Do stents prevent reversal?

I've seen this phenomenon several times now: A highly-motivated Track Your Plaque participant with a stent in one artery will do all the right things--lose weight, achieve 60:60:60 in basic lipids, identify and correct hidden lipoprotein disorders, take fish oil, correct vitamin D, etc.

Follow-up heart scan shows dramatic reduction in scoring in the two arteries without stents--30% per artery. But the artery with the stent will show marked increase in scoring above and/or below the stent. (It's impossible to tell what happens in or around the stent itself from a calcium scoring standpoint, since steel looks just like calcium on a CT heart scan.) In other words, there is marked plaque growth in the vicinity of the stent, despite the fact that dramatic reversal of atherosclerosis has occurred in other arteries without stents.

Should we take this to mean that a stent destroys the opportunity for atherosclerotic plaque reversal in the stented artery? I don't know, but I fear this may be true. What dangers does this different sort of plaque pose? Is it the result of the injury imposed at time of stent implantation, some modification of flow or biologic responses as a result of the presence of the stent?

These are all unanswered questions. But I believe that it is yet another suggestive piece of evidence that the best stent is no stent at all.

At what score should I have a heart cath?

This question comes up frequently: At what specific heart scan score should a heart catheterization be performed? In other words, is there a specific cut-off that automatically triggers a need for catheterization?

In my view, there is no such score. We can't say, for instance, that everybody with a score above 1000 should have a catheterization. It is true that the higher your score, the greater the likelihood of a plaque blocking flow. A score of 1000 carries an approximately 25-30% likelihood of reduced blood flow sufficient to consider a stent or bypass. This can nearly always be settled with a stress test. Recall that, despite their pitfalls for uncovering hidden heart disease in the first place, stress tests are useful as gauges of coronary blood flow.

But even a score of 1000 carries a 70-75% likelihood that a procedure will not be necesary. This is too high to justify doing heart catheterizations willy-nilly.

Unfortunately, some my colleagues will say that any heart scan score justifies a heart cath. I believe this is absolutely, unquestionably, and inexcusably wrong. More often than not, this attitude is borne out of ignorance, laziness, or a desire for profit.

Does every lump or bump justify surgery, radiation, and chemotherapy on the chance it could represent cancer? Of course not. There is indeed a time and place for these things, but judgment is involved.

In my view, no heart scan score should autmatically prompt a major heart procedure like heart catheterization in a person without symptoms.

Niacin makes NY Times

In the wake of the crash and burn of Pfizer's torcetrapib, media attention has turned up the miracles of . . .good old niacin. The NY Times carried a well-written report on niacin in its recent report, An Old Cholesterol Remedy Is New Again.


(Read the entire report at http://www.nytimes.com/2007/01/23/health/23consume.html?em&ex=1169701200&en=670fa84ae2ea648c&ei=5087%0A)

Among their comments:

...torcetrapib worked primarily by increasing HDL, or good cholesterol. Among other functions, HDL carries dangerous forms of cholesterol from artery walls to the liver for excretion. The process, called reverse cholesterol transport, is thought to be crucial to preventing clogged arteries.

Many scientists still believe that a statin combined with a drug that raises HDL would mark a significant advance in the treatment of heart disease. But for patients now at high risk of heart attack or stroke, the news is better than it sounds. An effective HDL booster already exists.

It is niacin, the ordinary B vitamin.

In its therapeutic form, nicotinic acid, niacin can increase HDL as much as 35 percent when taken in high doses, usually about 2,000 milligrams per day. It also lowers LDL, though not as sharply as statins do, and it has been shown to reduce serum levels of artery-clogging triglycerides as much as 50 percent. Its principal side effect is an irritating flush caused by the vitamin’s dilation of blood vessels.

Despite its effectiveness, niacin has been the ugly duckling of heart medications, an old remedy that few scientists cared to examine. But that seems likely to change.

“There’s a great unfilled need for something that raises HDL,” said Dr. Steven E. Nissen, a cardiologist at the Cleveland Clinic and president of the American College of Cardiology. “Right now, in the wake of the failure of torcetrapib, niacin is really it. Nothing else available is that effective.”

In 1975, long before statins, a landmark study of 8,341 men who had suffered heart attacks found that niacin was the only treatment among five tested that prevented second heart attacks. Compared with men on placebos, those on niacin had a 26 percent reduction in heart attacks and a 27 percent reduction in strokes. Fifteen years later, the mortality rate among the men on niacin was 11 percent lower than among those who had received placebos.

'Here you have a drug that was about as effective as the early statins, and it just never caught on,' said Dr. B. Greg Brown, professor of medicine at the University of Washington in Seattle. 'It’s a mystery to me. But if you’re a drug company, I guess you can’t make money on a vitamin.'



Of course, you and I don't have to wait for the media to endorse something. I'm nonetheless thrilled that this hugely helpful vitamin is gaining greater recognition. My preferred form nowadays is over-the-counter SloNiacin (Upsher Smith). Weve seen no liver side-effects and a minimal quantity of flushing. It's also reasonably priced, $13.99 for 100 tablets of 500 mg at Walgreen's. That's a lot cheaper than prescription Niaspan at $130 for 60 tablets.

Perhaps the notoriety will cut back on the silly responses from some physicians that I still hear about from patients: "My doctor said to stop the niacin because it's going to destroy my liver."

Wheat: the nicotine of food

Yes, we know that wheat contributes to creating small LDL, drops HDL, raises triglycerides, and VLDL. We also know it indirectly slows the clearance of after-eating fats from the blood (curious, I know). Wheat products also increase inflammation (C-reactive protein), raise blood sugar, and contribute tremendously to diabetes.

What many people don't know is that wheat products also have an addictive quality: have one donut and you want another. It's true for bread, breakfast cereals, pretzels, cookies, etc. How many times have you had just one Oreo cookie?

Curiously, elimination of wheat products, unlike elimination of nicotine, usually causes the cravings to disappear. In other words, if you stop smoking cigarettes, the desire to smoke doesn't go away. With wheat products, the often overwhelming desire for more wheat products often just goes away.

But most people are simply unable to dramatically reduce or eliminate wheat products from their daily diet and therefore struggle each and every day with excessive cravings for bagels, donuts, cookies, breads, etc.

Try this useful experiment: Eliminate wheat products for a month and see what happens. Most people drop blood pressure, lose the tummy excess, feel more alert, see a drop in blood sugar, experience improvements in lipoproteins, and regain control over appetite.

Good time for a heart attack?

Man Has Heart Attack At Right Place, Right Time

If Robert Ricard had picked the wrong restaurant for lunch, he might have died.

The 71-year-old Michigan man suffered a heart attack shortly after ordering a glass of wine with friends at Bentley's Roadhouse on Saturday.

Luckily, a disaster medical team was sitting nearby.



A TV station in Michigan reported the above story. You've heard these "if it wasn't for ___, so and so would have died" stories. They're reported in all cities at one time or another.

What amazes me about these common local stories is that they're accepted at all. The question that comes to my mind is "Why couldn't the heart attack have been averted in the first place?" Early identification then, as close as humanly possible, elimination of risk would have been a preferable path.

Of course, it may not be the role of the media to cast judgement on why and how the entire episode could have been completely prevented from occurring. But you shouldn't fall into the same trap of complacency. We cannot expect others to save us when the "big one" hits. Your best assurance is to never have one in the first place.

How good is the South Beach Diet?

I'm a fan of the South Beach Diet.

Though it is billed as a program for weight loss (for which it is very effective), it is really a program for health. The basic approach of South Beach involves:

Eat good fats — Choose good fats from olive oil, canola oil, peanut oil, flaxseed oil, walnut oil, avocados, nuts, and fish. Omega-3 (fish oil) supplements are also fine.


Eat good carbs — Good carbs include high-fiber, nutrient-dense fruits, vegetables, legumes, and whole grains.

Eat lean protein — Good sources include eggs, low-fat dairy, nuts, seeds, legumes, skinless white-meat poultry, fish, shellfish, lean cuts of meat, and vegetarian options such as tofu.

(From The South Beach Diet, Dr. Arthur Agatston)


There's no doubt that South Beach can yield dramatic weight loss. In my experience, the success in weight loss depends on 1) how unhealthy your diet was in the first place, and 2) how long you can stick to Phase I, the inital phase during which weight loss is most dramatic. Some people have to periodically cycle back to Phase I to break a "plateau" or to lose faster.

But South Beach is also healthy. It has all the ingredients of a healthy eating program: Low saturated and hydrogenated fats, rich in monounsaturated fats, high fiber, low- to moderate- glycemic index, vegetables and fruits, lean proteins.

The Atkins' diet, in contrast, while very effective for weiglht loss, is an unhealthy process. I've seen lots of bladder infections, constipation, skin rashes, and kidney stones. That's just in the short term. If you stick to the "induction phase" (the no carbohydrate, low fiber, indiscriminate fat initial phase) for an extended period, I suspect that other adverse internal phenemena also develop that might not show for years, like cancer. But--it does work for weight loss!

South Beach's Phase I is also carbohydrate restricted, but steers you towards healthier foods, such as healthy oils from olive and canola, raw or dry roasted nuts, and lean proteins and vegetables.

What really makes South Beach special, however, are its clever recipes. Dr. Arthur Agatston (the author) involved chefs from the restaurants in the South Beach area of Miami to help create healthy yet delicious recipes. We've tried many of them and, while they are different from traditional fare, are delicious and satisfying for the most part.

Criticisms? None, really. But, when my patients choose South Beach (which I often encourage), I often have to impress on them that the Track Your Plaque program is not about weight loss. It is about seizing control of a potentially life-threatening disease. It is a far more important goal with greater implications. Weight loss is just one aspect of a coronary plaque control effort. For this reason, we sometimes have to make changes in the South Beach program to allow for correction of specific lipoprotein patterns.

The most common modification is in people with small LDL particles. This pattern often does indeed respond to weight loss and/or niacin. However, it occasionally persists despite these efforts. We then will ask the patient to continue to restrict the re-introduction of wheat products, though it is allowed after Phase I in South Beach. In other words, for this specific and sometimes difficult to control lipoprotein pattern, a spedific modification of the off-the-shelf South Beach program is sometimes necessary. Of course, the diet is created to suit everybody. Lipoprotein analysis permits detailed insight into your patterns and it's only to be expected that specific modifications might be needed.

But, as written, you can do quite well in your plaque control program by sticking to South Beach.

Be patient with niacin

Mel's HDL started at 37 mg/dl one year ago. Mel had several other abnormal lipoprotein patterns along with his HDL (inc. small LDL and Lp(a)), but HDL was clearly a crucial factor in his panel.

With a heart scan score of 1166, we needed to raise Mel's HDL to the Track Your Plaque target of 60 mg/dl. So Mel started niacin, our number one method to raise HDL, in addition to reducing his exposure to wheat products and other high glycemic index foods; increasing his physical activity; trying to reduce his excess tummy fat; fish oil; dark chocolate (2 oz per day) and red wine (1-2 glasses per day, preferably dark French reds). The form of niacin we often choose is SloNiacin (Upsher Smith), available over-the-counter for about $12-14 per 100 tablets.

Mel started out with niacin 500 mg per day at dinner, increased to 1000 mg at dinner after four weeks. Although this is usually too soon to reassess HDL, Mel insisted. His HDL 41 mg/dl. Mel's disappointment was palpable. He was the usual type A personality: he wanted his HDL higher--now! So Mel insisted that we increase niacin to 1500 mg per day. (We never go higher than this if low HDL or small LDL is the indication for niacin; only when Lp(a) is present do we go higher.)

Six months into this process, HDL: 45 mg/dl. Still a sluggish response.

One year later, HDL: 68 mg/dl. Finally!

That is typical for niacin, as well as combination of lifestyle changes Mel made. None of them result in an immediate rise in HDL; all take months to 1-2 years to exert full HDL-raising effect.

Think of HDL as the 82-year old grandma who takes a long time to cross the street-she does get there!

Note: Doses of niacin >500 mg per day should be taken with medical supervision.

Can vitamin D be a SOLE risk factor?

Here's a crazy question. It occurred to me as I was talking to Drew, a slender, active 54-year old dentist with no bad habits including no smoking.

Drew's heart scan score was 222. His lipoprotein analysis mostly revealed a lot of nothing, which is unusual. The only pattern that showed up was a modestly high LDL of 122 mg/dl with a very slight excess of small LDL. That's it. I would not be satisfied that these were sufficient cause for Drew's level of coronary plaque.

Drew's 25-OH-vitamin D3 level: 15 ng/ml--severe deficiency--despite the fact that his doctor had suggested that he take a vitamin D2 preparation. In other words, Drew had been profoundly deficient, probably for years.

Given the unimpressive cholesterol and lipoprotein values, could vitamin D serve as a trigger for coronary plaque all by itself?

I don't have an answer and know of nobody else who does. However, my opinion is that vitamin D is indeed a potent risk that can cause heart disease as a sole risk factor.

Perhaps it's another piece of circumstantial evidence suggesting that vitamin D has an enormous influence on health, including coronary plaque. Interestingly, the only other health problem Drew has had is prostate cancer, treated a few years ago with prostate removal and radiation. Good evidence suggests that vitamin D deficiency escalates risk of prostate cancer substantially.

By the way, I've seen people taking vitamin D2 preparations, called "ergocalciferol," who are every bit as deficient as those who take no vitamin D at all. Avoid D2 or ergocalciferol preparations: they're worthless.

Does fish oil raise LDL cholesterol?

Katie had an LDL (conventionally calculated) of 87 mg/dl, HDL of 48 mg/dl.

She added fish oil, 6000 mg per day. Three months later her LDL was 118 mg/dl, HDL 54 mg/dl. In other words, LDL increased by 31 mg. What gives?

Several studies have, indeed, shown that fish oil raises LDL cholesterol, usually by 5-10 mg/dl. Occasionally, it may be as much as 20-30.

Unfortunately, many physicians often assume that it's the (minor) cholesterol content of fish oil capsules, or some vague, undesirable effect of fish oil. It's nothing of the kind.

Since we based Katie's program on (NMR) lipoprotein analysis, not conventional lipids (HDL, calculated LDL, triglycerides, total cholesterol), I knew that Katie also had a severe excess of intermediate-density lipoprotein, or IDL, and very-low density lipoproteins, VLDL. This signifies that after a meal, dietary fats persist for 12, 24,or more hours. Fish oil is a very effective method to clear IDL and VLDL, though sometimes it also causes a shift of some IDL and VLDL into the LDL class. Thus, the apparent increase in LDL.

Another contributor: Conventional LDL is a calculated value, not measured. The calculation for LDL is thrown off by any reduction in HDL or rise in triglycerides. In Katie's case, the rise in HDL from 48 to 54 means that calculated LDL is becoming more accurate and rising towards the true measured value. At the start, Katie's true measured LDL was 122 mg/dl, 35 mg higher than the calculated value. Calculated LDL is therefore approximating measured LDL more accurately as HDL rises.

The most important lesson to learn is that, if LDL rises significantly on fish oil and you haven't had lipoproteins formally measured, there may have been a substantial postprandial abnormality like IDL that was unrecognized.

Heart disease is everywhere

If you ever need convincing that heart disease is everywhere, you should do what I do: subscribe to Google Alerts and have them forward news anytime the search phrase "heart attack" crosses the web. (Just go to Google, click on "more" to the right of the search bar, and follow the links.)


Some recent samples:


Workmates resuscitate driver after heart attack

A woman coal mine truck driver had a heart attack and required resuscitation with a defibrillator 3 times on the way to the hospital.





Heart attack kills groom at reception
A 34-year old man died during his wedding reception, leaving behind his 26-year old new wife.






Heart attack ruled as cause of crash

An Alabama man drove his pick-up truck into oncoming traffic while suffering a heart attack.






Heart-attack victim to return to Hamburg stage


Country music artist, Michael Harding, suffered a heart attack and cardiac arrest during a performance. He is apparently recovered and returning to the stage.



That's just a sample from the last two days. While you and I are carry on a conversation on reversal of heart disease, our neighbors and friends drop over every day. Even though I witness successful heart disease reversal routinely, the rest of the world is not participating.

Pass it on: Coronary disease is identifiable, preventable, controllable, and reversible.
All posts by william-davis

Emmer, einkorn, and agribusiness

10,000 years ago, Neolithic humans did not obtain wheat products from the bagel shop, grocery store, or Krispy Kreme. They obtained wheat by locating a nearby wild-growing field of wild emmer or einkorn wheat grass, then harvesting it with their stone sickles.

Neolithic humans, such as the Natufians of the Fertile Crescent, carried their freshly-cut wheat home, then ground it by hand using homemade mortar and pestle. As yeast-raised bread was still some 5000 years in the future, emmer and einkorn wheat was not used to bake bread, but was consumed as a porridge in bowls. Einkorn has the simplest genetic code of 14 chromosomes, while emmer has 28 chromosomes.

A third variety of wheat appeared on the scene around 9000 years ago, a natural hybridization between emmer and goat grass, yielding the 42-chromosome Triticum aestivum species. Egyptians learned how to cause wheat to rise around 3000 BC, yielding bread, rather than the unleavened flatbreads of their predecessors.

From the original three basic varieties of wheat available to Neolithic man, over the past 30 years wheat has exploded to over 25,000 varieties. Where did the other 24,997+ strains come from?

In the 1980s, thousands of new wheat strains arose from hybridization experiments, many of them conducted in Mexico. Then, in the late 1980s, genetic engineering quietly got underway in which geneticists inserted or deleted single genes, mostly designed to generate specific characteristics, such as height, yield per acre, drought resistance, but especially resistance to various pesticides and weed killers. The fruits of these efforts were introduced into the market in 1994. Most of the genetically modified foods were thought to be only minor modifications of the unmodified original and thus no safety testing in animals or humans was conducted.

We now have many thousands of wheat strains that are different in important ways from original emmer, einkorn, and Triticum aestivum wheat. Interestingly, it has been suggested that einkorn wheat fails to provoke the same immune response characteristic of celiac disease provoked by modern wheat gluten, suggesting a different amino acid structure in gluten proteins. Another difference: Emmer wheat is up to 40% protein, compared to around 12% protein for modern wheat.

In other words, the wheat of earlier agricultural humans, including the wheat of Biblical times, is NOT the wheat of 2010. Modern wheat is quite a different thing with differing numbers of chromosomes, different genes due to human manipulation, varying gluten protein composition, perhaps other differences.

Somewhere in the shuffle and genetic sleight-of-hand that has occurred over the last 30 years, wheat changed. What might have been the "staff of life" has now become the cause of an incredible array of diseases of "wheat" intolerance.

Near-death experience with nattokinase

This is a true story that I personally witnessed.

A 60-some year old man heard that nattokinase "thinned the blood." So he had been taking it for the past 6 months.

One week before he came to see me, he abruptly became quite breathless. He was unable to walk more than 20 feet or bend over to tie his shoes due to the breathlessness.

He came to see me in the office. I was alarmed by how breathless he was without signs of heart failure or other obvious explanation. I sent him for an immediate CT pulmonary angiogram. Within 30 minutes, we had the diagnosis: a large "saddle" pulmonary embolus, meaning a large blood clot that straddled the right and left main pulmonary arteries. One wrong move and . . . bang! He would have been dead within a couple of minutes, since a large clot can completely occlude the large arteries feeding the lung, essentially corking any blood circuiting through the lungs and back to the left side of the heart. (Causing, incidentally, electromechanical dissociation, in which the heart keeps beating for a few minutes but no blood is being pumped. CPR can keep you alive for a few minutes, then it's over.)

When I advised the patient of the diagnosis (after initiating the REAL anticoagulants), he said, "But I was taking nattokinase!"

Exactly. Blood clots are no laughing matter. They are potentially fatal events. Betting your life on some company's advertisement is nothing short of foolish.

Anyone who reads The Heart Scan Blog knows that I am an avid supporter of nutritional supplements. I even write articles and consult for the supplement industry. But I truly despise hearing unfounded marketing claims that some supplement companies will make in the pursuit of a fast buck.

There is no doubt that we need better, safer methods to deal with dangerous blood clots, whether in the lung, pelvis, or other areas. But, before anyone takes a leap based on the extravagant marketing claims made by a supplement manufacturer, you want to be damn sure there are real data--not marketing claims, REAL data--before you use something like nattokinase in place of a proven therapy.

Don't confuse the very interesting, though unpalatable, natto with nattokinase. Natto contains vitamin K2 and some other interesting compounds, including nattokinase.

Blame the gluten?

Wheat is among the most destructive components of the human diet, a food that is responsible for inflammatory disease, diabetes, heart disease, several forms of intestinal diseases, schizophrenia, bipolar illness, ADHD, behavioral outbursts in autistic children . . . just to name a few.

But why?

Wheat is mostly carbohydrate. That explains its capacity to cause blood sugar to increase after eating, say, a turkey sandwich on whole wheat bread. The rapid release of sugars likely underlies its capacity to create visceral fat, what I call "wheat belly."

But neither the carbohydrate nor the other components, like bran and B vitamins, can explain all the other adverse health phenomena of wheat. So what is it in wheat that, for instance, worsens auditory hallucinations in paranoid schizophrenics? Is it the gluten?

First of all, what is gluten?

Gluten protein is the focus of most wheat research conducted by food manufacturers and food scientists, since it is the component of wheat that confers the unique properties of dough, allowing a pizza maker to roll and toss pizza crust in the air and mold it into shape. The distinctive “doughy” quality of the simple mix of wheat flour and water, unlike cornstarch or rice starch, for instance, properties that food scientists call “viscoelasticity” and “cohesiveness,” are due to the gluten. Wheat is mostly carbohydrate, but the 10-15% protein content is approximately 80% gluten. Wheat without gluten would lose its unique qualities that make it desirable to bakers and pizza makers. Gluten is also the component of wheat most confidently linked to immune diseases like celiac.

The structure of gluten proteins has proven frustratingly elusive to characterize, as it changes over time and varies from strain to strain. But an understanding of gluten structure may be part, perhaps most, of the answer to the question of why wheat provokes negative effects in humans.

The term “gluten” encompasses two primary families of proteins, the gliadins and the glutenens. The gliadins, one of the protein groups that trigger the immune response in celiac disease, has three subtypes: a/ß-gliadins, ?-gliadins, and ?-gliadins. The glutenins are repeating structures, or polymers, of more basic protein structures.

Beyond gluten, the other 20% or so of non-gluten proteins in wheat include albumins, prolamins, and globulins, each of which can also vary from strain to strain. In total, there are over 1000 other proteins that serve functions from protection of the grain from pathogens, to water resistance, to reproductive functions. There are agglutinins, peroxidases, a-amylases, serpins, and acyl CoA oxidases, not to mention five forms of glycerinaldehyde-3-phosphate dehydrogenases. I shouldn’t neglect to mention the globulins, ß-purothionin, puroindolines a and b, tritin, and starch synthases.

As if this protein/enzyme smorgasbord weren’t enough, food processors have also turned to fungal enzymes, such as cellulases, glucoamylases, xylanases, and ß-xylosidases to enhance leavening and texture. Many bakers also add soy flour to enhance mixing and whiteness, which introduces yet another collection of proteins and enzymes.

In short, wheat is not just a simple gluten protein with some starch and bran. It is a complex collection of biological material that varies according to its genetic code.

While wheat is primarily carbohydrate, it is also a mix of gluten protein which can vary in structure from strain to strain, as well as a highly variable mix of non-gluten proteins. Wheat has evolved naturally to only a modest degree, but it has changed dramatically under the influence of agricultural scientists. With human intervention, wheat strains are bred and genetically manipulated to obtain desirable characteristics, such as height (ranging from 18 inches to over 4 feet tall), “clinginess” of the seeds, yield per acre, and baking or viscoelastic properties of the dough. Various chemicals are also administered to fight off potential pathogens, such as fungi, and to activate the expression of protective enzymes within the wheat itself to “inoculate” itself against invading organisms.

From the original two strains of wheat consumed by Neolithic humans in the Fertile Crescent 9000 years ago (Emmer and Einkorn), we now have over 200,000 strains of wheat virtually all of which are the product of genetic manipulations that have modified the protein structure of wheat. The extraordinary complexity of wheat proteins have therefore created a huge black box of uncertainty in pinpointing which protein causes what.

But there's an easy cure for the uncertainty: Don't eat it.

Glycemic gobbledygook

The concept of glycemic index is meant to help determine what foods raise blood sugar a lot vs. what foods raise blood sugar a little. Dr. Jennie Brand-Miller's searchable database can be found here.

I have to admit that glycemic index provided me with a sense of false assurance for some years. It screwed up my health until I came to understand the issues a lot better.

For those of you just starting out in nutritional conversations, glycemic index (GI) represents a comparison of the blood glucose area-under-the-curve (AUC) over 2 hours after consuming 50 grams of the food in question compared to the AUC of glucose or white bread. Volunteers involved in developing these values are healthy people who are generally of normal weight.

Glucose, by definition, has a GI of 100. An equal quantity of sucrose (50% glucose, 50% fructose) has a GI of 60, lower than glucose. An equal quantity of whole wheat bread has a GI of 68-77 (Yes: The GI of whole wheat is higher than sucrose). Non-carbohydrate foods, such as eggs or avocado, have no GI since they do not impact on blood glucose.

Because the GI is also sensitive to how much carbohydrate is contained, the concept of Glycemic Load (GL) was introduced:

GL = (GI x amount of carbohydrate) / 100

GL is therefore the GI that incorporates the glycemic potential of the food of interest. GI does not vary with portion size; GL varies with portion size.

Let's take whole wheat pasta, a food regarded by most people as a healthy choice. Whole wheat pasta has a GI of 55--fairly low--and a GL of 29. A serving of 180 g (approximately 6 oz cooked) provides 50 g carbohydrates.

People who advocate that low-glycemic index foods would say that this is a desirable profile and should therefore replace high-glycemic index foods.

I say WRONG. First of all, most of us are not slender 20-somethings. We will therefore not show the same response as a young, slender person (like the GI volunteers), but will show exagerrated blood sugar responses. So this much low-glyemic index whole wheat pasta will typically yield a blood sugar of 120-200 mg/dl in non-diabetic people, high enough to trigger glycation. Sure, a high-glycemic index food, such as white flour birthday cake with plenty of sugary icing, might trigger a blood sugar of 140-250 mg/dl, much worse. But that doesn't make the lower blood sugar following pasta any less bad--it's still terrible.

Another issue: GI is assessed over a 2-hour timeline. What if blood sugar remains high in a sustained way, say, over 6 hours? That's precisely what whole wheat pasta will do: Keep blood sugar high for an extended period.

So not only does a low-glycemic index food like pasta increase blood sugar in most of us extravagantly, it does so in a sustained way.

Lastly, low-glycemic index pasta still triggers small LDL particles to an extreme degree, as I discussed in the previous Heart Scan Blog post, Small LDL: Complex vs. simple carbohydrates.

Don't be false reassured by the notion of low GI or GL. In fact, I'd go so far as to say that NO glycemic index is a GOOD glycemic index (or load). The foods we want to dominate our diet are the foods that aren't even listed in the GI database.

Man walks after removing wheat

No, this isn't some National Enquirer headline like "Woman delivers alien baby."

Tom is a 26-year old man with a complex medical condition, a malformation he was born with and has had reconstructed. Aside from this, he leads a normal life: works, is married, and is, in fact, quite intelligent.

He came to me for an opinion regarding his overall health. Tom was worried that his congenital condition would impair his long-term health and longevity prospects, so he wanted to optimize all other aspects of his health.

But, when I examined Tom, he could barely get himself up on the exam table without wincing in pain. When I asked him to walk, he hobbled a few steps, again clearly in pain. When I asked him what hurt, he said "everything." He said that all his joints hurt just to move.

He told me that his several doctors over the years didn't know why he was in such pain: It wasn't rheumatoid arthritis, gout, pseudogout, or any of the other inflammatory joint diseases that might account for virtually incapacitating this 26-year old man. Even the rheumatologists were stumped. It was also unrelated to his repaired congenital condition. So Tom went on with his life, barely able to even go for a walk with his wife without pain, slowing him down to the pace of an 80-year old.

So I suggested that he eliminate all wheat products. "I don't know for a fact whether it will work, Tom. But the only way to find out is to give it a try. Why not try a 4-week period of meticulously avoiding wheat? Nothing bad will come of it."

He and his wife look perplexed, but were so desperate for a solution that they agreed to give it a try.

Tom returned 6 weeks later. He walked into the room briskly, then bounded up on the exam table. He told me that, within days, all his joint pains had completely disappeared. He could walk, stretch, do all the normal physical things with none of the pain he had suffered previously.

Tom told me, "I didn't think it could be true. I thought it was just a coincidence. So I had a sandwich about 2 weeks into it. In about 5 minutes, I got about half my pains back."

Tom now remains wheat-free and pain-free, thankfully with no discernible joint impairment.

So, yes, Tom walked freely and without pain simply by eliminating wheat from his life.

Is it an immune phenomenon? Does wheat gluten trigger some inflammatory reaction in some people? There is surely something like this underlying experiences like Tom.

Wheat contains far more than gluten. Modern wheat is a collection of hundreds of different proteins, though gluten is the most plentiful, the one that confers the "viscoelasticity" of dough. But there's plenty more to wheat than gluten or celiac disease.

AGEing gracefully

Advanced Glycation End-products, or AGEs, have the potential to change our entire conversation about diet.

AGEs come from two principal sources:

1) Endogenous--Glucose-protein interactions that arise from high blood glucose levels

2) Exogenous--From diet

The first is sensitive to glucose levels: the higher the glucose level, the greater the AGE formation. The second depends on the quantity of AGE in the food consumed.

A compelling body of evidence points towards AGEs as an agent of aging, as well as kidney dysfunction, dementia, and atherosclerosis. Some of the observations made include:

--If AGEs are infused into an experimental animal, it develops atherosclerosis, kidney disease, and other "diseases of senescence" within weeks to months.

--In endothelial cells (cells lining arteries), AGE induces expression of adhesion molecules and inflammatory signals. In fibroblasts, AGE provokes collagen production. In smooth muscle cells, AGE triggers migration and proliferation. In monocytes and macrophages, AGEs induce chemotaxis and release of inflammation mediators. In short, AGEs have been implicated in just about every step leading to atherosclerosis.

--In humans, greater quantities of AGEs are present in diabetics, pre-diabetics and people with insulin resistance. We all know that these people develop atherosclerosis, kidney disease, cataracts, and other conditions at an accelerated rate.

--Foods containing greater quantities of AGEs cause endothelial dysfunction, i.e., artery constriction via blockade of nitric oxide and other mechanisms.

Short of taking agents that block AGE activity, how can you minimize the absorption or production of AGEs? There are two general strategies:

1) Keep blood glucose low--The Whitehall study demonstrated increased cardiovascular mortality with a postprandial (actually 2-hour post- 50-gram glucose challenge) blood sugar of 83 mg/dl. Lower blood glucose, less glycation. Less carbohydrates in the diet, the lower the blood sugar, the less the glycation. Studies like Whitehall demonstrate that glycation begins with glucose values within the normal range. Thus, aging occurs even with normal glucose levels. It occurs faster with higher glucose levels.

2) Choose and prepare foods with lower AGE content. Food content of AGEs is a major determinant of blood AGE levels. Fats and meats are the primary dietary source of AGEs, particularly if cooked at high temperature (broiling, frying). While this does not mean that meats and fats need to be avoided, it can mean that limiting serving size of meats and fats, while being selective in how they are prepared, are important. This can mean cutting your meats in thinner slices or smaller pieces to permit faster cooking, eating rare when possible (not poultry, of course), avoiding cooking with sauces that contain sugar (which enhances AGE formation). Is this an argument in favor of sashimi?

Minimizing exposure to AGEs, endogenous or exogenous, has the potential to slow the aging process, or at least to lessen the likelihood of many of the phenomena of aging.

More on this to come.

Small LDL: Simple vs. complex carbohydrates

Joseph is a whip-smart corporate attorney, but one who accepts advice at his own pace. He likes to explore and consider each step of the advice I give him.

Starting (NMR) lipoprotein panel on no treatment or diet change:

LDL particle number 2620 nmol/L (which I would equate to 262 mg/dl LDL cholesterol)
Small LDL 2331 nmol/L--representing 89% of LDL particle number, a severe dominance of small LDL

I advised him to eliminate wheat, cornstarch, and sugars, while limiting other carbohydrate sources, as well. Joseph didn't like this idea very much, concerned that it would be impractical, given his busy schedule. He also did a lot of reading of the sort that suggested that replacing white flour with whole grains provided health advantages. So that's what he did: Replaced all sugar and refined flour products with whole grains, but did not restrict his intake of grains.

Next lipoprotein panel with whole grains replacing white refined flour:

LDL particle number 2451 nmol/L
Small LDL 1998 nmol/L--representing 81.5% of LDL particle number.

In other words, replacing white flour products with whole grain products reduced small LDL by 14%--a modest improvement, but hardly great.

I explained to Joseph that any grain, complex, refined, or simple--will, just like other sugars and carbohydrates, still provoke small LDL. Given the severity of his patterns, I suggested trying again, this time with full elimination of grains.

Next lipoprotein panel with elimination of whole grains:

LDL particle number 1320 nmol/L
Small LDL 646 nmol/L
--48.9% of total LDL particle number, but a much lower absolute number, a reduction of 67.6%.

This is typical of the LDL responses I see with elimination of wheat products on the background of an overall carbohydrate restriction: Big drops in precisely measured LDL as LDL particle number (i.e., an actual count of LDL particles, not LDL cholesterol) and big drops in the number of small LDL particles.

You might say that wheat elimination and limitation of carbohydrate intake can yield statin-like values . . . without the statin.

Is Cocoa Puffs no longer heart healthy?

Until recently, Cocoa Puffs enjoyed the endorsement of the American Heart Association (AHA) as a heart-healthy food.

For a price, the AHA will allow food manufacturers to affix a heart "check mark" signifying endorsement by the AHA as conforming to some basic "heart healthy" requirements.

Odd thing: The list of breakfast cereals on the check mark program has shrunk dramatically. When I last posted about this, there were around 50-some breakfast cereals, from Cocoa Puffs to Frosted Mini Wheats. Now, the list has been trimmed down to 17:

Berry Burst Cheerios-Triple Berry
Cheerios
Cheerios Crunch
Honey Nut Cheerios
Kashi Heart to Heart Honey Toasted Oat Cereal
Kashi Heart to Heart Oat Flakes & Wild Blueberry Clusters
Kashi Heart to Heart Warm Cinnamon Oat Cereal
Multi Grain Cheerios
Oatmeal Crisp Crunchy Almond
Oatmeal Crisp Hearty Raisin
Quaker Cinnamon Life
Quaker Heart Health
Quaker Life
Quaker Life Maple & Brown Sugar
Quaker Oat Bran
Quaker Oatmeal Squares - Brown Sugar
Quaker Oatmeal Squares - Cinnamon


According to sales material targeted to food manufacturers, the American Heart Association boasts that "The American Heart Association’s heart-check mark is the most recognized and trusted food icon today . . . Eighty-three percent of consumers are aware of the heart-check mark. Sixty-six percent of primary grocery shoppers say the heart-check mark has a strong/moderate influence on their choices when shopping."

So, is Cocoa Puffs no longer heart healthy?

I suspect that agencies like the AHA, the USDA, the American Diabetes Association as starting to understand that they have blundered big time by pushing low-fat, having contributed to the nationwide epidemic of obesity and diabetes, and that it is time to quietly start backpedaling.

While it's a step in the right direction, judging from the above list of breakfast cereal "survivors" of the check mark program, the criteria may have been tightened . . . but not that much.

Fractures and vitamin D

This is a bit off topic, but it's such an interesting observation that I'd like to pass it on.

Over the past several years, there have been inevitable bone fractures: People slip on ice, for instance, and fracture a wrist or elbow. Or miss a step and fracture a foot, fall off a ladder and fracture a leg.

People will come to my office and tell me that their orthopedist commented that they healed faster than usual, often faster than anyone else they've seen before. My son was told this after he shattered his hand getting slammed against the boards in hockey; his orthopedist took the screws and cast off much sooner than usual since he judged that healing had occured early. (My son was taking 8000 units vitamin D in gelcap form; I also had him take 20,000 units for several days early after his injury to be absolutely sure he had sufficient levels.)

My suspicion is that people taking vitamin D sufficient to enjoy desirable blood levels (I aim for a 25-hydroxy vitamin D level of 60-70 ng/ml) heal fractures much faster, abbreviating healing time (crudely estimated) by at least 30%.

For any interested orthopedist, it would be an easy clinical study: Enroll people with traumatic fractures, randomize to vitamin D at, say, 10,000 units per day vs. placebo, watch who heals faster gauged by, for instance, x-ray. My prediction: Vitamin D will win hands down with faster healing and perhaps more assured fusion of the fracture site.

T3 for accelerating weight loss

Supplementation of the thyroid hormone, T3, is an underappreciated means to lose weight.

Thyroid health, in general, is extremely important for weight control, since even subtle low thyroid hormone levels can result in weight gain. The first step in achieving thyroid health is to be sure you are obtaining sufficient iodine. (See Iodine deficiency is real and Healthy people are the most iodine deficient) But, after iodine replacement has been undertaken, the next step is to consider your T3 status.

I've seen T3 ignite weight loss or boost someone out of a weight loss "plateau" many times.

Endocrinologists cringe at this notion of using T3. They claim that you will develop atrial fibrillation (an abnormal heart rhythm) and osteoporosis by doing this. I have yet to see this happen.

Adding T3 revs up metabolic rate at low doses. The idea is to push free T3 hormone levels to the upper limit of normal, but not to the hyperthyroid range. While an occasional person feels a little "hyper" like they've had a pot of coffee, most people just feel energized, clear-headed, and happier. And weight trends down much more readily.

Taking T3 by itself with no effort at weight loss generally yields only a modest weight reduction. However, T3 added to other weight reducing efforts, such as wheat elimination and exercise, accelerates the weight loss effect considerably. 5 lbs lost will likely be more like 8 to 10 lbs lost; 10 lbs lost will likely be more like 15 to 20 lbs, etc.

It's also my suspicion that more and more people are developing a selective impairment of T3, making it all the more important. I believe that you and I are being exposed to something (perchlorates, bisphenol A, perflurooctanoic acid, and others?) that may be impairing the 5'-deiodinase enzyme that converts the T4 thyroid hormone to the active T3. Relative lack of T3 leads to slowed metabolism, weight gain, and depressed mood. While avoiding or removing the toxin impairing 5'-deiodinase would be ideal, until we find out how to do this, taking T3 is a second best.

The tough part: Finding a prescriber for your T3.