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.

Wheat-free 2007


Long ago, most of us made the change of reducing saturated fat in our diet. Few people now rely on butter (despite the idiotic butter vs. margarine controversy), full-fat dairy products, fried foods, and greasy meats. That's a healthy change, since saturated fat has conclusively been tied to various cancers, high blood pressure, rise in LDL, and is calorie-dense.

But if there were just one change you were to make beyond a reduction in saturated fat, a change that would translate into dramatic health benefits, it would be a drastic reduction, even elimination, of wheat products.

People do indeed eat enormous quantities of wheat flour-containing products. U.S. per capita consumption of wheat flour was 110 pounds in the early 1970s, and rose to 141 pounds in 1991. It's even higher now. 20% or more of most people's caloric intake every day is provided by wheat flour products.

Wheat containing foods are tasty and convenient. Witness the popularity of bagel shops, the goodie counter at Starbuck's, the proliferation of crackers, breads, and breakfast cereals at the grocery store. Patients are horrified when I suggest that they find a substitute for the sandwiches they eat every day. Even Mom said they were okay!

You're unlikely to hear much about this from the popular press. The wheat industry is enormous and exerts extraordinary clout, just like the drug industry. Texas alone farms 6 million acres of wheat, yielding over $2 billion for the state's economy. The "wheat chain" is complex and far-reaching: growers, processors, food manufacturers, the transportation industry, retailers, chemical producers, and on and on. Wheat futures are traded on the Chicago Board of Trade. Wheat is a major export industry for the U.S.

Of course, these are not evil people, intent on corrupting your health. In fact, most of them are probably working under the perception that they are raising a healthy product. The point is that the notion that wheat is healthy is deeply entrenched in the minds and economy of the U.S. Don't expect to hear unbiased commentary on the health effects of wheat products from most media sources.

What can you expect if you sharply reduce or eliminate wheat? The majority of people:

--Feel like a cloud has been lifted from their thinking.
--Don't experience the afternoon blah or tired feeling after lunch.
--Lose weight, sometimes substantial quantities.
--Raise HDL.
--Reduce small LDL.
--Reduce triglycerides, particularly if they start >100 mg/dl.
--Reduce blood sugar.

The reduction in small LDL can be especially impressive.

For most people, reducing or eliminating wheat is a sacrifice, a major change in food choices and even a loss of convenience. But the health benefits for most people can be dramatic.

Is vitamin D a "vitamin"?

Vitamins are crucial participants in the body's reactions and are obtainable from food. Vitamin C, for example, comes from citrus fruits and vegetables. Vitamin K comes from green vegetables. The B vitamins are found in meats, soy, dairy products, and grains. Vitamin A comes from carrots, squash, and other orange and green colored vegetables.

How about vitamin D? What foods contain vitamin D? The list includes:


Food International Units(IU) vitamin D per serving

Cod liver oil, 1 Tablespoon 1,360
Salmon, cooked, 3½ ounces 360
Mackerel, cooked, 3½ ounces 345
Tuna fish, canned in oil, 3 ounces 200
Sardines, canned in oil, drained, 1¾ ounces 250

Milk, nonfat, reduced fat, and whole, vitamin D fortified, 1 cup 98
Margarine, fortified, 1 Tablespoon 60
Pudding, prepared from mix and made with vitamin D fortified milk, ½ cup 50
Cheese, Swiss, 1 ounce 12

Ready-to-eat cereals fortified with 10% of the DV for vitamin D, ¾ cup to 1 cup servings (servings vary according to the brand) 40

Egg, 1 whole (vitamin D is found in egg yolk) 20
Liver, beef, cooked, 3½ ounces 15

(Modified from the Office of Dietary Supplements, National Institutes of Health)


You'll note that the only naturally-occurring food sources of vitamin D are the modest quantities in fish, egg yolks, and liver. All the other vitamin D-containing foods like cereal, milk, and other dairy products have vitamin D only because humans add it.

It takes me (personally) 6000 units of vitamin D per day to bring my blood level to an acceptable 50 ng/ml. To obtain this from eating salmon, I would have to eat 58 ounces, or 3 1/2 pounds of salmon--every day. Or, I could eat 30 cans of tuna fish.

If I didn't want to eat loads of fish every day, I could drink 60 glasses of milk every day. After I recovered from the diarrhea, my vitamin D might be adequate, provided the milk indeed contained the amount stated on the label (which it often does not when scrutinized by the USDA).

If vitamin D is a vitamin, how are humans supposed to get sufficient quantities? I don't know anybody who can eat 3 1/2 lbs of salmon per day, nor drink 60 glasses of milk per day. But aren't vitamins supposed to come from food?




The problem is that vitamin D is not really a vitamin, it's a hormone. If your thyroid hormone level was low, you'd gain 20, 30, or more pounds in weight, your blood pressure would skyrocket, you'd lose your hair, become constipated, develop blood clots, be terribly fatigued. In other words, you'd suffer profound changes. Likewise, if thyroid hormone levels are corrected by giving you thyroid hormone, you'd experience profound correction of these phenomena.

That's what I'm seeing with vitamin D: restoration of this hormone to normal blood levels (25-OH-vitamin D3 50 ng/ml) yields profound changes in the body.

If there's one thing that I've come across lately that packs extraordinary potential to help us in reducing heart scan scores, it's the vitamin--sorry, the hormone--cholecalciferol, or D3.

Heart scan curiosities 3


Note the shape of the chest in this 64-year old man. The front of his chest (upper portion of scan) is concave. In other words, if you were looking at this man (shirtless, of course) face to face, his chest would bow inward, rather than the usual outward configuration. The official name for this is "pectus excavatum".





Compare this to the normal chest in the second image, in which the chest is convex. Face to face, the chest would bow slightly outward.















What does it matter? The pectus excavatum in and of itself has no importance, just a curiousity. (I personally find this surprising, given the fact that the heart actually appears squashed by the sternum, or chest wall.) However, it is commonly associated with a "floppy" mitral valve (also called mitral valve prolapse), a common congenital disorder of the mitral valve often accompanied by a slender build, loose joints, and even a nervous disposition. Occasionally, in its more severe forms, the aorta is also enlarged. (This man's aorta is not enlarged.)

So, while we can't actually visualize the mitral valve by a CT heart scan, we can surmise that he likely has a floppy mitral valve, is slender, is probably a nervous sort, and has long limbs with loose joints. He probably required braces as a child, since many people have a phenemenon of "crowded teeth". The roof of his mouth, or hard palate, probably unusually high up in the mouth. He probably has a "weak chin", meaning a less prominent protuberance of his chin. His fingers and toes are likely unusually long and slender.

It could mean that some attention and exploration of how floppy his mitral valve might be could be useful, e.g., an ultrasound or echocardiogram. He might even require oral antibiotics at the time of any oral or some gastrointestinal procedures, since floppy valve are more susceptible to blood infections when potentially "dirty" orifices are instrumented.

All that from a heart scan!

Gratitude

The holidays and the end of the year may be a good time to reflect on how grateful we should be for having the freedom to discuss the ideas we share on this Blog, the Track Your Plaque website, online and offline.

Although I rant and rave against the status quo in heart disease, the shameful profiteering of my colleagues and hospitals, the cut-throat marketing practices of drug and device manufacturers, I am truly grateful that, in the U.S., I have the extraordinary freedom to say these things. You have the freedom to agree or disagree and none of us pays a price for truth.

I've been reflecting myself a great deal on this idea of happiness and gratitude being a critical component of coronary plaque regression and dropping your heart scan score. (See The Heart Scan Blog from earlier this week.) The more I think about this, the more I think that it is indeed true: Harboring anger and resentment, regrets, irritability, all those petty emotions that most of us know are not good for us, erode our chances for success in dropping your heart scan score.

We could rationalize it this way: Anger and other negative emotions are adrenaline-driven states, also characterized by activation of the "sympathetic" nervous system. (Despite its name, the sympathetic system is not sympathetic, as in compassionate; its the "fight-or-flight" activator that accelerates heart rate and blood pressure.)

Happiness, contentment, and gratitude are "parasympathetic" states characterized by slower heart rates, deeper respiration, greater variation in beat-to-beat heart rates (a powerful predictor for health and the basis for the HeartMath program of Lew Childre), lower blood pressure, and even a subtle change in brain waves. In other words, happiness is not just a mental and emotional state, it is a constellation of physical phenomena.

Even though I pick on Dr. Dean Ornish for his stubborn adherence to the outdated low-fat mantra, I do agree with him on the value of happiness. His book, Love and Survival, articulates this concept. Ornish has even said on several occasions that it wasn't the diet that was most important but the connection and warmth that was created by the comraderie created by participation in the Ornish Program group sessions.

I am personally grateful that the concepts I promote are gaining a following and that I can say so without fear of prosecution. I am grateful that Track Your Plaque followers are not just sharing our concepts, but obtaining genuine and powerful health advice that will help keep them home and healthy, away from hospitals, procedures, and the dangers of heart disease.

I hope you share in my gratitude and are thankful for all the truly wonderful things that surround us. I wish you all a wonderful holiday and long, healthy life filled with gratitude.

A Track Your Plaque failure

We recently had a man suffer a heart attack after beginning the program. Let me tell you the details.

Jerry's heart scan score 781, age 53. Multiple lipoprotein abnormalities: HDL 32 mg/dl, triglycerides 279 mg/dl, nearly all of his LDL was in small particles with an "effective" LDL (LDL particle number), and very high IDL. So Jerry added fish oil 6000 mg per day, niacin, and vitamin D to the statin drug prescribed by his primary physician. Jerry added oat bran, ground flaxseed, and tried to eat fish at least once per week.

However, Jerry continued to smoke. He'd smoked for 40 years (!), up to 2 packs per day, and just reasoned that it was too late to quit. He also continued to indulge in the packaged, processed foods that were part of his convenience story business.

Jerry's stress test was normal--no chest pain, normal EKG, normal images of blood flow, though he was somewhat breathless, likely from his lung disease from smoking.

Two months into his program, he abruptly experienced severe crushing pain in his chest. Because he was traveling, he ended up in a small local hospital. A failed angioplasty led to urgent coronary bypass surgery.

Jerry's alive. Now he's a non-smoker. He's got the pursed lips and peculiar breathing pattern that smokers get, but he's breathing.

Lesson: In the face of the most powerful program for heart disease known, it can still be overpowered by Twinkies, Hoho's, pretzels, chips--and cigarettes.

The new year is approaching. Be grateful for another year of healthy life and commit to a new year of even greater health. If you're a smoker, there's no choice: you've got to quit.

Are you more like a dog or a rabbit?

Dr. William Roberts, editor of the American Journal of Cardiology and cardiovascular pathologist, is a perennial source of clever ideas on heart disease.
In a recent editorial, Dr. Roberts comments:








"Because humans get atherosclerosis, and atherosclerosis is a disease only of herbivorers, humans also must be herbivores. Most humans, of course, eat flesh, but that act does not make us carnivores. Carnivores and herbivores have different characteristics. (1) The teeth of carnivores are sharp; those of herbivores, flat (humans have some sharp teeth but most are flat for grinding the fruits, vegetables, and grains we are built to eat). (2) The intestinal tract of carnivores is short (about 3 times body length); that of herbivores, long (about 12 times body length). (Since I am 6 feet tall my intestinal tract should be about 60 feet long. As a consequence, if I eat bovine muscle [steak], it could take 5 days to course through those 20 yards.) (3) Body cooling for carnivores is done by panting because they have no ability to seat; although herbivores also can pant, they cool their bodies mainly by sweating. (4) Drinking fluids is by lapping them for the carnivore; it is by sipping them for the herbivore. (5) Vitamin C is made by the carnivore's own body; herbivores obtain their ascorbic acid only from their diet. Thus, although most human beings think we are carnivores or at least conduct their lives as if we were, basically humans are herbivores. If we could decrease our flesh intake to as few as 5 to 7 meals a week our health would improve substantially."



You can always count on Dr. Bill Roberts to come up with some clever observations.

I think he's right. Some of the most unhealthy people I've known have been serious meat eaters. Most of the vegetarians have been among the healthiest. (I say most because if a vegetarian still indulges in plenty of junk foods like chips, crackers, breakfast cereals, breads, etc., then they can be every bit as unhealthy as a meat eater.)

Should you become a vegetarian to gain control over coronary plaque and other aspects of health? I don't believe you have to. However, modern livestock raising practices have substantially modified the composition of meats. A steak in 2006, for instance, is not the same thing as a steak in 1896. The saturated and monounsaturated fat content are different, the pattern of fat "marbling" is different, the lean protein content is different. Meat is less healthy today than 100 years ago.

Take a lesson from Dr. Roberts' tongue-in-cheek but nonetheless provocative thoughts. Pardon me while I chew on some carrots.

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.