Rerun: To let low-carb right, you must check POSTPRANDIAL blood sugars

2. April 2010 William Davis (12)

Checking postprandial (after-eating) blood sugars yields extraordinary advantage in creating better diets for many people.

This idea has proven so powerful that I am running a previous Heart Scan Blog post on this practice to bring any newcomers up-to-date on this powerful way to improve diet, lose weight, reduce small LDL, reduce triglycerides, and reduce blood pressure.

To get low-carb right, you need to check blood sugars

Reducing your carbohydrate exposure, particularly to wheat, cornstarch, and sucrose (table sugar), helps with weight loss; reduction of triglycerides, small LDL, and c-reactive protein; increases HDL; reduces blood pressure. There should be no remaining doubt on these effects.

However, I am going to propose that you cannot truly get your low-carb diet right without checking blood sugars. Let me explain.

Carbohydrates are the dominant driver of blood sugar (glucose) after eating. But it's clear that we also obtain some wonderfully healthy nutrients from carbohydrate sources: Think anthocyanins from blueberries and pomegranates, vitamin C from citrus, and soluble fiber from beans. There are many good things in carbohydrate foods.

How do we weigh the need to reduce carbohydrates with their benefits?

Blood sugar after eating ("postprandial") is the best index of carbohydrate metabolism we have (not fasting blood sugar). It also provides an indirect gauge of small LDL. Checking your blood sugar (glucose) has become an easy and relatively inexpensive tool that just about anybody can incorporate into health habits. More often than not, it can also provide you with some unexpected insights about your response to diet.

If you’re not a diabetic, why bother checking blood sugar? New studies have documented the increased likelihood of cardiovascular events with increased postprandial blood sugars well below the ranges regarded as diabetic. A blood sugar level of 140 mg/dl after a meal carries 30-60% increased (relative) risk for heart attack and other events. The increase in risk begins at even lower levels, perhaps 110 mg/dl or lower after-eating.

We use a one-hour after eating blood sugar to gauge the effects of a meal. If, for instance, your dinner of baked chicken, asparagus brushed with olive oil, sauteed mushrooms, mashed potatoes, and a piece of Italian bread yields a one-hour blood sugar of 155 mg/dl, you know that something is wrong. (This is far more common than most people think.)

Doing this myself, I have been shocked at the times I've had an unexpectedly high blood sugar from seemingly "safe' foods, or when a store- or restaurant-bought meal had some concealed source of sugar or carbohydrate. (I recently had a restaurant meal of a turkey burger with cheese, mixed salad with balsamic vinegar dressing, along with a few bites of my wife's veggie omelet. Blood sugar one hour later: 127 mg/dl. I believe sugar added to the salad dressing was the culprit.)

You can now purchase your own blood glucose monitor at stores like Walmart and Walgreens for $10-20. You will also need to purchase the fingerstick lancets and test strips; the test strips are the most costly part of the picture, usually running $0.50 to $1.00 per test strip. But since people without diabetes check their blood sugar only occasionally, the cost of the test strips is, over time, modest. I've had several devices over the years, but my current favorite for ease-of-use is the LifeScan OneTouch UltraMini that cost me $18.99 at Walgreens.

Checking after-meal blood sugars is, in my view, a powerful means of managing diet when reducing carbohydrate exposure is your goal. It provides immediate feedback on the carbohydrate aspect of your diet, allowing you to adjust and tweak carbohydrate intake to your individual metabolism.

LDL glycation

1. April 2010 William Davis (11)

The proteins of the body are subject to the process of glycation, modification of protein structures by glucose (blood sugar). In the last Heart Scan Blog post, I discussed how glycated hemoglobin, available as a common test called HbA1c, can serve as a reflection of protein glycation (though it does not indicate actual Advanced Glycation End-products, or AGEs, just a surrogate indicator).

There is one very important protein that is subject to glycation: Apoprotein B.

Apoprotein B, or Apo B, is the principal protein of VLDL and LDL particles. Because there is one Apo B molecule per VLDL or LDL particle, Apo B can serve as a virtual VLDL/LDL particle count. The higher the Apo B, the greater the number of VLDL and LDL particles.

Because Apo B is a protein, it too is subject to the process of glycation. The interesting thing about the glycation of Apo B is that its "glycatability" depends on LDL particle size: The smaller the LDL particle, the more glycation-prone the Apo B contained within.

Younis et al have documented an extraordinary variation in glycatability between large and small LDL, with small LDL showing an 8-fold increased potential.

Think about it: Carbohydrates in the diet, such as wheat products and sugars, trigger formation of small LDL particles. Small LDL particles are then more glycation-prone by up to a factor of 8. Interestingly, HbA1c is tightly correlated with glycation of Apo B. Diabetics with high HbA1c, in particular, have the greatest quantity of glycated Apo B. They are also the group most likely to develop coronary atherosclerosis, as well as other consequences of excessive AGEs.

No matter how you spin it, the story of carbohydrates is getting uglier and uglier. Carbohydrates, such as those in your whole grain bagel, drive small LDL up, while making them prone to a glycating process that makes them more likely to contribute to formation of coronary atherosclerotic plaque.

High HbA1c: You're getting older . . . faster

28. March 2010 William Davis (16)

Over the years, we all accumulate Advanced Glycation End-products, or AGEs.

AGEs are part of aging; they are part of human disease. AGEs are the result of modification of proteins by glucose. AGEs form the basis for many disease conditions.

Accumulated AGEs have been associated with aging, dementia, cataracts, osteoporosis, deafness, cancer, and atherosclerosis. Most of the complications of diabetes have been attributable to AGEs.

There's one readily available method to assess your recent AGE status: HbA1c.

Hemoglobin is the oxygen-carrying protein of red blood cells. Like other proteins, hemoglobin becomes glycated in the presence of glucose. Hemoglobin glycation increases linearly with glucose: The higher the serum or tissue glucose level, the more glycation of hemoglobin develops. Glycated hemoglobin is available as the common test, HbA1c.

Ideal HbA1c is 4.5% or less, i.e., 4.5% of hemoglobin molecules are glycated. Diabetics typically have HbA1c 7.0% or greater, not uncommonly greater than 10%.

In other words, repetitive and sustained high blood glucose leads to greater hemoglobin glycation, higher HbA1c, and indicates greater glycation of proteins in nerve cells, the lens of your eye, proteins lining arteries, and apoprotein B in LDL cholesterol particles.

If AGEs accumulate as a sign of aging, and high blood sugars lead to greater degrees of glycation, it only follows that higher HbA1c marks a tendency for accelerated aging and disease.

Indeed, that is what plays out in real life. People with diabetes, for instance, have kidney failure, heart disease, stroke, cataracts, etc. at a much higher rate than people without diabetes. People with pre-diabetes likewise.

The higher your HbA1c, the greater the degree of glycation of other proteins beyond hemoglobin, the faster you are aging and subject to all the phenomena that accompany aging. So that blood glucose of 175 mg/dl you experience after oatmeal is not a good idea.

The lesson: Keep HbA1c really low. First, slash carbohydrates, the only foods that substantially increase blood glucose. Second, maintain ideal weight, since normal insulin responsiveness requires normal body weight. Third, stay physically active, since exercise and physical activity exerts a powerful glucose-reducing effect. Fourth, consider use of glucose-reducing supplements, an issue for another day.

While HbA1c cannot indicate cumulative AGE status, it can reflect your recent (preceding 60 to 90 days) exposure to this age-accelerating thing called glucose.

If your doctor refuses to accommodate your request for a HbA1c test, you can perform your own fingerstick test.

Slash carbs . . . What happens?

26. March 2010 William Davis (20)

Cut the carbohydrates in your diet and what sorts of results can you expect?

Carbohydrate reduction results in:

Reduced small LDL--This effect is profound. Carbohydrates increase small LDL; reduction of carbohydrates reduce small LDL. People are often confused by this because the effect will not be evident in the crude, calculated (Friedewald) LDL that your doctor provides.

Increased HDL--The HDL-increasing effect of carbohydrate reduction may require 1-2 years. In fact, in the first 2 months, HDL will drop, only to be followed by a slow, gradual increase. This is the reason why, in a number of low-carb diet studies, HDL was shown to be reduced.--Had the timeline been longer, HDL would show a significant increase.

Decreased triglycerides--Like reduction of small LDL, the effect is substantial. Triglyceride reductions of several hundred milligrams are not at all uncommon. In people with familial hypertriglyceridemia with triglyceride levels in the thousands of milligrams per deciliter, triglyceride levels will plummet with carbohydrate restriction. (Ironically, conventional treatment for familial hypertriglyceridemia is fat restriction, a practice that can reduce triglycerides modestly in these people, but not anywhere near as effectively as carbohydrate restriction.) Triglyceride reduction is crucial, because triglycerides are required by the process to make small LDL--less triglycerides, less small LDL.

Decreased inflammation--This will be reflected in the crude surface marker, c-reactive protein--Yes, the test that the drug industry has tried to convince you to take statins drugs to reduce. In my view, it is an absurd notion that you need to take a drug like Crestor to reduce risk associated with increased CRP. If you want to reduce CRP to the floor, eliminate wheat and other junk carbohydrates. (You should also add vitamin D, another potent CRP-reducing strategy.)

Reduced blood pressure--Like HDL, blood pressure will respond over an extended period of months to years, not days or weeks. The blood pressure reduction will be proportion to the amount of reduction in your "wheat belly."

Reduced blood sugar--Whether you watch fasting blood sugar, postprandial (after-meal) blood sugars, or HbA1c, you will witness dramatic reductions by eliminating or reducing the foods that generate the high blood sugar responses in the first place. Diabetics, in particular, will see the biggest reductions, despite the fact that the American Diabetes Association persists in advising diabetics to eat all the carbohydrates they want. Reductions in postprandial (after-eating) blood sugars, in particular, will reduce the process of LDL glycation, the modification of LDL particles by glucose that makes them more plaque-causing.

You may notice that the above list corresponds to the list of common plagues targeted by the pharmaceutical industry: blood pressure, diabetes (diabetes being the growth industry of the 21st century), high cholesterol. In other words, high-carbohydrate, low-fat foods from the food industry create the list of problems; the pharmaceutical industry steps in to treat the consequences.

In the Track Your Plaque approach, we focus specifically on elimination of wheat, cornstarch, and sugars, the most offensive among the carbohydrates. The need to avoid other carbohydrates, e.g., barley, oats, quinoa, spelt, etc., depends on individual carbohydrate sensitivty, though I tend to suggest minimal exposure.

Normal fasting glucose with high HbA1c

23. March 2010 William Davis (24)

Jonathan's fasting glucose: 85 mg/dl

His HbA1c: 6.7%

Jonathan's high HbA1c reflects blood glucose fluctuations over the preceding 60-90 days and can be used to calculate an estimated average glucose (eAG) with the following equation:

eAG = 28.7 X A1c – 46.7

(For glucose in mmol/L, the equation is eAG = 1.59 × A1C - 2.59)

Jonathan's HbA1c therefore equates to an eAG of 145.59 mg/dl--yet his fasting glucose value is 85 mg/dl.

This is a common situation: Normal fasting glucose, high HbA1c. It comes from high postprandial glucose values, high values after meals.

It suggests that, despite having normal glucose while fasting, Jonathan experiences high postprandial glucose values after many or most of his meals. After a breakfast of oatmeal, for instance, he likely has a blood glucose of 150 mg/dl or greater. After breakfast cereal, blood glucose likely exceeds 180 mg/dl. With two slices of whole wheat bread, glucose likewise likely runs 150-180 mg/dl.

The best measure of all is a postprandial glucose one hour after the completion of a meal, a measure you can easily obtain yourself with a home glucose meter. Second best: fasting glucose with HbA1c.

Gain control over this phenomenon and you 1) reduce fasting blood sugar, 2) reduce expression of small LDL particles, and 3) lose weight.

Can you handle fat?

21. March 2010 William Davis (19)

No question: Low-carbohydrate diets generate improved postprandial lipoprotein responses.

Here's a graph from one of Jeff Volek's great studies:

Participants followed a low-carb diet of less than 50 g per day carbohydrate ("ketogenic") with 61% fat. The curves were generated by administering a 123 g fat challenge with triglyceride levels assessed postprandially. The solid line represents the postprandial response at the start; dotted line after the 6-week low-carb effort.

Note that:

1) The postprandial triglyceride (area-under-the-curve) response was reduced by 29% in the low-carb diet. That's a good thing.

2) The large fat challenge generated high triglycerides of greater than 160 mg/dl even in the low-carb group. That's a bad thing.

In other words, low-carb improves postprandial responses substantially--but postprandial phenomena still occur. Postprandial triglycerides of 88 mg/dl or greater are associated with greater heart attack risk because they signify the presence of greater quantities of atherogenic (plaque-causing) postprandial lipoproteins.

A full discussion of these phenomena can be found in the Track Your Plaque Special Report, Postprandial Responses: The Storm After the Quiet!, part of a 3-part series on postprandial phenomena.

Statin stupid

19. March 2010 William Davis (0)

If we followed the lead of the pharmaceutical industry and my cardiology colleagues, we would all subscribe to the "statins for all" philosophy. There is now $2 billion of clinical "research" to back up this "evidence-based" practice.

I do not endorse this "statins for all" philosophy. I believe it is a product of the raw profiteering of the pharmaceutical industry, who are adept at recruiting physicians to their cause.

But lost in the confusion of tainted studies and over-the-top media saturation is the fact that there are small groups of people who likely do obtain benefit from statin drugs. They would certainly benefit from better informed scrutiny of their lipoprotein and metabolic abnormalities. But treatment may involve statins.

This is entirely distinct from the "statins for all" argument, the simpleminded rule that primary care physicians and cardiologist are told to follow.

Groups who may indeed benefit from statin therapy include:

Homozygous or heterozygous familial hypercholesterolemia--Lacking a receptor for LDL particles, LDL piles up to very high levels in these people. LDLs of 300+ are common and lead to heart disease and stroke at relatively young ages.

Combined mixed hyperlipidemia--Among the one or more genetic defects underlying this condition involves excessive production of apoprotein B and VLDL particles. This leads to high risk for heart disease.

People unable to follow a diet to correct their lipid disorder--I have 80+-year old patients, for instance, who say, "I've eaten this way for 82 years. I'm not going to change now!" In the absence of diet and other efforts (e.g., omega-3 fatty acids from fish oil), drugs may be the answer.

In other words, of the $27 billion annual bill for statin drugs, perhaps a tiny fraction is truly necessary. The majority of people taking statin drugs would not really need them if they had the real answers. But don't let that confuse us: There are some people who do indeed benefit.

Butter and insulin

19. March 2010 William Davis (83)

In a previous post, Atkins Diet: Common Errors, I commented on butter's unusual ability to provoke insulin responses. I offer this as a possible reason why, after a period of effective weight loss on a low-carbohydrate program, inclusion of some foods, such as butter, will trigger weight gain or stall weight loss efforts.

This develops because of butter's insulin-triggering effect, doubling or tripling insulin responses (postprandial area-under-the-curve). If insulin is triggered, fat gain follows.

Here's one such study documenting this effect: Distinctive postprandial modulation of ß cell function and insulin sensitivity by dietary fats: monounsaturated compared with saturated fatty acids

López et al 2008

From Lopez et al 2008. Mean (± SD) plasma glucose, insulin, triglyceride, and free fatty acid (FFA) concentrations during glucose and triglyceride tolerance test meal (GTTTM) with no fat (control), enriched in monounsaturated fatty acids (MUFAs) from refined olive oil (ROO meal), with added butter, with a mixture of vegetable and fish oils (VEFO) or with high-palmitic sunflower oil (HPSO). N = 14.

The postprandial (after-eating) area-under-the-curve is substantially greater when butter is included in the mixed composition meal. This effect is not unique to butter, but is shared by most other dairy products.

Fat, in general, does not make you fat. But butter makes you fat.

Vitamin D as a cardiovascular risk factor gains ground

18. March 2010 William Davis (0)

If you were reading The Heart Scan Blog back in 2007, or read my Life Extension article on vitamin D deficiency as a cardiovascular risk factor, you already knew that vitamin D deficiency is rampant and adds to cardiovascular risk.

Results of a study from the Intermountain Medical Center Heart Institute in Utah bolster the concept that vitamin D deficiency is a cardiovascular risk factor, vitamin D normalization/supplementation reduces cardiovascular risk.

Science Daily reported:

For the first study, researchers followed two groups of patients for an average of one year each. In the first study group, over 9,400 patients, mostly female, reported low initial vitamin D levels, and had at least one follow up exam during that time period. Researchers found that 47 percent of the patients who increased their levels of vitamin D between the two visits showed a reduced risk for cardiovascular disease.

In the second study, researchers placed over 31,000 patients into three categories based on their levels of vitamin D. The patients in each category who increased their vitamin D levels to 43 nanograms per milliliter of blood or higher had lower rates of death, diabetes, cardiovascular disease, myocardial infarction, heart failure, high blood pressure, depression, and kidney failure. Currently, a level of 30 nanograms per milliliter is considered "normal."

Over the past 4 years, people in our program have been enjoying the extravagant benefits of vitamin D restoration. Cardiovascular benefits are becoming better documented and the bone health, cancer-preventing, insulin-normalizing, mood-adjusting, and anti-inflammatory effects likewise.

Atkins Diet: Common errors

18. March 2010 William Davis (74)

No doubt: The diet approach advocated by the late Dr. Robert Atkins was a heck of a lot closer to an ideal diet than the knuckleheaded advice emitting from the USDA, American Heart Association, American Diabetes Association, and the Surgeon General's office.

But having just spent a week with Atkins low-carbers, here are some common errors that I see many make, errors that I believe have long-term health consequences, including impairment of weight loss.

Excessive consumption of animal products--Non-restriction of fat often leads to over-reliance on animal products. Higher intakes of red meats (heme proteins?) have been strongly associated with increased risk for colon and other gastrointestinal tract cancers. It is not a fat issue; it is an animal product issue. We should consume less meat, more vegetables and other plant-sourced foods.

Consumption of cured meats--Cured, processed meats, such as sausage, hot dogs, salami, bologna, and bacon, have a color fixative called sodium nitrite, an additive that has been confidently linked to gastrointestinal cancers. Risk is likely dose-dependent: The more you ingest, the greater the long-term risk.

Overconsumption of dairy products--Dairy products, especially milk, yogurt, cottage cheese, and butter, are potent insulinotropic foods, i.e., foods that trigger insulin release. There can be up to a tripling of insulin (area-under-the-curve) levels. This is not good in a world populated with tired, overworked pancreases, exhausted from a lifetime of high-carbohydrate eating.

Too many calories--While I agree that "a calorie is a calorie" and "calories in, calories out" are faulty concepts, I have anecdotally observed that long-time low-carbers often trend towards unlimited consumption of food, a phenomenon that seems to result in weight gain, especially in the sedentary. I wonder if this is a reflection of the insulinotropic action of dairy products and other proteins, compounded by the poor insulin responsiveness that develops with lack of physical activity. Factor into this conversation that lower calorie intake extends life, probably substantially (Sirt-2 activation and related phenomena, a la resveratrol). If lower calorie intake extends life, unlimited calorie intake likely shortens life.

Please don't hear this as low-carb bashing--it is not. It is a call to improve diets and not stumble into common traps that can impair heart health, weight loss, and longevity.

All posts by william-davis

Why average cholesterol values can be so bad

30. August 2007 William Davis (23)

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?

28. August 2007 William Davis (4)

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

27. August 2007 William Davis (13)

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

24. August 2007 William Davis (1)

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)?

24. August 2007 William Davis (17)

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

23. August 2007 William Davis (4)

(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

23. August 2007 William Davis (0)

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

22. August 2007 William Davis (22)

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?"

17. August 2007 William Davis (1)

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

17. August 2007 William Davis (7)

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.