Report from Washington II

16. July 2006 William Davis (0)

Today's discussions at the Society for Cardiovascular Computed Tomography (SCCT) focused on atherosclerotic "plaque characterization".

As CT scanners get better and better at imaging the various components of plaque, some fascinating issues emerge:

--CT heart scans provide insights into what exactly is contained in an individual's atherosclerotic plaque that are not often provided even during heart catheterization. In other words, CT heart scanning is, in many instances, superior to heart catheterization, since it provides images of the artery wall, not just the internal contents.

--Progression (i.e., increase) in heart scan score is a powerful predicter of heart attack risk. Dr. Matthew Budoff of UCLA argued persuasively that the annual rate of increase in score is probably the most accurate measure of risk available, superior to cholesterol and calculated measures like the Framingham risk score.

--Coronary calcium scoring remains the best method to gauge total plaque throughout the entire coronary tree. In a person free of symptoms, the risk of a cardiac "event" (heart attack, death, procedures) is low and additional imaging (like CT angiography) is generally unnecessary.

Dr. Budoff, among the true thought leaders in CT heart scanning, also recounted his perspective on the history of heart scans. He noted that the questions asked through the years have evolved:

1995-2000 Should we do coronary calcium scans?

2000-2002 Do high or low risk patients benefit from coronary calcium scoring?

2003-2004 What is the better scanner, EBT or MDCT?

2006 How often should we perform coronary calcium imaging?

I believe that Dr. Budoff summarizes wonderfully where the Track Your Plaque programs fits into the overall scheme of things: Serial (repeated)CT heart scans to gauge progression or reversal is the wave of the future. We shouldn't just be interested in identifying persons at risk for heart attack. We should also be interested in showing the person at risk exactly how to reduce or eliminate that risk.

Report from Washington

14. July 2006 William Davis (0)

I'm presently attending the Society for Cardiovascular Computed Tomography meetings in Washington, DC, along with 500 of my colleagues. It's exciting to see how interest in CT scanning for heart disease has balloonned in the past couple of years.

Several trends are noticeable today, based on the content and tone of the discussions:

--CT scanning of the heart, and imaging in general, is just getting started. In other words, the capabilities for CT scanners and other devices to detect heart disease (coronary and otherwise) are where the gasoline engine was in the 19th century. Scanning is getting faster, easier, safer, and more precise. Just as few people in 1905 could have predicted that automobiles would be computer-enhanced, high-speed, ubiquitous devices with several per household, the potential for CT imaging for heart disease is truly in its infancy.

--CT coronary angiography (so-called "64-slice CT scans") are not screening tests for hidden coronary disease in people without symptoms. I was grateful that this point has been made and reiterated by several speakers, as this is consistent with our views. Simple CT heart scans for coronary calcium scoring, in contrast, are screening tests. When the radiation exposure of CT angiograms are reduced to tolerable levels, then they may be used as screening tests. We are probably 3-4 years away from this point.

--Both stress testing and heart catheterizations will be partially replaced by CT scanning. In particular, over the next decade, you will see a dramatic drop in unnecessary catheterizations, i.e,, far less people saying "I had a heart cath but they told me that it was normal."

There has been heavy focus on applications of CT scanning for acute settings, particularly the emergency room and hospitals.

What has surprised me is that there is virtually no conversation whatsoever about the preventive uses of CT heart scanning. So far, only Dr. Daniel Berman of UCLA has shown that he has "seen the light": CT scans are a crucial tool for identification of early coronary plaque, and this tells us whether prevention is necessary and with what intensity.

There has been, however, no discussion at all about quantification of plaque in a program of reversal. Perhaps that should come as no surprise, given the imaging-technology focus of this convention. For most of my colleagues, prevention is also not terribly interesting. Identification and treatment of acute disease like impending heart attack is.

Of course, applying the information from your CT heart scan to empower you in a program and reversal is what the Track Your Plaque program is all about. I hope you see the light. I admit that it's not always easy to follow what we are advocating here. Perhaps not too different than telling someone in his horse-drawn buggy that one day he'll be driving a sleek car with onboard computerized mapping, air-conditioning, and micro-chips to modulate engine performance. He's probably tell us we're nuts.

I'll continue to update if any news relevant to our interests crops up in these meetings.

What about the Track Your Plaque failures?

14. July 2006 William Davis (0)

I’d love to tell you that the Track Your Plaque program track record is of 100% success. It’s not.

It is very successful. But we’ve had some people who have failed and failed BIG. These are the people who've undergone bypass surgery, received one or more stents, or had heart attacks. Lesser failures are the people who’ve had large, undesirable increases in heart scan scores of >30% in one year. (The expected rate of increase in your heart scan score without preventive efforts is 30% per year, on average.)

What can we learn from those failures? There were several characteristics that stand out among this small group:

· Non-compliance--meaning they just didn’t stick with it. They started out right but then rapidly lost interest in maintaining all the pieces of the program and neglected their fish oil, niacin, gain weight, etc. Matthew did this and ended up with three stents to his left anterior descending. His slow start was due to skepticism that the program worked and just plain forgetfulness.

· Extreme stress--One of our earliest failures was a 38-year old man whose heart scan score doubled in one year, despite doing everything right. But three family members, all close to him, died within the space of six months, including his mother and a brother. I regard this as one of those instances in which we were powerless, unfortunately, though it is a graphic example of the power of unresolved stress and grief.

· Having a “better way”--These are the couple of people who were convinced that they had a better way to control their heart scan score. David firmly believed that his two dozen supplements and exercise program would drop his score. Instead, they permitted a 42% increase. Lee relied exclusively on chelation, along with several supplements of his own design. Lee had three-vessel bypass surgery.

· Starting too late--Gerome started with a score of 1179, but also was having chest pressure with emotional stress. His stress test was abnormal, with the entire upper half of his heart not receiving blood with exercise on a stress nuclear study (“anterior ischemia”). Gerome received four bypass grafts. Unfortunately, Gerome never really had a chance to engage in the Track Your Plaque program, since his health and safety were in jeopardy as soon as he started.

Have we had any big failures of people who did everything right, were compliant, were not subject to extreme stress (more than just job stress, or financial worries), didn’t neglect the basic requirements of the Track Your Plaque program, and had sufficient time (at least 6 months to 1 year)? No, thankfully, we have not.

No one who has stuck to the program has had a big failure.

Be smarter than your cardiologist

12. July 2006 William Davis (0)

“Do you need a stent?”

Sad to say, but that sentence condenses the wisdom of over 90% of practicing cardiologists.

Prevention of heart disease means take Lipitor or some other statin and cutting the saturated fat in your diet. That’s it. Maybe throw in exercise.

Regression of coronary plaque? That phrase has only entered the conversation since the AstraZeneca-supported trial of Crestor succeeded in achieving 8% regression of plaque (Track Your Plaque Members: See News) as demonstrated by intracoronary ultrasound.

In other words, in the minds of my colleagues, it can’t be true until a drug company tells them it’s true. It’s beyond me why this brainwashing of otherwise intelligent people has occurred, but it is blatantly evident in practice.

Fish oil is another example. The spectacular benefits of fish oil have been known for 20 years. But only recently has it become a “mainstream” practice to recommend fish oil, largely because a drug manufacturer has put a preparation through the rigors of FDA approval (Omacor) and is now marketing directly to physicians. All of a sudden, fish oil is a good thing? No, it’s just achieved legitimacy in the eyes of practitioners because it graces marketing literature.

If you’re reading this, you’re likely interested in coronary plaque regression using the only tool available for you to measure, track, and regress coronary plaque: CT heart scans. Intracoronary ultrasound will achieve the same goal, but it is an invasive procedure performed at heart catheterization, involves threading a wire and imaging probe all the way down the artery, involves real risk of tearing the inner lining of the artery, and is costly (around $14,000-$20,000 for the entire package). Do it every year? That’d be nuts.

If you’re thinking about coronary plaque regression, using fish oil, concerned about patterns like low HDL and small LDL, aware of the vitamin D deficiency issue as a coronary risk factor, etc., you are far more aware than the vast majority of practicing cardiologists. They are interested in what new brand of anti-coagulant to use during their heart catheterization (because the product representative gushes about the new agent—only $1200 a dose!). Or, they are interested in gaining the procedural skills to put in a new device like a biventricular pacemaker. Regress/reverse coronary plaque? What for?

You already know that a conversation about coronary plaque reversal will not be obtained in your cardiologist’s office. Your family practice doctor or internist? Fat chance! Knee arthritis, pap smears, pneumovax inoculations, sore throats, gout, back pain—they’re spread far too thin to know anything more than the most superficial amount about coronary plaque control. Most know nothing.

That’s where we come in. That’s our mission: Educate people about the extraordinary tools that you have available to you, all in the cause of control or reversal of coronary plaque.

Why am I here?

11. July 2006 William Davis (0)

Frank came to the office for an opinion, sent by his (proactive) family physician.

"I really don't know why I'm here, to be honest."

Two years earlier, Frank had a heart attack, survived and received two stents to his circumflex coronary artery. He now took Zocor and his LDL cholesterol was a reasonably favorable 89 mg, total cholesterol 183 mg.

"I walk with my wife every other day. I've been avoiding fish fries. You'll never see me eat fast food."

Frank was correct: If we were going to engage in the conventional approach to coronary disease, Frank was on the right track. We would have postponed his next heart attack or procedure by a couple of years. Stroke, aneurysm, and other atherosclerotic manifestations would be set back, likewise, a few years.

Would Frank have profound control over his disease? Absolutely not. In fact, his disease had probably advanced a huge amount just in the two years since his stents were placed and he was on his "prevention" program. Without his current effort, his coronary plaque would be expected to grow 30% per year. On Zocor and his modest lifestyle efforts, plaque growth was probably in the 14-28% per year range.

So I explained the unique Track Your Plaque approach to Frank. First, we start with a CT heart scan to establish where he was starting. Although he had two stents in his circumflex artery, we still had two other arteries (LAD, right coronary) to score and track.

We then attempt to identify all hidden causes of his heart disease and then correct them.

Of course, Frank had multiple hidden causes:

--HDL too low at 38 mg/dl
--Small LDL-severe, in fact, with 95% of all LDL particles in the small category
--Triglycerides too high
--Excesses of several triglyceride-containing particles (VLDL, IDL)
--Pre-diabetes--Frank had both a borderline high blood sugar and a high insulin level. This is a sure-fire stimulus to coronary plaque growth.
--A severe deficiency of vitamin D (<20 ng/ml)
--An excessivelyhigh blood pressure during exercise--With a blood pressure of 190/102 on the treadmill.

There were others(!), but that was the bulk of the causes behind Frank's coronary disease.

Once Frank recognized that there was indeed a huge panel of hidden causes for heart disease, not just too much fat in his diet and LDL cholesterol, he jumped into the program head first.

The message: The conventional approach is absurdly oversimplified, a certain path to failure for the majority of people. Even if you don't have known coronary disease like Frank, but just have a heart scan score >zero, the same principles apply to you.

Catheterization to “define coronary anatomy”

10. July 2006 William Davis (0)

Gary is an avid jogger. On an average day, he runs 5-6 miles at a good clip. On two occasions recently, however, Gary experienced an ache in his left shoulder at mile 4. It was a toothache-like feeling, but he kept on going without difficulty.

Gary also had a heart scan score of 370.

Upon hearing of Gary’s score and his shoulder sensation, the cardiologist who saw him advised a heart catheterization “to define coronary anatomy”. (This is a real incident.)

What exactly does that mean? Why would Gary’s cardiologist need to define it?

In my view, this is an absurd notion. No one needs to “define coronary anatomy”. This catch-all phrase is commonly used to justify heart procedures. I believe what the cardiologist is saying is that it’s the easiest (for the cardiologist) and perhaps most generously reimbursed method to determine whether Gary’s symptoms are warning of an impending heart attack or not.

The problem is that the question can also be answered quite well by doing a stress test. Though not perfect diagnostic tests, stress tests are useful when symptoms are present that are doubtful in nature. Gary’s left shoulder ache could have been related to his heart, but the likelihood was that it was not. A stress test would have answered the diagnostic question quite adequately.

Instead, this man was subjected to an invasive test that was likely unnecessary. This happens dozens, if not hundreds, of times per day just around here. Nationwide, it is an epidemic of malpractice.

There are, indeed, times when a person should proceed directly to a heart catheterization. This is commonly and appropriately performed when a person develops unstable heart symptoms, such as chest discomfort or breathlessness at rest while not doing anything physical, or if the frequency is increasing, or if a stress test shows an important abnormality. There is no question that heart procedures can be lifesaving at times.

The problem is that thousands of people every year are scared into these procedures inappropriately. Beware!

It doesn't matter what I eat!

9. July 2006 William Davis (0)

"How are your food choices?" I asked.

"What does it matter, doc? I take Lipitor. Doesn't that take care of it? I eat what I want!"

So declared Matthew. What he "wanted" was pretty much the diet of a teenager: pizza, cheeseburgers, soft drinks, snacks. His "beer belly" (visceral fat) gave it away. So did his blood work that showed flagrant lipoprotein abnormalities--small LDL, an HDL of 37 mg, and a severe after-eating flood of fat represented by increased "intermediate-density lipoprotein" (IDL).

Like many people, Matthew had been persuaded (or chose to believe) that LDL cholesterol was the sole cause for heart disease. Lipitor was therefore was all he needed. It must be great--how else could they afford all those slick TV commercials?

Well, it is definitely not true. In fact, with the persistence of Matthew's abnormal lipoprotein patterns, we should expect his heart scan score to continue to grow by 30%--the very same rate of increase as if he were taking nothing.

Specifically, Lipitor and drugs like it do not:

--Raise HDL.

--Correct or reduce the proportion of small LDL.

--Block after-eating flood of fat, nor do they accelerate clearance of unhealthy fats persisting in the bloodstream after eating.

Yes, what you eat does have real consequences, even if you take a statin drugs. In fact, the foods you ingest have a remarkably rapid and dramatic effect on what your blood contains. Any diabetic who checks his/her blood sugar knows this. They eat a slice of whole wheat toast and watch their blood sugar skyrocket.

Mind what you eat. Make it enjoyable, of course. But drugs do not provide impunity.

People with higher scores need to try harder

8. July 2006 William Davis (0)

Sam is a 69-year retired physician. He was thoroughly enjoying retirement: golf, travelling, going out to dinner two or three times a week, spending weekends with his grandchildren. His lifestyle tended towards overindulgence, but he managed to stay fit and trim. At 6 ft 1 inch, he weighed 194 lbs and could still run 3 miles without too much difficulty. Not as good as his marathon-running days, but still not too bad for 69.

Sam's heart scan score in 2003 was a concerning 1983--extensive plaque. His doctor wasn't much help in interpreting the scan and so Sam simply chose to ignore it.

A chance conversation with a physician friend 18 months later made Sam think that perhaps this shouldn't be ignored. That's when he came to my office.

I find that sometimes the best way to motivate someone to take action is to demonstrate just how fast plaque grows if action isn't taken. So I advised Sam to get another scan first, since 18 months had passed. His score: 2441, or a 23% increase.

Sam was now starting to catch on. We made several changes in his prevention program (starting from virtually nothing). He did undergo a stress nuclear (thallium type) of test, which he passed without difficulty--normal blood flow in all heart territories despite the extensive plaque.

But, for some reason, Sam simply allowed himself to drift back to old habits: poor choices in food, overindulging in hard liquor, missing his fish oil and other supplements, and his medication, sometimes up to several days a week.

Sam started having unusual feelings in his chest. He described a sort of nervousness along with skipped heart beats. So we repeated a stress test. This time, a large area of reduced blood flow in the front of his heart ("anterior left ventricle") was detected. Sam ended up receiving three stents in a difficult procedure.

The moral: If you're starting out with a lower heart scan score of, say, 100 or 200, maybe you'll get by without trying too hard--maybe. But if your score is higher, say, several hundred or in the thousands, you got to try harder.

You're starting later in the process. Your disease will allow you very little slack. Let your guard down and it will get you. Control over your plaque is, indeed, very possible--we do it all the time. Score reduction is also possible. But your effort must be more serious and consistent.

Money can't buy health

6. July 2006 William Davis (1)

Fallen Enron CEO, Kenneth Lay, was pronounced dead early this a.m. after suffering a heart attack.

Mr. Lay apparently had no history of heart disease and there's been no indication that symptoms provided any warning. His death was therefore classified as "sudden cardiac death".

Yet here's a man previously worth hundreds of millions of dollars with access to any test or medical system he desired--many times over. Even more recently, with his wealth reduced following his legal troubles, he and his wife managed to put away $4 million dollars to ensure an income from the interest through annuities, untouchable by the courts.

Detecting Mr. Lay's heart disease would have cost him around a few hundred dollars or whatever it costs for a CT heart scan in his city. This would have alerted his (hopefully knowledgeable) doctor that he was a time-bomb. Pile on all the stress he'd been suffering, whether deserved or no, and the diagnosis would have required little thought.

Instead, Mr. Lay has joined the thousands of Americans who will die this year because of failing to get a simple, 30-second test that costs one-tenth the cost of a stress test. Mr. Lay wasn't as lucky as former President Bill Clinton, whose doctors likewise blundered their way through and missed obvious levels of heart disease.

All Mr. Lay needed was better information: get a heart scan, then follow a program of prevention like the Track Your Plaque program. You may not have hundreds of millions of dollars, but you have the information on how to not follow in Ken Lay's footsteps. Track Your Plaque--and stay alive.

What's important, what's not in your plaque-control program

6. July 2006 William Davis (0)

Sometimes it's hard to know what is really important in your plaque-control or plaque-reducing efforts.

There are, indeed, crucial make-it-or-break-it factors that are necessary to gain control over plaque. If you hope to stack the odds of reducing your heart scan score as much as possible in your favor, then fish oil, vitamin D, 60-60-60 in the way of standard lipids, elimination of small LDL, etc. -- all the elements of the Track Your Plaque program--are necessary.

But there's lots of things that sidetrack people. I spend much of my day fielding questions from patients about all the things that either provide very little benefit for plaque control, or provide none at all.

Among the things that we have found to be too weak or useless for plaque control, or are "non-issues", include:

--Caffeine--Go ahead and enjoy a couple cups a day (though not a pot). The effect is too trivial to make much difference.

--Hawthorne--Yes, it may dilate coronary arteries modestly, but not enough to make any difference.

--Garlic--with the possible exception of a specific preparation called Aged Garlic Extract (an acqueous, non-oil-based, extract from Kyolic), garlic's effects are too tiny to help, e.g., drop in blood pressure 1-2 points. Use it, but don't expect much. Aged Garlic Extract may be an exception, in that a single study from UCLA suggested specific effects on slowing coronary plaque growth. We await more info on this.

--Anti-oxidants--There is no shortage of extravagant claims about the benefits of anti-oxidants. Unfortunately, there's very little human exerience with pine bark extract, pycnogenol, grapeseed extract, and so on. Is the purported benefit from anti-oxidation or through some other means, e.g., enhancement of nitric oxide synthase? No data.

--Policosanol--If you've followed the Track Your Plaque Special Reports, you already know what a disappointment this agent has been, despite the too-good-to-be-true clinical data. It doesn't work.

--"No-flush niacin"--Unfortunately, no flush, no effect. This high-priced supplement is still sold widely in the U.S. despite its complete lack of efficacy. It does not work in humans. (It works great in rats!)

Track Your Plaque continues to try to be the arbiter of truth in what works, what doesn't in truly stopping or reversing your coronary plaque. The proof positive? Stopping or dropping your heart scan score.

All posts by william-davis

Fish oil: What's the difference?

10. December 2010 William Davis (27)

Ultra-purified, pharmaceutical grade, molecularly distilled. Over-the-counter vs. prescription. Gelcap, liquid, emulsion.

There's a mind-boggling variety of choices in fish oil today. A visit to any health food store, or any "big box" store for that matter, will yield at least several, if not dozens, of choices, all with varying and often extravagant claims of purity and potency.

So what's the real story?

Given the analyses conducted over the years, along with my experience with dozens of different preparations, I believe that several conclusions can be reached about fish oil:

Fish oil is free of contamination with mercury, dioxin, PCBs, or furans. To my knowledge, only one fish oil preparation has been found to have a slight excess of PCBs. (This is different from cod liver oil that has been found by one source to have a slight excess of PCBs.)

Oxidative breakdown products differ among the various brands. Consumer Lab (http://www.consumerlab.org/), for instance, has found that several widely available brands of fish oil contained excessive oxidative breakdown products (TOTOX). You can perform you own simple test of oxidative breakdown products: Sniff it. Your fish oil should pass the "sniff test." High quality fish oil should smell non-fishy to lightly fishy. Rancid fish oil with excessive quantities of oxidative breakdown products will smell nasty fishy.

FDA approval does not necessarily mean greater potency, purity, or effectiveness. It just means that somebody assembled the hundreds of millions of dollars to obtain FDA approval, followed by lots of marketing savvy to squash the competition.

This means that there are a number of excellent fish oil products available. My favorites are the liquid fish oils from Pharmax, Nordic Naturals, and Barleans. Capsules from Carlson, PharmaNutrients, and Fisol have also performed consistently. The "big box" capsules from Sam's Club and Costco have also performed well and are wonderfully affordable.

Wheat-free pie crust

9. December 2010 William Davis (17)

I've been working on wheat-free yet healthy recipes these past two months.

You can buy wheat-free, gluten-free foods at the store, of course. But the majority of these products are unhealthy because cornstarch, rice starch, potato starch, or tapioca starch are commonly used in place of wheat. Recall that these are among the few foods that increase blood glucose higher than even wheat.

Here's a simple recipe for wheat-free pie crust that works best for cheesecake, pumpkin pie, and cream pies, but not for berry or other fruit pies like apple.

You will need:
?
1½ cups ground pecans
6 tablespoons melted butter?or melted coconut oil
1 teaspoon vanilla extract?
2 teaspoons cinnamon
1 medium egg
2 tablespoons Truvia™ or ½ teaspoon stevia extract or ½ cup Splenda®

Mix all ingredients thoroughly in bowl. Pour mixture into pie pan and press onto bottom and sides.

Fill pie crust with desired filling. You can fill it with your favorite cheesecake recipe (e.g., Neufchatel or cream cheese, sour cream, eggs, vanilla, and stevia; add pumpkin for pumpkin cheesecake) and bake, usually at 350 degrees F for one hour.

Yes, the butter provokes insulin and artificial sweeteners can trigger appetite. But, for the holidays, a slice or two of pie made with this crust will not increase blood sugar nor trigger the uncontrolled impulse eating that wheat crust will trigger.

Have a cookie

9. December 2010 William Davis (0)

Here's a great insight dating all the way back to 1966 from one of the early explorations in lipoproteins from the National Institutes of Health lab of Levy, Lees, and Fredrickson:

The nature of pre-beta (very low density) lipoproteins

The subject is a 19 year old female (among the total of 11 in the this small, diet-controlled study) who was first fed a low-carbohydrate (50 grams per day), low-cholesterol diet; followed by a high-carbohydrate (500 grams per day), low-fat (5 grams per day) diet.

To B or not to B

5. December 2010 William Davis (11)

Apoprotein B (apo B) is the principle protein that resides in LDL particles along with other proteins, phospholipids, triglycerides, and, of course, cholesterol.

There's a curious thing about apo B. Just like one child per family in China or one television per household in 1950s America, there is only one apo B for every LDL particle.

So measuring apo B, in effect, provides a virtual count of LDL particles. (Actually, VLDL particles, the first lipoprotein to emerge from the liver, also have one apo B per particle but LDL particles far outnumber VLDL particles.) While apo B structure can show limited structural variation from individual to individual, the effect on measured apo B is negligible.

One apo B per LDL particle . . . no more, no less. What about the other components of LDL particles?

The other components of LDL particles are a different story. Cholesterol and triglycerides in LDL particles vary substantially. Diet has profound effects on cholesterol and triglyceride content of LDL particles. A diet rich in carbohydrates, for instance, increases triglycerides in LDL particles while reducing cholesterol. This means that measuring cholesterol in the LDL fraction will be misleading, since cholesterol will be falsely low. LDL cholesterol is therefore a flawed means to assess the behavior and composition of LDL particles. In particular, when LDL particles become enriched in triglycerides, they go through a process that transforms them into small LDL particles, the variety most likely to cause atherosclerosis.

In other words, when the worst situation of all--an abnormal abundance of small LDL particles develops--it is usually not signalled by high LDL cholesterol.

Because apo B is not sensitive to the composition of LDL particles--high cholesterol, low cholesterol, high triglycerides, etc.--it is a superior method to characterize LDL particles. While apo B doesn't tell you whether LDL particles are big, small, or in between, it provides a count of particles that is far more helpful than measuring this deeply flawed thing called "LDL cholesterol."

(Even better: Count LDL particles and measure LDL size, since size gives us insight into sensitivity to oxidation, glycation, adhesiveness, ability to trigger inflammatory pathways via monocyte chemoattractant protein, various interleukins, tunor necrosis factor and others. This is why cholesterol panels should go the way of tie dye shirts and 8-track tapes: They are hopelessly, miserably, and irretrievably inaccurate. Cholesterol panels should be replaced by either apoprotein B or lipoprotein measures.)

Put lipstick on a dwarf

2. December 2010 William Davis (24)

Today, virtually all wheat products are produced from the Triticum aestivum dwarf mutant.

You might call it "multi-grain bread,""oat bread," or "flaxseed bread." You could call it "organic," "pesticide-free," "non-GMO," or "no preservatives." It might be shaped into a ciabatta, bruschetta, focaccia, or panini. It might be sourdough, unleavened, or sprouted. It could be brown, black, Pumpernickel, or white. It could be shaped into a roll, bun, bagel, pizza, loaf, pretzel, cracker, pancake, brioche, baguette, or pita. It could be matzah, challah, naan, or Communion wafers.

No matter what you call it, it's all the same. It's all from the dwarf mutant Triticum aestivum plant, the 18-inch tall product of hybridizations, backcrossings, and introgressions that emerged from genetics research during the 1960s and 70s.

According to Dr. Allan Fritz, Professor of Wheat Breeding at Kansas State University, and Dr. Gary Vocke at the USDA, over 99% of all wheat grown today is the dwarf variant of Triticum aestivum. (For you genetics types, Triticum aestivum is the hexaploid, i.e., 3 combined genomes, product of extensive hybridizations, while ancestral einkorn is a diploid, i.e., a single genome, grass. Hexaploid Triticum aestivum contains the especially hazardous "D" genome, the set of genes most commonly the recipient of genetic manipulations to modify the characteristics of flour, such as gluten content. Einkorn contains only the original "A" genome.)

No matter what you call it, add to it, how you shape it, etc., it's all the same. It's all the dwarf mutant product of tens of thousands of hybridizations.

You can put lipstick on a pig, but it's still a pig. By the way, lipstick may contain wheat.

What the Institute of Medicine SHOULD have said

1. December 2010 William Davis (47)

The news is full of comments, along with many attention-grabbing headlines, about the announcement from the Institute of Medicine that the new Recommended Daily Allowance (RDA) for vitamin D should be 600 units per day for adults.

What surprised me was the certainty with which some of the more outspoken committee members expressed with their view that 1) the desirable serum 25-hydroxy vitamin D level was only 20 ng/ml, and 2) that most Americans already obtain a sufficient quantity of vitamin D.

Here's what I believe the Institute of Medicine SHOULD have said:

Multiple lines of evidence suggest that there is a plausible biological basis for vitamin D's effects on cancer, inflammatory responses, bone health, and metabolic responses including insulin responsiveness and blood glucose. However, the full extent and magnitude of these responses has not yet been fully characterized.

Given the substantial observations reported in several large epidemiologic studies that show an inverse correlation between 25-hydroxy vitamin D levels and mortality, there is without question an association between vitamin D and mortality from cancer, cardiovascular disease, and all cause mortality. However, it has not been established that there are cause-effect relationships, as this cannot be established by epidemiologic study.

While the adverse health effects of 25-hydroxy vitamin D levels of less than 30 ng/ml have been established, the evidence supporting achieving higher 25-hydroxy vitamin D levels remains insufficient, limited to epidemiologic observations on cancer incidence. However, should 25-hydroxy vitamin D levels of greater than 30 ng/ml be shown to be desirable for ideal health, then vitamin D deficiency has potential to be the most widespread deficiency of the modern age.

Given the potential for vitamin D's impact on multiple facets of health, as suggested by preliminary epidemiologic and basic science data, we suggest that future research efforts be focused on establishing 1) the ideal level of 25-hydroxy vitamin D levels to achieve cancer-preventing, bone health-preserving or reversing, and cardiovascular health preventive benefits, 2) the racial and genetic (vitamin D receptor, VDR) variants that may account for varying effects in different populations, 3) whether vitamin D restoration has potential to exert not just health-preserving effects, but also treatment effects, specifically as adjunct to conventional cancer and osteoporosis therapies, and 4) how such vitamin D restoration is best achieved.

Until the above crucial issues are clarified, we advise Americans that vitamin D is a necessary and important nutrient for multiple facets of health but, given current evidence, are unable to specify a level of vitamin D intake that is likely to be safe, effective, and fully beneficial for all Americans.

Instead of a careful, science-minded conclusion that meets the painfully conservative demands of crafting broad public policy, the committee instead chose to dogmatically pull the discussion back to the 1990s, ignoring the flood of compelling evidence that suggests that vitamin D is among the most important public health issues of the age.

Believe it or not, this new, though anemic, RDA represents progress: It's a (small) step farther down the road towards broader recognition and acceptance that higher intakes (or skin exposures) to achieve higher vitamin D levels are good for health.

My view: Vitamin D remains among the most substantial, life-changing health issues of our age. Having restored 25-hydroxy vitamin D levels in over 1000 people, I have no doubt whatsoever that vitamin D achieves substantial benefits in health with virtually no downside, provided 25-hydroxy vitamin D levels are monitored.

Coronary calcium: Cause or effect?

28. November 2010 William Davis (25)

Here's an interesting observation made by a British research group.

We all know that coronary calcium, as measured by CT heart scans, are a surrogate measure of atherosclerotic plaque "burden," i.e., an indirect yardstick for coronary plaque. The greater the quantity of coronary calcium, the higher the heart scan "score," the greater the risk for heart attack and other unstable coronary syndromes that lead to stents, bypass, etc.

But can calcium also cause plaque to form or trigger processes that lead to plaque formation and/or instability?

Nadra et al show, in an in vitro preparation, that calcium phosphate crystals are actively incorporated into inflammatory macrophages, which then trigger a constellation of inflammatory cytokine release (tumor necrosis factor-alpha, interleukins), fundamental processes underlying atherosclerotic plaque formation and inflammation.

Here's the abstract of the study:
Proinflammatory Activation of Macrophages by Basic Calcium Phosphate Crystals via Protein Kinase C and MAP Kinase Pathways:

A Vicious Cycle of Inflammation and Arterial Calcification?

Basic calcium phosphate (BCP) crystal deposition underlies thedevelopment of arterial calcification. Inflammatory macrophagescolocalize with BCP deposits in developing atherosclerotic lesionsand in vitro can promote calcification through the release of TNF alpha. Here we have investigated whether BCP crystals can elicit a proinflammatory response from monocyte-macrophages.BCP microcrystals were internalized into vacuoles of human monocyte-derived macrophages in vitro. This was associated with secretion of proinflammatory cytokines (TNF, IL-1ß and IL-8) capable of activating cultured endothelial cells and promoting capture of flowing leukocytes under shear flow. Critical roles for PKC, ERK1/2, JNK, but not p38 intracellular signaling pathways were identified in the secretion of TNF alpha, with activation of ERK1/2 but not JNK being dependent on upstream activation of PKC. Using confocal microscopy and adenoviral transfection approaches, we determined a specific role for the PKC-alpha isozyme.

The response of macrophages to BCP crystals suggests that pathological calcification is not merely a passive consequence of chronic inflammatory disease but may lead to a positive feed-back loop of calcification and inflammation driving disease progression.

This observation adds support to the notion that increasing coronary calcium scores, i.e., increasing accumulation of calcium within plaque, suggests active plaque. As I say in Track Your Plaque, "growing plaque is active plaque." Active plaque means plaque that is actively growing, inflamed and infiltrated by inflammatory cells like macrophages, eroding its structural components, and prone to "rupture," i.e., cause heart attack. Someone whose first heart scan score is, say, 100, followed by another heart scan score two years later of 200 is exposed to sharply increasing risk for cardiovascular events which may, in part, be due to the plaque-stimulating effects of calcium.

Conversely, reducing coronary calcium scores removes a component of plaque that would otherwise fuel its growth. So, people like our Freddie, who reduced his heart scan score by 75%, can be expected to enjoy a dramatic reduction of risk for cardiovascular events.

Less calcium, less plaque to rupture, less risk.

Wheat one-liners

26. November 2010 William Davis (22)

If you're having difficulty convincing a loved one or someone else that wheat should be eliminated from the human diet, here are some useful one-liners to use:

Wheat makes your boobs big.
(This is true. Priceless for women to use on their husbands.)

Wheat causes dementia.
(And confirmed on examination of brain tissue at autopsy. Yes, autopsy.)

Wheat makes you look pregnant.
(The visceral fat of a wheat belly does a darn good imitation of a near-term infant.)

The first sign of wheat intolerance can be wetting your pants.
(Cerebellar ataxia, i.e., destruction and atrophy of the cerebellum, caused by wheat leads to loss of coordination and bladder control. Average age of onset: 53 years old.)

White flour bad, whole grain better; just as Marlboros are bad, Salems are better.
(The flawed syllogism that led to the "eat more healthy whole grain" colossal blunder.)

Wheat is the only food with its very own mortality rate.
(Celiac disease, osteoporotic hip fractures, and the neurologic diseases triggered by wheat can be fatal.)

"Wheat" is no longer wheat; it's the dwarf mutant that came from genetics research in the 1960s.
(Over 99% of all wheat today comes from the 18-inch tall dwarf mutant.)

Wheat increases blood sugar higher than nearly all other foods.
(Higher than Milky Way bars, higher than Snickers bars, higher than table sugar.)

There you have it: A full arsenal of one-liners to shoot at your husband, wife, or friend when they roll their eyes at your refusal to consume this thing called "wheat."

The happy homeotherm

24. November 2010 William Davis (14)

If you were a "cold blooded" poikilotherm unable to regulate internal body temperature, you would have to sun yourself on rocks to raise your body temperature, just like turtles and snakes. When it got cold, your metabolic rate would slow and you might burrow into the mud to hide.

You and I, however, are homeotherms, terrestrial animals able to regulate our own internal body temperature. Principal responsibility for keeping your body temperature regulated falls with the thyroid gland, your very own thermoregulatory "thermostat."

But internal body temperature, even in a homeotherm, varies with circadian rhythm: Highest temperature occurs in the early evening around 8 p.m.; the low temperature nadir occurs at around 4 a.m.

The notion that normal human temperature is 98.6 degrees Fahrenheit is a widely-held fiction, a legacy of the extraordinary experience of 19th century German physician, Carl Reinhold August Wunderlich, who claims to have measured temperatures of one million people using his crude, uncalibrated thermometer to obtain axillary (armpit) body temperatures.

Dr. Broda Barnes was a 20th century American proponent of using the nadir body temperature to gauge thyroid function. Like Wunderlich, Barnes also used axillary temperatures.

Modern temperature assessments have employed radiotransmitting thermistors that are swallowed, with temperatures tracked as the thermistor travels through the stomach, duodenum, small intestine, large intestine, rectum, then peek-a-boos back out. Such internal "core temperature" assessments have shown that:

--Axillary temperatures do not track with internal core temperatures very well, often veering off course due to external factors.
--Axillary temperatures are subject to ambient temperatures, such as room temperature, and are affected by clothing.
--Axillary temperatures are more susceptible to physical activity, e.g., increased with exercise or physical work.

Even right vs. left axillary temperatures have been shown to vary up to 2 degrees Fahrenheit.

Studies such as this demonstrate that normal oral temperature upon arising is around 97.2-97.3 degrees Fahrenheit. While we lack data correlating thyroid function with circadian temperature variation, the a.m. nadir does indeed, as Dr. Barnes originally suggested, seem to track thyroid status quite well: lower with hypothyroidism, higher with normal or hyperthyroidism.

I have been using 97.3 degrees F orally as the cutoff for confirming or uncovering thyroid dysfunction, particularly when symptoms or blood tests (TSH, free T3, free T4) are equivocal, a value that has held up well in the majority of cases. I find it helpful when, for instance, someone complains of cold hands and feet and has normal TSH (1.5 mIU/L or less in my view) but low free T3. An a.m. oral temperature of, say, 95.7 degrees F, suggests that there will be a favorable response to T3 supplementation. And it nearly always plays out that way.

Wouldn't it be interesting to know if there was insight into thyroid status provided by also examining the circadian behavior of temperature (e.g., height or timing of the peak)?

Statin buster?

19. November 2010 William Davis (20)

Merck recently reported preliminary results with its drug-in-development, anacetrapib.

After six months of treatment, participants showed:

LDL cholesterol was reduced from 81 mg/dl to 45 mg/dl in those taking anacetrapib, and from 82 mg/dl to 77 mg/dl in the placebo group.

HDL increased from 41 mg/dl to 101 mg/dl in the drug group, from 40 mg/dl to 46 mg/dl in those on placebo.

As you'd expect, the usual line-up of my colleagues gushed over the prospects of the drug, salivating over new speaking opportunities, handsomely-paid clinical "research" trials, and plenty of nice trips to exotic locales.

Anacetrapib is a cholesteryl-ester transfer protein inhibitor, or CETP inhibitor, much like its scrapped predecessor, torcetrapib . . . you know, the one that went down in flames in 2006 after 60% excess mortality occurred in people taking the drug compared to placebo. The hopes of many investors and Pfizer executives were dashed with torcetrapib's demise. The data on torcetrapib's lipid effects were as impressive as Merck's anacetrapib.

These drugs block the effects of the CETP enzyme, an enzyme with complex effects. Among CETP's effects: mediating the "heteroexchange" of triglycerides from triglyceride-rich VLDL particles that first emerge from the liver for cholesterol from LDL particles. This CETP-mediated process enriches LDL particles with triglycerides, which then make LDL a target for action by another enzyme, hepatic lipase, that removes triglycerides. This yields a several nanometer smaller LDL particle, now the number one most common cause of heart disease in the U.S., thanks to conventional advice to cut fat intake and increase consumption of "healthy whole grains."

With effects like this, anacetrapib, should it hold up under the scrutiny of FDA-required trials and not show the same mortality-increasing effects of torcetrapib, will be a huge blockbuster for Merck if release goes as scheduled in 2015. It will likely match or exceed sales of any statin drug. Statin drugs have achieved $27 billion annual sales, some of it deserved. Anacetrapib will likely handily match or exceed Lipitor's $12 billion annual revenue.

More than increasing HDL, CETP inhibition is really a strategy to reduce small LDL particles.

As with many drugs, there are natural means to achieve similar effects with none of the side-effects. In this case, similar effects to CETP inhibition, though with no risk of heightened mortality, is . . . elimination of wheat, in addition to an overall limitation of carbohydrate consumption. Not just low-carb, mind you, but wheat elimination on the background of low-carb. For instance, eliminate wheat products and limit daily carbohydrate intake to 50-100 grams per day, depending on your individual carbohydrate sensitivity, and small LDL drops 50-75%. HDL, too, will increase over time, not as vigorously as with a CETP inhibitor, but a healthy 20-30% increase, more with restoration of vitamin D.

Eliminating wheat and adjusting diet to ratchet down carbs is, of course, cheap, non-prescription, and can be self-administerd, criteria that leave the medical world indifferent. But it's a form of "CETP inhibition" that you can employ today with none of the worries of a new drug, especially one that might share effects with an agent with a dangerous track record.

All posts by william-davis

Fish oil: The natural triglyceride form is better

2. February 2011 William Davis (43)

If you have a choice, the triglyceride form of fish oil is preferable. The triglyceride form, i.e., 3 omega-3 fatty acids on a glycerol "backbone," is the form found in the body of fish that protects them from cold temperatures (i.e., they remain liquid at low ambient temperatures).

Most fish oils on the market are the ethyl ester form. This means that the omega-3 fatty acids have been removed from the glycerol backbone; the fatty acids are then reacted with ethanol to form the ethyl ester.

If the form is not specified on your fish oil bottle, it is likely ethyl ester, since the triglyceride form is more costly to process and most manufacturers therefore boast about it. Also, prescription Lovaza--nearly 20 times more costly than the most expensive fish oil triglyceride liquid on a milligram for milligram basis--is the ethyl ester form. That's not even factoring in reduced absorption of ethyl esters compared to triglyceride forms. Remember: FDA approval is not necessarily a stamp of superiority. It just means somebody had the money and ambition to pursue FDA approval. Period.

Taking any kind of fish oil, provided it is not overly oxidized (and thereby yields a smelly fish odor), is better than taking none at all. All fish oil will reduce triglycerides, accelerate clearance of postprandial (after-eating) lipoprotein byproducts of a meal (via activation of lipoprotein lipase), enhance endothelial responsiveness, reduce small LDL particles, and provide a physical stabilizing effect on atherosclerotic plaque.

But if you desire enhanced absorption and potentially lower dose to achieve equivalent RBC omega-3 levels, then triglyceride forms are better.

Here are cut-and-pasted abstracts of two of the studies comparing forms of fish oil.

Bioavailability of marine n-3 fatty acid formulations.

Dyerberg J, Madsen P, Moller JM et al.

Department of Human Nutrition, Faculty of Life Sciences, University of Copenhagen, Copenhagen, Denmark.

Abstract

The use of marine n-3 polyunsaturated fatty acids (n-3 PUFA) as supplements has prompted the development of concentrated formulations to overcome compliance problems. The present study compares three concentrated preparations - ethyl esters, free fatty acids and re-esterified triglycerides - with placebo oil in a double-blinded design, and with fish body oil and cod liver oil in single-blinded arms. Seventy-two volunteers were given approximately 3.3g of eicosapentaenoic acid (EPA) plus docosahexaenoic acid (DHA) daily for 2 weeks. Increases in absolute amounts of EPA and DHA in fasting serum triglycerides, cholesterol esters and phospholipids were examined. Bioavailability of EPA+DHA from re-esterified triglycerides was superior (124%) compared with natural fish oil, whereas the bioavailability from ethyl esters was inferior (73%). Free fatty acid bioavailability (91%) did not differ significantly from natural triglycerides. The stereochemistry of fatty acid in acylglycerols did not influence the bioavailability of EPA and DHA.

(Full text of the Dyerberg et al study made available at the Nordic Naturals website here.)

Eur J Clin Nutr 2010 Nov 10.

Enhanced increase of omega-3 index in response to long-term n-3 fatty acid supplementation from triacylglycerides versus ethyl esters.

Neubronner J, Schuchardt JP, Kressel G et al.

Institute of Food Science and Human Nutrition, Leibniz Universität Hannover, Am Kleinen Felde 30, Hannover, Germany.

Abstract

There is a debate currently about whether different chemical forms of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are absorbed in an identical way. The objective of this study was to investigate the response of the omega-3 index, the percentage of EPA+DHA in red blood cell membranes, to supplementation with two different omega-3 fatty acid (n-3 FA) formulations in humans. The study was conducted as a double-blinded placebo-controlled trial. A total of 150 volunteers was randomly assigned to one of the three groups: (1) fish oil concentrate with EPA+DHA (1.01?g+0.67?g) given as reesterified triacylglycerides (rTAG group); (2) corn oil (placebo group) or (3) fish oil concentrate with EPA+DHA (1.01?g+0.67?g) given as ethyl ester (EE group). Volunteers consumed four gelatine-coated soft capsules daily over a period of six months. The omega-3 index was determined at baseline (t(0)) after three months (t(3)) and at the end of the intervention period (t(6)). The omega-3 index increased significantly in both groups treated with n-3 FAs from baseline to t(3) and t(6) (P < 0.001). The omega-3 index increased to a greater extent in the rTAG group than in the EE group (t(3): 186 versus 161% (P < 0.001); t(6): 197 versus 171% (P < 0.01)). Conclusion: A six-month supplementation of identical doses of EPA+DHA led to a faster and higher increase in the omega-3 index when consumed as triacylglycerides than when consumed as ethyl esters.

Diarrhea, asthma, arthritis--What is your wheat re-exposure syndrome?

30. January 2011 William Davis (52)

Have you experienced a wheat re-exposure syndrome?

As I recently discussed, gastrointestinal distress--cramps, gas, diarrhea--is the most common "syndrome" that results from re-exposure to wheat after a period of elimination.

Others experience asthma, sinus congestion and infections, mental "fogginess" and difficulty concentrating, or joint pains and/or overt swelling.

Still others say there is no such thing.

Let's take a poll and find out what readers say.

Marathoners, triathletes, and heart disease

30. January 2011 William Davis (0)

Curious thing: People with lipoprotein(a) gravitate towards elite levels of exercise.

I tell my lipoprotein(a) patients that, if they want to see a lot of other people with lipoprotein(a), go to a marathon or triathlon.

This effect applies more to males than to females, just as the fascination with numbers seems to be confined to men, too. That's why I've posted in past about the "prototypical" lipoprotein(a) male.

I believe this is a big part, perhaps the only, reason why there seems to be a modest increased risk for cardiovascular events despite high exercise levels in marathoners. It has nothing to do with the exercise itself; it has to do with the kind of people who choose to exercise at this level.

The best fish oil

29. January 2011 William Davis (30)

The best fish oils available are the liquid forms. Contrary to many people's expectations, the best liquid fish oils have no fishy odor or taste.

I use a lot of liquid fish oils because of the higher doses we use in the Track Your Plaque program, as well as our strategy of high-dose fish oil to reduce lipoprotein(a). Women, in particular, don't like taking the oodles of capsules required to achieve the higher doses we need. So the ladies really like the liquid forms.

The best liquid fish oils are non-fishy, highly-concentrated, and come in the better absorbed triglyceride form. Many capsules, including prescription Lovaza, are the less well-absorbed ethyl ester form. Several studies, such as this one, have now demonstrated that the naturally-occurring triglyceride form yields higher blood (RBC) levels of omega-3 fatty acids, likely due to more efficient digestion via pancreatic lipase.

While there are many good forms of fish oil and only a few bad, these are the best of the best:

Pharmax
The Pharmax Finest Pure Fish Oil with Essential Oil of Orange contains 1800 mg EPA + DHA per teaspoon. This is the preparation I've been taking.

Nordic Naturals
The Nordic Naturals lemon-flavored ProOmega Liquid contains 2752 mg EPA + DHA per teaspoon, the most concentrated of any fish oil I've seen.

(This list is not exclusive. These are just two brands I've used extensively with good results.)

These highly-concentrated, triglyceride forms are more expensive, due to their concentrated nature. 1 teaspoon Pharmax fish oil, for example, provides an equivalent quantity of omega-3 fatty acids as 6 standard fish oil capsules on a milligram for milligram basis, but more like 8 to 9 capsules when absorption efficiency is factored in. The triglyceride form is also more laborious to manufacture. On our Track Your Plaque Marketplace, our Pharmax 500 ml runs $58.95 list. (500 ml provides 100 teaspoons or 600-capsule equivalent.)

Note that, minus the protection of the capsule, liquid fish oils will oxidize if not refrigerated. So be sure to keep your liquid fish oil in the fridge.

What do Salmonella, E coli, and bread have in common?

28. January 2011 William Davis (22)

Say you happen to eat some chicken fingers contaminated with bacteria because the 19-year old kid behind the counter failed to wash his hands after using the toilet, or because the kitchen is poorly managed with unwashed counters and cutting boards, or because the food is undercooked. You get a bout of diarrhea and cramps, along with a desire to banish chicken from your life.

Here's yet another odd wheat phenomenon: About 30% of people who eliminate wheat from their lives experience an acute food poisoning-like effect on re-exposure. You've been wheat-free for, say, 6 months. You've lost 25 lbs from your wheat belly, you've regained energy, joints feel better. You go to an office party where they're serving some really yummy looking bruschetta. Surely a couple won't hurt! Within a hour, you're getting that awful rumbling and unease that precede the explosion.

The majority of people who experience a wheat re-exposure syndrome will have diarrhea and cramps that can last from hours to days, similar to food poisoning. (Why? Why would a common food trigger a food poisoning-like effect? It happens too fast to attribute to inflammation.) Others experience asthma attacks, joint pains that last 48 hours to a week, mental fogginess, emotional distress, even rage (in males).

Wheat re-exposure in the susceptible provides a tidy demonstration of the effects of this peculiar product of genetic research. So if you are wheat-free but entertain an occasional indulgence, don't be surprised if you have to make a beeline to the toilet.

The world of intermediate carbohydrates

28. January 2011 William Davis (0)

There are clear-cut bad carbohydrates: wheat, oats, cornstarch, and sucrose. (Fructose, too, but in a class of bad all its own.)

Wheat: The worst. Not only does wheat flour increase blood sugar higher than nearly all other carbohydrates, it invites celiac disease, neurologic impairment, mental and emotional effects, addictive (i.e., exorphin) effects, asthma, irritable bowel syndrome, acid reflux, sleepiness, sleep disruption, arthritis . . . just to name a few.

Oats: Yeah, yeah, I know: "Lowers cholesterol." But nobody told you that oats, including slow-cooked oatmeal, causes blood sugar to skyrocket.

Cornstarch: Like wheat, cornstarch flagrantly increases blood sugar.It also stimulates appetite. That's why food manufacturers put it in everything from soups to frozen dinners.

Sucrose: Not only does sucrose create a desire for more food, it is also 50% fructose, the peculiar sugar that makes us fat, increases small LDL particles, increases triglycerides, slows the metabolism of other foods, encourages diabetes, and causes more glycation than any other sugar.

But there are a large world of "other" natural carbohydrates that don't fall into the really bad category. This includes starchy beans like black, kidney, and pinto; rices such as white, brown, and wild; potatoes, including white, red, sweet, and yams; and fruits. It includes "alternative" grains like quinoa, spelt, triticale, amaranth, and barley.

For lack of a better term, I call these "intermediate" carbohydrates. They are not as bad as wheat, etc., but nor are they good. They will still increase blood glucose, small LDL, triglycerides, etc., just not as much as the worst carbohydrates.

The difference is relative. Say we compare the one-hour blood glucose effects of 1 cup of wheat flour product vs. one cup of quinoa. Typical blood sugar after wheat product: 180 mg/dl. Typical blood sugar after quinoa: 160 mg/dl--better but still pretty bad.

Some people are so carb-sensitive that they should avoid even these so-called intermediate carbohydrates. Others can have small indulgences, e.g., 1/2 cup, and not generate high blood sugars.

Heroin, Oxycontin, and a whole wheat bagel

25. January 2011 William Davis (27)

For a substantial proportion of people who remove wheat from their diet, there is a distinct and unpleasant withdrawal syndrome. Here are the comments of Heart Scan Blog reader, Scott, from Texas:

Hello Dr. Davis,

I've been experimenting with diet, converging upon a Paleo type diet, but I keep running into problems. I have isolated the problem to cutting out wheat.

Sugar, rice, fruit, corn, potatoes, etc. are relatively ok to add or remove from the diet, but cutting out wheat in particular brings on a moderate headache with heavy fatigue all day long. This resembles the wheat withdrawal symptoms I found on your blog. As I write this, I'm on day 8 of wheat-free. I consume a fair variety of meat and veggies each day with a moderate amount of white rice for carbs. Perhaps a bowl of corn flakes with milk and half a bar of dark chocolate a day. I've learned from experience over the past 5 months or so that none of these foods affect the withdrawal. It's purely wheat.

My question is, what is the range of times for withdrawal symptoms that you've heard from different people? Has there been anyone who never recovered from the wheat withdrawal symptoms even after many months?

It's very tough to get work done like this, and even though my body and head feel much healthier in general, my sinuses have cleared, don't have to take a big nap after I eat, etc., I don't want to go down a path where this is the way things are going to be forever.

People who have never experienced wheat withdrawal pooh-pooh the effect. But, for about 30% of people, wheat withdrawal is a real, palpable, and sometimes incapacitating experience.

Beyond removing an exceptionally digestible carbohydrate that yields blood sugar rises higher than nearly any other known food (due to the unique amylopectin structure of wheat-derived carbohydrate), wheat withdrawal is a form of opiate withdrawal, somewhat like stopping heroin, Oxycontin, and other opiates. Stop eating whole wheat toast for breakfast, whole grain sandwiches for lunch, or whole grain pasta for dinner, and the flow of exorphins, i.e., exogenous morphine-like compounds, stops. You experience dysphoria (sadness, unhappiness), mental "fog," inability to concentrate, fatigue, and decreased capacity to exercise. It is milder than withdrawal from prescription opiates. Unlike withdrawal from more powerful opiates like heroine, there are, thankfully, no seizures or hallucinations. There are also no deaths.

In my experience, most people get through with wheat withdrawal in about 5 days. An occasional person will struggle for as long as 4 weeks. Thankfully for Scott, I've never seen it last longer than 4 weeks. (Interestingly, people who survive the withdrawal syndrome are often prone to a peculiar re-exposure phenomenon that I will discuss in future, i.e., they get sick upon re-exposure.)

The modern dwarf mutant variant of Triticum aestivum (that our USDA urges us to eat more of) contains greater proportions of gluten proteins compared to wheat pre-1970; glutens are the source of wheat-derived exorphins.

Incidentally, a drug company should be releasing a drug in the next year that will contain naltrexone, an oral opiate blocking drug, for a weight loss indication. They claim it is a blocker of the "mesolimbic reward system." I say it's a blocker of wheat exorphins.

The five most powerful heart disease prevention strategies

24. January 2011 William Davis (39)

You've seen such lists before: 5 steps to prevent heart disease or some such thing. These lists usually say things like "cut your saturated fat," eat a "balanced diet" (whatever the heck that means), exercise, and don't smoke.

I would offer a different list. You already know that smoking is a supremely idiotic habit, so I won't repeat that. Here are the 5 most important strategies I know of that help you prevent heart disease and heart attack:

1) Eliminate wheat from the diet--Provided you don't do something stupid, like allow M&M's, Coca Cola, and corn chips to dominate your diet, elimination of wheat is an enormously effective means to reduce small LDL particles, reduce triglycerides, increase HDL, reduce inflammatory measures like c-reactive protein, lose weight (inflammation-driving visceral fat), reduce blood sugar, and reduce blood pressure. I know of no other single dietary strategy that packs as much punch. This has become even more true over the past 20 years, ever since the dwarf variant of modern wheat has come to dominate.

2) Achieve a desirable 25-hydroxy vitamin D level--Contrary to the inane comments of the Institute of Medicine, vitamin D supplementation increases HDL, reduces small LDL, normalizes insulin and reduces blood sugar, reduces blood pressure, and exerts potent anti-inflammatory effects on c-reactive protein, matrix metalloproteinase, and other inflammmatory mediators. While we also have drugs that mimic some of these effects, vitamin D does so without side-effects.

3) Supplement omega-3 fatty acids from fish oil--Omega-3 fatty acids reduce triglycerides, accelerate postprandial (after-meal) clearance of lipoprotein byproducts like chylomicron remnants, and have a physical stabilizing effect on atherosclerotic plaque.

4) Normalize thyroid function--Start with obtaining sufficient iodine. Iodine is not optional; it is an essential trace mineral to maintain normal thyroid function, protect the thyroid from the hundreds of thyroid disrupters in our environment (e.g., perchlorates from fertilizer residues in produce), as well as other functions such as anti-bacterial effects. Thyroid dysfunction is epidemic; correction of subtle degrees of hypothyroidism reduces LDL, reduces triglycerides, reduces small LDL, facilitates weight loss, reduces blood pressure, normalizes endothelial responses, and reduces oxidized LDL particles.

5) Make exercise fun--Not just exercise for the sake of exercise, but physical activity or exercise for the sake of having a good time. It's the difference between resigning yourself to 30 minutes of torture and boredom on the treadmill versus engaging in an activity you enjoy and look forward to: go dancing, walk with a friend, organize a paintball tournament outdoors, Zumba class, plant a new garden, etc. It's a distinction that spells the difference between finding every excuse not to do it, compared to making time for it because you enjoy it.

Note what is not on the list: cut your fat, eat more "healthy whole grains," take a cholesterol drug, take aspirin. That's the list you'd follow if you feel your hospital needs your $100,000 contribution, otherwise known as coronary bypass surgery.

Topping up your vitamin D tank

22. January 2011 William Davis (17)

Now that my vitamin D replacement experience dates back nearly 5 years, I've been witnessing an unusual phenomenon:

The longer you take vitamin D, the less you need.

Let me explain. You take 10,000 units D3 in gelcap form. 25-hydroxy vitamin D levels, checked every 6 months, have remained consistently between 60 and 70 ng/ml. Three years into your vitamin D experience and 25-hydroxy vitamin D level rises to 98 ng/ml--an apparent need for less vitamin D.

So we cut your intake from 10,000 units per day to 8000 units per day. Another 25-hydroxy vitamin D level 6 months later: 94 ng/ml. We cut dose again to 6000 units, followed by another 25-hydroxy vitamin D level of 66 ng/ml.

This has now happened in approximately 20% of the people who have been taking vitamin D for 3 or more years. I know of no formal analysis of this effect, what I call the "topping up" phenomenon. Reasoned simply, it seems to me that, once your vitamin D "tank" is topped up (i.e., tissue stores have been replenished), it requires less to keep it full.

No one has experienced any adverse consequence of this topping up effect though it has potential for some people to develop toxic levels if 25-hydroxy vitamin D levels are not monitored long-term. In my office, I measure 25-hydroxy vitamin D levels every 6 months.

It means that long-term monitoring of 25-hydroxy vitamin D is crucial to maintain favorable and safe levels.

Thirteen catheterizations later

21. January 2011 William Davis (16)

When I first met her, Janet couldn't stop sobbing. She'd just been through her 10th heart catheterization in two years.

It started with chest pains at age 56, prompting her first heart catheterization that uncovered severe atherosclerotic blockages in all three coronary arteries. Her cardiologist advised a bypass operation.

Six months after the bypass operation, Janet was back with more chest pains, just as bad as before. Another heart catherization showed that two of the three bypass grafts had failed. The third bypass graft contained a severe blockage that required a stent, along with multiple stents in the two now unbypassed arteries.

In the ensuing 18 months, Janet returned for 8 additional catheterizations, each time leaving the hospital with one or more stents.

Janet's doctor was puzzled as to why her disease was progressing so aggressively despite Lipitor and the low-fat diet provided by the hospital dietitian. So he had Janet undergo lipoprotein testing (NMR):

LDL particle number: 3363 nmol/L
Small LDL particle number: 2865 nmol/L
HDL cholesterol: 32 mg/dl
Triglycerides: 344 mg/dl
Fasting blood glucose 118 mg/dl
HbA1c 5.8%

Unfortunately, Janet's doctor didn't understand what these values meant. He pretty much threw his arms up in frustration. That's when I met Janet.

From her lipoprotein panel and other values, it was clear to me that Janet was miserably carbohydrate-sensitive and carbohydrate-indulgent, as demonstrated by the extravagant quantity (2865 nmol/L) and proportion (2865/3363, or 85%) of small LDL, the form of LDL particles created by carbohydrate exposure. Janet struggled with depression over the years and had been using carbohydrate foods as "comfort" foods, often resorting to cookies, pies, cakes, breads, and other wheat-containing foods for emotional solace.

It took a bit of persuasion to convince Janet that it was low-fat, "healthy whole grains," as well as comfort foods, that had led her down this path. I also helped Janet correct her severe vitamin D deficiency, mild thyroid dysfunction, and lack of omega-3 fatty acids.

Since meeting Janet and instituting her new prevention program, she has undergone three additional catheterizations (performed by another cardiologist), all performed for chest pain symptoms that struck during periods of emotional stress. All showed . . . no significant blockage. (Apparently, the repeated "need" for stents triggered a Pavlovian response: chest pain = "need" for yet more stents.)

In short, correction of the causes of coronary atherosclerotic plaque--small LDL, vitamin D deficiency, omega-3 fatty acid deficiency, and thyroid dysfunction--and Janet's disease essentially ground to a halt.

Imagine, instead, that Janet had undergone 1) a heart scan to identify hidden coronary plaque 5-10 years before her first heart procedure, then 2) corrected the causes before they triggered symptoms and posed danger. She might have been spared an extraordinary amount of life crises, hospital procedures, expense (nearly $1 million), and emotional suffering.