Wheat hip

You've heard of wheat belly. How about wheat hip?

Recall that the innocent appearing wheat belly is actually a hotbed of inflammatory activity beneath the surface. The visceral fat of the wheat belly, i.e., fat kidneys, fat liver, fat intestines, fat pancreas, produces abnormal inflammatory signals, such as various interleukins, tumor necrosis factor, and leptin. These are the inflammatory signals that create insulin resistance and diabetes, heart disease, hypertension, and cancer.

These same inflammatory mediators are able to enter the joint spaces, such as those in your hips, knees, and hands. This leads to osteoarthritis, the exceptionally common form of arthritis that affects 1 in 7 Americans. In particular, the level of leptin in joints mirrors that in blood, a phenomenon that has been associated with joint destruction.

The previously widely-held notion that arthritis is simply a wear-and-tear phenomenon due to the mechanical stress of excess weight is proving to be an oversimplification. Arthritis is also part of the carbohydrate-driven, weight-increasing, inflammatory condition of insulin resistance or metabolic syndrome.

Throw into this cytokine storm the fact that glycation, i.e., glucose modification of proteins, also causes cartilage destruction. The cells of human cartilage lack the ability to divide, so the cartilage cells you had at age 18 are the cartilage cells that you will hopefully still have at age 80. However, high blood sugars (glucose) glycate the proteins in cartilage. (Wheat raises blood glucose higher than almost all other foods, higher than a Milky Way bar, higher than a Snickers bar.) The process is irreversible and cumulative. Because cartilage has next to no capacity for repair or regeneration, it becomes brittle. Over years, it essentially crumbles, leading to the "bone on bone" that prompts conversations about total hip and total knee replacement.

So that ciabatta or blueberry muffin in your mouth takes you a step or two closer to joint destruction via heightened inflammation arising from the visceral fat of the wheat belly, worsened by glycation of high blood sugars after carbohydrate consumption.

My solution: Lose the ciabatta.

Men's lingerie is on the second floor

Consume wheat products, like poppyseed muffins, raisin bagels, and whole grain bread, and you trigger the 90- to 120-minute glucose-insulin cycle.

Blood glucose goes way up (more than almost any other known food), triggering insulin release from the pancreas. Glucose enters cells as a result, blood glucose plummets. You get hungry, shaky, and crabby, reach for another wheat or other sugar-generating food to start the roller coaster ride all over again.

Repetitive insulin triggering grows this thing I call a "wheat belly," the protuberant, hang-over-the-belt fat you see everywhere nowadays. Wheat belly fat is really visceral fat. Visceral fat means you have fat kidneys, fat intestines, fat pancreas, and fat liver, all causing the belly to protrude in the familiar way we've all come to recognize.

Visceral fat is special fat. Unlike the fat in the backside, thighs, or arms, visceral fat triggers inflammatory responses that are evident in such measures as tumor necrosis factor, interleukins, and leptin, as well as drops in the protective hormone, adiponectin.

Visceral fat also, oddly, triggers estrogen release. Estrogen triggers growth of breast tissue. That's why females with wheat bellies have up to four-fold (400%) greater likelihood of breast cancer.

Men also experience excess estrogen from the visceral fat wheat belly, causing "man boobs." This B-cup phenomenon means that inflammation is raging beneath the surface, all due to this thing you're wearing around your waist.

I wasn't aware until recently that male breast reduction surgery is a booming business growing at double-digit rates. So are special clothes to help men conceal their expansive breasts.

Perhaps the USDA is in cahoots with Playtex.

10,000 units of vitamin D

Joanne started with a 25-hydroxy vitamin D level of 23 ng/ml--severe deficiency.

What made this starting value even worse was that it was drawn in August after a moderately sunny summer spent outdoors. (Last summer, not this summer.) It therefore represented her high for the year, since vitamin D levels trend lower as fall and winter set in. This suggests that her winter level was likely in the teens or even single digits. In addition, note that, at age 43, Joanne has lost much of her ability to activate vitamin D in the skin.

So I advised that she take 6000 units of an oil-based gelcap per day, a dose likely to generate the desired blood level, which I believe is 60-70 ng/ml.

Four months later, her 25-hydroxy vitamin D level: 39.9 ng/ml--still too low. So I advised her to increase her dose to 10,000 units per day. Several months later, her 25-hydroxy vitamin D level: 63.8 ng/ml--perfect.

However, on hearing that she was taking 10,000 units vitamin D per day, Joanne's primary care physician was shocked: "What? Stop that immediately! You're taking a toxic dose!" So Joanne called me to find out if this was true.

No, of course it's not true. It's not the dose that's toxic, but the blood level it generates. Although it varies, vitamin D toxicity, as evidenced by increased blood calcium levels, generally does not even begin to get underway until at least 120-130 ng/ml, perhaps higher. Rarely, a dose of 2000 units per day will generate a level this high. In others, it may require 24,000 or more units per day to generate such a high level.

So it's not the dose that's toxic, but the blood level of 25-hydroxy vitamin D it generates.

Provided you and/or your doctor are monitoring 25-hydroxy vitamin D blood levels, the dose is immaterial. It's the blood level you're interested in.

No more Lovaza

That's it: I will NEVER ever write another prescription for Lovaza.

I actually very rarely write a prescription for Lovaza, i.e., prescription fish oil. But this was the last straw.

I advised a patient that we've had good success using high-doses of fish oil to reduce lipoprotein(a), Lp(a). 6000 mg per day of the omega-3 component (EPA + DHA) from fish oil reduces Lp(a) in 60% of people after one year. (Recall that Lp(a) is the most aggressive known lipid-related cause of heart disease.)

The two preparations I generally suggest are either the very affordable Sam's Club Members Mark Triple-Strength Fish Oil with 900 mg EPA + DHA per capsule: 7 capsules per day. Another great product (my personal favorite because of its extreme purity--it doesn't even smell like fish oil): Pharmax Finest Pure Fish Oil with 1800 mg EPA + DHA per teaspoon: 3 to 3 1/2 teaspoons per day.

Both preparations work great and are quite affordable, given the high dose. For the Sam's Club preparation, it will cost around $30 per month, while the Pharmax liquid will run around $49 per month.

Well, the woman's husband insisted on a prescription for Lovaza. One Lovaza capsule contains 784 mg EPA + DHA per capsule: 7 to 8 capsules per day.

Here are some prices for Lovaza from online pharmacy discounters:
Prescription Giant: $78.99 for 30 capsules ($2.63 per capsule)
Planet Drugs Direct: $135 for 100 capsules ($1.35 per capsule)

These are lower than the prices I obtained in past by calling local pharmacies in my area, quite a bit lower, in fact.

Filling the Lovaza prescription at Prescription Giant will therefore cost $552.93 to $631.92 per month; at Planet Drugs Direct it will cost $283.50 to $324.00 per month. At local pharmacies, a similar 7 to 9 capsules Lovaza per day will cost upwards of $800 to $900 per month.

The patient's husband insisted on the Lovaza prescription because he knew that his insurance would cover it. When I pointed out that this was a large cost that would have to be borne by others in their healthcare premiums, he said that didn't matter to him.

I hesitated, but ended up writing the prescription for 7 Lovaza capsules per day. As soon as I handed to him, I regretted it. In fact, I am embarassed and angry at myself for having given in.

So I vowed: I will NEVER EVER write another prescription for Lovaza.

I do not believe that we should spread the excessive profiteering of the pharmaceutical industry around on the backs of people who pay their healthcare insurance premiums, just so that a few people, like this selfish couple, can save a few dollars a month.

This is your brain on wheat II

In the original Heart Scan Blog post, This is your brain on wheat, I discussed how opioid peptides (i.e., small proteins that act like opiates such as heroine or morphine) that result from digestion of wheat cause unique effects on the human brain, particularly addictive behaviors. I also briefly reviewed how elimination of wheat has been shown to reduce auditory hallucinations and other psychotic behaviors in a subset of people with paranoid schizophrenia.

These two phenomena, addictions and schizophrenia, are most likely the result of exorphins that cross the blood-brain barrier. Exorphins--exogenous morphine-like compounds--can be blocked by opiate-blocking drugs like naloxone and naltrexone. Naloxone is used in hospitals to reverse morphine or heroine overdoses; naltrexone is being repackaged into a weight loss drug, since blocking wheat-derived exorphins reduces appetite. (Yes: The USDA tells us to eat more wheat, the drug industry sells us the antidote.)

There's another way that wheat can affect the brain and nervous system: immune-activated damage.

This is similar to the effect seen in celiac. There's even overlap with some of the antibody markers used to diagnose celiac, like the anti-gliadin antibodies and the anti-endomysium antibodies.

The most common immune neurological syndrome consequent to wheat consumption is cerebellar ataxia, a condition in which an immune response causes damage to the Purkinje cells of the cerebellum, the portion of the brain responsible for balance and coordination. This results in stumbling, incoordination, incontinence, and eventually leads to reliance on a cane or walker and wearing a diaper. Average age of onset: 53 years. A shrunken, atrophied cerebellum can be seen on an MRI of the brain.

Problem: Most people with central nervous system damage caused by wheat do not have any intestinal symptoms, like diarrhea and abdominal pain, the sort of symptoms usually associated with celiac disease. It means the first sign of wheat-induced brain damage may be bumping into walls and wetting your pants.

There's no such thing as a "no-carb" diet

When I tell patients how I advise a wheat-free, cornstarch-free, sugar-free diet on the background of a low-carbohydrate diet, some people ask: "But can I live on a no-carb diet?"

Well, there's no such thing as a "no-carb" diet. Low-carb, yes. No-carb, no.

Here are the carbohydrate contents of various "low-carb" foods:

Gouda cheese--3 oz contains 1.65 grams carbohydrates
Mozzarella cheese--1 cup contains 2.89 grams carbohydrates
Walnuts--4 oz (56 nuts) contains 2.96 grams carbohydrates
Almonds--4 oz contains 1.38 grams carbohydrates
Sour cream--one-half cup contains 3.31 grams carbohydrates
Red wine--3.5 oz glass contains 2.69 grams carbohydrates
Eggplant--1 cup cooked contains 8.33 grams carbohydrates
Green pepper--1 medium-sized raw contains 5.52 grams carbohydrates
Cucumber--1 medium contains 4.34 grams carbohydrates
Tomato--1 medium contains 4.82 grams carbohydrates

(Nutrition data from USDA Nutrient Database)

In other words, foods thought to be "low-carb" actually contain a modest quantity of carbohydrates.

Such modest quantities of carbohydrates may not be enough to trip your blood sugar. But add up all the "low-carb" foods you consume over the course of a day and you can easily achieve 30 grams or more carbohydrates per day even without consuming any higher carbohydrate foods.

Why doesn't your doctor try to CURE diabetes?

Imagine you have breast cancer. You go to your doctor and she says, "As your pain worsens, we'll help you with pain medication. We'll fit you with a special bra to accommodate the tumor as it grows. That's all we're going to do."

"What?" you ask. "You mean just deal with the disease and its complications, but you're not going to help me get rid of it . . . cure it?"

It would be incredibly shocking to receive such advice. Then why is that the sort of advice given when you are diagnosed with diabetes?

Say you go to the doctor. Lab values show a fasting blood sugar of 156 mg/dl, HbA1c (a reflection of your previous 60 days average glucose) of 7.1%. Both values show clear-cut diabetes.

Your doctor advises you to 1) start the drug metformin, then 2) talk to the diabetic teaching nurse or dietitian about an American Diabetes Association (ADA) diet.

The ADA diet prescribed encourages you to increase carbohydrates and cut fats at each meal and maintain a consistent intake so that you don't experience hypoglycemic (low blood sugar) episodes. You follow the diet, which causes you to gain 10-15 lbs per year, increasing your "need" for diabetes medication. You doctor adds Actos, then Januvia, then injections of Byetta.

Three years and 34 lbs later, you are not responding well to the drug combination with blood sugars rarely staying below 200 mg/dl. You've developed protein in your urine ("proteinuria"), lost 30% of your kidney function, and you are starting to lose sensation in your feet. So the doctor replaces some of your medication with several insulin injections per day.

This formula is followed millions of times per year in the U.S. So where along the way did your doctor mention anything about a "cure"?

Adult diabetes is the one chronic disease that nobody cares to cure. Treat it, maintain control over blood sugars, but cure it? Most physicians say it's impossible.

The tragedy is that diabetes is a curable condition. I've seen it happen many times. Physicians dedicated to curing diabetes like low-carb expert, Dr. Mary Vernon, have cured it countless times. Dr. Eric Westman and colleagues have been building the case for the carbohydrate-restricted cure for diabetes with studies such as this. In this last study, of the 8 participants on insulin + medications at the start of the study, 5 no longer required medications at the close of the study--they were essentially non-diabetic.

I tell patients that diabetes, in fact, is a disease you choose to have or not to have--provided you are provided the right diet and tools. Sadly, rarely are diabetics told about the right diet and tools.

That's why Cadbury Schweppes has been a major contributor to the American Diabetes Association, as are other processed food manufacturers and the drug industry, all who stand to profit from maintaining the status quo.

The cure? Eliminate or at least dramatically reduce carbohydrates, the foods that increase blood sugar.

Note: If you have diabetes and you are taking any prescription agents, such as glyburide, glipizide, insulin, and some others, you will need to discuss how to manage your medications if you reduce carbohydrates. The problem is finding a doctor or other resource to help you do this.

LDL pattern B

Here's a Q&A I stumbled on in the Forum of MedHelp, where people obtain answers from presumed health "experts."

Question:

My VAP test results in July 07 identified an LDL Pattern B.
Overall results:
Total 150
HDL 75
LDL 61
Trig 60
HDL-2 17
LP(a) 6.0
LDL Pattern B

Medications:
Lipitor 10mg
Zetia 10mg
Altace 10mg
Atenolol 50mg
Plavix 75mg
Aspirin 81mg

I had several heart attacks which resulted in CABG performed May 2000. I am a 53 year old white male , 6'1", 190 pounds, exercise every day, watch my diet and feel great. Everything looks OK except my LDL Pattern B. Is there any therapy to improve the Patten B?


Answer from CCF, MD:
Your results indicate an LDL pattern B, which generally indicates small atherogenic LDL particles which may cause increased risk for CAD. However, there are several problems with LDL patterning: 1) its unreliability (of LDL pattern testing ), 2) unclear clinical evidence regarding regarding the usefulness of LDL patterns and particle size. The majority of evidence regarding the progression of atherosclerosis is with LDL lowering and to an smaller extent HDL raising.

All available clinical evidence shows that any particles in the VLDL, IDL, or LDL range are atherogenic, and there is no evidence that whether belonging to pattern A or B one is more atherogenic than others.

Subclass studies have proliferated over the last few years, but many of these studies were funded or subsidized either by suppliers of the assays as a method to expand their use and move them into mainstream practice, or by pharmaceutical companies in an attempt to claim some advantage over other therapeutic agents.
Thus, current data on LDL subclasses are at best incomplete and at worst misleading, suffering from publication bias, and now given the recent results of the Ensign et al. study, unreliable.

Your LDL, and HDL are at goal. The Lpa level is still not clearly linked as a modifiable risk factor for CAD, although elevated levels are now know to be linked to stroke.

Continue with your present treatments: aspirin, plavix, ateonol and altace are all essential medications.



Wow. The extent of ignorance that pervades the ranks of my colleagues is frightening.

Contrary to the response, LDL particle size assays are quite reliable and accurate. I've performed many thousands of lipoprotein assays and they yield reproducible and clinically believable results. For example, eliminate wheat, oats, cornstarch, and sugars and small LDL drops from 2400 nmol/L to 893 nmol/L (NMR)--huge drops. If repeated within a short period of time, the second measure will correspond quite closely.

The data are also quite clear: Small LDL particles (i.e., "pattern B") are a potent predictor of cardiovascular events. What we lack are the treatment trials that show that reduction of small LDL results in reduced cardiovascular events. The reason for this is that small LDL research is not well-funded, since there is no prescription drug to treat small LDL, only nutritional means. Niacin (as Niaspan) is as close as it comes for a "drug" to reduce small LDL. But diet is far more effective.

Given the questioner's fairly favorable BMI of 25.1 and his history of aggressive heart disease, it is virtually certain that he has what I call "genetic small LDL," i.e., small LDL that occur on a genetically-determined basis (likely due to variants of the cholesteryl-ester transfer protein, or CETP, or of hepatic lipase and others).

Ignoring this man's small LDL will, without a doubt, consign him to a future of more heart attacks, stents, and bypass. Maybe by that time the data supporting the treatment of small LDL will become available.

What increases blood sugar more than wheat?

Take a look at these glycemic indexes (GI):


White bread 69
Whole wheat bread 72
Sucrose 59
Mars bar 68
White rice 72
Brown rice 66


I've made issue in past of whole wheat's high GI--higher than white bread. Roughly in the same glycemic league as bread are shredded wheat cereal, brown rice, and a Mars candy bar.

With few exceptions, wheat products have among the highest GIs compared to the majority of other foods. For instance:


Kidney beans 29
Chick peas 36
Apple 39
Ice cream 36
Snickers Bar 40


Yes, by the crazy logic of glycemic index, Snickers is a low-glycemic index food.

While I do not believe that low GI makes a food good or desirable, since low GI foods still provoke high blood sugars, small LDL particles, trigger glycation, and other abnormal phenomena, they are clearly less obnoxious than the items in the first list.

Take a look at this list:

Cornflakes 80
Rice cakes 80
Rice Krispies 82
Rice pasta, 92
Instant potatoes 83
Tapioca 81



Starches that are dried and/or pulverized, such as cornstarch, potato starch, rice starch, and tapioca starch (cassava root) will increase blood sugar even more than wheat. Foods with these starches have GI's of 80-100.

Cornstarch, potato starch, rice starch, and tapioca starch: Sound familiar? These are the main starches used in "gluten-free" foods. A hint of the high GI behavior of these dried starches is seen in the GI for cornflakes of 80.

So remember: Wheat-free is not the same as gluten-free. Gluten-free identifies junk carbohydrates masquerading as healthy because they don't contain one unhealthy ingredient, i.e. wheat.

Add Boston Globe to the list of heart scan blunders

Yet another piece of mass media misinformation hit the airwaves today. This time it's not from the New York Times or the LA Times, both of which have previously mangled the issues surrounding heart scans. This time it's from the Boston Globe.

In an article titled What is a calcium scan for heart disease, and who should undergo the test?, the report states:

". . . calcium scans may not be a good idea, or prove terribly useful, for most people. For one thing, the scans expose a patient to significant radiation - equivalent to roughly 50 chest X-rays" said Dr. Warren Manning, chief of noninvasive cardiac imaging at Beth Israel Deaconess Medical Center."

As many before him, Dr. Manning is confusing two tests: CT coronary angiography and CT heart scanning. Perhaps we can't blame him: This technology has had its weakest following in the northeast, for reasons not entirely clear to me. (In fact, Track Your Plaque followers have had the greatest struggle obtaining heart scans in that part of the country.) Nonetheless, you'd think he'd have his simple facts straight before talking to the press. Unfortunately, hospital public relations departments will usually just grab whoever they can willing to talk to the press--regardless of their expertise or lack of.


The story goes on to say:

. . ." it's not clear what to do with the results from a calcium scan. If you have diabetes, high cholesterol, high blood pressure, or a family history of heart disease, you already know - or should know - that you are at increased risk of heart problems and should lower these risk factors. So, a calcium scan provides little additional information," Manning said.

"Moreover, even a high score doesn't necessarily mean that the calcified plaque in your arteries is obstructing blood flow, said Dr. Adolph Hutter, a cardiologist at Massachusetts General Hospital."

"The vast majority of people with high calcium tests don't have obstructions and they do fine long-term. So you'd have to test lots and lots of people to prevent one heart attack or sudden death," said Manning.

And if you get a low calcium score, a sign of little or no calcification of plaques, that's not very useful, either, because it could be wrong, or it could be right but lull you into believing you do not have to exercise and watch your diet, cholesterol, and blood pressure levels. "You can still be at risk even if your calcium test is negative," Hutter said.



It is truly shocking how little many (not all, thank goodness) of my colleagues really know about 1) heart scans, 2) coronary disease prevention, and 3) prevention in general. These same "experts" likely advocate high-dose statin drugs and low-fat diets for people at risk. They likely refer patients to the American Heart Association for diet advice and themselves obtain a lot of information from the pharmaceutical industry. The notion of identification, tracking, and purposeful reversal of coronary plaque is entirely foreign to this bunch.

"The vast majority of people with high calcium tests don't have obstructions and they do fine long-term. So you'd have to test lots and lots of people to prevent one heart attack or sudden death." Well, take a look at a graph from a database of 25,000 people undergoing heart scans then observed for several years afterwards:




You can see quite clearly from the curves that heart scan scores very clearly predict your future (if no preventive action is taken). The higher the score, the greater the likelihood of heart attack and death. How much clearer can it get?

The most recent addition to this literature is the PREDICT study which concluded:

Hazard ratios relative to CACS [coronary artery calcium scores] in the range 0-10 Agatston units (AU) were: CACS 11-100 AU, 5.4 (P = 0.02); 101-400 AU 10.5 (P = 0.001); 401-1000 AU, 11.9 (P = 0.001), and >1000 AU, 19.8 (P < 0.001).

In other words, a heart scan score of >1000 is associated with a 20-fold increased risk of cardiovascular events (without preventive efforts). That kind of predictive power and quantitative confidence simply cannot be squeezed out of blood pressure and cholesterol values.

How about the 2008 University of California-Irvine study from the New England Journal of Medicine (do the northeast docs even pay attention to something that is published in their own neighborhood?) that reported:

There were 162 coronary events, of which 89 were major events (myocardial infarction or death from coronary heart disease). In comparison with participants with no coronary calcium, the adjusted risk of a coronary event was increased by a factor of 7.73 among participants with coronary calcium scores between 101 and 300 and by a factor of 9.67 among participants with scores above 300 (P<0.001 for both comparisons). Among the four racial and ethnic groups, a doubling of the calcium score increased the risk of a major coronary event by 15 to 35% and the risk of any coronary event by 18 to 39%.

How about the Prospective Army Coronary Calcium (PACC) project (men average age 43 years):

"In these men, coronary calcium was associated with an 11.8-fold increased risk for incident coronary heart disease (CHD) (p = 0.002) in a Cox model controlling for the Framingham risk score. Among those with coronary artery calcification, the risk of coronary events increased incrementally across tertiles of coronary calcium severity (hazard ratio 4.3 per tertile)."

Calcium score provided additional information even after factoring in the Framingham risk score.

That's just a sample of the studies. There are a number more.

Add to these conversations the fact that, unlike reducing blood pressure or LDL cholesterol, the heart scan score is a quantification of the disease itself. It can also be tracked over time to gauge the success or failure of prevention efforts. To believe that blood pressure reduction or LDL cholesterol reduction is sufficient to eliminate risk is something only a fool would believe.



Contary to the above statements, the data are clear:

--The higher the heart scan score, the greater the risk. This has been demonstrated beyond any shadow of a doubt in at least a dozen published studies. In fact, heart scan scores outshine lipid/cholesterol values several-fold.

--A person with a zero score has a nearly zero risk for cardiovascular events over a 5-year timeline.

--Heart scans are the only quantitative test available of coronary atherosclerotic plaque. This means that they can be repeated to gauge progression or regression. Cholesterol does not do that. Stress tests do not do that.

--Heart scans are not the same as CT coronary angiography.

--The lack of "need" for a procedure does not equate to the absence of disease.

The power of heart scans is that they can uncover evidence for coronary atherosclerotic plaque 10 years before a cardiac disaster strikes. Witness Tim Russert's heart scan score of 210 in 1998 at age 48. 10 years later, you know what happened.

Beware the camipaign of misinformation and ignorance that continues that is hell-bent on maintaining the procedural status quo or locking us into a "drugs for all" mentality.

What's worse than sugar?

There are a number of ways to view the blood sugar-raising or insulin-provoking effect of foods.

One way is glycemic index (GI), simply a measure of how high blood sugar is raised by a standard quantity of a food compared to table sugar. Another is glycemic load (GL), a combination (multiplied) of glycemic index and carbohydrate content per serving.

Table sugar has a GI of 65, a GL of 65.

Obviously, table sugar is not good for you. The content of white table sugar in the American diet has exploded over the last 100 years, totaling over 150 lb per year for the average person. (Humans are not meant to consume any.)

What is the GI of Rice Krispies cereal, organic or not? GI = 82-- higher than table sugar. GL is 72, also higher than table sugar.

How about Corn Flakes? GI 81, GL 70--also both higher than sugar.

How about those rice cakes that many dieters will use to quell hunger? GI 78, GL 64.

How about Shredded Wheat cereal? GI 75, GL 62.

All of the above foods with GI's and GL's that match or exceed that of table sugar are made of wheat and cornstarch. Some, like Shredded Wheat cereal and rice cakes, don't even have any added sugar.

Stay clear of these foods if you have low HDL, high triglycerides, high blood sugar, or small LDL. Or, for that matter, if you are human.

Keep the eloquent words of New York University nutritionist, Marion Nestle, author of the book, Food Politics, in mind:

“Food companies—just like companies that sell cigarettes, pharmaceuticals, or any other commodity—routinely place the needs of stock holders over considerations of public health. Food companies will make and market any product that sells, regardless of its nutritional value or its effect on health. In this regard, food companies hardly differ from cigarette companies. They lobby Congress to eliminate regulations perceived as unfavorable; they press federal regulatory agencies not to enforce such regulations; and when they don’t like regulatory decisions, they file lawsuits. Like cigarette companies, food companies co-opt food and nutrition experts by supporting professional organizations and research, and they expand sales by marketing directly to children, members of minority groups, and people in develop countries—whether or not the products are likely to improve people’s diets.” ??

Are sterols the new trans fat?

By now, I'm sure you're well-acquainted with the hydrogenated, trans fat issue.

Hydrogenation of polyunsaturated oils was a popular practice (and still is) since the 1960s, as food manufacturers sought a substitute for saturated fat. Bubbling high-pressure hydrogen through oils like cottonseed, soybean, and corn generates trans fatty acids. These man-made fatty acids, while safe in initial safety testing, proved to be among the biggest nutritional mistakes of the 20th century.

Trans fatty acids have been associated with increased LDL cholesterol, reduction in HDL, oxidative reactions, abnormal rigidity when incorporated into cell membranes, and cancer. Trans fats still dominate many processed foods like chips, cookies, non-dairy creamers, food mixes, and thousands of others. They're also found prominently in fast foods.

Fast forward to today, and most Americans have become aware of the dangers of trans fats and many try to avoid them.

But I worry there is yet another substance that has worked its way into the American processed food cornucopia that has some potential for repeating the trans fat debacle: sterol esters.


Sterols are naturally-occurring oils found in vegetables, nuts, and numerous other foods in small quantities. Most of us take in 200-400 milligrams per day just by eating plant-sourced foods.

Curiously, the chemical structure of sterols are very similar to human cholesterol (differing at one carbon atom). Sterols, by not fully understood means, block the intestinal absorption of cholesterol. Thus, sterol esters, as well as the similar stanol esters, have been used to reduce blood levels of total and LDL cholesterol.

So far, so good.

The initial commercial products, released in the late 1990s, were Take Control (sterol) and Benecol (stanol), both of which were marketed to reduce cholesterol when 2-3 tbsp are used daily, providing 3400 – 5100 mg of sterol or stanol esters, about 10- to 20-fold more than we normally obtain from foods. Several clinical trials have conclusively confirmed that these products reduce cholesterol levels.

They do indeed perform as advertised. Add either product to your daily diet and LDL cholesterol is reduced by about 10-15%. In fact, in the original Track Your Plaque book, these products were advocated as a supplemental means of reducing LDL when other methods fell short.

In 2008, there are now hundreds of products that have additional quantities of sterol esters in them, such as orange juice, mayonnaise, yogurt, breakfast cereals, even nutritional supplements. Most of these products proudly bear claims like "heart healthy." Stanol esters have not enjoyed the same widespread application. (I believe there may be patent issues or other considerations. However, it's the sterols that are the principal topic here, not stanols.)

Now, here's where it gets a bit tricky. There is a rare (1 per million) disease called sitosterolemia, a genetic disorder that permits the afflicted to absorb more than the usual quantity of sterols from the intestine. While you and I obtain some amount of sterols from plant-based foods, absorption is poor, and we absorb <10% of sterols ingested. However, people with sitosterolemia absorb sterols far more efficiently, resulting in high blood levels of sterols that result in coronary disease and aortic valve disease, with heart attacks occurring as young as late teens or 20s. Treatment to block sterol absorption are used to treat these people.

There are also a larger number, though still uncommon (1/500) of people who have only one of the two genes that young people with sitosterolemia have. These people may have an intermediate capacity for sterol absorption.

Okay, so what does this have to do with you? Well, if you and I now take in 10-20 times greater amounts of sterol esters, do our blood levels of sterols increase?

Several studies now suggest that, yes, sterol blood levels increase with sterol ingestion. One study from Finland, the STRIP Study, showed that children who had double usual sterol intake increased blood levels by around 50%.

Similarly, a Johns Hopkins study in adults with only one of the genes ("heterozygotes") for sitosterolemia increased sterol blood levels by between 54-116% by ingesting 2200 mg of sterols added per day, despite reduction of LDL cholesterol levels.

Even people with neither gene for sitosterol hyperabsorption can increase their blood levels of sterols. But the crucial question: Do the blood levels of sterols that occur in unaffected people or in heterozygotes increase the risk of coronary heart disease? The answer is not known.

Despite the several clinical trials performed with sterol esters, all of them have examined LDL and total cholesterol reduction as endpoints, not cardiovascular events. It is conceivable that, while sterol esters reduce cholesterol, risk for heart disease is increased due to higher blood levels of sterols.

The question is not settled. For now, it is just a suspicion. But that's enough for me to steer clear of processed foods supplemented with these uncertain sterol esters. My previous recommendations for sterol ester products will be removed with the next edition of Track Your Plaque. Until we have solid evidence that there are no adverse cardiovascular effects of sterol esters, in my view they should not be part of anyone's heart-disease prevention program.

(The same argument does not seem to apply to stanol esters, such as that contained in butter-substitute Benecol, since stanol esters are not absorbed at all and remain confined to the intestine.)

The Diabetes Gold Rush

Lou came into the office. Clearly, his program had gone sour.

Lou had initially obtained wonderful control over his heart scan score of 1114, having reversed modestly in his first three years of effort through correction of his multiple causes (including low HDL, severe small LDL, Lp(a), and a diabetic tendency).

But Lou now came into the office red-faced and sporting a big bulging abdomen. Blood sugar? Now in the overtly diabetic range. Lou said that his primary care doctor had suggested that he start on three new medications (glucophage, injectable Byetta, and Actos) to control his blood sugar. His doctor also told him to increase his intake of fibers by eating more "healthy" breakfast cereals like Cheerios.

Lou had apparently done just that (added "healthy" fiber-rich foods) even before his doctor had suggested it. (Lou failed to remember the several conversations we'd had about healthy eating.) Unfortunately, Lou also failed to connect his increased intake of "healthy fiber-rich foods" and his growing abdominal girth (his "wheat belly").

Here's the dirty little secret: Much of the world wants you to be diabetic. It is the health gold rush of this century. "Go West, young man!"




To find out what I mean, you need only ask: Who profits when people become diabetic? That's easy:

The pharmaceutical industry--Diabetes is a booming growth industry, a source of tens of billions of dollars of revenue, poised for enormous growth as the population ages and gets fatter. It is common for a newly-diagnosed diabetic to be given new prescriptions for two or three drugs with a monthly cost of $300. Of course, the chronic nature of the disease make this far more profitable than, say, a two week course of antibiotics. Presently, 70 new drugs are under development.

Diabetes drug maker Novo Nordisk reported a 25% increase in revenues in 2007 from diabetic agents in the North American market, along with near $2 billion increase in profit for the year. Merck's recently-released DPP-4 inhibitor, Januvia, has already sold $668 million in 2007 and is growing rapidly.

The medical device and supply industry. Take a look at the Medtronic quarterly earnings report, detailing the breakdown of their record-setting quarterly revenue of $3.7 billion:

Diabetes revenue of $269 million grew 12 percent driven by sales
of consumables, the accessories required by insulin pump users, and
continuous glucose monitoring products. Revenue from international
sales grew 31 percent over the same quarter last year.


That's what I call a growth industry.

The processed food industry. The food industry is as big or bigger than the drug industry. ADM, Kraft, General Mills all have annual revenues in the $12-50 billion range. There are plenty of others.

When we're told, for instance, that Cheerios reduces cholesterol, we're not told that it skyrockets blood sugar or triggers small LDL. When we're sold whole wheat crackers, Cocoa Puffs (which the American Heart Asscociation says is heart-healthy), or granola bars, hunger is stimulated, impulse to eat more grows, blood sugar escalates, we get fat, we get diabetic. It's a simple formula.

So be aware that there is little incentive among corporate giants in the food, medical device, or drug industries to encourage behaviors that decrease the incidence of diabetes. In fact, there is enormous financial incentive to make sure that diabetes continues to grow at the startling rate it has over the last decade.

To be sure, the drug and medical device industry will also develop better tools to deal with diabetes and its complications. But the very best way to deal with diabetes is to not develop it in the first place.

What else is there?

This question comes up frequently:

Aren't there any alternatives to heart scans performed on a CT or EBT device?

Yes, there are.

First of all, heart scans are performed best on an electron-beam CT device (EBT) or a 64-slice multi-detector CT (MDCT) device. (While they are also obtainable through less-than-64 slice CT devices (e.g., 16 slices and less), I would advise against it because of the excessive radiation exposure and poor accuracy.) CT heart scans are not to be confused with now more popular CT coronary angiograms, which are performed on the same devices but require intravenous x-ray dye and many times more radiation.(See CT scans and radiation exposure and Heart scan frustration.) Heart scans currently form the basis for the Track Your Plaque program, a program of tracking plaque in the hopes of stopping or reversing the otherwise inevitable 30% per year increase.

Let's confine our discussion to people without symptoms, meaning people like you and me sitting at home, not in an emergency room having chest pain or other similar acute symptomatic presentation.

Among the other ways to uncover hidden coronary plaque:

--Heart catheterization--to yield a coronary angiogram. Yes, this does tell us whether coronary plaque is present. However, it is invasive, expensive, and crude. (I've performed 5000 over my career; they are crude, though useful, tools in acute settings like unstable symptoms or heart attack, a different situation.) Coronary angiography is also non-quantitative. While they provide a value like "40% blockage mid-way in right coronary" or "90% blockage in left anterior descending" they do not provide a trackable lengthwise index of total plaque volume. Identifying severe blockages in people with symptoms leads to stents, bypass surgery and the like, but it is not practical nor of long-term usefulness in apparently, healthy people without symptoms.

--Carotid ultrasound--Here's is where a lot of confusion comes from. Standard carotid ultrasound (U/S) performed in virtually every hospital and many clinics will yield crude qualitative results, e.g., "16-49% stenosis (blockage) in right internal carotid artery". The crude value range is because much of carotid U/S is based on flow velocities, not just direct visualization of the plaque itself ("2-D imaging). However, if carotid stenosis of any degree is identified, the likelihood of silent coronary plaque is much greater.

Limitations: The qualitative, non-quantitative nature of carotid U/S make it difficult to follow long-term in a precise way. Also, this is carotid plaque, not coronary plaque. It makes it very difficult to follow carotid plaque as an indirect means of tracking coronary plaque. The two arterial territories, carotid and coronary, do not track together: there are divergences in many people, with carotid plaque absent in some people with advanced coronary plaque, carotid plaque more susceptible to different risk factors than coronary. So carotid U/S is helpful for its own purposes, but not terribly helpful for coronary tracking.

How about carotid intimal-medial thickness (CIMT) obtained also with carotid U/S? CIMT is a useful index of bodywide atherosclerosis. CIMT is simply a measure not of plaque (and is measured in regions of the carotid artery away from plaque), but of the thickness of the lining of the carotid arteries. Everybody has a measurable CIMT, but it thickens as atherosclerosis grows. CIMT is a radiation-free test that takes several minutes.

Limitations: Hardly anybody does it outside of research protocols. I know of no hospital or clinic in my area that performs CIMT, though it is slowly being adopted in some centers. It is also difficult to rely on repeated tests, because there is substantial variation when one technologist or another performs it. CIMT is also a flawed index of coronary plaque. When CIMT is compared to heart scan scores, CT coronary angiography, or conventional coronary angiography, CIMT correlates about 60-70% with the degree of coronary atherosclerosis.

CIMT is therefore a useful test for research, but a distant 2nd choice--if you can obtain it.

--Ankle-brachial index (ABI)--ABI is a crude measure, simply a comparison of the blood pressure (obtained with a blood pressure cuff) in the legs divided by blood pressure in the arms. The ratio is called ABI. Any ABI <1.0, meaning less pressure in the legs compared to the arms, is indirectly indicative of advanced coronary disease. ABI is, in fact, a very powerful predictor of cardiovascular events. If ABI is <1.0, your future risk for heart attack is very high, even in the absence of symptoms.

Limitations: The vast majority of people with heart disease, even those having undergone stents or bypass surgery, have normal ABI's. Virtually all people with high heart scan scores have normal ABI's. In other words, ABI is a measure of very advanced atherosclerosis only.

--Stress tests--I lump all stress tests together in their various forms, e.g., stress thallium, stress Cardiolite, stress Myoview, persantine/adenosine Cardiolite, dobutamine echocardiography, etc. Stress tests are tests of coronary blood flow, not of plaque. Stress tests are useful in people with symptoms, like chest pain or breathlessness, since stress tests are provocative tests that can help determine whether reduced coronary blood flow is the cause behind a symptom, or whether hiatal hernia, esophagitis, gallstones, pleurisy, musculoskeletal causes, or some other process is behind symptoms.

Limitations: Stress test are virtually useless in people without symptoms. This is why people like Tim Russert and Bill Clinton, both without symptoms, underwent several (Russert 3, Clinton 5) nuclear stress tests---all normal. You know what happened to them. Stress tests do not reliably uncover hidden coronary plaque in people without symptoms. Stress tests are, like coronary angiograms, non-quantitative. They are normal or abnormal.


Outside of experimental settings, that's it.

You can probably see why I advocate CT heart scans for tracking plaque. I do not advocate heart scans because I sell them (I don't), because scan centers pay me to say these things (they don't, and in fact my relationship with my usual heart scan centers has become deeply contentious, though I still endorse the technology). I say that heart scans are superior because they are, in 2008, the only way to 1) identify and 2) track coronary plaque that is easy, safe, low-radiation, and reasonably priced (<$200 in Milwaukee at 5 centers).

The need for a technology that allows tracking of plaque, not just initial identification, is also an important distinction. People who've had some measure of atherosclerosis all catch on to this eventually. "Can I reverse it?" is an inevitable question once the disease is identified in some way. So a tool for tracking over time to gauge the success or failure of a program of prevention can be assessed.

Perhaps in 10 years, another technology will emerge as the preferred means to do the same, but better. If that proves true, we will convert to that technology. But today heart scans performed on CT heart scans are the only rational way to both detect, then track, coronary atherosclerotic plaque.

Let's gamble with your health

Let's play a game.

I'm going to list some lipid patterns and you tell me whether or not the person with these values has heart disease.

Patient 1

Total cholesterol 150 mg/dl
LDL cholesterol 75 mg/dl
HDL 50 mg/dl
Triglycerides 125 mg/dl


Patient 2

Total cholesterol 300 mg/dl
LDL cholesterol 200 mg/dl
HDL cholesterol 35 mg/dl
Triglycerides 325


Patient 3

Total cholesterol 300 mg/dl
LDL cholesterol 100 mg/dl
HDL cholesterol 25 mg/dl
Triglycerides 875 mg/dl



Let's say that any one of these profiles is yours. Should you be getting your affairs in order, preparing for your cardiac catastrophe? Should you demand a stress test from your doctor, hoping that it will shed some light on your dilemma? Should you go ahead and go to the all-you-can-eat rib restaurant, content that you will be attending your granddaughger's wedding in 2020 in full health?

If you can tell, you're a lot better at this than I am.

I provide consultation to other physicians and patients on complex hyperlipidemias in my area. In other words, if someone has a difficulty to manage lipid disorder, the doctor sends the patient to me.

Managing these wildly variable values is the easy part. Deciding whether or not heart disease is concealed within the patient . . . well, that's the hard part.

Let's take it a step further: Suppose all three profiles also have 50% of all LDL particles as the abnormal small particles. And they all have a lipoprotein(a) level of 50 mg/dl, an abnormally high level.

How about now: Can you tell whether any or all of these people have hidden heart disease?

What if they are 20 years old? Does that make a difference?

What if they are all females over 65 years--how about now?

If the only tool you have to divine the presence of hidden heart disease is a lipid panel, or even a lipoprotein panel, then the best you can manage is to hazard a guess based on statistical probability. You also assume that this "snapshot" represents the sorts of values someone has had for their entire lives. You cannot factor in the fact that the first person gained 60 lbs in the last three years since completing menopause. You can't factor in that patient 2 smoked two packs of cigarettes a day for 25 years, but quit 10 years ago.

It's also foolhardy to believe that every known cause of heart disease is currently identifiable and revealed by modern-day blood testing.

A heart scan is simply a means to quantify the sum-total of risk factors--causes--that have exerted an effect up until the moment of your scan. It will reveal the quantity of coronary atherosclerotic plaque present, regardless of whether you stopped smoking 20 years ago or lost 30 lbs last year.

For these reasons, nothing can replace the value of quantifying plaque: not cholesterol, not the Framingham risk calculation, not measures of small LDL or lipoprotein(a), not the presence or absence of symptoms. In 2008, the method of choice for measuring plaque remains a CT heart scan. Perhaps in 10 years it will be some other method.

As always, let me remind Heart Scan Blog viewers that I make this point NOT to sell heart scans, which I have no reason whatsoever to do. I say this because we require a tool to track this potentially fatal disease. We require a yardstick for tracking progression or regression. The only tool that suits these purposes in 2008 is a CT heart scan.

Who knows what

You know that cynical old saying:


It’s not what you know, it’s who you know.

In other words, knowing the right person provides you strategic advantage in business, social advancement, etc.

In health, it was often true. Knowing who the better doctors were, for instance, in your city might provide you with access to better care.

Enter the Information Age. You now have access to medical information equal to that of your doctor. You now have access to patient discussions about doctors, their practices, their performance records. There is now a depth and breadth of information on health that was never available before.

I’d therefore turn the old saying into the new Health 2.0 version:


It’s not who you know, it’s what you know.


In health, information now reigns supreme, not knowing somebody else who has the right connections.

Positive: Everybody now theoretically has access to an equal amount of information, since you can access information on any topic just as easily as I can.

Negative: It puts more of the burden on you. If you screw up in health, perhaps you didn’t try to get the best information hard enough.

I love this new development, this emergence of empowerment in health. I call it self-directed health, the individual capacity to exert enormous influence over the quality of your healthcare.

This is obviously a work in progress. All the answers and tools for self-directed care, self-empowerment are not yet available, some haven’t even yet been imagined.

But they are coming.

“Too many false positives”

“Do you really think I need a heart scan?” asked Terry.

“My doctor said that heart scans show too many false positives. He says that many people end up getting unnecessary heart catheterizations because of them.”

At age 56, Terry was becoming increasingly frightened. His father had suffered his first heart attack at age 53, Terry’s paternal uncle had a heart attack at age 56, his paternal grandfather a heart attack at age 50.

Is this true? Do heart scans yield too many false positives, meaning abnormal results when there really is no abnormality?

No, it is not. What Terry’s doctor is referring to is the fact that, in the decades-long process that leads to heart attack, heart scans have the ability to detect early phases of developing coronary atherosclerotic plaque.

Let’s take Terry’s case, for example. Given his family history, it is quite likely that he does indeed have coronary atherosclerotic plaque. Will it be detectable by performing a stress test? Probably not. In fact, Terry jogs and feels well while doing so. While a stress test abnormality that fails to reach conscious perception is possible, it’s fairly unlikely given his exercise routine.

Will Terry’s coronary atherosclerotic plaque be detectable by heart catheterization? Very likely. But why perform an invasive hospital procedure just as a screening test? Should a woman wishing to undergo a screening test for breast cancer undergo breast removal? Of course not.

Is waiting for symptoms a rational way to approach diagnosis of heart disease? Well, when symptoms appear, it means that coronary blood flow is reduced. Stents and bypass surgery may be indicated. The risk of heart attack and death skyrocket. Sudden death becomes a real possibility.

In the 30 or so years required to establish sufficient coronary plaque to permit the appearance of symptoms or the development of an abnormality detectable by stress testing, there were many years when the disease was early--too early to generate symptoms, too early to be detectable by stress testing.

That’s when heart scans uncover evidence for silent coronary atherosclerotic plaque.

Should we call this a “false positive” just because it doesn’t also correlate with “need” for a catheterization, stent, bypass operation or result in heart attack within the next few weeks?

The detection of early plaque is just that: early disease detection.

Imagine, for instance, that the breast cancer that will grow into a palpable nodule or mass detectable by mammogram is detectable by a special breast scan 15 years before it becomes a full-blown tumor, metastasizing to other organs. What if effective means to halt that earliest evidence of cancer could put a stop to this devastating disease decades ahead of danger? Is this a “false positive” too?

In my view, this is the knuckleheaded thinking of the conventional practitioner: “Don’t bother me until you’re really sick.” Prevention is a practice that has become fashionable only because of the push of the drug industry. Nutrition is an afterthought, a message conceived through consensus of “experts” with suspect motivations and allegiances.

So, no, heart scans do not uncover “false positives.” They uncover early disease--true positives--years before it is detectable by standard tests or by the appearance of catastrophe. But that is the whole point: Early detection means getting a head start on prevention.

Do heart scans lead to unnecessary heart catheterizations? Yes, sadly they do. But not because heart scans are false positive. It happens because of unscrupulous or ignorant cardiologists who use the information wrongly. In my view, heart scans should NEVER lead directly to heart catheterization in an asymptomatic patient. Heart scans, as helpful as they are, do not modify the standard reasons for performing heart procedures.

If a car mechanic is dishonest and fixes a carburetor that didn't need fixing, should we condemn all car mechanics? No, of course not. We only need to develop the means to weed out the bad apples. The same applies to heart scans.

Triglycerides divided by five

Here's a bit of lipid tedium that might nonetheless help you one day decipher the meaning of shifts in your cholesterol panel.

Recall from prior discussions that conventional LDL cholesterol is a calculated value. Contrary to popular opinion, LDL is usually not measured, but calculated from the Friedewald equation:

LDL cholesterol = Total cholesterol - HDL cholesterol - triglycerides/5

For the sake of simplicity, let's call total cholesterol TC; HDL cholesterol HDL, and triglycerides TG.

We've also talked in past how a low HDL makes calculated LDL inaccurate, sometimes wildly so. (See Low HDL makes Dr. Friedewald a liar.)

Here's yet another source of inaccuracy of the Friedewald-calculated LDL: any increase in triglycerides.

Let's say, for instance, that starting lipid panel shows:

TC 170 mg/dl
LDL 100 mg/dl
HDL 50 mg/dl
TG 100 mg/dl



You're advised to follow a standard low-fat, whole grain-rich diet advocated by "official" agencies (the diet I bash as knuckleheaded). Another panel a few months later shows:

TC 230 mg/dl
LDL 140 mg/dl
HDL 50 mg/dl
TG 200 mg/dl



(Obviously, I've oversimplified the response for the sake of argument. HDL would likely go down, LDL would change more depending on body weight, small LDL tendencies, and other factors. You'd also likely get fat.)

Now your doctor declares that your LDL has gone up and you "need" a statin agent.

Nonsense, absolute nonsense.

What has really happened is that the increased dietary intake of wheat and other "healthy whole-grain foods" has caused triglycerides to skyrocket. LDL increases, in turn, by a factor of TG/5, or 40 mg/dl. Thus, LDL has been inflated by the triglyceride-raising effect of whole grains.

This is yet another reason why the standard lipid panel, full of hazards and landmines, needs to be abandoned. But calculated LDL in particular is an exercise in frustration.

Though the example used is hypothetical, I've witnessed this effect thousands of times. I've also seen many people placed on statin drugs unnecessarily, due to the appearance of a high LDL cholesterol that really represented increased TG/5, usually induced by an excessive carbohydrate intake, including those commonly misrepresented as healthy such as whole grains.

Who reads The Heart Scan Blog?

In the Heart Scan Blog, I am often guilty of speaking out loud of my varied thoughts on this crazy thing that we've created called the cardiovascular healthcare machine. But I discuss it in the context of asking "How could this be done better--better outcomes, more patient-friendly, more accessible . . . more do-it-yourself?

The last part is the part that throws most people. Do-it-yourself? My colleagues would claim I'm nuts, suggesting that coronary heart disease is something manageable by yourself. In the conventional pathway, after all, coronary disease is that unpredictable, poorly detected by standard tests, condition that then leads to heart catheterization, stents, bypass , and the like.

Several factors distinguish the readers of The Heart Scan Blog that surprised me:

--Nearly 60% are women
--There are a disproportionate number of Asian people. (Can someone explain this to me?)
--A great number have graduate degrees

I believe this tells me that The Heart Scan Blog appeals to a somewhat more sophisticated audience. This, to some degree, warms my heart, since it means that I've captured the attention of some people who may be more discriminating and thoughtful in their Internet surfing.

However, I also lament the fact that these conversations are not achieving the mainstream. After all,