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.

All posts by william-davis

How much omega-3s are enough?

8. May 2007 William Davis (7)

The basic dose we advocate for the Track Your Plaque program is 1200 mg per day of EPA + DHA, the essential omega-3 fatty acids.

1200 mg EPA+DHA is generally obtainable by taking 4 capsules of 1000 mg of fish oil, since the majority of preparations contain 180 mg EPA and 120 mg DHA per capsule.

But how will you know if a higher dose wouldn't be even better?

The principal parameter to look at is triglycerides. If triglycerides remain above 60 mg/dl, we usually consider increasing fish oil.

Another measure that's very important is intermediate-density lipoprotein, or IDL, also called "remnant lipoproteins" on a VAP panel. Persistence of any IDL or remnant lipoproteins is reason to consider more fish oil. Most commonly, if there is some persistence of either, we increase fish oil to 6000 mg per day of a standard preparation, or 1800 mg/day of EPA+DHA.

The only time we see persistence of IDL or remnant lipoproteins with this higher dose is when triglycerides are really high. If starting triglycerides are, for instance, 500 mg/dl, then even this higher dose may be insufficient. This is when more highly concentrated preparations of fish oil may be necessary, occasionally even the prescription form, Omacor. (We currently use Omacor only when high doses of EPA+DHA are required, most because of its outrageous cost. Two capsules per day costs around $120 per month; three capsules per day to provide 1800 mg/day of EPA+DHA costs $180 per month. I think this is outrageous and so we use it only when absolutely necessary.)

You might even argue that a higher dose of 1800 mg EPA+DHA, or 6000 mg of a standard capsule, might be preferable for more assured reduction of heart attack risk--even when triglycerides and IDL are perfectly under control. I wouldn't argue with you. But you won't observe any measurable feedback that tells you that a heightened effect is being obtained. I take that dose myself, in fact, despite the fact that elimination of wheat products and weight loss was sufficient to drop my triglycerides to the target level. I figure it's a small additional effort for added peace of mind.

Repentance for past sins

7. May 2007 William Davis (0)

If you are new to the Track Your Plaque program and would like to jump start your effort, or if you are struggling with losing weight and excess weight is a part of the situation that created your CT heart scan score, then don't forget about fasting.

Fasting is the cessation of eating. However, recall from the Track Your Plaque Special Report, Fasting: Fast Track to Control Plaque at http://www.cureality.com/library/fl_04-012fasting.asp, there are many variations on fasting that permit some intake of healthy foods. (Thus, they are not, in the strict sense, "fasting". Accurate or no, there are variations that may be more palatable or do-able in the real world by real people.)

My personal favorite method to fast is to use a low-sugar, low-fat soy milk such as Light Silk, available at most major grocery stores. This high-protein, low-fat, low-sugar soy milk takes the edge off hunger and provides a minimal quantity of calories. A minimum of 72 hours is required for substantial results. (My one reservation about this brand of soy milk is that the Fanatic Cook claims that the manufacturer, Dean Foods, is a factory farm operation that abuses livestock--a discussion for another day.)

Fasting yields more than weight loss. It refreshes your appreciation for food. It reawakens you to the amount and quality of food you've been putting in your body. Fasting also allows you to recognize just how bad you might feel from the diet you were eating.

You also emerge from a fast with a reduced appetite and a renewed sense of appreciation for food. It makes the discipline of healthy eating a lot easier when you break your fast.

I tell people that fasting is not punishment. It is a form of enlightenment, of re-experiencing food and life. Fasting allows you to "catch up" on all the indiscretions you've been guilty of over the years.

It also provides enormous advantage in gaining control over coronary plaque.

A fanatic for Fanatic Cook

6. May 2007 William Davis (1)

If you haven't already done so, I'd urge you to peruse the wonderfully insightful, sophisticated, and biting commentary provided by the Fanatic Cook Blog at http://fanaticcook.blogspot.com.

She (I assume it's a she) has been discussing the proposed Safe Food Act recently, an effort to address all the dangers in foods that have come to attention lately, like melamine in pet food and E. coli in bagged spinach. Her most recent post is:

Nebraska Farm Bureau Thinks Food Safety Act Bad Idea, the latest in a series of posts exploring this issue.

I'd like to know who the Fanatic Cook is, or "Bix" as she calls herself. (I assume it's a "she" but I don't really know that for a fact.) I've corresponded with her and she prefers to remain anonymous for unspecified reasons. I'd like to know who this person is both for a more secure sense of credibility, as well as I'd simply like to know who can write so intelligently and why. I suspect that she's a professional nutrition scientist or something along those lines, since the level of insight into many scientific issues is quite impressive. Her Blogs will make great material for a book, if compiled and organized. Watch out for this one.

Erectile dysfunction and coronary plaque

6. May 2007 William Davis (5)

Erectile dysfunction (ED), previously known as "impotence," and coronary atherosclerotic plaque go hand in hand.

A recent study in men with advanced coronary disease showed that 93% experienced ED. The participants in the Track Your Plaque program, for the most part, do not have advanced coronary atherosclerosis, but have an earlier form detected by a CT heart scan.

What proportion of men with asymptomatic coronary plaque as measured by a CT heart scan have ED? Around 50%. In other words, it's not a rare occurrence.

The conversation about ED (and even its renaming from impotence) really gained momentum with the development of ED-drugs like Viagra and Cialis. The drugs are reasonably effective and safe. However, you will hear little about all the strategies that can either precede your need for these drugs and/or enhance your response to these drugs if the response is partial. That part of the conversation, of course, doesn't yield loads of drug company revenues.

One of the most helpful and specific nutritional supplements available that can partially restore the nitric oxide-deficiency of ED is l-arginine. L-arginine is the body's source of nitric oxide (NO), the master dilator (relaxing agent) for all arteries of the body. NO dilates penile arteries, it dilates coronary arteries. Lack of NO disables the penile capacity for erection and encourages growth of coronary atherosclerotic plaque. Track Your Plaque Members are already familiar with l-arginine as a facilitator of coronary plaque regression.

We will detail the supplements that you can use safely in your Track Your Plaque program to both enhance erectile function if you suffer ED, as well as impact positively on coronary health, in an upcoming and detailed Special Report on the www.cureality.com website.

An exercise in optimism

5. May 2007 William Davis (0)

Followers of the Track Your Plaque program already know that maintaining an optimistic viewpoint is important in gaining control over coronary plaque.

In fact, I believe that, in many cases, a sense of optimism may make or break your CT heart scan score-reducing efforts. Pessimists rarely drop their score, while optimists do so all the time.

This week posed a challenge to my optimism. I spent the last week on jury duty hearing the details of a murder case. For four days, I listened to blow-by-blow testimony about the totally pointless, unprovoked death of a young man by a drug-dealing thug. Much of the witness testimony was from people who shared the hopeless, violent world of the defendant.

I was, however, completely impressed by the dedication of the prosecuting attorney, a 50-some year old man who was clearly deeply dedicated to his mission and didn't once provide any indication that he was grandstanding or looking for some personal glory. He was doing his job and trying to obtain justice for the fallen victim. I was equally impressed by the judge, who seemed unfazed by the events but carefully explained why the system worked the way it did. After the trial, he provided some further insights to us jury members and I saw him as a human being who, like the prosecutor, was trying to make a small contribution to making the world better.

Though many of the witnesses who testified against the defendant shared his world, I was impressed with their courage in coming forward. They face the threat of reprisals, I'm sure, for coming forward to the law and testifying against a known career criminal. Several of them said that they were not after any reward, but simply wished to do the right thing and provide testimony that proved damning against the defendant.

I acted as the jury foreman and I was proud of how the jury members listened carefully, asked intelligent and probing questions, and then helped us render a confident and expeditious sentence: guilty.

If anything, despite the tragic circumstances, I was much heartened at how all the participants in this process played their part and justice (at least in the legal sense) was served.

Let optimism prevail, even in dire circumstances.

No need to re-invent the wheel

2. May 2007 William Davis (0)

I seem to be repeating myself lately, but I think this does bear repeating:

There's no need to re-invent the wheel when it comes to gaining control over your heart scan score.

The Track Your Plaque program is the most powerful approach known to help you gain control over your coronary atherosclerotic plaque and CT heart scan score, bar none. While 100% of people do not drop their score, more and more people every week are doing so. (One of the admitted weaknesses of the Track Your Plaque website is our failure to list more success stories; we're working on it.)

The basic program is quite simple:

--The Rule of 60 for lipids (LDL 60 mg/dl; HDL 60 mg/dl or greater; triglycerides 60 mg/dl or less)

--Identify hidden causes of plaque, esp. small LDL, Lp(a), and IDL, followed by specific corrective action

--Fish oil--minimum 1200 mg per day of EPA + DHA

--Normal vitamin D3 blood levels (We aim for 25-OH-vitamin D3 of 50-60 ng/ml)

--Normal blood sugar (<100 mg/dl)

--Normal blood pressure (<130/80)

--An optimistic attitude

Much of the other stuff--vitamin K, matrix metalloproteinase reducing strategies, flavonoid strategies, exercise-induced hypertension, etc.--are, for the majority, fluff. Their real role is in people who may have failed in stopping the rise of their heart scan score just doing the basics of the program.

If you neglect the basics, hoping to find some magic potion, I'm afraid the overwhelming likelihood is that you will fail. I've seen it happen time and again. Someone will come to my office with an extraordinary list of supplements--hawthorne, dozens of anti-oxidants, EDTA, concentrated flavonoid preparations, and on and on. Not only is it shockingly expensive to do this, it's also unnecessary and foolhardy. This kind of unfocused, hocus-pocus in the hopes of getting it right fail time after time.

The Track Your Plaque program, while not foolproof, is the best I know of. Stick to the basics and wander off when the basics fail. But there's extraordinary power in just achieving the basics.

Are we a front for drug companies?

2. May 2007 William Davis (3)

I was shocked recently when someone accused me and the Track Your Plaque website of being nothing more than a front for the drug industry, that we are promoting concepts with the hidden pharmacuetical agenda behind us.

Don't make me laugh. How in the world that kind of impression could be gotten from either the Heart Scan Blog or the Track Your Plaque website is beyond me.

But I occasionally do need to state explicity: We do not promote drugs, neither this Blog nor the Track Your Plaque website has ever sought nor been backed by pharmaceutical money. The only money that supports this website is our own and that from paying Track Your Plaque members.

In fact, I am quite proud of the unbiased content and commentary on both venues. I challenge anyone to point out how and where there is any suggested relationship to a hidden source of commercial backing. I assure you, there is none.

If I say a drug is worth you and your doctor considering, then I say so with a true belief in it, not because somebody or some company paid me to say so. If I say a drug stinks, I believe that too. If we use a specific supplement in the program, it's because we believe it truly adds value to a plaque-reversal program. We receive no money from drug, supplement, or other commercial interests to promote their products. Period.

What is "normal"?

1. May 2007 William Davis (2)

When it comes to laboratory values and medical testing, a common dilemma is knowing what is "normal." Let me explain.

First of all, when you receive a laboratory result for a test, a "reference range" or "normal range" is usually provided. Where did that range come from?

It varies from test to test. For instance, a low potassium is easy, because low potassium levels can lead to life threatening consequences, e.g., dangerous heart rhythms. High potassium likewise, because dangerous phenomena develop when potassium generally exceeds 5.5 mg/dl or so.

But what about something like HDL or LDL. Here's where confusion reigns. Often, "normal" is obtained by taking the average and saying that any value plus or minus two standard deviations (remember that painful class?) represents normal or reference range.

If that were true, what if we applied that principle to body weight. If we weighed several thousand adult women, the average would be in the neighborhood of 172 lbs (no kidding). Does that mean that 172 lbs plus or minus two standard deviations is normal? No, of course not.

There is therefore a distinction between "normal" and "desirable". For HDL cholesterol, your laboratory report might say that an HDL cholesterol of 40-60 mg/dl is normal. But is it desirable? I don't think so. The most frequent HDL level for a male with a heart attack is 42 mg/dl--hardly desirable.

Let's take triglycerides. The average triglyceride level in the U.S. is somewhere around 140 mg/dl. For those of us who do a lot of lipoprotein testing, we can tell you that triglycerides at this level, though generally regarded as being within the normal range, are associated with flagrant and obvious excesses of several abnormal lipoprotein particles that contribute to coronary plaque growth (VLDL and often IDL; small LDL; drop in HDL and shift towards small HDL).

So, always take the so-called "normal" or "reference" values on a lab report as crude guidelines that often have little or nothing to do with health or desirability. Unfortunately, many physicians are not aware of this and will declare any value within the normal or reference range as okay. An HDL of 40 mg is not okay. A triglyceride level of 140 mg is also not okay.

What is okay? What is desirable? That depends on the parameter being examined. From a basic lipid standpoint, of course, we regard desirable as 60-60-60. Desirability from a lipoprotein standpoint we will cover in a more thorough Track Your Plaque Special Report in future.

The wisdom of the masses

1. May 2007 William Davis (0)

My sister sent me these quotes:

"We don't like their sound, and guitar music is on the way out."

Decca Recording Co. rejecting the Beatles, 1962

"Stocks have reached what looks like a permanently high plateau."

Irving Fisher, Professor of Economics, Yale University, 1929

"Airplanes are interesting toys but of no military value."

Marechal Ferdinand Foch, Professor of Strategy, Ecole Superieure de Guerre, France

"Everything that can be invented has been invented."

Charles H. Duell, Commissioner, US Office of Patents, 1899

No doubt, conventional wisdom can often be laughably (tragically?) wrong. The problem is that, as absurd as all the above sentiments seem to us now and in retrospect, they represented the view of many people years ago. These views were held by many, including many people in positions of power and decision-making responsibility.

A more relevant but nonetheless laughable and widely held belief in 2007: coronary heart disease should be treated with hospital procedures.

Why is a disease that requires 30 years to develop treated only at the final moments with a procedure? Do you only change your car's oil when the engine is on its last legs? Or, do periodic, relatively effortless oil changes during the life of the car make better sense?

I witness just how brainwashed the public has become with this crazed notion when I meet someone socially at, say a fundraiser or cocktail party. When they ask what I do, I tell them I'm a cardiologist. The invariable response: "Oh, what hospital do you work out of?"

I tell them I don't, that I take care of the majority of heart disease right from the office. 99% of the time I get a puzzled look. If we had comic bubbles above our heads revealing our internal thoughts, it would read "Yeah, right. What a kook."

The notion that coronary heart disease is something that is manageable with simple tools for the majority of us in the early stages is entirely foreign to almost everybody. The hospitals and the medical industry have so succeeded in dazzling the public with images of staff in scrubs, rushing from emergency to emergency, lights flashing, scalpels flying. . . how can you possibly accomplish this at home or anywhere outside of the high-tech world of the hospital?

Well, I'm a cardiologist and I do it every day. We all need a figurative dose of electroshock therapy to shake ourselves of this crazy notion.

How important is l-arginine?

30. April 2007 William Davis (13)

Perhaps more than any other supplement, l-arginine causes frustration and confusion. It’s difficult to find, sometimes quite expensive, and some preparations cause loose stools.

Just how necessary is it?

L-arginine, you’ll recall, is a source of nitric oxide, or NO. Though it’s the same stuff as in car exhaust, NO provides a critical signaling role in your body’s cells that regulate a multitude of functions. Among the important roles of NO is to powerfully dilate, or relax, arteries. A constant flow of NO is required for health, particularly since each molecule persists only a few seconds.

L-arginine is the body’s source of nitric oxide. In addition, a peculiar but very effective blocker of l-arginine called asymmetric dimethylarginine, or ASDM, has recently been discovered to prevent the production of NO. Varied conditions like hypertension, diabetes, high cholesterol, excessive saturated fat or processed carbohydrate intake all lead to heightened levels of ASDM, often several-fold greater levels, and thereby effectively blocking NO production.

The “Arginine Paradox” is the name that some researchers in this field have given to the unusual property of l-arginine supplementation to “overpower” the blocking effects of ASDM. This is somewhat unusual in biologic systems in that an agent that blocks a receptor cannot usually be outmuscled by providing excess material for a reaction. Kind of like hoping that your car runs faster simply by topping up the gas tank.

Concrete observable benefits have been made for l-arginine in clinical trials, such as arterial relaxation that results in arterial enlargement (which can actually be seen in the cath lab); anti-inflammatory effects; reduction of blood pressure; enhancement of insulin responses, etc. All of these effects can be connected to beneficial properties that may facilitate atherosclerotic plaque regression and, indeed, there are limited data to document that this is true.

Drug companies may be greedy, but they’re not stupid. They’ve been vigorously pursuing this line of research for some years, a research path that led inadvertently to the erectile dysfunction agent, sildenafil (Viagra), and all its subsequent competitors. (Erectile dysfunction is another expression of endothelial dysfunction, since male erections are driven by the ability to dilate penile arteries.) The wonderful properties of NO enhancement continue to occupy research labs around the world.

Wow. So what’s the reluctance? In the early years of the Track Your Plaque program (meaning just a short 7-8 years ago), I was thoroughly convinced that l-arginine was a crucial, necessary part of a plaque regression program. Without it, you would rarely succeed. With it, the odds were tipped in your favor.

However, something curious has emerged recently. I’ve seen more and more people dropping their heart scan scores. Not just a little bit, but a huge amount. Witness our most recent record holder, Neal, who dropped his score 51% in 15 months. Just five years ago, this magnitude of reversal was unimaginable. Granted, Neal is our record holder, but others are obtaining 10, 18, 24, 30% drops in scores all the time. Many have done it without l-arginine.

Now, how about the people who have failed to stop a rising score? Would they do better with l-arginine as part of the mix? I believe so, but sometimes we never quite know except in retrospect. It has been a great dilemma for us trying to predict from the starting gate who will or who won’t drop their heart scan score.

My view from the trenches is that l-arginine packs its greatest atherosclerosis-fighting punch in the first year or two of use, when “endothelial dysfunction” is likely to be present (abnormal artery constriction). But as all other strategies take hold—fish oil, correction of lipid and lipoprotein abnormalities, weight loss (big effect), vitamin D (another very big effect), etc.—endothelial behavior improves over time. Perhaps l-arginine becomes a less necessary component over time.

There’s no doubt that uncertainty still surrounds the use and science surrounding l-arginine. However, if you’re interested in stacking the odds in your favor, particularly during the first year or two of your plaque-reducing efforts, I think that l-arginine is worth considering. It is cumbersome, it can be expensive, some preparations may even be foul. But in the big picture of life, with hospitals trying every possible ploy to get your body on a table for a procedure, doctors perverting their mission by signing employment contracts with hospitals and agreeing to usher you into the hospital as a paying patient whenever possible, and drug companies viewing you and me as a market for medications which may or may not be helpful, l-arginine is surely not that big a burden.