Blast triglycerides

15. May 2009 William Davis (0)

The conventional answers to high triglycerides levels are generally: low-fat diet, a fibrate drug (Tricor, Lopid), a statin drug, and--most recently--prescription fish oil.

This is the regimen to take if you want the drug industry to get even richer and more powerful than they already are. After all, what CEO of a pharmaceutical company can stand to have his salary and benefits slashed to below $200 million this year? It's outrageous!

If you really want to blast the heck out of your triglycerides and achieve numbers like 50 mg/dl, then the regimen to consider consists of:

--Elimination of sugars, wheat, and cornstarch
--Fish oil--Sam's Club would do fine at $8 for 350 capsules, or the high-potency at $14.99 for 180 capsules (at 680 mg EPA +DHA, nearly the same potency as prescription Lovaza at 842 mg)
--Vitamin D supplementation sufficient to achieve normal blood levels (60-70 ng/ml)

Those three strategies alone can reduce triglycerides far more than any drug combination. In fact, it is rare for someone with triglycerides as high as 900 mg/dl to not reduce them to the <100 mg/dl range.

Cheerios: Prescription required?

13. May 2009 William Davis (15)

Followers of The Heart Scan Blog know my feelings about Cheerios:

Can you say "sugar"?

Cheerios and heart health

There's an interesting tussle going on between the makers of Cheerios, General Mills, and the FDA.

The FDA says that the Cheerios' package claims of:

• "you can Lower Your Cholesterol 4% in 6 weeks"
• "Did you know that in just 6 weeks Cheerios can reduce bad cholesterol by an average of 4 percent? Cheerios is ... clinically proven to lower cholesterol. A clinical study showed that eating two 1 1/2 cup servings daily of Cheerios cereal reduced bad cholesterol when eaten as part of a diet low in saturated fat and cholesterol."

constitute a medical claim, i.e., trying to promote Cheerios as a drug.

I'm glad that the FDA has come down on General Mills. But I find this entire episode laughable: The debate is over the purported health benefits of what I would regard as pure junk food, no better in my view than claiming that a cupcake has health benefits, or a carton of ice cream.

In my experience, Cheerios does not 1) reduce risk for heart disease, nor 2) reduce cholesterol.

It does, however, cause blood sugar to skyrocket and increase the small type of LDL--you know, the type that causes heart disease.

"Placebos are frequently of value"

12. May 2009 William Davis (1)

The treatment of angina pectoris, generally speaking, is unsatisfactory.

Any procedure that relieves mental tension is valuable. Since patients suffer particularly during the winter, I encourage winter vacations in a southern climate.

I insist that obese patients lose weight, and have found small doses of benzedrine, 10 to 20 mg. daily, helpful in curbing the appetite.

I generally forbid smoking. This is a particularly disturbing task for many patients to carry out. In such cases, I suggest that 3 or 4 cigarettes be smoked daily, knowing full well that regardless of what I say or recommend, the patients is going to continue to smoke.

Innumerable drugs, most of which are of questionable value, have been used to prevent attacks of angina pectoris. In fact, placebos are frequently of value.

Testosterone--The male sex hormone has been effective in my experience. Whether it acts as a vasodilator or merely by promoting a sense of well-being is not known.

Alcohol--Alcohol (whiskey, brandy, rum) has been used for many years in the treatment of angina pectoris. I have prescribed it in moderate quantity--an ounce several times a day--and while I have not made alcoholics of any of my patients, I also have not cured any of them with it. Preparations, such as creme de menthe, are of value in relieving "gas" of which so many patients complain.

From Heart Disease Diagnosis and Treatment

Emanuel Goldberger, MD

1951

Iodine is not salt

12. May 2009 William Davis (3)

I've noticed a point of confusion recently, something I hadn't noticed in my patients before: Because of the public health advice from the FDA, American Heart Association, and Surgeon General's office to reduce sodium/salt intake, people have thought this meant reducing iodine, too.

I believe that people have drawn an equation in their minds:

Sodium = iodine

Of course, they are two entirely unrelated things.

Recall that the only reason iodine is added to many (not all) salt products is because it was a public health solution to solve the substantial nationwide iodine deficiency prevalent during the 20th century. But it was a solution conceived in 1924, when the FDA thought this was the best way to get iodine into Americans. And it worked.

Unfortunately, sodium does indeed present adverse effects in some people. As a result, "get your iodine from salt" has evolved into "reduce your sodium intake." Everyone forgot about the iodine: They forgot about the large disfiguring goiters, the poor school performance in iodine-deficient schoolchildren, the mentally-impaired offspring of iodine-deficient mothers.

So don't confuse sodium with iodine. You may need less of the former, but more of the latter.

For more on this, see "Help keep your family goiter free."

"You can't reduce coronary plaque"

10. May 2009 William Davis (9)

"I told my cardiologst that I stumbled on a program called 'Track Your Plaque' that claims to be able to help reduce your coronary calcium score.

"My cardiologist said, 'That's impossible. You cannot reduce coronary plaque. I've never seen anyone reduce a heart scan score."

Who's right here?

The commenter is right; the cardiologist is wrong.

I would predict that the cardiologist is among the conventionally-thinking, "statins drugs are the only solution" group who follows his patients over the years to determine when a procedure is finally "needed." In fact, I know many of these cardiologists personally. The primary care physicians are completely in the dark, usually expressing an attitude of helplessness and submitting to the "wisdom" of their cardiology consultants.

Quantify and work to reduce the atherosclerotic plaque? No way! That's work, requires thinking, some sophisticated testing (like lipoprotein testing), even some new ideas like vitamin D. "They didn't teach that to me in medical school (back in 1980)!"

Welcome to the new age.

Atherosclerotic plaque is 1) measurable, 2) trackable, and 3) can be reduced.

We do it all the time. (Amy still holds our record: 63% reduction in plaque/heart scan score.)

Though I pooh-pooh the value of statin drug studies, there's even data from the conventional statin world documenting coronary plaque reversal. The ASTEROID Trial of rosuvastatin (Crestor), 40 mg per day for one year, demonstrated 7% reduction of atherosclerotic plaque using intracoronary ultrasound.

I have NEVER seen a heart attack or appearance of heart symptoms (angina, unstable angina) in a person who has reversed coronary plaque (unless, of course, they pitched the whole effort and returned to bad habits--that has happened). Stick to the program and coronary risk, for all practical purposes, been eliminated.

A heart scan score is not a death sentence. It is simply a tool to empower your prevention program, a measuring stick to gauge plaque progression, stabilization, or regression. Don't accept anything less.

Lethal lipids

8. May 2009 William Davis (15)

There's a specific combination of lipids/lipoproteins that confers especially high risk for heart disease. That combination is:

Low HDL--generally less than 50 mg/dl

Small LDL--especially if 50% or more of total LDL

Lipoprotein(a)--an aggressive risk factor by itself

This combination is a virtual guarantee for heart disease, often at a young age. It's not clear whether each risk factor exerts its own brand of undesirable effect, or whether the combined presence of each cause some adverse interaction.

For instance, lipoprotein(a), or Lp(a), by itself is the most aggressive risk factor known (that nobody's heard about--there's no blockbuster revenue-generating drug for it). Each Lp(a) molecule is a combination of an LDL cholesterol molecule with a specific genetically-determined protein, apoprotein(a). If the LDL component of Lp(a) is small, then the combination of Lp(a) with small LDL is somehow much worse, kind of like the two neighborhood kids who are naughty on their own, but really bad when they're together.

Interestingly, the evil trio responds as a whole to many of the same corrective treatments:

Niacin--increases HDL, reduces small LDL, and reduces Lp(a)

Elimination of wheat, cornstarch, and sugars--Best for reducing small LDL; less potent for Lp(a) reduction.

High-fat intake--Like niacin, effective for all three.

High-dose fish oil--Higher doses of EPA + DHA north of 3000 mg per day also can positively affect all three, especially Lp(a).

If you have this combination, it ought to be taken very seriously. Don't let anybody tell you that it is uncorrectable--just because there may be no big revenue-generating drug to treat it on TV does not mean that there aren't effective treatments for it. In fact, some of our biggest successes in reducing heart scan scores have had this precise combination.

"Get regressive"

6. May 2009 William Davis (0)

This caught my eye:

Niaspan, prescription niacin, now sold by Abbott Laboratories, is now promoting its advantages in regressing coronary plaque:

In patients with a history of coronary artery disease (CAD) and hypercholesetgerolemia, Niaspan (niacin), in combination with a bile acid-binding resin, is indicated to slow progression or promote regression of atherosclerotic disease.

And the new slogan: "Get regressive."

Interestingly, the new marketing campaign is based on relatively old data. They base this new claim on 3 studies:

1) Cholesterol-Lowering Atherosclerosis Study (CLAS)--a 1987

CRP House of Cards

4. May 2009 William Davis (15)

Lew has coronary plaque with a heart scan score of 393. At age 53, that's in the 90th percentile (higher score than 90% of men in his age group).

On our search for causes of his coronary plaque, we identify low HDL of 41 mg/dl, high triglycerides of 202 mg/dl, small LDL (83% of total), calculated LDL of 133 mg/dl, and severe vitamin D deficiency with a starting blood level of 25-hydroxy vitamin D of 19 ng/ml.

His c-reactive protein: 4.1 mg/dl--above the cut-off of 2.0 mg/dl that the pharmaceutical industry is targeting as a mandate for statin therapy, particularly given the JUPITER data.

Lew instead eliminates wheat and other small LDL-provoking foods and, as a result, loses 28 lbs in 3 months; adds omega-3 fatty acids from fish oil; supplements vitamin D sufficient to increase his blood level to 70 ng/ml.

Along with dramatic correction of his starting abnormalities, his c-reactive protein: 0.4 mg/dl--no statin drug.

In my view, increased CRP is nothing more than a surrogate for the inflammatory phenomena that arise from high-carbohydrate diets, overweight, and small LDL. Correct those and CRP drops off a cliff. In fact, it is exceptionally rare for CRP to not drop to very low levels following this formula.

I believe that CRP is one more item on the list of reasons--the house of cards--the pharmaceutical industry is building to persuade us to take more and more statin drugs. LDL not low enough? Take more statin. Diabetic with low cholesterol? Take a statin. Inflammation? Take a statin.

Enough already.

At-home blood tests

2. May 2009 William Davis (6)

Our at-home blood tests are proving a hit.

So far, vitamin D is the number one most popular test, no surprise.

Second--to my surprise--is DHEA. I would have predicted it would have been thyroid testing.

Our male and female hormone panels are also proving popular.

I've personally been using the thyroid and vitamin D testing to monitor my levels. I increased my Armour thyroid based on a low free T3 value, while my vitamin D was perfect at 77 ng/ml on 8000 units vitamin D3 (cholecalciferol) per day.

The process of performing the blood spots is straightforward. The finger pricks are virtually painless using the automatic spring-loaded finger stick devices:

The number of blots to make depends on how many tests you'd like. Just a vitamin D test requires 2 blots. If 6 or more tests are ordered at a time, then all 12 blots should be made. (Two spring-loaded lancets are provided in each kit.)

If you are interested in any of our at-home blood tests, go here.

Our own Heart Hawk has posted an editorial on about blood spot testing on Health Central:

Simple, affordable home blood testing is a real game-changer in the arena of informed, self-directed healthcare. For the first time broad access to home blood testing, on a scale similar to that enjoyed by persons who routinely test their blood sugar, is available to virtually everyone and it removes doctors as the gatekeepers of these tests. Even private insurance companies and Medicare are beginning to understand the potential for improving healthcare and decreasing costs and are slowly beginning to expand coverage of home blood testing much as they do for diabetics or persons taking anti-coagulants.

"Help keep your family goiter free"

1. May 2009 William Davis (10)

People ask, "If I need iodine, should I go back to iodized salt?"

First of all, how did this notion of iodized salt originate?

In 1924, J. Edgar Hoover was appointed head of the FBI, Marlon Brando and Doris Day were born, and Calvin Coolidge was elected President of the United States. Half of American households had a car, while 1 in 4 Americans were illiterate.

In the 1920s, cities were a fraction of their current size and a third of the U.S. population, or 36 million people, lived in small rural communities.

Goiters were also wildly prevalent in 1924. Up to a third of the population in some areas of the country, particularly the Midwest, suffered from goiters, thyroid glands that enlarged due to lack of iodine.

Goiters were not only unsightly, but sometimes grotesque, causing a visible bulge in the front of the neck. Occasionally, they would grow so big that it compressed adjacent structures, like the trachea, and would have to be surgically removed. Goiters were commonly associated with thyroid dysfunction, especially low thyoid or hypothyroidism, that resulted in low IQ's in schoolchildren, debilitation in adults. Women of childbearing age delivered retarded children.

So iodine deficiency in early 20th century America was a big problem. How to solve this enormous public health problem in a large nation without television, few radios, no internet, with a largely rural and often illiterate population?

Thus was iodized salt born, a simple, technologically available solution that could be implemented on a large scale nationwide at low cost. The FDA chose this route in 1924, figuring that it was the best way to ensure that most Americans could obtain sufficient iodine through liberal use of iodized salt. Public health officials urged Americans to use salt. Morton's salt label proudly bore the slogan "Help keep your family goiter free!"

It worked. Goiters largely became a thing of the past.

How about today? The American Heart Association recommends limiting salt, recently announcing that they would like to limit intake to 1500 mg per day. The American Medical Association has been lobbying the FDA to set lower salt limit guidelines. The FDA has been clamping down on food manufacturers to reduce the quantity of salt in processed foods.

Why limit salt? The concern is that there are segments of the population (not all) that are salt sensitive, particularly African Americans, people with certain genetic forms of high blood pressure, conditions that cause water retention, and any degree of heart or kidney failure. Salt in these peoplem, in fact, can be disastrous.

So adding iodine to salt was the solution to epidemic goiter. And it worked.

But salt is not a perfect solution, just one that served its purpose back in 1924. What we need is a 21st century solution.
You will find that in the various iodine supplements at your health food store. My favorite is kelp--inexpensive, available, and a form that mimics the way Japanese people obtain iodine (though by eating seaweed, rather than with tablets).

Image of kelp courtesy Wikipedia

All posts by william-davis

What to eat: Part I

6. April 2010 William Davis (0)

I've spent a good number of Heart Scan Blog posts detailing what foods to limit or avoid.

The list of unquestionably bad foods to avoid include foods made of wheat, cornstarch, and sugars. Fructose is proving to be an exceptionally bad form of sugar, worse than any other. I've issued warnings about levels of carbohydrates that can be determined by postprandial testing.

In response to several requests to clarify what foods to eat, this post begins a series discussing what foods are good to eat.

I believe that a strong case can be made for eating vegetables in nearly all its varied forms, from cucumbers to peppers to leafy vegetables to eggplant to alliums like onions. The only form we avoid are red and white potatoes due to the blood sugar-increasing effects.

While this seems obvious, I am impressed how many people who follow low-carb diets find themselves following a high-animal product diet with vegetables as the sideline. It should be the other way around: A high vegetable diet with animal products as the sideline.

Vegetables are your principal source of:

1) Flavonoids and polyphenols--e.g., anthocyanins and catechins. All the recently appreciated effects of flavonoids and polyphenols highlight the wonderful effects of compounds originating in plant foods. This includes the anthocyanins and resveratrol in red wine; the catechins and epicatechins cocoa and green tea; the hydroxytyrosol, phenolic acid, and flavonoids of olive oil.

2) Fiber--Fiber is essentially a plant phenomenon, since there is virtually none in chicken, fish, and beef. The benefits of fiber are, I believe, undisputed. Neglecting fiber can, at the very least, lead to a nasty case of hemorrhoids. At the worst, it is related to various cancers, especially colon cancer.

3) Vitamin C--While vitamin C may be old and boring in light of new, exciting discoveries like flavonoids, neglect leads to bad things.

Vegetables are generally classified as carbohydrate foods, since they are low in protein and fat. But this is the source of carbohydrates you do not want to sacrifice in a low-carbohydrate diet. There's just too much good from vegetables.

Notice that I didn't say "fruits and vegetables." This is a fundamental mistake made by many: Oveconsumption of fruits. I've even seen people who follow an otherwise good diet develop diabetes--just from too much fruit.

Vegetables should be the cornerstone of the human diet. But I'll bet you knew that already.

Carbohydrates and LDL

4. April 2010 William Davis (16)

There's a curious and powerful relationship between carbohydrates and LDL particles. Understanding this relationship is crucial to gaining control over heart disease risk.

(Note that I did not say "LDL cholesterol"--This is what confuses people, the notion that cholesterol is used as a surrogate marker to quantify various lipoproteins, including low-density lipoproteins, LDL. I'm NOT interested in the cholesterol; I'm interested in the behavior of the low-density lipoprotein particle. There's a difference.)

Carbohydrates:

1) Increase triglycerides and very low-density lipoprotein particles (VLDL)
2) Triglyceride-rich VLDL interact with LDL particles, making them smaller. (A process mediated by several enzymes, such as cholesteryl-ester transfer protein.)
3) Smaller LDL particles are more oxidizable--Oxidized LDL particles are the sort that are taken up by inflammatory white blood cells residing in the artery wall and atherosclerotic plaque.
4) Smaller LDL particles are more glycatable--Glycation of LDL is an important phenomenon that makes the LDL particle more atherogenic (plaque-causing). Glycated LDLs are not recognized by the LDL receptor, causing them to persist in the bloodstream longer than non-glcyated LDL. Glycated LDL is therefore taken up by inflammatory white blood cells in plaque.

Of course, carbohydrates also make you fat, further fueling the fire of this sequence.

The key is to break this chain: Cut out the carbohydrates. Cut carbohydrates and VLDL and triglycerides drop (dramatically), VLDL are unavailable to transform large LDL into small LDL, small LDL is no longer available to become oxidized and glycated, blood sugar is reduced to allow less glycation. Voila: Less atherosclerotic plaque growth.

Yet the USDA, American Heart Association, and the Surgeon General's office all advise you to eat more carbohydrates. The American Diabetes Association tells you to eat 70 grams or so carbohydrates per meal. (Yes: Diabetes, the condition that is MOST susceptible to these carbohydrate effects.) Follow their advice and you gain weight; triglycerides and VLDL go up; calculated (Friedewald) LDL may or may not go up, but true measured LDL (NMR LDL particle number or apoprotein B) goes way up; small LDL is triggered . . . You know the rest.

The dance between carbohydrates and LDL particles requires the participation of both. Allow one partner to drop out of the dance and LDL particles will sit this dance out.

Strange but true: Part II

4. April 2010 William Davis (0)

Here's the second part of the Heart Scan Blog post I wrote a couple of years back describing the wacky origins of this thing that has so changed the face of heart care in the U.S., the cardiac catheterization.

Heart catheterization: Strange, but true

3. April 2010 William Davis (1)

It's a couple of years old, but this post from March, 2008, remains relevant.

It details the curious origins of heart catheterization, the procedure that has saved some lives, but also been responsible for the proliferation of unnecessary heart procedures.

The modern era of heart disease care was born from an accident, quirky personalities, and even a little daring.

The notion of heart catheterization to visualize the human heart began rather ignominiously in 1929 at the Auguste-Viktoria Hospital in Eberswalde, Germany, a technological backwater of the day. Inspired by descriptions of a French physician who inserted a tube into the jugular vein of a horse and felt transmitted heart impulses outside the body, Dr. Werner Forssmann, an eager 25-year old physician-in-training, was intent on proving that access to the human heart could be safely gained through a surface blood vessel. No one knew if passing a catheter into the human heart would be safe, or whether it would become tangled in the heart’s chambers and cause it to stop beating. On voicing his intentions, Forssmann was ordered by superiors not to proceed. But he was determined to settle the question, especially since his ambitions captured the interest of nurse Gerda Ditzen, who willingly even offered to become the first human subject of his little experiment.

Secretly gathering the necessary supplies, he made his first attempt in private. After applying a local anesthetic, he used a scalpel to make an incision in his left elbow. He then inserted a hollow tube, a catheter intended for the bladder, into the vein exposed under the skin. After passing the catheter 14 inches into his arm, however, he experienced cold feet and pulled it out.

One week later, Forssman regained his resolve and repeated the process. Nurse Ditzen begged to be the subject, but Forssmann, in order to allow himself to be the first subject, tricked her into being strapped down and proceeded to work on himself while she helplessly watched. After stanching the oozing blood from the wound, he threaded the catheter slowly and painfully into the cephalic vein, up through the bicep, past the shoulder and subclavian vein, then down towards the heart. He knew that simply nudging the rubber catheter forward would be sufficient to direct it to the heart, since all veins of the body lead there. With the catheter buried 25 inches into his body, Forssmann untied the fuming Ditzen. Both then ran to the hospital’s basement x-ray department and injected x-ray dye into the catheter, yielding an image of the right side of his heart, the first made in a living human.

Thus, the very first catheterization of the heart was performed.

An x-ray image was made to document the accomplishment. Upon hearing of the experiment, Forssmann was promptly fired by superiors for his brazen act of self-experimentation. Deflated, Forssmann abandoned his experimentation and went on to practice urology. He became a member of the Nazi party in World War II Germany and served in the German army. Though condemned as crazy by some, physicians in Europe and the U.S., after hearing of his experience, furthered the effort and continued to explore the potential of the technique. Forssmann himself was never invited to speak of his experiences outside of Germany, as he had been labeled a Nazi.

Many years after his furtive experiments, the once intrepid Dr. Forssmann was living a quiet life practicing small town medicine. He received an unexpected phone call informing him that he was one of three physicians chosen to receive the 1956 Nobel Prize for Medicine for his pioneering work performing the world’s first heart catheterization, along with Drs. André Cournand and Dickinson W. Richards, both of whom had furthered Forssmann’s early work. Forssmann remarked to a reporter that he felt like a village pastor who was made a cardinal.

Strange, but true.

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.