL for the U.S. is 132 mg.) Likewise, HDL was a favorable 63 mg.

Lipoprotein analysis told the story loud and clear. His LDL particle number, a far more precise measure of LDL, was 2448 nmol/l. This means that his true LDL was more like 240-250 mg! (You can get a sense for what the true LDL is from LDL particle number by dropping the last digit: 2448 becomes 244.) Conventional LDL was therefore inaccurate by over 100 mg.

He also had a severe small LDL particle pattern. The cause of his coronary plaque was a large excess of small LDL particles. LDL cholesterol (and total cholesterol, likewise) didn't even hint at this pattern. Nor did his favorable HDL.

Think of LDL particle number as an actual count of LDL particles per volume, e.g., number of particles per cc of blood. This makes it easier to conceptualize. LDL particle number is the measure you get when you have an NMR lipoprotein profile, our preferred method of lipoprotein testing. If this is unavailable to you, apoprotein B is a reasonable second choice, though not as accurate in my view. More info on NMR is available at their website, www.lipoprofile.com.

How to make a $1 million in cardiology

26. May 2006 William Davis (0)

Want to make a $1,000,000 as a cardiologist in the next year? It's easy. All you have to do is:

1) Perform heart catheterizations or other procedures on anybody you can, even if it's not necessary. Perform them even if the patient has no symptoms and the stress test is normal.

2) Perform heart catheterizations if the patient is too timid or ill-informed to object.

3) Insert coronary stents in blockages, even when they're minor and it's not necessary.

4) Turn every heart procedure into a revenue-producing stream by looking for other profit opportunties, such as minor kidney artery blockages.

5) Heart disease is frightening. Scare the heck out of patients by exagerrating the dangers so they'll go through testing and procedures gratefully.

Sound absurd? Well, it would be if these weren't all true.

These are real examples, as awful as it sounds. I've witnessed all these behaviors. Not just occasionally, but with regularity.

Just today, I encountered a colleague who performs heart catheterizations routinely (up to several per day) when any symptom is present and the stress test is entirely normal. This is grossly inappropriate.

Your protection is being better-informed and avoid being sucked into the vast and frightening cardiovascular machine of revenue-yielding procedures. Part of your protection is to get a CT heart scan, then engage in a program of heart disease prevention.

Doctor, do I have lipoprotein (a)?

25. May 2006 William Davis (0)

I met Joyce today for a 2nd opinion. She told me about this conversation she'd had with her cardiologist:

"Doctor, do you think I could have lipoprotein (a)? I read about how it can cause heart attacks even when cholesterol is controlled."

"What does it matter? Even if you have it, there's nothing we can do about it. There's no treatment for it."

Joyce was understandably groping for some means to prevent her coronary disease from causing more danger. At 56, she'd already survived a heart attack that resulted in two stents to her left anterior descending. Around 9 months later, she received a 3rd stent to another artery.

Her doctor had put her on Pravachol and said that was enough. "We know that cholesterol causes heart disease and the Pravachol reduces it. Why do we need to know anything more?"

So Joyce came to me for another view. I explained to her that there are, in fact, several ways to deal with lipoprotein(a). It is, without a doubt, among the more difficult patterns to manage--but not impossible. In fact, we have a growing list of participants in the Track Your Plaque program who have stopped or reduced their heart scan scores.

I continue to be horrified at the level of ignorance that prevails among my colleagues, the cardiologists, and the primary care community. If your doctor gives you advice like this, get a new doctor.

All posts by william-davis

Why healthy can make us fat

13. September 2007 William Davis (0)

Brian Wansink, author of Mindless Eating: Why we eat more than we think (see yesterday's Heart Scan Blog post), also has a Blog. Despite the bland advice offered on much of the Prevention Magazine and website, Wansink's Food Think Blog is a winner.

In a recent post, Wansink quotes a report from Science Daily that described a study he recently published in the Journal of Consumer Research. Wansink's study describes how just applying the label "healthy" to fast food choices increased consumers' calorie intake:

"When we see a fast-food restaurant like Subway advertising its low-calorie sandwiches, we think, 'It's OK: I can eat a sandwich there and then have a high-calorie dessert,' when, in fact, some Subway sandwiches contain more calories than a Big Mac."

In one study, Chandon and Wansink had consumers guess how many calories are in sandwiches from two restaurants. They estimated that sandwiches contain 35% fewer calories when they come from restaurants claiming to be healthy than when they are from restaurants not making this claim.

The result of this calorie underestimation? Consumers then chose beverages, side dishes, and desserts containing up to 131% more calories when the main course was positioned as "healthy" compared to when it was not--even though, in the study, the "healthy" main course already contained 50% more calories than the "unhealthy" one.

"These studies help explain why the success of fast-food restaurants serving lower-calorie foods has not led to the expected reduction in total calorie intake and in obesity rates," the authors write.

Interesting. In fact, I've had many patients say that they eat at Subway or similar chains and choose the "healthy" options. "That's got to be better than a cheeseburger and fries!" Perhaps not. (Of course, you can't leave Subway or other fast food operation feasting on wheat products.)

Wansink can be counted on for some truly fascinating observations into many behaviors that are subconscious but explain at least part of the reason why we're so fat. Though his Blog has a relatively short history of posts, there's lots of great commentary.

Pierre Chandon and Brian Wansink. "The Biasing Health Halos of Fast Food Restaurant Health Claims: Lower Calorie Estimates and Higher Side-Dish Consumption Intentions" Journal of Consumer Research, October 2007.

Outsmarting the enemy

12. September 2007 William Davis (2)

"Everyone--every single one of us--eats how much we eat largely because of what's around us. We overeat not because of hunger but because of family and friends, packages and plates, names and numbers, labels and lights, colors and candles, shapes and smells, distractions and distances, cupboards and containers. This list is almost as endless as it's invisible.

Invisible?

Most of us are blissfully unaware of what influences how much we eat . . . We all think we're too smart to be tricked by packages, lighting, or plates. We might acknowledge that others could be tricked, but not us. That is what makes mindless eating so dangerous. We are almost never aware that it is happening to us."

So opens Brian Wansink's book, Mindless Eating: Why we eat more than we think.

Wansink studies consumer behavior at Cornell University. He's the guy who scrutinizes in excruciating detail why we eat what we do, what factors determine what we eat like food color and smell, the company we keep, product packaging. He works without food industry funding, though there are plenty of researchers who do this sort of research funded by the likes of Kraft, Nabisco, and Kellogg's.

His book is packed full of the conclusions he and his team have come to over the years studying our buying and eating habits. While this information could (and is) be easily used by the food industry to coerce us to eat more and more, understanding many of the concepts Wansink talks about can also open your eyes to their clever tactics.

He especially details how our internal satiety signals fail us when external cues are present that easily trip us up. He talks about one experiment he ran in which soup bowls were rigged with concealed rubber tubes in the bottom that continually replenished the soup as the person consumed it. Thus, with the bowl continually refilled, the eater had no idea how much he or she had consumed. When the quantity of soup eaten from the endless bowl was compared to people eating from standard bowls, there was as much as a three-fold increase in the quantity and calories eaten.

Just be aware that, while Wansink is an expert in consumer eating behavior, he is not necessarily an expert in nutrition. Just as a card shark can show you lots of clever tricks to hoodwink your opponent, he might not be the best person to teach you how to play bridge.

For a great hint at some of the interesting and all-too-human observations Wansink makes, the online Prevention Magazine posted a brief video:

http://link.brightcove.com/services/link/bcpid1155399889/bclid1171884988/bctid1113465050

We might not be able to stop Big Food from selling garbage foods, but we can at least be armed with insight into how we are subconsciously coerced into eating more.

Test Of Scanner Saves A Doctor's Life

11. September 2007 William Davis (5)

Read the story online at http://www.courant.com/news/health/hc-luckydoc.artsep10,0,7572510.story?coll=hc_features_promo

I personally hate these stories, the ones that turn heart scans into drama by describing how someone had a heart scan, then turned out to have so much coronary plaque that they had to have bypass surgery.

But I point this one out because the story is related in an interesting way. It highlights the utter ignorance that operates in heart disease detection.

The story highlights how a 50-year-old, 5 ft 8, 150 lb slender, exercising neurologist underwent a CT coronary angiogram in a newly installed device in a Hartford, Connecticut hospital (not a heart scan) that detected entirely unsuspected severe and diffuse coronary disease. You know the rest: abnormal stress test, heart catheterization, bypass surgery of the hapless doctor-now-patient, followed by grateful patient saying things like "This machine saved my life."

It probably is true. You've seen these stories before. I've witnessed these sorts of headline-makers for the past decade. I remain surprised that it still happens.

The doctor is not some ignorant, uninformed man who can't even fill out his income tax forms. Yet how does a man like this walk around with life-threatening disease and not know it? Why does it still make headlines?

Anyway, despite all my jawing about heart scans and early heart disease detection, many physicians and the public remain in the stone age of heart disease. Even though this neurologist's story made headlines, the many other people who 1) identified their heart disease earlier with a simple heart scan, then 2) took action to put a stop to it, do not make headlines. But that's the way to go.

Why isn't the rest of the story being told? Why was this man's heart disease uncovered only in its late phases? Hartford, Connecticut is not some backwater. I've been there. It's a major city with large hospitals and a University Medical Center. But a professional with presumed knowledge of health and his doctor(s) allowed this to happen?

In other words, this is not a story of success, but of failure--failure to identify coronary disease years earlier when preventive action would have prevented bypass. But that's not such a compelling headline, is it?

As an aside, I'll bet you that this man has lipoprotein(a), a severe small LDL pattern, and severe deficiency of vitamin D. Correct these and it's unlikely he'll need bypass again. But that's kind of boring, isn't it?

The great food industry deception

8. September 2007 William Davis (1)

I'd forgotten what a powerful report Peter Jennings and ABC News produced about the enormous deception perpetrated by the food industry and its effects on health until Dr. Joe Mercola posted the YouTube clips from the report on Mercola.com.

(This is not meant to be an endorsement of everything Dr. Mercola has to say. He says lots of things; I agree with only a fraction of it. But this is a gem.)

Although made in 2004, the report remains every bit as relevant today as it was then. It concerns me deeply that, despite reports like this being broadcast to Americans, the obesity epidemic continues unabated. In fact, it's worse just in the short three years since then.

Be aware of what the food industry is up to. They intensively market high profit margin foods to us--and especially our children--to increase sales. As Jennings points out, the U.S. government (USDA) is, for a variety of reasons both good and bad, complicit with this massive deception. While many media reports continue to focus on lack of exercise as the root cause for the obesity epidemic, it is really the active and purposeful selling of processed junk foods to Americans that is principally to blame.

By the way, how many of these foods proudly boast the American Heart Association Check Mark of approval?

Part 1

Part 2

Part 3

Part 4

Part 5

Dr. Joseph Prendergast and l-arginine

7. September 2007 William Davis (21)

In response to a discussion started by Track Your Plaque Member, Rich, on the Member Forum, I tracked down Dr. Joseph Prendergast, who had posted a video on his unique experiences, both personal and professional, with l-arginine.

Dr. Prendergast describes some of this in a brief webcast. Here, I quote Rich:

“This 90-second video by a Palo Alto physician (internal/endocrine, diabetes specialist) will totally blow your mind.

http://enews.endocrinemetabolic.com/2007/08/16-12-years.html

You will see in the link below that he reversed his personal atherosclerotic disease, diagnosed in abdominal aorta at age 37—completely reversed. He's now much older."

http://www.endocrinemetabolic.com/about/press/larginine.pdf

I contacted Dr. Prendergast to find out more.

Dr. Joseph Predergast is founder of the Endocrine Metabolic Medical Center in Palo Alto, California, focused on providing care for people with diabetes. In addition to the website, he provides Blogs and newsletters, though most of his conversation is about diabetes issues. Dr. Predergast’s website is located at http://www.endocrinemetabolic.com.

I asked Dr. Prendergast several questions about his l-arginine experience. His brief answers are below.

1) What dose of l-arginine have you employed in your patients and why this dose?

The dose is 3 - 6 grams as suggested by the Stanford Cardiovascular Research Department Chairman John Cooke. http://med.stanford.edu/profiles/John_Cooke/

2) I gather that you have preference for specific preparations of l-arginine. Can you say why some preparations seem superior to others in your experience?

I started with pharmaceutical l-arginine from the pharmacy. I gradually began to add components that would augment the power of the l-arginine and have gone through 12–15 different products. I have completely reversed my own very severe atherosclerosis discovered at age 37 and there has been less than 0.05% cardiovascular disease in my endocrine practice in almost 17 years. Both my exams were evaluated with CT technology. I am now using ProArgi9 Plus that includes several anti-aging components and will likely never switch. http://www.synergyworldwide.com/synergycorp/home.aspx

3) Are you employing any other unique practices in your patients to reduce cardiovascular events?

Withdrawing as many prescription drugs as possible.

Interesting. Of course, I also advocate l-arginine as a facilitator of atherosclerotic plaque regression, though I am not as ebullient about its use as Dr. Prendergast.

Instead, I see l-arginine as a method that yields forced normalization of “endothelial dysfunction,” the abnormal constriction and other effects that develop when abnormal lipoproteins and unhealthy food by-products are present in the circulation. Endothelial dysfunction is an inevitable accompaniment of plaque.

However, unlike Dr. Predergast’s experience, despite our use of doses higher than he uses, I have never seen plaque regression just using l-arginine alone. Nonetheless, it’s good to hear that others are seeing at least some positive effects.

By the way, we have also had some positive posts on our Forum about the ProArgi9 product he uses.

Dr. Dwight Lundell on omega-3s and CLA

7. September 2007 William Davis (15)

An interview with Dr. Dwight Lundell, cardiac surgeon and author of the new book, "The Cure for Heart Disease."

Dr. Lundell comes to us with a unique pedigree. He is a cardiothoracic surgeon practicing in the Phoenix, Arizona, area. Despite having performed thousands of coronary bypass operations, including numerous "off-pump" procedures earning him a place in the Beating Heart Hall of Fame and a listing in Phoenix Magazine’s Top Doctors for 10 years, more recently Dr. Lundell has turned his attentions away from traditional surgical treatment and towards prevention of heart disease and.

In particular, Dr. Lundell is a vocal advocate for omega-3 fatty acids from fish oil and conjugated linoleic acid, or CLA.

When I heard about Dr. Lundell’s unique perspectives, I asked him if he’d like to tell us a little more about his ideas. Here follows a brief interview with Dr. Lundell.

You’re a vocal advocate of the role of omega-3 fatty acids from fish oil in heart disease prevention. Can you tell us how you use it?

In my book, I recommend 3 g of fish oil daily. This would normally yield about 1000 mg of EPA and DHA depending on the concentration of the supplement. This is approximately the dose that reduced sudden cardiac death by 50%, and all cause death, by 25% in patients with previous heart attack.

In patients with signs of chronic inflammation such as heart disease, obesity, arthritis, metabolic syndrome or depression or in those patients with elevation of CRP, I would recommend higher doses, 2000 to 3000 mg per day of EPA and DHA. The FDA has approved up to 3400 mg for treating patients with severely elevated triglycerides.

I personally take a 2000 mg EPA and DHA per day because I have calcium in my coronary arteries.

Of course, in the Track Your Plaque program we track coronary calcium scores. Do you track any measures of atherosclerosis in your patients to chart progression or regression?

Carotid ultrasound with measurement of IMT [intimal-medial thickness] has been shown to be a good surrogate marker for coronary disease, as has vascular reactivity in the arm. CT scanning with calcium scoring is a direct marker of coronary disease. CT does not differentiate between stable or unstable plaque but there is no good noninvasive way of doing this.

The dramatic value of CT scan calcium scoring is to demonstrate to people that they actually do have coronary disease and to motivate them to make the necessary lifestyle and nutritional changes to reduce it. CT scan with calcium scoring is a direct way to measure the progression or regression of coronary artery disease. If there is a choice between a direct measurement and indirect measurement, always choose the direct method.

Every patient treated with CLA in my clinic, experienced significant reductions in C-reactive protein. These patients were also on a weight-loss program, so I can't prove whether it was the CLA or the weight-loss that improved their inflammatory markers. In the animal model for arteriosclerosis, CLA has a dramatic effect of reducing and preventing plaque. This has not yet been proven in humans.

Normally, when people lose weight 20% or more of the loss is lean body mass (muscle) this lowers the metabolic rate and frustrates further weight-loss. My patient, from teenagers to retirees, lost no lean body mass and continued to have satisfactory weight-loss when CLA was used as part of the plan.

In reading your book, your use of conjugated linoleic acid (CLA) as a principal ingredient struck me. Can you elaborate on why you choose to have your patients take CLA?

My enthusiasm for CLA is based on:

1) Safety?this is of paramount importance. Animal toxicity studies have been done, as well as multiple parameters measured in human studies, both of these are well reviewed recently in the American Journal of Clinical Nutrition (2004:79(suppl)1132s). CLA, a naturally-occurring substance, is not toxic or harmful to animals or humans. The only negative report is by Riserus in Circulation (2002), where he found an elevated c- reactive protein; however, he used a preparation that is not commercially available and not found in nature as a single isomer.

2) Effectiveness?also critically important. A recent meta-analysis [a reanalysis of compiled data] in the American Journal of Clinical Nutrition (2007; 85:1203-1211) demonstrated the effectiveness of CLA in causing loss of body fat in humans. The study also reconfirmed the safety of CLA.

Since we now know that atherosclerosis is an inflammatory disorder, any strategy that reduces low-grade inflammation without significant side effects would seem to be beneficial in the treatment and prevention of atherosclerosis. CLA not only has antioxidant properties, but it modulates inflammatory cascade at multiple points. CLA reduces PGE2 (in much the same way as omega-3) CLA also has been shown to reduce IL-2, tumor necrosis factor-alpha and Cox–2. It reduces platelet deposition and macrophage accumulation in plaques. It also has some beneficial effect in the PPAR [peroxisome proliferator-activated receptors, important for lipid and inflammatory-mediator metabolism] area.

Part of the effect of CLA may be because it reduces fat mass and thus the amount of pro-inflammatory cytokines produced by fat cells.

I reiterate and fully admit that CLA has not been shown to have any effect on atherosclerosis in human beings. However, the results in the standard animal models for atherosclerosis (rabbits, hamsters,APO-E knockout mice) are very dramatic.

From all I know, it appears that the effective dose for weight loss and the animal studies in atherosclerosis would be equal to about 3 g of CLA per day. The anti-inflammatory properties of CLA seem to work better in the presence of adequate blood levels of omega-3.

I’m curious how and why a busy cardiothoracic surgeon would transform his practice so dramatically. Was there a specific event that triggered your change?

The transition from a very busy surgical practice to writing and speaking about the prevention of coronary disease has not been particularly easy, but it has been very interesting. I can't really point to any specific epiphany, it was a general feeling of frustration that we were not making any progress in curing heart disease, which is what I thought I was doing when I began my medical career.

Of course, I enjoyed the technical advances, the dramatic life-saving things that you do and I did on a daily basis. American medicine is spectacularly good at managing crises and spectacularly horrible at preventing those crises.

The lipid hypothesis is old and tired, even the most aggressive statin therapy reduces risk of heart attack by about 30% in a relatively small subset of people. It's interesting that we're now looking at statins as an anti-inflammatory agent.

Thanks, Dr. Lundell. We look forward to future conversations as your experience with CLA and heart disease prevention and reversal develops!

More about Dr. Lundell's book, The Cure for Heart Disease can be found at http://www.thecureforheartdisease.net.

Note: We are planning a full Special Report on CLA for the Track Your Plaque website in future.

High-tech heart attack proofing

5. September 2007 William Davis (7)

I was reminiscing the other day about what I was taught about heart disease in medical school some 20 years ago.

In the 1980s, the world was still (and remains) fascinated with this (then) novel "solution" to heart disease called coronary bypass surgery. As medical students, we all fought for a chance to watch a bypass operation being performed. And there was lots of opportunity. I was a medical student at St. Louis University School of Medicine, a center that boasted of a busy thoracic surgery service, performing up to 10 bypass operations every day.

Back then, coronary angioplasty was just a twinkle in Andreas Gruentzig's eye, still contemplating whether it was possible to put an inflatable device in the blockages of coronary arteries to re-establish blood flow. Risk detection for heart disease consisted of EKGs, screening for symptoms, detection of heart failure, and tests that are long forgotten in the dust bin of medical curiosities, tests like systolic-time intervals, phonocardiography (using amplified sound to detect abnormal heart sounds), and detailed physical examination. Treatment for heart attack involved nitroglycerin and extended bedrest. Bypass surgery would come after you recovered.

In other words, NONE of the tools we now use in the Track Your Plaque program for heart disease control and reversal were available just twenty years ago. There was no lipoprotein testing, no CT heart scans. Nobody recognized the power of omega-3 fatty acids (although epidemiologic observations were just beginning to suggest that eating fish might be the source of reduced risk for heart attack and cardiovascular death). Vitamin D? Why, that's in your milk so your babies don't get rickets.

So much of what we do today was not available then, nor were they even in the crystal ball of forward-looking people. I certainly had no idea whatsoever that I'd be talking and obsessing today about reversal of heart disease based on what I saw and learned back then.

Things have certainly come a long way and all for the better. The problem is that much of the world is stuck in 1985 and haven't yet heard that coronary disease is a manageable and reversible process. They've been sidetracked by the fiction propagated by the likes of Dr. Dean Ornish, the nonsense of low-fat diets aided and abetted by the food manufacturing industry and the USDA, the extravagant claims of some practitioners and the supplement industry. They haven't yet stumbled on the real-life experiences that are chronicled here in this Blog and the accompanying Track Your Plaque website.

Our program has been criticized for being too "high-tech," involving too many sophisticated measures like small LDL, lipoprotein(a) treatment, vitamin D blood levels. But when you see a woman reduce her heart scan score 63%, or a school principal's score plummet 51%, then that's reward in itself.

It's all about plaque

5. September 2007 William Davis (0)

Just to keep my finger on the pulse of what is being said in the world of heart disease by the media, I subscribe to many publications.

Conversations abound about cholesterol, low-fat diets, now low-carb diets, not smoking, inflammation, etc. No doubt, these all have some importance in the conversation.

But the great majority of discussions fail to identify the one truly crucial factor to identify and track: coronary atherosclerotic plaque.

Sugar for breakfast

2. September 2007 William Davis (17)

We were reviewing Stuart's diet because of his persistent small LDL, low HDL, modestly elevated triglycerides, and blood sugar of 107 mg/dl.

"I've changed my diet, doc. No kidding. We never fry our foods. No butter, no goodies. I don't know what else I can possibly do."

"Okay. Let's review your diet. What did you have for breakfast?"

"Orange juice, a big glass. Gotta get my potassium. Then cereal like Cheerios or Shredded Wheat, sometimes Kashi or Raisin Bran, always in skim milk. Gotta have my one slice of toast, no butter. I'll put some fruit preserves on it. You know, real fruit. Only whole wheat bread, never white. On Sundays, we always go out for pancakes, but now we order only whole wheat."

Many of us have gotten into a peculiar habit: Having what amounts to pure sugar for breakfast. Perhaps there's a little fiber thrown in with it, but many people indulge in breakfasts that are sugar and plenty of it. That's precisely what Stuart is doing: A breakfast that, while it doesn't contain a huge amount of sugar outside of the orange juice, is promptly converted to sugar. If we were to check his blood sugar just after his standard breakfast, it would rise substantially.

This pattern has become deeply ingrained into the American psyche. Some people will act like I've suggested we overthrow the government when I suggest that breakfast cereals need to be eliminated from their lives. We all share memories of Tony the Tiger, the leprechaun on Lucky Charms ("They're magically delicious!), reading the brightly colored boxes often including games and prizes. Breakfast cereals seem as American as apple pie. But the wheat and corn content ensures a big rise in blood sugar, the sort that create small LDL, low HDL, etc.--all the patterns Stuart is showing--and make us fat.

Orange juice? Too much sugar all at once. Get your potassium from whole vegetables and fruits, not from orange juice. (Bananas are another problem source of potassium for similar reasons despite being a whole fruit.)

Toast? Any diabetic who monitors their blood sugar after meals will tell you: Even one slice of bread, ANY bread, skyrockets blood sugar. Add the fruit preserves made with sugar syrup and it's doubly worse.

Pancakes? Even if made with plenty of fiber, blood sugars go absolutely berserk after a meal like this, especially if maple syrup is added.

In other words, the seemingly healthy breakfast Stuart eats guarantees that he fails to control all his patterns that contribute to his coronary plaque growth.

After I pointed out Stuart's dietary faux pas, he asked, "Then what the heck can I eat?"

"There's actually lots of good choices: Eggs (preferably free-range, if available, or the 'omega-3' enriched) or Egg Beaters; oat products, but true oat products like slow-cooked oatmeal, or the best of all, oat bran, used as a hot cereal; ground flaxseed as a hot cereal with added fruit, berries, nuts; a handful of raw almonds, walnuts, pecans; some cheese, preferably traditional fermented cheese and not processed; low-fat cottage cheese; low-fat yogurt that you flavor yourself with berries and nuts; raw seeds like sunflower and pumpkin.

"Try and save some of your dinner foods for breakfast. For instance, save some green peppers and onions from your salad and put it in your scrambled eggs along with some olive oil. Save some of the chicken and add it to your breakfast. Save some of the cooked vegetables and have them as they are. You'll be surprised how filling dinner foods can be when eaten for breakfast."

It's not that tough. But Stuart and many other people need to break the hold that the food manufacturers have created. If you're hoping to seize hold of your heart scan score, get rid of the sugar foods in your morning, even the ones cleverly disguised as healthy.

The Low-Carb Man

31. August 2007 William Davis (4)

If ever there was an enthusiastic disciple of deceased Dr. Robert Atkins of Atkins' Diet fame, it's Mr. Jimmy Moore.

Jimmy tells the story of how he was transformed by the Atkins' approach, losing 180 lbs in the course of one year. He continues to develop this conversation, in many ways elaborating on the conversation in more sophisticated ways than even Atkins did in his lifetime.

Though we've agreed to disagree on some points of nutrition, Jimmy and I had a recent discussion about heart disease, the mis-guided ways of conventional cardiac care,and the evils of processed carbohydrates. We do differ on the role of saturated fat in heart disease and health, but beyond that difference I was impressed (reading his Blog and listening to his many webcasts) with his level of understanding of the issues. Jimmy is not some over-enthusiastic dieter. He has a grasp of the issues that exceeds that of 99% of my colleagues.

If you are interested in reading our discussion or just perusing a really fun, informative Blog/website, go to LivinLaVidaLowCarb.com. The interview is posted at:

http://livinlavidalocarb.blogspot.com/2007/08/davis-wanna-cut-plaque-in-your-arteries.html

See Jimmy Moore's before and after pictures at http://livinlavidalocarb.blogspot.com/2005/07/my-before-pictures.html. He's quite an entertaining read.