Why average cholesterol values can be so bad

Jack had been told again and again that there was absolutely nothing wrong with his cholesterol panel. His numbers:

Total cholesterol 198 mg/dl

LDL cholesterol 119 mg/dl--actually below the national average (131 mg/dl).

HDL 48 mg/dl--actually above the average HDL for a male (42 mg/dl).

Triglycerides 153 ng/dl--right at the average.


So his primary care physician was totally stumped when Jack's heart scan revealed a score of 410.


Lipoprotein analysis (NMR) told an entirely different story:

LDL particle number 1880 nmol/l (take off the last digit to generate an approximate real LDL, i.e., 188 mg/dl).

Small LDL 95% of all LDL particles, a very severe pattern.

A severe excess of intermediate-density lipoprotein (218 nmol/l), suggesting that dietary fats are not cleared for 24 hours or so after a meal.

And those were just the major points. In other words, where conventional cholesterol values, or lipids, failed miserably, lipoprotein analysis can shine. The causes for Jack's high heart scan score become immediately apparent, even obvious. Jack's abnormalities are relatively easy to correct--but you have to know if they're present before they can be corrected. A shotgun statin drug approach could only hope to correct a portion of this pattern, but would unquestionably fail to fully correct the pattern.

As I've said before, standard cholesterol testing is a fool's game. You can squeeze a little bit of information out of them, but there's so much more information that can be easily obtained through lipoprotein testing like Jack had.

Cholesterol trumps heart scan?

Lela's heart scan score: 449--very high for a 49-year old, peri-menopausal woman. Her score placed her flat in the 99th percentile, or the worst 1% of women her age.

Lela first consulted her primary care physician. Her doctor looked at the result puzzled. "Now wait a minute. Your cholesterol numbers have been great." After a pause, her doctor (a woman) declared the heart scan wrong. "Tests aren't perfect. The heart scan is simply wrong. I'm going to believe the cholesterol numbers and there's no way you have heart disease."

Is that right? Can cholesterol numbers trump your heart scan score? Can the heart scan simply be wrong?

The answer is simple: NO.

The heart scan is not wrong. The heart scan is right. What is wrong with this picture is that standard cholesterol testing commonly and frequently fails to identify people at risk for heart disease.

What if this woman smoked? That wouldn't be revealed in her cholesterol panel. Or had high blood pressure, increased inflammatory responses like C-reactive protein, had increased small LDL or lipoprotein(a), was severely deficient in vitamin D? None of that would be revealed by cholesterol numbers.

So, no, the heart scan is not wrong. The cholesterol numbers are not wrong. The doctor's interpretation of the data is wrong.

Please do not allow false reassurances offered by those who do not understand the technology steer you wrong.

This woman proved to have an entire panel of hidden causes of her coronary plaque uncovered. No surprise.

Boycott LabCorp

Track Your Plaque Members have been following this conversation on the Track Your Plaque Forum.

A good number of people have had their blood drawn for NMR lipoprotein analysis through laboratories operated by the Laboratory Corporation of American, or LabCorp. When the results were returned, the very important page 2 of the report was withheld. Many of us have communicated with the company, only to be given some corporate-speak about internal policy.

I have personally expressed my dissatisfaction, my outrage, at this silly policy. Why would laboratory results that you or your insurance paid for be denied to you? It is my understanding that, on request, you are legally entitled to the information. The page 2 information is provided by the laboratory (Liposcience, Inc.) that actually performs the testing. LabCorp does nothing more than draw the blood, prepare the specimen, then convey and dilute the results that Liposcience reports to them.

My personal suspicion is that the LabCorp people do this to 1) make the results appear that they actually performed the tests and not farmed to an outside laboratory (Liposcience), and 2) not further confuse and befuddle the bungling primary care physician who barely understands cholesterol issues to begin with. "LDL, HDL, triglycerides . . . What now--a bunch of new information, bars even!?

To me, this LabCorp policy is criminal. In fact, I wonder if this has the substance to justify a class action lawsuit against LabCorp. I believe that we can easily make a case that crucial health information is being systematically denied to people.

If this has affected you, or if you share in the frustration of many people who have had watered down lipoprotein results provided, write to:


Ken Younts, VP of Sales at LabCorp. Yountsk@labcorp.com


Or, write to:

Tom MacMahon
Chairman of the Board

David P. King
President and Chief Executive Officer

Laboratory Corporation of America Holdings
358 South Main Street
Burlington, NC 27215



Thanks to the Track Your Plaque Members who have already participated in this campaign and written to the LabCorp people. And thanks to our Members who uncovered the contact information.

Until then, please BOYCOTT LABCORP LABORATORIES. Please do not use LabCorp Laboratories if you can avoid it. Simply ask the laboratory staff who operates the lab and they should tell you. It is your right to know.

Useless low-fat diets

If you would like to read an ironic testimonial to the futility of conventional low-fat diets, read:

Cutting Cholesterol, an Uphill Battle on the New York Times website at http://www.nytimes.com/2007/08/21/health/21brod.html?_r=2&adxnnl=1&oref=slogin&ref=health&adxnnlx=1187928650-f0mfyzGTFdsLmtInHcGPUw

In this story, author and columnist Jane Brody recounts her struggles with her cholesterol levels. She describes how she followed an increasingly strict low-saturated fat diet, hoping to reduce LDL cholesterol. But she saw the opposite occur: LDL climbed from an initial 134 to 171, a level that caused her doctor to prescribe a statin drug.

Yet she states that "About 85 percent of the cholesterol in your blood is made in your body. The remaining 15 percent comes from food. But by reducing dietary sources of saturated fats and cholesterol and increasing consumption of cholesterol-fighting foods and drink, you can usually lower the amount of harmful cholesterol in your blood."

Had Ms. Brody and her doctor been just a bit better informed and performed lipoprotein analysis instead, they would have seen some obvious phenomena:

--All the increase in LDL was in the fraction of small particles, the sort highly likely to cause heart attack.

--The conventional LDL that she quotes is a calculated value that miserably misrepresents the real LDL when actually measured. Her calculated LDL of 171 mg/dl, in fact, was probably more like 220 to 250 mg/dl--much higher than they think.


Of course, Ms. Brody turns to her conventionally-thinking physician who then predictably prescribes a statin drug.

Ms. Brody's well-articulated story achieves the ironic, unintended result of proving the idiocy of the conventional low-fat diet. The low-fat diet, as currently practiced by most people, raises LDL cholesterol and escalates risk for heart disease. In fact, Ms. Brody probably increased her risk far more than suggested by a 30 mg increase in LDL.

One of my favorite blogs, the Fanatic Cook, has a tremendously insightful post on Ms. Brody's misadventures.

If all she did was eliminate all wheat flour containing products and reduce the overall glycemic index of her diet, she would witness an enormous drop in LDL cholesterol, both calculated and measured.

I hope that Ms. Brody survives her diet mistakes and her doctor's ignorance.

Do statin drugs reduce lipoprotein(a)?

Alex had lipoprotein(a), Lp(a), at a high level. With a heart scan score of 541 at age 53, treatment of this pattern would be crucial to his success.

Part of Alex's treatment program was niacin. However, Alex complained about the niacin "flush" to his primary care physician. So, his doctor told him to stop the niacin and replace it with a statin drug (Vytorin in this case).

Is this a satisfactory replacement? Do statin drugs reduce Lp(a)?

No, they do not. In fact, that's how I often meet people who have Lp(a): Their doctor will prescribe a statin drug for a high LDL cholesterol that results in a poor response. The patient will be told that statin drugs don't work for them. In reality, they have Lp(a) concealed in the LDL that makes the LDL resistant to treatment.

Lp(a) responds to a limited number of treatments, like niacin, testosterone, estrogen, and DHEA. But not to statin drugs.

Now, statin drugs may still pose a benefit through LDL reduction. But they do virtually nothing for the Lp(a) itself. Unfortunately, most practicing physicians rarely go any farther than Lipitor, Zocor, Vytorin, and the like.

If your doctor tries to shove a statin drug on you as a treatment for Lp(a), put up a fight. Voice your objections that statins do not reduce Lp(a).

Breakfast cereals and toilet paper



















(Image courtesy of Brandon Blinkenberg and Wikipedia.)


What do breakfast cereals and toilet paper have in common?

You guessed it: They both belong in the toilet.

If you would like some insight into why your friends and neighbors have protruding bellies that conceal any glimpse of their toes, have to conduct that peculiar side-to-side gait that now characterizes many Americans' walking style, and are pre-diabetic or diabetic, look no further than your supermarket cereal aisle.

The Fanatic Cook has some particularly biting comments about this strangely American phenomenon at http://fanaticcook.blogspot.com.

Breakfast cereals range in quality from awful to bad. I don't know of any that fit into the Track Your Plaque program that aims to eliminate the risk of heart disease.

Another lipoprotein hurdle

A number of our Track Your Plaque Members have encountered unexpected difficulty obtaining the 2nd page of their NMR Lipoprofile lipoprotein results when their blood was drawn in a LabCorp laboratory. This is the page that displays the lipoprotein subclasses in graphic format: VLDL, IDL, LDL, and HDL subclasses.

If you are unable to view page 2, you're stuck with the averaged values displayed on page 1. In my view, page 1 is is a drastically "watered down" version that sacrifices some crucial information, particularly if you use NMR lipoprotein analysis in a serial fashion, comparing one study to the next over time.

Why would LabCorp do this? The response I received from a Mr. Theo McCormick, Director of Marketing at LabCorp, was some corporate-speak about . . . Actually, I'm not sure what he was saying. (Members can read the complete Track Your Plaque conversation in the Forum.)

In my view, withholding this information is none of their business. If you or your insurance company paid for the test, then the information is yours to view. This would be like saying that "Sure you paid for the blood test, but we decided that you really won't know what to do with it, so we're keeping it from you."

Please send your objections to the contact info below. Several of the Members who have participated in the Track Your Plaque Forum conversation have already done so. It can only help to add to the growing objections to this silly and unfair practice.

Alternatively, just boycott any laboratory associated with LabCorp. If they are capable of such ridiculous withholding of information, who knows what else these people do?


Contact info:


Theo McCormick, Director of Marketing
Laboratory Corporation of America
1904 Alexander Drive
Research Triangle Park, NC 27709
Phone 919-572-7454 (Direct)
919-361-7700 Main
Fax 919-361-7149
theo_mccormick@labcorp.com

Until we hear about some real action from them, please DO NOT USE ANY LABCORP LABORATORY.

More on aortic valve disease and vitamin D

I hope I'm not getting my hopes up prematurely, but I believe that I've seen it once again: Dramatic reversal of aortic valve disease.

This 64-year old man came to me because of a heart scan score of 212. Jack proved to have small LDL, lipoprotein(a), and pre-diabetes. But there was a wrench in the works: Because of a new murmur, we obtain an echocardiogram that revealed a mildly stiff ("stenotic") aortic valve, one of the heart valves within the heart that can develop abnormal stiffness with time.

You can think of aortic valve disease as something like arthritis--a phenomenon of "wear and tear" that progresses over time, but doesn't just go away. In fact, the usual history is that, once detected, we expect it to get worse over the next few years. The stiff aortic valve eventually causes symptoms like chest pains, breathlessness, lightheadedness, and in very severe cases, passing out. For this reason, when symptoms appear, most cardiologists recommend surgical aortic valve replacement with a mechanical or a bio-prosthetic ("pig") valve.

Now, Jack's first aortic valve area (the parameter we follow by echocardiogram representing the effective area of the valve opening when viewed end on) was 1.6 cm2. A year later: 1.4 cm2. One year later again: 1.1 cm2.

In other words, progressive deterioration and a shrinking valve area. Most people begin to develop symptoms when they drop below 1.0 cm2.

Resigned to a new valve sometime in the next year or two, Jack underwent yet another echocardiogram: Valve area 1.8 cm2.

Is this for real? I had Jack come into the office. Lo and behold, to my shock and amazement, the prominent heart murmur he had all along was now barely audible.

I'm quite excited. However, it remains too early to get carried away. I've now seen this in a handful of people, all with aortic valve disease.

Aortic valve stenosis is generally regarded as a progressive disease that must eventually be corrected with surgery--period. The only other strategy that has proven to be of any benefit is Crestor 40 mg per day, an intolerable dose in my experience.

If the vitamin D effect on aortic valve disease proves consistent in future, even in a percentage of people, then hallelujah! We will be tracking this experience in future.

"How often do you call an ambulance?"

I asked one of the CT technologists at Milwaukee Heart Scan what quesetions are often asked by people undergoing their first CT heart scan.

"That's easy," she said. " 'How often do you call an ambulance?' "

She went on. "People are very scared when they have their heart scan. In fact, some people don't even want to see their heart scan images and don't want to know their score--even after they paid $200 for the scan!"

I think she's right. People often remember the headlines that some heart scan centers have used: "Heart scan saved so and so's life!," when a high score led to a heart catheterization, stents, or bypass surgery. It's the sort of headline that gives people the impression that ambulances pull up to the scan center whenever a score is high.

So, how often is an ambulance called to the scan center? Never. Not once. A CT heart scan score is NEVER an emergency.

Emergencies occur in other places when people can't breathe, or are having pain in their chest, or pass out, emergencies that should not take anyone to a heart scan center. When heart scans are used properly, it is the person without symptoms who undergoes a scan to look for hidden heart disease. This cannot lead to an emergency.

Of course, that doesn't mean that a high score shouldn't prompt quick action in the next few days or weeks, like seeing your doctor to discuss the results, undergoing a stress test, discussing how to stop the score from progressing.

But call an ambulance? Forget about it.

If you are contemplating a scan but are scared that it could lead to a 911 call, don't let that stop you. But, in the event that you go to an unscrupulous center or get bad information, be sure to be armed with the best information possible. One good start would be to take look at our free downloadable book, What does my heart scan show? available for free on the www.cureality.com website.

Oat vs. wheat

Here's a fascinating 2002 study by Dr. Brenda Davy and colleagues at Colorado State University that examined the NMR lipoprotein differences between a diet enriched in oats and one enriched with wheat. (Davy BM, Davy KP, Ho RC 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. Am J Clin Nutr 2002; 76:351-358.)

36 sedentary, overweight men (average BMI around 30--obese), aged 50-75 years, were given a diet enriched with either oat bran (as oatmeal and oat bran, providing 5.5 grams of beta-glucan) or wheat (as a hot cereal or Frosted Mini-Wheats), with equivalent calories in each group. All underwent baseline NMR lipoprotein analysis.

Three months later, there were no differences in "anthropometrics" like weight, waist size, or BMI (though there was a trend towards larger waistlines in the wheat group). The NMR lipoprotein analysis was repeated.



Comparison of the lipoprotein changes revealed:

--LDL cholesterol: Down 2.5% with oats, up 8.0% with wheat.

--LDL particle number: Down 5% with oats, up 14.2% with wheat.

--Small LDL: Down 17.3% with oats, up 60.4% with wheat.

--Triglycerides: Down 7.6% with oats, up 22.0% with wheat.



The across-the-board differences between the wheat and oat effects were astounding. In particular, note the extraordinary effect on small LDL particles: wheat triggered a 60% increase.

Similar studies yielding similar results have been conducted elsewhere, including Dr. Ronald Krauss' group at University of California-Berkeley.

Now, this was a study conducted under the somewhat artificial circumstances of a study. But imagine this sort of habitual intake continues, not for just three months, but for years. After all, wheat has expanded and metastasized to all three meals, snacks, every day, 7 days a week in most Americans' diet.

What a wonderfully graphic representation of the undesirable effects of wheat products. When you see Mini-Wheats, Shredded Wheat, whole grain bread, whole wheat bread, whole wheat crackers, Raisin Bran, and the thousands of other wheat-containing products that promise health, run the other way. Grab some oat bran on the way out.
All posts by william-davis

I'll supply the tar if you supply the feathers

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


DIRECT-TO-CONSUMER PHARMACEUTICAL ADVERTISING HAS:

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

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

Needlessly increased healthcare costs
81 (50%)

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


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

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

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

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

What goes up can't come down

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

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

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

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

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

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

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

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


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

Davis W, Rockway S, Kwasny M.

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

Gretchen's postprandial diet experiment

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









Gretchen describes her experience:

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

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

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

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

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

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

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

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

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

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

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



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

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

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

More of Gretchen's thoughts can be found at:

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

After-eating effects: Carbohydrates vs. fats

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.

The Paleo approach to meal frequency

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.

Even mummies do it


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.

Life Extension article on iodine

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.

The healthiest people are the most iodine deficient

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.

It's the score, stupid

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.