Large new clinical study launched to study. . .niacin


Oxford University has issued a press release announcing plans for a new clinical trial to raise HDL cholesterol and reduce heart attack risk. 20,000 participants will be enrolled in this substantial effort. The agent? Niacin.

How is that new? Well, this time niacin comes with a new spin.

Dr. Jane Armitage, formerly with the Heart Protection Study that showed that simvastatin (Zocor) reduced heart attack risk regardless of starting LDL, is lead investigator. She hopes to prove that niacin raises HDL cholesterol and thereby reduces heart attack risk. But, this time, niacin will be combined with an inhibitor of prostaglandins that blocks the notorious "flushing" effect of niacin.

The majority of Track Your Plaque participants hoping to control or reverse coronary plaque take niacin. Recall that niacin (vitamin B3)is an extremely effect agent that raises HDL, dramatically reduces small LDL, shifts HDL particles into the effective large fraction, reduces triglycerides and triglyceride-containing particles like IDL and VLDL. Several studies have shown that niacin dramatically reduces heart attack. The HATS Study showed that niacin combined with Zocor yielded an 85-90% reduction in heart attack risk and achieved regression of coronary plaque in many participants.

In our experience, approximately 1 in 20 people will really struggle using niacin. Flushes for these occasional people will be difficult or even intolerable. Should Dr. Armitage's study demonstrate that this new combination agent does provide advantages in minimizing the hot flush effect, that will be a boon for the occasional Track Your Plaque participant who finds conventional niacin intolerable.

But you already have access to niacin, an agent with an impressive track record even without this new study. And you have a reasonably effective prostaglandin inhibitor, as well: aspirin. Good old aspirin is very useful, particularly in the first few months of your niacin initiation to blunt the flush.

Although this study is likely to further popularize niacin and allow its broader use, it's also a method for the drug companies to profit from an agent they know works but is cheap and available.

You don't have to wait. You already have niacin and aspirin available to you.

The dark side of CT heart scans

"I just got a heart scan!" declared Eric to his doctor. He handed the report to him.

"Oh my. Your score is 154." The doctor paused, then looked at Eric with a serious look on his face. "If we're going to understand whether or not you're in danger, you'll need a heart catheterization."


I've seen this happen countless times. How can I say this diplomatically? THIS IS WRONG!! In my view, it's absolutely criminal for this to happen. Physician ignorance, profiteering, whatever--it is wrong.

There's very few reasons why someone who has no symptoms should go directly to the cath lab for a procedure. (A rare exception might be an exceptional quantity of plaque in the left mainstem artery, e.g., >100. This is highly unusual.)

Even a nuclear stress test (e.g., thallium) at this level of scoring is only 10-15% likely to be abnormal. That means 85-90% likelihood of being normal. There's rare reasons to perform a heart catheterization in a person with no symptoms and an entirely normal stress test. The vast majority of people like Eric do not need a heart catheterization to discern risk.

If Eric's doctor had been up-to-date on the published literature on the prognostic value of heart scans, he could have advised Eric what the risks were--without a catheterization. Many doctors simply don't want to be bothered. Or, they opt for the more profitable method--a hospital procedure.

Always discuss your heart scan with your doctor--but be armed with information in case your doctor is uninformed or unscrupulous. Unfortunately, that's not uncommon. The Track Your Plaque program is your advocate, a source for unbiased information.

The dirty little secret about aneurysms

Jake had an abdominal aneurysm identified--by accident.

While getting a CT scan of his abdomen for unexplained abdominal pain, a 4.4 cm aneurysm was discovered. Jake's abdominal pain eventually passed without explanation, but he was left with this aneurysm.

Jake's primary care doctor referred him to a surgeon. "It's too small to require surgery right now. Wait a few years and it'll probably get bigger. When it gets to around 5.5 cm, that'll be the time to operate. Let's schedule an abdominal ultrasound or CT scan every 6 months."

Jake then got himself a heart scan. His high score of 879 then led him to my office. Lipoprotein testing, a stress test, correction of his lipoprotein patterns, changes in lifestyle followed. One year later, Jake's heart scan score was unchanged.

How about his abdominal aneurysm? 4.2 cm--a modest quantity of regression. When Jake's surgeon learned of the change, he just shrugged. "Okay, we'll just watch it from here."

Shockingly, the conversation surrounding aneurysms is just like the one Jake received: Let's just watch it grow until you need surgery.

If you've every seen anyone have abdominal aneurysm surgery, you know it is an awful, painful, barbaric process with high risk for major complications like kidney failure and loss of the legs. Waiting for an aneurysm to grow is a lousy solution. Surgeons point out that, although surgery is imperfect, it's better than the alternative: rupture, which is catastrophic with a 50% chance of dying.

But what about stopping the growth of the aneurysm? Or even reversing, or shrinking, it?

Surgeons say it can't be done. Yet we've done it--many times. And it's not that difficult.

The steps to take are very similar to that in the Track Your Plaque program for coronary plaque regression, with a few different strategies. Suppression of inflammation, for instance, plays a more important role and blood pressure must be abolutely normal, even during exercise.

More to come on this important topic in the future, including an upcoming Special Report on the www.cureality.com membership website.

Heart scan scores dropping like stones!!

I saw two instances of dramatic coronary plaque regression today.

John, a 53-years old mechanical lift operator, dropped his heart scan score from 479 to 323--a 32% regression of coronary plaque volume!

Eric, a 50-year consulting engineer, dropped his heart scan score from 668 to 580--a 13% reduction.

Both men did nothing special beyond the principles advocated in the Track Your Plaque program. Recall that, without preventive efforts, your heart scan score is expected to increase by 30% per year. Both men are well on their way to freedom from risk of coronary "events".

Two less people to feed the revenue-hungry hospital procedure system! We need many more like them.

Pre-diabetes: An explanation for explosive coronary plaque growth

Art's first CT heart scan in March, 2006 yielded a concerning score of 1336. He felt fine--no chest discomfort, no breathlessness, etc.

Art agreed to take the statin cholesterol drug his primary care doctor prescribed. He also agreed to take the fish oil, niacin, and some of the nutritional supplements that we advised. But Art just couldn't bring himself to make the commitment to lose weight.

At the start of his program, Art--at 5 ft. 8 inches--was 40 lbs overweight (212 lb). This was important since his blood sugar wavered in the pre-diabetic range, going as high as 130 mg. (The American Diabetes Assn. defines diabetes as a blood glucose of 126 mg or greater.)

One year later, Art's lipid and lipoprotein values were corrected to perfection. But he still weighed in at a hefty 209 lbs--essentially no change. His blood sugar likewise hovered in the 120's.

I felt Art need to be prodded, so I asked him to undergo another heart scan. His score: 1935--a 600 point increase, or 45%!

Only now has Art begun to comprehend to power of diabetes and pre-diabetes to fan the flames of plaque growth. Recent published data, in fact, show that the majority of recently diagnosed diabetics already have well-established coronary artery disease.

Don't let this happen to you. Do not dismiss diabetic patterns as they will catch up to you. If Art can lose the 30-40 lbs in the abdominal weight that is creating the diabetic pattern, he will likely succeed in stopping plaque growth. Otherwise, it's just a matter of time before his heart attack, stent, or bypass.

Who cares if you're pre-diabetic?

Marta is a smart lady. She's worked in hospital laboratories for the last 23 years and knows many of the ins and outs of lab tests and their implications.

After years of being told that her cholesterol was acceptable, she needed to undergo urgent bypass surgery after experiencing severe breathlessness that proved to be a small warning heart attack at age 57. But this made Marta skeptical of relying on cholesterol to identify heart disease risk.

I met Marta two years after her bypass surgery when she was seeking better answers. And, indeed, she proved to have several concealed sources of heart disease: small LDL particles, Lipoprotein(a), intermediate-density lipoprotein (IDL--a very important abnormality that means she is unable to clear dietary fats from her blood), among others. But she was also mildly diabetic with a blood sugar of 131 mg (normal < or = 100 mg). This had not been previously recognized.

As I'm a cardiologist and our program focuses on reversal and control of coronary plaque, I asked Marta to return to her primary care doctor to continue the conversation about diabetes. She was a bit frightened but followed through.

"Well, you're not urinating excessively. And your long-term measure of blood sugar, hemoglobin A1C, is still normal. I wouldn't worry about it. We'll just watch it."

I guess I should know better. What the poor primary care doctor doesn't know is that pre-diabetes and mild diabetes are potent risks for heart disease. In fact, some of the most explosive rates of plaque growth occur when these patterns are present. It's well established that risk for heart attack in a diabetic is the same as that of someone who's already suffered a prior heart attack--very high risk, in other words.

Marta's primary care doctor's advice would be like inquiring about cancer and the doctor says "Let's just wait until it's metastatic--then we'll start to worry." Of course, this is insane.

Pre-diabetes and mild diabetes should not be ignored or just "watched". Even though the blood sugar itself may not be high enough to endanger you, the hidden patterns underlying your body's unresponsiveness to insulin creates a torrent of hidden coronary risk.

For better answers, Track Your Plaque members can read "Shutting Off Metabolic Syndrome" at http://www.cureality.com/library/fl_dp001metabolic.asp on the www.cureality.com website. ("Metabolic syndrome" is the name commonly given to the constellation of abnormalities associated with pre-diabetes and diabetes.)

Don't get smug!

It may sound silly, but after someone succeeds in stopping their heart scan score from increasing or reduces their score, I warn them to not get smug. Let me explain.

I'll tell you about Jack. I met Jack a few years ago after he had a heart scan at age 39. His score: 1441! A score this high at his age obviously puts him in the 99th percentile. Also recall that a score >1000 carries a 25% annual risk for heart attack.

This captured Jack's attention. At the start, his lipoproteins were disastrous with numerous abnormal patterns. Jack committed to the program. After one year, his lipoproteins were around 80-90% corrected towards perfection. He'd lost 27 lbs, was exercising six days a week, and felt great.

Jack's repeat score one year later: 1107--over a 300 point drop! A huge success. He was ecstatic.

Unfortunately, work and life in general distracted him. Jack allowed himself to drift back to old habits, indulging in fast food 2 or 3 times a week, slacking on exercise such that it became sporadic, half-hearted efforts, and regained 15 lbs. He even failed to show up for appointments and we lost contact for two years.

One day, Jack simply decided to see where he stood, so he got himself another heart scan. The score: 2473--over a doubling from his reduced score.

The message: Long-term consistency is key, even after you've achieved control over your score. Stick with your program--and don't get smug!

Holidays are dangerous!

If you're on holiday from work today, make sure you're not on holiday from your health, too.

Too often, people come back to the office telling me that the holidays simply got out of hand--cookouts, picnics, family gatherings, etc.--and they simply couldn't avoid overeating, overdrinking, sitting around--and gaining 3-5 lbs in a weekend. (Our record is 10 lbs in a weekend!)

I don't want to harp on this issue and ruin your holiday, but I can't stress how important it is that you don't allow this to happen to you. Weight gained in a brief space of time has exceptionally destructive effects. Ever see the movie "Super Size Me"? It's an entertaining and well-done yet graphic portrayal of the damaging effects of rapid weight gain.

Enjoy your time off. Relax, enjoy your family and friends--but continue to pay attention to choosing the right foods, don't overeat, take time out to do something (or several things) physical. It'll pay off hugely in the long run.

More on carotid plaque...

Although not a perfect test, carotid ultrasound is an exceptionally easy and accessible test. Using high-frequency sound, clear images are available for most people.

I say it's not perfect because the way it's done in 2006 makes it a non-quantitative test. It is a qualitative test. In other words, you may find out that there's a 30% blockage ("stenosis"), at the far end of the common carotid artery on the right side. Unfortunately, this gives you an isolated measure of diameter of the plaque compared to the artery. What it does not tell you is what the volume of the entire plaque is. That's a far more accurate measure (and one that is incorporated into your heart scan score, by the way).

Nonetheless, carotid ultrasound is easy, very safe, and available in most hospitals and many clinics. One difficulty: most insurance companies will not allow you to go through a carotid ultrasound scan as a "screening" procedure, i.e., a test just to see if you have a carotid plaque. They will generally pay if you're having symptoms of a stroke or "mini-stroke" (transient ischemic attack, or "TIA"), have an abnormal sound in your carotid ultrasound detected by your doctor (a carotid "bruit"), or some other unusual indications. Sometimes, a resourceful physician will muster up a diagnosis based on something in your history (e.g., left arm numbness, a common and often benign complaint that can also signal stroke).

Another option are the mobile scanners or some hospital services that offer carotid screening, usually for a very modest price. Drawback: Sporadic availability, difficulty in obtaining serial scans, and imprecise reporting since it's viewed as a screening test. But it's better than nothing.

My hope is that, as screening services using safe imaging techniques like ultrasound propagate and increase in direct availability to the public, you'll be able to circumvent the obstacles imposed by your insurance company and even, sometimes, your doctor. But try your doctor first.

Carotid plaque can be shrunk

Rose, a 64-year old woman, just had a 70% carotid blockage identified by a screening ultrasound. When the result was given to her doctor, he prescribed Lipitor and told Rose that an ultrasound would be required every year. She would need carotid surgery, an "endarterectomy", if the blockage worsened.

"Can't I reduce the amount of blockage I have?" asked Rose.

"No. Once you've got it, it doesn't get any better."


Is this true? Once you've got carotid plaque, you can only expect it to get worse and it can't be reduced?

This is absolutely not true. In fact, compared to coronary plaque, carotid plaque is easier to reduce!

Of course, the Track Your Plaque program is designed to help you control or reduce coronary plaque. But, in our experience, people who have both coronary and carotid plaque will show far greater and faster reduction of carotid plaque. Dramatic reductions are sometimes seen. I've personally seen 50-70% blockages reduced to <30% on many occasions.

The requirements to achieve reduction of carotid plaque are very similar to the approach we use to reduce coronary plaque. One difference is that hypertension may play a more important role with carotid plaque and needs to be reduced confidently to the normal range before carotid plaque is controlled.

I find it shocking that the attitude like the one provided by this physician continue to prevail. Unlike coronary plaque, which has a relatively small body of scientific literature documenting how it can be reduced, carotid plaque actually enjoys a substantial clinical literature. Part of the reason is that the carotids are more easily imaged using ultrasound. (Heart structures can be seen with ultrasound, but not the coronary arteries.)

Numerous agents have been shown to contribute to reduction of carotid plaque: statin drugs, niacin, fish oil, the anti-diabetic "TZD" drugs (Actos, Avandia), several anti-hypertensive drugs, vitamin E, pomegranate juice, and several others.

It outrages me to hear stories like this. Rose is not the only one.

Don't accept the flip dismissals or the over-enthusiastic referral for carotid procedures. Insist on a conversation about plaque regression.


Note: Although I am a vigorous advocate of atherosclerotic plaque regression, this does not mean that if you have a severe (70% blockage or greater), or if there are symptoms from your carotid disease, that you should engage in a program of reversal. You must always take the advice of your doctor if your safety is in question.
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.