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.

I'll supply the tar if you supply the feathers

30. November 2009 William Davis (13)
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

28. November 2009 William Davis (13)
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

27. November 2009 William Davis (11)
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

25. November 2009 William Davis (17)
In the ongoing debate over whether it's fat or carbohydrate restriction that leads to weight loss and health, here's another study from the Oxford group examining the postprandial (after-eating) effects of a low-fat vs. low-carbohydrate diet. (Roberts R et al, 2008; full-text here.)

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

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

Blood was drawn over 6 hours following the test meal.




Roberts R et al. Am J Clin Nutr 2008

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

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

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

Vitamin D and autism

17. August 2007 William Davis (1)
This has nothing to do with coronary plaque reversal, nor directly with the Track Your Plaque program, but I found Dr. John Cannell's discussion about the possible relationship between vitamin D and autism so compelling that I thought I just had to pass it on.

So, below are Dr. Cannell's latest thoughts. He takes some criticisms along with praise. I think we owe him a lot for continuing to doggedly promote the benefits of vitamin D.




Vitamin D Newsletter


August, 2007



Dear Dr. Cannell:

I saw an article from a Toronto newspaper about autism and vitamin D. I am currently searching for a vitamin D specialist in the Washington D.C. area to perform a medical work up on my daughter to look for vitamin D-related disorders. The reason I am in search of a vitamin D specialist is that I believe I have stumbled upon a complex relationship in my daughter involving her foot pain, vitamin D, and her autism.

In April 2006, a few weeks after my 3-year-old profoundly autistic daughter began refusing her daily PediaSure drink, she began having excruciating foot spasms lasting from 10-30 minutes at a time, several times a week. She would throw herself on the floor, curl her toes, slam her heels against the floor, and rub the tops of her feet against the carpet, all while screaming the entire time. These were horrible for her to endure, and horrible for my wife and myself to watch. This went on for a year.

From what I read, the symptom was perhaps like foot spasms associated with carpopedal syndrome or tetany. But her blood work did not support that at all. Calcium level was normal (10.2 mg/dL); 25-Hydroxy-vitamin D low (23.5 ng/ml); 1,25 dihydroxy-vitamin D normal (24.7). Despite some vitamin D deficiency, I was assured by medical professionals that nothing supported a vitamin D cause of these particular spasms, so vitamin D was dismissed. Because her calcium level was normal, they told me she did not have tetany, and vitamin D could not be the cause of the pain.

All medical consultants were stymied. I made another research effort and found a 2003 article on WebMD that stated vitamin D has been found to have some link to basic, unexplained muscle and bone pain. By chance, vitamin D was the next supplement we had at home to begin giving my daughter to treat her autism. So, in April 2007 we began giving my 4 year-old profoundly autistic daughter Vitamin D supplements. Her foot spasms which had plagued her for a year diminished within days and disappeared within three weeks. She has not had a spasm in over two months.

In addition, we noted clear improvements in her autistic condition which appear to be from the vitamin D supplements. Eye contact went from zero to fantastic. Her vocalizations increased markedly (still only babbling; she remains completely nonverbal). She appears even happier than previously (she has always been a somewhat happy child). (Please note that my wife and I have tried many dietary supplements over the past 1.5 years guided by a doctor and dietician who both specialize in autism. We honestly state that this is the only thing that has ever had a positive effect on my daughter. We have seen nothing else work.)

My daughter and vitamin D have a complicated relationship. By all counts, looking at her lab work and general condition, vitamin D should have played no role in those excruciating foot fits. And yet it is apparently exactly what is involved in them. And, my wife and I believe at the same time her autistic condition has improved from the vitamin D. The foot fits and her autism appear linked; it was not just a coincidence that this autistic child has those mysterious foot spasms, and the link appears to be vitamin D.

And so I wonder if this is just the tip of the iceberg, if perhaps there is more to know about my child's relationship with vitamin D and what that might mean for her autism. Does she have a specific vitamin D-related disorder? If so, might direct treatment of it also improve her autism further? These are the questions I would like to pose to a vitamin D specialist who could perform a medical work up on my daughter. Please let me know if you know of anyone in the Northern Virginia/Washington DC area. Also, where is the best place to get vitamin D? Thank you for your time.

Sincerely,
Paul, Washington, D.C.



Dear Paul:

I know of no such specialist in the Washington area, indeed no vitamin D/autism expert exists in the world. As far as a specific "vitamin D disorder," linking her spasms, autism, and vitamin D, the world's English language medical literature contains no description of such a disorder. From your daughter's case, it sounds as if PediaSure was her only regular source of vitamin D. If so, her spasms began two weeks after stopping the small amount of vitamin D contained in PediaSure. The spasms continued for a year, ending a few days after you started giving her vitamin D again, this time in the form of a supplement. Several weeks after restarting vitamin D, both you and your wife noticed an improvement in her autism. To my knowledge, this "case report" - your daughter's - is the first ever published.

As no medical literature has ever been published on any of this, all you can do is give her enough vitamin D to get her 25-hydroxy-vitamin D, known as 25(OH)D, into high normal ranges and then wait and hope. Vitamin D's extraordinary mass-action pharmacology implies that simply providing more substrate ([25(OH)D] will help children with low enzyme activity produce more activated vitamin D (calcitriol) in their brains. The vitamin D theory of autism is not simply that vitamin D deficiency in gestation or early childhood causes the disorder. Instead, the theory holds that a quantitative or qualitative abnormality exists in the enzyme system that activates vitamin D.

It could as simple as the normal variation in the enzyme, an enzyme whose activity would vary in a normal or Gaussian distribution, much like height. Some people are tall, some are short, most are in the middle. The same may be true of the enzyme that forms activated vitamin D (calcitriol), some children have a lot of enzyme and some only a little; most are in the middle. As the substrate [25(OH)D] the enzyme metabolizes fell over the last 20 years with sun-avoidance, more and more children on the low end of the enzyme curve are effected by marginally low 25(OH)D levels, explaining both its genetic basis and exploding incidence.

At this point, all your daughter needs is a physician willing to periodically measure her 25(OH)D. Then you can safely supplement your daughter with doses higher than the current Upper Limit for children (2,000 IU/day). You did not tell me your daughter's weight but, assuming she weighs about 30 pounds, even without 25(OH)D blood tests, you can safely give her 50 mcg/day which is 2,000 IU per day. In fact, the U.S. government says this dose is safe for children over the age of one. Life Extension Foundation sells 250 of the 1,000 IU capsules for about ten bucks with powdered vitamin D inside. The powder is tasteless and dissolves easily in juice. Bio Tech Pharmacal, of Fayetteville, Arkansas, told me they were going to be making a 1,000 IU capsule. Or you can get 1,000 IU capsules in a pharmacy or at Costco and crush them. A Canadian firm is now making vitamin D liquid, called Ddrops, with 1,000 IU per drop, but their mail order web site is not yet easily accessed. Beware of cod liver oil; do not use it because vitamin A inhibits the actions of activated vitamin D, and due to the potential for low-grade vitamin A toxicity.

Remember, more and more researchers now believe autism is a progressive, inflammatory, disorder. That is, the inflammation probably progressively destroys brain tissue as the child ages. As I said in my recent paper, I think there is a chance that vitamin D may have a treatment effect in young autistic children if given in adequate doses, due to its anti-inflammatory properties, and its ability to upregulate glutathione, the master antioxidant that also chelates (binds) and then helps excrete heavy metals like mercury. Unfortunately, I see no way, even if the vitamin D/autism theory turns out to be true, that vitamin D can regenerate brain tissue. However, if it stops the inflammation, and cell death, the brain could then begin to develop and learn. These are big ifs. However, you have nothing to lose by trying, the worst that will happen is that it will not help and vitamin D will be added to the long list of false-hope treatments.

Actually, there is a worse possibility. Say the parents of a three-year-old autistic child decide today that vitamin D is nonsense, another false hope, and that I'm a quack. They decide not to give vitamin D supplement their autistic child, who is probably - like your child - vitamin D deficient. Then, it turns out five years from now that scientific evidence shows vitamin D does indeed help. By that time, the child will be eight and will have suffered additional, irreparable, brain damage. In my mind, that is more tragic than another false hope.



Dear Dr. Cannell:

After that article appeared in the Toronto paper, I started my four-year-old son on 1,000 IU of vitamin D two weeks ago. So far the only thing I noticed is that after about ten days, he didn't seem so miserable. The thing that has always broken my heart is that look of sadness and suffering on his face. After about two weeks of vitamin D, I noticed he seemed less miserable. I wouldn't say he looks happy now but that look of misery seems to be gone. Will it come back? I'm not sure I can take it if it comes back. What else might happen? Also, last summer we noticed he seemed to get better, but then he got worse in the fall. We never thought about it until we read about vitamin D.

Susan, Toronto, Canada




Dear Susan:

I don't know. I think all parents have had their heart pierced by that look at one time or another. I would advise increasing the dose to 2,000 IU per day, making sure it is cholecalciferol and not ergocalciferol, and having your doctor order a 25(OH)D every two months to see if he needs higher doses. You want to get his blood level up to between 50 ng/ml and 80 ng/ml (In many countries outside of the USA, that would be reported as between 125 and 200 nmol/L.) and keep it there, summer and winter, and that may take more than 2,000 IU/day in the winter. If vitamin D has a treatment effect, it will take many months to see its full effect. As you noted, if the theory is correct, autistic children who spend time outdoors in the summer should show some seasonal improvements - if they don't wear sunblock and they expose enough of their skin to generate significant amounts of vitamin D.



Dear Dr. Cannell:

I resent you calling autism a tragedy. My son is not a tragedy and I'm glad he was born and is in our lives. He is our joy. Autism is not a tragedy.

Emma, London, England.




Dear Emma:

I'm glad he is your joy and I believe you. I'm new to the autism field and was not aware how much thought and speech control exists in the discussion of the disease. Nevertheless, I have a few politically incorrect questions. If autism is a joy, I assume you would like other parents to have an autistic child? If autism is such a joy, why is there a huge industry forming to prevent and treat it? At the risk of sounding insensitive - apparently one of the most serious charges leveled in the autism debate - autism is a tragedy. As I pointed out in my paper, research shows that having an autistic child, puts the family under more emotional stress than having a child with a fatal illness.



Dear Dr. Cannell:

Who are you to write an article on autism? You didn't even publish it in a medical journal. You are not with a university. You have not published very much. You have no expertise on autism. No autism experts support your theory. There is no evidence to support the theory. Shouldn't you leave this to experts before you give parents more false hopes?

Mary, Trenton, New Jersey.



Dear Mary:

You are right, I am a nobody; just ask my ex-wife. In the Toronto Globe, I explained why I have not yet submitted the paper. As far as giving false hopes, I've thought about that charge. Right now, regardless of what advocacy groups say, autism is rather hopeless. That is, no treatment, including vitamin D, has been shown to materially affect the clinical course of autism. As a psychiatrist, my observation is that people would rather live with a false hope than with no hope.

Furthermore, if autistic children began taking vitamin D, the worse that can happen is that a period of false hope will followed by dashed hopes and then parents will be back to hopelessness. In the meantime, they will have made their child vitamin D sufficient. Vitamin D deficiency is a serious problem in childhood.
Postgrad Med J. 2007 Apr;83(978):230-5.

The Telegraph, Why is Vitamin D So Vital?

As far as the theory having no support from experts, Dr. Richard Mills, research director of the National Autistic Society in England, was quoted in the Telegraph article on the autism/vitamin D theory: "There has been speculation in the past about autism being more common in high-latitude countries that get less sunlight and a tie-up with rickets has been suggested - observations which support the theory."

Finally, you said there is no evidence to support the theory. I assume you meant there is no proof. The first statement is absolutely false, the second absolutely true. As I detailed in my paper, there is a lot of evidence to support the theory. In fact, if anyone can come up with an autism fact, that the theory cannot explain, I'd like to know about it. Even the announcement of a link between television viewing and autism supports the theory. Furthermore, the TV/autism link is actually evidence of a treatment effect. That is, if autistic children who play outside in the sunshine more - watching less TV - have less severe illness, it may be due to the Sun-God, who bestows her precious gift of calcitriol into the brains of children playing outside in her sunlight but not into the brains of children watching TV inside in the darkness.
Natl Bur Econ Res Bull Aging Health. 2007 Winter;(18):2-3.

As far as proof the theory is true, there is, of course, none. In medicine, proof means randomized controlled human trials, the gold standard for proof. However, proof is the last step, not the first. First comes evidence, then comes a theory, then comes researchers disproving those theories. It works that way. Sometimes we never get to the last step, proof. For example, please point me to a single randomized controlled human trial proving cigarette smoking is dangerous? Instead, the convincing evidence of smoking's dangerousness lies in epidemiological studies, not randomized controlled trials. Proof, or disproof, of the autism vitamin D theory will take years, years during which young autistic brains will continue to suffer irreparable damage. Perhaps vitamin D' powerful anti-inflammatory actions will help prevent that damage, perhaps not.

It's something of a Pascal's wager, betting on vitamin D instead of the existence of God, risking your child's brain instead of eternal damnation. "If you believe vitamin D helps autism and turn out to be incorrect, you have lost nothing -- but if you don't believe in vitamin D and turn out to be incorrect, your child will suffer irreparable brain damage."

John Cannell, MD
The Vitamin D Council
9100 San Gregorio Road
Atascadero, CA 93422

This is a periodic newsletter from the Vitamin D Council, a non-profit trying to end the epidemic of vitamin D deficiency. If you don't want to get the newsletter, please hit reply and let us know. This newsletter is not copyrighted. Please reproduce it and post it on Internet sites. Remember, we are a non-profit and rely on donations to publish our newsletter and maintain our website.

Michael Pollan Podcast

15. August 2007 William Davis (3)
I just found this great podcast of an April, 2006 National Public Radio (NPR) interview with Omnivore's Dilemma author, Michael Pollan:

Author Michael Pollan: 'The Omnivore's Dilemma'

available at http://www.npr.org/templates/story/story.php?storyId=5342514

The Science Friday segment is a great encapsulation of all the fascinating spins this wonderfully insightful author has on human eating habits and the developing distortions of food choices, much magnified by the food manufacturing industry.

One of my favorite comments from Pollan: "The USDA should be called "The Department of Corn," referring to the ubiquitous dissemination of corn products into livestock and human foods that has increasingly led to the enormous health problems we're all facing in 2007.

Are you addicted to fructose?

13. August 2007 William Davis (1)
Try a little experiment:

Side by side, try a yogurt made with fructose or high fructose corn syrup as one of the first ingredients on the label along with a yogurt made without fructose.

Yoplait and Dannon brands, for instance, fit the bill for fructose. Several brands do not use fructose products. Many of these are the unflavored or unsweetened versions. You may therefore have to add some blueberries, strawberries, or some other fruit for some flavor. ( I doubt that you would add high fructose corn syrup.) Add nuts, seeds, flaxseed, or oat bran to either.

Many people who do this will notice a peculiar effect: The fructose or high fructose corn syrup containing product is, to most, delicious. It also triggers a desire for more. You can't have just one--you've got to have another, or you've got to eat something else.

The non-fructose containing product is more likely to generate satiety, a feeling that you've had enough.

If you experience this effect, the solution is simple: avoid fructose and high fructose corn syrup. I believe that the most worrisome health effect of fructose is this hunger-increasing aspect, difficult to document, perhaps impossible to measure, but a great boon to the food industry who practice an "eat more" philosophy to increase revenues year after year.

Perhaps you will also see weight drop (since you will be more satisfied), see triglycerides drop (since fructose raises triglycerides), and maybe obtain all the downstream benefits of reduced triglycerides (higher HDL, less small LDL, less VLDL, more rapid clearance of post-prandial lipoproteins).

Most people who follow this idea gain better control over appetite, lose weight, and do better in health, including in their Track Your Plaque program.

Chicken Little

11. August 2007 William Davis (1)
Clinical studies can be designed in a number of ways. The ease and cost of these studies differ dramatically, as does the confidence of the findings.

The most confident way to design a clinical study is to tell neither the participants nor the investigator(s) what treatment is being offered, then to administer treatment or placebo. Neither the people doing the research nor the participants know what they are receiving. Of course, there needs to be some way to find out what was given at the end of the study in order to analyze the outcome.

This is called a “double-blind, placebo-controlled” clinical study. While not perfect since it tends to examine a treatment phenomenon in isolation (e.g., the effects of a single drug in a select group of people), it is the best sort of study design that is most likely to yield confident results, both negative and positive. This sort of design is followed, for instance, for most prescription drugs.

There are pitfalls in such studies, of course, and some have made headlines lately. For instance, beyond tending to examine single conditions in a select group of participants, a double-blind, placebo-controlled study can also fail to uncover rare effects. If a study contains 5000 participants, for instance, but a rare complication develops in 1 person out of 20,000, then it’s unlikely such an ill-effect will be observed until larger numbers of people are exposed to the agent.

Another pitfall (though not so much of study design, but of human greed) is that study outcomes that are not favorable can be suppressed by simply failing to publish the results. This has undoubtedly happened numerous times over the years. For this reason, a registry has been created for all human clinical trials as a means to enforce publication of outcomes, both favorable and unfavorable.

Despite its weaknesses, the double-blind, placebo-controlled study design remains the most confident way to show whether or not some treatment does indeed yield some effect. It is less prone to bias from either the participant or the investigator. Human nature being what it is, we tend to influence results just to suit our particular agenda or interests. An investigator who knows what you are given, drug or placebo, but owns lots of stock in the company, or is hoping for special favors from the pharmaceutical company sponsor, for instance, is likely to perceive events in a light favorable to the outcome of the study.

Now, most studies are not double-blind, placebo-controlled studies. These are notoriously difficult studies to engineer; raise lots of ethical questions (can you not treat a person with an aggressive cancer, for instance, and administer a placebo?); often require substantial numbers of participants (thousands), many of whom may insist on payment for devoting their time, bodies, and perhaps even encountering some risk; and are tremendously expensive, costing many tens of millions of dollars.

For this reason, many other study designs are often followed. They are cheaper, quicker, may not even require the active knowledge or participation of the group being studied. That’s not to say that the participants are being tricked. It may simply be something like trying to determine if there are more heart attacks in people who live in cities compared to rural areas by comparing death rates from heart attack from public records and population demographic data. Or, a nutritional study could be performed by asking people how many eggs they eat each week and then contacting them every month for 5 years to see if they’ve had a heart attack or other heart event. No treatment is introduced, no danger is added to a person’s established habits. Many epidemiologic studies are performed this way.

The problem is that these other sorts of study designs, because they generate less confident results, are not generally regarded as proof of anything. They can only suggest the possibility of an association, an hypothesis. For real proof to occur, a double-blind, placebo-controlled may need to follow. Alternatively, if an association suggested by a study of lesser design might, by reasons of a very powerful effect, be sufficient. But this is rare. Thalidomide and catastrophic birth defects are an example of an association between a drug and fetal limb malformation that was so clear-cut that no further investigation was required to establish a causative association. Of course, no one in their right mind would even suggest a blinded study.

Where am I going with this tedious rambling? Lately, the media has been making a big to-do about several studies, none of which are double-blind, placebo-controlled, but were cross-sectional sorts of observations, the sorts of studies which can only suggest an effect. This happened with Dr. Steve Nissen’s study of Avandia (rosiglitazone) for pre-diabetes and risk for heart attack and the recent study suggesting that cancer incidence is increased when LDL cholesterol is low. Both were observations that suggested such associations.

Now, those of you following the Heart Scan Blog or the www.cureality.com website know that we do not defend drug companies nor their drugs. In fact, we’ve openly and repeatedly criticized the drug industry for many of its practices. Drugs are, in my opinion, miserably overused and abused.

But, as always, I am in the pursuit of truth. Neither of these studies, in my view, justified the sort of media attention they received. They are hypothesis-generating efforts—that’s it. You might argue that the questions raised are so crucial that any incremental risk of a drug is simply not worth it.

Despite the over-reaction to these studies, good will come of the fuss. I do believe that heightened scrutiny of the drug industry will result. Many people will seek to avoid prescription drugs and opt for healthy changes in lifestyle, thus reducing exposure to costs and side-effects.

But beware of the media, acting as our Chicken Little, reporting on studies that prove nothing but only raise questions.

200 point drop in heart scan score

11. August 2007 William Davis (0)
Some of the math-savvy will have noticed that we often report drops in CT heart scan scores on a percentage basis. Unfortunately, it this were a competition (which, of course, it is not), this would be unfair.

A score of 50, for instance, that drops "only" 25 points would represent a 50% drop in score.

But someone with a score of 1050 who drops his or her score the same quantity, or 25, will have dropped their score less than 5%.

In other words, the magnitude of your starting score determines how large a percentage drop you achieve, even when the absolute, or real, quantity of plaque reversal is the same as someone who begins with a lower score.

I qualify this discussion in this vein because of Grady's story. Grady, a soon-to-retire attorney, started with a heart scan score of 1151. On the Track Your Plaque program, he saw his score drop nearly 200 points--200 points!

But, if we gauged Grady's success just on a percentage basis, he dropped his score only a measly 17% or so. (Imagine the headlines if this program were sponsored by a drug manufacturer. The Track Your Plaque program proudly has nothing to do with the drug industry.)

Of course, the Track Your Plaque program is not a competition. It is an effort to help everyone possible, the more the better. Even if Grady failed to set a new Track Your Plaque record gauged on a percentage basis, he will have achieved an extraordinary advantage in health: the virtual elimination of the dangers of heart disease.

With this drop in score, Grady's risk for heart attack plummets from a spine-chilling 25% per year to nearly zero. (I know of NO other program that can claim such a track record.)

Grady's full story will be reported in the August, 2007 Track Your Plaque newsletter. To subscribe or to just view when it is posted, go to www.cureality.com website, click on the upper right hand corner What Does My Heart Scan Show? graphic, which then takes you to the page to view the newsletter. Or, Track Your Plaque Members can just go to the Library and click on newsletter archives.

How tough is the Track Your Plaque 60-60-60 target?

9. August 2007 William Davis (3)
One of the basic requirements that stack the odds in your favor of stopping or dropping your CT heart scan score is to achieve basic lipid targets of 60-60-60.

In other words, we generally see best results when LDL is reduced to 60 mg/dl, HDL raised to 60 mg/dl, triglycerides reduced to 60 mg/dl. Now, these are not absolute requirements. Someone can have a spectacular drop in heart scan score even with an HDL of 56, LDL of 71. But the "Rule of 60" provides a useful target that is easy to remember, packs real power, and is clearly beyond that achieved with conventional approaches.

People often ask, "Just how tough is it to get to these targets?"

It's really not that tough. Interestingly, whenever I tell my cardiologist or primary care colleagues that I advocate these 60-60-60 targets, they declare that it's tough, perhaps impossible, except for the most highly motivated.

I agree that it requires motivation. A cigarette-smoking, TV-addicted, 70-lb overweight, chip- and pretzel-eating couch potato is not going to achieve them.

On the other hand, you don't have to be a marathon running vegetarian to do it, either.

Most people, in fact, engaged in the Track Your Plaque program achieve the 60-60-60 targets---or exceed them. It's not uncommon, for instance, for HDL to skyrocket to 80 or 90 mg/dl with many of our strategies. (Of course, if your starting HDL is 20 or 25 mg/dl, 80 or 90 is not possible with current technology.)

But it certainly does require more than the "Take Lipitor and stick to your low-fat diet" approach that is the mantra repeated in the vast majority of medical offices across the U.S. For instance, reducing LDL to 60 mg/dl when starting at 170 mg/dl will require addition of oat bran and other soluble or viscous fibers; raw almonds and walnuts; perhaps the use of Benecol butter substitute; reduction or elimination of wheat products if small LDL comprises a substantial proportion of LDL particles. Reducing triglycerides requires the generous use of omega-3 fatty acids from fish oil. Attention to vitamin D must be a part of the effort.

So, yes, it is not as simple as the conventional approach. But the results are far superior in reducing or eliminating heart attack and in dropping your heart scan score.

But it can be done. We do it every day.

Vitamin D2 belongs in the garbage

8. August 2007 William Davis (15)
It happened yet again.

Mel came to the office. CT heart scan score: 799--quite high, enough to pose a real threat very soon. Thus, no time to lose in instituting an effective prevention program.

We do the usual--identify the six causes of coronary plaque; begin fish oil, show him how to correct his plaque causes. You've heard it before.

Vitamin D blood level in March: 17 ng/ml--severe deficiency.

Vitamin D replacement needs to be a part of his coronary plaque control program. So I suggested 6000 units per day of an oil-based preparation of vitamin D3 (cholecalciferol). Conveniently, there is a Vitamin Shoppe outlet across the street from my office. I just point and tell people to go across the street.

Mel did just that. However, he also informed his primary care physician about his vitamin D deficiency. His primary physician promptly told him he needed to take a prescription form of vitamin D and not to bother with just a supplement.

So Mel stopped his vitamin D capsules and started taking vitamin D prescription "medication." Mel figured, naturally, that if it requires a prescription, it must be better. Unfortunately, Mel and his doctor failed to pass the change in strategy onto us.

So, four months later, Mel got repeat vitamin D blood level: 19 ng/ml.

I've seen this too many times. The prescription form of vitamin D is nonsense. There's hardly any effect on blood levels of vitamin D3 at all. The body's conversion of this non-human form of D is extremely inefficient and therefore virtually useless. While it raises the blood level of vitamin D2 (ergocalciferol) and thereby total D (D3 + D2), there is negligible effect on the real human and active form, D3.

How and why this preparation got through the FDA process to obtain approval as a drug is beyond me, though I am not a defender of FDA practices and politics.

This notion that "if it's a prescription, it must be better" is a fiction perpetuated by the drug industry. The same principle gets tossed around with fish oil, hormones like estrogens and testosterone, and others. Often, the principal difference between prescription and non-prescription is patent protection. Patent protection provides profit protection. Selling a product without patent protection can be risky business. It's certainly less profitable.

As always, getting at the truth is sometimes the most difficult job of all. Prescription vitamin D belongs in the garbage. Vitamin D capsules (gelcaps) do the job and do it well, over and over, with reliable, consistent and substantial rises in blood levels of 25-OH-vitamin D3. I take 6000 units per day (3 2000 unit capsules) that cost me $5.99 for a bottle of 120 capsules, or about $4.50 a month.

And nobody--nobody--pays me to say this. I say it because I believe it's true.

Angioplasty vs. Track Your Plaque

5. August 2007 William Davis (10)
What does angioplasty have over the Track Your Plaque program?

Well, first of all, the Track Your Plaque program has a lot to boast about. What other approach can claim to have reduced heart disease 30, 40, 51, and now 63%? That's as close to a cure that's ever--EVER--been achieved. Statin drug manufacturers can talk about an occasional 1, 2, or 5% reversal. We're talking 10 times more.

The Track Your Plaque program also uses as little prescription medication as necessary. Fish oil, vitamin D, coenzyme Q10, niacin--some of the frequent tools used for plaque reversal in our program. Yes, we do use prescription medications, but only when there is truly a benefit and nutritional strategies have failed to achieve the goals we're seeking. We do not endorse shotgun prescription approaches conceived of by some marketing department at a pharmaceutical company.

So what possible advantage can coronary angioplasty have? Why don't more people embrace a program like Track Your Plaque that has already proven itself enormously effective?

Because angioplasty is easy. There's little worrying ahead of time. Just wait for the symptoms or other problem to appear, go to the hospital and get your procedure. You can live the free and easy life beforehand--no exercise, no diet efforts, no nutritional supplements. Just be sure to go to the hospital when suspicious symptoms strike. (Of course, you gamble that you survive the appearance of symptoms, a process 30-50% of people fail to survive.)

That means you can eat all you want, drink all you want, save the money you otherwise might have thrown away on supplements, pocket the monthly costs of an exercise club membership, etc. Go to the hospital when you experience the sensation of an anvil on your chest or of suffocation, let the emergency room do their thing, meet your cardiologist, go to the catheterization laboratory, get two or three stents, go home the next day!

Why bother with a prevention program, especially one that requires involvement, learning, and effort like Track Your Plaque?

Because it's your way to stack the odds enormously in your favor of 1) surviving the appearance of symptoms, 2) avoiding the prospect of heart procedures, which are not as clean and easy as they often seem, 3) have a longer lasting durability than a stent which could buy you a couple of years before your next procedure or heart catastrophe, and 4) it's the right thing to do for the sake of the huge societal cost of heart disease.

Many of you have the equivalent of a cure for heart disease at your fingertips. Unless you have a soft spot in your heart for hospitals, cardiologists, or the pharmaceutical or medical device industry, there isn't a choice.

Plaque is like money

3. August 2007 William Davis (0)
In case anyone missed this in the June, 2007 Track Your Plaque Newsletter, I'm again posting how we calculate the annual rate of score increase, should it occur.

For instance, say your score in January, 2005, is 100. In November, 2006, you undergo another scan and the score is 140. Obviously, your score has increased an undesirable 40%. But what is the annual rate of score increase, the amount of increase per year?

In this example, the annual rate of score increase is 19%--not anywhere near as bad as the 40% that can scare the heck out of you.

Obviously, the best rate of heart scan score increase is a negative number, i.e., a drop in score from, say 100, to 60. You might even eliminate the need for this calculation altogether if you drop your score.

Nonetheless, whenever there is a score increase over an uneven period of time, a fraction of year(s), this is the method we use to annualize the calculation. The equation we use is a modified form of the annual compound interest equation using continuous compounding, since that’s how coronary atherosclerotic plaque grows--just like money. The difference is, of course, is that while you might want more money, you certainly don't want more plaque.

You will need a calculator for this calculation, one with an exponential “y to the power x” function. For ease, calculate "1/t first, then use it as the “x” exponent on your yx function and "(score 2 / score 1)" as the "y".


Annual rate of plaque growth (APG) = ( score 2 / score 1 ) 1/t - 1

Multiply the result by 100 to yield a percent.


“Score 1” is your 1st heart scan score, “score 2” is your 2nd (or any subsequent heart scan score); “t” is the amount of time between the two scans expressed in years in decimal form. Time between scans should be expressed in years or fractions of years. To obtain the time interval in fractions of years, simply divide the number of months between scans by 12 (e.g., 18 months / 12 = 1.5 years ; 22 months / 12 = 1.83 years).

It’s not as tricky as it looks. For example, if your first heart scan score is 300 and your next scan 16 months later (or 16/12 = 1.33 years) is 372, then:

Annual rate of plaque growth (APG) = ( 372 / 300 ) 1/1.33 - 1 = 0.175

Multiply 0.175 x 100 = 17.5% annual rate of plaque growth


Some scan centers will do the calculation for you as part of a repeat scan. However, the equation can be used if you're left on your own, or if you go to a different scan center. If this is too much effort, perhaps it's just another reason to add to the list of reasons to drop your heart scan score!

Triglycerides: What is normal?

1. August 2007 William Davis (2)
In The Track Your Plaque program, we advocate decreasing triglycerides to 60 mg/dl or less.

That's the level of triglycerides that minimize the presence of triglyceride-containing undesirable lipoproteins causing plaque, such as small LDL, VLDL, and the after-eating persistence of IDL (intermediate-density lipoprotein, a bad player). (The enzyme, cholesteryl-ester transfer protein, or CETP, is responsible for exchanging one triglyceride molecule for one cholesterol molecule between HDL and other lipoprotein particles. Thus, an excess of triglyceride availability permits CETP to operate unrestrained, creating more undesirable lipoproteins. This was the basis for Pfizer's now defunct CETP inhibitor, torcetrapib.)

Of course, this triglyceride target is far below that of the conventional guidelines. The Adult Treatment Panel-III of the National Cholesterol Education Panel suggests a triglyceride level of 150 mg/dl is okay.

In my view, a level of 150 mg/dl is highly abnormal, permitting the persistence of multiple lipoprotein particles and virtually guarantees plaque growth. In short, triglycerides of 150 are awful.

Curious thing: Successful participants in our program, i.e., people who achieve desirable weight, reduce processed carbohydrate junk foods and saturated fat sources, and aim for the 60-60-60 targets for conventional lipids, commonly end up with triglyceride levels of 25-50 mg/dl.

We have seen many people drop their heart scan scores just by achieving a triglyceride level of 60 mg/dl or less. So achieving a lower level below 60 is not necessarily a requirement for coronary plaque regression.

But it makes me wonder if a triglycere level of 30s or 40s is the level for perfect health. These are levels ordinarily regarded as impossibly low. When colleagues see the numbers we readily and routinely achieve, they declare that the numbers are spurious, temporary, or just flukes. "No way you can do that all the time!"

This level also seems to, in virtually all cases, eliminate the triglyceride-containing undesirable lipoproteins small LDL, IDL, etc., and allow full conversion of HDL into the healthy, large fraction.

Should we move the Track Your Plaque triglyceride target to below 45 mg/dl or even lower? I don't think so, but it makes me wonder.
All posts by william-davis

Wheat-free and weight loss

13. October 2007 William Davis (14)
With a heart scan score of 1222, Leslie could be in deep trouble in short order.

At 64 years old, Leslie had gained nearly 40 lbs since she'd given up a lot of her activities caring for a husband who'd developed psychological difficulties and stopped contributing to the household duties. A tall woman at 5 ft 9 inches, she held her 202 lbs well, but her lipoprotein patterns were a disaster:

--LDL particle number 2482 nmol/l--an equivalent LDL cholesterol of 248 mg/dl (drop the last digit)
--HDL 38 mg/dl
--Triglycerides 241 mg/dl
--90% of LDL particles were small
--Lipoprotein(a) 240 nmol/l

Blood sugar was in the pre-diabetic range at 112 mg/dl, C-reactive protein was high at 3.0 mg/l, blood pressure was somewhat high at 140/84.

Now, with the exception of lipoprotein(a), these patterns are exquisitely weight-sensitive. A reduction in weight would yield effects superior to any medication I could give her.

Processed wheat products were a big problem for Leslie: whole wheat bread, pretzels for snacks, whole wheat pasta. Yes, they sound healthy, even endorsed by the American Heart Association, often bearing "heart healthy" labels on the packages. Don't you believe it.

In particular, Leslie had the number one cause for heart disease in America: small LDL particles, a pattern that is magnified 30-70% by wheat products. Endorsed by the Heart Association? (As I often tell people, if you want heart disease, follow the diet advocated by the American Heart Association.)

Leslie was skeptical, worried that she would be hungry all the time and would have virtually nothing left to eat. Instead, when she returned to the office three months later, she reported that eating was easy, finding healthy foods not containing wheat was easier than she thought, she felt great, finding more energy than she'd had in years.

She'd also shed 30 lbs.

Leslie's lipoprotein patterns also reflected the weight loss. She achieved her 60:60:60 Track Your Plaque lipid targets, small LDL shrunk dramatically, blood sugar and blood pressure were back in normal ranges.

I see results like Leslie's several times every week. For those of us with patterns like Leslie's, or just obesity that accumulates in the abdomen, going wheat-free is among the most powerful single strategies I know of.

If you need convincing, try an experiment. Eliminate--not reduce, but eliminate wheat products from your diet, whether or not the fancy label on the package says it's healthy, high in fiber, a "healthy low-fat snack", etc. This means no bread, pasta, crackers, cookies, breads, chips, pancakes, waffles, breading on chicken, rolls, bagels, cakes, breakfast cereal. I find elimination of wheat easier than just cutting back. I believe this is because wheat is powerfully addictive. It's very similar to telling an alcoholic that a drink now and then is okay--it just doesn't work. They need to be alcohol-free. Most of us need to be wheat-free, not just cut back.

You won't be hungry if you replace the lost calories with plenty of raw almonds, walnuts, pecans, sunflower and pumpkin seeds; more liberal use of healthy olive oil, canola oil and flaxseed oil; adding ground flaxseed and oat bran to yogurt, cottage cheese, etc.; and more lean proteins like lean beef, chicken, turkey, fish, and eggs.

The majority of people who go wheat-free lose weight, sometimes dramatically. Most people also feel better: more energy, more alert, better sleep, less mood swings. Time and again, people who try this will tell me that the daytime grogginess they've suffered and lived with for years, and would treat with loads of caffeine, is suddenly gone. They cruise through their day with extra energy.

Even without weight loss, going wheat-free usually raises HDL, reduces the dreaded small LDL dramtically. It also reduces triglycerides, blood sugar, C-reactive protein, blood pressure. Blood sugar control in diabetics is far easier, with less fluctuations and sharp rises in blood sugar.

Success at this also yields great advantage for your heart scan score control and reversal efforts.

Collective wisdom

12. October 2007 William Davis (5)

As public consciousness and knowledge about health issues grows, thanks to the internet and other media, I predict that:

1) Hospitals will recede into a role of acute and catastrophic care ONLY, dropping the charade of providing health, which they do NOT.

2) Doctors and other health professionals will begin to see themselves as providers of acute and catastrophic care, also. They will stop providing day to day care, such as treating high blood pressure, cholesterol, breast exams, and other preventive maintenance.

3) Instead, preventive care will be self-provided. The public will have acquired sufficient savvy and know-how to manage issues like blood pressure themselves. They will need the assistance of helpful information resources, web-based for the most part. Much preventive care can, in fact, be algorithm-driven, just like following a simple recipe.

All the worries about runaway health care costs will be much reduced, since excessive testing driven by liability worries will disappear, repeated office visits for day-to-day issues will go away. Yes, you will need a doctor and hospital for a broken leg, car accident, unexpected cancer, or non-compliance or neglect of prevention.

But osteoporosis, high blood pressure, nutrition, weight loss, hormone management, cholesterol issues, minor complaints will all be managed by people themselves with the assistance of web-based knowledge systems.

I already sense this sort of phenomeonon developing, though in its infancy, in venues like the Track Your Plaque Forum and other health portals, places where the information being discussed exceeds the quality of information you can obtain from your doctor. Over and over again, for instance, the sophistication and knowledge demonstrated by our Track Your Plaque Forum discussions shows that the public is capable of far more understanding of health issues than many previously believed. Most of our members could carry on a credible conversation with trained lipid experts. The knowledge base of our members exceeds that of 98% of most of my colleagues when it comes to heart scans, lipoproteins, and nutrition.

I am in awe of Wikipedia, the popular online encyclopedia. Five 20- and 30-somethings have created a knowledge base that has now eclipsed Encyclopedia Britannica in size and scope, with equivalent accuracy, and relatively little cost. I'd like to see the same phenomenon occur in health care information, helping to usurp the current paternalistic "I'll tell you what to do" model.

Success--Slow but sure

12. October 2007 William Davis (5)
John is a gentleman.

At age 76, he continues to teach at a local college. He's a delight to talk to, having written several scholarly books on religious topics. He's a fountain of knowledge on religious history and the roots of faith.

John is one of those incurably optimistic people, always greeting me with a smile and a warm handshake. I can't help but linger for a hour or so to talk with John, unfortunately disrupting my office schedule miserably.

John is another Track Your Plaque success story. Though he didn't set any records in reduction of his heart scan score, he did it simply by adhering to the program over a period of two years, succeeding slowly but surely.

John's first heart scan score: 1190, a score that carries as much as a 25% annual risk for heart attack. Among the list of causes was an LDL cholesterol in the 170 mg/dl range, along with an LDL particle number that verified the accuracy of LDL.

Among John's suggested treatments was a statin drug, since I was not confident he could reduce LDL with diet and nutritional modifications sufficiently to safely reduce both LDL and his risk for heart attack. But he proved terribly intolerant to any dose of any statin, with incapacitating and strange side-effects, like head-to-toe itching, abdominal cramps and diarrhea. It was clear: John needed to do the program without benefit of a statin drug.

I therefore asked John to maximize all efforts that reduce LDL, 70% of which were small LDL paricles despite his very slender build. He used oat bran and ground flaxseed daily, raw nuts, a soy protein smoothie every morning, and eliminated wheat and other high-glycemic index foods (including the Oreos he loved to snack on). Because the mis-adventures with statin drugs wasted nearly a year, I asked John to undergo another heart scan. Score 2: 1383, a 16% increase.

I asked John to keep on going. Thankfully, he did manage to tolerate fish oil, niacin (though it required over a year just to get to a 1000 mg per day dose), and vitamin D. With all these efforts, he did reduce LDL to the 80-90 mg/dl range. Of course, John's unflagging optimism was crucial. He did express his occasional anxiety over his heart scan score, but dealt with it in a logical, philosophical way. He understood that there was no role for prophylactic stents or bypass, and he accepted that much of his program rested on his ability to adhere to the strategies we advised.

Another year later, a 3rd heart scan: 1210, a 12% reduction.

I'm very proud of John and his success. When you think about it, he succeeded in conquering heart disease with some very simple tools, minus statin drugs. It can be done, but requires consistency and patience--and an optimistic outlook.

Vitamin D and octagenarians

10. October 2007 William Davis (28)
Roger practically bounced in his chair vibrating with energy.

"It must be the vitamin D! I haven't felt like this in years. I can work around the yard all day and still have energy left over."

At age 84, Roger started out with pretty good health, despite a prosthetic valve and bypass surgery 5 years earlier. He looked 74, perhaps younger.

I've seen this effect now in about 20 octagenarians. A Track Your Plaque Member mentioned this same effect in his father-in-law in a discussion in our Forum. Most are taking around 6000-8000 units per day (gelcap, of course). The average dose of vitamin D tends to be higher in this age group, since by age 80, you've essentially lost the capacity to convert 7-hydrocholesterol to active vitamin D3 in the skin. Most octagenarians start with 25-OH-vitamin D3 levels of 10 ng/ml or less--profound deficiency.

I believe the effect is real, having now witnessed it multiple times. Unfortunately, my observations are too informal to qualify as a study. (I wouldn't even know how to quantify this. I suppose some sort of muscle and coordination testing might yield quantifiable measures.) However, there are some data emerging that show less fractures, falls, improved coordination, and perhaps improved memory and mentation with vitamin D supplementation, though doses often used in studies tend to be lower than what we are using in practice.

I haven't been so excited about the effects of a nutritional supplement in a long time. Vitamin D continues to yield surprises every day in its array of positive and powerful effects.

Could we say that vitamin D restores youthfulness?

NY Times Jane Brody misses the mark

9. October 2007 William Davis (6)


NY Times' health columnist, Jane Brody, recently wrote a bit of fluff for her paper:

"CT Scans of the Heart Come With Trade-Offs


In her report, she says:

Coronary CT scans are being sold directly to the public, and they have found a market in health-conscious people who can afford them. But screening exams can have downsides. They can cause needless worry, and they sometimes reveal other potential conditions that require invasive procedures like biopsies to diagnose.

I soon learned that among the strongest proponents of CT scans of coronary arteries were physicians with financial ties to drug companies that make statins and others connected to imaging centers that would profit directly from widespread CT screenings.


She then goes on to discuss how the Framingham scoring calculation can tell you whether or not you are at low-, intermediate-, or high-risk for heart disease. She therefore concludes that heart scans are therefore irrelevant for the majority of people. She then proceeds to take a statin agent.

This sort of nonsense continues to get published, despite the clear lack of real "digging" for the truth. She clearly fell for the conventional arguments that continue to mis-guide the majority of people, myths like:

--the Framingham scoring system is reliable--Reliable it is NOT; it is susceptible to substantial "misclassification" bias, meaning people who appear low risk can actually be high risk, and people at high risk can actually be low risk. Among the latest studies that question the scoring system is Family history of premature coronary heart disease and coronary artery calcification: Multi-Ethnic Study of Atherosclerosis (MESA). This study pointed out how the Framingham scoring system, which leaves out family history, can cause people classified as low risk to actually have substantial heart scan scores. This is crucial. A heart scan gets beyond the uncertainties and shows with >95% certainty whether or not hidden coronary atherosclerotic plaque is present.

--"Coronary risk" is a dynammic phenomenon, subject to changes in a person's life. What if, for instance, a person smoked for 20 years, quit 10 years ago, lost 30 lbs, dropped their blood pressure as a result of the weight loss, then relied on the Framingham Risk Calculator to determine risk. They would likely be classified as low- risk, since risk factors now appear favorable. This person could easily have a heart scan score of 500, or 700, or 1000, levels that carry a cardiovascular event risk of 5-25% per year, hardly low-risk, because much of their risk accumulated earlier in life and is no longer revealed by an assessment of risk factors.

--There are sources of risk that have nothing to do with Framingham, such as lipoprotein(a), which is often revealed by family history; the presence of small LDL, which co-varies with HDL and triglycerides, but can behave independently also; and, my favorite, deficiency of vitamin D. This would explain part of the 60-70% of people who are typically mis-classified by Framingham.


Where did Ms. Brody get the idea that proponents of heart scans had ties to drug companies? I think she's barking up the wrong tree on that one. Of course, she ends up on a statin drug. For my part, I am a critic of statin drugs. Yes, they play a role, but they are miserably misused and abused by practicing physicians, based on the endless onslaught of drug company-sponsored trials that have served to distort their usefulness.

If I were Ms. Brody, I would be quaking in my shoes, not knowing what my true risk for heart disease was, relying on the--at best--30% reduction in heart attack risk of Lipitor or other statin drug. Ms. Brody: You are not cured, you're simply wearing a superficial Band-Aid. If you want to know your true risk for heart attack, and you want a precise value that you can track over time, the answer is simple: Reject the conventional notion and get a heart scan.

"There must be a mistake"

9. October 2007 William Davis (2)
Neal is our current male record holder for greatest reduction in heart scan score. (Yes, the ladies have the lead!)

You may remember that this 40-year old man reduced his heart scan score from 339 to 161--a 51% drop. If you haven't yet read his story, go to

http://www.cureality.com/library/fl_07-001nealt51.asp


Neal reminded me of the experience he had when he underwent his second heart scan. Both scans had been performed at the same scanning center. At this center, the radiologists provide the added service of sitting down with people and actually going over the images and results.

After the scan, the radiologist pulled up the result from Neal's first scan for comparison. "There must be a mistake! This score is lower. Scores never drop."

The radiologist was apparently stumped, unable to provide an explanation. However, Neal then proceeded to tell the radiologist that we had warned Neal that this could happen and that he might even be told that it was due to error of some sort. This yielded a puzzled look on the radiologist but no further comment.

Of course it's not a mistake. It's something we achieve on purpose. Curiously, I still get comments that this is impossible, heart scan scores never drop, etc. Of course, those of you following this conversation know this is completely untrue. Heart scan scores DO drop, and sometimes drop enormous amounts, as it did for Neal.

I would have liked the radiologist to have had the lightbulb of understanding go off in his head when he realized that a reduction in heart scan score is a cause for celebration. Unfortunately, this radiologist's reaction is all too common: disbelief, confusion, dismissal.

Heart disease reversal is simply not in the realm of understanding of most doctors, radiologists and cardiologists alike. By conventional thought, if you have it, it just gets worse. "Maybe some high-dose Lipitor might help."

Ironically, when they see it right in front of their eyes, plain as day on the computer screen, they don't understand what has happened. It's Greek to them.

Should this happen to you, don't be surprised. Just bite your tongue, because you know better.

Jimmy Moore Interview: Is saturated fat the villain we thought?

7. October 2007 William Davis (45)
Enter "weight loss" or "low carb" in your web search and you can't help but stumble across the prolific and widely-connected Jimmy Moore.

On his Blog, Livin' la Vida Lo Carb , Jimmy conducts a wide-ranging and informative discussion of the benefits of a low carbohydrate diet, a la Atkins. Though his initial claim to fame was the 180 lbs he lost in his first year of dieting on this approach, Jimmy has extended the conversation and built a considerable community of like-minded individuals, all of whom are participating in this grand "experiment."

Anybody who looks at lipoproteins and associated factors in health will quickly come to the conclusion that processed carbohydrates are the culprits in much of heart disease, diabetes, and heart disease. But I have had a hard time dismissing the ill-effects of saturated fat. After all, we've all been taught--drilled--with the idea that saturated fats cause LDL cholesterol to go higher, cause arterial constriction, growth of atherosclerotic plaque, inflammation, even cancer.

But there does indeed seem to be a growing sentinment that this long-held dogma may not be true. So I went to the ever-entertaining and informative Jimmy Moore, an able spokesman for these concepts.




TYP: It's certainly impossible to argue with the success you had in weight loss and the health you've regained on your program.

I think that the approach we use in diet in the Track Your Plaque program and the nutrition approach you advocate overlap to a great extent. We both emphasize plenty of vegetables, fruits, healthy oils, nuts, etc. The major point of difference seems to lie in saturated fat: We say restrict it, you say don't restrict it. Could you elaborate?





JM: Thank you for inviting me to your blog today, Dr. Davis. I have nothing but deep respect and admiration for the work you are doing to help educate others about how to keep their heart health in tip-top shape. Keep fighting the good fight, my friend.

While we do agree on probably 99% of the basic tenets of what I describe as
"livin' la vida low-carb," the issue of saturated fat to me is one where we
indeed do not. It's not a deal breaker regarding my support for what you do
just as I'm sure you would say the same regarding your backing of what I do. If
we all agreed on everything, then what a boring world this would be!

My thinking on saturated fat has evolved since I started eating this way nearly
four years ago. Like most people, I was terrified to eat ANY fat at all because
of the abject fear that people like Dr. Dean Ornish and other so-called health
"experts" instilled in me about how dangerously unhealthy it is to consume it.
This fat phobia is arguably the single biggest contributor to the ongoing
obesity crisis our world faces today.

With that said, you and I both know fat consumption is a part of a healthy
lifestyle. There are just too many benefits to the body that come from the
consumption of fats and even saturated fats such as coconut oil, butter, lard,
nuts, seeds, and animal fat when it is combined with a restricted carbohydrate
intake.

An intriguing study was presented at a scientific conference in November 2006 by two highly-respected researchers--Dr. Stephen Phinney from the University of California at Davis and Dr. Jeff Volek from the University of Connecticut--who conducted a side-by-side comparison of the amount of saturated fat in the blood of people on a low-carb diet with those following those highly-touted low-fat diets. What they found was the low-carb study participants had "significantly less" saturated fat in their blood than the low-fatties did.

Here are the actual numbers from the study:

- LOW-FAT/HIGH-CARB DIETERS: lowered saturated fat by 24%
- LOW-CARB/HIGH-FAT DIETERS: lowered saturated fat by 57%
- Eating 3X the saturated fat cut the amount in the blood in half

In an interview I conducted at my blog with Dr. Volek last year (here's the
link: http://livinlavidalocarb.blogspot.com/2006/09/volek-high-carb-low-fat-diet-useless-to.html),
he said the conventional wisdom regarding fat, especially saturate fat, is dead
wrong while the significance of carbs is all but ignored by those who claim to
understand the metabolic response mechanism.

Here's what Dr. Volek said in my interview:

"Eating fat does not make you fat, storing fat makes you fat. And carbohydrates play a major role in storing fat. So the level of dietary carbohydrate is really the most important factor to control because it dictates what happens to fat. Carbs are dominant and fat is passive. When carbohydrates are low, fat tends to be burned, and when carbohydrates are high dietary fat tends to be stored. The same holds true for the atherogenic effects of saturated fat. The body handles saturated fat better when carbohydrates are low."

Long-time low-carb practitioner and current President of the American Society of Bariatric Physicians (ASBP) Dr. Mary C. Vernon from Lawrence, Kansas confirms the findings of Dr. Volek and Dr. Phinney in a succinct recap of what their research showed.

Here's what she said:

"Eating fat (whatever kind) does not make you fat. It does not increase blood
stream saturated fat. Eating carbs does make you fat. Eating carbs does put
saturated fat in your blood stream."

To me, as a simple layperson with no medical background, it's all a matter of who you believe. Do we continue to buy into the low-fat propaganda machine and assume that what they are telling us about saturated fat is true? Or do we instead start paying closer attention to the latest research that is coming out about saturated fat that doesn't exactly line up with the edicts of the last three decades? The choice for me is a simple one.

And if you haven't read the brand new Gary Taubes book entitled GOOD CALORIES, BAD CALORIES yet, then it is REQUIRED reading to arm yourself with the research studies about fat. After you read that book, it will be almost impossible for ANYONE to believe fat, including saturated fat, is unhealthy.



TYP: In our program, we advocate a wheat-free approach for many people, because of the addictive potential of wheat products, as well as the flagrant creation of the small LDL pattern that wheat products create, thereby adding to atherosclerotic plaque growth. However, many people express a concern over a lack of fiber in their diets if they eliminate whole wheat bread, pasta, Fiber One, Raisin Bran cereal, etc.

Have you encountered any phenomena of low-fiber on your approach?

JM: What an excellent question and I even wrote a humorous blog post about the importance of fiber intake called "Allow Your Bowel To Shake, Rattle, And Roll" (http://livinlavidalocarb.blogspot.com/2006/06/allow-your-bowel-to-shake-rattle-and.html).

Fiber consumption is another one of those issues that not everyone who advocates
a controlled-carb approach agrees is necessary. I'm on the side that it IS a healthy part of your diet and should be consumed in high enough quantities to keep you regular...something many people think is impossible on a low-carb diet.
Not true! I take a fiber supplement like FiberCon, eat plenty of high-fiber vegetables, drink lots of water, and even consume high-fiber, low-carb products that help me maintain high levels of fiber in my diet (see my favorite ones in this post: http://livinlavidalocarb.blogspot.com/2007/04/there-are-plenty-of-low-carb-fiber.html).

As for consuming the highly-touted "healthy whole grain" cereals that you
mentioned, what a travesty that would be for people trying to manage their
weight and health. While the cereal manufacturers have had a heyday in their
marketing efforts promoting their whole grain content, it's all just a big fat
ruse on the public trying to convince them that these cereals are somehow healthy for their bodies. Sure, they're better than the sugary cereals, but all those grains are metabolized as sugar inside the body, so you might as well be eating Lucky Charms and Fruit Loops!

Many of these "healthy" cereals contain as many carbohydrates in a single bowl
without the milk as I would eat in an entire day. Raisin Bran, for example, which used to be my favorite cereal before my low-carb lifestye, has a whopping 47 grams of carbohydrates. Needless to say, I don't touch that with a ten-foot pole nowadays because I would surely gain weight and get back on the blood sugar rollercoaster ride that I was on prior to beginning the Atkins diet on January 1, 2004. Plus, all those carbs just make you hungrier sooner, so it's better just to eat some delicious eggs cooked in butter, a couple of slices of sausage, and tomato slices to start your day off right. You'll get enough fiber in your body the rest of your day.



TYP: 180 lbs of weight loss in your first year is absolutely astounding.

I take it that you've continued this trend and have lost more weight since your early success. What role did exercise play during your first year and subsequently?
How are your food choices today different from that first year?

JM: Yes, that weight loss was indeed one of the greatest accomplishments I have ever experienced in my life. It was a hard-fought battle that even included a 10-week period where I was stalled with no weight loss. But I knew my chosen diet was the right one for me because I felt better than I ever had on a diet, was never hungry because I ate every 2-3 hours, and could see myself doing this for the rest of my life. So far, so good!

It has been close to four years since I began this journey and I am indeed continuing this pathway to better health. My low weight in 2004 was 230 pounds and I currently weigh 225 pounds. As long as I keep my carbs reduced, I am able to maintain my weight right where it is. I've had minor fluctuations in both directions where I got down to as low as 215 pounds at one point (but didn't feel good at that weight) and as high as 252 pounds (when I was allowing myself one too many high-carb foods here and there).

There's a balance that people need to find for themselves and it's different for
all of us. I am one of the unlucky people who has to keep his carbohydrate
intake below 50g daily or I gain. It's just a fact of life that I've come to
grips with and realize is a necessity in order to manage my weight for the rest
of my life. But I wouldn't have it any other way!

Exercise was indeed a part of my low-carb weight loss success in 2004 as I
forced myself to do cardio every single day as a commitment to this journey. In
hindsight, that was probably not the best thing for me to do since the body has
a rather peculiar way of telling you it needs to wiggle and move spontaneously
on its own rather than forcing the issue. But I consider the exercise I did to
be such an integral part of my success that I dedicated an entire chapter of my
book to the subject.

Today, my daily cardio routine is out the window and I choose instead to engage
in activities outside the gym that let me burn calories and have some fun in the
process. I regularly play volleyball, basketball, and referee flag football at
my church which all give me quite a workout. I'm very physically active and fit
on my 6'3" body and just enjoy burning off all this excess energy that I have
been given since losing nearly have my weight! I do want to get into a little
more organized resistance training routine soon to try to shape and tone some
areas of my body that still show signs of that 410-pound man I used to be
(although the loose, hanging skin in my abdomen and inner thighs isn't going to
get any better with exercise since the elasticity has been ruined from being
stretched out so far). Here is a link to some posts and pictures I have written
about this subject:
http://lowcarblinks.blogspot.com/2007/04/theme-based-low-carb-links-loose-skin.html

As for my food choices today compared to my weight loss year in 2004, they
haven't really changed a whole lot. This was a lifestyle change in every sense
of the phrase and I've learned to implement this way of eating into a permanent
and healthy diet that I can and will gladly live with forever and ever amen. I
probably eat more berries, melons, and nuts today than I did then, but otherwise
it's the identical diet.



TYP: I'm sure that you are as impressed as I am that much of the wisdom in healthy eating doesn't always come from doctors or clinical studies, but from the collective wisdom that emerges from this national experiment (inadvertent, for the most part) in eating. Your Livin' La Vida Low-Carb is, in my view, a perfect example of the sort of wisdom that is helping all of us understand what happened to our health over the last 20 years.

Does the approach you advocate today differ in any substantial way from the diet as originally articulated by Dr. Atkins?

JM: Actually, my personal diet is precisely based on the teaching of the late great Dr. Robert C. Atkins in his classic bestseller DR. ATKINS' NEW DIET REVOLUTION (DANDR) book. But most people are surprised when they learn I do not necessarily advocate the Atkins diet as the nutritional approach for everyone.

Nope, I sure don't!

Instead, my philosophy is simple: Find the diet plan that will work for YOU, read and research everything you can about that chosen plan, follow that plan exactly as prescribed by the author of that book, and then KEEP doing that plan for the rest of your life. If you do that, then there's no reason why you can't succeed just like I did.

Anyone interested in doing the low-carb lifestyle and needs help finding which
plan is right for them, let me HIGHLY encourage you to pick up a copy of Dr. Jonny Bowden's LIVING THE LOW-CARB LIFE (read my review: http://livinlavidalocarb.blogspot.com/2005/05/must-have-book-for-everybody-doing-low.html).
It's the perfect overview of low-carb living with a comparison and recap of the
major plans.

THANK YOU again for allowing me to share my story with you and your readers, Dr.
Davis!

TYP: And thanks to you, Jimmy!



For more on Jimmy Moore's lively and informative discussion of these issues, go to

Livin' la Vida Lo Carb

Also, watch "Livin' La Vida Low-Carb on YouTube"

Join the conversation at Jimmy's new low-carb forum called "Livin' La Vida
Low-Carb Discussion" at LowCarbDiscussion.com


Also, Jimmy's 2005 book on his weight loss experience:
"Livin' La Vida Low-Carb: My Journey From Flabby Fat To
Sensationally Skinny In One Year"

Mammogram of the heart

6. October 2007 William Davis (3)
Some people have called CT heart scans the "mammogram of the heart." The analogy contains a lot of wisdom.

First of all, both--mammograms and CT heart scans--are screening tests, one for cancer, of course, the other for coronary atherosclerotic plaque. Both are performed in specific age groups, mammograms in women 40 years and over (generally), heart scans in women 50 years and over (generally).


















Mammograms: Left, normal; right, a small mass. (Courtesy Nat'l Institutes of Health and Wikipedia.)



Both are also meant to be repeated periodically when normal as a surveillance process.

Both use low quantities of radiation of about 0.3-0.4 mSv (the most real-life measure of total body exposure), a modest quantity of radiation.

Both are good for their purposes, though not perfect. Can a mammogram performed properly miss a small cancerous mass? Sure it can, but it's still unusual. Can a CT heart scan miss the non-calcified plaque prone to rupture? Sure it can, but this is also unlikely (<5% probability).

Given the exorbitant costs of medical tests, both are quite inexpensive. On the flip side, they are both also quite unprofitable for the centers providing the tests. Unfortunately, this means that mammography centers and heart scan centers come and go because of the difficulties of the profit-side of these services.

Both tests initially struggled to gain acceptance among the medical community. In 1960, for instance, mammograms were performed on standard x-ray devices, the same as that used to perform chest x-rays--low precision, high radiation back then. In 1969, dedicated mammography devices made the scene. However, it took over 10 years for even these new dedicated devices to become widely used. Use of mammograms has gradually increased over the ensuing 20 years. In other words, 47 years have passed since the introduction of mammography.

CT heart scans, of course, have had a shorter history of approximately 20 years, since engineer, Dr. Douglas Boyd, first invented the "ultra-fast" EBT devices, the first devices with sufficient scanning speed to scan the heart and coronary arteries.

One interesting difference between the two: In a woman between the age of 50 and 60, the likelihood of detecting cancer is 1 in 237. The likelihood of detecting coronary atherosclerotic plaque? About 1 in 4. Coronary disease eventually kills 1 in 3 females, hugely overshadowing breast cancer in frequency.


Progress on both fronts, one in cancer detection, the other in atherosclerotic coronary plaque detection. But still lots more progress to go.

Dr. Susie Rockway on conjugated linoleic acid (CLA)

5. October 2007 William Davis (7)
I’m fascinated by the perspectives that nutritionists (free-thinking ones, at least), food scientists, and biochemists bring on nutrition and nutritional supplements.

A few months ago, I met a fascinating nutritionist/biochemist named Susie Rockway, PhD. Dr. Rockway brings a world of experience in the world of nutritional supplements, clinical trials with supplements, and their development. She has special expertise in conjugated linoleic acid (CLA), having been among the scientists who initially developed CLA as a supplement. We are also exploring CLA as a possible addition to the Track Your Plaque program and wanted to get Dr. Rockway’s perspectives.

So I asked Dr. Rockway if she’d answer a few questions for us.






TYP: Dr. Rockway, we understand that you are particularly excited about the prospects of CLA for FAT loss and perhaps for regression of atherosclerosis. Can you tell us about the origins of your interest in CLA and why you're so enthusiastic?

Dr. Rockway: I have been fascinated with this unique fatty acid since the early 1990’s when CLA was first being discussed as nature’s most potent anti-carcinogen. I was then working in the granting/funding section of the National Dairy Council and saw this molecule as truly one of the future functional fats that would likely benefit people (next to omega-3’s!)

I think the benefits of CLA have just begun to be investigated—animal studies are extraordinary for showing fat reduction, lean mass (muscle) increases, immune enhancements, blood glucose normalization, anti-inflammatory properties and plaque reduction!

Human data to date is very encouraging for fat reduction. As a nutritionist seeing the massive increase in abdominal fat (stomach fat) in the world population and the direct relationship to cardiovascular disease, I see CLA as a great supplement to take to help this. Of course eating lots of vegetables, fruit, lean protein and whole grain products is also a must for maximizing good health.

I am studying the impact of CLA in reducing muscle loss in aging women—a condition known as sarcopenia. As we lose muscle with age, we lose strength, falls increase, we become frailer, and eventually many of us lose our independence. Along with the muscle atrophy, most people gain fat—never a good thing! So, if CLA can reduce fat and increase muscle, our bodies are more likely to withstand the hurdles that life throws at us much more efficiently.

So, how can you not be excited about this very bioactive molecule?




TYP: What are your specific areas of interest in nutrition and health?

Dr. Rockway: I strive to understand the role of bioactive molecules that can be taken to improve the aging process and enhance health.

As a trained nutritional biochemist, we tend to look at cell metabolism in a very ideal sense: what we learned in our biochemistry texts years ago where all substrates, proteins, enzymes, etc. are made exactly when we need them, where all cells behave as they should.

Unfortunately, little research has been devoted to understanding the changes in metabolism as we age. Do we still produce everything as efficiently as when we were 20? I suspect not. So, I think we need a little help, and supplements are a key to getting there.

Two nutrients that I think are emerging as “super nutrients” are the fatty acids found in fish oil (EPA and DHA) and vitamin D. Where we know these two nutrients are essential for life, we are seeing that they play a huge role in the QUALITY of life. Mood, depression, PMS, wound healing, bone growth, atherosclerosis, and arthritis are clinical areas where we see a direct benefit with doses of omega-3 and Vitamin D that are probably much greater than the RDA. Our current requirements for nutrients are really based on fixing deficiencies and not maximizing health, and maximizing health is where I’m at.

Thus, I am very interested molecules like CLA as mentioned above, and other bioactive ingredients such as plant derived ingredients (phytochemicals) called flavonoids that may well help explain why people who have diets high in fruits and vegetables are less likely to have certain cancers and heart disease. Reducing oxidative stress through foods that provide these active molecules (think colored fruits and veggies) is a new and exciting area of research.



TYP:The big "diet experiment" in America has clearly steered people in the wrong direction, usually by 50 or more pounds. As a scientist in nutrition, what are your thoughts?

Dr. Rockway: The American Heart Association was keen 20 years ago to promote the low-fat diet for all Americans as the key way to reduce cholesterol levels and decrease chance of heart disease, the number one killer of men and women. However, I must admit the nutritional community bought into this one, too. Unfortunately, the general public took this message to reduce percent fat in their diet (and they did a bit), but increased overall calories instead—and a large portion of the increased calories was from simple carbohydrates. I’m convinced that this in itself has been part of the huge rise in obesity…we simply eat more food and it’s not the healthy kind of food either.

When you increase sugar intake beyond what you burn off, you will store some of it as glycogen in the liver and muscles, but you will convert most of the excess into fat—and that we can store very efficiently! The fat that is made in the liver is sent to the blood as VLDL’s which are the precursor to the class of lipids called low density lipoproteins (LDL) that are the “lethal” type of cholesterol circulating in our blood.

So, Americans now have to listen to a new message that they need to eat more fruits and vegetables in hopes they will cut down on fast foods—tending to be high in fat (saturated particularly), low in fiber and low in nutrients and other high calorie dense foods. We nutritionists have our work cut out for us, that’s for sure.



TYP: We are especially excited that nutritionists are assuming a leading role in shining light on the confusion in diet and nutrition that has characterized the last 40 years. Do you have a sense for the emerging important issues for the next 10 years?

Dr. Rockway: Certainly, the scientists in the nutritional field are well aware of the problems facing this nation—it’s in fixing them that we fall short!

We aren’t very well coordinated to get a single message out, nor do we all agree on what that message should be. I feel that people need to eat healthy MOST OF THE TIME, exercise all of the time, and take supplements that have clear evidence of benefit. Lots of my colleagues would not concur with supplement use. Our bodies were designed to move a lot and eat a lot…we just do the latter now and are paying the price!

One emerging and very exciting area that we have to teach Americans is that all fat is not bad. The different types of fat—omega-6 vs. omega-3, are where we need to focus our education.

Decreasing the corn oil we pour on everything needs to go out the window! Consume olive oil and eat fish or take fish oil supplements—we simply have tons and tons of research showing the benefits of reducing the ratio of omega-6 to omega-3. Did you know that cattle that are grass fed actually have less omega-6 in their tissues and more CLA? But most cattle are fed corn-based diets, so we have perturbed their natural selection of food and their fat composition.

See, it all comes back to CLA!


TYP: Thanks, Susie!




Susie Rockway, Ph.D., C.N.S.

Dr. Susie Rockway is an experienced scientist with accomplishments in both the academic and food and supplement industry business directing science/technology research. Her background includes faculty appointments at the graduate level in teaching and research at Rush University Medical Center and industrial experience managing basic and applied research studies.

Dr. Rockway received her Ph.D. in Nutritional Sciences, Biochemistry from the University of Arizona. Dr. Rockway has authored several publications in journals such as the Physiological Genomics, Journal of Nutrition, the Journal of Food Science, International Archives of Occupational and Environmental Health and has published chapters on nutrition on inflammatory bowel diseases. She is a member of the American Society for Nutrition, American Oil Chemists Society, the Institute of Food Technology, American College of Nutrition and is a Certified Nutrition Specialist.

We're also proud to add Dr. Rockway to our panel of Track Your Plaque Experts.

Which is better?

4. October 2007 William Davis (12)
If you have the common pattern of high LDL particle number (NMR) with small LDL--a pattern highly related to coronary plaque--which is better:




Lipitor or a combination of fish oil, vitamin D, and elimination of wheat?


Lipitor quite effectively reduces LDL particle number, usually on the order of 40% or so. Effect on LDL particle size: None. Side-effects: plenty, including muscle aches (inevitable in my experience, not the ridiculous 2% they claim) and occasionally mental effects such as impaired short-term memory.

Lipitor does seem to exert a modest effect on reduction of C-reactive protein, around 30%. It also reduces cardiovascular events by 30%.



A combination of fish oil, vitamin D, and elimination of wheat:

Reduces LDL particle number commonly by a similar 40% (though variable, depending on body weight). There is substantial improvement in LDL particle size, a large drop in C-reactive protein, often >50%, a 30% or more reduction in cardiovacular events.



On this combination, however, you also:

--Lose weight, often substantially.

--Improve bone health, esp. osteoporosis and arthritis.

--Reduce cancer risk from the vit D supplementation.

--Reduce risk of stroke.

--Reduce postprandial (after-eating) abnormalities like intermediate-density lipoprotein.

--Reduce winter blues.

--Experience more energy.

--Obtain increased clarity of thought (from elimination of wheat).

--Reduce blood pressure.


Oh, and there's no muscle aches.