All posts by william-davis

Indian buffet

24. February 2011 William Davis (56)

I took my family to a local all-you-can-eat Indian buffet. It was delicious.

I confined my food choices mostly to vegetables and soups. Within about 30 minutes, I started to get that odd buzz in my head that usually signals a high blood sugar.

When I got home, my fingerstick blood glucose: 173 mg/dl. Darn it! Must have been cornstarch or other sugars in the sauces.

I got on my supine stationary bike and pedaled for 40 minutes at a moderate pace while I played Modern Warfare on XBox. (A great way, by the way, to fit in some low- to moderate-intensity exercise while occupying your brain. My wife often has to yell at me to get off, it's so much fun.)

Blood glucose at the conclusion of exercise: 93 mg/dl-- a nice 80 mg/dl drop.

This is a useful strategy to use in a pinch when you've either been inadvertently exposed to more carbohydrate than you can tolerate, or if you'd like to blunt the adverse glucose effects of a bowl of ice cream or other carbohydrate indulgence.

Should we explore the idea of a "morning-after" pill, or actually a "meal-after" pill, a supplement pill or liquid that blunts or eliminates the blood glucose rise after a meal? I've considered such an idea, but have been fearful that people would start to use it habitually. Thoughts?

American Heart Association diet makes a monkey out of you

21. February 2011 William Davis (38)

Heart Scan Blog reader, Roger, brought this New York Times article to my attention.

In an effort to develop a better experimental model for obesity than mice, scientists have turned to monkeys and other primates. The emerging observations are eerily reminiscent of what you and I witness just by going to the local grocery store or fast food outlet:

"'It wasn’t until we added those carbs that we got all those other changes, including those changes in body fat,' said Anthony G. Comuzzie, who helped create an obese baboon colony at the Southwest National Primate Research Center in San Antonio."

"Fat Albert, one of her monkeys who she said was at one time the world’s heaviest rhesus, at 70 pounds, ate “nothing but American Heart Association-recommended diet,” she said."

Yes, indeed: The American Heart Association diet makes monkeys fat. Extrapolate this a little higher on the evolutionary ladder and guess what?

This is one of the many reasons why, when I have a patient who is counseled by the hospital dietitian on the American Heart Association diet, I advise them to 1) ignore everything the dietitian told them, and then 2) follow the wheat-free, cornstarch-free, sugar-free, whole food diet I advocate.

Not unexpectedly, much of this primate research is not being devoted to just manipulating diet to achieve weight loss and health, but to develop new drugs to "treat" obesity.

Would you like a banana?

Construct your glucose curve

19. February 2011 William Davis (24)

In a previous Heart Scan Blog post, I discussed how to make use of postprandial (after-meal) blood sugars to reduce triglycerides, reduce small LDL, increase HDL, reduce blood pressure and inflammatory measures, and accelerate weight loss.

In that post, I suggested checking blood glucose one hour after finishing a meal. However, this is a bit of an oversimplification. Let me explain.

A number of factors influence the magnitude of blood glucose rise after a meal:

--Quantity of carbohydrates
--Digestibility of carbohydrates--The amylopectin A of wheat, for example, is among the most digestible of all, increasing blood sugar higher and faster.
--Fat and protein, both of which blunt the glucose rise (though only modestly).
--Inclusion of foods that slow gastric emptying, such as vinegar and fibers.
--Body weight, age, recent exercise

Just to name a few. Even if 10 people are fed identical meals, each person will have a somewhat different blood glucose pattern.

So it can be helpful to not just assume that 60 minutes will be your peak, but to establish your individual peak. It will vary from meal-to-meal, day-to-day, but you can get a pretty good sense of blood glucose behavior by constructing your own postprandial glucose curve.

Say I have a breakfast of oatmeal: slow-cooked, stoneground oatmeal with skim milk, a few walnuts, blueberries. Blood glucose prior: 95 mg/dl. Blood glucose one-hour postprandial: 160 mg/dl.

Rather than taking a one-hour blood glucose, let's instead take it every 15 minutes after you finish eating your oatmeal:

In this instance, the glucose peak occurred at 90-minutes after eating. 90-minute postprandial checks may therefore better reflect postprandial glucose peaks for this theoretical individual.

I previously picked 60-minutes postprandial to approximate the peak. You have the option of going a step better by, at least one time, performing your own every-15-minute glucose check to establish your own curve.

Why is type 1 diabetes on the rise?

16. February 2011 William Davis (43)

Type 1 diabetes, also called "childhood" or "insulin-dependent" diabetes, is on the rise.

Type 2 diabetes, or "adult," diabetes, is also sharply escalating. But the causes for this are easy-to-identify: overconsumption of carbohydrates and resultant weight gain/obesity, inactivity, as well as genetic predisposition. A formerly rare disease is rapidly becoming the scourge of the century, expected to affect 1 in 3 adults within the next several decades.

Type 1 diabetes, on the other hand, generally occurs in young children, not uncommonly age 3 or 4. Type 1 diabetes also shares a genetic basis to some degree. But the genetic predisposition should be a constant. Obviously, lifestyle issues cannot be blamed in young children.
Then why would type 1 diabetes be on the rise?

For instance, this study by Vehik et al from the University of Colorado documents the approximate 3% per year increase in incidence in children with type 1 diabetes between 1978 and 2004:

(From Vehik 2007)

(For an excellent discussion of the increase in type 1 diabetes in the 20th century, see this review.)

This is no small matter. Just ask any parent of a child diagnosed with type 1 diabetes who, after recovering from hearing the devastating diagnosis, then has to stick her child's fingers to check glucose several times per day, mind carefully what he or she eats or doesn't eat, watch carefully for signs of life-threatening hypoglycemic episodes, not to mention worry about her child's long-term health. Type 1 diabetes is a life-changing diagnosis for both child and parents.

Various explanations have been offered to account for this disturbing trend. Some attribute it to the increase in breast feeding since 1980 (highly unlikely), exposure to some unidentified virus, or other exposures.

I'd like to offer another explanation: wheat.

Lest you accuse me of becoming obsessed with this issue, let me point out the four observations that lead me to even consider such an association:

1) Children diagnosed with celiac disease, i.e., the immune disease of wheat gluten exposure, have 10-fold greater likelihood of developing type 1 diabetes.

2) Children diagnosed with type 1 diabetes are 10-fold more likely to have abnormal levels of antibodies (e.g., transglutaminase antibodies) to wheat gluten.

3) Experimental models, such as in these mice genetically susceptible to type 1 diabetes, showed a reduction of type 1 diabetes from 64% to 15% with avoidance of wheat.

4) The increase in type 1 diabetes corresponds to the introduction of new strains of wheat that resulted from the extensive genetics research and hybridizations carried out on this plant in the 1960s. In particular, unique protein antigens (immune-provoking sequences) were introduced with the dwarf variant attributable to alterations in the "D" genome of modern Triticum aestivum.

Proving the point is tough: Would you enroll your newborn in a study of wheat-containing diet versus no wheat, then watch for 10 years to see which group develops more type 1 diabetes? It is a doable study, just a logistical nightmare. Perhaps the point will be settled as more and more people catch onto the fact that modern wheat--or this thing we are being sold called "wheat"--is a corrupt and destructive "foodstuff" and eliminate it from their lives and the lives of their young children from birth onwards. Then a comparison of wheat-consuming versus non-wheat-consuming populations could be made. But it will be many years before this crucial question is settled.

Yet again, however, the footprints in the sand seem to lead back to wheat as potentially underlying an incredible amount of human illness and suffering. Yes, the stuff our USDA puts at the bottom, widest part of the food pyramid.

Apo E4 and sterols: Lethal combination?

11. February 2011 William Davis (24)

Phytosterols, or just "sterols" to its friends and neighbors, are a group of cholesterol-like compounds that are abundant in the plant world. Lately, however, sterols have proliferated in the processed food supply, thanks to the observation that sterols reduce LDL cholesterol when ingested by humans.

This must mean that sterols are good for you.

Uh oh. Wait a minute: There is a rare disease called sitosterolemia in which there is unimpeded intestinal absorption of all sterols ingested through diet. They must have really low LDL cholesterols! Nope. They develop coronary disease--heart attacks, angina, etc.--in their late teens and 20s. In other words, if sterols gain access to your bloodstream, they are bad. Very bad.

Conventional thinking is that only a modest quantity of dietary sterols gain access to the bloodstream. But there are two potentially fatal flaws in this overly simplistic line of thinking:

1) What happens when you load up your diet with "heart healthy" sterols, such as those in "heart healthy" margarines, mayonnaise, and yogurt, effectively increasing sterol intake 10-fold?

2) What happens in people with the genetic pattern, apo E4, that is carried by 25% of the general population that permits much greater intestinal absorption of sterols?

My prediction: Despite the fact that sterols reduce LDL, they may, in certain genetically-susceptible people, such as those with apo E4, increase risk for heart disease: heart unhealthy.

Here are two studies that suggest that greater sterol absorption in people without sitosterolemia are at higher risk for heart disease:

Alterations in cholesterol absorption/synthesis markers characterize Framingham offspring study participants with CHD

Plasma sitosterol elevations are associated with an increased incidence of coronary events in men: results of a nested case-control analysis of the Prospective Cardiovascular Münster (PROCAM) study

Glucomania

8. February 2011 William Davis (52)

As I suggested in a previous Heart Scan Blog post, a glucose meter is your best tool to:

1) Lose weight
2) Cure diabetes
3) Reduce or eliminate small LDL particles
4) Achieve anti-aging or age-slowing effects

But it means getting hold of a glucose meter and applying it in a very different way.

Diabetics typically check fasting morning glucose and again several times during the day to assess medication effects. But you and I can measure blood glucose to assess the immediate effects of food choices--two very different approaches.

The concept is simple: Check a blood glucose just prior to a food or meal of interest, then one hour after finishing.

Let's take two hypothetical breakfasts. First, oatmeal, a so-called "low-glycemic index" food. Slow-cooked, stone ground oatmeal with skim milk, a handful of walnuts, just a few blueberries.

Blood glucose just prior: 95 mg/dl
Blood glucose one hour after finish: 175 mg/dl

I made those numbers up, but this is a fairly typical response for many adults. (This is why "low-glycemic index" is an absurd notion.) This kind of response causes 1) glycation, the adverse effects of glucose modification of proteins that leads to cataracts, kidney disease, cartilage damage and arthritis, atherosclerosis, skin wrinkles, etc., 2) high insulin response that cascades into fat deposition, especially visceral fat ("wheat belly"), and 3) glucotoxicity, i.e., direct damage to the pancreas that can, over years, lead to diabetes.

Next day, let's try a breakfast of 3-egg omelet made with green peppers, sundried tomatoes, and olive oil.

Blood glucose just prior: 95 mg/dl
Blood glucose one hour after finish: 93 mg/dl

This is a meal of virtually zero-glycemic index. This kind of response triggers none of the effects experienced following the oatmeal. Repeated over time and you fail to trigger glycation, you stop provoking insulin, and visceral fat mobilizes rather than accumulates: you lose weight, particularly around the middle.

We therefore aim to keep the one-hour blood glucose 100 mg/dl or less. If you start with a high fasting blood glucose of, say, 118 mg/dl, then we aim to keep the one-hour after-eating blood glucose no higher than the pre-meal.

It works. Plain and simple.

This makes the primary care docs crazy: "How dare you check your blood sugar! You're not diabetic." In truth, blood glucose meters are relatively simple devices to use. The test strips and lancets will cost a few bucks. (The meters themselves are either low-cost or free, just like Gillette sometimes sends you a beautiful new razor for free but expects you to buy the blades). These are direct-to-consumer products. While a prescription written by your doctor for a glucose meter and supplies helps insurance cover the costs, you can easily get these devices without a prescription. Some stores, like Target, keep their devices out on the shelves with the shampoo and bath soap.

Warning: Anyone taking diabetes drugs will have to consult with their doctors about the safety of such an approach. Because this approach can actually cure diabetes in some people, if you are taking some diabetes drugs, especially glyburide, glipidize, and glimepiride, you can experience dangerously low blood sugars, just as any non-diabetic taking these drugs would.

Diarrhea, runny noses, and rage: Poll results

6. February 2011 William Davis (19)

Here are the results of the week-long poll asking the question:

Have you experienced a wheat re-exposure syndrome?

Yes, undesirable gastrointestinal effects 223 (41%)
Yes, asthma or sinus problems 51 (9%)
Yes, joint pains and/or swelling 85 (15%)
Yes, emotional or other nervous system effects 59 (10%) No, nothing, nada 107 (19%)

No. Wheat is sacred and you're all nuts 13 (2%)

There are several interesting observations to make from this informal poll. First, as I have observed, the most common wheat re-exposure syndrome is gastrointestinal, usually involving cramps, diarrhea, and lame explanations to your dinner partner.

Second most common: joint pains and/or swelling.

Third: asthma or sinus congestion.

The incidence of emotional or nervous system effects surprised me a bit. I didn't expect 10% of people to share this effect. This is an effect I also experience personally, along with the gastrointestinal consequences.

To be sure, this is a skewed poll, since many people likely come to this blog in the first place because of such issues. But I was nonetheless impressed with the relatively modest proportion of people who did not share such a re-exposure syndrome: only 19%.

Beyond the interesting numbers provided by readers, a good many also provided some fascinating and graphic comments. Here's a sample:

Sassy said:

Reflux -- starts a day later and goes for up to a week. And Bloat:2-5 inches on my waistline in a day, lasting up to three. Miserable. And why, having experienced this once, have I done it often enough to verify the connection with certainty? I am working on that one.

Anonymous said:

Wheat increased hunger with even with only a small amount. Crackers in soup was enough to set it off.

Also, when I was trying to get off wheat, I noticed that 2 eggs and 2 bacon and I could go 5 hours before hunger, or 2 eggs and 2 bacon and toast was good for three hours before hunger. That was the final step to giving up wheat. Now three years and 59 Kg [130 lbs!] loss later, there is no doubt in my mind that wheat is evil, and I do not regard it as suitable for human food. I speculate that it increases ghrelin or cortisol.

Anna said:

For me, in the two years since I began eating Gluten-Free (Low Carb for 6 years), the few times I've had re-exposure to wheat, I've experienced fast onset and intense abdominal pain (known exposure during the daytime) and heartburn, indigestion, intense nausea, and disrupted sleep (exposures during evening meal not discovered until the next day).

My husband wants to think he's fine with wheat (though I know that he has at least one gene that predisposes to celiac), but IMO, he isn't. He eats no wheat at home because that's the default, and he's OK with that. But if he goes out to dinner at a restaurant that serves "good" artisan bread, he will indulge in a few bites (he does restrict his carb intake, so it's still a limited amount). More often than not, he will sleep fitfully on those nights, snore more, and wake in the night with indigestion. He wants to bury his head in the sand and will only acknowledge the discomfort being due to eating too many carbs, not the wheat itself. I notice he sleeps fine if he eats a small amount of potato or rice. Go figure.

Our 12 yo son has been eating GF for two years also. About 6 months into GF, he unknowingly ate wheat a number of times (licorice candy laces at a friend's house), which resulted in outbreaks of canker sores in his mouth each time. He also exhibits mood and behavior changes when he eats wheat, which is what prompted me to test him for gluten intolerance in the first place.

Mark said:

If I go for 3-4 days without wheat, grains or sugar and then go out and binge on a pizza and ice cream or something like that I become explosive within 20 minutes to an hour. It's like a wheat and sugar rage.(I'm not saying this is an excuse for rage, I'm saying it has happened to me and I believe partly do to re-exposure) It seems the combination of the wheat plus sugar can be the worst.

I get red rashes around my neck sometimes right away and sometimes up to a day or later and sometimes get bad diarrhea.

I think it can be almost dangerous to cut things like gluten and sugar suddenly out of the diet without being very serious about keeping them out. I have found it very hard to cut out wheat without binging on it later after 4 or 5 days. I don't believe that my symptoms are just psychological either.

I was also diagnosed with ADHD as a young kid and then rediagnosed with adult ADHD by 3 different doctors. I also have bouts of mania at times too. I am considering trying to go completely gluten/refined carbohydrate free to see if it helps with the symptoms and gives me some relief.

I have never been tested for celiac or gluten intolerance but I would like to be. I think it would help explain to my girlfriend, family and friends why I can't go out and eat pizza or have a beer or ice cream. Right now they all think I'm a hypochondriac. At times I have experienced an intense fatigue the next day like I can't wake up and also sharp pains in my body and headaches.

Anonymous said:

I ditched wheat a year ago after my wife was diagnosed celiac. I immediately experienced a number of health improvements (blood lipids, sleep, allergies, etc.).

Fast forward: We all suffered some inadvertent wheat exposure yesterday via some chocolate covered Brazil nuts (of all things). This accidental A-B-A experimental design resulted in the following:

1. My celiac wife experienced what she calls "the flip" within an hour of exposure (i.e., intense GI distress).
2. My five-year old son went to bed with some wicked reflux.
3. I woke up with some twinges in my lower back and an ache in my football-weary left shoulder. I was also complaining to my wife about fuzzy-headedness that refused to respond to caffeine or hydration. I could only describe it as "carb flu"...

And then I read your post!

Anne said:

Depression, agitation and brain fog if I get glutened. Some times this comes with abdominal pain and a rash on my back - I think it is dose dependent. Cross contamination with wheat is a big issue when eating out. Needless to say, I eat out infrequently and then try to stick with the restaurants that are the most aware of gluten issues.

Terrence said:

Several weeks ago, I started Robb Wolf's 30 day challenge.

The first two weeks were brutal - calling it a withdrawal flu was a massive understatement. So, I thought I would try some wheat and see what happened (could not be worse, I thought). Well, it was.

I still felt extremely crappy, but I was now MASSIVELY GASSY - AMAZINGLY GASSY, for about 48 hours - flatulence on wheels, in spades. I did not go out at all in those 48 hours - when the gas came on, it went out, LONG, and QUICKLY and LOUDLY.

I am easing back into wheat and grain free. I am gluten free today and tomorrow (Sunday and Monday). I expect to try a small amount of wheat on Thursday, then maybe a little more the following Thursday.

Donald said:

I have limited wheat consumption severely over the last 8 months. I have lost 120 pounds, no longer have bouts of illness, asthma, depression, or low energy. I also take vitamin D and other supplements that have helped (many are from your blog recommendations).

Last week I ate a small piece of cake and dessert pizza. Shortly thereafter I started sneezing, had a scratchy throat, and runny nose. I called off sick the next day for fear of being contagious. My symptoms subsided quickly and I am now attributing them to the processed flour eaten at my work luncheon. I think it was an allergic reaction since I recall having much more severe symptoms fairly regularly in my wheat eating days. Those were attributed to an "allergy" of unknown origin back then.

John said:

I suffered from Ankylosing Spondylitis, Iritis, Plantar Fasciits, etc for a number of years. I restricted carbs, especially wheat and I've been symptom free for the past two years now.

Lori said:

I found wheat to be one of the worst things for giving me gas bloating and acid reflux, and I'd had sinus and nasal congestion my whole life. When I ate that cookie, it just re-introduced old problems. I can occasionally eat a gluten-free, grainy goody at my party place without any side effects. I also have a little sprouted rice protein powder every day.

Another odd thing about wheat: it was hard for me to stop eating it once I started. I could go through a whole box of cookies in one sitting, even though I wasn't a binge eater. But I can have a couple of gluten-free cookies and stop.

Paul said:

Except for one slip up this recently past holiday season, I've been sugar-grain-starch free since July 2008. Mental fog was the most noticable re-exposure symptom I had.

My mom has had the worst acid-reflux for 40-plus years. It had become so bad that she was on three medications just to deal with the symptoms. After much training and coaxing, I finally got across to her how to totally get off wheat. Not at all to my surprise, after being wheat free for a few weeks, she lost weight and her acid reflux was GONE!

But she had been addicted to wheat for so long, she relapsed, and the reflux fire soon returned. Wheat must be akin to heroin with some people. Even though they know it's very bad for them, they can't help themselves.

Onschedule said:

Re-exposure often leads to diarrhea for me, or such a heavy feeling of tiredness that all I can do is lay down and pass out. A local pizzeria makes a darn good pie, but since I started practicing wheat-avoidance, I can't keep my eyes open after eating there. I can't say for sure that it's the wheat causing it, but definitely something in the crust. Diarrhea, on the other hand, is definitely triggered by the wheat for me.

My mom complained of gastric reflux for years, but never filled the prescriptions that her doctors would give her. I suggested wheat-avoidance- gastric reflux disappeared within 3 days and hasn't returned (has been 6 months now). I've already commented elsewhere on this blog about how much weight and bloating she has lost...

Steve said:

Interesting that I should sit down, turn on my computer and find your poll. Having gone several weeks, maybe months, avoiding gluten, I took my daughter and her boyfriend out to eat because my wife has been working late at the office lately. Although I was thinking I would just eat my steak and chicken, I succumbed to the temptation of eating about a dozen greasy, breaded shrimp that my daughter and her boyfriend ordered. It's 1:39am and I still do not feel sleepy. My left nostril is completely blocked, my stomach feels bloated, really, really full and I've been burping. In your poll I checked sinus problems but could have chose gastrointestinal or nervous problems just as well.

A few weeks ago my daughter brought home a pizza and, once again, despite my knowing that I shouldn't, I ate a couple of pieces. I was sick for two days. The pain in what I think was my transverse colon was so bad I thought I might have to go to ther emergency room. Before I ate the pizza I had never gone grain-free that long before. I did this after reading Robb Wolf's book.

I AM CONVINCED. No more wheat for me! Please, Lord, give me strength.

LV said:

What don't I experience! I typically avoid wheat (and gluten for that matter) as I'm pretty sure it makes me sick, but when I slip (or someone else slips me some) I end up with massive amounts of joint swelling and tenderness, diarhea, cramping, gas, bloating and brain fog. I'm absolutely miserable. Just that alone is enough to keep me off gluten. I have RA, so if I have repeated exposures I'll have a flare which SUCKS!

A carpenter is only as good as his tools

4. February 2011 William Davis (18)

A carpenter wouldn't build a house using just his bare hands. You shouldn't stumble your way through nutritional blunders without the proper tools to guide you.

Best tool to lose weight:

Best tool to cure diabetes:

Best tool to reduce small LDL particles:

Best tool for anti-aging:

Observing blood sugar excursions after eating is proving to be among the most powerful tools I have come across.

The perfect Frankengrain

4. February 2011 William Davis (25)

Pretend I'm a mad food scientist. I'd like to create a food that:

1) Wreaks gastrointestinal havoc and cause intractable diarrhea, cramps, and anemia.
2) Kills some people who consume it after a long, painful course of illness.
3) Damages the brain and nervous system such that some people wet their pants, lose balance, and lose the ability to feel their feet and legs.
4) Brings out the mania of bipolar illness.
5) Amplifies auditory hallucinations in people with paranoid schizophrenia.
6) Makes people diabetic by increasing blood sugars.
7) Worsens arthritis, such as osteoarthritis and rheumatoid arthritis.
8) Triggers addictive eating behavior.
9) Punishes you with a withdrawal process if you try to remove it from your diet.

I will develop a strain that is exceptionally hardy and tolerates diverse conditions so that it can grow in just about any climate. It should also be an exceptionally high yield crop, so that I can sell it cheaply to the masses.

Now, if my evil scheme goes as planned, I will then persuade the USDA that not only is my food harmless, but it is good for health. If they really take the bait, they might even endorse it, create a diet program around it.

Dag nabit! Such a plan has already been implemented. Another evil food scientist already beat me to the punch. The food is called wheat.

Diabetes: A study in aging

3. February 2011 William Davis (0)

Diabetics experience long-term health difficulties, including atherosclerosis/heart attacks, peripheral vascular disease, hypertension, cataracts, kidney disease, neuropathies, male erectile dysfunction, osteoarthritis, and colorectal cancer. They also die, on average, 10 years earlier than non-diabetics.

In effect, diabetics compress their lives into a shorter period of time. They experience all the "complications" of aging at a younger age. People without diabetes, of course, can develop atherosclerosis, cataracts, kidney disease, etc., but they tend to do so later in life compared to diabetics.

One index of the rate of aging (but not chronologic age itself) is hemoglobin A1c, or HbA1c, a "moving average" of glycated hemoglobin, i.e., glucose-modified hemoglobin. Blood glucose glycates hemoglobin linearly and irreversibly; measuring HbA1c thereby provides an index of the last 60 or so days average blood glucose.

To put HbA1c values into perspective:

Average HbA1c of hunter-gatherers: 4.5%
Average HbA1c for Americans: 5.6%
American Diabetes Association definition of diabetes: 6.5% or greater
American Diabetes Association definition of adequate control of diabetes: 7.0% or less

Why do diabetics age faster? There are likely several reasons. One important reason is glycation, as indexed by HbA1c. Glycated proteins in the lens of the eye causes cataracts. Glycated proteins in cartilage leads to arthritis. Glycated LDL particles (apo B) leads to atherosclerosis. Glycated nerve cells causes neuropathy. And so on.

If glycation underlies many of the phenomena of aging, then we might surmise that:

1) The less you glycate, the slower you age.
2) The more you glycate, the faster you age.

Therefore, the higher the HbA1c, the faster you are aging.

What foods increase HbA1c? Carbohydrates. That bowl of slow-cooked, stone ground oatmeal? A one-hour after-eating blood sugar of 170 mg/dl is common. Your doctor says that's okay because it's below 200 mg/dl and you don't "need" medication yet.

Fatal underdose

27. April 2008 William Davis (8)

Since vitamin D has been the topic of a fair amount of media coverage, I've received many questions about this fascinating "nutrient." A day doesn't go by without several nurses, friends, even fellow physicians stopping me to ask about vitamin D.

When I inform them that the average dose for females in this region (upper Midwest) is 4000-5000 units per day, 5000-6000 units per day for males, they are all surprised. "Then why did they say just take your multivitamin every day, or just drink your milk on the news?"

Many people are even more surprised, sometimes completely turned off, when they hear that, to be truly confident of adequate vitamin D dosing, a blood level of 25(OH) vitamin D3 needs to be checked. Now we're talking real hassle!

But there is no other way to do it. In order to obtain the full potential benefits of vitamin D, such as reduction in blood sugar and sensitization to insulin, reduction in cancer risk (especially prostate, colon, and breast), reductions in blood pressure, increased bone density, not to mention markedly increasing the likelihood of stopping or reducing your heart scan score, then achieving a desirable blood level of 25(OH) vitamin D is necessary.

Checking a blood level of vitamin D is no more difficult than having a cholesterol test, unless, of course, your doctor balks at the idea. (Time for a new doctor if that occurs.)

All too often, someone will be convinced they are taking a sufficient dose of vitamin D of, say 2000 units per day, only to discover that their blood level of 25(OH) vitamin D is something like 17 ng/ml--severe deficiency, sufficient to leave them exposed to all the undesirable consequences of vitamin D deficiency. Even though 2000 units per day represents 500% of the Institute of Medicine's recommended Adequate Intake for adults, to those familiar with the Track Your Plaque program it likely sounds like a child's dose.

Many variables enter into the equation in your body that determines your need for vitamin D: body size (heavier or larger people need more, with obese people often requiring enormous doses); sex (men need more than women); age (aging results in dramatic loss of ability to activate vitamin D in the skin); race; skin color (darker skinned people require more). Trying to guess your need is a fool's game. It's also a game that can seriously compromise your health and your hopes of ever stopping or reducing your heart scan score.

The message is clear: You cannot guess what your vitamin D need is. You cannot properly judge your vitamin D requirement by your age, body size, sex, or any other characteristic. Having a tan or a lack of a tan is a lousy indicator, as well. A simple blood level of 25(OH) vitamin D is an absolute necessity to gauge your vitamin D status, both before starting and while on your supplement.

Members of Track Your Plaque: Watch for the 30-some page booklet, The Track Your Plaque Complete Handbook on Vitamin D and Heart Health, which will be released in the next day or two.

Copyright 2008 William Davis, MD

Is direct-to-consumer drug marketing a failure?

23. April 2008 William Davis (4)

According to the poll just completed by 80 participants on The Heart Scan Blog, 50% of respondents said they were less likely to take a drug after viewing an advertisement for it. A whopping 3 (4%) said that they would be more likely to take the drug after viewing an advertisement.

I find that interesting. If half the people responding are less likely to become customers of a drug company, then how does the drug industry justify running around-the-clock, every-few-minute ads? Spending by the drug industry for direct-to-consumer (DTC) advertising has ballooned over the past few years, and is now well over $30 billion dollars per year.

Unfortunately, despite the views of the highly-educated, curious, think-for-yourself, health information-seeking sorts of people who read this blog, drug companies still come out on top by DTC advertising. Estimates vary, with a 2006 U.S. Government Accountability Office study reporting that, for every $1 DTC advertising, sales are increased by $2.20. A 2000 Harvard study showed a higher return of $4.40 for every advertising dollar spent.

I'm sure the drug companies themselves have a very tight accounting handle on their own set of figures. We may not be terribly fond of these people and their often suspect tactics, but they're not stupid. They are certainly not stupid when it comes to making money.

Interestingly, 80% of the funds spent on DTC advertising focus on the 20 or so most popular drugs, all of which are used for treatment of chronic conditions like high cholesterol and high blood pressure, markets that are large and long-term. It pays very little to advertise drugs that may serve small markets for a short period. The implicit message is that this is not at all about informing the public. It is about advertising to grow revenues and profits--pure and simple.

It makes me wonder what the results of our poll would have been had we conducted it in 2000 before many people hadn't yet been brought to the brink of vomiting from the endless onslaught of commercial after commercial, complete with smarmy spokespeople (a la Lipitor's Dr. Robert Jarvik). What will it show in two years? Will the broader public join the more informed people who read this blog and become increasingly inured to the hard sell tactics?

For further discussion of this topic, click here for a reprint of an August, 2007 New England Journal of Medicine study, A Decade of Direct-to-Consumer Advertising of Prescription Drugs provides background, along with commentary on the impact of DTC drug marketing since the FDA allowed it 10 years ago. (Because it is a study and not an editorial, the editors fall short of making any recommendations for improvement or calling for a moratorium.)

Copyright 2008 William Davis, MD

Cheerios and heart health

22. April 2008 William Davis (11)

Anna responded to the Heart Scan Blog post, Can you say "sugar"? with the following wonderfully telling comment:

A measured bowl of Cheerios and a bit of milk (whole, because it's what I had), equal to 75 grams of carbohydrate, gave me the highest ever blood glucose reading from a food (not counting glucose solution from a Glucose Tolerance Test). I was attempting a "homemade" version of a 3 hr GTT before going to my doctor with my concerns about my BG.

My BG started to rise very fast within 15 minutes after eating the cereal, peaked at about 250 mg/dL at 45 minutes, then slowly dropped. By about 60-75 minutes, I experienced strong hunger and carb cravings as the BG began to slowly drop, and by about 2.5 hours after eating, my BG had suddenly dropped quite low (in the low 70s) and I had developed a nasty hypoglycemic feeling (shaky, irritable, craving sugary foods, headache, etc.).

It's hard for me to see "heart healthy" Cheerios (or any other highly processed breakfast cereal) as anything other than a bowl of pre-digested sugar that contributes to roller coaster blood glucose and insulin levels, which a great way to start anyone's day. Certainly, I don't do well with Cheerios because I clearly have a damaged glucose regulatory system (probably a diminished or absent first phase insulin response, but I can't imagine that it is doing any good for people with healthy glucose regulation, either.

I banned prepared cold cereals from our house. If my 9 yr old son gets cereal at all at home, it's whole groats (not even rolled or steel cut because those aren't truly "whole grain" anymore), soaked overnight in some water and a tsp of plain yogurt (soaking neutralizes phytates and reduces cooking time), then cooked about 8-10 minutes (water added as necessary). Sometimes I add a bit of quinoa or almond meal prior to soaking to boost the protein content a bit. I garnish with a pat of butter, some heavy cream, and a dusting of cinnamon. If I'm feeling *really* indulgent, I drizzle about 1 tsp of Grade B maple syrup on top (Grade B is stronger in flavor and so less can be used). I don't eat this cereal myself, and truthfully, I'd rather my son not, either, but he sometimes wants cereal. It's the least damaging compromise I can come up with that we can both live with.

I have also seen diabetic effects from Cheerios: rises in blood sugar, exagerration of small LDL, drops in HDL, rises in triglycerides. Yes, it may reduce LDL a small quantity, but so what?

The Cheerios "heart healthy" claim is based on a piece of research apparently performed by Dr. Donald Hunninghake at the University of Minnesota and reported in 1998:

A study conducted at the University of Minnesota Heart Disease Prevention Clinic and published as "Cholesterol-Lowering Benefits of a Whole Grain Oat Ready-to-Eat Cereal" in the May issue of the Nutrition in Clinical Care journal in 1998, showed that people can lower their blood cholesterol by an average of 3.8% over six weeks by enjoying 3 cups of cold cereal made with 100% whole grain oats everyday as part of the meals and snacks in a healthy lower-fat diet.

(Unfortunately, I could not locate the actual publication. It doesn't mean it doesn't exist; I just couldn't locate it. Perhaps it's in a small journal not entered into the online publication database.)

The purported effects of Cheerios should not be confused with that of actual, intact oat bran, as suggested by studies such as those of Brenda Davy et al, High-fiber oat cereal compared with wheat cereal consumption favorably alters LDL-cholesterol subclass and particle numbers in middle-aged and older men, in which significant reductions in LDL particle number and small LDL (NMR) were obtained. (This study was also supported by Quaker Oats.) Several studies have shown that oat bran does indeed reduce LDL cholesterol, sometimes as much as 30-50 mg/dl. Cheerios can not even come close to this.

If Cheerios were nothing more than finely pulverized oats, then perhaps it wouldn't be so bad. But add corn starch and sugar, and you have ingredients that have potential to distort LDL particle size and yield blood sugar-escalating effects like those described by Anna.

The gravity of perpetuating these myths is brought home by a testimonial posted on the website for Cheerios:

“I had unexpected open heart surgery a year ago. As I adopted heart health habits during my recovery, I realized that I should have been eating the Cheerios cereal I carried around in a plastic baggie so many years for my kids!”

Beverly
Scotch Plains, NJ

It makes me shudder.

Copyright 2008 William Davis, MD

The IF Life: Intermittent fasting

21. April 2008 William Davis (4)

There's a wonderful blog called The IF Life: Intermittent Fasting and Instant Freedom. It is written by personal trainer (and apparently former corporate bigshot), Mike O'Donnell.

Mike has a great take on brief, intermittent fasting that I found helpful and I believe you will also.

Intermitent Fasting 101: How to Start, Part I

The biggest question people have is how to effectively use IF (intermittent fasting) to achieve their goals and maximum results. These results and goals can vary by each person with fat loss, muscle gain, better health, improved performance in your sport of choice and more. With that comes the individuality of what is a person’s insulin resistance, current body composition (bodyfat%), daily lifestyle, eating habits, macronutrient ratios (carbs/protein/fat), type of exercise program, frequency and volume of training, recovery demands, and so forth. You are unlikely to find 2 people with the same set of parameters and same exact responses to an IF protocol. What does this mean? Well just that we need to start with a basic IF program, and then learn how to monitor results and adjust as we go. Even down the road things will change as you will improve health, lower insulin resistance and maybe change performance and recovery needs. So nothing is ever just one set way. Life is dynamic (always changing and evolving) and so should be the way we see our own journey for health and fitness.

What is IF?

For those that may not be familiar to the term, intermittent fasting is just taking times of fast (no food) and working them into your lifestyle. This can be either daily or a couple times a week (will get into that more below). Benefits include improving insulin resistance (which you will hear alot about as being the #1 key marker in so many health factors including weight loss, muscle gain, performance, recovery, anti-ageing and disease prevention) and giving the body a chance to do some internal cleaning (or housework), which can lead to improved immune function and overall health. If you want to see studies of all the benefits of IF/CR, please the resources page.

How do I begin to IF?

Is there only one set way in which to do IF? No. I could easily come up with 10 different IF protocols based on 10 people’s individual’s needs, lifestyle, exercise, goal, macronutrient ratios, and so forth. We will keep it simple and give the 2 most frequent and basic options.

Daily Fasting: Typically done every day and only giving the person a smaller eating window in which to get their calories. (for example, a 18hr daily fast would mean someone would only eat every day between the hours of Noon and 6pm). You will see varying times from 15-19 hours for daily fasting.
Fasting 1-3x a week: This could also be called alternate day fasting/calorie restriction (for those doing it every other day). This is just fasting of usually longer periods 18-24 hours but only 1-3x a week. Many variations to play with here.
“But which one is better and how to I do it now if I want…….”. Whoa, slow down. I know many have questions but let’s still try to keep this simple for now and expand into more specifics later. So far many people have experimented with both types of IF and have seen great results. But you also have to take into account all the other variables such as what is the person eating in that window? Is is junk food? Is it low carb? How many times a week are they doing it? Are they overweight and wanting just fat loss? Are they lower bodyfat but looking for improved performance and health? How many times a week are they exercising? What kind are they doing and what intensity? The list can go on and on, but let’s start to analyze the 2 types of IF and let you decide which one best suits your lifestyle.

Daily Fasting (15-19 hours):

The Advantages are:

--simple eating strategies for every day
--even people that may not eat 100% clean foods can see weight loss due to the smaller window and lower calorie total per day

The Disadvantages are:

--Can possibly lower metabolism if calories are too low for too long (not what you want if your #1 goal is weight loss)
--Not getting enough food in the smaller window may also lead to muscle loss for more active people (not good)
Fasting 1-3x a week:

The advantages are:

--Allows a person to make sure they are getting enough calories on the non-fasting days, and then just keeps to a simple small feed window (if any) on the IF days.
--Simple thinking for people who do not have experience in how to eat clean to eat one day, and then eat in a smaller window the following day (alternate day fasting/CR). This can achieve fat loss for people who are mostly overweight and may not be too active. (of course don’t get me wrong, that eating healthy is our main goal but this can be a good step for some people to start their weight loss jounrey and learn how to make better choices as they go)

Disadvantages:

--Doesn’t force a person to make better choices with their food (as one could probably eat junk one day, and then fast the next and still lose weight). Not something we want long term because this is not going to improve your other health markers (diseases prevention, insulin resistance) like a good IF program on healthy foods.

Again I can’t say it enough, as there are so many variables to play with in an IF program. Some people may say “well it didn’t work for me” or “I didn’t gain any muscle”. Well unless I know everything about what you do for exercise daily, your total calories, when you eat and your macronutrient ratios (protein/carbs/fats), I can’t even begin to help. IF is a simple tool to start with, but you have to take full responsibility for your own health and progress and learn when it is not working and when to change things up! Like I said, if it is NOT working then stop IF and rethink your attack plan (or get a professional to coach you on it).

So to sum up, here are some examples of what you can play with:

Daily Fasting of 15-19 hours. I would highly suggest that if you do this make sure you are recovering from your exercise and start only Mon-Fri and give yourself the weekends to eat all day (hopefully with healthy choices of course)

Fast 1-2x a week to start if you have never done any fasting or do not know how to eat healthy and control your macronutrients. Start with 1-2 days a week with fasts of 18-20 hours (I wouldn’t start with 24 hr fasts to begin as most people can not handle the hunger cravings and in turn will just end up eating all the wrong foods when they do eat) and say eat only from say 1pm-6pm for example. Drink lots of water (add lemon, your liver will appreciate it! and it will help with the hunger). For example, fast Wed and Sun (or whatever days fit into your schedule)

Or you can do a mixed approach and fast every other day for a small eating window. For example eat all day Mon, only 12-6pm on Tues, all day Wed, 12-6pm on Thurs, etc. Start with bigger eating windows and make them smaller as you get used to fasting. This approach may work for people who have alot of weight to lose and can not (I should really say “will not” as everything is a choice!) eat 100% healthy for the moment. This approach may not work for more advanced people who have a high activity level unless you are getting a ton of health calories in that fasting window.
“So What Do I Eat on the Fasting Days?”

That’s the best part, you should be able to eat unlimited healthy foods (healthy proteins, fats, veggies, fruit, nuts…see Paleo Diet in the resources page). If you are eating more processed foods, breads and other high calorie intakes then you may have to monitor and control portions. Please know this is NOT about chronic calorie restriction or starving yourself. When I do weeks of eating 1-7pm, I am eating a ton of protein and veggies (complex carbs pwo also). I am hardly starving myself. I am not taking in 4000 cal a day however, so my daily average of say 2200-2500 cal is still low compared to the alternative. If you want to lose weight of course you will need a calorie deficit to pull the “stored energy” out of fat cells. That is the advantage to eating “Paleo”, you can’t over eat on protein, healthy fats, fruits (in moderation) and veggies. If you are making bad choices or starving yourself on IF, you may lose the effectiveness or slow progress. All goes back to the fact that if it is not working, then change something up! (there is always something that can be changed…and food choices is the #1 place to start!) I don’t count calories, and by eating natural foods that have been around for 100s of years….I don’t need to! (eating healthy natural foods will not only help you lose weight but also improve your health and lower your risks of diseases….so eating for health should always be the #1 goal in any program)

Hopefully this will give a good overview while trying to keep it simple. Remember it’s your journey to take, measure progress and adjust things that are not working. Start with one approach, and modify it. Who knows, your approach may change every couple months and that is ok. Life is always changing and so should your approach to health and fitness (as the body always responds better to change than sticking with the same eating/exercise approach for a long period of time).

Can you say "sugar"?

20. April 2008 William Davis (11)

All of these products bear the American Heart Association Check Mark of approval emblem, signifying that they are "heart healthy":

Kellogg's Frosted Mini-Wheats cereal

Ingredients:WHOLE GRAIN WHEAT, SUGAR, STRAWBERRY FLAVORED CRUNCHLETS (SUGAR, CORN CEREAL, CORN SYRUP, MODIFIED CORN STARCH, PARTIALLY HYDROGENATED COTTONSEED AND/OR SOYBEAN OIL, CITRIC ACID, GLYCERIN, NATURAL AND ARTIFICIAL FLAVOR, RED #40, BLUE #2), NATURAL AND ARTIFICIAL STRAWBERRY AND CREME FLAVOR, SORBITOL, GELATIN, REDUCED IRON, NIACINAMIDE, ZINC OXIDE, RED #40, PYRIDOXINE HYDROCHLORIDE (VITAMIN B6), RIBOFLAVIN (VITAMIN B2), THIAMIN HYDROCHLORIDE (VITAMIN B1), FOLIC ACID, BLUE #1, AND VITAMIN B12. TO MAINTAIN QUALITY, BHT HAS BEEN ADDED TO THE PACKAGING.

Orville Redenbacher popcorns

Dora the Explorer Cereal

Cheerios

The following requirements must be met to gain approval of the Check Mark program:

1) total fat 3.0 grams or less per serving

2) saturated fat 1.0 gram or less per serving

3) 20 grams or less cholesterol per serving

4) 480 mg or less sodium per serving

5) "Jelly Bean Rule": 10% of the Daily Value of 6 nutrients (e.g., fiber, vitamins A and C, etc.) must also be contained in each serving.

Had the Check Mark program focused on genuine nutrition and rated products by:

1) Healthy oil content

2) Sugar content or sugar-equivalents, i.e., glycemic index or load

3) Impact on HDL, small LDL, triglycerides

none of these products would have made the list, not even close.

Warfarin is scary stuff

19. April 2008 William Davis (16)

Gilbert is a 58-year old high school science teacher.

When I first met Gil, he'd been having bouts of atrial fibrillation and had required various medications to suppress recurrences of the rhythm. However, because his rhythm proved somewhat difficult to control, his electrophysiologist (heart rhythm specialist) prescribed warfarin to reduce the risk of stroke. With atrial fibrillation, because of blood stagnation (in the left atrial appendage) in the heart, there is a stroke risk of approximately 8% per year. Warfarin reduces this risk substantially, to about 2%.

I met Gil because he had a cholesterol disorder. In my practice, the first step in gauging the implications of a lipid or lipoprotein disorder is to obtain a heart scan. If the heart scan score is zero, great. It means that we have plenty of time to treat the disorder since risk for cardiovascular events is near zero also; it means less intensive efforts less intensive efforts are necessary. But if the heart scan score is, say, 1200, then an aggressive approach in short order is required, since the risk for heart attack may as high as 20-25% per year, even in the absence of symptoms.

Gil's heart scan score: 787--high and posing a risk for heart attack of about 5-10% per year without preventive efforts. Gil did indeed prove to have a complex lipoprotein disorder, as well as high blood pressure, vitamin D deficiency, and several other potential contributors to coronary plaque.

Gil did just about everything right: He exercised, followed the recommended diet, achieved better than the Track Your Plaque 60-60-60, lost 18 lbs of abdominal fat.

Gil's rhythm stabilized for several months, only to have atrial fibrillation break through again. So Gil's electrophysiologist re-prescribed warfarin.

18 months later, Gil's 2nd heart scan score: 1410--a near doubling. Unsettling to Gil and to us, to say the least.

How can this happen in the face of perfect lipids/lipoproteins, correction of hidden causes like lipoprotein(a) and inflammation, along with a vigorous lifestyle effort?

I fear that the culprit might be warfarin.

Warfarin, better known by its brand name, Coumadin, may have some effects that intersect with the Track Your Plaque mission of reducing coronary plaque.

It is no secret that, beyond the obvious risk of bleeding from blood thinning, warfarin also may:

--Accelerate aortic valve calcification
--Accelerate calcification of the framework of the mitral valve (the mitral "anulus")
--Accelerate osteoporosis
--Induce an artificial situation of vitamins K1 and K2 deficiency.

The vitamin K1 deficiency is the route by which blood thinning is achieved. However, the K2 deficiency may have undesirable consequences, among which are the above list of various pathologic calcifications.

I therefore wonder if warfarin dramatically accelerated the coronary calcium that we track to gauge the progression of coronary atherosclerosis. One experience is hardly sufficient reason to sound the alarm. It is also difficult to pinpoint the cause of the explosive growth in Gil's coronary calcium specifically on warfarin.

That all said, I am quite certain it was the warfarin.

Unfortunately, some people are unavoidably committed to warfarin, such as those with specific genetic blood clotting disorders, prosthetic valves, prior deep vein thromboses and pulmonary emboli, etc.--serious reasons. Until an alternative emerges, warfarin remains a necessity for some people. (No, nattokinase is NOT an alternative, at least not one that would permit survival.)

My personal policy is that warfarin be used only when absolutely necessary and the gains markedly outweight the risks--including that of possible accelerated calcification of multiple sites.

Whether we will be able to get Gil off warfarin and potentially gain control over his coronary disease/plaque/calcium remains to be seen. I sure hope so.

Caraballo PJ, Heit JA, Atkinson EJ et al. Long-term use of oral anticoagulants and the risk of fracture. Arch Intern Med 1999; 159 (15): 1750–6. PMID 10448778.

Pilon D, Castilloux AM, Dorais M, LeLorier J. Oral anticoagulants and the risk of osteoporotic fractures among elderly. Pharmacoepidemiol Drug Saf 2004;13(5): 289–294.PMID 15133779.

Gage BF, Birman-Deych E, Radford MJ, Nilasena DS, Binder EF. Risk of osteoporotic fracture in elderly patients taking warfarin: results from the National Registry of Atrial Fibrillation 2. Arch Intern Med 2004; 166(2):241–246.PMID 16432096.

Copyright 2008 William Davis, MD

Lipoprotein(a) Research Foundation

16. April 2008 William Davis (18)

There is no longer any doubt that lipoprotein(a) is a major causal factor in heart disease:

Meta-analysis (combined re-analysis) of 27 prospective studies:
Danesh J et al. Lipoprotein(a) and Coronary Heart Disease: Meta-Analysis of Prospective Studies

Lp(a) and "subclinical" atherosclerosis
Brown SA et al. The relation of lipoprotein[a] concentrations and apolipoprotein[a] phenotypes with asymptomatic atherosclerosis in subjects of the Atherosclerosis Risk in Communities (ARIC) Study.

Lp(a) and oxidized LDL
Tsimikas S et al. Oxidized phospholipids, Lp(a) lipoprotein, and coronary artery disease.

Lp(a) predicts peripheral vascular disease
Valentine RJ et al. Lp(a) lipoprotein is an independent, discriminating risk factor for premature peripheral atherosclerosis among white men.

Peltier M et al.Elevated serum lipoprotein(a) level is an independent marker of severity of thoracic aortic atherosclerosis.

Lp(a) across various populations
Gambhir JK et al. Association between lipoprotein(a) levels, apo(a) isoforms and family history of premature CAD in young Asian Indians.

Weber M et al. Metabolic factors clustering, lipoprotein cholesterol, apolipoprotein B, lipoprotein (a) and apolipoprotein E phenotypes in premature coronary artery disease in French Canadians.

Lp(a) and stroke risk
Jurgens G et al. Lipoprotein(a) serum concentration and apolipoprotein(a) phenotype correlate with severity and presence of ischemic cerebrovascular disease.

Willeit J et al. Lipoprotein(a) and asymptomatic carotid artery disease. Evidence of a prominent role in the evolution of advanced carotid plaques: the Bruneck Study.

From just about any direction, Lp(a) has been conclusively associated with atherosclerotic disease. We have more than enough data proving association.

But there are two areas of desperate need:

1) Data on effective treatments.

2) Raising awareness of this widely unknown (among the public) and ignored (among health professionals) genetic condition.

Treatment remains a real struggle. In a recent detailed Track Your Plaque Special Report, Unique Treatment Strategies for Lipoprotein(a) Reduction, we summarized the treatment approaches that have some power to reduce Lp(a) and/or its potential for causing heart disease. But, even armed with an appreciation for the world's scientific literature on this genetic condition, full control remains difficult for many people.

Track Your Plaque's HeartHawk has Lp(a) and he has struggled with this pattern for the last several years. He details some of his thoughts in a recent blog post.

More research and clinical studies are required and we need it soon if we hope to gain better control over this genetic pattern that affects up to 20% of people with coronary or vascular disease. Much of the needed research is sophisticated, background work similar to that being done by Dr. Santico Marcovina at University of Washington, Dr. Angelo Scanu at the University of Chicago, and Dr. Sally McCormick in New Zealand.

However, much of the needed research also consists of brief clinical experiences that detail whether or not there is an effect of various potential agents. Larger experiences, for instance, with potential treatment agents such as various phospholipid fractions, acetylcysteine, antibiotic regimens, some hormonal treatments, etc. could be performed quickly and simply. These studies would not require the $20 or $30 million typically spent by a drug company for a study, nor the several hundred million dollars to gain FDA approval of a new agent. They would simply be examinations of existing agents. These studies still cost money, require expertise, staff, and equipment. But the cost is a tiny fraction of the drug industry's investment in research. But it also means that investment return is nil from a drug manufacturer's perspective. Yet there are literally dozens, perhaps hundreds, of agents that hold some promise but have not been thoroughly studied.

For instance, if a specific modification of the phosphatidylcholine molecule were to generate a substantial Lp(a) reducing effect, Merck, Pfizer, and AstraZeneca would yawn--it is non-patent protectable, cannot be protected from competitors through the costly FDA approval process, and therefore is simply not worth their investment--regardless of whether it works or not.

(This is yet another example of how the drug industry, as well as hospitals and many health professionals, have lost sight of their real mission: to alleviate disease, not to profit from sickness.)

HeartHawk and I have discussed on a number of occasions whether a Lipoprotein(a) Research Foundation should be formed, an organization that seeks to fund the smaller research efforts that may accelerate productive research in Lp(a) and perhaps yield useful strategies faster than hoping for somebody to simply stumble on a treatment, or wait for the drug industry to create a unique, patentable entity that returns billions.

I'd like to propose that our Track Your Plaque program begin to fund such an effort. But a lot more help will be needed, particularly to generate the money to fund genuine, high-quality research from high-quality researchers.

If any readers of the Heart Scan Blog have any thoughts or insights into this process of creating a foundation, we'd appreciate your input.

More on ASTEROID

16. April 2008 William Davis (3)

Since we are on the topic of the ASTEROID trial and rosuvastatin, I'd make one more point before I start to sound like I'm plugging this drug (which I definitely am not).

In an informative Roundtable Discussion (open to subscribers to the American Journal of Cardiology; sorry) amongst Dr. Steve Nissen, principal investigator behind ASTEROID; and Drs. Vincent Friedewald, Christie Ballantyne, P. Shah, and William Roberts, Dr. Nissen made some interesting comments:

Dr. Shah: In ASTEROID, was the magnitude of atheroma volume change seen across different levels of LDL-C and HDL-C?

Dr. Nissen: No. There was no plaque regression seen in the 17 persons with LDL-Cs >/= 100 mg/dl, and there was little change in persons with LDL-Cs of 70 to 100 mg/dl. Only in persons with LDLs less than or equal to 70 mg/dl was there significant regression. The study was not powered to look for an HDL-C(which increased by 14.7%)-raising effect.

Interesting. In other words, ASTEROID, in a fairly internally consistent way, suggests that the lower the LDL is reduced, the more likely plaque regression is obtained. This is consistent with the Track Your Plaque experience, in which we've advocated reducing (calculated) LDL cholesterol to 60 mg/dl for the past several years.

Unfortunately, the message that the ASTEROID Trial sponsors, AstraZeneca, as well as the roundtable discussion panel (later in the discussion) try to make is that there is something magical about Crestor, that it yields benefits superior to other statin agents or other means of reducing LDL.

I disagree with this message. In the Track Your Plaque experience, we do aim for a similar LDL target. But we also employ a number of other strategies. We have also succeeded in regressing plaque without use of any statin drugs (though, admittedly, many people do require statin drugs to obtain LDLs in this range). We also witness magnitudes of reversal that often far exceed that seen in ASTEROID.

The Rountable Discussion is unfortunately tainted, as is the ASTEROID Trial itself, with deep drug industry financial involvement of the Roundtable participants. In fact, the discussion begins with a listing of the financial disclosures of the participants, a listing that occupies a full column of a two-column page. The potential biases of the participants doesn't necessarily invalidate the arguments, but to me suggests that participants are more likely to argue in favor of the sponsor's drug, or that participants were chosen because of these biases.

Why bother to even mention the ASTEROID Trial in a venue (the Heart Scan Blog, that is) that purports to seek unvarnished, unbiased truth in coronary plaque reversal? Because useful information can sometimes be found in unlikely places. Just like the four-year old child who blurts out an unexpected pearl of wisdom, so it can happen with the gobbledy-gook that emerges from the drug industry.

Every once in a while, they are worth paying attention to.

LDL cholesterol, statins, and plaque regression

13. April 2008 William Davis (12)

The ASTEROID Trial reported in 2006 examined the effects of LDL cholesterol reduction using the statin drug, rosuvastatin (Crestor), with coronary atherosclerosis quantified and tracked with intracoronary ultrasound. The Track Your Plaque report, New study confirms: LDL of 60 mg reverses plaque, on the ASTEROID Trial provides commentary on the results.

Though I remain skeptical that a statin-only treatment strategy can reverse coronary plaque in the majority of people, I do believe that the AstraZeneca-sponsored ASTEROID Trial does add to the wisdom on heart disease management. More importantly, it has served to raise awareness among both the public and my physician colleagues that atherosclerosis is indeed a potentially reversible condition.

Specifically, the ASTEROID results confirm that, either directly or indirectly, LDL cholesterol reduction achieved with statin agents does correspond to increasing degrees of plaque reversal. The mean (calculated) LDL cholesterol achieved in ASTEROID was 60 mg/dl, the same as the Track Your Plaque suggested LDL target.

Though the ASTEROID Trial is not news, I stumbled on a chart posted on the ASTEROID Trial website that clearly highlights how a number of other studies beyond ASTEROID have fallen into this pattern:

The graph reveals a linear relationship: The greater the reduction in LDL cholesterol with statin drugs, the greater the plaque regression ("change in percent atheroma volume"). (Several other studies not included in the graph also cluster into the same linear relationship.)

I am no supporter of drug companies, nor a defender of their policies and practices. But I do believe that their data can serve to teach us a few lessons. For instance, here is an (cherry-picked, to be sure) example of intracoronary ultrasound cross-sectional images before and after two years of rosuvastatin, 40 mg daily:

The color-coded/outlined atherosclerotic coronary plaque is shown shrinking, while the "lumen," or the path for blood to flow, enlarges. The reduction in coronary plaque is irrefutable. (The small circle within the lumen with the white halo surrounding it is the ultrasound catheter.)

If you and I were to choose a single treatment approach to coronary disease reversal, then 40 mg of rosuvastatin is probably at the top of the list. However, in the Track Your Plaque program, we do not advocate a single treatment strategy. While the Crestor-only approach is relatively straightforward--one pill a day--few people, in my experience, can tolerate this dose for any length of time. Patients invariably have to stop the drug or reduce the dose severely due to muscle aches when I've had patients try it. Contrary to the ASTEROID results, in my experience the majority of people, perhaps all, eventually give up with this improbable "one-size-fits-all" scheme.

The Track Your Plaque approach, while more complicated and involves several nutritional supplements and strategies, in my view addresses more causes of coronary plaque, is better tolerated, and provides health benefits outside of just LDL cholesterol reduction. It also minimizes or eliminates the need for prescription medication.

Studies cited in graph:

1.Nissen S et al. N Engl J Med 2006;354:1253-1263.
2 Tardif J et al. Circulation 2004;110:3372-3377.
3 Nissen S et al. JAMA 2006;295 (13):1556-1565
4 Nissen S et al. JAMA 2004;292: 2217–2225.
5 Nissen S et al. JAMA 2004; 291:1071–1080

When is a calorie not a calorie?

10. April 2008 William Davis (8)

One ounce of raw almonds (about 23 nuts) contains:

6 grams protein

14 grams fat

6 grams carbohydrate

3.5 grams fiber

For a total of 163 calories per ounce.

(From the USDA Nutrient Database)

Calorie content of foods is determined by summing up the calories from each constituent: 1 gram of fat = 9 calories; 1 gram protein = 4 calories; 1 gram carbohydrate = 4 calories. Calorie content can also be directly measured using a device called a burn calorimeter, in which the amount of energy released from a specific food is measured by literally burning it and gauging precisely how much energy is released.

The problem with both of these methods is that it is assumed that all foods are digested with equal efficiency. That is, it assumes that a potato chip is as readily digested and absorbed as energy from table sugar, a pretzel, oatmeal, a piece of steak, or a handful of nuts. In real life, of course this is not true. Different foods are absorbed with varying efficiency.

For a long time I've suspected that some foods are very inefficiently absorbed. I've particularly suspected that raw nuts are relatively poorly absorbed and thus yield only a fraction of the calories ingested.

Among the studies recently reported at the Federation of the Association of Societies for Experimental Biology (FASEB) meetings I attended in San Diego this past week were several devoted to almonds.

One study, to my surprise, documented this phenomenon. In Manipulation of lipid bioaccessibility of almonds influences postprandial lipemia in healthy human subjects, it was determined that, of 100 calories ingested from the fat fraction of almonds, only about half was actually absorbed. The remaining half passed out in the stool. (They did this by collecting stool samples and comparing the fat composition after eating the different almonds prepartions. This is not discussed in the limited text of the abstract.) In addition, postprandial (after-eating) surges in triglycerides were much less with whole almonds compared to the oil separated from the nut (i.e., broken down into almond oil + defatted almond flour). The researchers attributed the difference to the inhibitory effects of the almond nut's "food matrix," or the structural properties of chewed foods.

Add to this the fact that, of 6 grams of carbohydrate per ounce of whole almonds, 3.5 grams are indigestible fibers. This means that 6 - 3.5 = 2.5 grams of digestible carbohydrates are present per ounce (assuming 100% release).

If we follow the reasoning that only about half the fat fraction of almonds are absorbed, and assume that the protein and carbohydrate (minus the indigestible fibers) are absorbed efficiently (100%), then we would re-calculate the calorie content of almonds to be 97 calories per ounce, or 40% less than calories calculated by composition or measured with a calorimeter.

If we were to assume that protein and carbohydrates were, like fats, inefficiently absorbed because of the effects of the food matrix, then one ounce of almonds yields 88 calories per ounce, or 46% less. This is, in fact, a likely scenario, since the food matrix is largely created by the cell wall and should impede digestive access to fat, protein, and carbohydrate equally.

My point? Almonds and other nuts at first appear to be calorically dense due to fat composition. However, this simplistic view of nuts is misleading because of the confounding effects of the food matrix. Stated differently: Whole foods yield less calories. And, judging by the postprandial triglyceride effects: Whole foods yield less undesirable effects, such as postprandial rises in triglycerides.

Some other observations with almonds included:

The effect of almonds on plasma lipids in persons with prediabetes This study confirmed the LDL-reducing and modest HDL-raising effects of almonds.

Almonds (Amygdalus communis L.) as a possible source of prebiotic functional food This curious observation suggests that almonds modify the bacterial flora of the intestinal tract in a positive way (like the cultures in yogurts).

Copyright 2008 William Davis, MD

I had a heart attack--and I don't know why!

25. October 2006 William Davis (0)

Kevin came to my office for another opinion.

A husband and father of two teenagers, Kevin had his first heart attack at age 39. Kevin received two stents to his right coronary artery. The entire process took place in a flurry with little explanation over 48 hours, start to finish.

He smoked a pack of cigarettes a day, but the only history of heart disease in his family was his father, who, also a smoker, had his heart disease uncovered in his late 70s.

His internist subsequently prescribed Zocor even though Kevin's LDL cholesterol was a relatively unimpressive 128 mg/dl.

Kevin subsequently asked his cardiologist, "Where did I get the heart disease from?"

"Cigarettes. And genetics. You can quit the first. There's nothing you can do about the second." End of explanation.

This left Kevin frightened and demoralized. If much of the cause of his heart disease couldn't be identified, why bother quitting smoking? Why not enjoy what time he had left?

Kevin was understandably shocked when I told him that genetic causes were 1)identifiable, 2)quantifiable, and 3) correctable.

Kevin's full lipoprotein analysis subsequently showed the most dire combination that commonly accounts for coronary disease in young people: Lp(a) with small LDL particles. This, along with smoking, fully accounted for this young father of two's heart disease.

Along with starting Kevin on a new program for correction of his patterns, I also persuaded him to get a heart scan. What usefulness is a heart scan after the fact? Plenty. Even though Kevin's right coronary was no longer "scorable" because the steel in the stent obscured our measurements, the two remaining unstented arteries would still yield a score. This provides a baseline for future comparison. Even after a stent, Kevin could "track his plaque".

Butter basics

24. October 2006 William Davis (3)

There’s lot of confusion about butter, margarines, and their substitutes. Butter/margarine substitutes that avoid the negative aspects and provide modest health benefits are available, but I find that people confuse what's what. So here’s a brief primer.

Butter--Avoid it. Plain and simple. Butter is a rich source of saturated fat. Of 11.5 grams total fat per tablespoon, 7.3 grams are saturated. It is not better than margarine, contrary to simple-minded reports from some media sources. Butter raises LDL cholesterol, raises blood pressure, and has been related to various cancers.

Margarine--Not better than butter, arguably worse. Some argue that the trans-fatty acids, or hydrogenated oils, used to solidify vegetable oils to make margarine solid are worse than butter. In addition to the ill-effects of butter, margarine reduces HDL and raises cancer risk, perhaps even more than saturated fats. Hydrogenation yields a very unnatural structure that modifies cellular behavior of the sort that may promote the appearance of cancer cells. More recently, however, some of the major manufacturers, like Blue Bonnet, have produced soft spread products without hydrogenation. These are reasonable substitutes when used sparingly.

Smart Balance--This is a product made with canola oil, a source of monounsaturates (the best oil source after omega-3s), but manufactured without hydrogenation and therefore has no trans-fats. It does have, in my view, a bit too much saturated fat (1.5 gm per tbsp. in the 37% Light Spread; 2.5 gm per tbsp in the 67% regular spread). This is a reasonable product to use in small quantities.

There is also a Smart Balance Omega PLUS product that contains added flaxseed oil and sterol esters. I do not recommend this product because of the sterol content (see below). I also object to the manufacturers who label their products “rich in omega-3s” when they mean linolenic acid (in flaxseed), which is converted to a trivial quantity of omega-3s. Linolenic acid may pose unique benefits of its own, but it should not be listed as an omega-3 source.

Benecol--This is a butter substitute that contains stanol esters, a substance that reduces total and LDL cholesterol. Two tablespoons a day reduces LDL around 20 mg/dl, more or less depending on your starting cholesterol.

There’s a light and regular spread. The light contains 20 calories less per tablespoon but somewhat less monounsaturates, but the same LDL-reducing stanol esters. The manufacturer does hydrogenate the oils, yielding 0.5 mg trans-fats per tablespoon--a small drawback.

Take Control--Similar to Benecol, but made with sterol esters. Take Control also reduces LDL cholesterol. However, data from several high-quality studies from Finland suggest that sterol esters may, in some people, be absorbed into the blood. This is potentially concerning. There is a rare disease called sitosterolemia that results in coronary disease in teenagers and young adults in their 20s from increased absorption of sterol esters. While you can’t acquire this genetic disease, some people have the capacity to absorb sterol esters from their intestines very efficiently. I find it very disturbing and I suggest that you stay away this product and other sterol-containing products like HeartWise orange juice and Smart Balance Omega PLUS until the issue is clarified and safety assured.

Brummel and Brown--A blend of vegetable oils (soybean and partially hydrogenated soybean) with calories and fats reduced by blending in yogurt. This is an okay product. The hydrogenation yields trans-fats below the FDA required declaration limit of 1.0 mg.

There’s also 1.0 mg each of saturated and monounsaturated fats. The calories are relatively low as a consequence of the added yogurt, only 45 calories per tablespoon. This makes the Brummel and Brown a reasonable choice.

Other products are making their way out to supermarkets. Look for the type of oil used. Canola, olive, and flaxseed are the best. Also look for trans-fats and saturated fat content; both should be low, preferably <1.0 mg per tablespoon, ideally none.

The best choice among the above products in my view is Benecol, though it’s also the most expensive. It will yield substantial drops in LDL cholesterol. All the products in our informal tastings taste a lot like butter, or at least as well as we can remember what butter tasted like! The key with all of these products is use in moderation, since they all provide between 45?80 calories per tablespoon.

Let Dr. Friedewald rest in peace

24. October 2006 William Davis (1)

In the 1960s, doctors struggled with the concept of cholesterol and its relationship to heart disease. It was becoming clear that higher levels of cholesterol were predictive of heart disease. It was also becoming clear that the low-density fraction of cholesterol, or LDL, was somewhat better than total cholesterol in predicting heart attack.

Cholesterol was easily measurable in the 1960s. LDL was not. So, Dr. Friedewald, a noted lipid researcher at the National Institutes of Health, proposed an easy method to calculate LDL cholesterol from total choleseterol, HDL, and triglycerides:

LDL cholesterol = Total cholesterol – HDL cholesterol – triglycerides/5

This simple manipulation would put LDL cholesterols into the hands of the practicing physician and the American public. Dr. Friedewald recognized that this calculation only represented an approximation of LDL cholesterol and that it was thrown off, sometimes substantially, by any abnormal rise in triglycerides or reduction in HDL. But it served its purpose at an age when most doctors hadn’t even heard of cholesterol and the public was still sold on whole milk and “farm-fresh” butter, and Chesterfields were the cigarette choice of most doctors.

The world has since changed. Most doctors have heard about cholesterol and, along with the public, have been drowned in drug company marketing for cholesterol-reducing drugs. Most people with some level of common sense and health awareness no longer use butter or whole milk, and no longer believe that the brand of cigarette you choose can be healthy. But we’re still using Dr. Friedewald’s original calculation for LDL cholesterol. When you get an LDL cholesterol from your clinic, doctor, or hospital, >99% of the time it is obtained using Dr. Friedewald’s calculation.

Is it because there’s nothing better available? No, it’s not. There’s two reasons why your neighborhood primary care physician or cardiologist is still using this dinosaur of testing called LDL:

1) The lag in science to practice is 20 years. Accept that most primary care doctors are 20 years behind the times on many issues, LDL cholesterol included.

2) Insurance companies vigorously discourage testing beyond conventional lipids. The array of objections we get from insurance companies is mind-boggling. It would be funny if human life and finances weren’t at stake. These “new” tests are “experimental”, “unproven”, not endorsed by standard guidelines, not approved by some internal committee, or simply “We don’t know what this test is” ?we’ve heard them all.

What are the tests that are superior to Dr. Friendewald’s calculated LDL? There are several, listed here in order of best to worst:

1) LDL particle number--the value generated by NMR lipoprotein testing. This is the gold standard, most reliable test available, and the one I recommend.

2) Apoprotein B--More widely available even from conventional laboratories in hospitals. Not as accurate as NMR LDL particle number, but a pretty good choice. Apo B is the principal protein in LDL, VLDL, and IDL particles, and so it’s a better reflector of risk from all of these lipoprotein fractions, not just LDL.

3) “Direct” LDL--This is LDL that is actually measured. Unfortunately, it ignores the issues of LDL size and has some other pitfalls, but it’s still better than calculated LDL

4) Non-HDL cholesterol--So-called because it incorporates all undesirable cholesterol-containing lipids except good HDL, thus “non-HDL”. This is another calculation, though better than LDL (because it sums up the risk from other apoprotein B-containing lipoproteins). Non-HDL is calculated from Total cholesterol – HDL. It’s therefore available from any standard lipid panel. It’s little used in everyday practice, however, because most people and their physicians find it confusing.

5) Friedewald calculated LDL--You can see that calculated LDL is last on a list of choices. Yet this is the measure that doctors use day in, day out. It’s the measure that drug companies base billions of dollars of revenue and profits on.

It’s an everyday occurrence in my office that calculated LDL is 89 mg/dl, but the real value is somewhere between 160 and 200 mg/dl. That’s a big difference. Imagine your realtor tells you your house’s estimated value is $200,000 and that’s what you sell it for to an eager buyer. After closing, you find out your house was really worth $300,000. You’d be upset. But that’s what you’re often getting with LDL cholesterol?a bum deal.

It’s part of the reason people will say, “My doctor said my cholesterol was fine and that no cause for my heart disease can be found. He said it was genetic.” In reality, they could have sky-high LDL cholesterol revealed by LDL particle number or apoprotein B.

Use LDL cholesterol in a pinch when you’ve got nothing else. It’s also helpful to gauge any treatment effect of diet, functional foods, drugs, etc. But it is a seriously flawed tool to diagnose your initial level of risk.

The key to losing weight

23. October 2006 William Davis (0)

I saw three people this past week, all of whom set off on an effort to lose substantial quantities of weight. And all seriously needed to.

All three started with at least 70 lbs. excess weight; all showed substantial weight-sensitive lipoprotein patterns like low HDL, small LDL, high triglycerides, VLDL, and pre-diabetic levels of blood sugar. They also all shared high blood pressure.

All three also had high heart scan scores. Kate’s score was just over 1200. Tom, a 58-year old real estate developer, had a score of nearly 600. Susan, the youngest of the three at 52, had a heart scan score of 377¾99th percentile at this age. Losing weight was an absolute requirement for their plaque control program. Because their lipoprotein abnormalities and pre-diabetic patterns were triggered by weight, weight loss would provide powerful correction. Each and every one of them would need to lose much of their excess weight¾at least 50 lbs¾if they hoped to halt the relentless progression of their heart scan scores.

All three of them returned after 6-8 weeks, and all had lost between 17-24 lbs: spectacular results.

There’s no secret to weight loss. Each of them achieved their weight loss in slightly different ways. But they also shared several critical ingredients in their weight-loss efforts:

1) All three dramatically slashed their intake of wheat flour-containing foods and other processed carbohydrates and did so consistently. All also avoided the usual high-fat, high caloric-density foods like butter, margarine, fried foods, greasy foods, nuts roasted in oil, etc. They concentrated on vegetables, salads, raw nuts, lean proteins (inc. turkey, chicken, fish, lean red meats, low-fat cottage cheese and yogurt).

2) They stopped using food as a reward or as a consolation tool.

3) Exercise for one hour a day at least 5 days a week. The exercise in 2 of 3 of these people was just walking. It wasn’t strenuous, it wasn’t expensive. The women both liked walking with friends or their spouse. Tom followed a more common male path of more strenuous work on his treadmill, elliptical, and biking at the fitness club. But they all did it religiously and missed rare sessions.

4) They refrained from any and all alcoholic beverages. Yes, there are some advantages to 1-2 glasses of wine per day, but it stalls weight loss efforts.

5) They didn’t allow themselves any major indiscretions. There were no binges, major pig-outs at weddings, barbecues, or all-you-can-eat buffets. They did allow themselves an occasional “treat” but did so in small portions.

That’s it. But for most people, that’s simply too much. Adhering to an effort to lose dramatic weight requires day-after-day consistency. Nobody can lose the equivalent of 70,000 calories (20 lbs.) just by skipping a meal, a 20-minute walk, skipping the mashed potatoes at dinner.

It can be done. You’ve just got to be consistent about it.

How can I get my lipoproteins tested?

20. October 2006 William Davis (0)

This question came up on our recent online chat session and comes up frequently in phone calls and e-mails.

If lipoprotein testing is the best way to uncover hidden causes of coronary heart disease, but your doctor is unable, unknowledgeable, or unwilling to help you, then what can you do?

There are several options:

1) Get the names of physicians who will obtain and interpret the test for you. Go to the websites for the three labs that actually perform the lipoprotein tests: www.liposcience.com (NMR); www.berkeleyheartlab.com (electropheresis or GGE); www.atherotech.com (VAP or centrifugation). None of them will provide you with the names of actual physicians. They will provide you with the name of a local representative who will know who the doctors in your area who are well-acquainted with their technology. I prefer this route to just having a representative identify a laboratory in your area where the blood sample can be drawn, because you will still need a physician to interpret the results¾this is crucial. The test is of no use to you unless someone interprets it intelligently and understands the range of treatment possibilities available. Don’t be persuaded by your doctor if he/she agrees to have the blood drawn but has never seen the test before. This will be a waste of your time. That’s like hoping the kid next door can fix your car just because he says he fixed his Mom’s car once. Interpretation of lipoproteins takes time, education, and experience.
2) Seek out a lipidologist. Lipidologists are the new breed of physician who has sought out additional training and certification in lipid and lipoprotein disorders. Sometimes they’re listed in the yellow pages, or you can search online in your area.
3) Contact us. I frankly don’t like doing this because I feel that I can only provide limited information through this method. I provide a written discussion of the implications and choices for treatment with the caveat to discuss them with your doctor, since I can’t provide medical advice without a formal medical relationship. We also charge $75 for the interpretation. But it’s a lot better than nothing.
4) Make do with basic testing. Basic lipids along with a lipoprotein(a), C-reactive protein, fibrinogen, and homocysteine would provide a reasonable facsimile of lipoprotein testing. You’ll still lack small LDL and postprandial (after-eating) information, but you can still do reasonably well if you try to achieve the Track Your Plaque targets of 60-60-60.

In 20 years, this will be a lot easier. But for now, you can still obtain reasonably good results choosing one of the above alternatives.

What do you think about those heart scans?

20. October 2006 William Davis (1)

52-year old Jerry came in for a stress test. He displayed the usual apprehension: fidgeting while he sat on the bed, examining his surroundings, asking lots of questions.

“Your doctor asked you have have a stress test?” I asked.

“All the males in my family have had heart attacks by age 56, so my doctor suggested I have a stress test,” Jerry explained.

Jerry went on to tell me that he had exercised vigorously this morning for 45 minutes without symptoms. He had, in fact, gone surfing just several weeks earlier and described how aerobically challenging it was keeping up with the 20 year olds. “But I did it!” he proudly declared.

As he neared the end of his brisk walk on the treadmill, Jerry asked, “What do you think about those heart scans?”

Jerry had asked his primary care physician the same question. His doctor had apparently told him that they were just a gimmick. “We’ll get you a real test.”

Of course, Jerry’s stress test proved entirely normal. The likelihood of an abnormal stress test with his history of vigorous exercise was <2%. I explained to Jerry that not getting heart scan would be a mistake. In fact, a heart scan was the only easily obtainable test that would uncover hidden heart disease. In truth, the stress test was a waste of time—and an unneeded exposure to radiation.

If Jerry’s heart scan score turned out to be zero, great! He was probably spared the genes from the other males in his family, and his risk of heart attack in the next decade was nearly zero.

If his heart scan turned out be 1000, then an urgent scramble to uncover the causes and correct them to create a truly effective prevention program would be crucial for his long term health. Or, perhaps his score lies somewhere in between, but Jerry would then know how far along he stood on his way to heart disease.

Don’t be a victim of the ignorance of your doctor. Despite all the attention heart scans have received, the majority of doctors remain miserably, inexcusably in the dark. I say inexcusable because CT heart scans can uncover the number one killer of Americans, the number one cause of all deaths in any primary care physician’s practices, and it’s laughably easy. How can a physician not advise patients on the value of heart scans?

If given a choice and you’re without symptoms, a heart scan is far and away the superior test.

Olive oil for gourmets

19. October 2006 William Davis (0)

"The finest extra-virgin olive oils should not be used as a medium for hot cooking, but rather as a condiment or a finisher on top of your favorite savory foods. They are expensive, but if stored properly they will last for up to a year..."

You all know that olive oil is among the preferred oils to use: rich in monounsaturates, low in saturates, high in polyphenols.

For a fascinating perspective for the olive oil gourmet, go to www.npr.org, the website for National Public Radio. (Scroll down to the article or enter olive oil into their site search.) Their article, "Like fine wines, fine olive oils boast subtle joys" provides an insightful discussion on squeezing maximum enjoyment out of this wonderful "functional food".

As we emerge from the mis-directed low-fat craze of the past 20 years, we're re-discovering the joys of healthy oils. You'll find some great thoughts here

Vitamin D must be oil-based

18. October 2006 William Davis (10)

As part of the Track Your Plaque coronary plaque reversal program, we advocate vitamin D supplementation. Vitamin D has been shown to reduce blood sugar and reduce pre-diabetic tendencies, reduce blood pressure (it's a renin antagonist, a blood pressure hormone), it's far more important for bone health than calcium, and it may help prevent colon cancer, prostate cancer, and multiple sclerosis.

And, oh yes, it may facilitate coronary plaque regression.

One lesson I've learned is that vitamin D MUST be taken as a oil-based capsule or gelcap. You'll recognize it as a transparent or translucent, sometimes opaque, capsule. The list of ingredients may say something like "cholecalciferol [vitamin D] in a base of soybean oil", indicating that the active ingredient is oil-based.

Oil-based vitamin D3 skyrockets blood levels of 25-OH-vitamin D3 in to the normal range reliably and easily.

Tablets are a different story. These are generally white powdery tablets. The rise in blood levels of vitamin D3 are minimal, sometimes none. Women will often say "I get vitamin D with my calcium tablets."

People taking this form almost always have blood levels of vitamin D that are low, as if they were taking nothing.
If you're going to take vitamin D, the oil-based tablets are the way to go. They're not necessarily any more expensive. We've had good experiences with the Nature's Life 2000 unit capsule, as well as preparations from Life Extension. We have had negative experiences with the preparations from GNC, Sam's Club, and Walgreen's, all tablets and non-oil-based.

When is LDL cholesterol NOT LDL cholesterol?

18. October 2006 William Davis (0)

Darlene had a high LDL cholesterol, at times as high as 200 mg/dl. Her primary care doctor first tried Mevacor, then Pravachol, then Zocor, then Lipitor. Every statin drug failed to reduce Darlene's LDL below 160 mg/dl, even when maximum doses were used. The higher doses also resulted in nearly intolerable muscle aches and weakness.

When we sent Darlene's blood sample off for lipoprotein analysis, a surprise came back: she had a high lipoprotein(a), or Lp(a). This explained a lot.

LDL cholesterol is not always just LDL cholesterol. One of the particles that can masquerade as LDL is Lp(a). Darlene's story is typical of many people who've had high cholesterol levels poorly responsive to the statin drugs. That's because their LDL conceals Lp(a), which does not respond to these agents. LDL cholesterol does drop some because there's also some real LDL mixed in.

A poor response to statin agents or to nutritional strategies to reduce LDL is a tip-off that Lp(a) may be hidden. The answer: just measure Lp(a)! If you and your doctor don't measure it, you won't know whether or not you have it. Rather than a statin drug, we put Darlen on niacin. Not only did her Lp(a) drop, but her LDL also plummeted.

What is a desirable triglyceride level?

17. October 2006 William Davis (0)

Though well-intended, the National Cholesterol Education Panel's Adult Treatment Panel, or ATP-III, (whew!) guidelines for cholesterol have been responsible for loads of misinformation.

The intention was to educate the internist or family doctor who treats sore throats, performs Pap smears, administers pneumovax vaccine, treats arthritic knees---and dabbles in heart disease prevention. The ATP-III guidelines are the "Cholesterol for Dummies" approach.

What standard guidelines definitely do not represent are the ideal values to achieve. They do not ensure protection from heart disease. This is particularly true of the ATP-III advice to keep triglycerides at or below the "desirable" level of 150 mg/dl.

In the Track Your Plaque program, we ask "What is necessary to tip the odds in favor of coronary plaque regresion or reduction of heart scan score?" This is not achieved with a triglyceride of 150. In fact, triglycerides at this level are associated with flagrant abnormalities of lipoprotein patterns. It usually means that processed carbohydrates, particularly wheat products, are occupying too prominent a role in your food choices. It could mean that you're making excessive use of processed foods containining high-fructose corn syrup. It will not respond to a low-fat diet. It will, however, respond vigorously to fish oil.

Triglycerides are a crucial aspect of your plaque control program. We aim for 60 mg/dl or less. The ideal level is actually 45 mg/dl. At this level, all abnormal triglyceride-containing lipoproteins finally go away.