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

Don't be satisfied with "deceleration"

16. November 2007 William Davis (2)

In the Track Your Plaque program, we aim to stop or reduce your heart scan score.

Recall that, without any preventive efforts, heart scan scores can be expected to increase at the average rate of 30% per year (faster at lower scores, slower at higher scores by a quirk of arithmetic).

I am continually surprised at how often people--that is, people not in the Track Your Plaque program--are often content with what I term "deceleration," or the slowing of plaque growth. In truth, most people are content with deceleration of plaque growth because they simply don't know that plaque continues to grow.

For instance, the BELLES Trial (Beyond Endorsed Lipid Lowering with EBT Scanning (BELLES)), reported in 2005 showed that 650 women participants continued to increase heart scan scores 15% whether they took "high-intensity" statin therapy in the form of Lipitor 80 mg or "low-intensity" statin therapy as pravastatin 40 mg, even though the group taking Lipitor experienced twice the amount of LDL reduction. In other words, heart scan scores continued to increase at the same rate of 15% per year regardless of the intensity of LDL lowering by statin drug.

Another study reported in 2006, Effect of intensive versus standard lipid-lowering treatment with atorvastatin on the progression of calcified coronary atherosclerosis over 12 months: a multicenter, randomized, double-blind trial reported similar results. Of the 471 participants, those taking Lipitor 80 mg per day experienced 27% per year plaque growth (LDL cholesterol 87 mg/dl); those taking 10 mg Lipitor experienced 25% plaque growth (LDL 107 mg/dl). The intensity of statin therapy made no difference on the rate of plaque growth.

In other words, if we are content to sit back and take Lipitor or other statin drug, follow the conventional American Heart Association low-fat, low-cholesterol diet, we will experience somewhere between 15 to 27% annual plaque growth--year after year.

No wonder that conventional advice offered by your friendly neighborhood doctor will avoid (postpone?) only one heart attack in four.

Such is the nature of coronary plaque deceleration: growth is modestly slowed, but is not stopped. Nor is it reversed.

In the Track Your Plaque program, we grade deceleration of plaque growth into three distinct stages out of a total of five. (See Winning Your Personal War with Heart Disease: The Track Your Plaque 5 Stages of Success.)

Why be satisfied with deceleration? Why not aim for a total stop to plaque growth? Why not aim for stage 5 of Track Your Plaque success: reversal?

Whole grains and half truths

14. November 2007 William Davis (13)

(For followers of the Heart Scan Blog, below is a re-posting of a recent post. I've moved it up to make it accessible to a number of patients that I asked to look at this post for some conversation about the concept of wheat-free diets.)

TV ads, media conversations, magazine articles, even advice from the American Heart Association and USDA (a la Food Pyramid) all agree: eat more whole grains, get more fiber.

What happens when you follow this advice to add more and more whole grains to your diet? Look around you: People gain weight, they become pre-diabetic and diabetic. Lipids and lipoprotein patterns emerge: increased triglycerides and VLDL, reduced HDL, small LDL. Blood sugar goes up, inflammatory responses are ignited. You feel crumby, cancer risk is increased.

"Official" agencies have urged us to eat more grains, get more fiber and most Americans have complied. We now have a nationwide health disaster that will eventually lead to more people with coronary plaque, more heart disease, more heart attack, more heart procedures.

This is why I've been urging patients to go wheat-free. It has proven an extraordinarily and surprisingly effective strategy for:

1) rapid and profound weight loss
2) raising HDL and reducing triglycerides, VLDL, and small LDL
3) reducing blood sugars, pre-diabetes and diabetes

So here I (re-) post just a sampling of the comments sent by readers of the Heart Scan Blog who have given this idea a try.

Barbara W said:

It's true! We've done it. My husband and I stopped eating all grains and sugar in February. At this point, we really don't miss them any more. It was a huge change, but it's worth the effort. I've lost over 20 pounds (10 to go)and my husband has lost 45 pounds (20 to go). On top of it, our body shapes have changed drastically. It is really amazing. I've got my waist back (and a whole wardrobe of clothes) - I'm thrilled.

I'm also very happy to be eating foods that I always loved like eggs, avocados, and meats - without feeling guilty that they're not good for me.

With the extremely hot weather this week in our area, we thought we'd "treat" ourselves to small ice cream cones. To our surprise, it wasn't that much of a treat. Didn't even taste as good as we'd anticipated. I know I would have been much more satisfied with a snack of smoked salmon with fresh dill, capers, chopped onion and drizzled with lemon juice.

Aside from weight changes, we both feel so much better in general - feel much more alert and move around with much greater flexibility, sleep well, never have any indigestion. We're really enjoying this. It's like feeling younger.

It's not a diet for us. This will be the way we eat from now on. Actually, we think our food has become more interesting and varied since giving up all the "white stuff". I guess we felt compelled to get a little more creative.

Eating out (or at other peoples' places) has probably been the hardest part of this adjustment. But now we're getting pretty comfortable saying what we won't eat. I'm starting to enjoy the reactions it produces.

Weight loss, increased energy, less abdominal bloating, better sleep--I've seen it many times, as well.

Dotslady said:

I was a victim of the '80s lowfat diet craze - doc told me I was obese, gave me the Standard American Diet and said to watch my fat (I'm not a big meat eater, didn't like mayo ... couldn't figure out where my fat was coming from! maybe the fries - I will admit I liked fries). I looked to the USDA food pyramid and to increase my fiber for the constipation I was experiencing. Bread with 3 grams of fiber wasn't good enough; I turned to Kashi cereals for 11 years. My constipation turned to steattorrhea and a celiac disease diagnosis! *No gut pains!* My PCP sent me to the gastroenterologist for a colonscopy because my ferritin was a 5 (20 is low range). Good thing I googled around and asked him to do an endoscopy or I'd be a zombie by now.

My symptoms were depression & anxiety, eczema, GERD, hypothyroidism, mild dizziness, tripping, Alzheimer's-like memory problems, insomnia, heart palpitations, fibromyalgia, worsening eyesight, mild cardiomyopathy, to name a few.

After six months gluten-free, I asked my gastroenterologist about feeling full early ... he said he didn't know what I was talking about! *shrug*

But *I* knew -- it was the gluten/starches! My satiety level has totally changed, and for the first time in my life I feel NORMAL!

Feeling satisfied with less is a prominent effect in my experience, too. You need to eat less, you're driven to snack less, less likely to give in to those evil little bedtime or middle-of-the-night impulses that make you feel ashamed and guilty.

An anonymous (female) commenter said:

My life changed when I cut not only all wheat, but all grains from my diet.

For the first time in my life, I was no longer hungry -no hunger pangs between meals; no overwhelming desire to snack. Now I eat at mealtimes without even thinking about food in between.

I've dropped 70 pounds, effortlessly, come off high blood pressure meds and control my blood sugar without medication.

I don't know whether it was just the elimination of grain, especially wheat, or whether it was a combination of grain elimnation along with a number of other changes, but I do know that mere reduction of grain consumption still left me hungry. It wasn't until I elimnated it that the overwhelming redution in appetite kicked in.

As a former wheat-addicted vegetarian, who thought she was eating healthily according to all the expert advice out there at the time, I can only shake my head at how mistaken I was.

That may be a record for me: 70 lbs!!

Stan said:

It's worth it and you won't look back!

Many things will improve, not just weight reduction: you will think clearer, your reflexes will improve, your breathing rate will go down, your blood pressure will normalize. You will never or rarely have a fever or viral infections like cold or flu. You will become more resistant to cold temperature and you will rarely feel tired, ever!

Ortcloud said:

Whenever I go out to breakfast I look around and I am in shock at what people eat for breakfast. Big stack of pancakes, fruit, fruit juice syrup, just like you said. This is not breakfast, this is dessert ! It has the same sugar and nutrition as a birthday cake, would anyone think cake is ok for breakfast ? No, but that is exactly the equivalent of what they are eating. Somehow we have been duped to think this is ok. For me, I typically eat an omelette when I go out, low carb and no sugar. I dont eat wheat but invariably it comes with the meal and I try to tell the waitress no thanks, they are stunned. They try to push some other type of wheat or sugar product on me instead, finally I have to tell them I dont eat wheat and they are doubly stunned. They cant comprehend it. We have a long way to go in terms of re-education.

Yes. Don't be surprised at the incomprehension, the rolled eyes, even the anger that can sometimes result. Imagine that told you that the food you've come to rely on and love is killing you!

Anne said:

I was overweight by only about 15lbs and I was having pitting edema in my legs and shortness of breath. My cardiologist and I were discussing the possible need of an angiogram. I was three years out from heart bypass surgery.

Before we could schedule the procedure, I tested positive for gluten sensitivity through www.enterolab.com. I eliminated not only wheat but also barley and rye and oats(very contaminated with wheat) from my diet. Within a few weeks my edema was gone, my energy was up and I was no longer short of breath. I lost about 10 lbs. The main reason I gave up gluten was to see if I could stop the progression of my peripheral neuropathy. Getting off wheat and other gluten grains has given me back my life. I have been gluten free for 4 years and feel younger than I have in many years.

There are many gluten free processed foods, but I have found I feel my best when I stick with whole foods.

Ann has a different reason (gluten enteropathy, or celiac disease) for wanting to be wheat-free. But I've seen similar improvements that go beyond just relief of the symptoms attributable to the inflammatory intestinal effects of gluten elimination.

Wccaguy said:

I have relatively successfully cut carbs and grains from my diet thus far.

Because I've got some weight to lose, I have tried to keep the carb count low and I've lost 15 pounds since then.

I have also been very surprised at the significant reduction in my appetite. I've read about the experience of others with regard to appetite reduction and couldn't really imagine that it could happen for me too. But it has.

A few weeks ago, I attended a party catered by one of my favorite italian restaurants and got myself offtrack for two days. Then it took me a couple of days to get back on track because my appetite returned.

Check out Jimmy Moore's website for lots of ideas about variations of foods to try. The latest thing I picked up from Jimmy is the good old-fashioned hard boiled egg. Two or three eggs with some spicy hot sauce for breakfast and a handful of almonds mid-morning plus a couple glasses of water and I'm good for the morning no problem.

I find myself thinking about lunch not because I'm really hungry but out of habit.

The cool thing too now is that the more I do this, the more I'm just not tempted much to do anything but this diet.

Going wheat-free, along with a reduction in processed sugary foods like Hawaiian Punch, sodas, and candy, is the straightest, most direct path I know of to lose weight, obtain all the health benefits listed by our commenters, as well as achieve the lipoprotein corrections we seek, like reduction of small LDL particles and rise in HDL, in the Track Your Plaque program.

Fasting and heart disease

14. November 2007 William Davis (10)

Followers of the Track Your Plaque program know that we advocate periodic fasts to reduce heart disease risk.

I came across an interesting report form an abstract presented at last week's American Heart Association meetings in Orlando:

(Read the report at HeartWire. You will need to register or sign-in.)

In this study, the investigators tried to determine why members of the Church of Jesus Christ of Latter-Day Saints (LDS) tended to have reduced risk of heart disease compared to others in the area but not in the LDS faith. While the reduced risk of heart disease in LDS members had been traditionally attributed to the no smoking policy advocated by the Mormon church, the investigators suspected that there was more to the reduced risk.

Of 515 people interviewed, periodic fasting, whether for religious or other reasons, was found to distinguish people who were less likely to have coronary disease by conventional catheterization (59% vs. 67%). (Since the study was published in only abstract form, it's not clear why all these people underwent heart catheterization in the first place.)

Nonetheless, it's an interesting observation and one consistent with the benefits we see when someone fasts: reduced blood pressure, reduced inflammatory responses, improved lipids and lipoproteins, weight loss.

Fasting can be an especially effective method to gain control over heart disease and coronary plaque if rapid control is desired. In fact, I wonder if the normally year-long process of plaque control that I advocate can be much abbreviated. Fasting, I believe, is a crucial component of rapid control, what I've talked about in Instant Heart Disease Reversal

There's also additional thoughts on fasting in my Heart Scan Blog post, For rapid success, try the "fast" track.

Fasting is not something to fear. It can be an enlightening process that can serve to abruptly sever bad habits, perhaps even turn the clock back on prior dietary and lifestyle excesses. My favorite variation on fasting is to use soy milk (yes, yes, I know! I can already hear the the soy bashers screaming!) as a meal substitute. It is an easy, less dramatic way that still maintains most of the benefit of a full, water-only fast.

Coronary arteries aren't what they seem

12. November 2007 William Davis (5)

Why do stress tests so often fail to detect coronary atherosclerotic plaque? Why do even heart catheterizations--the "gold standard"--fail to disclose the full extent of plaque within the walls of coronary arteries?

We owe much of the explanation of these phenomena to Dr. Seymour Glagov, retired professor of pathology at the University of Chicago.

When studying the coronary arteries of people who died, he observed that people commonly had plenty of atherosclerotic plaque lining the artery wall, yet it did not necessarily impinge on the artery "lumen," or the internal path for blood to flow.

The only time the lumen became obstructed by plaque was when either 1) plaque grew to overwhelming levels and was severe and extensive, or 2) when a plaque had "ruptured," meaning its thin covering had been penetrated and eroded by the underlying plaque tissue like a volcano emerging from the surface and erupting.

This groundbreaking observation, now dubbed "the Glagov phenomenon," explains why someone can have a normal stress test on Tuesday but erupt a plaque on Wednesday.

The Glagov phenomenon also explains why heart scans can detect plaque when both stress tests and heart catheterizations fail to do so. Many physicians will then interpret this to mean that the heart scan was wrong. With the Glagov phenomenon in mind, you can see that the heart scan is not wrong, it is simply detecting coronary atherosclerotic plaque at a stage that is not yet detectable by the other methods.

In the illustration, you can see that the lumen of the vessel is maintained--despite the artery on the left having minimal plaque, the artery on the right containing moderate plaque. If either artery were examined by a test that relies on blood flow--stress test or heart catheterization--both would appear normal. But a test that examines the artery wall, such as a heart scan, would readily detect the artery on the right and probably even the artery on the left.

I am very grateful to Dr. Glagov and his insight into this important process. Otherwise, we might still be floundering around trying to understand the apparent discrepances between these tests that simply provide different perspectives on the same problem.

Heart disease reversal a big "No No"

11. November 2007 William Davis (7)

I dare you: Ask your doctor whether coronary heart disease can be reversed.

My prediction is that the answer will be a flat "NO." Or, something like "rarely, in extraordinary cases," kind of like spontaneous cure of cancer.

There are indeed discussions that have developed over the years in the conventional scientific and medical literature about reversal of heart disease, like Dean Ornish's Lifestyle Heart Trial, the REVERSAL Trial of atorvastatin (Lipitor) and the ASTEROID Trial of rosuvastatin (Crestor). Reversal of atherosclerotic plaque in these trials tends to be small in scale and sporadic.

Of course, the medical literature is swamped with studies that have nothing to do with reversal, like what stent is best, what platelet-inhibiting intravenous drug is best, when should angioplasty or stents be used and when, do implantable defibrillators save lives, improvements in coronary bypass techniques, etc. There are tens of thousands of these studies for every study that focuses on the question of atherosclerotic plaque reversal.

The concept of reversal of heart disease has simply not gained a foothold in the lexicon nor in the thinking of practicing physicians. Heart disease is a relentlessly, unavoidably, and helplessly progressive disease in their way of thinking. Perhaps we can reduce the likelihood of cardiovascular events like heart attack and death with statin drugs and beta blockers. But reverse heart disease ? In your dreams!

We need to change this mentality. Heart disease is a reversible phenomenon. Atherosclerosis in other territories like the carotid arteries is also a reversible pheneomenon. Rather than throwing medicines and (ineffective) diets at you (like the ridiculous American Heart Association program), what if your doctor set out from the start not just to reduce events, but to purposefully reduce your heart's plaque? While it might not succeed in everyone, it would certainly change the focus dramatically.

After all, isn't this the theme followed in cancer treatment? If you had a tumor, isn't cure the goal? Would we accept an oncologist's advice to simply reduce the likelihood of death from cancer but ignore the idea of ridding yourself completely of the disease? I don't think so.

Then why accept "event reduction" as a goal in heart disease? We shouldn't have to. Heart disease reversal--elimination--should be the goal.

Demystification

11. November 2007 William Davis (2)

Once upon a time, remember how medical information was mysterious, hospitals were places where frightening, inscrutable things happened, diseases were strange maladies that struck without reason, and obtaining information about health was like hunting for buried treasure? The full extent of many peoples' understanding of health came through relatively anemic sources like Readers' Digest. (Remember "I am Joe's Colon"?)

Compare this to what we have now. If I wanted to obtain information about ankylosing spondylitis (a rare genetic disease of the spine), a Google search yields 1.46 million citations. Not all the information, of course, is helpful or relevant, but there's certain to be a bounty of information that far exceeds what you could have uncovered 40 years ago.

Suppose you enter the search phrase "antithrombin III" into your Google search. Citations: over 900,000. (The number of search citations, in fact, exceeds the number of Americans with a deficiency of this blood clotting protein!)

The same is true with heart disease. There was a time, not more than 30-40 years ago, when information about the heart and heart disease was hard to come by. The most you would find were superficial discussions about heart attacks, what chest pain means, descriptions of bypass surgery. Ask your doctor, you'd likely receive a brief, cursory response about how you probably shouldn't worry it.

Even during medical school in the 1980s, I remember struggling to get answers to my questions from faculty during medical school and medical training. It was as if providing too much information would eliminate the advantage superiors wielded over trainees.

The same selfish sentiment, the "I know something you don't know" mentality reminiscent of a schoolboy's "naa na na naa naa!" unfortunately persists. But it is rapidly disintegrating. Soon it will join the junk heap of medical mis-information accumulated over the years (a big pile, to be sure). The internet and, I'll admit (grudgingly), the media, have been responsible for demystifying the formerly mysterious and indecipherable world of health.

You now have, at a moment's disposal, access to an extraordinary array and breadth of health information that was inconceivable just a few years ago.

Times are changing. Doctors no longer hold the monopoly over health information. The public--YOU--are rapidly becoming the arbiters of health, the informed consumers of a soon-to-be retail product called health care, and the increasingly savvy judges of what should join the mainstream path of health. It is all part of this wave of change that I've been advocating: the emerging concept of self-empowerment in healthcare.

Added to the junk heap of health-mistakes-of-years-past will be medical protectionism over health information, heart procedures, drug industry excesses, nutritional mis-information, among others. The demystification of health information will open the floodgates of individual insight into health. It delivers control over your own health destiny straight into your own lap.

Everything has omega-3

8. November 2007 William Davis (5)

Walking the supermarket aisles, you may have lately noticed that numerous new products are appearing sporting "omega-3s" on the label.

Some products simply contain alpha-linolenic acid, a tiny amount of which is converted to the biologically active omega-3s, EPA and DHA. Natural Ovens' Brainy Bagel, for instance, carries a claim of "620 omega-3."

I find this confusing and misleading, since people will often interpret such a claim to mean that it contains 620 of EPA and DHA, similar to two capsules of standard fish oil (1000 mg capsules). Of course, it does NOT. I find this especially troublesome when people will actually stop or reduce their fish oil, since they've been misled into thinking that products like this bread contain active omega-3 fatty acids that yield all the benefits of the "real stuff."

Other products actually contain the omega-3, DHA, though usually in small quantities. Breyer's Smart with DHA is an example, with 32 mg DHA per container.

I find products with actual DHA (from algae) a more credible claim. However, the Center for Science in the Public Interest (CSPI) has looked at the actual contents of DHA in some of these products and found some discrepancies, including amounts of DHA less than the labeled amount and claims of omega-3 wihtout specifying DHA vs. linolenic acid. (It's probably linolenic acid, if it's not specified.)

All in all, the addition of DHA to food products is a nice way to boost your intake of this healthy omega-3. However, keep in mind that these are processed, often highly processed, foods and you will likely pay a premium for the little boost. For now, stick to fish oil, the real thing.

For a brief summary of the CSPI report and a link to the Nutrition Action Newsletter, see Omega-3 Madness: Fish Oil or Snake Oil.

Are cardiologists the enemy?

7. November 2007 William Davis (12)

I'm sitting at dinner with two colleagues. One is a cardiology colleague, another an internist who, in addition to practicing general internal medicine, also takes heart disease prevention very seriously. He has, in fact, participated in the Track Your Plaque program and dropped his heart scan score substantially.

"Why don't we see you in the cath lab much?" my cardiology colleague asked me. He was puzzled, since he knew my background in cath lab work from years before, spending day and night doing procedure after procedure. He spends virtually all his days there.

"Well, my patients simply don't have events any more. Heart attacks and angina among people in my program are just about non-existent. They don't have symptoms and they don't have to go to the hospital. I can't remember the last time that I was woken up in the middle of the night for an urgent procedure for one of my patients."

The internist across the table smiled and expressed his agreement. "That's the same thing I'm seeing: No heart attacks, very few if any referrals to cardiologists for procedures. I remember when it was a several times a week thing. Now, almost never. "

Looking at my cardiology colleague, I saw the usual cardiologist reaction: Eyes searching left and right and behind us for something more interesting. Certainly, talking about a virtual cure for coronary heart disease was just too damn dull.

Such is the attitude of 98% of my colleagues: If it doesn't generate a revenue-producing procedure, why bother? Prevention is for general practitioners, the line of thinking goes. "And anyway, I'm too busy doing procedures! I don't ahve time to talk about prevention and health!" Of course, the poor general practitioner is already overloaded with caring for arthritis, flu, diabetes and all the new drugs for diabetes, headaches, vaccinations, diarrhea, and . . .oh, yes, heart disease prevention.

Are cardiologists the enemy? No, of course they are are not. But they often act like they are. Talking to cardiologists is like going to the car dealer with your checkbook out, pen in hand. The salesman gets to write the check himself and you just sign it. Talk to a cardiologist and more often than not you will end up with a heart procedure--whether or not you need it.

Unfortunately--tragically--they often forget what they are supposed to be doing: Taking care of a disease by preventing it. Putting in a defibrillator is not preventing a disease. Putting in three stents, laser angioplasty, and thrombectomy are not ways of preventing a disease.

I'm thankful for my internist friend who sees the light. Coronary heart disease is a an easily measurable, quantifiable, preventable, and REVERSIBLE process for many, if not most, people when provided the right tools. But don't ask your neighborhood cardiologists to give you those tools.

Are CETP inhibitors kaput?

6. November 2007 William Davis (9)

Was torcetrapib’s crash and burn fatal for this class of drug?

At the 2007 American Heart Association meetings in Orlando, Florida, Dr. Philip Barter of Sydney, Australia, presented an update of the ILLUMINATE drug trial for the once-promising drug, torcetrapib, the billion-dollar bet that Pfizer made on its first entry into the new drug class.

You may recall that the crash and burn of Pfizer’s torcetrapib in December 2006 made headlines and prompted enormous disappointment for many patients and doctors who had hoped for a new drug choice to raise HDL cholesterol. Pfizer executives (heads flew!) and investors were also disappointed, anticipating release of a drug that might have become the number one biggest selling drug in the world—ever, surpassing even Lipitor's® $13 billion annual sales.

Torcetrapib is the first among the “cholesteryl-ester transfer protein inhibitors,” or CETP-inhibitors, drugs that block the exchange of cholesterol and triglycerides between HDL and VLDL particles and prevent formation of the unwanted small LDL particles. Preliminary efforts suggested that effects were positively enormous.

However, the 15,000-participant trial was abruptly terminated after 550 days when an excess of deaths were identified among the group taking the experimental drug: 59 deaths in control group; 93 deaths in the torcetrapib group.

In addition, cardiovascular events were 24% greater in the torcetrapib group, numbering 373 compared to 464 in the no-torcetrapib group, including a substantially greater number of heart attacks and hospitalizations. Another surprise came in the way of cause of death among some of the torcetrapib patients, with an excess of deaths due to cancers (twice as many in the torcetrapib group), strokes, and infections.

Why the divergence: enormous improvements in cholesterol values, yet increase in adverse effects including more heart attack? Deeper digging by the principal investigators uncovered unexpected distortions of electrolytes like sodium and potassium. They then re-analyzed blood samples from participants on both sides of the trial and discovered that participants taking torcetrapib experienced significant rise in the blood pressure hormone, aldosterone. This, they surmised, also likely accounted for the 4 mmHg average rise in blood pressure among those taking the experimental drug. (This is the same pathway blocked by blood pressure drugs like ACE inhibitors lisinopril and enalapril, ARBs like losartan.)

Simultaneously (what a coincidence!) with the torcetrapib data, investigators at competing drug manufacturer, Merck, reported encouraging data with their version of CETP inhibitor, anacetrapib. In a phase II FDA trial of 589 patients, anacetrapib reduced LDL-C levels by up to 40% and increased HDL-C up to 139%.

Spokesman Daniel Bloomfield, M.D., of Merck Research Laboratories reported that "The favorable lipid effects seen in this study with multiple doses of anacetrapib were significant, and confirm the continued evaluation of the clinical benefits of CETP inhibitors in the treatment of dyslipidemia." Quick to distinguish this drug from torcetrapib’s track record of dangerous effects on blood pressure, he added that "the decreased LDL-C concentrations, increased HDL-C concentrations and no demonstrable increase in blood pressure seen with anacetrapib are particularly encouraging results of this study."

However, the data reported only an 8 week expereince. Given the experience with torcetrapib, longer term data will obviously be required to assess safety. After Pfizer spent over $1 billion and sacrificed lives to obtain this experience, Merck will need to tread carefully.

It will clearly be many years before we have a confident answer on whether the CETP-inhibitor class of drugs will be a safe choice for correction of cholesterol abnormalities, especially low HDL. Are we helpless until then?

Though CETP inhibitors offer the potential for a one-stop opportunity to raise HDL substantially, there are still many strategies available to raise HDL.

Strategies that raise HDL and are available today include:
• Weight loss—to your ideal weight. A very effective strategy.
• Reduction in processed carbohydrates—like breads, pasta, cookies, pretzels, etc. Note that very low-fat diets reduce HDL. Often a huge effect.
• Fish oil—A small effect, more dramatic when triglycerides are high.
• Niacin—Vitamin B3, the best we have at present. Doses of 500-1500 mg per day raise HDL 20–50%; work with your doctor if you are contemplating niacin. We use this agent everyday and have had great success; good hydration is key to minimize the annoying “hot-flush” effect.
• Dark chocolate—40 grams, or about 2 inches square, a delicious way to squeeze out a little rise in HDL.
• Alcoholic beverages—Red wines are almost certainly the preferred route, rich in flavonoids.
• Exercise—HDL-raising effects vary, but can sometimes be as much as 10–20 mg.
• Other drugs—Though not commonly used for this effect, drugs like pioglitazone (for diabetes and pre-diabetes); fibrates (Tricor® or fenofibrate; Lopid® or gemfibrozil); and Pletal® or cilostazol are occasionally prescribed.
• Vitamin D—You won’t find validation of this effect in any scientific study, but our emerging experience in our heart disease reversal program is suggesting that this neglected nutrient can exert powerful HDL-raising effects. In fact, supplementing vitamin D has made my life much easier.

And, last I checked, none of these HDL-raising strategies are ever fatal.

Roto Rooter for plaque

4. November 2007 William Davis (4)

Joe, a machinist, was frightened and frustrated.

With a heart scan score of 1644 at age 61, his eyes bulged when I advised him that, if preventive efforts weren't instituted right away, his risk for heart attack was a high as 25% per year. Joe had "passed" a stress test, thus suggesting that, while coronary plaque was present--oodles of it, in fact--coronary blood flow was normal. Thus, there would be no benefit to inserting three stents, say, or a bypass operation.

(Illustration courtesy Wikipedia)

"I don't get it, doc. Why can't you just take it out? You know, like Roto-Rooter it out? Or give me something to dissolve it!"

Of course, if there were such a thing, I'd give it to him. But, of course, there is not. It doesn't mean that there haven't been efforts in this direction over the years. Among the various attempts made to "Roto-Rooter" atherosclerotic plaque have included:

Coronary endarterectomy
This is a drastic procedure rarely performed anymore but enjoyed some popularity in the 1980s and 1990s. Coronary endarterectomy was performed during coronary bypass surgery, but few thoracic surgeons performed it. Milwaukee's Dr. Dudley Johnson was the foremost practitioner of this procedure (retired a few years ago after his own bypass operation) with a mortality in excess of 25%. A very dangerous procedure, indeed. The technical hurdle, beyond the tedium and length of time required to remove plaque that had a tendency to fragment, was blood clot formation after tissue was exposed upon plaque removal. I saw many lengthy hospital stays and deaths following this procedure.

Coronary atherectomy
This is an angioplasty-type procedure that has gone through several variations over the years.

In the early 1990s, transluminal extraction atherectomy (TEC) was a technique involving low-rpm drill bits with a suction apparatus that was used to clear soft debris, usually from large coronary arteries or, more commonly, bypass grafts. Then came direction atherectomy, in which a steel housing contained a sharp drill bit that captured atherosclerotic plaque in an aperture along the housing length and stuffed it into a nosecone, retrieved once the device was removed.

Then came high-speed rotational atherectomy in which a diamond-tipped drill bit rotated up to 200,000 rpm and essentially pulverized plaque to flow downstream and, presumably, eventually captured by the liver for disposal. Rotational atherectomy is still in use on occasion. Laser angioplasty, usually using the excimer wavelength, vaporizes plaque. I did plenty of all of these back in the early and mid-1990s.

While all atherectomy procedures sound clever, they are all plagued by the same problem: vigorous return of plaque. Remove plaque, it grows back. There are few instances today in which atherectomy is still performed.

Chelation
This involves a metal-binding, or "chelating," agent like EDTA normally used in conventional practice for lead poisoning. Usually administered IV, some have also advocated oral use. People who use chelation also tend to believe in faith healing and other practices based on faith, not science. There is an international trial that is nearing completion that should provide the final word on whether there is any role to intravenous chelation.

There are numerous other oral treatments that claim a Roto-Rooter-like effect. Nattokinase, for example--an outright, unadulterated, and unqualified scam.

Unfortunately, the helpless, ignorant, and gullible are many. When frightened by the specter of heart disease, there are plenty of people who will willingly pay for the hope provided by clever ads, fast-talking salespeople, and unscrupulous practitioners.

So, Joe, there is no Roto-Rooter for coronary atherosclerotic plaque, at least one that is safe, doesn't involve a life-threatening effort, provides results that endure beyond a few months, and truly works.

The Track Your Plaque program may not be easy. There are obvious common hurdles to adhering to these concepts: obtaining lipoprotein testing, getting intelligent interepretation of the results, persuading your doctor to measure vitamin D blood levels, battling the onslaught of prevailing food propaganda that confuses and misleads. The Track Your Plaque program also requires time, at least a year.

But it's the best program there is. Do you know of anything better?

All posts by william-davis

The world according to the Wheat Foods Council and the Whole Grains Council

23. April 2010 William Davis (26)

You might get a kick out of what the Wheat Foods Council and the Whole Grains Council recommend for a sample meal plan:

Breakfast: Whole grain raisin toast

Lunch: Sandwich on whole grain
Snack: Rye bread crackers
Dinner: Whole grain pasta with your favorite sauce

Breakfast: Whole grain waffles

Lunch: Hamburger on whole grain bun

Snack: Graham crackers

Dinner: Whole grain homemade pizza on whole grain pita crust

Remember Morgon Spurlock's documentary movie, Super Size Me? (If you haven't already seen it, Super Size Me is viewable for free on Hulu.) Spurlock conducts a self-inflicted 30-day experiment of eating at McDonald's fast food restaurants every day. In short, the results on Spurlock's weight and health are disastrous.

How about Wheat Belly: The Movie? We would chronicle our star through a 30-day course of meals served up by the Wheat Foods and Whole Grains Councils, all featuring wonderful wheat products in every meal. We could measure blood sugar, triglycerides, LDL, small LDL, weight, etc.

Any predictions?

Why bananas increase cholesterol

21. April 2010 William Davis (0)

Anything that increases postprandial (after-eating) blood sugar will increase the number of LDL particles in the blood.

An increase in LDL particles is an important factor in causing heart disease: The greater the number of LDL particles, the more opportunity they have to interact with the walls of arteries, contributing to atherosclerosis.

Carbohydrates increase small LDL, especially if postprandial sugar is increased. Here's another way carbohydrates increase LDL particles: The duration of time LDL particles hang around in the blood stream is doubled.

When blood sugar increases, such as after the 30 grams carbohydrates in a medium-sized banana, glycation of LDL particles occurs. This means that a gglucose (sugar) molecule reacts with a lysine residue in the apoprotein B of the LDL particle. This induces a change in conformation that makes it less readily recognized by the LDL receptor. Thus, the glycated LDL particle persists for a longer period of time in the blood stream.

LDL particles are therefore cleared less efficiently, numbers of LDL particles increase.

Plant-based or animal-based?

19. April 2010 William Davis (78)

The ideal diet for heart and overall health restricts carbohydrate intake. I say this because carbohydrates:

Make you fat--Carbohydrates increase visceral fat, in particular.
Increase triglycerides
Reduce HDL
Increase small LDL particles
Increase glycation of LDL
Increase blood pressure
Increase c-reactive protein

Reducing carbohydrates reverses all the above.

But here's a common mistake many people make when following a low-carbohydrate diet: Converting to a low-carb, high-animal product diet.

It accounts for a breakfast of a 3-egg omelette with cheese and butter, 4 strips of bacon, 2 sausages, cream in coffee. Low-carb? It certainly is. But it is a purely high-animal product, no-plant-based meal.

I believe a strong argument can be made that a low-carbohydrate but plant-based diet with animal products as the side dish is a better way to go.

Consider that:

1) Animal products have little to no fiber, while plant-based products like spinach, avocado, and walnuts and other raw nuts have substantial quantities.

2) Plant products are a source of polyphenols and flavonoids--This encompasses a large universe of nutrients, from epigallocatechins in tea, polymeric procyanidins from cocoa, to hydroxytyrosol from olives, and anthocyanins from red wine and eggplant. The inflow of these beneficial compounds needs to be frequent and generous, not piddly amounts taken infrequently.

3) Vitamin C--While it's easy to obtain, the fact that you and I need to obtain vitamin C from frequent ingestion of plant sources suggests that humans were meant to eat lots of plants. While it may require a few months of deficiency before your teeth fall out, imagine what low-grade deficiency can do over a long period.

4) Vitamin K1--Rich in green vegetables, vitamin K1 is virtually absent in animal products.

5) Tocotrienols--I've been watching the data on this fascinating family of powerful oil-soluble antioxidants unfold for 20 years. Tocotrienols come only from plants. (I recently had an extended conversation with the brilliant biochemist, Dr. Barrie Tan, who is incredibly knowledgeable about tocotrienols, having developed several methods of extraction from plants, including his discovery of the highly concentrated source, annatto. Be sure to watch for future conversations about tocotrienols.)

6) Meats and dairy yield a net acid load--While plant foods are net basic. At the very least, this yields risk for osteoporosis, since acids are ultimately buffered by basic calcium salts from the bones. Tissue and blood pH is a tightly regulated system; veering off just a teensy-weensy bit from the normal pH of 7.4 to an acidic pH of, say, 7.2, leads to . . . death. In short, pH control is very important. A net acid challenge from animal products is a lot like drinking carbonated soda, a huge acid challenge that leads to osteoporosis and other health issues.

Conversely, a pure plant-based diet has its own set of problems. Eating a pure plant-based diet can lead to deficiencies of vitamin B12, omega-3 fatty acids (no, linolenic acid from flaxseed will NOT cut it), vitamin K2, carnitine, and coenzyme Q10.

So, rather than a breakfast of 3-egg omelet with bacon, sausage, cream, and cheese, how about a handful of pecans, some blueberries, and a 2-egg omelet made with basil-olive oil pesto? Or a spinach salad with walnuts, feta cheese, and lots of olive oil?

Fat is not the demon

16. April 2010 William Davis (36)

So my patient, Dane, generously volunteered to be on the Dr. Oz show, as I discussed previously.

What we didn't know, nor did the producer who contacted us mention, that Dane would be counseled by low-fat guru Dr. Dean Ornish on a strict low-fat diet. The teaser introduction essentially tells the entire story.

Ironically, that is the exact opposite of the dietary program that I advocate. I rejected the 10% fat diet long ago after I became a type II diabetic, gained 30 lbs, and suffered miserable deterioration of my cholesterol values on this diet. I also witnessed similar results in many hundreds of people, all following a strict low-fat diet. In fact, elimination of wheat--whole, white, or otherwise--along with limitation or elimination of all other grains has been among the most powerful health strategies I have ever witnessed.

I now regret having subjected my patient to this theatrical misinformation. Dane is a smart cookie--That's probably why he was not allowed more than a "yes" or "no" during Dr. Oz's monologue, else Dane might have pitched in about some ideas that would have tripped Oz and Ornish up.

In their defense, if we took 100 Americans all following a typical 21st century diet of fast food, white bread buns, Coca Cola and other soft drinks, chips, barbecue sauce, and French fries, converting to a plant-based, high-carbohydrate, grain-rich diet is indeed an improvement. People will, at first, lose weight and enjoy an initial response. (The occasional person with the Apo E4 genetic pattern, heterozygote or homozygote, may even enjoy long-term benefits, a topic for another day.)

But the majority of people, in my experience, after an initial positive response to an Ornish-like low-fat, high-carbohydrate diet will either plateau (stay overweight, have low HDL, high triglycerides, plenty of small LDL, and high blood sugars) or deteriorate, much as I did.

Thankfully, Dane has been a good sport about this, understanding that this is essentially show business. I believe he understands that the information was all well-intended and, after all, we are all working towards the same goal: reduction of heart disease risk.

By the way, regardless of which diet you follow, it is, in my view, absurd to believe that diet alone will do it. What about vitamin D normalization, thyroid normalization (thyroid disease is incredibly common), omega-3 fatty acids from fish oil, identification of hidden sources of risk (something that is unlikely in Ornish, since small LDL particles skyrocket on a low-fat diet), postprandial glucoses, etc., all the pieces we focus on to gain control over coronary plaque? Eating green peppers and barley soup alone is not going to do it.

Near-fatal brush with nattokinase

14. April 2010 William Davis (0)

Here is precisely why I have spoken out against nattokinase: People may put faith in this "supplement" when there are virtually no data to support its use in such dangerous conditions as pulmonary embolism.

Pulmonary embolism occurs when a large volume of blood clots in the veins of the pelvis, abdomen, and into the legs. A clot breaks off and lodges in the pulmonary arteries of the lungs. This can be fatal within minutes to hours, the victim struggling to breathe, since oxygen is not transferred to the blood and it causes terrible pain in the chest.

The treatments are fairly obnoxious: intravenous anticoagulants (blood thinners), followed by oral blood thinners like warfarin. While they carry risk of bleeding and other long-term risks, it's better than dying.

Would you bet that a "nutritional supplement" manufacturer's vague claims and lack of data are sufficient proof to treat a life-threatening condition? You're a fool if you are.

Anyone reading these pages knows that I am a vigorous supporter of nutritional supplements. I even consult for the nutritonal supplement industry. But I am also an advocate of TRUTH, not BS.

Here is a woman from England who inquired whether she should stop her husband's warfarin in favor of nattokinase. This is precisely the sort of thing that can happen because of the campaign of misinformation behind nattokinase.

Dr. Davis,

Thank you for your very interesting blogs, which I came across searching for natural alternative treatments to warfarin.

My husband has been following the low carb, high fat, real food regime over the past few years. He got off all the blood pressure and cholesterol drugs and never felt better. He even got his blood sugar down from a recorded high that we are aware of 13 nmol/L (234 mg/dol) to 6.1 nmol/L 109.8 mg/dl).

We were on holiday in the Caribbean. Just before our return home, we did a trip to a neighbouring island that included non-alcoholic fruit punches. They tasted great, but were very sweet. I broke my normal refusal to drink these things, but only had a couple of glasses. (After all, we were on holiday!) My husband believes he consumed around 1.5 litres of the stuff and now realises he was feeding his body a very toxic product – fructose. That night, he had an incredible toxic response and we only got him onto the plane with a visit to the hospital and a pain killer injection.

The symptoms of pulmonary embolism only showed 2 weeks later . . . and warfarin treatment was started. We would both like to use an alternative therapy if we can find someone with experience to provide the support.Do you know of any studies that support alternative options?

Do you know of any practitioners in the England who support a non-drug approach with an understanding of nutrition who we may be able to receive advice and support?

FB
York, England

Glucophobia: The Novel

13. April 2010 William Davis (25)

Just kidding: No novel here. However, there is indeed a story to tell that should scare the pants off you.

If you haven't yet gathered that carbohydrates are a macronutrient nightmare, let me recount the list:

Carbohydrates increase small LDL particles
Or, in the cholesterol-speak most people understand, "carbohydrates increase cholesterol." It's counterintuitive, but carbohydrates increase LDL substantially, far more than any fat.

Carbohydrates increase blood sugar
Eggs don't increase blood sugar, nor do chicken, raw almonds, onions or green peppers. But a bowl of oatmeal will send your blood sugar skywards.

Carbohydrates make you fat
Carbohydrates, whether in the form of wheat flour in your whole wheat bread, sucrose in your ice cream, fructose in your "organic Agave nectar," or high-fructose corn syrup in your dill pickles. They all provoke de novo lipogenesis, or fat formation. They also stimulate insulin, the hormone of fat storage.

Carbohydrates cause glycation
High blood sugar, like the kind that develops after a bowl of oatmeal, triggers glycation, or modification of proteins by glucose (blood sugar). This is how cataracts, kidney disease, and atherosclerotic plaque develop. Small LDL is 8-fold more glycation prone than large LDL, providing a carbohydrate double-whammy.

Your glucose meter remains the single best tool to gauge the quality of your diet. Many people have horror stories of the shocking experiences they've had when they finally get around to checking their postprandial glucose.

Drama with the Dr. Oz Show

11. April 2010 William Davis (27)

A producer from the Dr. Oz show recently contacted my office. They asked whether we could supply them with a volunteer patient from either my practice or the Track Your Plaque program who would be willing to appear on the show and discuss heart disease prevention. They needed someone to commit within 24 hours.

Despite the short notice, we identified a volunteer. He flew to New York the following week where he was interviewed along with several other men and women, all of whom had heart disease (heart attacks, stents, etc.). However, as this young man is very slender and follows most of the Track Your Plaque principles (e.g., vitamin D and omega-3 fatty acid supplementation; no wheat, cornstarch, or sugars, no restriction of fat, etc.), he apparently received less attention than the overweight, I-know-nothing-about-diet interviewees.

Then there was an odd turn of events: Dr. Dean Ornish, apparently a friend of Dr. Oz, will be providing the dietary counseling. The producer had made no mention of Dr. Ornish.

Now that's an odd collision of philosophies: Our Track Your Plaque version of low-carb with the guru of low-fat, Dr. Ornish.

The following week, Dr. Ornish called me and graciously asked whether I was okay with this. I'm not sure just how much he knew about the philosophy I advocate, nor how much I have bashed his program as a destructive approach to diet, nor whether he knew that I gained 30 lbs on the Ornish diet, along with a drop in HDL to 27 mg/dl, increased triglycerides to 350 mg/dl, and type II diabetes that I've talked about on this blog and the Track Your Plaque book and website. I suspect he knew little to none of this.

Anyway, I tried to diplomatically explain that my patient's cause for coronary plaque was small LDL particles that he expressed despite his very slender build, likely from excessive carbohydrates, controlled with carbohydrate restriction. Dr. Ornish maintained his usual arguments: Grains are good, provided they are whole grains, heart disease is "reversed" with his diet program, etc. (I didn't want to challenge him in a phone call and tell him that he never actually reversed coronary plaque, but just reversed endothelial dysfunction. But, as Dr. Ornish is not a cardiologist, I wasn't sure how far his understanding of these issues went.)

We agreed to disagree. This leaves my poor patient in an odd position: Being asked by Dr. Ornish and the Dr. Oz show to follow a low-fat program for the sake of entertainment, or adhering to the advice we follow that has so far served him well, given his small LDL particle size tendencies.

We'll see where this little drama leads.

Response from Nature Made

10. April 2010 William Davis (31)

Here's the response from Nature Made when I emailed them about my concern that there appears to be no vitamin D in their vitamin D gelcaps.

It is the usually CYA corporate-speak that says nothing. The grammatical errors make it clear that this was a "canned" response.

Date: April 9, 2010
From: Marissa Reyes, Consumer Affairs Department
Subject: Reference #346236

Dear William Davis, MD:

We recently received your e-mail regarding Nature Made products. We regret to
hear that the quality standards of our company. [?]

Our company is called Pharmavite, and we manufacture Nature Made nutritional
supplements. We have been in business since 1971. We are committed to quality
control, and have very high quality standards. Our Quality Control personnel
sample and test all raw materials as they enter our plant, and again assay the
finished product, before final packaging.

Dietary Supplements are regulated under the FDA through DSHEA (Dietary
Supplement Health & Education Act of 1994). The United States Pharmacopoeia
(USP) establishes standards for the composition of drugs and nutritional
supplements. This voluntary non governmental organization was set up in 1820
and has officially been recognized by federal law since 1906. Standards
established by USP for products are legally enforceable by the FDA. At
Pharmavite we participate in the USP Dietary Supplement Verification Program
(DSVP). Many of our products have earned the DSVP seal and additional products
are currently being evaluated. Our DSVP certified products will have the DSVP
seal on the product label.

Our Nature Made Vitamin D 400 IU tablets have been reviewed by the USP and bears
the DSVP symbol on the label. Although the USP has not reviewed all of the
Nature Made Vitamin D supplements, all of our products go through the same
rigorous quality testing at Pharmavite. The products which have earned the seal
help us to demonstrate the high quality of our products.

We would like to look into the product(s) your patients have been using. If you
could provide the UPC and lot numbers of the product(s), we will be happy to
review our records. In addition, if you would like us to test the product(s)
that you currently have, we will be pleased to send a prepaid postage mailer so
you may return the product(s) to us so that our Quality Control Department can
examine it. Please let us know if you would like us to send you the prepaid
postage mailer.

We thank you for contacting us and hope that you will continue to use and enjoy
Nature Made products with complete confidence.

Sincerely,
Marissa Reyes
Consumer Affairs Coordinator
Pharmavite, LLC
MR:346236-10

Patients who come to the office do not provide me with the bottles nor lot numbers. In past, when I've gone to the trouble of doing this (with other companies, not Nature Made), it has come to nothing helpful. The information gets passed on to the company and we hear nothing and never learn if there was a problem, or receive some more corporate-speak letter saying everything was fine. This is obviously a liability-avoidance tactic: Admitting that something was wrong would open them up to legal risk. So, frankly, I can't be bothered.

So we are left with the unsatisfying experience of relying on street-level experiences.

For now, my advice: Avoid Nature Made vitamin D. Too many people have had blood tests demonstrating that they are not obtaining any vitamin D.

By the way, the Nature Made brand of fish oil is among the very few problem brands of fish oil we've encountered. Fish oil should be only mildly fish in smell and generally should not cause stomach upset and excessive belching if properly purified. Nature Made is excessively fishy when you smell it, suggesting oxidation. We've had repeated (dozens) of patients who have experienced difficulties with this brand. Rather than dealing with the frustrating gobbledy-gook of this company, just avoid their products.

What to Eat: The diet is defined by small LDL

9. April 2010 William Davis (15)

I approach diet from the perspective of small LDL particles.

Small LDL particles have exploded in frequency and severity in Americans. It is not at all uncommon to see 70% or more small LDL particles (i.e., 70% of total LDL particle number or Apo B) on lipoprotein testing. (I saw two people today who began with over 95% small LDL.)

Small LDL particles are:
--More likely to persist in the bloodstream longer than large LDL particles.
--More likely to adhere to components of atherosclerotic plaque.
--More likely to gain entry to plaque.
--More likely to be taken up by inflammatory white blood cells which, in turn, become the mast cells that fill coronary plaque.
--More likely to be oxidized.
--More likely to be glycated (8-fold more likely than large)

To add insult to injury, foods that trigger small LDL formation--i.e., carbohydrates--also cause high postprandial blood sugars. High postprandial blood sugars, in turn, glycate small LDL. That combination of events accelerates 1) plaque growth, 2) plaque instability, and 3) aging.

So carbohydrates trigger this sequence, carbohydrates of all stripes and colors. Not just "white" carbohydrates, but ALL carbohydrates. It's all a matter of degree and quantity. So, yes, even quinoa, bulghur, and sorghum trigger this process. I've only recently appreciated just how bad oats and oatmeal are in this regard--really bad.

Foods that trigger small LDL also trigger higher blood sugars; foods that trigger higher blood sugars also trigger small LDL. Small LDL and blood sugar are two different things, but they track each other very closely.

So, in the Track Your Plaque approach to diet, we craft diet based on these simple principles:

1) Eliminate wheat, cornstarch, and sugars--These are the most flagrant triggers of small LDL, blood sugar, and, therefore, LDL glycation.
2) The inclusion of other carbohydrates, such as oatmeal, quinoa, rye, etc. depends on individual sensitivity. Individual sensitivity is best gauged by assessing one-hour postprandial glucose.

Stay tuned for more in this series. Also, Track Your Plaque Members: We will be having an in-depth webinar detailing more on thees principles in the next couple of weeks.

Is it or isn't it vitamin D?

7. April 2010 William Davis (63)

Jackie takes 10,000 units of vitamin D(3) per day as a gelcap.

Her starting 25-hydroxy vitamin D blood level was 18.1 ng/ml. Severe deficiency, no surprise.

On her 10,000 units per day, Vitamin Shoppe brand, her 25-hydroxy vitamin D level was 76.2 ng/ml--perfect. It stayed in this range for about two years.

She then changed to the Nature Made brand gelcaps she picked up at Walgreen's. Repeat 25-hydroxy vitamin D level: 23 ng/ml.

This has now happened with five different people, all taking the Nature Made brand.

If you are taking this brand of vitamin D, please be on the alert. You might consider a 25-hydroxy vitamin D blood level to be sure it actually has the vitamin D it's supposed to have.

Or, change brands.