And you thought gasoline was expensive

2. June 2009 William Davis (5)

In 1995, the Palmaz coronary stent was introduced, the brainchild of Drs. Julio Palmaz and Richard Schatz. Medical device manufacturer, Johnson & Johnson, priced the device at $2500 per stent.

Let's put this into perspective: At just 0.05 grams per 15 millimeter stent, that put the price of the common stainless steel used to manufacture the stent at $22,650,000 per pound.

Only after several competing stents finally made it to market did J&J reduce its price to its bargain price of $1200, or $10,872,000 per pound. And to think that most of us were shocked to find out that the U.S. military paid $200 for a hammer.

Since 1995, a competitive market for stents has developed, pushing prices down. Now, you can purchase a brand-new coronary stent for as little as $4,000,000 per pound.

Medical device manufacturers have been guilty of a degree of greed that would make many Wall Street bankers blush. That's why I call medical devices "the industry of infinite markups."

"Hey buddy, wanna buy some exorphins?"

31. May 2009 William Davis (18)

Dr. Christine Zioudrou and colleagues at the National Institutes of Mental Health got this conversation going back in 1979 with their paper, Opioid peptides derived from food proteins: The exorphins.

Exorphins are exogenously-derived peptides (i.e., short amino acid sequences obtained from outside the body) that exert morphine-like properties. Mimicking the digestive process that occurs in the gastrointestinal tract using the gastric enzyme, pepsin, and hydrochloric acid (stomach acid), Zioudrou et al isolated peptides from wheat gluten with morphine-like activity. They followed this research path because of the apparent association of wheat and mental illness.

In the bioassays used, wheat-derived exorphins competed successfully with the endogenous opiate, met-enkephalin. Interestingly, casein-derived (i.e., casein milk protein) exorphins were also identified that also displayed opiate-binding activity, though less powerfully. The morphine-like activity was also blocked by the drug, naloxone (the same stuff given to people exposed to morphine overdose).

Among the many devastating effects of celiac disease , the immune disease that develops from wheat gluten exposure, are mental and emotional effects, such as anxiety, fatigue, mental "fog," depression, bipolar illness, and schizophrenia, that disappear with removal of gluten. Many parents of autistic children also advocate wheat-free diets for similar reasons.

Among the many wonderful comments posted on the last Heart Scan Blog post, "I can't do it," was Anne's:

I am not the Anne in your post, but I was addicted to wheat. It was my favorite food. I lived on and for breads. Then I discovered I was gluten sensitive and I did go through a withdrawal of about 4 days. After 4 days I noticed my health problems were disappearing. Depression, brain fog and joint pain are 3 of the many symptoms that disappeared. That was 6 yrs ago.

Tell Anne that I had dreams about bread in the beginning - they will pass. Now the donuts, breads, cookies and cakes in the stores and at work don't even look good. In fact, I don't like the smell of bread anymore. It takes time, but the cravings do pass.

Combine wheat"s exorphin-driven addictive potential with its flagrant blood sugar-increasing properties, and you have a formula that:

1) makes you fat
2) increases likelihood of diabetes, and
3) makes you want to keep on doing it.

Reminds me of nicotine.

My personal view: I have absolutely no remaining doubt that wheat products have no place in the human diet. Not only does the research provide a plausible basis for its adverse health effects, but having asked hundreds of people to remove it from their habits has yielded consistent and remarkable health benefits. Just read the reader comments here and here.

"I can't do it"

30. May 2009 William Davis (20)

Anne sat across from me, bent over and sobbing.

"I can't do it. I just can't do it! I cut out the breads and pasta for two days, then I start dreaming about it!

"And my husband is no help. He knows I'm trying to get off the wheat. But then he brings home a bunch of Danish or something. He knows I can't help myself!"

Having asked hundreds of people to completely remove wheat from their diet, I witness 30% of them go through such emotional and physical turmoil, not uncommonly to the point of tears. For about 10-20% of people who try, it is as hard as quitting cigarettes.

Make no mistake about it: For many people, wheat is addictive. It meets all the criteria for an addictive product: People crave it, consuming it creates a desire for more, lacking it triggers a withdrawal phenomenon. If wheat were illegal, there would surely be an active underground trafficking illicit bagels and pretzels.

Withdrawal consists of fatigue and mental fogginess that usually lasts 5-7 days. Just like quitting smoking, wheat withdrawal is harmless but no less profound in severity.

People who lack an addictive relationship with wheat usually have no idea what I'm talking about. To them, wheat is simply a grain, no different than oats.

But wheat addicts immediately know who they are. They are the ones who can't resist the warm dinner rolls served at the Italian restaurant, need to include something made of wheat at every meal, and crave it every 2 hours (matching the cycle of blood sugar peaks and valleys, the "valley" triggering the craving). When they stop the flow of immediately-released glucose that comes from wheat (with blood sugar peaks that occur higher and faster than table sugar), irresistible cravings kick in. Then watch out: They'll bite your hand off if you reach for that roll before they do.

Break the cycle and the body is confused: Where's the sugar? The body is accustomed to receiving a constant flow of easily-digested sugars.

Once the constant influx of sugars ceases, it takes 5-7 days for metabolism to shift towards fat mobilization as a source of energy. But along with fat mobilization comes a shrinking tummy, reducing the characteristic wheat belly.

If you try to quit smoking, you've got "crutches" like nicotine patches and gum, Zyban, Chantix, hypnosis, and group therapy sessions. If you try and quit wheat, what have you got? Nothing, to my knowledge. Nothing but sheer will power to divorce yourself from this enormously destructive, diabetes-causing, small LDL-increasing, inflammation-provoking, and addictive substance.

Spontaneous combustion, vampires, and goitrogens

26. May 2009 William Davis (17)

What do the following have in common:

Lima beans
Flaxseed
Broccoli
Cabbage
Kale
Soy
Millet
Sorghum?

They are all classified as goitrogens, or foods that have been shown to trigger goiter, or thyroid gland enlargement. Most of them do this either by blocking iodine uptake in the thyroid gland or by blocking the enzyme, thyroid peroxidase. This effect can lead to reduction in thyroid hormone output by the thyroid gland, which then triggers increased thyroid stimulating hormone (TSH) by the pituitary; increased TSH acts as a growth factor on the thyroid, thus goiter.

Add to this list of goitrogens the flavonoid, quercertin, found in abundance in red wine, grapes, apples, capers, tomatoes, cherries, raspberries, teas, and onions. Most of us obtain around 30 mg per day from our diet. Quercetin, often touted as a healthy flavonoid alongside resveratrol (e.g., Yang JY et al 2008), has been shown to be associated with reduced risk for heart disease and cancer. Many people even take quercetin as a nutritional supplement.

Quercetin has also been identified as a goitrogen (Giuliani C et al 2008).

What to make of all this?

Most of these observations have been made in in vitro ("test tube") preparations or in mice. Rabbits who consume a cabbage-only diet can develop goiter.

How about humans? The few trials conducted in humans have shown little or no effect. In most instances, the adverse effects of goitrogens have been eliminated with supplemental iodine. In other words, goitrogens seem to exert their ill thyroid effects when iodine deficiency is present. Restore iodine . . . no more goitrogens (with rare exceptions).

Should we as humans adopt a diet that avoids apples, grapes, tomatoes, red wine, tea, onions, soy etc. on the small chance that we will develop goiter?

I believe that we should avoid these common food-sourced goitrogens with as much enthusiasm as we should be worried about spontaneous combustion of humans or the appearance of vampires on our front porches. We are as likely to suffer low thyroid activity from quercetin or other "goitrogens" as we are to experience the "mitochondrial explosions" that are purported to set innocent people afire.

Magnesium and you-Part II

25. May 2009 William Davis (17)

Blood magnesium levels are a poor barometer for true body (intracellular) magnesium.

Only 1% of the body’s magnesium is in the blood, the remaining 99% stored in various body tissues, particularly bone and muscle. If blood magnesium is low, cellular magnesium levels are indeed low—very low.

If blood magnesium is normal, cellular or tissue levels of magnesium may still be low. Unfortunately, tissue magnesium levels are not easy to obtain in living, breathing humans. In all practicality, a blood magnesium test only helps if it’s low, while normal levels don’t necessarily mean anything and may provide false reassurance.

Short of performing a biopsy to measure tissue magnesium levels, several signs provide a tip-off that magnesium may be low:

• Heart arrhythmias—Having any sort of heart rhythm disorder should cause you to question whether magnesium levels in your body are adequate, since low magnesium levels trigger abnormal heart rhythms. In fact, in the hospital we give intravenous magnesium to quiet down abnormal rhythms.
• Low potassium— Low magnesium commonly accompanies low potassium. Potassium is another electrolyte depleted by diuretic use and is commonly deficient in many conditions (e.g., excessive alcohol use, hypertension, loss from malabsorption or diarrhea). Like magnesium, potassium may not be fully replenished by modern diets.
• Muscle cramps— Magnesium regulates muscle contraction. Leg cramps, or “charlie-horses”, painful vise-like cramps in calves, fingers, or other muscles, are a common symptom of magnesium deficiency. (Leg cramps that occur with physical activity, such as walking, are usually due to atherosclerotic blockages in the leg or abdominal arteries, not low magnesium.)
• Migraine headaches—Reflective of magnesium’s role in regulating blood vessel tone, low magnesium can trigger vascular spasm in the blood vessels of the brain. In some emergency rooms, they will actually administer intravenous magnesium to break a migraine.
• Metabolic syndrome—Magnesium plays a fundamental role in regulating insulin responses. Metabolic syndrome (low HDL, high triglycerides, small LDL, high blood pressure, increased blood sugar, excessive abdominal fat, etc.) is triggered by insulin responses gone awry and is clearly linked to low magnesium levels.

The absence of any of these tell-tale signs does not necessarily mean that tissue levels of magnesium are normal.

Then how do you really know? There really is no easy, available method to gauge body magnesium. As a practical solution, we therefore have aimed for maintaining serum levels of >2.1 mg/dl or RBC magnesium (a surrogate for tissue levels) of >6.0 mg/dl. (Going too high is not good either, so occasional monitoring really helps. However, I've only seen this once in a psychotic woman who drank ungodly amounts of magnesium-containing antacids for no apparent reason; she almost ended up on a respirator due to respiratory suppression by the magnesium level of 11 mg/dl!)

In all practicality, because of magnesium’s crucial role in health, its widespread deficiency in Americans, and the growing depletion of magnesium in water, supplemental magnesium is necessary for nearly everyone to ensure healthy levels.

More on magnesium to come.

Lethal Lipids II

22. May 2009 William Davis (7)

I call the combination of low HDL, small LDL, and lipoprotein(a) "lethal lipids," since the trio is an exceptionally potent predictor for heart disease. Uncorrected, the combination is a virtual guarantee of heart disease.

Ed is a perfect example of someone who came to my office recently with this pattern. His starting values:

HDL: 34 mg/dl

Small LDL: 78% of total LDL
NMR: Small LDL 1655 nmol/L; total LDL particle number 2122 nmol/L)

Lipoprotein(a): 205 nmol/L

The atherogenicity, or plaque-causing potential, of this pattern was reflected in Ed's heart scan score of 2133.

You can readily see that, of this combination, only HDL cholesterol would be adequately identified through conventional lipid testing. Small LDL and lipoprotein(a) need to be specifically measured via lipoprotein testing.

And, contrary to the drug industry's "statin drugs for everybody" motto, this pattern, while improved with statin therapy, is not shut off.

Specific correction of each abnormality is required. For instance, niacin addresses all three: increases HDL, reduces small LDL, and (usually) reduces lipoprotein(a). A standard low-fat diet makes this pattern worse by reducing HDL, increasing small LDL, and (usually) increasing lipoprotein(a).

"You've got 10 minutes"

20. May 2009 William Davis (0)

There's a new trend in office healthcare in Milwaukee: Time-restricted office visits.

I'm told by several physicians who are employed by a major healthcare system here in town that they are peridically watched--physically watched by an administrator--to make sure that they do not exceed the allotted 10 minutes of time. My cardiologist colleagues, I gather, were at first incredulous at such intrusions into their practices, but apparently had no choice: They were employees.

Goiter, goiter everywhere

20. May 2009 William Davis (25)

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

The question:

Do you used iodized salt?

The responses:

Yes, I use iodized salt every day
94 (28%)

Yes, I use iodized salt occasionally
56 (16%)

No, I do not use any iodized salt
41 (12%)

No, I use a non-iodized salt (sea salt, Kosher)
126 (37%)

No, I use a non- or low-sodium substitute
15 (4%)

Thanks for your responses.

If only 28% of people are regular users of iodized salt, that means that the remainder--72%--are at risk for iodine deficiency if they are not getting iodine from an alternative source, such as a multivitamin or multimineral.

Even the occasional users of salt can be at risk. The common perception is that occasional use is probably sufficient to provide iodine. This is probably not true and not just because of the lower quantity of ingestion. Occasional users of salt tend to have their salt canister on the shelf for extended periods. The iodine is then lost, since iodine is volatile. In fact, iodine is virtually undetectable four weeks after a package is opened.

In my office, now that I'm looking for them much more systematically and carefully, I am finding about 2 people with goiters every day. They are not the obvious grotesque goiters of the early 20th century (when quack therapies like the last post, the Golden Medical Discovery, were popular). The goiters I am detecting are small and spongy. Yesterday alone I found 5 people with goiters, one of them visible to the eye and very distressing to the patient.

It seems to me that iodine deficiency is more prevalent than I ever thought. It is also something that is so simple to remedy, though not by increasing salt intake. Kelp tablets--cheap, available--have been working quite well in the office population. My sense is that the Recommended Daily Allowance of 150 mcg per day for adults is low and that many benefit from greater quantities, e.g., 500 mcg. What is is the ideal dose? To my knowledge, nobody has yet generated that data.

Thyroid issues being relatively new to my thinking, I now find it incredible that endocrinologists and the American Thyroid Association are not broadcasting this problem at the top of their lungs. This issue needs to be brought to the top of everyone's attention, or else we'll have history repeating itself and have goiters and thyroid dysfunction galore.

For more on this topic, see the previous Heart Scan Blog post, "Help keep your family goiter free."

Goiter and the Golden Medical Discovery

17. May 2009 William Davis (19)

Thick neck, or goitre . . . consists of an enlargement of the thyroid gland, which lies over and on each side of the trachea, or windpipe, between the prominence known as "Adam's apple" and the breast bone. The tumor gradually increases in front and laterally, until it produces great deformity, and often interferes with respiration and the act of swallowing. From its pressure on the great blood vessels running to and from the head, there is a constant liability to engorgement of blood in the brain, and to apoplexy, epilepsy, etc.

The causes of the affection are not well understood. The use of snow water, or water impregnated with some particular saline or calcareous matter, has been assigned as a cause. It has also been attributed to the use of water in which there is not a trace of iron, iodine, or bromine. . . The disease is often due to an impeded circulation in the large veins of the neck, from pressure of the clothing, or from the head being bent forward, a position which is often seen in school children.

Treatment

We have obtained excellent results in many cases, not too far advanced, by a method of treatment which consists in the employment of electrolysis. . . Many cases at the present time are operated upon with entire success.

Those who are afflicted with this disease and unable to avail themselves of special treatment cannot do better than to take Doctor Pierce's Alterative Extract, or Golden Medical Discovery, and apply over the skin around the tumor, night and morning, the following, which may be prepared at any drug store:

Resublimed Iodine--One dram
Iodide of Potassium--Four drams
Soft Water--Three ounces

Apply to the tumor, twice daily, with feather or camel hair pencil.

From The People's Common Sense Medical Adviser by R.V. Pierce, MD; 1918.

Magnesium and you-Part I

15. May 2009 William Davis (11)

If this were 10,000 B.C., you'd get your drinking water from streams, rivers, and lakes, all rich in mineral content. Humans became reliant on obtaining a considerable proportion of daily mineral needs from natural water sources.

21st century: We obtain drinking water from a spigot or plastic bottle. Pesticides and other chemicals seep into the water supply. Municipal water purification facilities have intensified water purification in most communities to remove contaminants like lead, pesticide residues, and nitrates. (For a really neat listing of the water quality of various cities, the University of Cincinnati makes this data available.)

But intensive water treatment also removes minerals like calcium and magnesium.

Many people have added water filters or purifiers to their homes,, like reverse osmosis and distillation, that are efficient at extracting any remaining minerals, converting “hard” into “soft” water. In fact, manufacturers of such devices boast of their power to yield pure water free of any “contaminant,” minerals like magnesium included. The magnesium content of water after passing through most commercial filters is zero.

Modern enthusiasm for bottled water has compounded the problem. Americans consumed a lot of bottled water, nearly 8 billion gallons last year. In the U.S., nearly all bottled water has little or no magnesium.

The result is that we can no longer rely on drinking water to provide magnesium. The Recommended Daily Allowance (RDA)—the amount required to prevent severe deficiency—for magnesium is 420 mg per day for men, 320 mg/day for women. In cities with the highest magnesium water content, only 30% of the RDA can be obtained by drinking two liters of tap water per day. In most cities, only a meager 10–20% of the daily requirement can be obtained. That leaves between 70–90% that needs to come from other sources. As a result, the average American ingests substantially less than the RDA.

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.