Are there any alternatives to niacin?

In the Track Your Plaque program, we tend to rely a great deal on niacin. When used properly, 90-95% of people will do just fine and achieve their lipid and lipoprotein goals with the help of niacin, along with their other efforts.

Unfortunately, around 5% of people simply can't take niacin without intolerable "hot flush" effects, or occasionally excessive skin sensitivity--itching, burning, etc.

Why does this happen? These 5% tend to be "rapid metabolizers" of niacin, i.e. they convert niacin (nicotinic acid, or vitamin B3) into a metabolite called nicotinuric acid. Nicotinuric acid is the compound responsible for the skin flush. Most people can slow or reduce the effects of nicotinuric acid by:

--Taking niacin with dinner, so that food slow tablet dissolution.

--Taking with plenty of water. Two 8-12 oz glasses usually eliminates the flush entirely in most people.

--Taking with an uncoated 325 mg tablet of aspirin in the first few weeks or months. Eventually, you will need to revert back to a better stomach tolerated dose of 81 mg, preferably enteric coated. But a full 325 mg uncoated can really help in the beginning, or when you have any niacin dose increases, e.g., 500 mg to 1000 mg.

But even with these very effective strategies, some people still struggle. That's when the question arises: Are there any alternatives to niacin?

Well, it depends on why niacin is being used. If you and your doctor are using niacin for:

Raising HDL--Then weight loss to your ideal weight; reduction of processed carbohydrates, especially wheat products; avoidance of hydrogenated ("trans") fats; a glass or two of red wine per day; dark chocolates (make sure first ingredient is chocolate or cocoa, not sugar), 40 gm per day; fish oil; exercise; other prescription agents (fibrates like Tricor; TZD agents for diabetes; cilostazol (Pletal)). Niacin is by far the most effective agent of all, but, if you're intolerant, raising HDL is still possible through a multi-faceted effort.

Reduction of small LDL--The list of effective strategies is the same as for raising HDL, but add raw almonds (1/4-1/2 cup per day), oat bran and other beta-glucan rich foods like oatmeal. Reduction of processed carbohydrates is especially important to reduce small LDL.

Reduction of Lipoprotein(a)--This is a tricky one. For men, testosterone and DHEA are effective alternatives; for women, estrogen and perhaps DHEA. Hormonal preparations of testosterone and estrogen are stricly prescription; DHEA is OTC. I have not seen the outsized benefits on lipoprotein(a) claimed by Rath et al by using high-dose vitamin C, lysine, and profile, unfortunately. We are clearly in need of better alternatives to treat this difficult and high-risk disorder.

Reduction of triglycerides/VLDL/IDL--I lump these three together since they all respond together. If you're niacin intolerant, maximixing your fish oil can be crucial for reduction of these patterns using doses above the usual starting 4000 mg per day (providing 1200 mg EPA+DHA). Reduction of processed carbohydrates, eimination of processed foods that contain high-fructose corn syrup, and weight loss to ideal weight are also very effective. "Soft" strategies with modest effects include green tea (>6 cups per day) or theaflavin 600-900 mg/day; raw nuts like almonds, walnuts, and pecans; exercise; soy protein.

Reduction of LDL--Lots of alternatives here including oat bran (3 tbsp per day), ground flaxseed (3 tbsp per day), soy protein (25 grams per day), Benecol butter substitute (for stanol esters), soluble fibers like pectin, psyllium, glucomannan; raw nuts like almonds, walnuts, and pecans.

In future, should torcetrapib become available (by prescription), this will add to our available tools for these areas when niacin can't be used. Until now, the alternatives to niacin depend on what you and your doctor are trying to achieve. In the vast majority of cases, HDL, small LDL, triglyceride, etc. goals for heart scan score control can be achieved, even when niacin is not well tolerated.

Is flaxseed oil a substitute for fish oil?


This question comes up so frequently that it's worth going over.

Flaxseed oil is a wonderful oil rich in linolenic acid, which may provide health benefits all by itself. Some authorities have speculated that the substantial reduction in heart attack seen in the Lyon Heart Study, the study that demonstrated the healthy power of the Mediterranean diet, is due to linolenic acid.

Flaxseed oil is also rich in monounsaturates and low in saturates, both desirable qualities. Of course, I'm talking here about flaxseed oil, to be distinguished from flaxseed , which are the intact seeds. The seeds themselves also contain the same oils, but contain other components, specifically lignan, a plant fiber with suspected health benefits like reduction in cancer risk.

Despite all flaxseed oil's wonderful properties, it is definitely not a substitute for fish oil. Why do we use fish oil for our coronary plaque control program (trying to reduce your heart scan score)? Several reasons. Fish oil:

--Dramatically reduces triglycerides, usually by 50% or more.
--Dramatically reduces specific lipoprotein classes like VLDL
--Dramatatically reduces, often eliminates, abnormal postprandial (after-eating) lipoprotein patterns, like IDL (intermediate-density lipoprotein)
--Has been conclusively shown to reduce risk of heart attack and death from heart attack (GISSI Prevenzione Trial).
--Has been shwon to reduce risk of stroke.
--Modifies blood clotting parameters, particularly a 20% reduction in fibrinogen.

Flaxseed oil, or linolenic acid concentrate for that matter, do not accomplish any of these effects, all crucial if you are to gain control over your coronary plaque.

Flaxseed oil and flaxseed remain wonderful nutritional agents for their own reasons. But they will not substitute for fish oil in your program. Only fish oil--the real thing--does the job.

If you have coronary artery disease . . . do you know why?

This conversation is aimed primarily at non-followers of the Track Your Plaque program, because if you were a follower, you’d already know the answer!

I saw a woman in the hospital today. She’d just survived her second heart attack one week earlier. At 51 years old, she was understandably shaken, perhaps terrified. She felt that her future was uncertain and, in fact, had discussed with her husband what he should do to prepare for a future without her.

One week earlier, she’d received three stents that successfully aborted her heart attack. But, as is always the case, the modest delays of ambulance transport, the emergency room preliminaries, then of mobilizing an available cardiologist and catheterization laboratory team, totaled nearly two hours before her stent procedure. Inevitably, a moderate amount of damage had been done to her heart.

Her first “event” had been very similar: very little warning, then 911 and the flurry of activity. Both times, the cardiologists (two different physicians) complimented the patient on her prompt action. Both also called her heart attacks “close calls”.

She defied the odds with two near-death events. So, when I met her a week after her last heart attack, I asked an obvious question: “Has anyone told you why you’re having these heart attacks?”

She looked completely puzzled at first. She then said, “No, not really. I just assumed it was genetic. My mother went through the same thing when she was my age. But she didn’t get as far as I have, since they didn’t have these procedures back then.”

To me, this seems inexcusable: This woman had experienced two brushes with death and no doctor had established a cause. Could this woman’s belief be true, that it’s just genetic?

While there are, indeed, genetic causes for heart disease, the vast majority of these genetic causes are 1) identifiable, and 2) correctable. Genetic does not necessarily mean hopeless. It just means that the usual equation of heart disease risk management (heart disease = LDL cholesterol = need for Lipitor) has limited value. It would be like giving penicillin to people for any and all infections. It will work occasionally, but it will fail miserably in a great many cases. Treating LDL cholesterol with statin drugs is just like that.

Perhaps this woman has lipoprotein(a), a serious genetic trait that predicts heart disease at a young age and is largely unaffected by statin drugs. Or, she may have a severe excess of small LDL, only partially suppressed by statins. If she has the combined pattern of lipoprotein(a) and small LDL, that means she has two statin-unresponsive and significant genetic traits. But they respond to niacin, specific nutritional strategies, and several other agents.

The message: If you have coronary disease, you need to insist on knowing why. “It’s genetic” is not an acceptable answer. “There’s no proof of any heart disease causes beyond cholesterol” is also nonsense. “Everyone gets heart disease, or “hardening of the arteries”, eventually. You just got it a little before everyone else” is also patently ridiculous.

Identifying the causes of your coronary disease (or coronary plaque if you’ve had a CT heart scan) is the first step in developing a program of treatment that provides you with control over this disease.

Have you tried inulin yet?

If you haven't yet tried it to facilitate weight loss, it's really worth giving the new inulin-containing product, Fiber Choice "Weight Management", a try.

Recall (from a prior Heart Scan Blog) that inulin is a vegetable-based fiber found in celery, green peppers, etc. that, when exposed to water, expands to many times original volume. This simple phenomenon yields satiety--a feeling of fullness.


The manufacturer of the product has also added green tea, which has been shown in two small clinical studies to enhance weight loss, though by a different route.

We've been advising patients to chew two of the strawberry flavored tablets one hour before every meal (or with breakfast if you eat immediately in the morning). You'll be satisfied with less food and you'll experience less intense food cravings.

Though no one so far has achieved a huge drop in weight, it does seem to enhance a slow, gradual weight loss larger than achieved by diet and exercise alone. And it's very safe and inexpensive. If you give it a try to help you lose weight, let us know what kind of results you've obtained.

Fish oil update on Life Extension

An article of mine came out in Life Extension Magazine and is available on the online version at:

http://www.lef.org/magazine/mag2006/sep2006_report_omega1_01.htm

This is an update on the heart health applications of fish oil.

Or, go to to www.lef.org and put fish oil into your on-site search and you'll come back to it in future.

Of course, it comes with Life Extension's promotion of its supplements.

Although it's not yet available online, the hard copy version of an article I wrote on homocysteine is available in the October, 2006 Life Extension Magazine. If you're not a member of their program, they'll send you a free copy just for signing up for it without obligation. Go to the home page of www.lef.org to do so. Or, Life Extension is available at newstands if you're in a rush or don't want to sign up for a free copy.

More on Vitamin D

If you haven't done so already, you should subscribe to Dr. John Cannell's free newsletter on vitamin D issues. His newest issue is available at:

http://www.vitamindcouncil.com/newsletter/2006-aug.shtml

A sign-up to subscribe is available on the same page.

I continue to be shocked and amazed at the prevalence and magnitude of vitamin D deficiency in the people I see every day. It's been a beautiful summer with very little rain. Most days have been in the 70-80 degree range--very comfortable to be outdoors in the sun and getting skin expoxure to activate vitamin D in the skin.

Yet, in the vast majority of people I see, summer blood levels of vitamin D are virtually indistinguishable from winter levels. Both hover around the 30 ng/ml range. Summer levels in Wisconsin people seem to be no more than 10 ng/ml higher than winter levels. This remains true even in people who spend a lot of their day outdoors gardening, walking, etc. wearing shorts and a short-sleeved shirt, i.e. with plenty of skin surface area exposed.

I'm at a loss to explain precisely why. Yes, it is Wisconsin. But a direct sun overhead, 75 degree day should be providing plenty of sun. My suspicious is that a combination of factors are at work: people are not spending as much time outdoors as they claim; they often seek shade; use sunscreen; and they're overweight. (Excess weight decreases vitamin D blood levels dramatically, yet another reason not to get fat!)

Read more about vitamin D by checking out Dr. Cannell's insightful comments on the unfolding vitamin D story. He holds nothing back.

Why not just get "perfect" lipids and call it a day?

What if you achieved the Track Your Plaque lipid targets: LDL cholesterol 60 mg/dl, HDL 60 mg/dl, and triglycerides 60 mg/dl?

After all, these are pretty stringent standards. Compared to national guidelines (the ATP-III Guidelines of the National Cholesterol Educational Panel), the Track Your Plaque 60-60-60 goals are laughably ambitious. There's a lot of wisdom hidden in those numbers. The triglyceride level of 60, for instance, is a level at which triglycerides become essentially unavailable for formation of triglyceride-containing lipoprotein particles such as small LDL and VLDL.

If you get to the 60-60-60 target, isn't that good enough? What if you just held your values there and went about your business? Will coronary plaque stop growing and will your CT heart scan score stop increasing?

Sometimes it will. But, unfortunately, many times it will not. The experience generated through clinical trials bear this out. Studies like the St. Francis Heart Study and the BELLES Trial both showed that just reducing LDL cholesterol is insufficient to stop plaque growth. Beyond the Track Your Plaque experience, there's no clinical trial experience that shows whether the 60-60-60 approach does any better.

In our experience, achieving 60-60-60 is indeed better than just reducing LDL. That makes sense. Just raising HDL from the average of 42 mg/dl for a male, 52 mg/dl for a woman adds advantage. Compound this with triglyceride reduction from the plaque-creating equation, and you've doubled success.

But there's even more. What if you had hidden patterns not revealed by conventional lipids? How about lipoprotein(a)? Small LDL? Postprandial (after-eating) abnormalities? Hypertensive effects (more common than you think)!

In 2006, stopping the increase in your heart scan score is, for most of us, not just a matter of taking Lipitor or its equivalent and sitting back. For nearly all of us, stopping the progression of your score is a multi-faceted effort.

Hospitals: Then and Now

It's 1920. The hospital in your city is a facility run by nuns or the church. It's a place for the very ill, often without hope of meaningful treatment, but nonetheless a place where surgeries take place, babies are born, the injured and chronically ill can find care. No one has health insurance and there's no Medicare. Everyone pays what they can. The hospital is accustomed to doling out plenty of care without compensation. For that reason, they welcome donations and sometimes will build new additions or other facilities in honor of a major donor.

Volunteeers are common, since the wards are understaffed and generally suffering from a shortage of trained nurses and personnel associated with the church. Drugs, such as they are, are often prepared from basic ingredients in the hospital pharmacy. Product representatives hawking medicines and devices are virtually unheard of.

Though their therapeutic tools are limited, the physicians are a proud group, dedicating their careers to healing. The majority of the medical staff volunteer large portions of their time to care for the poor who come to the hospital with very advanced stages of disease: metastatic tumors, advanced heart failure, debilitating strokes, overwhelming septicemia, etc.

Hospitals are usually governed by a board of clergy and physicians who make decisions on how to apply their limited resources and continually seek charitable donations.


Fast forward to present day: Hospitals are high-tech, professional facilities with lots of skilled people, complicated equipment,and capable of complex procedures. While they still house people with advanced illnesses, the floors are also filled with people with much earlier phases of disease. In general, they do a good job, with quality issues scrutinized by a number of official agencies to police practices, incidence of hospital-related infections, medication errors, care protocols, etc.

The hospital of 2006 is a more more effective place than the hospital of 1920. But its aims and operations are different, also. Though some churches are still involved in hospitals, more and more are owned by publicly-traded companies that answer to shareholders--shareholders who want share value to increase. Though donations are still sought, much of the revenues are obtained by concentrating on profitable, large-ticket procedures. More procedures are often generated by advertising.

Because they operate to generate profits, several hospitals in a single city or region compete with one another. The 21st century has therefore witnessed the phenomenon of hospital-owned physicians: more and more practicing physicians are employees of their hospital. That way, the physician brings all his patients and procedures to his hospital, not to a competitor. The top of the funnel is the primary care physician, who tends to see all disease when it first occurs. The primary care physician then sends the patient to the specialist, who is obliged (by contract) to perform his/her procedure in the hsopital paying their salary.




Representatives from companies manufacturing and selling expensive hospital equipment and drugs are everywhere, falling over themselves to gain attention of the physicians using their equipment and the hospital buyers who make purchasing decisions. Millions of dollars can be transacted with just one sale.

The number of volunteers has dwindled. The poor and uninsured are commonly diverted elsewhere, often to a government-funded, and often second-rate, institution. Hospitals measure success by comparing annual revenues and numbers of major procedures.

The hospital of 2006 is a vastly different place than 1920. If you're expecting charitable treatment, compassion, and selfless care, you're in the wrong century. In 2006, the hospital is a business. You don't expect charitable treatment at Wal-Mart or from your car dealer. Don't expect it from your hospital. They are businesses and you are a customer. Recognize this fact, lose the nostalgia for the hospitals of yesterday, and a lot more will become clear to you.

The dreaded small LDL particle

Brian is a 59-year old landscape architect whose starting CT heart scan score was 276.

Brian's food choices at the start were deplorable: a pound of sausage per week, sometimes more; butter on anything and everything; up to two pounds of cheese per week; hot dogs; etc. His lipoproteins were accordingly just as miserable: low HDL, high triglycerides, excessive (postprandial, or after-eating) IDL. Small LDL was a particularly stand-out pattern, with 95% of all LDL particles in the small category.

Brian made a dramatic turnaround in lifestyle and corrected all of his patterns--except for small LDL. After one year, small LDL still occupied 95% of all LDL particles, even though the quantity of LDL had been reduced. In order to help convince Brian that correction of his small LDL was going to be necessary to achieve control oover coronary plaque, I suggested that he undergo another heart scan. His score: 435, or a 57% increase.

Each day that passes, I gain more and more respect for small LDL as a cause for coronary plaque growth. Conventional thought among lipid experts is that small LDL should no longer be a factor if total LDL (e.g., LDL particle number) is reduced. But our experience suggests otherwise: when small LDL persists, we tend to see continued, sometimes frightening, plaque growth.

I therefore asked Brian to intensify his efforts: additional weight loss off his somewhat prominent abdomen (since visceral fat increases small LDL), further reduce wheat products and processed carbohydrates, increase niacin (to 1500 mg per day), and use more raw almonds and oat bran.

Don't let small LDL get the best of you. It is a nasty, sometimes persistent abnormality that has impressive effects on plaque growth.

Winning Through Intimidation

Do you remember the book, Winning Through Intimidation by author Robert J. Ringer?



In his 1984 bestseller, author Ringer details how to succeed in business by overwhelming clients and competition by appearing hugely successful and powerful. Rather than a business card, he'd hand out an elegant book to represent himself. He'd show up in a limousine to a meeting, even when he could barely afford it. He used these tactics, even when he was a small-fry, in commercial real estate and built a successful business following such techniques.

This reminds me a lot of what happens in conventional medical practice: The large and successful hospitals, filled with trained staff and technology, exude legitimacy and success. How can they possibly be wrong? Such overwhelming know-how and multiple levels of expertise mustbe right!

Let's be grateful that we do have access to such high-tech, capable care. Unfortunately, just as Mr. Ringer used deceptive practices to appear something he wasn't, this is also true in hospitals. Not all physicians have your best interests in mind. Their principal concern is how profitable your care can be for them--can you be persuaded to have your stent, bypass, etc.. After all, look around you: Aren't all this equipment and personnel impressive? Aren't you intimidated?

The patient that most recently drove home this issue for me recently was a smart and capable executive who came in for consultation. He had been told by his internist that a surgery (to replace his aorta, a HUGE procedure) was probably necessary. In my view, it was not--his process was simply not that far progressed. The risks for danger over the next several years was virtually nil. Unfortunately, this man, now confused and worried, sought an opinion from the chief of thoracic surgery (in the usual white coat and with professorial demeanor, I'm sure) in a major metropolitan hospital (in Chicago), who promptly rushed him off to the operating room.

The pathology report, cleverly not mentioned in any other of the hospital documentation, showed what I had suspected: this man had mild disease that wasn't even close to requiring surgery. But, with all that technology, $100,000 or so of costs, chief of surgery who looked the part, etc.--they must be right!

Robert Ringer's concepts only ring too true for hospitals and some of the unscrupulous physicians in practice. Don't allow yourself to be intimidated.

Diabetes: Better than hedge funds

Diabetes is where the action is.

While, for virtually all of history, type 2 diabetes was an uncommon condition of adults, the disease has spread so much to all levels of American society that even kids are now developing the adult form. Researchers from the Center for Disease Control and Prevention predict that, by 2050, one in three adults will be diabetic.

The diabetes market is booming, handily surpassing growth of the oil industry, the housing market, even technology. It makes Bernie Madoff’s billions look like small potatoes. In health, few markets are growing as fast as diabetes—-not osteoporosis, not heart disease, not cancer.

Americans are getting fat from carbohydrate consumption, becoming diabetic along with it. While kids hanging around the convenience store gulp down 26 teaspoons of sugar in 32-ounce sodas and 56-grams-of-sugar in 16-ounce frozen ices, health-minded adults are more likely eating two slices of 6-teaspoons sugar-equivalent “healthy whole grain” bread, wondering why last year’s jeans are too tight.

The U.S. is not the only nation affected. Globally, 2.8% of the world’s population are diabetic, a number expected to double over the next 20 years.

Pharmaceutical companies boast double-digit growth for diabetes drugs, growth rates that keep profit-hungry investors happy. Merck’s Januvia, for instance, introduced in 2006, recently catalogued 30% growth in sales, with annual sales approaching $1 billion. Recently FDA-approved Victoza, requiring once-a-day injection, is expected to reap $4 billion in sales per year for manufacturer Novo Nordisk. Such numbers can only warm a drug company CEO’s heart.

Most diabetics don’t just take one medication, but several. A typical regimen for an adult diabetic after a couple of years of treatment and following the dietary advice of the American Diabetes Association includes metformin, Januvia, and Actos, a triple-drug treatment that costs around $420 per month. Two forms of insulin (slow- and fast-acting), along with two or three oral medications, is not at all uncommon.

“Collateral” revenues from the other health conditions that develop from a diet rich in “healthy whole grains,” such as drugs for hypertension, drugs to slow the progression of kidney disease in diabetes, drugs for “high cholesterol,” and drugs for high triglycerides, and you have a pharmaceutical drug bonanza. You, too, would throw all-expenses-paid, fly-the-entire-sales-force-to-the-Caribbean sales meetings.

The global diabetes market has already topped $25 billion and is growing at double-digit rates. Forget the Internet, gold stocks, or solar energy—-diabetes is where the money is. This fact has not been lost on the very market-savvy pharmaceutical industry. As with any successful business, they have devoted substantial resources to develop and grow this booming business.

270 lb man in diapers

Alex is a big guy: 6 ft 4 inches, 273 lbs.

On 10,000 units per day of vitamin D in gelcap form, his 25-hydroxy vitamin D level was 38.4 ng/ml. One year earlier, his 25-hydroxy vitamin D level, prior to any vitamin D supplementation was 9.8 ng/ml.

According to the latest assessment offered by the Institute of Medicine (IOM):

Vitamin D need for a 13-month old infant: 600 units per day

Vitamin D need for a 6 ft 4 in, 273 lb male: 600 units per day

I paint this picture to highlight some of the absurdity built into the smug assumptions of the IOM's report. It would be like trying to fit a large, full-grown man into the diapers of a 13-month old. Few nutrients or hormones (in fact, I can't think of a single one) are required in similar quantity by an infant or toddler and a full grown adult. However, according to the IOM's logic, their vitamin D needs are identical, regardless of age, body size, skin color, genetics, etc. One size fits all.

Just as the original RDA assessment by the Institute of Medicine kept thinking about vitamin D somewhere in the Stone Age, so does this most recent assessment.

90% small LDL: Good news, bad news

Chris has 90% small LDL particles.

On his (NMR) lipoprotein panel, of the total 2432 nmol/L LDL particles ("LDL particle number"), 2157 nmol/L are small, approximately 90% (2157/2432).

Bad news: Having this severe excess of small LDL particles virtually guarantees heart attack and stroke in Chris' future.

Good news: It means that Chris potentially has spectacular control over his lipoprotein and lipid values, achieving statin-like values without statin drugs.

Typically, extravagant quantities of small LDL particles are accompanied by low HDL, high triglycerides, and pre-diabetes or diabetes. Chris' HDL is 26 mg/dl, triglycerides 204 mg/dl; HbA1c 5.9% (a reflection of prior 60-90 days average blood glucose; desirable 4.8% or less), fitting neatly into the expected pattern.

Chris' pattern tells me several things:

1) He overconsumes carbohydrates, since carbohydrates trigger this pattern.
2) He likely has a genetic susceptibility to this effect (e.g., a variant of the gene for cholesteryl ester transfer protein, perhaps hepatic lipase). Only the most gluttonous and overweight carbohydrate consumers can generate this high a percentage small LDL without an underlying genetic susceptibility.
3) Provided he follows the diet advised, i.e., elimination of all wheat, cornstarch, oats, and sugars, he is likely to have an extavagant drop in LDL particle number. Should he achieve the goal I set of small LDL of 300 nmol/L or less, his LDL particle number will likely be around 500 nmol/L. This translates to an LDL cholesterol of 50 mg/dl . . . 50 mg/dl.

In many people, this notion of taking statin drugs for "high cholesterol" is an absurd oversimplification. But it is a situation that, for many, is wonderfully controllable with the right diet.

The American Heart Association has a PR problem

The results of the latest Heart Scan Blog poll are in. The poll was prompted by yet another observation that the American Heart Association diet is a destructive diet that, in this case, made a monkey fat.

Because I am skeptical of "official" organizations that purport to provide health advice, particularly nutritional advice, I thought this poll might provide some interesting feedback.

I asked:

The American Heart Association is an organization that:

The responses:
Tries to maintain the procedural and medication status quo to benefit the medical system and pharmaceutical industry for money
240 (64%)

Doesn't know its ass from a hole in the ground
121 (32%)

Is generally helpful but is misguided in some of its advice
79 (21%)

Accomplishes tremendous good and you people are nuts
6 (1%)


Worrisome. Now, perhaps the people reading this blog are a skeptical bunch. Or perhaps they are better informed.

Nonetheless, one thing is clear: The American Heart Association (and possibly other organizations like the American Diabetes Association and USDA) have a serious PR problem. They are facing an increasingly critical and skeptical public.

Just telling people to "cut the fat and cholesterol" is beginning to fall on deaf ears. After all, the advice to cut fat, cut saturated fat, cut cholesterol and increase consumption of "healthy whole grains" in 1985 began the upward ascent of body weight and diabetes in the American public.

Believe it or not, my vote would be for something between choices 1 and 3. I believe that the American Heart Association achieves a lot of good. But I also believe that there are forces within organizations that are there to serve their own agendas. In this case, I believe there is a substantial push to maintain the procedural and medication status quo, the "treatments" that generate the most generous revenues.

I believe that I will forward these poll results to the marketing people at the American Heart Association. That'll be interesting!

The formula for aortic valve disease?

I've discussed this question before:

Can aortic valve stenosis be stopped or reversed using a regimen of nutritional supplements?

I had a striking experience this past week. Don has coronary plaque and began the Track Your Plaque program. However, discovery of a murmur led to an echocardiogram that measured his effective aortic valve area at 1.5 cm2. (Normal is between 2.5-3.0 cm2.)

Because of his aortic valve issue, I suggested that, in addition to the 10,000 units of vitamin D required to increase his 25-hydroxy vitamin D level to 70 ng/ml, he also add vitamin K2, 1000 mcg per day, along with elimination of all calcium supplements. (I asked Don to use a K2 supplement that contained both forms, short-acting MK-4 and long-acting MK-7.)

One year later, another echocardiogram: aortic valve area 2.6 cm2--an incredible increase.

This is not supposed to happen. By conventional thinking, aortic valve stenosis can only get worse, never get better. But I've now witnessed this in approximately 10% of the people with aortic valve stenosis. The majority just stop getting worse, an occasional person gets worse, while a few, like Don, get better.

Aortic valve stenosis is to the aortic valve as degenerative arthritis is to your knees: A form of wear-and-tear that leads to progressive dysfunction. When the aortic valve becomes stiff enough (i.e., "stenotic"), then it leads to chest pains, lightheadedness or losing consciousness, heart failure, and, eventually, death. Bad problem.

Aortic stenosis typically starts in your 50s with calcification of the valve, getting worse and worse until the calcium makes the valve "leaflets" unable to move. The treatment: a new valve, a major undertaking involving an open heart procedure.

What if taking vitamins D and K2 and avoiding calcium do not just reverse or stop aortic valve stenosis once established, but prevents it in the first place? Tantalizing possibility.

Pressures on my time being what they are, I've not had the freedom to put together a prospective study to further examine this fascinating question. But it is definitely worth pursuing.

Blood glucose 160

What happens when blood glucose hits 160 mg/dl?

A blood glucose at this level is typical after, say, a bowl of slow-cooked oatmeal with no added sugar, a small serving of Cheerios, or even an apple in the ultra carb-sensitive. Normal blood sugar with an empty stomach, i.e., fasting; high blood sugars after eating.

Conventional wisdom is that a blood sugar of 160 mg/dl is okay, since your friendly primary care doctor says that any postprandial glucose of 200 mg/dl or less is fine because you don't "need" medication.

But what sort of phenomena occur when blood sugars are in this range? Here's a list:

--Glycation (i.e., glucose modification of proteins) of various tissues, including the lens of your eyes (cataracts), kidney tissue leading to kidney disease, skin leading to wrinkles, cartilage leading to stiffness, degeneration, and arthritis.
--Glycation of LDL particles. Glycated LDL particles are more prone to oxidation.
--VLDL and triglyceride production by the liver, i.e., de novo lipogenesis.
--Small LDL particle formation--The increased VLDL/triglyceride production leads to the CETP-mediated reaction that creates small LDL particles which are, in turn, more glycation- and oxidation-prone.
--Glucotoxicity--i.e., a direct toxic effect of high blood glucose. This is especially an issue for the vulnerable beta cells of the pancreas that produce insulin. Repeated glucotoxic poundings by high glucose levels lead to fewer functional beta cells.

A blood glucose of 160 mg/dl is definitely not okay. While it is not an immediate threat to your health, repeated exposures will lead you down the same path that diabetics tread with all of its health problems.

Indian buffet

I took my family to a local all-you-can-eat Indian buffet. It was delicious.

I confined my food choices mostly to vegetables and soups. Within about 30 minutes, I started to get that odd buzz in my head that usually signals a high blood sugar.

When I got home, my fingerstick blood glucose: 173 mg/dl. Darn it! Must have been cornstarch or other sugars in the sauces.

I got on my supine stationary bike and pedaled for 40 minutes at a moderate pace while I played Modern Warfare on XBox. (A great way, by the way, to fit in some low- to moderate-intensity exercise while occupying your brain. My wife often has to yell at me to get off, it's so much fun.)

Blood glucose at the conclusion of exercise: 93 mg/dl-- a nice 80 mg/dl drop.

This is a useful strategy to use in a pinch when you've either been inadvertently exposed to more carbohydrate than you can tolerate, or if you'd like to blunt the adverse glucose effects of a bowl of ice cream or other carbohydrate indulgence.

Should we explore the idea of a "morning-after" pill, or actually a "meal-after" pill, a supplement pill or liquid that blunts or eliminates the blood glucose rise after a meal? I've considered such an idea, but have been fearful that people would start to use it habitually. Thoughts?

American Heart Association diet makes a monkey out of you

Heart Scan Blog reader, Roger, brought this New York Times article to my attention.

In an effort to develop a better experimental model for obesity than mice, scientists have turned to monkeys and other primates. The emerging observations are eerily reminiscent of what you and I witness just by going to the local grocery store or fast food outlet:

"'It wasn’t until we added those carbs that we got all those other changes, including those changes in body fat,' said Anthony G. Comuzzie, who helped create an obese baboon colony at the Southwest National Primate Research Center in San Antonio."

"Fat Albert, one of her monkeys who she said was at one time the world’s heaviest rhesus, at 70 pounds, ate “nothing but American Heart Association-recommended diet,” she said."

Yes, indeed: The American Heart Association diet makes monkeys fat. Extrapolate this a little higher on the evolutionary ladder and guess what?

This is one of the many reasons why, when I have a patient who is counseled by the hospital dietitian on the American Heart Association diet, I advise them to 1) ignore everything the dietitian told them, and then 2) follow the wheat-free, cornstarch-free, sugar-free, whole food diet I advocate.

Not unexpectedly, much of this primate research is not being devoted to just manipulating diet to achieve weight loss and health, but to develop new drugs to "treat" obesity.

Would you like a banana?

Construct your glucose curve

In a previous Heart Scan Blog post, I discussed how to make use of postprandial (after-meal) blood sugars to reduce triglycerides, reduce small LDL, increase HDL, reduce blood pressure and inflammatory measures, and accelerate weight loss.

In that post, I suggested checking blood glucose one hour after finishing a meal. However, this is a bit of an oversimplification. Let me explain.

A number of factors influence the magnitude of blood glucose rise after a meal:

--Quantity of carbohydrates
--Digestibility of carbohydrates--The amylopectin A of wheat, for example, is among the most digestible of all, increasing blood sugar higher and faster.
--Fat and protein, both of which blunt the glucose rise (though only modestly).
--Inclusion of foods that slow gastric emptying, such as vinegar and fibers.
--Body weight, age, recent exercise

Just to name a few. Even if 10 people are fed identical meals, each person will have a somewhat different blood glucose pattern.

So it can be helpful to not just assume that 60 minutes will be your peak, but to establish your individual peak. It will vary from meal-to-meal, day-to-day, but you can get a pretty good sense of blood glucose behavior by constructing your own postprandial glucose curve.

Say I have a breakfast of oatmeal: slow-cooked, stoneground oatmeal with skim milk, a few walnuts, blueberries. Blood glucose prior: 95 mg/dl. Blood glucose one-hour postprandial: 160 mg/dl.

Rather than taking a one-hour blood glucose, let's instead take it every 15 minutes after you finish eating your oatmeal:


In this instance, the glucose peak occurred at 90-minutes after eating. 90-minute postprandial checks may therefore better reflect postprandial glucose peaks for this theoretical individual.

I previously picked 60-minutes postprandial to approximate the peak. You have the option of going a step better by, at least one time, performing your own every-15-minute glucose check to establish your own curve.

Why is type 1 diabetes on the rise?

Type 1 diabetes, also called "childhood" or "insulin-dependent" diabetes, is on the rise.

Type 2 diabetes, or "adult," diabetes, is also sharply escalating. But the causes for this are easy-to-identify: overconsumption of carbohydrates and resultant weight gain/obesity, inactivity, as well as genetic predisposition. A formerly rare disease is rapidly becoming the scourge of the century, expected to affect 1 in 3 adults within the next several decades.

Type 1 diabetes, on the other hand, generally occurs in young children, not uncommonly age 3 or 4. Type 1 diabetes also shares a genetic basis to some degree. But the genetic predisposition should be a constant. Obviously, lifestyle issues cannot be blamed in young children.
Then why would type 1 diabetes be on the rise?

For instance, this study by Vehik et al from the University of Colorado documents the approximate 3% per year increase in incidence in children with type 1 diabetes between 1978 and 2004:


(From Vehik 2007)

(For an excellent discussion of the increase in type 1 diabetes in the 20th century, see this review.)

This is no small matter. Just ask any parent of a child diagnosed with type 1 diabetes who, after recovering from hearing the devastating diagnosis, then has to stick her child's fingers to check glucose several times per day, mind carefully what he or she eats or doesn't eat, watch carefully for signs of life-threatening hypoglycemic episodes, not to mention worry about her child's long-term health. Type 1 diabetes is a life-changing diagnosis for both child and parents.

Various explanations have been offered to account for this disturbing trend. Some attribute it to the increase in breast feeding since 1980 (highly unlikely), exposure to some unidentified virus, or other exposures.

I'd like to offer another explanation: wheat.

Lest you accuse me of becoming obsessed with this issue, let me point out the four observations that lead me to even consider such an association:

1) Children diagnosed with celiac disease, i.e., the immune disease of wheat gluten exposure, have 10-fold greater likelihood of developing type 1 diabetes.

2) Children diagnosed with type 1 diabetes are 10-fold more likely to have abnormal levels of antibodies (e.g., transglutaminase antibodies) to wheat gluten.

3) Experimental models, such as in these mice genetically susceptible to type 1 diabetes, showed a reduction of type 1 diabetes from 64% to 15% with avoidance of wheat.

4) The increase in type 1 diabetes corresponds to the introduction of new strains of wheat that resulted from the extensive genetics research and hybridizations carried out on this plant in the 1960s. In particular, unique protein antigens (immune-provoking sequences) were introduced with the dwarf variant attributable to alterations in the "D" genome of modern Triticum aestivum.

Proving the point is tough: Would you enroll your newborn in a study of wheat-containing diet versus no wheat, then watch for 10 years to see which group develops more type 1 diabetes? It is a doable study, just a logistical nightmare. Perhaps the point will be settled as more and more people catch onto the fact that modern wheat--or this thing we are being sold called "wheat"--is a corrupt and destructive "foodstuff" and eliminate it from their lives and the lives of their young children from birth onwards. Then a comparison of wheat-consuming versus non-wheat-consuming populations could be made. But it will be many years before this crucial question is settled.

Yet again, however, the footprints in the sand seem to lead back to wheat as potentially underlying an incredible amount of human illness and suffering. Yes, the stuff our USDA puts at the bottom, widest part of the food pyramid.
Cureality | Real People Seeking Real Cures

Can I see your linea alba?

As more and more people are eliminating wheat from their diet and losing their "wheat bellies," i.e., the muffin top around their waists along with the visceral fat beneath, I am frequently seeing something I haven't seen in years: the linea alba.

Linea alba, or "white line," refers to the band of connective tissue running vertically from sternum to pubic area. It underlies the depression that separates the horizontal abdominal rectus muscles of the "six pack" abdomen.

It's like digging in your closet and finding something you thought you'd lost years earlier. Surprise! It's been there all along. Buried deep beneath the abdominal fat from dozens of deep-crust pizzas, whole wheat pasta, and whole grain sandwiches is this pleasing anatomical feature long lost from most peoples' anteriors.


Can you see your linea alba?

Dwarf mutant wheat

Here's my 12-year old standing next to dwarf wheat grown near my house. The wheat is full-grown, harvested about 2 weeks after I took this photo.

Wheat is no longer the 4-foot tall "amber waves of grain" of the 20th century. Over 99% of all wheat grown worldwide is now the 18- to 24-inch tall dwarf. New size, new biochemistry, new effects on humans. I call it dwarf "mutant" wheat despite its lack of extra limbs or eyes because of the dramatic transformation required to breed this unique synthetic plant. 

Short-stature means less stalk, faster growing. The stockier stalk also means that the heavy seed head won't cause the plant to "buckle," as 4-foot tall wheat used to. 





The thousand-plus proteins of wheat that have been transformed to generate this dwarf mutant also changed wheat's relationship to consuming humans.

Medical education in the days of Big Pharma

I received this detailed email from an unexpected source: a 3rd-year medical student.

In her email, Theresa describes her frustrations in what she is witnessing for the first time, proceeding through her training and getting exposed to the realities of medical life.

Medical training, particularly clinical training from the 3rd and 4th years of medical school, onwards through internship, residency, and fellowship training, consists largely of bullying, "pimping" (meaning rapid-fire grilling of questions at trainees), and sleep deprivation. It is an extended hazing period meant to demoralize and inculcate the trainee into following the lead of superiors. Buck the system and you're . . . out. Imagine you've just sunk $190,000 and 8 years of college into getting to your internship. You are not going to chance being thrown out on principle. So you just swallow your pride, go along with the game, and echo all the answers they want you to repeat.

While Theresa laments the sad state of modern American pharmaceutical- and procedure-obsessed medicine, she provides me with hope that some young people training to practice medicine today will carve out their own paths, not the one laid for them by the pharmaceutical industry, nor fall for the temptation of higher-paying procedural specialties like orthopedics and cardiology. I am impressed with her ability to see this so early in her career.


Dr. Davis,

I am a 3rd year medical student at ________ University. I came across
your blog today, and I'm very glad I did. I appreciate the value of your time,
so I want to be as succinct as possible while still getting across what I'm
really thinking and feeling:

From what I gathered exploring your blog for a while this afternoon, the
wellness strategies you incorporate into your practice are some of the exact
things I want to do with my future patients. Personally, I strongly believe in
staying healthy by eating right, staying active, etc. For instance, I don't eat
grains or much in the way of starches and sugars. So I love the fact that you
are helping your patients make these powerful and foundational changes in their
lives.

As I'm sure was your experience, a full appreciation of nutrition and lifestyle
as a first-line health strategy is not something that was taught to me in
medical school. I came to school with this deep conviction already in my heart
and mind, and now, on my 3rd year rotations, I am still conflicted and at a loss
as to how I'm going to be able to practice medicine the way I want to, which is
to incorporate these all-important principles into the care of my patients.

What I've come to understand about the medical field today is that the
information that exists is primarily subsidized by the pharmaceutical industry,
and dictated to medical professionals as "evidence-based" treatment guidelines
and recommendations by organizations with sincere and official sounding names
like American Heart Association and American Cancer Society. Add to that the
pressure of potential malpractice litigation and the complexities of the
insurance reimbursement game, and it seems to me like what you get is a bunch of
diagnostic and medication management algorithms that any half-trained monkey
could follow. In his sleep. Which I guess would be alright if at least they
weren't algorithms based on misguided, self-serving, profit-seeking Big Pharma,
Food Inc, insurance conglomerates, and agri-politics (I think I just made that
word up.)

A lot of well-intentioned physicians are just parroting the party
line, as their patients dutifully and gratefully chomp down their statins and
diabetes drugs and blood pressure pills. And I'm sorry, but "diabetes
education" programs with curriculum put together by drug companies? How is that
even legal? Massive corporations raking in massive profits that are dependent
on uncontrolled blood sugars telling people how to best control their blood
sugars?!

Anyway, forgive my rant. What I'm getting at is this: How can I practice
medicine, with the freedom to educate/coach/treat my patients with diet and
lifestyle changes to mitigate/reverse their chronic health conditions? Without
feeling like I automatically have to first and foremost prescribe the litany of
drugs dictated by "evidence-based" guidelines? Without excessive fear of
litigation or loss of credibility among my peers? Without having to lie through
my teeth to my patients, and tell them that eating low-fat and heart-healthy
whole grains is the best way (implication also being the only scientifically
proven way) to control their diabetes, lower their cholesterol, etc, etc, etc?

I want my patients to have the full benefit of honest nutrition and lifestyle
information, and medications and surgery as necessary. I'm afraid that there
isn't room for this kind of holistic emphasis in the medical profession today.
Are there residencies that include this kind of training or at least respect
these "unconventional" philosophies? Are there clinics or practice groups that
would allow me to practice with this emphasis, or is there a bias against docs
who do not necessarily conform to the party position? Will I have no other
option but to go it alone under the auspices of my own shingle? How do you
handle these kinds of issues in your professional life?

Sincerely,
Theresa M.


A ray of hope! Perhaps Theresa is just the first among many more medical students who refuse to submit to the brainwashing practices of the pharmaceutical industry, the same mind manipulation that has hopelessly turned most of my colleagues into their unwitting puppets.

I'll be interested in watching how Theresa's experience unfolds. I've asked her to keep us informed every so often.

The Great Low-Carb Connector

The effusive Jimmy Moore of Livin' La Vida Low-Carb asked me to help get the word out about his new podcast subscription service, The Livin' La Vida Low-Carb Show Fan Club.

Jimmy has been The Great Connector for the low-carb discussion, from his ubiquitous online and social media presence, to his annual low-carb cruise. He has also broadcast first class interviews of nutritional notables like Gary Taubes, Dr. Robert Lustig, and blogger Stephan Guyenet. His Fan Club expands listener involvement in the podcast process and, potentially, greater access to his guests:

My faithful listeners have long been asking me about how they can become even more engaged in the behind-the-scenes workings of the show to get the inside scoop about what’s coming next. I’ve heard people ask specifically for access to transcripts of the most popular podcasts, a listing of the interviews I’m currently working on with the ability to ask questions of those guests, to have sneak peek of audio from not-yet-released interviews and more. My amazing podcast producer, Kevin Kennedy-Spaein, and I have been discussing how to best do this for a while in an effort to meet the demands of our biggest fans and we think we’ve got just the answer for you. Introducing The Livin’ La Vida Low-Carb Show Fan Club!

This is for all intents and purposes the quintessential destination for people who can’t get enough of this podcast that goes much deeper than discussion about the low-carb lifestyle. Yes, I speak with a lot of people who are supporters of carbohydrate-restricted diets, but I also talk with fitness gurus, people who support alternative eating plans, those who have interesting theories and beliefs regarding health and much more. Wouldn’t you love to have a chance to know who’s coming up in my schedule to be able to ask them questions BEFORE I interview them? Keep in mind that my interviews are pre-recorded and air sometimes as much as 5-6 months afterwards. Members of the “fan club” would know all about who’s coming and likely will have their question asked on the air just for signing up to be a part of this exciting new addition to “The Livin’ La Vida Low-Carb Show.”


Jimmy is the guy who is bringing this disparate and widely-spread community together. He's the guy we all know, he knows "everybody." I'm looking forward to seeing how this new project makes a more involved, personal delivery of interaction possible.

New Track Your Plaque record!

The record for the largest drop in heart scan score (by percentage of starting score) has been held for around three years, with 63% reduction in score.

Well, the longstanding record was broken this week: 75% reduction in score.

At the start, Freddie has disastrous lipid values:

LDL cholesterol 263 mg/dl
HDL 26 mg/dl
Triglycerides 323 mg/dl
Total cholesterol 354 mg/dl

Lipoproteins (NMR) were worse:

LDL particle number 3360 nmol/L
Small LDL 2677 nmol/L

Heart scan score: 732

Interestingly, Freddie had virtually no vitamin D in his body, with a 25-hydroxy vitamin D level that was unmeasurable.

Freddie was miserably intolerant to statin drugs, with even the smallest dose resulting in intolerable muscle aches. That's when his doctor sent him to me.

Because I felt that the dominant abnormality in Freddie's lipids and lipoproteins was small LDL particles, representing 80% of total LDL particle number, we focused his program on correcting this parameter. Freddie's program was therefore focused elimination of wheat, cornstarch, oats, and sugars, along with an eventual vitamin D dose of 20,000 units to finally achieve a 25-hydroxy vitamin D level of 66 ng/ml. No statin drug in sight.

43 lbs of weight loss and 18 months later, a second heart scan score: 183--a 75% reduction.

While the rest of the world continues to insist that coronary calcium (heart scan) scores cannot be reduced, I am seeing records being broken. I add Freddie's experience to the rapidly growing list of people who have not just stopped coronary plaque from growing, but are seizing control and reducing it, sometimes to dramatic degrees.

The Anti-AGEing Diet

Advanced Glycation End-products, AGEs, are a diverse collection of compounds that have been associated with endothelial dysfunction, cataracts, kidney disease, and atherosclerosis in both animal models and human studies. Not all involve glycation nor glucose, but the catch-all name has stuck.

There are a number of actively-held theories of aging, such as the idea that aging is the result of accumulated products of oxidative injury; a genetically pre-programmed script of declining hormones and other phenomena; genetic "mis-reading" that results in disordered gene expression, debris, and uncontrolled cell proliferation (e.g., cancer); among others.

One of the fascinating theories of aging is, cutely, the AGEing theory of aging, i.e., the accumulation of AGE debris in various tissues. Such AGEs have been recovered in lenses from the eyes, atherosclerotic plaque in arteries, kidney and liver tissue, even brain tissue of people with Alzheimer's dementia. AGEs perform no known useful physiologic function: They are relatively inert once formed (especially polymeric AGEs), they do not participate in communication, they make no contribution of significance. They simply gum up the works--debris. (AGEs are to health as the USDA food pyramid is to dietary advice: material for the junkyard.)

There are two general ways to develop AGEs:

1) Endogenous--High blood glucose (any blood sugar above 100 mg/dl) will permit glycation of the various proteins of the body. The higher the blood glucose, the more glycation will proceed. Glycation also occurs at low velocity at blood glucose levels below 100 mg/dl, though this would therefore represent the "normal," expected rate of glycation. Endogenous glycation explains why people with diabetes appear to age and develop all the phenomena of aging faster than non-diabetics (kidney disease, eye diseases, atherosclerosis, dementia, etc.). Hemoglobin A1c, HbA1c, is a readily-obtainable blood test that can show how enthusiastically you have been glycating proteins (hemoglobin, in this case) over the last 2 to 3 months.

A low-carbohydrate diet is the nutritional path that limits endogenous glycation leading to AGE formation. Restricting the most obnoxious carbohydrates, the ones that increase blood sugar the most, such as wheat, cornstarch, rice starch, potato starch, tapioca starch, and sucrose, will limit endogenous AGE formation.

2) Exogenous--AGEs (here especially is where the "AGE" label is misleading, since many other reactions besides glycation lead to such compounds) are formed with cooking at high temperatures, especially meats and animal products. Therefore, a rare steak will have far less than a well-done steak. A thoroughly baked piece of salmon will have greater AGE content than sashimi.

The forms of cooking that increase AGE content the most: roasting,deep-frying, and barbecuing. Temperatures of 350 degrees Fahrenheit and greater increase AGE formation.

Therefore, cooking foods at lower temperature (e.g., baking, sauteeing, or boiling), eating meats rare whenever possible (not chicken or pork, of course), eating raw foods whenever possible (e.g., nuts) are all strategies that limit exogenous AGE exposure. And minimize or avoid butter use, if we are to believe the data that suggest that it contains the highest exogenous AGE content of any known food.

If we connect the dots and limit exposure to both endogenous and exogenous AGEs, we will therefore not trigger this collection of debris that is likely associated with disease and aging. So following a low-AGE diet may also be an anti-aging strategy.

The New Track Your Plaque Diet, soon to be released on the Track Your Plaque website, has incorporated strategies to limit both endogenous as well as exogenous AGEs.

Butter: Just because it's low-carb doesn't mean it's good

The diet I advocate in the Track Your Plaque program to gain control over the factors that lead us to coronary plaque and heart attack is a low-carbohydrate diet. We begin with elimination of wheat, cornstarch, oats, and sugars in the context of an overall carbohydrate-reduced diet. We refine the program by monitoring postprandial (after-meal) glucoses.

But not everything low-carb is good for you. Fried sausages, for instance, are exceptionally unhealthy, despite having little to no carbohydrates.

An emerging but potentially very powerful issue is that of Advanced Glycation End-products, or AGEs. There are two general varieties of AGEs: endogenous (formed within the body) and exogenous (formed in food that is consumed).

Endogenous AGEs form in the body as a result of high blood glucose, i.e., glycation. When exposed to any blood glucose level of 100 mg/dl or greater, some measure of glycation will develop due to a reaction between glucose and various proteins, e.g., proteins in the lens of the eye, forming cataracts over time.

Exogenous AGEs form in food, generally as a result of heating to high-temperature. (AGEs is really a catch-all term; there are actually a number of reactions that occur in foods, not all of them involving sugars. However, the "AGE" label is used to signify all the various related compounds. The values quoted here are from Dr. Helen Vlassara's Mt. Sinai Hospital laboratory; reference below.)

Beef cooked to high-temperature yields plentiful AGEs. One gram of roast beef, for instance, contains 306,238 units. This means that an 8-oz serving yields 13.8 million units AGEs. Compare this to a boiled egg with 573 units per gram, raw tomato with 234 units per gram.

Butter contains an impressive 264,873 units AGEs per gram, the highest content per gram in the entire list of 250 foods tested in the Mt. Sinai study. A couple pats of butter (10 g) therefore contains 2.64 million units. A stick of butter that you might add to cake batter to make a cake therefore yields 30 million units of AGEs.

So there's nothing wrong with the fat of butter. It's AGEs that appear to be responsible for the endothelial dysfunction/artery-constricting, insulin-blocking, oxidation and inflammation reactions that are triggered. Among all of our food choices, butter is among the worst from this viewpoint.

Throw in the peculiar "insulinotrophic" effect of butter, and you have potent distortion of metabolic pathways, courtesy of the butter on your lobster.

(AGE data from Goldberg 2004. In this analysis, carboxymethyllysine was the marker used for AGE content.)

Incidentally, the new Track Your Plaque diet will soon be released as chapter 9 of the new Track Your Plaque book on the website.

Einkorn now in Whole Foods

I just saw this at Whole Foods: einkorn pasta.

In my einkorn bread experience (In search of wheat: We bake einkorn bread), I was spared the high blood glucose and neurologic and gastrointestinal effects of conventional whole wheat grain (dwarf Triticum aestivum). I shared the einkorn bread  with four other people with histories of acute wheat sensitivities, only one of whom experienced a mild diffuse joint reaction, the other three not experiencing any symptoms.

Anyone wishing to try einkorn can now obtain commercial pasta from Jovial, an Italy-based manufacturer. It comes in spaghetti, linguine, rigatoni, fusilli, and penne rigate shapes.

Eli Rogosa, founder of The Heritage Wheat Conservancy, tells me that, in her experience, celiac suffers seem to not experience immunologic phenomena triggered by conventional wheat.

However, we've got to be careful here. The so-called ("diploid") "A" genome of einkorn shares many of the same genes as the ("hexaploid") "ABD" genomes of modern wheat, including overlap in the sequences coding for the 50-or so different glutens and glutenins. Most of the genes that code for the glutens that cause celiac and related illnesses reside in the "D" genome that are absent in the einkorn "A" genome. However, the "A" genome still codes for glutens. So there is potential for activating celiac disease in some people. Insufficient research has been devoted to this question. It is a question of extreme importance to people with celiac and other immune-mediated conditions, since re-exposure to the wrong form of gluten can increase risk of intestinal lymphoma 77-fold, as well as risk of other gastrointestinal cancers.

So einkorn should not be viewed as a cure-all for all things wheat, but as something to consider for a carbohydrate indulgence. Yes, indeed: It is a carbohydrate, with 61 grams ("net") carbs per 4 oz (uncooked) serving.
Should anyone give it a try, please be sure to report back your experience, especially if you have a history of wheat intolerance. If you have a glucose meter, pre- and 1-hour post values are the ones to measure to gauge the blood sugar effects of consumption. Because pasta tends to cause long sustained blood sugar rises, another value at 2-4 hours might be interesting.

Noodles without the headaches

If you are looking for a wheat-free noodle or pasta, shirataki noodles are worth a try.

Shirataki noodles are low-carbohydrate (less than 3 g per 8 oz package) and, of course, do not trigger all the unhealthy effects of wheat--no blood sugar/insulin provocation, no addictive brain effects (exorphins), no gluten-mediated inflammatory effects.

(I advise avoiding gluten-free pasta alternatives made with rice flour and other common gluten alternatives, since they trigger blood sugar, small LDL, and growth of visceral fat just like wheat.)

I made a stir-fry using the shirataki-tofu noodles, shown below. (Tofu is added to make the noodles more noodly in consistency, as opposed to the chewier non-tofu variety.) The noodles were a lot like the ramen I used to eat as a kid. They were filling and tasted great in the sesame oil, soy sauce, tofu, and vegetables I used.


The noodles are easy to use. Just drain liquid out of package. (The noodles come in water.) Rinse in collander 30 seconds, then boil for 3 minutes. Add to your stir-fry or other dish. Some manufacturers, such as House Foods, also have angel hair and fettucine style noodles.

You're fried

If I could invent a food that illustrates nearly all of the shortcomings of the American diet, it would be French fries, the familiar fixture of fast food.

What we have come to view as French fries contain just about every one of the unhealthy ingredients that lead us down the path of obesity, diabetes, heart disease, high blood pressure, etc.

Let's take them one by one:

Potato starch--Potato starch exerts an effect on blood sugar similar to that of table sugar, only worse. (Glycemic index french fries 75; glycemic index sucrose 65.)

Advanced Glycation End-products (AGEs)--AGEs form when proteins and fats are subjected to high temperature cooking; the longer the high temperature, the more the food reaction creating AGEs proceeds. AGEs are the likely culprit in roasted and fried foods that made it appear that saturated fats were bad, when it was really AGEs all along. AGEs have been shown to block insulin's effects, increase blood sugar, cause endothelial dysfunction and high blood pressure.

Acrylamides--Acrylamides, like AGEs, are created through high-temperature heating. French fries are unusually rich in AGEs. Brewed coffee also contains a small quantity, while French fries contain 82-fold greater quantities, among the highest of all known sources of acrylamides.

Oxidized oils--The amount of oxidized oils will depend on what sort of oil was used for frying. As more restaurants are trying to get away from hydrogenated oils, many are turning back to polyunsaturates. Others are turning to commercial-grade oils that contain both hydrogenated and polyunsaturates. If oils are permitted to oxidize, then they will trigger oxidative phenomena in your body upon consumptions, e.g., LDL oxidation (Staprans 1994).

In other words, the innocent appearing French fry unavoidably triggers oxidation, all the phenomena triggered by high blood glucose (high insulin, glycation, visceral fat accumulation), along with the cascade of effects arising from AGEs and acrylamides.

Top your French fries with some ketchup made with high-fructose corn syrup that exagerrates AGE formation, visceral fat, and distorts postprandial (after-eating) effects.

Is it any wonder that we've lost control over diet?