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.

Bosom buddies

Male breast reduction surgery is a booming business. While most industries are in a downward tailspin, breast reduction surgery in men is growing at double-digit rates.

Other efforts, some legitimate, some not, are also cropping up, all intended to help men deal with this embarassing problem:

Exercise programs to reduce male breast size.

Liposuction--Not just for the belly!

Plastic surgery

Gynexin--a supplement that purportedly reduces male breast size.

Conventional medical treatment also includes estrogen blocking drugs, the same ones used to treat breast cancer, drugs like tamoxifen. There's even clothing intended to make breasts less obvious.


While male breast enlargement--"gynecomastia"--can occasionally occur due to rare endocrinologic problems, such as high prolactin hormone levels (hyperprolactinemia) or somewhat more commonly as failed testosterone production (hypogonadism), the vast majority of men who suffer with this problem simply have high estrogen levels.

Makes sense: Women develop larger breasts during development mostly due to increased levels of estrogen. A parallel situation in men likewise stimulates breast tissue.

So where does the excess estrogen come from?

Visceral fat converts testosterone to estrogen. Men with excess visceral fat therefore develop low levels of testosterone and high levels of estrogen. Estrogen levels can, in fact, be substantially higher compared to slender males.

So what foods cause the accumulation of visceral fat and, thereby, increased estrogen and decreased testosterone?

Foods that increase blood glucose and insulin to the greatest degree are the foods that begin this cascade. The common foods that increase blood sugar the most? Here's a list, starting with most blood glucose-insulin provoke at the top, least at the bottom:

Gluten-free foods (dried, pulverized cornstarch, rice starch, potato starch, tapioca starch)
Whole wheat bread
Sucrose
Milky Way bars
Snickers bars

So the whole wheat sandwiches you've been eating increase blood sugar and insulin, leading to visceral fat. (And, yes, whole wheat bread increases blood sugar higher than Milky Way bars and Snickers bars.) The more visceral fat grows, the more resistant to the effects of insulin you become, further escalating blood sugar. Estrogen increases, testosterone drops, mammary gland tissue grows, normal male breasts grow to B- or C-cup size.

Yet again, an entire industry is growing from the unintended consequence of conventional advice. In this instance, the advice to "eat more healthy whole grains" leads to this booming industry of male breast reduction efforts from surgery to medications to clothing. The REAL solution: Eliminate the foods that start the process in the first place.

Don't be a dipstick

If I want to know how much oil is in my car's engine, I check the dipstick.

The dipstick provides a gauge of the amount of oil in my engine. If the dipstick registers "full" because there an oil mark at one inch, I understand that there's more than one inch of oil in my engine. The dipstick provides an indirect gauge of the amount of oil in my engine.

That's what cholesterol was meant to provide: A gauge, a "dipstick," for the kind of lipoproteins (lipid-carrying proteins) in the bloodstream.

Lipoproteins are a collection of particles that are larger than a single cholesterol molecule but much smaller than a red blood cell. Lipoproteins consist of many components: various proteins, phospholipids, lots of triglycerides, as well as cholesterol. In the 1960s, methods to characterize lipoproteins were not widely available, so the cholesterol in lipoproteins were used as a "dipstick" to assess low-density lipoproteins ("LDL cholesterol") and high-density lipoproteins ("HDL cholesterol"). (Actually, even "LDL cholesterol" was not measured, but was derived from "total cholesterol," the quantity of cholesterol in all lipoprotein fractions.)

Some other component of lipoproteins could have been measured instead of cholesterol, such as apoprotein B, apoprotein C, or others, all meant to act as the "dipstick" for various lipoproteins.

Relying on cholesterol to characterize lipoproteins provides a misleading picture. Imagine watching cars go by at high speed while standing on the side of the highway. You want to count how many people--not cars, but people--go by in a given amount of time. Because you cannot make out the detail of each and every car whizzing by, you count the number of cars and assume that each car carries two people. Whether it's rush hour, Sunday morning, late evening, rainy, sunny, or snowing, you make the same assumption: two people per car.

That's what cholesterol does: It is assuming that each and every lipoprotein particle (car) carries the same amount of cholesterol (people).

But that may, obviously, not be true. A bus goes by carrying 25 people. Plenty of cars may carry just the driver. People carpooling may be in cars carrying 3 or 4 people. Assuming just 2 people per car can send your estimates way off course.

That is precisely what happens when your doctor tries to use conventional cholesterol values (total cholesterol, LDL cholesterol) to gauge the lipoproteins in your bloodstream. Measuring cholesterol can also provide the false impression that cholesterol is the cause of heart disease, even though it was originally meant to simply serve as a "dipstick."

What we need to do is to characterize lipoproteins themselves. We can distinguish them by size, number, density, charge, and the type and form of proteins contained within. It provides greater insight into the composition of lipoproteins in the blood. It provides greater insight into the causes underlying coronary atherosclerotic plaque. It can also tell us what dietary changes trigger different particle patterns and how to correct them.

Until you have a full lipoprotein analysis, you can never know for certain 1) if you will have heart disease in your future, or 2) how your heart disease was caused.

Unfortunately, the vast majority of doctors are perfectly content to just count cars going by and assume two people per car, i.e., confine assessment of your heart disease risk using cholesterol . . . just as drug industry marketing has instructed them.

It's not your job to educate your doctor. If he or she refuses to provide access to lipoprotein testing to better determine your heart disease risk, then consider going out on your own. Many of our Track Your Plaque program followers have obtained lipoprotein testing on their own through Direct Labs.

The ultimate insurance company cost savings

I had a very disturbing conversation with a physician who is employed by an insurance company last week.

I admitted a patient in the hospital for very clear-cut reasons. She is one of my few non-compliant patients, doing none of the strategies I advocate--no fish oil, no vitamin D, no correction of her substantial lipoprotein abnormalities, not even medication. Much of this was because of difficult finances, some of it is because she is from the generation (she is in her late 70s) that tends to ignore preventive health, some of it is because she is a kind of happy-go-lucky personality. So her disease has been progressive and, now, life-threatening, including an abdominal aneurysm near-bursting in size (well above the 5.5 cm cutoff). The patient is also a sweet, cuddly grandmother. I have a hard time bullying nice little old ladies.

While she was in the hospital, the social worker told me that her case was being reviewed by her insurer and would likely be denied. Their medical officer wanted to speak to me.

So the medical officer called me and started asking pointed questions. "Why did you do that test? You know that she's not been compliant. Are you sure you want to do that? I don't think that's a good idea." In other words, this was not just a review of the case. This was an opportunity for the insurance company to intervene in the actual care of the patient.

Then the kicker: "Have you considered not doing anything and . . . just letting nature take its course?"

At first, I was stunned. "You mean let the patient die?"

Expressed in such blatant terms, while he was trying to be diplomatic, made him back down. "Well, uh, no, but she is a high-risk patient."

Anyway, this was the first instance I've encountered in which the insurance company is not just in the business of reviewing a case, but actually trying to intervene during the hospital stay, to the point of making the ultimate healthcare cost savings: Letting the patient die.

Unfortunately, never having had an experience like this before, I did not think to record the conversation or take notes. I am wondering if this is an issue to be taken up by the Insurance Board . . . or is this a taste of things to come as the health insurers fall under increasing pressure with the legislative changes underway?

Salvation from halogenation

Iodine is a halogen.

On the periodic table of elements (remember the big chart of the elements in science class?), the ingenious table that lays out all known atomic elements, elements with similar characteristics are listed in the same column. The elegant genius of the periodic table has even allowed prediction of new, undiscovered elements that conform to the "laws" of atomic behavior.

Column 17 (also called "group VIIa") contains all the halogens, of which iodine is one member. Other halogens include fluorine, chlorine, and bromine.

Odd phenomenon in biologic systems: One halogen can often not be distinguished from another. Thus, a chlorinated compound can cleverly disguise itself as an iodinated compound, a brominated compound can mimic an iodinated compound, etc.

What this means in thyroid health is that, should sufficient iodine be lacking in the body, i.e., iodine deficiency, other halogens can gain entry into the thyroid gland.

While a polychlorinated biphenyl (PCB) molecule may be recognized as an iodinated compound, it certainly doesn't act like an iodinated compound once it's in the thyroid's cells and can disrupt thyroid function (Porterfield 1998). Another group of chlorine-containing compounds, perchlorates, that contaminate groundwater and are found as pesticide residues in produce, are extremely potent thyroid-blockers (Greer 2002). Likewise, bromine-containing compounds, such as polybrominated diphenyl ethers (PBDEs), widely used as flame retardants, also disrupt thyroid function (Zhou 2001). Perfluorooctanoic acid (PFOA), found in Teflon non-stick cookware and stain-resistant products,  has been associated with thyroid dysfunction (Melzer 2010). PFOA, incidentally, can disrupt thyroid dysfunction that will not show up in the TSH test used by primary care physicians and endocrinologists to screen for thyroid dysfunction. (In fact, the presumed champions of thyroid health, the endocrinology community, have proven a miserable failure in translating and implementing the findings from  toxicological science findings to that of preserving or restoring thyroid health. They have largely chosen to ignore it.)

We therefore navigate through a world teeming with halogenated thyroid blocking compounds. We should all therefore avoid such exposures as perchlorates in produce by rinsing thoroughly or purchasing organic, avoid non-stick cookware, avoid use or exposure to pesticides and herbicides.

Another crucial means to block the entry of various halogenated compounds into your vulnerable thyroid: Be sure you are getting sufficient iodine. While it doesn't make your thyroid impervious to injury, iodine circulating in the blood in sufficient quantities and residing in sufficient stores in the thyroid gland provides at least partial protection from the halogenated impostors in your life.

I make this point in the context of heart disease prevention, since even the most subtle degrees of thyroid dysfunction can easily double, triple, or quadruple heart disease risk. See related posts, Is normal TSH too high? and Thyroid perspective update.

Lipitor-ologist

One of the things I do in practice is consult in complex hyperlipidemias, the collection of lipoprotein disorders that usually, but not always, lead to atherosclerosis.

First order of business: Make the diagnosis--familial combined hyperlipidemia, hypoalphalipoproteinemia, lipoprotein(a), familial heterozygous hypercholesterolemia, familial hypertriglyceridemia, hyperapoprotein B with metabolic syndrome, etc. These are the disorders that start with a genetic variant, e.g., a missing or dysfunctional enzyme or signal protein, such as lipoprotein lipase or apo C3.

I then ask: What can be done that is easy and safe and preferably related to diet and lifestyle?

By following an effective diet, many of these abnormalities can be dramatically corrected, sometimes completely. Familial hypertriglyceridemia, for instance, an inherited disorder of lipoprotein lipase in which triglyceride levels can exceed 1000 mg/dl, high enough to cause pancreatic damage, responds incredibly well to carbohydrate restriction and over-the-counter fish oil. I have a number of these people who enjoy triglyceride levels below 100 mg/dl--unheard of in conventionally treated people with this disorder.

Then why is it that, time after time, I see these people in consult, often as second or third opinions from lipidologists (presumed lipid specialists) or cardiologists, when the only solutions offered are 1) Lipitor or other statin drug, and 2) a low-fat diet? Occasionally, an aggressive lipidologist might offer niacin, a fibrate drug (Tricor or fenofibrate), or Lovaza (prescription fish oil).

Sadly, the world of lipid disorders has been reduced to prescribing a statin drug and little else, 9 times out of 10.

I don't mean to rant, but I continue to be shocked at the incredible influence the drug industry has over not just prescribing patterns, but thinking patterns. Perhaps I should say non-thinking patterns. The drugs make it too easy to feel like the doctor is doing something when, in truth, they are doing the minimum (at best) and missing an opportunity to provide true health-empowering advice that is far more likely to yield maximum control over these patterns with little to no medication.

All in all, I am grateful that there is a growing discipline of "lipidology," a specialty devoted to diagnosing and treating hyperlipidemias. Unfortunately, much of the education of the lipidologist is too heavily influenced by the pharmaceutical industry. Not surprisingly, the drug people favor "education" that highlights their high-revenue products.

Seeing a lipidologist is still better than seeing most primary care physicians or cardiologists. Just beware that you might be walking into the hands of someone who is simply the unwitting puppet of the pharmaceutical industry.

Robb Wolf's new Paleo Solution

The Paleo Solution: The Original Human Diet


The Paleo Solution: The Original Human Diet

I have to say: I'm impressed. If you would like insight into why a "Paleo" nutritional approach works on a biochemical level--why you lose weight, burn fat, and gain overall better health--then Robb's book is worth devoting a few hours to, of not a reread or two.

Robb has a particular knack for organizing and presenting information in a way that makes it immediately accessible. You will gain an appreciation for how far American nutritional habits have veered off course.

Because Robb brings expertise from his academic biochemistry background, as well as personal trainer and educator running a successful gym in northern California, NorCal Strength and Conditioning, he delivers a book packed with information that is extremely easy to convert to immediate action in health and exercise. He seems to anticipate all the little problems and objections that people come up with along the way, dealing with them in his characteristic lighthearted way, providing practical, rational solutions.

Robb's book nicely complements what Dr. Loren Cordain has written in his The Paleo Diet: Lose Weight and Get Healthy by Eating the Food You Were Designed to Eat and The Paleo Diet for Athletes: A Nutritional Formula for Peak Athletic Performance. (My wife is now reading The Paleo Diet for Athletes and loves it. I'm going to add Robb's book to her reading list for her to read next.)

If nutrition has you stumped, if the USDA food pyramid still sounds like a reasonable path, or if you just would like to understand nutrition a little bitter, especially its biochemical ins and outs, Robb's book is a wonderful place to start.

Human foie gras

If you want to make foie gras, you feed ducks and geese copious quantities of grains, such as corn and wheat.

The carbohydrate-rich diet causes fat deposition in the liver via processes such as de novo lipogenesis, the conversion of carbohydrates to triglycerides. Ducks and geese are particularly good at this, since they store plentiful fats in the liver to draw from during sustained periods of not eating during annual migration.

Modern humans are trying awfully hard to create their own version of foie gras-yielding livers. While nobody is shoving a tube down our gullets, the modern lifestyle of grotesque carbohydrate overconsumption, like soft drinks, chips, pretzels, crackers, and--yes--"healthy whole grains" causes fat accumulation in the human liver.

Over the past few years, there has been an explosion of non-alcoholic fatty liver disease and non-alcoholic steatosis, two forms of liver disease that result from excess fat deposition. The situation gets so bad in some people that it progresses to cirrhosis, i.e., a hard, poorly-functioning liver that paints a very ugly health picture. The end-result is identical to that experienced by longstanding alcoholics.



While Hannibal Lecter might celebrate the proliferation of human fatty livers with a glass of claret, fatty liver disease is an entirely preventable condition. All it requires is not eating the foods that create it in the first place.

Let go of my love handles

When is fat not just fat?

When it's visceral fat. Visceral fat is the fat that infiltrates the intestinal lining, the liver, kidneys, even your heart. It's the stuff of love handles, the flabby fat that hangs over your belt, or what I call "wheat belly."

Unlike visceral fat, the fat in your thighs or bottom is metabolically quiescent. Thigh and bottom fat may prevent you from fitting into your "skinny jeans," but its mainly a passive repository for excess calories.

Visceral fat, on the other hand, is metabolically active. It produces large quantities of inflammatory signals ("cytokines"), such as various interleukins, leptin, and tumor necrosis factor, that can trigger inflammatory responses in other parts of the body. Visceral fat also oddly fails to produce the protective cytokine, adiponectin, that protects us from diabetes, cancer, and heart disease.

Visceral fat also allows free fatty acids to leave and enter fat cells, resulting in a flood of fatty acids and triglycerides (= 3 fatty acids on a glycerol "backbone") in the bloodstream. This worsens insulin responses ("insulin resistance") and contributes to fatty liver. The situation is worsened when the very powerful process of de novo lipogenesis is triggered, the liver's conversion of sugar to triglycerides.

Visceral fat is also itself inflamed. Biopsies of visceral fat show plenty of inflammatory white blood cells (macrophages) infiltrating its structure.

So what causes visceral fat? Anything that triggers abnormal increases in blood glucose, followed by insulin, will cause visceral fat to grow.

It follows logically that foods that increase blood glucose the most will thereby trigger the greatest increase in visceral fat. Eggs don't lead to visceral fat, nor do salmon, olive oil, beef, broccoli, or almonds. But wheat, cornstarch, potato starch, rice starch, tapioca starch, and sugars will all trigger glucose-insulin that leads to visceral fat accumulation.

Fructose is also an extravagant trigger of visceral fat. Fructose is found in sucrose (50% fructose), high-fructose corn syrup, agave syrup, maple syrup, and honey.

Increased visceral fat can be suggested by increased waist circumference. The inflammatory hotbed created by excess visceral fat has therefore been associated with increased likelihood of heart attack, cardiovascular mortality, diabetes, cancer, and total mortality.

So I'm not so worried that you can't squeeze your bottom into your size 8 jeans. I am worried, however, when you need to let your belt out a notch . . . or two or three.

Surviving a widow maker

Gwen came to me 5 years ago. In her late 60s, she'd been having feelings of chest pressure for the past 4 weeks with small physical efforts, such as climbing a flight of stairs or lifting her grandchildren.

She sat in my office, heaving small sobs, accompanied by her daughter.

Gwen had already undergone a heart catheterization at a hospital near home by a cardiologist who I knew to be honest and competent. She'd been told that she had a 90% stenosis ("blockage") of her proximal left anterior descending (LAD) coronary artery. He called it a "widow maker," since closure of the artery at this point can be fatal within minutes. He advised bypass surgery as soon as possible. Though a stent could be placed at this location, he felt that its proximity to the left main stem (i.e., the "trunk" that divides into the LAD and circumflex arteries) might be jeopardized by expanding a stent in this bulky plaque, what I felt was a reasonable concern.

I reviewed the images that she brought with her. Yes, indeed: a widow maker. The portion of the left ventricle (heart muscle) fed by the LAD was also impaired ("hypokinetic"), reflecting reduced flow through the artery.

I advised Gwen that her first cardiologist's advice was sound: This was a potentially dangerous and severe condition. Either a bypass or stent should be performed near-future, the less delay the better.

But Gwen and her daughter would have no talk of any more procedures. She'd come to me because she heard about the (then rudimentary) effort I'd been making at reversing coronary plaque. "I admire your commitment, Gwen, but I am concerned that there may not be sufficient time to implement a program of prevention or reversal. Prevention is very powerful, but very slow. When symptoms like yours are active, also, it can mean that we won't have full control over the plaque causing the symptoms. This risks closure of the vessel, since flow characteristics in the plaque are abnormal. I think that you should go through a stent or bypass. We can then start your prevention/reversal program once we know you're safe."

Gwen would still have none of it. I asked her to return in a few days after thinking it over. In the meantime, we drew her lipoprotein blood samples while she added fish oil, l-arginine (back then I used a lot of l-arginine for its endothelial health effects), and began the Track Your Plaque diet a la 2004. This was in addition to the aspirin, beta blocker, and statin prescribed by the first cardiologist.

Several days later, Gwen and her daughter returned, as committed as ever to not having a procedure and proceeding with our prevention/reversal efforts.

So off we went. I was nervous about Gwen's safety, but she had clearly made her mind made up. Gwen's lipoprotein analysis revealed a severe small LDL pattern along with markers for prediabetes (high insulin, high blood glucose, hypertension, along with the loose tummy of visceral fat). So I counseled her intensively in diet and added niacin.

Within 2 weeks, Gwen no longer had chest pain. Whether this was due to her efforts or to some resolution of an intraplaque phenomenon (e.g., resorption of internal plaque hemorrhage), I don't know. But her symptoms did not return.

As the program evolved, we added the new strategies along the way--vitamin D supplementation; elimination of all wheat along with other changes in diet; iodine and thyroid normalization; as well as discontinuing l-arginine after the initial two years. She also got rid of the statin drug after losing around 20 lbs on the diet.

It's now been six years with her "widow maker" and Gwen has been fine: no recurrence of her symptoms, all stress tests performed have been normal, reflecting normal blood flow in her coronary arteries.

Should ALL people with symptomatic widow makers undergo such an effort and avoid procedures? No, not yet. Prevention and reversal efforts are indeed powerful, but slow. Some people just may not have sufficient time to accomplish what Gwen did. The fact that Gwen showed evidence for reduced flow in the LAD worried me in particular. There is no question that mortality benefits for stenting or bypass of this location are not as large as previously thought (see here, for instance), but each case needs to be viewed individually, factoring in flow characteristics in the artery, appearance of "stability" or "instability" of the plaque itself, not to mention commitment of the person.

But it can be done.

Fred Hahn's Slow Burn

I just had a workout with personal trainer and fitness expert, Fred Hahn. After a workout that quickly taught me that I had a lot to learn about exercise and strength training, Fred and I had a nice low-carbohydrate dinner at a Manhattan restaurant and shared ideas.

Fred is coauthor of Slow Burn Fitness Revolution: The slow motion exercise that will change your body in 30 minutes a week, written in collaboration with the Drs. Eades, Michael and Mary Dan. Fred also blogs here.

I had heard about Fred's "slow-burn" concept in past, but made little of it. I then met Fred on Jimmy Moore's low-carb cruise this past year, where I gave a talk on how carbohydrate-reduced diets reduce small LDL particles. Fred provided a group demonstration on his slow-burn techniques. I watched the demonstration, even tried it a few times back home in the gym, but never really applied them, losing patience most of the time and just going back to my usual routine.

Well, Fred showed me today how to do his slow-burn. In a nutshell, it is the slow, methodical use of weight resistance until the muscle is exhausted. It involves slow movement--e.g., 5 seconds for a lat pulldown from top to bottom--repeated until exhaustion using a weight that allows, perhaps, 6 repetitions over a 60-second effort.

I've been strength training since I was a teenager. I've seen lots of bad training techniques, injuries, and hocum when it comes to how to use resistance training techniques. But I believe that Fred Hahn's slow-burn technique really provides something unique that I hadn't experienced before.

For one, the burn is nothing like I've felt before. Two, there appears to be nearly zero risk for injury, since the usual momentum-driven, herky-jerky motion often employed with weight machines is entirely gone. Three, if what Fred is seeing is true--enhanced visceral (abdominal) fat loss, reduced blood glucose, increased HDL, decreased LDL/total cholesterol--then there's something really interesting going on here.

I also discovered that Fred is no ordinary personal trainer. He has insights into metabolism that I found truly impressive. After all, he's been hanging around with Mike Eades, who's a pretty sharp guy. What Mike Eades is to metabolic insights is what Fred Hahn is to exercise physiology.

I'm going to take Fred's slow burn training insights home with me. I'll let you know how it goes. Some aspects I'd like to explore: Will strength, muscle mass, and blood sugar responses change?



Fred Hahn's latest book, adapting slow burn techniques for kids.