More on being wheat-free

Reducing or even eliminating the wheat in your diet can dramatically enhance the phenomenon of insulin resistance.

Insulin resistance is the evil process that lies behind low HDL, high triglycerides, small LDL particles, and VLDL and IDL. It’s also the process that makes us tired after meals, heightens inflammation that raises your risk of heart disease, stroke, diabetes, and caner. Insulin resistance is the culprit behind the bulge hanging over some 100,000,000 American belts.

Show me a person with a protruding abdomen and I’ll show you a bread lover, or some other form of wheat.

Why do I pick on wheat so much? Many of you among the more nutrition-minded would point out that wheat is just one group of food items among many other high-glycemic index foods, i.e., foods that yield a vigorous surge in blood sugar (glucose), followed by a sharp decline. Wheat enjoys the high-glycemic index company of corn, rice (white and brown), potatoes, among others.

I pick on wheat because, for most Americans, wheat is 90% of the high-glycemic index problem. (I’m assuming you’ve at least eliminated or dramatically reduced highly-processed sweets like candy, cookies, soft drinks, cakes, etc. That’s a no-brainer.) It’s not uncommon to have a wheat-based product with every meal, a wheat-based snack, 7 days a week. But few people have corn products (i.e., corn starch products) three times a day. Or rice three times a day.

Wheat has traded places with saturated fat sources as the chief scourge of diet. In 1985, we had dinners of spare ribs, cheeseburgers, French fries, and butter on our mashed potatoes. Hardly anybody eats that like anymore, at least amongst the web-savvy set.

Wheat has assumed the previous exalted role as chief scourge as a consequence of the low-fat consciousness of the 80s and 90s. It has since ballooned in importance in diet and, as a result, skyrocketed as a cause of obesity, insulin resistance, and coronary plaque growth.

What if you're already slender and have none of the above issues, especially small LDL particles? Then don't sweat the wheat issue.

Note: My comments on being wheat-free should not be confused with gluten sensitivity or celiac disease. These are allergies to wheat gluten that, if undiagnosed, wreak havoc on health to extremes. This phenomenon is separate and distinct from the far more prevalent issue I’m discussing.

Can you break the “Rule of 60”

In the Track Your Plaque program, we aim for conventional lipid values (LDL cholesterol, HDL cholesterol, and triglycerides) of 60—60—60, i.e., LDL 60 mg/dl, HDL 60 mg/dl or greater, triglycerides 60 mg/dl. Most participants do indeed reach these target values.

When I tell this to colleagues, they’re stunned. “You can’t possibly get those numbers in most people.” And I can sympathize with their plight. After all, they are stuck with relatively lame tools: statin drugs, the American Heart Association diet. I’d be surprised if they ever achieved 60—60—60.

But can you drop your heart scan score even if you don’t reach the 60—60—60 targets? Yes, you can. The Rule of 60 is only a guideline, a tool that helps more people achieve our goals. The Rule of 60 does not guarantee reversal (drop in heart scan score), nor does not achieving the targets completely destroy your chances.

We have had many people drop their scores even if they haven’t reached the targets. On the other hand, we’ve also had people who failed at first, only to see success once they achieved the 60 mg/dl targets.

But which one are you? That’s the problem. We possess limited capacity to predict who will or who will not drop their scores from the start. We know that there are factors that stack the odds in your favor (e.g., optimism, lack of Lp(a), ideal weight, vitamin D >50 ng/ml, etc.). We know that there are factors that make it tougher (overweight, Lp(a), pessimistic attitude, underappreciated hypertension, higher heart scan scores, etc.) But at the start, we just don’t know who truly needs to adhere to the Rule of 60. So we suggest that everyone, at least in the beginning, aim to achieve it.

I had an exception the other day. Rich did everything by the Track Your Plaque book. However, a starting low HDL of 27 only rose to 37 after one year of effort—way below our 60 mg/dl target. Yet a repeat heart scan showed 23% reduction.

Why would Rich be so successful despite a persistently very low HDL? There may be a number of reasons. One explanation could be that conventional measures of HDL fail to distinguish between what HDLs truly work and what do not. Look at ApoA1 Milano; remember this story? The people in the secluded mountain village of Limone-Sul-Garde in northern Italy have HDL cholesterols of 8-15 mg/dl yet do not experience excess vascular atherosclerosis, suggesting that what little HDL they have is super-effective.

Yes, large HDL seem to be more healthy and effective than small HDL, but perhaps there’s more to it. However, nobody has a HDL effectiveness test ready for us to use.

In the meantime, we continue to suggest that the Track Your Plaque Rule of 60 be considered as a means of making plaque reversal as likely as possible. You and your doctor can always adjust in future, depending on your heart scan score results.

Non-profit hospitals

Hospitals hide behind a veil of non-profit.

Ostensibly operating for the public good, most hospitals enjoy all the business advantages of non-profit status. This means that any profits that flow to the bottom line at the end of the year are not subject to tax. Hospitals point out that profit margins are modest, often ranging from 2-6%.

What they don’t tell you is that, regardless of non-profit status, lots of money can be paid out along the way. A hospital CEO who pays himself $4 million dollars a year can work for this non-profit organization. He can also direct the hospital in business expansion: pharmacies, extended-care facilities, medicine and medical supply distributorships. Your friendly hospital CEO, as well as his many administrators, can hold positions in hospital subsidiaries, complete with salaries and perks.

Yes, most hospitals are officially non-profit. But that’s a designation for tax purposes. It does not mean that hospitals are non-lucrative.

I believe that it’s time for hospitals to drop the façade of “Saint” in their names or other religious names—Methodist, Baptist, Jewish, All Saints’. More accurate would be something like “ABC Medical Enterprises, Inc.” That way, the public would be quicker to recognize that they are dealing with a business run by people eager to make more money.

Wheat five times a day

Terri couldn't understand why her weight wouldn't drop.

At 5'3", 208 lbs., she had the typical mid-abdominal excess weight that went with small LDL, low HDL, high triglycerides, a post-prandial (after-eating) fat clearance disorder, high blood sugar, increased c-reactive protein, and high blood pressure.

She claimed to have tried every diet and all had failed. So we reviewed her current "strict" diet:

"For breakfast, I had Shredded Wheat cereal in skim milk. No sugar, just some cinnamon and a little Splenda. For lunch, I had low-fat turkey breast sandwich--no mayonnaise--on whole wheat bread. For snacks, I had pretzels between breakfast and lunch, and a whole wheat bagel with nothing on it before dinner. For dinner, we had whole wheat pasta with tomato sauce and a salad. While we watched TV, I did have a couple of whole wheat crackers.

"I don't get it. I didn't butter anything, I didn't sneak any sweets, cakes, I didn't even touch cookies. And I love cookies!"

Did you see the pattern? I pointed out to Terri that what she was doing, in effect, was eating sugar 5 or more times a day. Many of her meals, of course, contained no sugar. All were low fat. But the excessive wheat content yielded quick conversion to sugar--glucose--immediately after ingestion.

Repeated surges of blood sugar like this trigger the excessive insulin response that yields low HDL, higher triglycerides, small LDL, etc., everything that Terri had.

Terri was skeptical when I suggested that she attempt an "experiment": Try a four week period of being entirely wheat-free. This meant more raw nuts and seeds, more lean proteins like low-fat yogurt and cottage cheese, chicken, fish, lean red meats, more vegetables and fruits.

After only two weeks, Terri dropped 5 1/2 lbs. She also reported that the mood swings she had suffered, afternoon sleepiness, and uncontrollable hunger pangs had all disappeared. The mental cloudiness that she had experienced chronically for years had lifted.

What happened was that the load of sugar from wheat products, followed by an insulin surge then a precipitous drop in sugar, and finally fogginess, irritability, and cravings for food all disappeared. With it, the entire panel of downstream phenomena (small LDL, CRP, etc.) all faded.

Though she started out intending to complete a four week trial, I believe that, having seen the light, she will continue to be wheat-free, or nearly so, for a lifetime.

The battle for natural hormones

The battle for preservation of availability of compounded natural hormones goes on.

It started with pharmaceutical manufacturer, Wyeth, who petitioned the FDA to disallow the mixing of pharmaceuticals, especially natural human hormones, by specially trained pharmacists at what are called "compounding pharmacies." These are pharmacies that have special equipment and where trained pharmacists can mix up specific preparations for dispensing. These are available by prescription.

For instance, I have been prescribing natural human testosterone and progesterone for nearly 10 years. I have found service to be excellent, with lots of learning materials provided to patients by the pharmacy. The pharmacists I've spoken to have been courteous and knowledgeable. Compounded hormones are also shockingly less expensive. While a testosterone patch from a pharmaceutical company costs around $4.00 per day, the same quantity of testosterone cream formulated by a compouding pharmacy costs around $0.50 per day--87.5% less.

Wyeth hides behind a smoke screen of concern over quality. But the price differences tells the entire story: they want to eliminate the inexpensive competition and hold us all hostage to the far more expensive, often inferior products that they produce. They'd sooner force a woman to use horse-derived Premarin than to allow her access to human estrogens and progesterone.

To me, this is an outrageous affront to our freedom of choice, both as consumers as well as a physician. If you feel as strongly as I do about opposing the unfair and bullying ways of Wyeth Pharmaceuticals and the FDA, the P2C2 association of compounding pharmacists makes writing a letter to your Senator easy by going to

http://iacprx.convio.net/site/PageServer?pagename=P2C2

Just enter your info and personalize the comments, and the e-mails will be generated for you.

Lipitor and memory

At first, I was skeptical. A book from a nutty author and physician named Duane Graveline kept on coming up in conversations with patients. His book, Lipitor: Thief of Memory , details his personal experience with dramatic changes in memory and thought while taking Lipitor.



Now this is a drug that I've seen used thousands of times. But I've now seen about a dozen people who have had distinct struggles with memory and clarity of thinking while taking Lipitor. Most took doses of 40 mg per day or more, though an occasional person takes as little as 10 mg. The association seems to be undeniable, since it improves after two weeks off the drug, recurs when resumed. Just today, I saw two people where this effect may be an issue.

Curiously, I've not seen it with any other statin agent. Unfortunately, uncovering any scientific data on the issue is a hopeless quest. Either it's very uncommon or, worse, the data has been suppressed.

Any way, I believe that Dr. Graveline was right: Lipitor, in a small number of people, does indeed seem to exert real detrimental effects on the mind.

If you take Lipitor, should you stop it in fear of long-term effects on your mental capacity? I think it's premature to toss the drug out based on this relatively uncommon relationship. This particular effect is likely to be idiosyncratic, i.e., peculiar to an occasional person but does not seem to apply to the majority, probably by some quirk of metabolism or penetrability of the barrier between the blood and nervous system tissue.

If, however, you feel that your thinking and memory have deteriorated on the drug, please speak to your doctor.

EKG's and heart disease


How helpful are EKG's for detecting hidden heart disease?

I pose this question because several patients asked this question just this week. It's also a frequent point of confusion and misperception.

Your EKG is nothing more than an expression of the surface electrical activity emitted by heart muscle activity. Multiple (12) leads are attached to the body simply to provide various "views" of this electical activity. EKG, or sometimes "ECG", is short for "electrocardiogram".

What modifies this surface electrical activity? Anything that modifies the electrical activity within the heart itself, or interferes with the detection of the activity. An old heart attack modifies the patterns of electrical conduction in the heart and that can change your EKG. An ongoing heart heart attack likewise. High blood pressure commonly creates changes in the EKG, as does lung disease. A bellyache can change your EKG, as can a stroke. (These non-heart-related phenomena probably are often due to changes in autonomic, or "automatic," nervous system activity.) The heart generates electrical activity in a predictable sequence that generates the heart beat, or "rhythm". EKG's are useful for monitoring heart rhythm, also.

Does having plaque in your coronary arteries have any effect on the EKG? None whatsoever, unless plaque rupture caused heart attack or is about to cause heart attack. So, you can have a horrendous CT heart scan score of, say, 3000, yet maintain a perfectly normal EKG, as long as the heart muscle is normal.

Then why bother with these iffy tests? They are indeed useful to diagnose the cause of active symptoms. For instance, go to the ER with chest pain and an EKG could show changes suggesting that the chest pain is a heart attack. EKG's are also useful for future comparison. Any change in EKG can suggest certain things, like new heart rhythm disturbances unrelated to coronary plaque.

Think of your EKG as just like buying a used car. Say I'm trying to sell you my 1999 Buick Century. It looks pretty good from the outside and I tell you that it has 70,000 miles and runs well. You ask to open the hood, look in the interior and take it out for a drive. I tell you no, you can't do that.

Would you buy the car? Of course you wouldn't. You were permitted only a very superficial examination of the car. You have no idea what's going on inside. Just because the paint job looks brand new doesn't mean the engine and transmission are good.

The same with your EKG: It's a superficial look at one aspect of this used car called your heart. If the EKG is normal, that's good, just like a good exterior on the Buick. But you cannot assume that the heart is otherwise normal.

View the EKG as a simple, superficial test that can only provide minimal reassurance, no matter how often you have it done.

A new Track Your Plaque record

Neal, a 40-year old school principal, and his young wife were terrified on learning of his CT heart scan score of 339, a concerningly high score for any age, particularly age 40.

To make matters worse, all of Neal's plaque was located in the critical left mainstem coronary artery, the shared stem of two of the three coronary arteries. A heart attack in this location is instantly fatal.

So, it was especially gratifying that Neal has set the Track Your Plaque record for largest magnitude of plaque reversal: 51% in his first year.

Studies that show a reduction in heart attack make the news. They talk about 1, 2, up to 6% regression, all achieved with high doses of statin drugs. Yet we are seeing huge, extraordinary quantities of heart disease reversal that haven't yet made headlines, amounts that far exceed those featured in the news. We should be encouraged by experiences like Neal's.

Watch for the upcoming Track Your Plaque newsletter for more details on Neal's story--how he came to the program, how he accomplished this huge effect, and why his experience was such a success. If you haven't yet subscribed, go to the www.cureality.com homepage and click on the upper right hand corner.

The Plavix Scam

Periodically, I'll see a flurry of TV ads for Plavix. It comes with a polished computer-animated cartoon that shows how platelets clump and form a blood clot, causing heart attack.

Imagine there's a pile of oil-soaked rags in a corner of your garage. I come by and tell you to get a good fire extinguisher to keep next to the rag pile in case they spontaneously ignite.

Does that make sense to you?

Wouldn't it be better to get rid of the oily rags and forget about the fire extinguisher?

Plavix is the fire extinguisher. The oil rags are your coronary plaque. The solution is to gain control over plaque behavior. Unfortunately, the TV ads (intentionally, I suspect) give the impression that blood clots just form out of the blue for no reason. Of course that's not true. It requires active, growing, inflamed atheroslcerotic plaque that ruptures, uncovering the "angry" and platelet-adhering material underneath the thin covering or endothelial lining.

Urging everybody to take Plavix is absurd. The TV ads urge many people who have no business taking the drug to take it. There are, without a doubt, groups of people who are better off taking Plavix and aspirin: people who are in the midst of heart attack, people who have unstable plaque, people with recent stents or bypass. Perhaps people at high risk for plaque rupture, e.g., extensive coronary plaque that has continued to grow.

These tactics are consistent with the experiences I've had with the sales representatives from the company (when I used to actually talk to sales reps; my office is now barred from them). The reps very aggressively would urge me to consider having everyone take Plavix. No kidding.


For us, i.e., for people who just have a heart scan score but interested in engaging in a powerful program of prevention and reversal, Plavix rarely provides any advantage. The answer is, just like our oily rag analogy, control the plaque, not put out the fire.

Lipoprotein(a) and small LDL

You won't find a lot of scientific validation for this, but it is my firm impression that small LDL, by some crazy means, has the capacity to "turn on" or "turn off" lipoprotein(a), Lp(a).

Recall that Lp(a) is a specific genetic trait, passed to us (if you have it) by mother or father. It falsely elevates LDL cholesterol and escalates heart disease risk more than just about any other known abnormality.

A frequent hint that Lp(a) might be present is a comment I hear often from patients: "My doctor said statin cholesterol drugs don't work for me. I tried them all and my cholesterol won't go down." Or, the result was substantially less than expected. That's because, when Lp(a) is lurking in your cholesterol value, it is unaffected by the statins.

It's been my in-the-trenches observation that, the more fully expressed the small LDL pattern becomes, the worse the Lp(a) behaves. In other words, if small LDL is suppressed effectively, Lp(a) doesn't seem to carry the same dangers as in someone who has plenty of small LDL. I don't know why this is. (I expect that the answer will come from someone like Dr. Marcovina at Stanford, who is at the forefront of Lp(a) structural research. Lp(a) is a complex molecule with several components. How and why it interacts with other particles remains a mystery.)

There are a little bit of data to confirm this. The Quebec Cardiovascular Study has presented some data to this effect, that the combination of small LDL particles and Lp(a) are a particularly lethal combination. We are trying to correlate our data from a CT heart score perspective to discern any statistical relationships.

This raises a very important therapeutic issue if you have Lp(a): the worst thing you can do if you have Lp(a) is become overweight. Excess abdominal fat is a huge trigger to create small LDL particles. Even though being overweight itself has no effect on the measured level of Lp(a), it activates small LDL which, in turn, throws gasoline on the Lp(a) fire.

If you have Lp(a), stay skinny.

What's that in your mouth?




Fat = triglycerides

In other words, eat fat, whether it's saturated, hydrogenated, polyunsaturated, or monounsaturated, and blood levels of triglycerides will go up over the next 6 hours. This remains true if there are carbohydrates in the meal, or if there are NO carbohydrates in the meal. It also remains true if you chronically consume fats.

While fats are the primary determinant of postprandial (after-eating) triglycerides, carbohydrates are the primary determinant of fasting triglycerides.

So, if your triglycerides are high on a fasting cholesterol (lipid) panel, it's most likely because you overconsume carbohydrates.


Thanks to cartoonist Eli Stein, who has generously allowed me to reprint his artwork on these pages. Mr. Stein has published his work in dozens of magazines and newspapers, including the Wall Street Journal, Barron's, and Good Housekeeping. More of his work can be found at Eli Stein Cartoons.

De Novo Lipo-what?

Humans have limited capacity to store carbohydrates. Beyond the glucose and glycogen in our blood and tissues, we have relatively little carbohydrate to draw from in time of energy need. That's why long-distance runners and triathletes have to carry sugar sources to keep blood sugar from plummeting.

Fat, of course, is different. We have virtually unlimited capacity to store energy as fat.

Because we have limited carbohydrate storage capacity, what can the body do with the excessive quantities of carbohydrates that Americans ingest? What becomes of a bagel for breakfast, wheat crackers for snacks, a whole wheat sandwich for lunch, pretzels, and whole wheat pasta that many people eat every day, not to mention the chips, soft drinks, and juices?

Excess carbohydrates are diverted to an interesting metabolic pathway called de novo lipogenesis (DNL). This refers to the liver's ability to make triglycerides from excessive carbohydrates in the diet. Triglycerides are packaged for release into the blood as VLDL. VLDL, in turn, interacts with other lipoproteins, creating small LDL particles, reduced HDL and smaller, less protective HDL. High VLDL will be measured on a standard cholesterol panel as higher triglycerides.

A University of California (Berkeley, San Francisco) group has done much of the work describing DNL.

A diet weighed towards carbohydrates, especially if 50% or greater calories are carbohydrate, is sufficient to provoke plenty of DNL, even in slender people. DNL is a big part of the reason why low-fat (and, thereby, high-carbohydrate) diets result in higher triglycerides. DNL really gets turned on many-fold if the carbohydrates are "simple," rather than "complex."

Overweight people, however, can demonstrate five-fold greater DNL even with lesser quantities of carbohydrate intake (e.g., 40% fat, 46% carbohydrate, 14% protein):





From Schwarz et al 2003. Mean (± SEM) fractional de novo lipogenesis in lean normoinsulinemic (NI), obese NI, and obese hyperinsulinemic (HI) subjects after 5 d of consuming a high-fat, low-carbohydrate diet and in different lean NI and obese HI subjects after 5 d of consuming a low-fat, high-carbohydrate diet. Values with different superscript letters are significantly different.


Excessive carbohydrates, a la standard low-fat diets, are good for nobody. The concept of de novo lipogenesis fills in a theoretical hole that now explains why people who eat carbohydrates have higher triglycerides, VLDL, and, eventually, insulin resistance and diabetes.

Gretchen's postprandial diet experiment II

I previously posted Gretchen's postprandial diet experiment, in which she consumed a low-fat diet for a day, followed by a low-carbohydrate diet for a day. Grethen monitored blood glucose and triglycerides with fingerstick checks. (Blood glucose can be checked on any widely available glucose monitor; triglycerides can be monitored with the Cardiochek device.)

Let's now discuss what happened.

On the low-carb, high-fat day, there was an initial surge in triglycerides to 250 mg/dl late morning, followed by a secondary peak several hours following dinner. Because fat is mostly triglycerides, Gretchen's high-fat (sausage, bacon, butter, whole-fat yogurt) breakfast provided a large quantity of triglycerides that needed to be absorbed. This generally occurs over approximately 6 hours, varying depending on body weight, how accustomed you are to fat, activity level during the day, the kind of fat in the meal. The high content of saturated fat in Gretchen's high-fat breakfast likely caused the somewhat slower drop in triglycerides over approximately 7 1/2 hours.

As Gretchen herself had noted, triglycerides the following day were lower, a typical low-carb response. Blood sugar throughout showed only minor variation, with only small postprandial increases.

Thus, Gretchen experienced what we'd expect with a low-carb, high-fat diet: an initial high surge in triglycerides, followed by a decline in fasting levels, while blood sugar shows a normal contour.







Now, the more confusing low-fat experience:



Blood glucose makes a striking peak at 200 mg/dl after the low-fat breakfast of pasta and rice, in contrast to the low-carb breakfast. Triglycerides behaved very differently from the low-carb experiment: While there was no initial postprandial surge, there was a late surge developing 6-24 hours later. The late surge continued into the next day, with fasting levels the following morning (210 mg/dl) exceeding the starting triglyceride level (60 mg/dl).

The one potentially confusing aspect of all this is Gretchen's late rise in triglycerides on the low-fat diet. This phenomenon is due to something called de novo lipogenesis, or the liver's conversion of carbohydrates to triglycerides that occurs when an excessive carbohydrate load comes through diet. Because the human body cannot store anything beyond a minor quantity of carbohydrates (as glucose and glycogen), carbohydrates are converted to fats.

Another factor causing the late triglyceride increase is insulin resistance, given the high blood sugar response. When insulin resistance is present, the activity of the enzyme, lipoprotein lipase, is reduced. Less lipoprotein lipase activity allows slower VLDL degradation, allowing VLDL (and thereby triglycerides contained in VLDL) to "stack up" in the blood. Thus, the higher triglycerides late after eating and into the next morning.

One issue to be aware of: Acute responses can differ from chronic responses. In other words, had Gretchen had the luxury (and time and money) to conduct the experiment over, say, 4 weeks, rather than a single day, there would be somewhat different responses. The best data on this come from Dr. Jeff Volek of the University of Connecticut, in which 4 weeks of low-carbohydrate eating modify fasting and postprandial responses over time.

Several conclusions can be made from Gretchen's experience:

1) Low-carb, high-fat acutely generates extravagant postprandial triglyceride responses.
2) Low-fat causes a late triglyceride surge and higher fasting triglycerides.
3) Low-fat leads to high blood sugars and, by implication, diabetes.


Both the low-carb and the low-fat responses are undesirable, both leading to increased risk for heart disease. Which is worse? I believe that low-fat is more destructive, since it leads over time to both high triglycerides and diabetes, while low-carb/high-fat only leads to postprandial triglyceride surges, at least acutely.

How to best balance the responses to reduce risk for heart disease? That's a discussion for future.


Again, my thanks to Gretchen and the substantial amount of effort that went into generating these numbers. More of Gretchens' own writing can be found on her blogs:
http://wildlyfluctuating.blogspot.com
http://www.healthcentral.com/diabetes/c/5068

A wheat-free 2010

A Heart Scan Blog reader sent this fascinating description of his wheat-free adventure.

Whenever I discuss this notion of going wheat-free and the incredible health effects that develop, I invariably receive comments or emails saying something like "I eat wheat and feel fine. That can't be true." The problem is that not everybody needs to go wheat-free. 20-30% of people can include wheat in their diet and suffer little more than weight gain, some not at all.

But stories like Michael's (below) are commonplace in my experience. I've had many patients who, at first, refused to believe that wheat exposure might be the underlying cause for health struggles. But they finally give it a try and find that rashes, arthritis, acid reflux, irritable bowel symptoms, mood swings, anger, etc. are miraculously improved or gone.

Anyway, hear what Michael has to tell us:


Dr. Davis,

I want to thank you. I was browsing the web a while back and happened to stumble upon your blog post about wheat belly. The first thing that caught my attention was that I thought you had somehow gotten a photograph of me. The young man you posted an image of looked exactly like me. So I read what you had to say. After reading, I thought "Four weeks isn’t so bad. I think I can handle this."

It has now been nine weeks and all I can say is that I am completely amazed. Let me say first that twice in the past twenty years I have been tested for allergies. The first time I was tested I showed a slight reaction to Timothy Grass, but not enough to cause me any problems. The second testing I did not show a reaction to anything. So, I have always assumed that my chronic sinus problem were due to sensitivities to environmental pollutions. Now I am not so sure. I would like to list for you everything that has happened to me since I eliminated wheat from my diet.

1. I have lost a total of 12 pounds in the last 9 weeks.
2. I have lost 1 ¼ inches of belly fat
3. I have lost a tremendous amount of fat from my neck.
4. My entire life I have had problems with oily hair. I could wash my hair and three hours later I looked as if I hadn’t washed in a week. Now my hair stays clean and soft for two to three days without shampoo.
5. My hair was always flat and stringy. Now it has lots of body.
6. I used to have thick layers of dry skin on my scalp. It would come loose in chunks as large as a fingernail. That dry scalp is gone.
7. I used to have dry flaky skin that seemed to secrete oil. That no longer happens. My skin is now soft and smooth.
8. I have lived with bad acne for at least 35 years. Now it is hard to find a pimple on my body.
9. I have always had to fight dehydration. That is no longer a problem.
10. I used to drink two large cups of coffee every morning just to be able to function. I now have enough energy that I have eliminated caffeine from my diet.
11. I sleep more soundly than ever before and my dreams are clear and vivid.
12. My thought processes are more active and clear than they have ever been.
13. My chronic sinus issue is now a thing of the past.
14. I used to have problems with getting the “shakes” if I had gone more than a couple of hours without eating. It was as if I was suffering from low blood sugar. I would even be afraid that I would pass out. Now all I feel is hunger. I can go all day without eating and never feel in danger of losing consciousness.


Today is Thursday. This past Monday my wife and I were eating out and I ordered a burger without a bun. What I didn’t realize was that the burger would arrive covered in onion rings. I knocked the mountain of onion rings onto the plate but there were still a couple that were embedded in the cheese. I decided, what the hell, a couple of onion rings shouldn’t make that much of a difference. I will not make that mistake again anytime soon. Within 30 minutes I felt like there was a steel spike going through my left eye socket. I don’t remember ever being in that much pain. My sinuses were exploding. This morning, as I write this, I still feel the vestiges of that pain. Just enough that I know it is there. But after two and a half days, I am at least able to function again.

I owe you a debt of gratitude. You may have just saved my life. In the very least you have given me the means to improve my life in ways that I never thought possible.

Thank you so much,
Michael B.



Now, if wheat exposure can do that in Michael, what damage can it do in other people?

Personally, I previously experienced many of the same symptoms that Michael suffered, all gone with wheat elimination.

My advice: If you have any inkling that you might have a wheat sensitivity, make a New Year's resolution to stay wheat-free for 4 weeks and see whether you can feel any difference. Not everybody will, but many will be telling us about the dramatic health turnarounds they experienced.

Lipoprotein lipase and you

Lipoprotein lipase can make the difference between having heart disease and not having it. Having sky-high triglycerides or normal triglycerides. It can mean dinner hanging around for over 12 hours in the bloodstream, rather than the usual 4-6 hours.

If you take niacin, you must exercise

We use a lot of niacin in the Track Your Plaque program.

Niacin:

--Increases HDL and shifts HDL towards the large, protective fraction

--Reduces small LDL--In fact, niacin is the best treatment we have to reduce small LDL after wheat elimination and carbohydrate reduction.

--Reduces fasting and postprandial (after-eating) triglycerides

--Reduces heart attack risk by 20-28%--even as a sole agent.


But . . . niacin also triggers higher blood sugar because it partially blocks the effects of insulin (insulin "resistance").

While the net effect of niacin remains positive, the provocation of insulin resistance is not such a good thing. Can it be minimized or eliminated?

Yes, through exercise. Here's one interesting observation in obese (BMI 34.0), sedentary men given placebo, exercise, niacin (1500 mg Niaspan, once per day), or niacin + exercise:





From Plaisance et al 2008.

Blood was drawn following a high-fat meal challenge. (Yes, a high-fat challenge, not a carbohydrate challenge. In this study, there were only 17 grams carbohydrates in the test meal, but 100 grams fat. More on this in future.) Exercise consisted of walking for 50 minutes at a moderate pace one hour prior to the meal challenge.

You can see from the graph that exercise partially corrected the increased insulin level provoked by niacin.

Judging from this and other studies, exercise can help minimize the insulin-blocking effects of niacin. It doesn't take much, just moderate exercise for at least 30 minutes.

Adequate sleep can also help, since sleep deprivation is a potent trigger for insulin resistance, only worsened in the presence of niacin. Vitamin D supplementation to achieve desirable blood levels (which I define as 60-70 ng/ml) is also an effective means to minimize this effect.

To track small LDL, track blood sugar

Here's a trick I learned after years of fussing over people's small LDL.

To gain better control over small LDL, follow blood sugars (blood glucose).

When you think about it, all the foods that trigger increases in blood sugar also trigger small LDL. Carbohydrates, in general, are the most potent triggers of small LDL. The most offensive among the carbohydrates: foods made with wheat. After wheat, there's foods made with cornstarch, sucrose (table sugar), and the broad categories of "other" carbohydrates, such as oats, barley, quinoa, sorghum, bulghur, etc.

Assessing small LDL requires a full lipoprotein assessment in which small LDL particles are measured (NMR, VAP, GGE). Not the easiest thing to do in the comfort of your kitchen.

However, you can easily and now cheaply check your blood sugar. Because blood sugar parallels small LDL, checking blood sugar can provide insight into how you respond to various foods and know whether glucose/small LDL have been triggered.

Here's how I suggest patients to do it:

1) Purchase an inexpensive blood glucose monitor at a discounter like Walmart or Walgreen's. You can buy them now for about $10. They're even sometimes free with promotional offers. You will also need to purchase lancets and test strips.

2) With a meal in question, check a blood sugar just prior to the meal, then again 60 minutes after finishing the meal. Say, for example, your pre-meal blood sugar is 102 mg/dl. You eat your meal, check it 60 minutes after finishing. Ideally, the postprandial (after-meal) blood sugar is no more than 102 mg/dl, i.e., no higher than pre-meal.

Perhaps you're skeptical that oatmeal in skim milk with walnuts and raisins will do any damage. So you perform this routine with your breakfast. Blood sugar beforehand: 100 mg/dl. Blood sugar 1 hour post: 163 mg/dl--Uh oh, not good for you. And small LDL will be triggered.

This approach is not perfect. It will not, for example, identify "stealth" triggers of blood sugar and small LDL like pasta, for the same reasons that pasta has a misleadingly low glycemic index: sugars are released slowly and not fully evident with the one-hour blood sugar.

Nonetheless, for most foods and meals, tracking your one-hour postprandial blood sugar can provide important insight into your individual susceptibility to sugar and small LDL-triggering effects.

C-reactive protein: Fiction from the drug industry?

C-reactive protein (CRP) is the liver product of inflammatory responses anywhere in the body. If there's an inflamed left knee, CRP will be increased. If viral bronchitis is making you cough, then CRP will be increased.

The argument put forward by the drug industry is that, because CRP indicates underlying inflammation, very low-grade levels that can be measured in the absence of overt inflammation like the sore knee or bronchitis is associated with increased risk for cardiovascular events. There are now many studies that conclusively demonstrate that, the higher the CRP, the greater the cardiovascular risk.

Naturally, any marker of risk is followed by the inevitable study: Do statin drugs reduce the excess cardiovascular risk of excessive CRP?

And, yes, indeed they do. My statin-crazed colleagues rave about the so-called "pleiotropic," or non-lipid, effects of statins. CRP reduction and the reduction of risk associated with CRP result with statin treatment.

But is life really statin vs. placebo, as most statin trials are constructed? Are there strategies that can outdo statins like Crestor for reduction of CRP?

Watch your fish oil labels

A quick quiz:

How much omega-3 fatty acids, EPA + DHA, are in each capsule of fish oil with the composition shown on the label below:





If you said 1340 mg (894 mg + 446 mg), sorry, but you're wrong. There are 670 mg EPA + DHA per capsule.

Did you notice that the composition, or "Supplement Facts," lists the contents of two capsules? Rather than the usual one capsule contents, this product label lists two capsules.

I don't know why some manufacturers or distributors do this. However, I have seen many people tripped up by this kind of labeling, taking half the omega-3 fatty acids they thought they were taking. This can be important when you are trying to obtain a specific dose of EPA + DHA to reduce triglycerides, reduce Lp(a), control abnormal heart rhythms, reduce bipolar mood swings, or other important effects.

I liken this to pulling up to a gas station where the sign says gasoline for $1.25. Wow! Can't beat that! You then find out that it's really $1.25 for a half-gallon, or $2.50 a gallon.

In truth, the labeling is accurate; it's just very easy to not notice the two capsule composition.

Why do I need a prescription for Olava?

Imagine this:





What is OLAVA?

Olava is prescription olive oil. It is the purest, highest concentration of olive oil available.




Why Do I Need a Prescription for OLAVA?

Studies show that olive oil contains essential fatty acids, "good" fats that:



--Contain natural compounds your body needs for good health but can't produce on its own.

--Has antioxidants that may provide protection from heart disease.



So, it is common for people to ask why they need a prescription for OLAVA if it is made from a natural ingredient--olive oil. It's time to get the facts about OLAVA. Learn why OLAVA is different from olive oil you can buy at a store.



OLAVA Is an FDA-Approved Medication

OLAVA is the only FDA-approved medicine made from olive oil that's proven, along with diet, to reduce risk for heart disease


The FDA enforces standards to make sure that prescription medications like OLAVA are safe, effective, and quality controlled.


The way OLAVA is manufactured is reviewed and approved by the FDA.


OLAVA uses a 10-step purification process that helps remove lead and other environmental toxins that can be present in olive oil.


Each 1-gram capsule of OLAVA contains 1000 mg of pure olive oil.


The FDA-approved dose of OLAVA is 4 capsules per day. It could take up to 2 tablespoons per day of regular olive oil to provide the same amount of active ingredients proven to lower heart disease risk.




What Else You Should Know About Olive Oil

Regular olive oil has not been approved by the FDA to treat any specific disease like heart disease.



Olive oil doesn't have specific dosing information; it has a food label.



Olive oil does not go through an FDA-approved manufacturing process.





Talk to Your Doctor About OLAVA

If you have very heart disease, you may need a prescription medicine, along with diet, to treat your condition. Talk to your doctor about OLAVA. Print a trial offer to use on your first prescription of OLAVA.