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.
I came across this Blog authored by a nutritionist when it was highlighted on Blogger as an interesting site:

The Fanatic Cook at http://fanaticcook.blogspot.com/

I was thoroughly impressed with the insightful and entertaining commentary. I'd highly recommend this site to you for reading on nutrition. In particular, her coenzyme Q10 column was exceptionally well written and clear.(http://fanaticcook.blogspot.com/2005/02/statins-and-not-well-publicized-side.html)

Also read her column, Super NonFoods at http://fanaticcook.blogspot.com/2005/07/super-nonfoods.html.

There's also oodles of recipes, all for the taking.

Eggs: Good, bad, or indifferent?

5. August 2006 William Davis (3)
Eggs have been in the center of the cholesterol controversy almost from the very start.

The traditional argument against eggs went that eggs, high in cholesterol (210-275 mg per egg)and with some saturated fat (1.5-2.5 grams per egg), raised blood cholesterol (and LDL). Out went the daily fried, scrambled, poached eggs that many Americans indulged in most mornings. (We replaced it with more breakfast cereals and other carbohydrate conveniences, then got enormously overweight.)





A large Harvard epidemiologic study in 1999 called this observation into question. They tracked the fate of 117,000 thousand people and then compared the rate of heart attack, death, and other cardiovascular events among various people correlated to the "dose" of eggs they ate. Egg intake varied from none to 7 or more per week. Lo and behold, people who ate more eggs appeared to not suffer more events.

This study, large and well-conducted by an internationally respected group of investigators, seem to reopen the gates for more egg consumption, though most Americans still consume eggs cautiously.

Deeper down in this study, however, was another observation: People with diabetes who ate 1 egg per day had double the risk of heart attack. Because this study was observational, no specific conclusion as to why could be drawn.

A new study conducted by a Brazilian group may shed some light. Healthy (non-diabetic) men were fed an emulsion of several eggs. Inclusion of plentiful yolks caused a dramatic slowing of fat clearance from the blood. Specifically, "chylomicron remnants" were abnormally persistent in the blood. Chylomicron remnants are potent causes of coronary plaque. (Chylomicron remnants can be measured fairly well by intermediate-density lipoprotein and VLDL by NMR, or IDL by VAP.)

Diabetics are know to have substantial disorders of after-meal fat clearance, including an excess of chylomicron remnants. Could the Brazilian observation be the explanation for the increased event rate in diabetics in the Harvard study? Interesting to speculate.

We continue to tell our patients that eating eggs in moderation is probably safe. After all, there are good things in eggs: the high protein in the egg white, lecithin in the yolk. It is the yolk's contents that are in question, not the white. Thus, you and I can eat all the egg whites (e.g., Egg Beaters) we want. It's the safety of yolks that are uncertain.

The abnormal after-eating effect suggested by the Brazilians opens up some very interesting questions and confirms that we should still be cautious in our intake of egg yolks. One yolk per day is clearly too much. What is safe? The exisitng information would suggest that, if you have diabetes, pre-diabetes, or a postprandial disorder (IDL, VLDL), you should minimize your egg yolk use, perhaps no more than 3 or so per week, preferably not all at one but spaced out to avoid the after-eating effect.

Others without postprandial disorders may safely eat more, perhaps 5 per week, but also not all at one but spaced out.

Track Your Plaque Members: Be sure to read our upcoming Special Report on Postprandial Disorders. It contains lots of info on what this important pattern is all about. Postprandial disorders are largely unexplored territory that hold great promise for tools to inhibit coronary plaque growth and drop your heart scan score. The Brazilian study is just one of many future studies that are likely to be released in future about this very fascinating area.




Hu FB, Stampfer MJ, Rimm EB, Manson JE, Ascherio A, Colditz GA, Rosner BA, Spiegelman D, Speizer FE, Sacks FM, Hennekens CH, Willett WC.A prospective study of egg consumption and risk of cardiovascular disease in men and women. JAMA 1999 Apr 21;281(15):1387-94.

Cesar TB, Oliveira MR, Mesquita CH, Maranhao RC. High cholesterol intake modifies chylomicron metabolism in normolipidemic young men. J Nutr. 2006 Apr;136(4):971-6.

Diabetes is Track Your Plaque's Kryptonite!

3. August 2006 William Davis (0)

If there's one thing I truly fear from a heart scan score reduction/coronary plaque regression standpoint, it's diabetes.

I saw a graphic illustration of this today. Roy came into the office after his 2nd heart scan. His first scan 14 months ago showed a score of 162. Roy started out weighing well over 300 lbs and with newly-diagnosed adult diabetes.

Roy put extraordinary effort into his program. He lost nearly 70 lbs by walking; cutting processed carbohydrates, greasy foods, and slashing overall calories. His lipoproteins, disastrous in the beginning, were falling into line, though HDL was still lagging in the low 40s, as Roy remains around 60 lbs overweight, even after the initial 70 lb loss.

Unfortunately, despite the huge loss in weight, Roy remains diabetic. On a drug called Actos, which enhances sensitivity to insulin, along with vitamin D to also enhance insulin response, his blood sugars remained in the overtly diabetic range.

Roy's repeat heart scan showed a score of 482--a tripling of his original score.

Obviously, major changes in Roy's program are going to be required to keep this rate of growth from continuing. But I tell Roy's story to illustrate the frightening power of diabetes to trigger coronary plaque growth.

Like Kryptonite to Superman (remember George Reeves crumbling and falling to his knees when the bad guys got a hold of some?), diabetes is the one thing I fear greatly when it comes to reducing your heart scan score. As you see with Roy's case, diabetes can be responsible for explosive plaque growth, more than anything else I know.

The best protection from diabetes is to never get it in the first place. (See my earlier Blog, "Diabetes is a choice you make".)

Boy, was I wrong!

1. August 2006 William Davis (0)
Around 10 years ago, I was talking to a balloon and stent manufacturer's representative, who was raving about some new device that was due for release to the market. Back then, the sky seemed the limit to cardiac device manufacturers, who were falling over themselves scrambling to design and market the next new device.

The angioplasty market then had ballooned (no pun intended) from nothing to a multi-billion dollar industry. Stents were just getting underway but clearly had potential for being at least as large.

But this was a time when preventive therapies were also beginning to get quite powerful. We had just gotten started doing CT heart scans and were excited about the possibilities, statin drugs were gaining evidence through clinical trials, and the power of many nutritional supplements was finally achieving validation. We were even learning the error of our prior low-fat ways.

So I broadly pronounced to the enthusiastic product representative, "In 10 years, balloons, angioplasty, and stents will occupy this little corner of cardiac care because prevention will have become so powerful. We won't talk about heart procedures. We'll talk about coronary plaque regression!"

I even advised the representative that he should consider a career change in anticipation of the coming wave of preventive strategies.

Was I ever wrong. Despite the power of heart disease prevention--which is indeed true--cardiac device and procedure technology has boomed, both in popularity as well as in revenue success. Device manufacturing and sales are hugely successful. Implanting devices into people is a hugely profitable enterprise.

Since my ill-timed comments to the salesman, Boston Scientific, a major manufacturer of stents and other cardiac devices, reported revenues of $6.2 billiondollars in 2005, a 12% increase over the prior year. Medtronic reported 2005 revenues of $11.3 billion, growing at 15% per year. Clearly, cardiac procedures are still quite popular--and profitable.

My timing was off, but not for long. The huge crest of change in preventive therapies is upon us. That's the premise behind the Track Your Plaque concept: heart disease prevention can't be found in a hospital, is not supported by cardiac device manufacturers, and is not being advocated by most cardiologists or primary care physicians. Yet the tools are getting better and better every day.

Those of you who succeed in halting or reducing your heart scan score are extremely unlikely to add to Boston Scientific's or Medtronic's revenues. Help me spread the word.

Don't forget how dangerous heart disease can be

29. July 2006 William Davis (0)
Sometimes it's easy to get smug when coronary plaque is a reversible process.

When you see people day in, day out, week in, week out, drop their heart scan scores, reversing what could be a dangerous disease, you can sometimes lose sight of just how dangerous coronary disease can be.

Whether I like it or not, I maintain a reasonably active role in hospitals out of necessity. I do need their services occasionally for people with advanced heart disease when I meet them (when regression is not the initial conversation for safety reasons), or valve disease is diagnosed, or someone shows up with congenital or heart muscle diseases. In other words, although we focus on coronary issues, there's more to heart disease than just coronary disease.

This unfortunate case just served to remind me how powerful coronary disease can be. Elizabeth, an active 67-year old, finally came to the hospital after suffering 6 months of chest pain and increasing breathlessness. She hated hospitals and hadn't seen a doctor in 30 years since she was successfully treated for cancer.

In those 30 years, she'd been quite active with family and a small business. But she also smoked 2 packs of cigarettes most of those years.

After she was admitted to the hospital, it became clear that Elizabeth had experienced one, if not several, heart attacks along the way. The entire front 2/3 of her heart was non-functional. If that wasn't bad enough, two of her heart valves were severely diseased and dysfunctional: Her aortic valve barely opened (aortic valve "stenosis", or stiffness) and the mitral valve leaked severely (mitral valve "insufficiency", or leakiness). All of this was confirmed with conventional testing in the hospital, including a heart catheterization.

Elizabeth ended up in emergency surgery--very unusual, by the way, for valve surgery of the sort she had--but died in the first few hours after her procedure. Her heart had simply been too damaged from her heart attacks, and the extraordinary stress of surgery that included two valves was too much. She died on the ventilator.

Coronary disease is a very serious matter. When I see cases like Elizabeth, it boosts my commitment to tell everyone that heart disease--when identified early enough--is a controllable, preventable, even reversible process. For poor Elizabeth, she was much too far down the path of severe, irreversible disease that control or reversal was simply not an option. She was in imminent danger of dying even upon arrival.

It's exciting yet sometimes frightening to know what you have in your hands: The means to control this monster called coronary disease. Use it wisely. But don't lose sight of what it can do it you permit it to grow, fester, and explode.

How many ways can you disguise sugar?

28. July 2006 William Davis (0)
I came across this shockingly silly report on AOL, who obtained their info courtesy Health Magazine:

The Best New Healthy Foods for Busy People
from Health

The foods on their list:

Kettle Brand Bakes Hickory Honey BBQ--the healthy claim is based on the lack of trans-fatty acids and low-fat.










Post Healthy Classics Raisin Bran Cereal Bars, Cranberry--Likewise, low-fat, sweet, and addictive means healthy to these people.




Amy’s Mediterranean Pizza With Cornmeal Crust --Please!!



Horizon Organic Colby Cheese Sticks --Because it's made by cattle without use of growth hormone or antibiotics, they declare this healthy. I guess we can ignore the saturated fat content and high total fat content.

100% Whole Grain Chips Ahoy! Cookies --You mean we can add the bran back to wheat products and make it healthy?!


This kind of mass-market marketing trickery leaves me incredulous. Don't believe it for a moment. This is typical of the food industry: Take one aspect of nutrition that is truly healthy, such as high-fiber, or low-fat, or organic. Then add undesirable, unhealthy ingredients. The current fad is to add lots of sugar and or sugar-equivalents (usually flour and other wheat products). Because there's one healthy ingredient, they'll call the end-product healthy, too.

If you want to see what health looks like if you indulge in "healthy" products like this, just look up and down the grocery aisles at your neighborhood grocery store. You're likely to see the results: Gross obesity, diabetes, and arthritis.

You won't, of course, see the huge acceleration of growth in coronary plaque, but it's there, ticking away.

To remind us what ideal body weight is: Watch an old movie!

26. July 2006 William Davis (0)
Jack was skeptical. At 273 lbs, 5 ft 11 inches, he felt that he was "just right".

"I feel fine. I don't see why you think I should lose weight," he declared. "In fact, when I lost 25 lbs a couple of years ago, everyone said I was too skinny!"

I showed Jack why: He had an HDL of 35 mg/dl, small LDL (over 90% of all LDL particles), an elevated blood sugar of 123 mg/dl (diabetes is officially 126 mg/dl or greater), high blood pressure, and increased inflammation (C-reactive protein). These were all manifestations that his body weight was too much for it to handle.




So I told Jack that we've all forgotten what ideal weight should look like. Our perception of "normal" has been so utterly and dramatically distorted by the appearance of our friends, family, co-workers, and other people around us that we've all lost a sense of what a desirable weight for health should be.




So I suggested to Jack that, if he wanted to rememember what ideal weight is and what people are supposed to look like, just watch old movies.

Old movies, like the 1942 production of Casablanca, or the 1952 production of Singin' in the Rain, show the body build that was prevalent in those days. Look at Humphrey Bogart or Gene Kelly--men with average builds, weighing 140-160 lbs--that's how humans were meant to look.

A report this morning on the Today Show showed the "after" photos of several people following bariatric (weight reduction) surgery. The "after" pictures, from the perspective of ideal weight and ideal health, remain hugely overweight.

We need to readjust our perceptions of weight. The average woman in the U.S. now weighs 172 lbs(!!!). Don't confuse average with desirable.

Diabetes is a choice you make

24. July 2006 William Davis (0)
Tim had heart disease identified as a young man. He had his first heart attack followed by a quadruple bypass surgery at age 38. Recurrent anginal chest pain and another small heart attack led to several stents over three procedures in the first four years after bypass.

Tim finally came to us, interested in improving his prevention program. You name it, he had it: small LDL, low HDL (28 mg/dl), lipoprotein(a), etc. The problem was that Tim was also clearly pre-diabetic. At 5 ft 10 inches, he weighed 272 lbs--easily 80 or more pounds overweight.

Tim was willing to make the medication and nutritional supplement changes to gain control over his seeminglly relentless disease. He even turned up his exercise program and lost 28 lbs in the beginning. But as time passed and no symptoms recurred, he became lax.

Tim regained all the weight he'd lost and some more. Now Tim was diabetic.

"I don't get it. I eat good foods that shouldn't raise my insulin. I almost never eat sweets."

I stressed to Tim that diabetes and pre-diabetes, while provoked acutely by sugar-equivalent foods (wheat products, breads, breakfast cereals, crackers, etc.), is caused chronically by excess weight. If Tim wants to regain control over his heart disease, he needed to lost the weight.

Unlike, say, leukemia, an unfortunate disease that has little to do with lifestyle choices, diabetes is a choice you make over 90% of the time. In other words, if you become diabetic (adult variety, not children's variety) as an adult, that's because you've chosen to follow that path. You've neglected physical activity, or indulged in too many calories or poor food choices, or simply allowed weight to balloon out of control.

But diabetes is also a path most people can choose not to take. And it is a painfully common choice: Nearly two-thirds of the adults in my office have patterns of pre-diabetes or diabetes when I first meet them.

Let me stress this: For the vast majority of adults, diabetes is a choice, not an inevitability.

I'll call the doctor when I feel bad!

24. July 2006 William Davis (0)
Max just had his heart scan. He sat down with the x-ray technologist at the work console while she pointed out the white areas in his coronary arteries that represented plaque.

"It looks like you're going to have a fairly high score," the technologist commented. "The final report will be available after one of our cardiologists reviews your images."

Max shrugged. "Well, I don't feel anything. I'm always running around with work, with my kids, stuff like that. That's better than any stress test. I guess I'll worry about it if it starts to bother me."


You'd be surprised how common this view remains: If it's not bothering you, then just forget about it. It's easy to do, since you have no symptoms, nothing to impair your physical activities. But what are the potential consequences of ignoring your heart scan? Here's a few:

--Prevention and plaque reversal efforts are most effective the earlier you start. From a heart scan score viewpoint, the lower your starting score, the easier it is to gain control over it. More people will succeed in reducing their score when the starting score is lower.

--The role of prevention of heart disease instantly crystallizes when you know your score. Your LDL cholesterol of 142 mg/dl or HDL of 41 mg/dl no longer seem like just numbers of borderline signficance. Instead, they become useful tools to gain control over plaque. They cast your numbers in a new and clear light.

--Knowing your heart scan score today gives you a basis for comparison in future. Your score of, say 250, today, can be 220 in one year. Without your preventive efforts, it will be 30% higher: 325. That's a big difference!

--Sudden death or heart attack--can occur in up to 35-40% of people with hidden heart disease--without warning.

Don't even bother getting a heart scan if you're going to ignore it. I've said it before and I'll say it again: A heart scan is the most important health test you can get--but only if you do something about it.
All posts by william-davis

"You've got 10 minutes"

20. May 2009 William Davis (0)
There's a new trend in office healthcare in Milwaukee: Time-restricted office visits.



I'm told by several physicians who are employed by a major healthcare system here in town that they are peridically watched--physically watched by an administrator--to make sure that they do not exceed the allotted 10 minutes of time. My cardiologist colleagues, I gather, were at first incredulous at such intrusions into their practices, but apparently had no choice: They were employees.



Goiter, goiter everywhere

20. May 2009 William Davis (25)
The results of the recent Heart Scan Blog poll are in.

The question:

Do you used iodized salt?

The responses:

Yes, I use iodized salt every day
94 (28%)

Yes, I use iodized salt occasionally
56 (16%)

No, I do not use any iodized salt
41 (12%)

No, I use a non-iodized salt (sea salt, Kosher)
126 (37%)

No, I use a non- or low-sodium substitute
15 (4%)


Thanks for your responses.

If only 28% of people are regular users of iodized salt, that means that the remainder--72%--are at risk for iodine deficiency if they are not getting iodine from an alternative source, such as a multivitamin or multimineral.

Even the occasional users of salt can be at risk. The common perception is that occasional use is probably sufficient to provide iodine. This is probably not true and not just because of the lower quantity of ingestion. Occasional users of salt tend to have their salt canister on the shelf for extended periods. The iodine is then lost, since iodine is volatile. In fact, iodine is virtually undetectable four weeks after a package is opened.

In my office, now that I'm looking for them much more systematically and carefully, I am finding about 2 people with goiters every day. They are not the obvious grotesque goiters of the early 20th century (when quack therapies like the last post, the Golden Medical Discovery, were popular). The goiters I am detecting are small and spongy. Yesterday alone I found 5 people with goiters, one of them visible to the eye and very distressing to the patient.

It seems to me that iodine deficiency is more prevalent than I ever thought. It is also something that is so simple to remedy, though not by increasing salt intake. Kelp tablets--cheap, available--have been working quite well in the office population. My sense is that the Recommended Daily Allowance of 150 mcg per day for adults is low and that many benefit from greater quantities, e.g., 500 mcg. What is is the ideal dose? To my knowledge, nobody has yet generated that data.

Thyroid issues being relatively new to my thinking, I now find it incredible that endocrinologists and the American Thyroid Association are not broadcasting this problem at the top of their lungs. This issue needs to be brought to the top of everyone's attention, or else we'll have history repeating itself and have goiters and thyroid dysfunction galore.

For more on this topic, see the previous Heart Scan Blog post, "Help keep your family goiter free."

Goiter and the Golden Medical Discovery

17. May 2009 William Davis (19)

Thick neck, or goitre . . . consists of an enlargement of the thyroid gland, which lies over and on each side of the trachea, or windpipe, between the prominence known as "Adam's apple" and the breast bone. The tumor gradually increases in front and laterally, until it produces great deformity, and often interferes with respiration and the act of swallowing. From its pressure on the great blood vessels running to and from the head, there is a constant liability to engorgement of blood in the brain, and to apoplexy, epilepsy, etc.

The causes of the affection are not well understood. The use of snow water, or water impregnated with some particular saline or calcareous matter, has been assigned as a cause. It has also been attributed to the use of water in which there is not a trace of iron, iodine, or bromine. . . The disease is often due to an impeded circulation in the large veins of the neck, from pressure of the clothing, or from the head being bent forward, a position which is often seen in school children.


Treatment

We have obtained excellent results in many cases, not too far advanced, by a method of treatment which consists in the employment of electrolysis. . . Many cases at the present time are operated upon with entire success.

Those who are afflicted with this disease and unable to avail themselves of special treatment cannot do better than to take Doctor Pierce's Alterative Extract, or Golden Medical Discovery, and apply over the skin around the tumor, night and morning, the following, which may be prepared at any drug store:

Resublimed Iodine--One dram
Iodide of Potassium--Four drams
Soft Water--Three ounces 


Apply to the tumor, twice daily, with feather or camel hair pencil.


From The People's Common Sense Medical Adviser by R.V. Pierce, MD; 1918.

Magnesium and you-Part I

15. May 2009 William Davis (11)
If this were 10,000 B.C., you'd get your drinking water from streams, rivers, and lakes, all rich in mineral content. Humans became reliant on obtaining a considerable proportion of daily mineral needs from natural water sources.

21st century: We obtain drinking water from a spigot or plastic bottle. Pesticides and other chemicals seep into the water supply. Municipal water purification facilities have intensified water purification in most communities to remove contaminants like lead, pesticide residues, and nitrates. (For a really neat listing of the water quality of various cities, the University of Cincinnati makes this data available.)

But intensive water treatment also removes minerals like calcium and magnesium.

Many people have added water filters or purifiers to their homes,, like reverse osmosis and distillation, that are efficient at extracting any remaining minerals, converting “hard” into “soft” water. In fact, manufacturers of such devices boast of their power to yield pure water free of any “contaminant,” minerals like magnesium included. The magnesium content of water after passing through most commercial filters is zero.

Modern enthusiasm for bottled water has compounded the problem. Americans consumed a lot of bottled water, nearly 8 billion gallons last year. In the U.S., nearly all bottled water has little or no magnesium.

The result is that we can no longer rely on drinking water to provide magnesium. The Recommended Daily Allowance (RDA)—the amount required to prevent severe deficiency—for magnesium is 420 mg per day for men, 320 mg/day for women. In cities with the highest magnesium water content, only 30% of the RDA can be obtained by drinking two liters of tap water per day. In most cities, only a meager 10–20% of the daily requirement can be obtained. That leaves between 70–90% that needs to come from other sources. As a result, the average American ingests substantially less than the RDA.

Blast triglycerides

15. May 2009 William Davis (0)
The conventional answers to high triglycerides levels are generally: low-fat diet, a fibrate drug (Tricor, Lopid), a statin drug, and--most recently--prescription fish oil.

This is the regimen to take if you want the drug industry to get even richer and more powerful than they already are. After all, what CEO of a pharmaceutical company can stand to have his salary and benefits slashed to below $200 million this year? It's outrageous!

If you really want to blast the heck out of your triglycerides and achieve numbers like 50 mg/dl, then the regimen to consider consists of:

--Elimination of sugars, wheat, and cornstarch
--Fish oil--Sam's Club would do fine at $8 for 350 capsules, or the high-potency at $14.99 for 180 capsules (at 680 mg EPA +DHA, nearly the same potency as prescription Lovaza at 842 mg)
--Vitamin D supplementation sufficient to achieve normal blood levels (60-70 ng/ml)

Those three strategies alone can reduce triglycerides far more than any drug combination. In fact, it is rare for someone with triglycerides as high as 900 mg/dl to not reduce them to the <100 mg/dl range.

Cheerios: Prescription required?

13. May 2009 William Davis (15)
Followers of The Heart Scan Blog know my feelings about Cheerios:


Can you say "sugar"?

Cheerios and heart health


There's an interesting tussle going on between the makers of Cheerios, General Mills, and the FDA.

The FDA says that the Cheerios' package claims of:

• "you can Lower Your Cholesterol 4% in 6 weeks"
• "Did you know that in just 6 weeks Cheerios can reduce bad cholesterol by an average of 4 percent? Cheerios is ... clinically proven to lower cholesterol. A clinical study showed that eating two 1 1/2 cup servings daily of Cheerios cereal reduced bad cholesterol when eaten as part of a diet low in saturated fat and cholesterol."

constitute a medical claim, i.e., trying to promote Cheerios as a drug.

I'm glad that the FDA has come down on General Mills. But I find this entire episode laughable: The debate is over the purported health benefits of what I would regard as pure junk food, no better in my view than claiming that a cupcake has health benefits, or a carton of ice cream.

In my experience, Cheerios does not 1) reduce risk for heart disease, nor 2) reduce cholesterol.

It does, however, cause blood sugar to skyrocket and increase the small type of LDL--you know, the type that causes heart disease.

"Placebos are frequently of value"

12. May 2009 William Davis (1)
The treatment of angina pectoris, generally speaking, is unsatisfactory.

Any procedure that relieves mental tension is valuable. Since patients suffer particularly during the winter, I encourage winter vacations in a southern climate.

I insist that obese patients lose weight, and have found small doses of benzedrine, 10 to 20 mg. daily, helpful in curbing the appetite.

I generally forbid smoking. This is a particularly disturbing task for many patients to carry out. In such cases, I suggest that 3 or 4 cigarettes be smoked daily, knowing full well that regardless of what I say or recommend, the patients is going to continue to smoke.

Innumerable drugs, most of which are of questionable value, have been used to prevent attacks of angina pectoris. In fact, placebos are frequently of value.

Testosterone--The male sex hormone has been effective in my experience. Whether it acts as a vasodilator or merely by promoting a sense of well-being is not known.

Alcohol--Alcohol (whiskey, brandy, rum) has been used for many years in the treatment of angina pectoris. I have prescribed it in moderate quantity--an ounce several times a day--and while I have not made alcoholics of any of my patients, I also have not cured any of them with it. Preparations, such as creme de menthe, are of value in relieving "gas" of which so many patients complain.


From Heart Disease Diagnosis and Treatment
Emanuel Goldberger, MD
1951

Iodine is not salt

12. May 2009 William Davis (3)
I've noticed a point of confusion recently, something I hadn't noticed in my patients before: Because of the public health advice from the FDA, American Heart Association, and Surgeon General's office to reduce sodium/salt intake, people have thought this meant reducing iodine, too.

I believe that people have drawn an equation in their minds:


Sodium = iodine


Of course, they are two entirely unrelated things.

Recall that the only reason iodine is added to many (not all) salt products is because it was a public health solution to solve the substantial nationwide iodine deficiency prevalent during the 20th century. But it was a solution conceived in 1924, when the FDA thought this was the best way to get iodine into Americans. And it worked.

Unfortunately, sodium does indeed present adverse effects in some people. As a result, "get your iodine from salt" has evolved into "reduce your sodium intake." Everyone forgot about the iodine: They forgot about the large disfiguring goiters, the poor school performance in iodine-deficient schoolchildren, the mentally-impaired offspring of iodine-deficient mothers.

So don't confuse sodium with iodine. You may need less of the former, but more of the latter.

For more on this, see "Help keep your family goiter free."

"You can't reduce coronary plaque"

10. May 2009 William Davis (9)
"I told my cardiologst that I stumbled on a program called 'Track Your Plaque' that claims to be able to help reduce your coronary calcium score.

"My cardiologist said, 'That's impossible. You cannot reduce coronary plaque. I've never seen anyone reduce a heart scan score."

Who's right here?

The commenter is right; the cardiologist is wrong.

I would predict that the cardiologist is among the conventionally-thinking, "statins drugs are the only solution" group who follows his patients over the years to determine when a procedure is finally "needed." In fact, I know many of these cardiologists personally. The primary care physicians are completely in the dark, usually expressing an attitude of helplessness and submitting to the "wisdom" of their cardiology consultants.

Quantify and work to reduce the atherosclerotic plaque? No way! That's work, requires thinking, some sophisticated testing (like lipoprotein testing), even some new ideas like vitamin D. "They didn't teach that to me in medical school (back in 1980)!"

Welcome to the new age.

Atherosclerotic plaque is 1) measurable, 2) trackable, and 3) can be reduced.

We do it all the time. (Amy still holds our record: 63% reduction in plaque/heart scan score.)

Though I pooh-pooh the value of statin drug studies, there's even data from the conventional statin world documenting coronary plaque reversal. The ASTEROID Trial of rosuvastatin (Crestor), 40 mg per day for one year, demonstrated 7% reduction of atherosclerotic plaque using intracoronary ultrasound.

I have NEVER seen a heart attack or appearance of heart symptoms (angina, unstable angina) in a person who has reversed coronary plaque (unless, of course, they pitched the whole effort and returned to bad habits--that has happened). Stick to the program and coronary risk, for all practical purposes, been eliminated.

A heart scan score is not a death sentence. It is simply a tool to empower your prevention program, a measuring stick to gauge plaque progression, stabilization, or regression. Don't accept anything less.

Lethal lipids

8. May 2009 William Davis (15)
There's a specific combination of lipids/lipoproteins that confers especially high risk for heart disease. That combination is:

Low HDL--generally less than 50 mg/dl

Small LDL--especially if 50% or more of total LDL

Lipoprotein(a)--an aggressive risk factor by itself


This combination is a virtual guarantee for heart disease, often at a young age. It's not clear whether each risk factor exerts its own brand of undesirable effect, or whether the combined presence of each cause some adverse interaction.

For instance, lipoprotein(a), or Lp(a), by itself is the most aggressive risk factor known (that nobody's heard about--there's no blockbuster revenue-generating drug for it). Each Lp(a) molecule is a combination of an LDL cholesterol molecule with a specific genetically-determined protein, apoprotein(a). If the LDL component of Lp(a) is small, then the combination of Lp(a) with small LDL is somehow much worse, kind of like the two neighborhood kids who are naughty on their own, but really bad when they're together.

Interestingly, the evil trio responds as a whole to many of the same corrective treatments:

Niacin--increases HDL, reduces small LDL, and reduces Lp(a)

Elimination of wheat, cornstarch, and sugars--Best for reducing small LDL; less potent for Lp(a) reduction.

High-fat intake--Like niacin, effective for all three.

High-dose fish oil--Higher doses of EPA + DHA north of 3000 mg per day also can positively affect all three, especially Lp(a).


If you have this combination, it ought to be taken very seriously. Don't let anybody tell you that it is uncorrectable--just because there may be no big revenue-generating drug to treat it on TV does not mean that there aren't effective treatments for it. In fact, some of our biggest successes in reducing heart scan scores have had this precise combination.
All posts by william-davis

Genetic vs. lifestyle small LDL

19. February 2010 William Davis (59)
Let me explain what I mean by "genetic small LDL." I think it helps to illustrate with two common examples.

Ollie is 50 years old, 5 ft 10 inches tall, and weighs 253 lbs. BMI = 36.4 (obese). Starting lipoproteins (NMR):

LDL particle number 2310 nmol/L
Small LDL: 1893 nmol/L (1893/2310 = 81.9% of total, a severe small LDL pattern)


Stan is 50 years old, also, 5 ft 10 inches tall, and weighs 148 lbs. BMI = 21.3. Starting lipoproteins:

LDL particle number 1424 nmol/L
Small LDL 1288 nmol/L (1288/1424 = 90.4% of total, also severe)


Both Ollie and Stan go on the New Track Your Plaque diet and eliminate wheat, cornstarch, and sugars, while increasing oils, meats and fish, unlimited raw nuts, and vegetables. They add fish oil and vitamin D and achieve perfect levels of both. Six months later, Ollie has lost 55 lbs, Stan has lost 4 lbs. A second round of lipoproteins:

Ollie:

LDL particle number 1810 nmol/L
Small LDL: 193 nmol/L (193/1810 = 10.6% of total)


Stan:

LDL particle number 1113 nmol/L
Small LDL 729 nmool/L (729/1113 = 65.4% of total)


Ollie has reduced, nearly eliminated, small LDL through elimination of wheat, cornstarch, and sugars, along with weight loss, fish oil, and vitamin D.

Stan, beginning at a much more favorable weight, reduced both total and small LDL with the same efforts, but retains a substantial proportion (65.4%) of small LDL.

Stan's pattern is what I call "genetic small LDL." Of course, this is a presumptive designation, since we've not identified the specific gene(s) that allow this (e.g., gene for variants of cholesteryl ester transfer protein, hepatic lipase, lipoprotein lipase, and others). But it is such a sharp distinction that I am convinced that people like Stan have this persistent pattern as a genetically-determined trait.

Carbohydrate sins of the past

17. February 2010 William Davis (15)
Fifty years ago, diabetes was a relatively uncommon disease. Today, the latest estimates are that 50% of Americans are now diabetic or pre-diabetic.

There are some obvious explanations: excess weight, inactivity, the proliferation of fructose in our diets. It is also my firm belief that the diets advocated by official agencies, like the USDA, the American Heart Association, the American Dietetic Association, and the American Diabetes Association, have also contributed with their advice to eat more “healthy whole grains.”

When I was a kid, I ate Lucky Charms® or Cocoa Puffs® for breakfast, carried Hoho’s® and Scooter Pies® in my lunchbox, along with a peanut butter sandwich on white bread. We ate TV dinners, biscuits, instant mashed potatoes for dinner. Back then, it was a matter of novelty, convenience, and, yes, taste.

What did we do to our pancreases eating such insulin-stimulating foods through childhood, teenage years, and into early adulthood? Did our eating habits as children and young adults create diabetes many years later? Could sugary breakfast cereals, snacks, and candy in virtually unlimited quantities have impaired our pancreas’ ability to produce insulin, leading to pre-diabetes and diabetes many years later?

A phenomenon called glucose toxicity underlies the development of diabetes and pre-diabetes. Glucose toxicity refers to the damaging effect that high blood sugars (glucose) have on the delicate beta cells of the pancreas, the cells that produce insulin. This damage isirreversible: once it occurs, it cannot be undone, and the beta cells stop producing insulin and die. The destructive effect of high glucose levels on pancreatic beta cells likely occurs through oxidative damage, with injury from toxic oxidative compounds like superoxide anion and peroxide. The pancreas is uniquely ill-equipped to resist oxidative injury, lacking little more than rudimentary anti-oxidative protection mechanisms.

Glucose toxicity that occurs over many years eventually leaves you with a pancreas that retains only 50% or less of its original insulin producing capacity. That’s when diabetes develops, when impaired pancreatic insulin production can no longer keep up with the demands put on it.

(Interesting but unanswered question: If oxidative injury leads to beta cell dysfunction and destruction, can antioxidants prevent such injury? Studies in cell preparations and animals suggest that anti-oxidative agents, such as astaxanthin and acetylcysteine, may block beta cell oxidative injury. However, no human studies have yet been performed. This may prove to be a fascinating area for future.)

Now that 50% of American have diabetes or pre-diabetes, how much should we blame on eating habits when we were younger? I would wager that eating habits of youth play a large part in determining potential for diabetes or pre-diabetes as an adult.

The lesson: Don’t allow children to repeat our mistakes. Letting them indulge in a lifestyle of soft drinks, candy, pretzels, and other processed junk carbohydrates has the potential to cause diabetes 20 or 30 years later, shortening their life by 10 years. Kids are not impervious to the effects of high sugar, including the cumulative damaging effects of glucose toxicity.

Saturated fat and large LDL

16. February 2010 William Davis (44)
Here's a half-truth I often encounter in low-carb discussions:

Saturated fat increases large LDL particles


For those of you unfamiliar with the argument, I advocate a low-carbohydrate approach, specifically elimination of all wheat, cornstarch, and sugars, to reduce expression of the small LDL pattern (not to mention reduction of triglycerides, relief from acid reflux and irritable bowel, weight loss, various rashes, diabetes, etc). Small LDL particles have become the most common cause for heart disease in the U.S., exploding on the scene ever since agencies like the USDA and American Heart Association have been advising the public to increase consumption of "healthy whole grains."

This has led some to make the pronouncement that saturated fat increases large LDL, thereby representing a benign effect.

Is this true?

It is true, but only partly. Let me explain.

There are two general categories of factors causing small LDL particles: lifestyle (overweight, excess carbohydrates) and genetics (e.g., variants of the gene coding for cholesteryl-ester transfer protein, or CETP).

If small LDL is purely driven by excess carbohydrates, then adding saturated fat will reduce small LDL and increase large LDL.

If, on the other hand, your small LDL is genetically programmed, then saturated fat will increase small LDL. In other words, saturated fat tends to increase the dominant or genetically-determined form of LDL. If your dominant genetically-determined form is small, then saturated fat increases small LDL particles.

So to say that saturated fat increases large LDL is an oversimplification, one that can have dire consequences in the wrong situation.

Is glycemic index irrelevant?

14. February 2010 William Davis (20)


University of Toronto nutrition scientist, Dr. David Jenkins, was the first to quantify the phenomenon of "glycemic index," describing how much blood sugar increased over 90 minutes compared to glucose. The graph is from their 1981 study, The glycemic index of foods: a physiologic basis for carbohydrate exchange. The research originated with an effort to characterize carbohydrates for diabetics to gain better control over blood sugar.

Since Dr. Jenkins’ original work, thousands of clinical studies have been performed by others exploring this concept. The food industry has also devoted plenty of effort exploiting it (e.g., low-glycemic index noodles, low-glycemic index cereals, etc.).

Most Americans are now familiar with the concept of glycemic index. You likely know that table sugar has a high glycemic index (60), increasing blood sugar to a similar degree as white bread (glycemic index 71). Oatmeal (slow-cooked) has a lower glycemic index (48), since it increases blood sugar less than white bread.

A number of studies have shown that when low glycemic index foods replace high glycemic index foods (e.g., whole wheat bread in place of cupcakes), people are healthier: less diabetes, less heart attack, less high blood pressure. Books have been written about glycemic index, touting its benefits for health and weight control. Health-conscious people will try to substitute low-glycemic index foods for high-glycemic index foods.

So what’s not to like here?

There are several fundamental flaws with the notion that low-glycemic index foods are good for you:

1) Check your blood sugar after a low-glycemic index food like oatmeal. Most non-diabetic adults will show blood sugars in the 140 to 200 mg/dl range. The more central (visceral) fat you have, the higher the value will be. In other words, an apparently “healthy” whole grain food like oatmeal can generate extravagantly high blood sugars. Repeated high blood sugars of 125 mg/dl or greater after eating increase heart disease risk by 50%.

2) Foods like whole wheat pasta have a low glycemic index because the blood sugar effect over the usual 90 minutes is increased to a lesser degree. The problem is that it remains increased for an extended period of up to several hours. In other words, the blood sugar-increasing effect of pasta, even whole grain, is long and sustained.

3) Low-glycemic index foods trigger other abnormalities, such as small LDL particles, triglycerides, and c-reactive protein (a measure of inflammation). While they are not as bad as high-glycemic index foods, they are still quite potent triggers.

Low-glycemic index foods trigger the very same responses as high-glycemic index foods—they’re just less bad. But less bad does not equate to good. Low-glycemic index foods cause weight gain, trigger appetite, increase blood pressure, and lead to the patterns that cause heart disease.

High-glycemic index foods are bad for you. This includes foods made with white flour (bagels, white bread, pretzels). Low-glycemic foods (whole grain bread, whole wheat crackers, whole wheat pasta) are less bad for you—but they are not necessarily good.

Don’t be falsely reassured by foods because they are billed as “low-glycemic index.” View low-glycemic index foods as indulgences, something you might have once in a while, since a slice of whole grain bread is really not that different from a icing-covered cupcake.

What Mr. Clinton did NOT do

12. February 2010 William Davis (36)
You've likely already heard that former President Bill Clinton underwent a heart catheterization today during which one of the bypass grafts to his coronary arteries was found to be occluded. The original coronary artery was therefore stented.

Dr. Alan Schwartz, Mr. Clinton's cardiologist, announced to the gathered press that Mr. Clinton had followed a good diet, had adopted a regular exercise program, but that his condition is a "chronic disease" like hypertension that is not cured by these efforts.



Needing a stent just 6 years after four bypass grafts are inserted is awfully soon. I would propose that it has less to do with having a "chronic disease" and more to do with all the things that Mr. Clinton likely is NOT doing. (In addition to all the other things that Mr. Clinton did not do.) In other words, in the Track Your Plaque world, procedures are a rarity, heart attacks virtually unheard of. I would wager that Mr. Clinton has been doing none of the following:

--Taking fish oil. Or, if his doctor was "advanced" enough to have advised him to take fish oil, not taking enough.
--Vitamin D--Followers of the Heart Scan Blog already know that vitamin D is the most incredible health find of the last 50 years, including its effects on reducing heart disease risk. Unless Mr. Clinton runs naked in a tropical sun, he is vitamin D deficient. A typical dose for a man his size is 8000 units per day (gelcap only!).
--Eating a true heart healthy diet. I'll bet Mr. Clinton's doctor, trying to do the "right" thing, follows the prudent course of advising a "balanced diet" that is low in fat--you know, the diet that causes heart disease. Judging by Mr. Clinton's body shape (central body fat), it is a virtual certainty that he conceals a severe small LDL pattern, the sort that is worsened by grains, improved with their elimination.
--Making sure that hidden causes are addressed--In addition to the "hidden" small LDL, lipoprotein(a) is another biggie. Lp(a) tends to be the province of people with greater than average intelligence. I believe Mr. Clinton qualifies in this regard. I would not be at all surprised if Mr. Clinton conceals a substantial lipoprotein(a) pattern, worsened in the presence of small LDL.
--Controlling after-meal blood sugars--Postprandial (after-eating) blood sugars are a major trigger for atherosclerotic plaque growth. There are easy-to-follow methods to blunt the after-meal rise of blood sugar. (This will be the subject of an in-depth upcoming Track Your Plaque Special Report.)
--Thyroid normalization--It might be as simple as taking iodine; it might involve a little more effort, such as supplemental T3. Regardless, thyroid normalization is an easy means to substantially reduce coronary risk and slow or stop coronary plaque growth.


It's not that tough to take a few steps to avoid bypass surgery in the first place. Or, if you've already had a procedure, a few additional steps (of the sort your doctor will likely not tell you about) and you can make your first bypass your only bypass.

Magnesium and arrhythmia

11. February 2010 William Davis (35)
Because magnesium is removed during municipal water treatment and is absent from most bottled water, deficiency of this crucial mineral is a growing problem.

Magnesium deficiency can manifest itself in a wide variety of ways, from muscle cramps (usually calves, toes, and fingers), erratic blood sugars, higher blood pressure, to heart rhythm problems. The abnormal heart rhythms that can arise due to magnesium deficiency include premature atrial contractions, premature ventricular contractions, multifocal atrial tachycardia, atrial fibrillation, and even ventricular tachycardia, fibrillation, and Torsade de Pointes (all potentially fatal). Magnesium is important!

Magnesium supplementation is therefore necessary for just about everybody to maintain normal tissue levels. (The exception is people with kidney disorders, who should not take magnesium without supervision, since they retain magnesium.)

Here is a Heart Scan Blog reader's dramatic rhythm-correcting response to magnesium supplementation:



Dr. Davis,

A few months ago, I contacted you inquiring if you had written any articles on arrhythmia. You were generous enough to answer and guide me to an LEF article you'd written in which you stressed fish oil and magnesium. I had been suffering with bad PVCs [premature ventricular contractions] for over 20 years, and they had gotten so bad recently that I was told my next options were ablation or pacemaker!

I was already on fish oil and had not seen any difference, and so I researched the magnesium you suggested more thoroughly and found a huge body of studies supportng its effect on arrhythmia. I also read many posts on heart forums with people having success with it. After getting advice from various bloggers, I tried magnesium taurate in the morning and Natural Calm (an ionized form of mag citrate) in the afternoon and evening. Within three days the PVCs were quite diminished and by 2 weeks totally gone! As long as I keep taking it, they never return---not even one irregular blip---even when I drink strong coffee! The magnesium also cleared up my restless leg syndrome, my eye twitching, and insomnia. (Apparently, I was the poster-girl for magnesium deficiency.)

I am so angry that after all these years of suffering, trying various medications, and seeing at least 4 different cardiologists that NOT ONE ever even mentioned trying magnesium. The generosity of the few minutes you took to answer my email and steer me in a helpful direction brought me total relief.

Thank you SO MUCH!

Warmly,
Catherine C.

Video teleconference with Dr. Davis

10. February 2010 William Davis (4)

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.

Thinner by Thursday

10. February 2010 William Davis (0)
You want to lose a few pounds . . . Okay, maybe 50 or 75.

Should you exercise? Lengthen you workout? Push the plate away, deny yourself seconds, use a smaller plate?

Of all the weight loss strategies I've tried in patients, there's only one that stands out as a means of obtaining immediate--meaning within 3 days--weight reduction.

Wheat elimination.

Omega-3 Index: 10% or greater?

9. February 2010 William Davis (19)
We've previously considered the question:

What is an ideal level of omega-3 fatty acids in the blood?

Recall that omega-3 levels in red blood cells (RBCs), a measure called the "omega-3 index," have been associated with risk for sudden cardiac death:





In a recent analysis, 265 people experiencing sudden death during a heart attack (ventricular fibrillation, successfully resuscitated) showed an omega-3 index of 4.88%, while 185 people not experiencing sudden death during a heart attack showed an omega-3 index of 6.08%.

We have more ambitious goals than just avoiding sudden death, of course! How about the omega-3 index associated with reduced risk for heart attack? A recent analysis of females from the Harvard School of Public Health suggested that RBC omega-3 levels as high as 8.99% were still associated with non-fatal heart attack (myocardial infarction), compared to 9.36% in those without heart attacks, suggesting that even higher levels are necessary to prevent non-fatal events.

Most recently, another study comparing 50 people after heart attack with 50 controls showed that people with heart attack had an omega-3 index of 9.57% vs 11.81% in controls--even higher. (This study was in a Korean population with higher fish consumption. There was also a powerful contribution to risk from trans fat RBC levels.) The investigators concluded: "The area under the receiver operating characteristic curve of fatty acid profiles was larger than that for traditional risk factors, suggesting that fatty acid profiles make a higher contribution to the discrimination of MI cases from controls compared with modified Framingham risk factors."

The data suggest that, while an omega-3 index of 7.3% is associated with reduced risk for sudden cardiac death, a higher level of 10% or greater is associated with less risk for heart attack. Surprisingly, fish consumption and fish oil intake account for only 47% of the variation in omega-3 index.

I believe the emerging data are becoming increasingly clear: If you desire maximal control over heart health, know your omega-3 index and keep it 10% or higher.

Let's soak 'em with fish oil

8. February 2010 William Davis (12)
If you don't think that charging drug prices for fish oil is wrong, take a look at a letter from an angry Heart Scan Blog reader:


Hello Dr. Davis,

My 44 year old brother had an MI [myocardial infarction, or heart attack] in June. He got pushed around due to "bad government insurance," a state-run program for the "uninsured": government pays 1/3, job pays 1/3, and individual pays 1/3.

What they didn't tell him is that there is no major medical coverage and little to no prescription coverage. We fought for 4 months to get him open heart surgery that the insurance was not going to pay for.

Now, with no assistance, terrible insurance, and no disability he has little to no income. He is a heavy equipment mechanic and is trying to be the "good American"-- take care of his bills, not file bankruptcy, etc.

Anyway, the doctors never seem to pay attention to what they prescribe. Lipitor was not working for him, due to side effects. Now they want to give him Zetia and Lovaza....Zetia at $114, and Lovoza is $169.85! Wow! For dead fish???? I think this is a little fishy! I looked up Lovaza, gee how nice, they will give you a $20 coupon....

Forget it, he can't afford this stuff. So I am enrolling in the Zetia program for him. And trying to get him OTC [over-the-counter] fish oil. The most prevalent fish oil around here (that I take myself is) Omega 3 Fish Oil that has EPA 410mg, DHA 274.

Thanks for your blog. It made me feel better that I wasn't the only one outraged by this stuff. I 've been a nurse for 20 years and it just never seems to get better. Thank you for your wisdom.

Sincerely JP, Tennessee


Had this reader not been aware that her brother could take fish oil as a nutritional supplement, he likely would have been denied the benefit of omega-3 fatty acids in slashing the risk for recurrent cardiovascular events. You and I can buy wonderfully safe and effective fish oil as a nutritional supplement, but there won't be a sexy drug representative to sell it, nor an expensive dinner and payment for a trip to Orlando to hear about it.