All posts by william-davis

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?

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?

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.

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.

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

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.

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 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.

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.

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.

The results of the latest Heart Scan Blog poll are in.

DIRECT-TO-CONSUMER PHARMACEUTICAL ADVERTISING HAS:

Increased public awareness of medical conditions and their treatment
19 (11%)

Has had little overall effect on health and healthcare
29 (18%)

Needlessly increased healthcare costs
81 (50%)

Further empowered the revenue-obsessed pharmaceutical industry
130 (81%)

Clearly, there's a lot of negative sentiment against direct-to-consumer (DTC) drug advertising.

It looks as if a small minority believe that good has come from DTC advertising, judging by the meager 11% who voted for increased awareness. In fact, the poll results are heavily weighed towards the negative: 50% voted for "needlessly increased healthcare costs," while an astounding 81% voted for "empowered the revenue-obsessed pharmaceutical industry."

It is, indeed, an odd situation: Pharmaceutical agents available only by prescription being hyped directly to the consumer.

Personally, I would vote for choices 1,3, and 4. While awareness has increased, it has come with a hefty price, not all of it well spent. I believe the pharmaceutical industry still adheres to the rule that, for every $1 spent on advertising, $4 is made in revenue. They are, in effect, printing money.

According to conventional wisdom, heart scan scores cannot be reduced.

In other words, say you begin with a heart scan score of 300. Conventional wisdom says you should take aspirin and a statin drug, eat a low-fat "heart healthy" diet, and take high blood pressure medications, if necessary.

If your heart scan score goes up in a year or two, especially at an annual rate of 20% or more, then you are at very high risk for heart attack. If the heart scan score stays the same, then your risk is much reduced. These observations are well-established.

But more than 99% of physicians will tell you that reducing your heart scan score is impossible. Don't even try: Heart scan scores can go up, but they can't go down.

Baloney. Heart scan scores can indeed go down. And they can go down dramatically.

It is true that, following conventional advice like taking a statin drug, following a low-fat diet, and taking aspirin will fail to reduce your heart scan score. A more rational approach that 1) identifies all causes of coronary plaque, 2) corrects all causes while including crucial strategies like omega-3 fatty acid supplementation, vitamin D supplementation, and thyroid function normalization, is far more likely to yield a halt or reduction in score.

While not everybody who undertakes the Track Your Plaque program will succeed in reducing their heart scan score, a growing number are enjoying success.

A small portion of our experience was documented this past summer. (I collected and analyzed the data with the help of Rush University nutrition scientist, Dr. Susie Rockway, and statistician, Dr. Mary Kwasny.)

Effect of a combined therapeutic approach of intensive lipid management, omega-3 fatty acid supplementation, and increased serum 25 (OH) vitamin D on coronary calcium scores in asymptomatic adults.

Davis W, Rockway S, Kwasny M.

The impact of intensive lipid management, omega-3 fatty acid, and vitamin D3 supplementation on atherosclerotic plaque was assessed through serial computed tomography coronary calcium scoring (CCS). Low-density lipoprotein cholesterol reduction with statin therapy has not been shown to reduce or slow progression of serial CCS in several recent studies, casting doubt on the usefulness of this approach for tracking atherosclerotic progression. In an open-label study, 45 male and female subjects with CCS of > or = 50 without symptoms of heart disease were treated with statin therapy, niacin, and omega-3 fatty acid supplementation to achieve low-density lipoprotein cholesterol and triglycerides < or = 60 mg/dL; high-density lipoprotein > or = 60 mg/dL; and vitamin D3 supplementation to achieve serum levels of > or = 50 ng/mL 25(OH) vitamin D, in addition to diet advice. Lipid profiles of subjects were significantly changed as follows: total cholesterol -24%, low-density lipoprotein -41%; triglycerides -42%, high-density lipoprotein +19%, and mean serum 25(OH) vitamin D levels +83%. After a mean of 18 months, 20 subjects experienced decrease in CCS with mean change of -14.5% (range 0% to -64%); 22 subjects experienced no change or slow annual rate of CCS increase of +12% (range 1%-29%). Only 3 subjects experienced annual CCS progression exceeding 29% (44%-71%). Despite wide variation in response, substantial reduction of CCS was achieved in 44% of subjects and slowed plaque growth in 49% of the subjects applying a broad treatment program.

Gretchen sent me the results of a little experiment she ran on herself. She measured blood glucose and triglycerides after 1) a low-fat diet and 2) a low-carb diet.

Gretchen describes her experience:

Several years ago I received a windfall of triglyceride strips that would expire in a week or so. I hated to waste them, so I decided to use them to test my triglyceride and BG responses to two different diets: low carb and low fat.

The first day I followed a low-fat diet. For breakfast I ate a lot of carbohydrate, including 1 oz of spaghetti cooked al dente and ¾ cup of white rice. For the rest of the day I ate less carbohydrate but continued to eat low fat.

The second day I followed a low-carb diet. For breakfast I ate a lot of fat, including a sausage, mushrooms fried in butter, 2 slices of bacon, and ¼ cup of the creamy topping of whole-milk yogurt. For the rest of the day I ate less fat, especially less saturated fat, but continued to eat low carb.

Both days I measured both BG and triglyceride levels every hour until I went to bed. On the low-carb day I had 3 meals. On the low-fat day, I was constantly hungry, had 4 meals, and kept snacking.

You can see the results in Figure 1. On the low-fat diet, after a “healthy” low-fat breakfast of low-glycemic pasta with low-fat sauce, my BG levels shot up to over 200 mg/dL and took more than 6 hours to come down. My triglycerides, however, remained low, and at first I thought perhaps the low-fat diet might be better overall. However, after about 6 hours, the triglyceride levels started to increase steadily, and by the next morning, they were higher than they had been the day before.
On the low-carb diet, my BG levels stayed low all day. However, after meals, the triglyceride levels skyrocketed. After meals they came down, and by the next morning they were lower than they had been the day before.

As I interpret these results, the high triglyceride levels after eating the high-fat meals represent chylomicrons, the lipoproteins that transport fat from your meals to the cells of your body. The high triglyceride levels the morning after eating the low-fat meals represent very low density lipoprotein, which takes the cholesterol your liver synthesizes when your intake of dietary cholesterol is low and distributes it to cells that need it, or again, to the fat for storage.

There are several interesting factors to consider here. First, when you have a lipid test done at the lab, it’s usually done fasting, which means first thing in the morning after not eating for 8 to 12 hours. It tells you nothing about what your triglyceride levels were all day.

Second, the low-carb diet resulted in lower fasting triglyceride levels, but much higher postprandial triglyceride levels. Which are more dangerous? I’m afraid I don’t know. You should also note that the high-fat, low-carb breakfast was extremely high in fat, including saturated fat. I don’t normally eat that much fat but wanted to test extremes.

Third, although the low-fat diet didn’t produce the very high postprandial triglyceride levels that the high-fat diet did, it produced extremely high BG levels that persisted for 6 hours. Some people think that it’s oxidized and glycated lipids that are the dangerous ones, so high BG levels and normal triglyceride levels might be more dangerous than very high triglyceride levels and normal BG levels. Note that high BG levels also contribute to oxidation rates.

Fourth, this shows the results of an experiment with a sample size of one. My physiology might not be typical. If you want to know how your own body’s lipids respond to different types of diets, you should get a lipid meter and test yourself. Unfortunately, your insurance is unlikely to want to pay for this, so it will be an expensive experiment.

The main point of this is that the results of different diets are complex. We have to eat. And what we eat can affect many different systems in our bodies. Finding the ideal diet that matches our own physiology and results in the best lipid levels as well as BG levels is a real challenge.

This was a lot of effort for one person. Thanks to Gretchen for sharing her interesting experience.

Gretchen makes a crucial point: Some of the effects of diet changes evolve over time, much as triglyceride levels changed substantially for her on the day following her experiment. Wouldn't it be interesting to see how postprandial patterns develop over time if levels were observed sequentially, day after day?

The stark contrast in blood sugars is impressive--Low-carb clearly has the advantage here. Are there manipulations in diet composition in low-carb meals that we can make to blunt the early (3-6 hour) postprandial lipoprotein (triglyceride) peak? That's a topic we will consider in future.

More of Gretchen's thoughts can be found at:

http://wildlyfluctuating.blogspot.com
http://www.healthcentral.com/diabetes/c/5068

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

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

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

Blood was drawn over 6 hours following the test meal.

Roberts R et al. Am J Clin Nutr 2008

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

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

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

Furthering our discussion of postprandial (after-eating) phenomenona, including chylomicron and triglyceride "stacking" (Grazing is for cattle and Triglyceride and chylomicron stacking), here's a comment from the recent Palet Diet Newsletter on the closely related issue, meal timing and frequency:

We are currently in the process of compiling meal times and patterns in the worlds historically studied hunter-gatherers. If any single picture is beginning to emerge, it clearly is not three meals per day plus snacking ala the typical U.S. grazing pattern. Here are a few examples:

--The Ingalik Hunter Gatherers of Interior Alaska: 'As has been made clear, the principal meal and sometimes the only one of the day is eaten in the evening.'
--The Guayaki (Ache) Hunter Gatherers of Paraguay: 'It seems, however, that the evening meal is the most consistent of the day. This is understandable, since the day is generally spent hunting for food that will be eaten in the evening."
--The Kung Hunter Gatherers of Botswana. "Members move out of camp each day individually or in small groups to work through the surrounding range and return in the evening to pool the collected resources for the evening meal."
--Hawaiians, Tahitians, Fijians and other Oceanic peoples (pre-westernization). 'Typically, meals, as defined by Westerners, were consumed once or twice a day. . . Oliver (1989) described the main meal, usually freshly cooked, as generally eaten in the late afternoon after the day’s work was over."

The most consistent daily eating pattern that is beginning to emerge from the ethnographic literature in hunter-gatherers is that of a large single meal which was consumed in the late afternoon or evening. A midday meal or lunch was rarely or never consumed and a small breakfast (consisting of the remainders of the previous evening meal) was sometimes eaten. Some snacking may have occurred during daily gathering, however the bulk of the daily calories were taken in the late afternoon or evening. This pattern of eating could be described as intermittent fasting relative to the typical Western pattern, particularly when daily gathering or hunting were unsuccessful or marginal. There is wisdom in the ways of our hunter gatherer ancestors, and perhaps it is time to re-think three squares a day.

In other words, the notion of "grazing," or eating small meals or snacks throughout the day, is an unnatural situation. It is directly contrary to the evolutionarily more appropriate large meal followed by periods of no eating or small occasional meals.

I stress this point because I see that the notion of grazing has seized hold of many people's thinking. In my view, grazing is a destructive practice that is self-indulgent, unnecessary, and simply fulfills the perverse non-stop hunger impulse fueled by modern carbohydrate foods.

Eliminate wheat, cornstarch, and sugars and you will find that grazing is a repulsive impulse that equates with gorging.

The full-text of the Paleo Diet Newsletter can be obtained through www.ThePaleoDiet.com. You can also read and/or subscribe to the new Paleo Diet Blog, just launched in November, 2009.

Graphic courtesy Parsemus Foundation

Lady Rai, nursemaid to Queen Nefertari of Egypt, died in 1530 BC, somewhere between the age of 30 and 40 years. Her mummy is preserved in the Egyptian National museum of Antiquities in Cairo.

A CT scan of her thoracic aorta revealed calcium, representing aortic atherosclerosis, reported by Allam et al (including my friend from The Wisconsin Heart Hospital, Dr. Sam Wann, who provided me a blow-by-blow tale of this really fascinating project). Ladi Rai and 14 other Egyptian mummies were found to have vascular calcification of a total of 22 mummies scanned. (The hearts of the mummies were too degenerated to make out any coronary calcium.)

But why would people of that age have developed atherosclerosis?

The authors of the study comment that "Our findings that atherosclerosis was not infrequent among middle-aged and older ancient Egyptians of high social status challenges the view that it is a disease of modern humans. . . Although ancient Egyptians did not smoke tobacco or eat processed food or presumably lead sedentary lives, they were not hunter-gatherers. [Emphasis mine.] Agriculture was well established in ancient Egypt and meat consumption appers to have been common among those of high social status."

Fascinating. But I don't think that I'd blame meat consumption. Egyptians were also known to have cultivated grains, including wheat, and frequently consumed such sweet delicacies as dates and figs. Egyptians were also apparently beer drinkers. Unfortunately, no beer steins were seen in any of the scans.

Here's a link to my recent article in Life Extension Magazine on iodine:

Halt on Salt Sparks Iodine Deficiency

Iodized salt, a concept introduced into the U.S. by the FDA in 1924, slowly eliminated goiter (enlarged thyroid glands), along with an enormous amount of thyroid disease, heart attack, mental impairment, and death. The simple addition of iodine to salt ensured that salt-using Americans obtained enough iodine sufficient to not have a goiter.

Now that the FDA, goiters long forgotten from their memories, urges Americans to reduce salt, what has happened to our iodine?

I talk at length about this issue in the Life Extension article.

Here's an informal observation.

The healthiest people are the most iodine deficient.

The healthier you are, the more likely you are to:

--Avoid junk foods--30% of which have some iodine from salt
--Avoid overuse of iodized salt
--Exercise--Sweating causes large losses of iodine.

So the healthy-eating, exercising person is the one most likely to show iodine deficiency: gradually enlarged thyroid gland (in the neck), declining thyroid function. Over time, if iodine deficiency persists, excessive sensitivity to iodine develops, as well as abnormal thyroid conditions like overactive nodules.

Even subtle levels of thyroid dysfunction act as a potent coronary risk factor.

Sal has had 3 heart scans. (He was not on the Track Your Plaque program.) His scores:

March, 2006: 439

April, 2007: 573

October, 2009: 799

Presented with the 39% increase from April, 2007 to October, 2009, Sal's doctor responded, "I don't understand. Your LDL cholesterol is fine."

This is the sort of drug-driven, cholesterol-minded thinking that characterizes 90% of primary care and cardiologists' practices: "Cholesterol is fine; therefore, you must be fine, too."

No. Absolutely not.

The data are clear: Heart scan scores that continue to increase at this rate predict high risk for cardiovascular events. Unfortunately, when my colleagues hear this, they respond by scheduling a heart catheterization to prevent heart attack--a practice that has never been shown to be effective and, in my view, constitutes malpractice (i.e., performing heart procedures in people with no symptoms and with either no stress test or a normal stress test).

It's the score, stupid! It's not the LDL cholesterol. Pay attention to the increasing heart scan score and you will know that the disease is progressing at an alarming rate. Accepting this fact will set you and your doctor on the track to ask "Why?"

That's when you start to uncover all the dozens of other reasons that plaque can grow that have nothing to do with LDL cholesterol or statin drugs.

Indian buffet

American Heart Association diet makes a monkey out of you

Construct your glucose curve

Why is type 1 diabetes on the rise?

Apo E4 and sterols: Lethal combination?

Glucomania

Diarrhea, runny noses, and rage: Poll results

A carpenter is only as good as his tools

The perfect Frankengrain

Diabetes: A study in aging

I'll supply the tar if you supply the feathers

What goes up can't come down

Gretchen's postprandial diet experiment

After-eating effects: Carbohydrates vs. fats

The Paleo approach to meal frequency

Angioplasty Special: Get it while it's hot!

Even mummies do it

Life Extension article on iodine

The healthiest people are the most iodine deficient

It's the score, stupid